start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=11
article-no=
start-page=2924
end-page=2937
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250901
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy and safety of esaxerenone with and without sodium–glucose cotransporter-2 inhibitor use in hypertensive patients with type 2 diabetes mellitus: a pooled analysis of five clinical studies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This pooled subanalysis of five multicenter, prospective, open-label, single-arm studies on esaxerenone aimed to evaluate the efficacy, organ-protective effects, and safety of esaxerenone in hypertensive patients with type 2 diabetes mellitus (T2DM), with and without concomitant sodium–glucose cotransporter-2 inhibitor (SGLT2i) therapy. In total, 283 and 279 patients were included in the safety (with SGLT2i, 148; without, 135) and full analysis sets (with SGLT2i; 145; without, 134), respectively. Significant changes in morning home systolic/diastolic blood pressure (SBP/DBP) from baseline to Week 12 were shown in the overall population (mean change: −11.9/−5.2 mmHg, both P < 0.001) and both SGLT2i and non-SGLT2i subgroups (−11.3/−4.8 and −12.5/−5.7 mmHg, respectively, all P < 0.001). Similar findings were observed in bedtime home and office SBP/DBP. The proportions of patients who achieved target home SBP/DBP < 135/85 mmHg were 71.2% (overall population) and 70.5% and 71.9% in the SGLT2i and non-SGLT2i subgroups, respectively. The urine albumin-to-creatinine ratio significantly improved from baseline to Week 12 in the overall population and SGLT2i subgroups (percentage change in geometric mean from baseline: −42.8%, −43.0%, and −42.6%, respectively, all P < 0.001). N-terminal pro-B-type natriuretic peptide levels improved in all groups. The incidence of serum potassium ≥5.5 mEq/L was 2.0% vs 5.2% in the SGLT2i vs non-SGLT2i subgroups. Esaxerenone demonstrated significant BP-lowering effects, and improved renal and cardiovascular parameters, regardless of SGLT2i use. Safety was consistent across groups, with the numerically lower incidence of serum potassium ≥5.5 mEq/L in the SGLT2i subgroup suggesting a potential mitigating effect of SGLT2is on the risk of hyperkalemia.
en-copyright=
kn-copyright=

en-aut-name=MotokiHirohiko
en-aut-sei=Motoki
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KuwaharaKoichiro
en-aut-sei=Kuwahara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KarioKazuomi
en-aut-sei=Kario
en-aut-mei=Kazuomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatsuyaTomohiro
en-aut-sei=Katsuya
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShimosawaTatsuo
en-aut-sei=Shimosawa
en-aut-mei=Tatsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsujitaKenichi
en-aut-sei=Tsujita
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SuzukiShoko
en-aut-sei=Suzuki
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SuedomiTomohiro
en-aut-sei=Suedomi
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TaguchiTakashi
en-aut-sei=Taguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Division of Cardiovascular Medicine, Department of Medicine, Jichi Medical University School of Medicine
kn-affil=

affil-num=6
en-affil=Katsuya Clinic
kn-affil=

affil-num=7
en-affil=Department of Clinical Laboratory, School of Medicine, International University of Health and Welfare
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University
kn-affil=

affil-num=9
en-affil=Data Intelligence Department, Daiichi Sankyo Co. Ltd.
kn-affil=

affil-num=10
en-affil=Primary Medical Science Department, Daiichi Sankyo Co. Ltd.
kn-affil=

affil-num=11
en-affil=Primary Medical Science Department, Daiichi Sankyo Co. Ltd.
kn-affil=
en-keyword=Esaxerenone
kn-keyword=Esaxerenone
en-keyword=Hypertension
kn-keyword=Hypertension
en-keyword=Morning home blood pressure
kn-keyword=Morning home blood pressure
en-keyword=Sodium–glucose cotransporter-2 inhibitor
kn-keyword=Sodium–glucose cotransporter-2 inhibitor
en-keyword=Type 2 diabetes mellitus
kn-keyword=Type 2 diabetes mellitus
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=9
article-no=
start-page=2413
end-page=2426
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy and safety of esaxerenone in hypertensive patients with chronic kidney disease, with or without type 2 diabetes mellitus: a pooled analysis of five clinical studies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Effective management of blood pressure (BP) and albuminuria are crucial for suppressing chronic kidney disease (CKD) progression and cardiovascular risks in hypertension. This pooled analysis evaluated the antihypertensive effects, organ-protective effects, and safety of esaxerenone in hypertensive patients with CKD by integrating five clinical studies of esaxerenone. Patients were divided based on type 2 diabetes mellitus (T2DM) status (with or without T2DM) and creatinine-based estimated glomerular filtration rate (eGFRcreat) (30 to <60 and ≥60 mL/min/1.73 m2). Significant changes in morning home BP from baseline at Week 12 were observed in the overall population (mean change −12.8/ − 5.4 mmHg), T2DM subgroups ( − 12.2/ − 4.5 and −14.5/ − 7.8 mmHg), and eGFRcreat subgroups ( − 12.5/ − 4.7 and −14.0/ − 6.9 mmHg) (all P < 0.001). Bedtime home and office BP showed similar tendencies. Urine albumin-to-creatinine ratio significantly improved from baseline at Week 12 in the overall population (mean change: −55.2%), T2DM subgroups ( − 56.5% and −52.0%), and eGFRcreat subgroups ( − 54.6% and −55.4%) (all P < 0.001). N-terminal pro-B-type natriuretic peptide levels significantly decreased in the overall population (percent change: −14.1%) and subgroup without T2DM ( − 25.3%). The incidence of serum potassium ≥5.5 mEq/L was lower in the subgroup with T2DM vs without T2DM (3.1% and 11.3%), potentially related to the use of sodium–glucose cotransporter 2 inhibitors. These findings highlight the sustained BP-lowering effect of esaxerenone throughout the day in hypertensive patients with CKD, irrespective of T2DM status, and its significant reduction in albuminuria. The data support the safety and efficacy of esaxerenone in this patient population, underscoring its potential as a valuable therapeutic option.
en-copyright=
kn-copyright=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MotokiHirohiko
en-aut-sei=Motoki
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KuwaharaKoichiro
en-aut-sei=Kuwahara
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KarioKazuomi
en-aut-sei=Kario
en-aut-mei=Kazuomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatsuyaTomohiro
en-aut-sei=Katsuya
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShimosawaTatsuo
en-aut-sei=Shimosawa
en-aut-mei=Tatsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsujitaKenichi
en-aut-sei=Tsujita
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SuzukiShoko
en-aut-sei=Suzuki
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SuedomiTomohiro
en-aut-sei=Suedomi
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TaguchiTakashi
en-aut-sei=Taguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Shinshu University School of Medicine
kn-affil=

affil-num=5
en-affil=Division of Cardiovascular Medicine, Department of Medicine, Jichi Medical University School of Medicine
kn-affil=

affil-num=6
en-affil=Katsuya Clinic
kn-affil=

affil-num=7
en-affil=Department of Clinical Laboratory, School of Medicine, International University of Health and Welfare
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University
kn-affil=

affil-num=9
en-affil=Data Intelligence Department, Daiichi Sankyo Co., Ltd.
kn-affil=

affil-num=10
en-affil=Primary Medical Science Department, Daiichi Sankyo Co., Ltd.
kn-affil=

affil-num=11
en-affil=Primary Medical Science Department, Daiichi Sankyo Co., Ltd.
kn-affil=
en-keyword=albuminuria
kn-keyword=albuminuria
en-keyword=chronic kidney disease
kn-keyword=chronic kidney disease
en-keyword=esaxerenone
kn-keyword=esaxerenone
en-keyword=morning hypertension
kn-keyword=morning hypertension
en-keyword=type 2 diabetes mellitus
kn-keyword=type 2 diabetes mellitus
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=5762
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250217
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hypoglycemia and hyperinsulinemia induced by phenolic uremic toxins in CKD and DKD patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Patients with end-stage renal disease have lower fasting plasma glucose and HbA1c levels, with significantly higher insulin levels. For a long time, it has been believed that this higher insulin level in renal failure is due to decreased insulin clearance caused by reduced renal function. However, here we reported that accumulation of the gut microbiota-derived uremic toxin, phenyl sulfate (PS) in the renal failure, increased insulin secretion from the pancreas by enhanced glucose-stimulated insulin secretion. Other endogenous sulfides compounds which accumulated as in the renal failure also increased glucose-stimulated insulin secretion from β-cell. With RNA-seq analyses and gene knock down, we demonstrated that insulin secretion evoked by PS was mediated by Ddah2. In addition, we also found that PS increased insulin resistance through lncRNA expression and Erk phosphorylation in the adipocytes. To confirm the relationship between PS and glucose metabolism in human, we recruited 2 clinical cohort studies (DKD and CKD) including 462 patients, and found that there was a weak negative correlation between PS and HbA1c. Because these trials did not measure fasting insulin level, we alternatively used the urinary C-peptide/creatinine ratio (UCPCR) as an indicator of insulin resistance. We found that PS may induce insulin resistance in patients with eGFR < 60 mL/min/1.73 m2. These data suggest that the accumulation of uremic toxins modulates glucose metabolism and induced insulin resistance in CKD and DKD patients. Considering HbA1c as a reflection of chronic hyperglycemia and UCPCR as a reflection of chronic hyperinsulinemia, our findings indicate that PS is negatively associated with hyperglycemia independent of CKD, and positively associated with hyperinsulinemia in DKD patients.
en-copyright=
kn-copyright=

en-aut-name=TonguYoshiyasu
en-aut-sei=Tongu
en-aut-mei=Yoshiyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KasaharaTomoko
en-aut-sei=Kasahara
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AkiyamaYasutoshi
en-aut-sei=Akiyama
en-aut-mei=Yasutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuzukiTakehiro
en-aut-sei=Suzuki
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HoHsin-Jung
en-aut-sei=Ho
en-aut-mei=Hsin-Jung
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoYotaro
en-aut-sei=Matsumoto
en-aut-mei=Yotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KujiraiRyota
en-aut-sei=Kujirai
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KikuchiKoichi
en-aut-sei=Kikuchi
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NataKoji
en-aut-sei=Nata
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KanzakiMakoto
en-aut-sei=Kanzaki
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SuzukiKenshin
en-aut-sei=Suzuki
en-aut-mei=Kenshin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WatanabeShun
en-aut-sei=Watanabe
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawabeChiharu
en-aut-sei=Kawabe
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MiyataYui
en-aut-sei=Miyata
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ItaiShun
en-aut-sei=Itai
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ToyoharaTakafumi
en-aut-sei=Toyohara
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SuzukiChitose
en-aut-sei=Suzuki
en-aut-mei=Chitose
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TanakaTetsuhiro
en-aut-sei=Tanaka
en-aut-mei=Tetsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=TomiokaYoshihisa
en-aut-sei=Tomioka
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=AbeTakaaki
en-aut-sei=Abe
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

affil-num=1
en-affil=Tohoku University School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Medical Biochemistry, School of Pharmacy, Iwate Medical University
kn-affil=

affil-num=10
en-affil=Department of Biomedical Engineering, Tohoku University
kn-affil=

affil-num=11
en-affil=Tohoku University School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=16
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=
en-keyword=CKD, DKD, Phenyl sulfate, Uremic toxin, Insulin secretion, Insulin resistance, Gut microbiota
kn-keyword=CKD, DKD, Phenyl sulfate, Uremic toxin, Insulin secretion, Insulin resistance, Gut microbiota
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=10
article-no=
start-page=e94951
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251019
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bladder Trigone as a Sensory Hub: A Narrative Review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The bladder trigone is an anatomically and functionally distinct region within the lower urinary tract (LUT), characterized by a dense network of afferent sensory fibers, specialized urothelial interactions, and prominent mechanotransduction mechanisms. Its intricate neuroarchitecture enables precise detection of bladder filling and coordination of micturition, whereas dysregulation of these pathways contributes to lower urinary tract symptoms (LUTS), including urgency, frequency, and bladder pain. Despite its recognized clinical relevance, the structural and functional basis of trigonal sensory signaling - and its role - remain incompletely understood.<br>
This review synthesizes current evidence on trigonal afferent organization, integrating data from anatomical mapping, receptor profiling, electrophysiological characterization, and translational research. Seminal anatomical observations are combined with recent advances in mechanotransduction and purinergic, peptidergic, and transient receptor potential (TRP) signaling to provide a comprehensive perspective. The trigone exhibits three principal afferent classes: (1) intraepithelial fibers penetrating umbrella cells, marked by P2X purinoceptor 3 (P2X3), transient receptor potential vanilloid 1 (TRPV1), calcitonin gene-related peptide (CGRP), and substance P (SP); (2) subepithelial plexuses surrounding microvasculature, enriched in vasoactive neuropeptides and exhibiting plastic hypertrophy in overactive bladder (OAB) and interstitial cystitis/bladder pain syndrome (IC/BPS); and (3) encapsulated corpuscular endings at the lamina propria-detrusor junction, expressing PIEZO1/2 and acid-sensing ion channels (ASICs) for rapid adaptation. In trigeminal dorsal root ganglion (DRG) neurons, high expression of PIEZO2, P2RX3, and voltage-gated sodium channel, type 1.8 (Nav1.8) was observed, revealing their role as the foundation for multisensory information processing. Functional assays highlight distinct mechanotransductive and chemosensory pathways, with aging, inflammation, and neurotrophic factors driving afferent plasticity underlying abnormal bladder sensation, such as urgency, frequency, and pain. Early clinical trials of P2X3 antagonists and intravesical TRPV1 inhibitors demonstrate promising symptomatic benefits. Collectively, evidence positions the bladder trigone as a critical sensory hub where neuronal, urothelial, and immune signals converge to regulate bladder sensation. Understanding its molecular and structural specialization may inform the development of region-specific neuromodulatory therapies targeting sensory urgency and afferent-driven bladder dysfunction.
en-copyright=
kn-copyright=

en-aut-name=SadahiraTakuya
en-aut-sei=Sadahira
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaruyamaYuki
en-aut-sei=Maruyama
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsuiYosuke
en-aut-sei=Mitsui
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SekitoTakanori
en-aut-sei=Sekito
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeTomofumi
en-aut-sei=Watanabe
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=bladder trigone
kn-keyword=bladder trigone
en-keyword=botulinum toxin
kn-keyword=botulinum toxin
en-keyword=lower urinary tract symptoms
kn-keyword=lower urinary tract symptoms
en-keyword=sensory afferents
kn-keyword=sensory afferents
en-keyword=varicosities
kn-keyword=varicosities
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=43
article-no=
start-page=9936
end-page=9941
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Harnessing the reactivity of captodative radicals: photocatalytic α-pyridination of glycyl derivatives through reversible radical coupling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Captodative radicals that are highly stabilized by the presence of both electron-donating and electron-withdrawing groups exhibit unique reactivity in organic syntheses. These radicals are known to be less reactive towards radical–radical coupling reactions due to the presence of a shielding occupied molecular orbital. Herein we describe a photocatalytic synthetic strategy for the coupling of two different captodative radicals, which are generated from glycyl derivatives and 4-cyanopyridines. An aromatization is incorporated as the driving force after a reversible radical–radical coupling process. This method can be applied to a wide variety of peptides, providing pharmaceutically relevant pyridyl-functionalized products under mild reaction conditions.
en-copyright=
kn-copyright=

en-aut-name=YamazakiKen
en-aut-sei=Yamazaki
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkimotoShuta
en-aut-sei=Akimoto
en-aut-mei=Shuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MiuraTomoya
en-aut-sei=Miura
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Division of Applied Chemistry, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Applied Chemistry, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Applied Chemistry, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=27
article-no=
start-page=6557
end-page=6563
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fluorescence detection of DNA with a single-base mismatch by a Tm-independent peptide nucleic acid (PNA) twin probe
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=There is a need to develop efficient methods for detecting target nucleic acids to enable the rapid diagnosis and early treatment of diseases. We previously demonstrated that a peptide nucleic acid (PNA) twin probe, consisting of two PNAs each containing a fluorescent dye, with pyrene at one end, detects target DNA sequence-specifically through pyrene excimer emission. In this study, to advance the development of this probe system, we further investigated the fluorescence properties of the PNA twin probe P1 and P2, and found that the excimer fluorescence was significantly reduced when a mismatched base in the DNA sequence was present at the site of P1 closest to the pyrene. In other words, this probe was found to detect single-base mismatches without taking into account the thermal stability of the PNA/DNA hybrid. The detection limit of this PNA twin probe for the single-base-mismatched DNA was 2.7 nM. In the future, this probe should lead to a method to detect point mutations in endogenous nucleic acids within cells.
en-copyright=
kn-copyright=

en-aut-name=IshiiKoki
en-aut-sei=Ishii
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShigetoHajime
en-aut-sei=Shigeto
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamuraShohei
en-aut-sei=Yamamura
en-aut-mei=Shohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImaiYoshitane
en-aut-sei=Imai
en-aut-mei=Yoshitane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Applied Chemistry, Kindai University
kn-affil=

affil-num=2
en-affil=Health and Medical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST)
kn-affil=

affil-num=3
en-affil=Health and Medical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST)
kn-affil=

affil-num=4
en-affil=Department of Applied Chemistry, Kindai University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Applied Chemistry, Kindai University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=5
article-no=
start-page=209
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250514
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel Anti-MRSA Peptide from Mangrove-Derived Virgibacillus chiguensis FN33 Supported by Genomics and Molecular Dynamics
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Antimicrobial resistance (AMR) is a global health threat, with methicillin-resistant Staphylococcus aureus (MRSA) being one of the major resistant pathogens. This study reports the isolation of a novel mangrove-derived bacterium, Virgibacillus chiguensis FN33, as identified through genome analysis and the discovery of a new anionic antimicrobial peptide (AMP) exhibiting anti-MRSA activity. The AMP was composed of 23 amino acids, which were elucidated as NH3-Glu-Gly-Gly-Cys-Gly-Val-Asp-Thr-Trp-Gly-Cys-Leu-Thr-Pro-Cys-His-Cys-Asp-Leu-Phe-Cys-Thr-Thr-COOH. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) for MRSA were 8 µg/mL and 16 µg/mL, respectively. FN33 AMP induced cell membrane permeabilization, suggesting a membrane-disrupting mechanism. The AMP remained stable at 30–40 °C but lost activity at higher temperatures and following exposure to proteases, surfactants, and extreme pH. All-atom molecular dynamics simulations showed that the AMP adopts a β-sheet structure upon membrane interaction. These findings suggest that Virgibacillus chiguensis FN33 is a promising source of novel antibacterial agents against MRSA, supporting alternative strategies for drug-resistant infections.
en-copyright=
kn-copyright=

en-aut-name=SermkaewNamfa
en-aut-sei=Sermkaew
en-aut-mei=Namfa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AtipairinApichart
en-aut-sei=Atipairin
en-aut-mei=Apichart
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=BoonruamkaewPhetcharat
en-aut-sei=Boonruamkaew
en-aut-mei=Phetcharat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KrobthongSucheewin
en-aut-sei=Krobthong
en-aut-mei=Sucheewin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AonbangkhenChanat
en-aut-sei=Aonbangkhen
en-aut-mei=Chanat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UchiyamaJumpei
en-aut-sei=Uchiyama
en-aut-mei=Jumpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YingchutrakulYodying
en-aut-sei=Yingchutrakul
en-aut-mei=Yodying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SongnakaNuttapon
en-aut-sei=Songnaka
en-aut-mei=Nuttapon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=School of Pharmacy, Walailak University
kn-affil=

affil-num=2
en-affil=School of Pharmacy, Walailak University
kn-affil=

affil-num=3
en-affil=School of Pharmacy, Walailak University
kn-affil=

affil-num=4
en-affil=Center of Excellence in Natural Products Chemistry (CENP), Department of Chemistry, Faculty of Science, Chulalongkorn University
kn-affil=

affil-num=5
en-affil=Center of Excellence in Natural Products Chemistry (CENP), Department of Chemistry, Faculty of Science, Chulalongkorn University
kn-affil=

affil-num=6
en-affil=Department of Bacteriology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency
kn-affil=

affil-num=8
en-affil=School of Pharmacy, Walailak University
kn-affil=
en-keyword=anionic AMP
kn-keyword=anionic AMP
en-keyword=AMP
kn-keyword=AMP
en-keyword=antimicrobial peptide
kn-keyword=antimicrobial peptide
en-keyword=antimicrobial resistance
kn-keyword=antimicrobial resistance
en-keyword=FN33
kn-keyword=FN33
en-keyword=genome
kn-keyword=genome
en-keyword=molecular dynamics simulations
kn-keyword=molecular dynamics simulations
en-keyword=MRSA
kn-keyword=MRSA
en-keyword=Virgibacillus chiguensis
kn-keyword=Virgibacillus chiguensis
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=9
article-no=
start-page=846
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240905
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Unveiling a New Antimicrobial Peptide with Efficacy against P. aeruginosa and K. pneumoniae from Mangrove-Derived Paenibacillus thiaminolyticus NNS5-6 and Genomic Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study focused on the discovery of the antimicrobial peptide (AMP) derived from mangrove bacteria. The most promising isolate, NNS5-6, showed the closest taxonomic relation to Paenibacillus thiaminolyticus, with the highest similarity of 74.9%. The AMP produced by Paenibacillus thiaminolyticus NNS5-6 exhibited antibacterial activity against various Gram-negative pathogens, especially Pseudomonas aeruginosa and Klebsiella pneumoniae. The peptide sequence consisted of 13 amino acids and was elucidated as Val-Lys-Gly-Asp-Gly-Gly-Pro-Gly-Thr-Val-Tyr-Thr-Met. The AMP mainly exhibited random coil and antiparallel beta-sheet structures. The stability study indicated that this AMP was tolerant of various conditions, including proteolytic enzymes, pH (1.2–14), surfactants, and temperatures up to 40 °C for 12 h. The AMP demonstrated 4 µg/mL of MIC and 4–8 µg/mL of MBC against both pathogens. Time-kill kinetics showed that the AMP acted in a time- and concentration-dependent manner. A cell permeability assay and scanning electron microscopy revealed that the AMP exerted the mode of action by disrupting bacterial membranes. Additionally, nineteen biosynthetic gene clusters of secondary metabolites were identified in the genome. NNS5-6 was susceptible to various commonly used antibiotics supporting the primary safety requirement. The findings of this research could pave the way for new therapeutic approaches in combating antibiotic-resistant pathogens.
en-copyright=
kn-copyright=

en-aut-name=SermkaewNamfa
en-aut-sei=Sermkaew
en-aut-mei=Namfa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AtipairinApichart
en-aut-sei=Atipairin
en-aut-mei=Apichart
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KrobthongSucheewin
en-aut-sei=Krobthong
en-aut-mei=Sucheewin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AonbangkhenChanat
en-aut-sei=Aonbangkhen
en-aut-mei=Chanat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YingchutrakulYodying
en-aut-sei=Yingchutrakul
en-aut-mei=Yodying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UchiyamaJumpei
en-aut-sei=Uchiyama
en-aut-mei=Jumpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SongnakaNuttapon
en-aut-sei=Songnaka
en-aut-mei=Nuttapon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=School of Pharmacy, Walailak University
kn-affil=

affil-num=2
en-affil=School of Pharmacy, Walailak University
kn-affil=

affil-num=3
en-affil=Center of Excellence in Natural Products Chemistry (CENP), Department of Chemistry, Faculty of Science, Chulalongkorn University
kn-affil=

affil-num=4
en-affil=Center of Excellence in Natural Products Chemistry (CENP), Department of Chemistry, Faculty of Science, Chulalongkorn University
kn-affil=

affil-num=5
en-affil=National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency
kn-affil=

affil-num=6
en-affil=Department of Bacteriology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=School of Pharmacy, Walailak University
kn-affil=
en-keyword=antimicrobial peptide
kn-keyword=antimicrobial peptide
en-keyword=antimicrobial resistance
kn-keyword=antimicrobial resistance
en-keyword=bacterial genome
kn-keyword=bacterial genome
en-keyword=biosynthetic gene cluster
kn-keyword=biosynthetic gene cluster
en-keyword=Klebsiella pneumoniae
kn-keyword=Klebsiella pneumoniae
en-keyword=Mangrove
kn-keyword=Mangrove
en-keyword=mass spectrometry
kn-keyword=mass spectrometry
en-keyword=NNS5-6
kn-keyword=NNS5-6
en-keyword=Paenibacillus thiaminolyticus
kn-keyword=Paenibacillus thiaminolyticus
en-keyword=Pseudomonas aeruginosa
kn-keyword=Pseudomonas aeruginosa
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=S1
article-no=
start-page=7
end-page=12
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Basic biology is not just “for the birds”: how avian studies have informed us about vertebrate reproduction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Avian reproductive physiology has been studied for centuries, largely because of the importance of birds as food animals. It is likely that the ubiquity and ease of access to domesticated chickens led to them being used in some of the first experiments on transplantation of endocrine structures—in this case, the testes. Since then, study of seasonal changes in reproductive physiology (photoperiodism) in different orders of bird species has led to advances in the understanding of endocrine regulation of reproductive physiology and behavior. These include mechanisms of adult neuroplasticity, sexual selection, sperm competition, stress physiology, and circadian physiology. Here, we focus mainly on the discovery in birds of a neuropeptide named gonadotropin-inhibitory hormone that mostly has inhibitory effects on reproduction. This hormone has since been shown to exist in all mammals studied to date, including humans (it is known as RFamide-related peptide in mammals). We discuss the history and implications of avian studies on gonadotropin-inhibitory hormone/RFamide-related peptide for human reproductive biology.
en-copyright=
kn-copyright=

en-aut-name=BentleyGeorge E.
en-aut-sei=Bentley
en-aut-mei=George E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=GnIH
kn-keyword=GnIH
en-keyword=RFamide
kn-keyword=RFamide
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=16
article-no=
start-page=7832
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synergistic Antimicrobial Activity of BrSPR20-P1 Peptide and Silver Nanoparticles Against Pathogenic Bacteria
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bacterial infection is a cause of life-threatening diseases. The emergence of antimicrobial-resistant bacteria exacerbates this situation, highlighting the need for the discovery of new antimicrobial agents. Our previous study identified a novel antimicrobial peptide, BrSPR20-P1 (P1), which showed potential activity against MRSA. Additionally, silver nanoparticles (AgNPs) exhibit broad-spectrum antibacterial activity, capable of killing multidrug-resistant bacteria. The combination of antimicrobial agents presents a novel strategy for combating these pathogens. This study aimed to evaluate the antibacterial activity of the combination of P1 and AgNPs. It revealed that the combinations showed synergy. The P1 and AgNP mixture at a concentration of 1 and 8 µg/mL (1:8) doubled the activity against S. aureus and MRSA, while that combination of 64 and 64 µg/mL (64:64) exhibited broad-spectrum activity, expanding to E. coli with a 32-fold increase. These combinations exhibited a bactericidal effect, showing the rapid killing of tested bacteria at 10× MIC, with killing rates during the first 3 h ranging from 4.04 ± 0.01 to 4.31 ± 0.03 h−1. The P1 and AgNP mixtures caused a low risk of antibacterial resistance up to 30 passages. It was demonstrated that the synergistic activity of P1 and AgNPs occurred through the disruption of cell walls and membranes, leakage of intracellular materials, and cell lysis. Additionally, the mixtures appeared to interact with bacterial genomic DNA, as indicated by a gel retardation assay. These activities of the combinations were concentration-dependent. The 1:8 µg/mL mixture caused low hemolysis and cytotoxicity and did not impede the wound healing process. In contrast, although the 64:64 µg/mL mixture showed excellent antibacterial efficacy, it was toxic to erythrocytes and mammalian cells. It implies that dose optimization is required to balance its efficacy and toxicity. Therefore, the P1 and AgNP combinations exhibit synergistic antimicrobial activity and have the potential to resolve bacterial infections.
en-copyright=
kn-copyright=

en-aut-name=ThonginThanyamai
en-aut-sei=Thongin
en-aut-mei=Thanyamai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SawatdeeSomchai
en-aut-sei=Sawatdee
en-aut-mei=Somchai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SongnakaNuttapon
en-aut-sei=Songnaka
en-aut-mei=Nuttapon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UchiyamaJumpei
en-aut-sei=Uchiyama
en-aut-mei=Jumpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WiwasukuTheanchai
en-aut-sei=Wiwasuku
en-aut-mei=Theanchai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SrichanaTeerapol
en-aut-sei=Srichana
en-aut-mei=Teerapol
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakphengTitpawan
en-aut-sei=Nakpheng
en-aut-mei=Titpawan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AtipairinApichart
en-aut-sei=Atipairin
en-aut-mei=Apichart
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil= School of Pharmacy, Walailak University
kn-affil=

affil-num=2
en-affil= School of Pharmacy, Walailak University
kn-affil=

affil-num=3
en-affil= School of Pharmacy, Walailak University
kn-affil=

affil-num=4
en-affil=Department of Bacteriology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=School of Science, Walailak University
kn-affil=

affil-num=6
en-affil=Drug Delivery System Excellence Center and Department of Pharmaceutical Technology, Faculty of Pharmaceutical Sciences, Prince of Songkla University
kn-affil=

affil-num=7
en-affil=Drug Delivery System Excellence Center and Department of Pharmaceutical Technology, Faculty of Pharmaceutical Sciences, Prince of Songkla University
kn-affil=

affil-num=8
en-affil= School of Pharmacy, Walailak University
kn-affil=
en-keyword=antimicrobial peptide
kn-keyword=antimicrobial peptide
en-keyword=Brevibacillus sp. SPR20
kn-keyword=Brevibacillus sp. SPR20
en-keyword=silver nanoparticle
kn-keyword=silver nanoparticle
en-keyword=synergistic effect
kn-keyword=synergistic effect
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=158
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250719
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oncolytic virus-mediated p53 activation boosts the antitumor immunity of a p53-transduced dendritic cell vaccine
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dendritic cells (DCs) transduced with replication-deficient, wild-type human p53-expressing adenovirus Ad-p53 (Ad-p53 DCs) induce p53-targeting cytotoxic T lymphocytes (CTLs). However, the antitumor efficacy of Ad-p53 DCs is diminished by weak p53 immunogenicity in tumor cells and poor immune responses. We developed a p53-armed oncolytic adenovirus, OBP-702, to induce tumor-specific p53 expression and antitumor immune response, suggesting a role for OBP-702 in enhancing the antitumor efficacy of Ad-p53 DCs. The combined effect of Ad-p53 DCs and OBP-702 was investigated using murine colon cancer (CC) tumor models. Ad-p53 DCs were obtained by stimulating bone marrow-derived cells with granulocyte-macrophage colony-stimulating factor, interleukin-4, and Ad-p53. Subcutaneous tumor models of CT26 (p53 wild-type) and MC38 (p53 mutant-type) murine CC cell lines were used to evaluate the therapeutic potential of combination therapy in the terms of tumor growth, abscopal effect, antitumor immune response, and presentation of p53 peptides in tumor cells. Combination therapy with Ad-p53 DCs and OBP-702 significantly suppressed the growth of p53-intact CT26 tumors at treated and untreated sites by inducing tumor-infiltration of CD8+ CTLs and CD11c+ DCs. OBP-702-infected tumor cells presented human p53 epitopes in the context of major histocompatibility complex molecules, which were recognized by CTLs induced by Ad-p53 DCs. Combination therapy significantly suppressed the growth of p53-mutant MC38 tumors by activating the antitumor immune response. Our results suggest that OBP-702-mediated presentation of p53 epitopes on tumor cells enhances the antitumor efficacy of Ad-p53 DCs against murine CC tumors by attracting p53-targeting CTLs.
en-copyright=
kn-copyright=

en-aut-name=YamadaMotohiko
en-aut-sei=Yamada
en-aut-mei=Motohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TazawaHiroshi
en-aut-sei=Tazawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuemoriKanto
en-aut-sei=Suemori
en-aut-mei=Kanto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OkadaNaohiro
en-aut-sei=Okada
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KajiwaraYoshinori
en-aut-sei=Kajiwara
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShojiRyohei
en-aut-sei=Shoji
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NagaiYasuo
en-aut-sei=Nagai
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=InoueHiroaki
en-aut-sei=Inoue
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HashimotoNaoyuki
en-aut-sei=Hashimoto
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KanayaNobuhiko
en-aut-sei=Kanaya
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KikuchiSatoru
en-aut-sei=Kikuchi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KurodaShinji
en-aut-sei=Kuroda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MichiueHiroyuki
en-aut-sei=Michiue
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=UrataYasuo
en-aut-sei=Urata
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Neutron Therapy Research Center, Okayama University Hospital
kn-affil=

affil-num=14
en-affil=Oncolys BioPharma, Inc
kn-affil=

affil-num=15
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=4
cd-vols=
no-issue=2
article-no=
start-page=101575
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Simplified Outcome Prediction in Patients Undergoing Transcatheter Tricuspid Valve Intervention by Survival Tree-Based Modelling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Patients with severe tricuspid regurgitation (TR) typically present with heterogeneity in the extent of cardiac dysfunction and extra-cardiac comorbidities, which play a decisive role for survival after transcatheter tricuspid valve intervention (TTVI).<br>
Objectives This aim of this study was to create a survival tree-based model to determine the cardiac and extra-cardiac features associated with 2-year survival after TTVI.<br>
Methods The study included 918 patients (derivation set, n = 631; validation set, n = 287) undergoing TTVI for severe TR. Supervised machine learning-derived survival tree-based modelling was applied to preprocedural clinical, laboratory, echocardiographic, and hemodynamic data.<br>
Results Following univariate regression analysis to pre-select candidate variables for 2-year mortality prediction, a survival tree-based model was constructed using 4 key parameters. Three distinct cluster-related risk categories were identified, which differed significantly in survival after TTVI. Patients from the low-risk category (n = 261) were defined by mean pulmonary artery pressure ≤28 mm Hg and N-terminal pro–B-type natriuretic peptide ≤2,728 pg/mL, and they exhibited a 2-year survival rate of 85.5%. Patients from the high-risk category (n = 190) were defined by mean pulmonary artery pressure >28 mm Hg, right atrial area >32.5 cm2, and estimated glomerular filtration rate ≤51 mL/min, and they showed a significantly worse 2-year survival of only 52.6% (HR for 2-year mortality: 4.3, P < 0.001). Net re-classification improvement analysis demonstrated that this model was comparable to the TRI-Score and outperformed the EuroScore II in identifying high-risk patients. The prognostic value of risk phenotypes was confirmed by external validation.<br>
Conclusions This simple survival tree-based model effectively stratifies patients with severe TR into distinct risk categories, demonstrating significant differences in 2-year survival after TTVI.
en-copyright=
kn-copyright=

en-aut-name=FortmeierVera
en-aut-sei=Fortmeier
en-aut-mei=Vera
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LachmannMark
en-aut-sei=Lachmann
en-aut-mei=Mark
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=StolzLukas
en-aut-sei=Stolz
en-aut-mei=Lukas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=von SteinJennifer
en-aut-sei=von Stein
en-aut-mei=Jennifer
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=RommelKarl-Philipp
en-aut-sei=Rommel
en-aut-mei=Karl-Philipp
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KassarMohammad
en-aut-sei=Kassar
en-aut-mei=Mohammad
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=GerçekMuhammed
en-aut-sei=Gerçek
en-aut-mei=Muhammed
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SchöberAnne R.
en-aut-sei=Schöber
en-aut-mei=Anne R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=StockerThomas J.
en-aut-sei=Stocker
en-aut-mei=Thomas J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OmranHazem
en-aut-sei=Omran
en-aut-mei=Hazem
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FettMichelle
en-aut-sei=Fett
en-aut-mei=Michelle
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TervoorenJule
en-aut-sei=Tervooren
en-aut-mei=Jule
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KörberMaria I.
en-aut-sei=Körber
en-aut-mei=Maria I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HesseAmelie
en-aut-sei=Hesse
en-aut-mei=Amelie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=HarmsenGerhard
en-aut-sei=Harmsen
en-aut-mei=Gerhard
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FriedrichsKai Peter
en-aut-sei=Friedrichs
en-aut-mei=Kai Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=RudolphTanja K.
en-aut-sei=Rudolph
en-aut-mei=Tanja K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=JonerMichael
en-aut-sei=Joner
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=PfisterRoman
en-aut-sei=Pfister
en-aut-mei=Roman
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=BaldusStephan
en-aut-sei=Baldus
en-aut-mei=Stephan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=LaugwitzKarl-Ludwig
en-aut-sei=Laugwitz
en-aut-mei=Karl-Ludwig
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=WindeckerStephan
en-aut-sei=Windecker
en-aut-mei=Stephan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=PrazFabien
en-aut-sei=Praz
en-aut-mei=Fabien
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=LurzPhilipp
en-aut-sei=Lurz
en-aut-mei=Philipp
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=HausleiterJörg
en-aut-sei=Hausleiter
en-aut-mei=Jörg
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=RudolphVolker
en-aut-sei=Rudolph
en-aut-mei=Volker
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

affil-num=1
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=2
en-affil=First Department of Medicine, Klinikum rechts der Isar, Technical University of Munich
kn-affil=

affil-num=3
en-affil=DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance
kn-affil=

affil-num=4
en-affil=Department of Cardiology, Heart Center, University of Cologne
kn-affil=

affil-num=5
en-affil=Department of Cardiology, Heart Center Leipzig, University of Leipzig
kn-affil=

affil-num=6
en-affil=Department of Cardiology, Inselspital Bern, Bern University Hospital
kn-affil=

affil-num=7
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=8
en-affil=Department of Cardiology, Heart Center Leipzig, University of Leipzig
kn-affil=

affil-num=9
en-affil=DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance
kn-affil=

affil-num=10
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=11
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=12
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=13
en-affil=Department of Cardiology, Heart Center, University of Cologne
kn-affil=

affil-num=14
en-affil=First Department of Medicine, Klinikum rechts der Isar, Technical University of Munich
kn-affil=

affil-num=15
en-affil=Department of Physics, University of Johannesburg
kn-affil=

affil-num=16
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=17
en-affil=Department of Cardiovascular Medicine, Okayama University
kn-affil=

affil-num=18
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=

affil-num=19
en-affil=DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance
kn-affil=

affil-num=20
en-affil=Department of Cardiology, Heart Center, University of Cologne
kn-affil=

affil-num=21
en-affil=Department of Cardiology, Heart Center, University of Cologne
kn-affil=

affil-num=22
en-affil=First Department of Medicine, Klinikum rechts der Isar, Technical University of Munich
kn-affil=

affil-num=23
en-affil=Department of Cardiology, Inselspital Bern, Bern University Hospital
kn-affil=

affil-num=24
en-affil=Department of Cardiology, Inselspital Bern, Bern University Hospital
kn-affil=

affil-num=25
en-affil=Department of Cardiology, Heart Center Leipzig, University of Leipzig
kn-affil=

affil-num=26
en-affil=DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance
kn-affil=

affil-num=27
en-affil=Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum
kn-affil=
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=transcatheter tricuspid valve intervention
kn-keyword=transcatheter tricuspid valve intervention
en-keyword=tricuspid regurgitation
kn-keyword=tricuspid regurgitation
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=10819
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A high-protein diet-responsive gut hormone regulates behavioral and metabolic optimization in Drosophila melanogaster
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Protein is essential for all living organisms; however, excessive protein intake can have adverse effects, such as hyperammonemia. Although mechanisms responding to protein deficiency are well-studied, there is a significant gap in our understanding of how organisms adaptively suppress excessive protein intake. In the present study, utilizing the fruit fly, Drosophila melanogaster, we discover that the peptide hormone CCHamide1 (CCHa1), secreted by enteroendocrine cells in response to a high-protein diet (HPD), is vital for suppressing overconsumption of protein. Gut-derived CCHa1 is received by a small subset of enteric neurons that produce short neuropeptide F, thereby modulating protein-specific satiety. Importantly, impairment of the CCHa1-mediated gut-enteric neuronal axis results in ammonia accumulation and a shortened lifespan under HPD conditions. Collectively, our findings unravel the crosstalk of gut hormone and neuronal pathways that orchestrate physiological responses to prevent and adapt to dietary protein overload.
en-copyright=
kn-copyright=

en-aut-name=YoshinariYuto
en-aut-sei=Yoshinari
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishimuraTakashi
en-aut-sei=Nishimura
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoShu
en-aut-sei=Kondo
en-aut-mei=Shu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanimotoHiromu
en-aut-sei=Tanimoto
en-aut-mei=Hiromu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiTomoe
en-aut-sei=Kobayashi
en-aut-mei=Tomoe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NiwaRyusuke
en-aut-sei=Niwa
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=2
en-affil=Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=5
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=6
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=7
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=8
en-affil=Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=100242
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Photochemical internalization of mRNA using a photosensitizer and nucleic acid carriers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=mRNA has great potential for therapeutic applications because it can encode a variety of proteins and antigens, in addition to advantages over DNA in terms of gene expression without genomic integration, nuclear localization, or transcription. However, therapeutic applications of mRNA require safe and effective delivery into target cells. Therefore, we aimed to investigate photochemical internalization (PCI) as a promising strategy for delivering mRNA to target cells. In this strategy, mRNA is taken up into cells by endocytosis, accumulates in endosomes, and is released in a light-dependent manner from the endosomes using an endosome-accumulating photosensitizer, aluminum phthalocyanine disulfonate (AlPcS2a), in combination with nucleic acid carrier molecules. We compared the efficacy of various nucleic acid carriers, including branched polyethyleneimine (bPEI) and poly{N'-[N-(2-aminoethyl)-2-aminoethyl] aspartamide} (PAsp(DET)) under the same conditions for PCI-based mRNA delivery. Our results indicated that bPEI and PAsp(DET) at low N/P ratios exhibited efficient light-enhancement of mRNA expression by PCI with AlPcS2a. Notably, bPEI exhibited the highest light-dependent mRNA delivery among the carriers evaluated (including cationic polymers, cationic peptides, and lipids), whereas PAsp(DET) showed promise for clinical use because of its lower toxicity compared with bPEI. This PCI strategy allows effective cytosolic mRNA delivery at low N/P ratios, thereby reducing cationic carrier molecule-induced cytotoxicity. This method allows spatiotemporal control of protein expression and holds potential for novel light-dependent mRNA therapies. Overall, this study provided valuable insights into optimizing mRNA delivery systems for therapeutic applications.
en-copyright=
kn-copyright=

en-aut-name=MaemotoHayaki
en-aut-sei=Maemoto
en-aut-mei=Hayaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SuzakiRyohei
en-aut-sei=Suzaki
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ItakaKeiji
en-aut-sei=Itaka
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biofunction Research, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=mRNA
kn-keyword=mRNA
en-keyword=Photochemical internalization
kn-keyword=Photochemical internalization
en-keyword=Photosensitizer
kn-keyword=Photosensitizer
END

start-ver=1.4
cd-journal=joma
no-vol=89
cd-vols=
no-issue=7
article-no=
start-page=930
end-page=938
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hemodynamic Changes After Wire Frame Occluders vs. Metal Mesh Devices for Atrial Septal Defect
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Transcatheter atrial septal defect (ASD) closure is the first treatment option for secundum ASD, but parameters for optimal device selection have not been established. We compared outcomes between occluders with a wire frame and metal mesh devices.<br>
Methods and Results: This study included secundum ASD patients implanted with a wire frame occluder (GORE®CARDIOFORM ASD occluder [GCA]; W.L. Gore & Associates) or metal mesh devices (Amplatzer septal occluder device [Abbott] and Occlutech Figulla Flex II device [Occlutech]). The presence of residual shunt and B-type natriuretic peptide (BNP) levels after implantation were compared. Of the 970 patients with either GCA (n=48) or a metal mesh device (n=922; control), 42 patients from each group were analyzed after propensity score matching. The prevalence of residual shunt was significantly lower in the GCA group 1 day and 1 month after implantation (P<0.001 and P=0.017, respectively), whereas there was no significant difference between the 2 groups 6 months later (P=0.088). BNP levels at 1 month were significantly higher in the GCA group (ratio of change 1.36; 95% confidence interval [CI] 1.01–1.83), but did not differ significantly between the 2 groups at 6 months (ratio of change 1.04; 95% CI 0.65–1.65).<br>
Conclusions: Patients implanted with a wire frame occluder had a lower prevalence of residual shunt and a greater increase in BNP levels in the early period after implantation.
en-copyright=
kn-copyright=

en-aut-name=NakashimaMitsutaka
en-aut-sei=Nakashima
en-aut-mei=Mitsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakayaYoichi
en-aut-sei=Takaya
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikiTakashi
en-aut-sei=Miki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakayamaRie
en-aut-sei=Nakayama
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AkagiTeiji
en-aut-sei=Akagi
en-aut-mei=Teiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Amplatzer septal occluder
kn-keyword=Amplatzer septal occluder
en-keyword=GORE® CARDIOFORM ASD occluder
kn-keyword=GORE® CARDIOFORM ASD occluder
en-keyword=Occlutech Figulla Flex II
kn-keyword=Occlutech Figulla Flex II
en-keyword=Transcatheter atrial septal defect closure
kn-keyword=Transcatheter atrial septal defect closure
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=バソヒビン2を標的としたペプチドワクチンは糖尿病性腎症に対して予防的効果を持つ
kn-title=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NAKASHIMAYuri
en-aut-sei=NAKASHIMA
en-aut-mei=Yuri
kn-aut-name=中島有理
kn-aut-sei=中島
kn-aut-mei=有理
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=9
article-no=
start-page=1559
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250503
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impacts of Dental Follicle Cells and Periodontal Ligament Cells on the Bone Invasion of Well-Differentiated Oral Squamous Cell Carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Oral squamous cell carcinoma (OSCC) frequently invades the jawbone, leading to diagnostic and therapeutic challenges. While tumor-bone interactions have been studied, the specific roles of dental follicle cells (DFCs) and periodontal ligament cells (PDLCs) in OSCC-associated bone resorption remain unclear. This study aimed to compare the effects of DFCs and PDLCs on OSCC-induced bone invasion and elucidate the underlying mechanisms. Methods: Primary human DFCs and PDLCs were isolated from extracted third molars and characterized by Giemsa and immunofluorescence staining. An in vitro co-culture system and an in vivo xenograft mouse model were established using the HSC-2 OSCC cell line. Tumor invasion and osteoclast activation were assessed by hematoxylin and eosin (HE) and tartrate-resistant acid phosphatase (TRAP) staining. Immunohistochemical analysis was performed to evaluate the expression of receptor activator of NF-kappa B ligand (RANKL) and parathyroid hormone-related peptide (PTHrP). Results: DFCs significantly enhanced OSCC-induced bone resorption by promoting osteoclastogenesis and upregulating RANKL and PTHrP expression. In contrast, PDLCs suppressed RANKL expression and partially modulated PTHrP levels, thereby reducing osteoclast activity. Conclusions: DFCs and PDLCs exert opposite regulatory effects on OSCC-associated bone destruction. These findings underscore the importance of stromal heterogeneity and highlight the therapeutic potential of targeting specific stromal-tumor interactions to mitigate bone-invasive OSCC.
en-copyright=
kn-copyright=

en-aut-name=ChangAnqi
en-aut-sei=Chang
en-aut-mei=Anqi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakabatakeKiyofumi
en-aut-sei=Takabatake
en-aut-mei=Kiyofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=PiaoTianyan
en-aut-sei=Piao
en-aut-mei=Tianyan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArashimaTakuma
en-aut-sei=Arashima
en-aut-mei=Takuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EainHtoo Shwe
en-aut-sei=Eain
en-aut-mei=Htoo Shwe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SoeYamin
en-aut-sei=Soe
en-aut-mei=Yamin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MinZin Zin
en-aut-sei=Min
en-aut-mei=Zin Zin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakanoKeisuke
en-aut-sei=Nakano
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NagatsukaHitoshi
en-aut-sei=Nagatsuka
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Oral Pathology and Medicine, Okayama University
kn-affil=
en-keyword=oral squamous cell carcinoma
kn-keyword=oral squamous cell carcinoma
en-keyword=dental follicle cells
kn-keyword=dental follicle cells
en-keyword=periodontal ligament cells
kn-keyword=periodontal ligament cells
en-keyword=bone invasion
kn-keyword=bone invasion
en-keyword=receptor activator of NF-kappa B ligand
kn-keyword=receptor activator of NF-kappa B ligand
en-keyword=parathyroid hormone-related peptide
kn-keyword=parathyroid hormone-related peptide
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=High-Resolution HPLC for Separating Peptide-Oligonucleotide Conjugates
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Peptide-oligonucleotide conjugates (POCs) are chimeric molecules that combine the specificity of oligonucleotides with the functionality of peptides, improving the delivery and therapeutic potential of nucleic acid-based drugs. However, the analysis of POCs, particularly those containing arginine-rich sequences, poses major challenges because of aggregation caused by electrostatic interactions. In this study, we developed an optimized high-performance liquid chromatography (HPLC) method for analyzing POCs. Using a conjugate of DNA and nona-arginine as a model compound, we systematically investigated the effects of various analytical parameters, including column type, column temperature, mobile-phase composition, and pH. A column packed with C18 resin with wide pores combined with butylammonium acetate as the ion-pairing reagent and an optimal column temperature of 80 degrees C provided superior peak resolution and sensitivity. The optimized conditions gave clear separation of POCs from unlinked oligonucleotides and enabled the detection of nucleic acid fragments lacking an alkyne moiety as a linkage part, which is critical for quality control. Our HPLC method is robust and reproducible and substantially reduces the complexity, time, and cost associated with the POC analysis. The method may improve the efficiency of quality control in the production of POCs, thereby supporting their development as promising therapeutic agents for clinical applications.
en-copyright=
kn-copyright=

en-aut-name=NaganumaMiyako
en-aut-sei=Naganuma
en-aut-mei=Miyako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsujiGenichiro
en-aut-sei=Tsuji
en-aut-mei=Genichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AmiyaMisato
en-aut-sei=Amiya
en-aut-mei=Misato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HiraiReira
en-aut-sei=Hirai
en-aut-mei=Reira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HiguchiYuki
en-aut-sei=Higuchi
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HataNaoko
en-aut-sei=Hata
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NozawaSaoko
en-aut-sei=Nozawa
en-aut-mei=Saoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WatanabeDaishi
en-aut-sei=Watanabe
en-aut-mei=Daishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakajimaTaeko
en-aut-sei=Nakajima
en-aut-mei=Taeko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=DemizuYosuke
en-aut-sei=Demizu
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=2
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=3
en-affil=YMC CO., LTD.
kn-affil=

affil-num=4
en-affil=YMC CO., LTD.
kn-affil=

affil-num=5
en-affil=YMC CO., LTD.
kn-affil=

affil-num=6
en-affil=YMC CO., LTD.
kn-affil=

affil-num=7
en-affil=YMC CO., LTD.
kn-affil=

affil-num=8
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=9
en-affil=YMC CO., LTD.
kn-affil=

affil-num=10
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Division of Pharmaceutical Science, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=2323
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A mini-hairpin shaped nascent peptide blocks translation termination by a distinct mechanism
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Protein synthesis by ribosomes produces functional proteins but also serves diverse regulatory functions, which depend on the coding amino acid sequences. Certain nascent peptides interact with the ribosome exit tunnel to arrest translation and modulate themselves or the expression of downstream genes. However, a comprehensive understanding of the mechanisms of such ribosome stalling and its regulation remains elusive. In this study, we systematically screen for unidentified ribosome arrest peptides through phenotypic evaluation, proteomics, and mass spectrometry analyses, leading to the discovery of the arrest peptides PepNL and NanCL in E. coli. Our cryo-EM study on PepNL reveals a distinct arrest mechanism, in which the N-terminus of PepNL folds back towards the tunnel entrance to prevent the catalytic GGQ motif of the release factor from accessing the peptidyl transferase center, causing translation arrest at the UGA stop codon. Furthermore, unlike sensory arrest peptides that require an arrest inducer, PepNL uses tryptophan as an arrest inhibitor, where Trp-tRNATrp reads through the stop codon. Our findings illuminate the mechanism and regulatory framework of nascent peptide-induced translation arrest, paving the way for exploring regulatory nascent peptides.
en-copyright=
kn-copyright=

en-aut-name=AndoYushin
en-aut-sei=Ando
en-aut-mei=Yushin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KoboAkinao
en-aut-sei=Kobo
en-aut-mei=Akinao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NiwaTatsuya
en-aut-sei=Niwa
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamakawaAyako
en-aut-sei=Yamakawa
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KonomaSuzuna
en-aut-sei=Konoma
en-aut-mei=Suzuna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiYuki
en-aut-sei=Kobayashi
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NurekiOsamu
en-aut-sei=Nureki
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TaguchiHideki
en-aut-sei=Taguchi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItohYuzuru
en-aut-sei=Itoh
en-aut-mei=Yuzuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=2
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=3
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=4
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=5
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=6
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=7
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=8
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=9
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=210
cd-vols=
no-issue=
article-no=
start-page=112952
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202503
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A microfluidic paper-based analytical device that uses gelatin film to assay protease activity via time readout
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Food processing, detergents, and pharmaceuticals frequently employ proteases, which are enzymes that break the chemical bonds of both proteins and peptides. In this work, we developed a microfluidic paper-based analytical device (µPAD) for protease activity assays via time readout. To accomplish this, we folded the µPAD to form layers, then inserted a water-insoluble gelatin film between the layers of paper to form the device. Lamination helps to maintain the gelatin film between the introduction zone, which is the upper layer, and the detection channel, which is the lower layer. Proteases decompose the gelatin film when it enters the introduction zone, which then allows it to flow into the detection channel. The protease activity in the sample solution determines the time required to dissolve the gelatin film, which leads to a linear relationship between the logarithm of the protease concentration and the time required to flow the solution a specific distance on the detection channel. The µPAD was used to measure proteases in concentrations that ranged from 0.25 to 1 mg L−1 for bromelain, 2.5 to 10 mg L−1 for papain, and 1 to 8 mg L−1 for trypsin. The limits of quantification for bromelain, papain, and trypsin were 0.41, 2.7, and 9.2 mg mL−1, respectively. The relative standard deviations for bromelain were smaller than 2 % for concentrations ranging from 0.5 to 1.0 mg L−1. We compared the µPAD to a commercially available protease activity assay kit, which relies on quenching fluorescein isothiocyanate-labeled casein. Both methods demonstrated the same order of activity: bromelain > papain > trypsin. The proposed device allowed the assay of bromelain in both pineapple pulp and juice, which were stored at room temperature. When first using the proposed device, the bromelain in the pulp gradually lost its activity, while the activity of the bromelain in the juice showed no significant change for five days. The µPAD requires no analytical instruments for quality control and monitoring of the protease activity in food.
en-copyright=
kn-copyright=

en-aut-name=RenJianchao
en-aut-sei=Ren
en-aut-mei=Jianchao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DanchanaKaewta
en-aut-sei=Danchana
en-aut-mei=Kaewta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KanetaTakashi
en-aut-sei=Kaneta
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Chemistry, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Chemistry, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Chemistry, Okayama University
kn-affil=
en-keyword=Microfluidic paper-based analytical device
kn-keyword=Microfluidic paper-based analytical device
en-keyword=Protease
kn-keyword=Protease
en-keyword=Enzyme assay
kn-keyword=Enzyme assay
en-keyword=Time readout
kn-keyword=Time readout
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=3
article-no=
start-page=817
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Interrelationships Between Plasma Levels of Brain Natriuretic Peptide and Prolonged Symptoms Due to Long COVID
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: Evidence for the usefulness of biomarkers that aid in diagnosis, assessment of severity, and prediction of prognosis in patients with long COVID is limited. The aim of this study was to clarify the characteristics of brain natriuretic peptide (BNP) in long COVID. Methods: We conducted a retrospective observational study of patients who visited the COVID-19 aftercare outpatient clinic at Okayama University Hospital from February 2021 to April 2024. Results: A total of 428 patients were enrolled in this study, and the patients were divided into a group with normal BNP (n = 314, <= 18.4 pg/mL) and a group with increased BNP (n = 114, >18.4 pg/mL). The long COVID group with increased BNP had a higher proportion of females (44.3% vs. 73.7%, p < 0.01) and an older median age (38 vs. 51 years, p < 0.01). Fatigue and brain fog were commonly manifested in both groups, while dyspnea was a more frequent complaint in the group with increased BNP. Various symptoms including fatigue, palpitations, and taste and/or olfactory disorders were associated with elevated BNP (23 to 24 pg/mL). Memory impairment was also linked to higher BNP (OR: 2.36, p = 0.05). In long COVID patients, plasma BNP elevation appears to be more pronounced in females and is often related to cardiogenic factors, in which inflammatory responses are also involved. Conclusions: Plasma BNP measurement may be useful for evaluating the severity of long COVID, especially in female patients and those with respiratory symptoms and/or memory impairment.
en-copyright=
kn-copyright=

en-aut-name=MasudaYohei
en-aut-sei=Masuda
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=brain fog
kn-keyword=brain fog
en-keyword=brain natriuretic peptide (BNP)
kn-keyword=brain natriuretic peptide (BNP)
en-keyword=COVID-19
kn-keyword=COVID-19
en-keyword=fatigue
kn-keyword=fatigue
en-keyword=long COVID
kn-keyword=long COVID
en-keyword=memory impairment
kn-keyword=memory impairment
en-keyword=post-COVID-19 conditions
kn-keyword=post-COVID-19 conditions
END

start-ver=1.4
cd-journal=joma
no-vol=326
cd-vols=
no-issue=6
article-no=
start-page=F1054
end-page=F1065
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240530
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetic nephropathy remains the leading cause of end-stage kidney disease in many countries, and additional therapeutic targets are needed to prevent its development and progression. Some angiogenic factors are involved in the pathogenesis of diabetic nephropathy. Vasohibin-2 (VASH2) is a novel proangiogenic factor, and our previous study showed that glomerular damage is inhibited in diabetic Vash2 homozygous knockout mice. Therefore, we established a VASH2-targeting peptide vaccine as a tool for anti-VASH2 therapy in diabetic nephropathy. In this study, the preventive effects of the VASH2-targeting peptide vaccine against glomerular injury were examined in a streptozotocin (STZ)-induced diabetic mouse model. The mice were subcutaneously injected with the vaccine at two doses 2 wk apart and then intraperitoneally injected with 50 mg/kg STZ for 5 consecutive days. Glomerular injury was evaluated 20 wk after the first vaccination. Treatment with the VASH2-targeting peptide vaccine successfully induced circulating anti-VASH2 antibody without inflammation in major organs. Although the vaccination did not affect blood glucose levels, it significantly prevented hyperglycemia-induced increases in urinary albumin excretion and glomerular volume. The vaccination did not affect increased VASH2 expression but significantly inhibited renal angiopoietin-2 (Angpt2) expression in the diabetic mice. Furthermore, it significantly prevented glomerular macrophage infiltration. The preventive effects of vaccination on glomerular injury were also confirmed in db/db mice. Taken together, the results of this study suggest that the VASH2-targeting peptide vaccine may prevent diabetic glomerular injury in mice by inhibiting Angpt2-mediated microinflammation.
en-copyright=
kn-copyright=

en-aut-name=NakashimaYuri
en-aut-sei=Nakashima
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MifuneTomoyo
en-aut-sei=Mifune
en-aut-mei=Tomoyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakadoiTakato
en-aut-sei=Nakadoi
en-aut-mei=Takato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HayashiHiroki
en-aut-sei=Hayashi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagamiHironori
en-aut-sei=Nakagami
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=New Industry Creation Hatchery Center, Tohoku University
kn-affil=

affil-num=8
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=albuminuria
kn-keyword=albuminuria
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=macrophages
kn-keyword=macrophages
en-keyword=peptide vaccine
kn-keyword=peptide vaccine
en-keyword=vasohibin-2
kn-keyword=vasohibin-2
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=
article-no=
start-page=1439705
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241211
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=HOMA-beta independently predicts survival in patients with advanced cancer on treatment with immune checkpoint inhibitors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Although immune checkpoint inhibitors (ICIs) are effective cancer drugs, ICI-induced diabetes is a rare but a life-threatening adverse event for patients. The deleterious action of ICI on pancreatic beta-cell function is a concern. However, the influence of ICI on insulin synthesis and secretion in patients with cancer without diabetes remains unknown. <br>
Methods: This study included 87 patients diagnosed with advanced cancer. Glucose metabolism markers (HbA1c, HOMA-IR) and indicators of insulin secretory capacity (HOMA-beta, C-peptide) were prospectively evaluated in patients with ICI-treated cancers to determine their association with cancer prognosis. <br>
Results: Patients with overall survival (OS) >= 7 months had substantially higher HOMA-beta levels at baseline (p=0.008) and 1 month after ICI administration (p=0.006) compared to those with OS <7 months. The median OS was significantly longer in patients with HOMA-beta >= 64.24 (13 months, 95%CI: 5.849-20.151, 37 events) than in those with HOMA-beta < 64.24 (5 months, 95%CI: 3.280-6.720, 50 events) (p=0.013). Further, the median progression-free survival (PFS) was significantly longer in patients with HOMA-beta >= 66.43 (4 months, 95%CI: 3.073-4.927, 33 events) than in those with HOMA-beta < 66.43 (2 months, 95%CI: 1.410-2.590, 54 events) (p=0.025). Additionally, multivariable logistic regression analysis revealed that a HOMA-beta value >= 64.24 independently predicted longer OS in ICI-treated patients. <br>
Conclusions: Pre-ICI HOMA-beta level is linked to longer OS in ICI-treated patients. This connection is significant and shows that insulin secretory capacity may predict ICI efficacy.
en-copyright=
kn-copyright=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakamotoAtsushi
en-aut-sei=Takamoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KanzakiHiromitsu
en-aut-sei=Kanzaki
en-aut-mei=Hiromitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NodaYohei
en-aut-sei=Noda
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KagawaSyunsuke
en-aut-sei=Kagawa
en-aut-mei=Syunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Urology, Fukuyama City Hospital
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Tsuyama Chuo Hospital
kn-affil=

affil-num=5
en-affil=Department of Urology, Fukuyama City Hospital
kn-affil=

affil-num=6
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=anti-PD1 immune checkpoint inhibitors
kn-keyword=anti-PD1 immune checkpoint inhibitors
en-keyword= insulin secretory capacity
kn-keyword= insulin secretory capacity
en-keyword= cancer prognosis
kn-keyword= cancer prognosis
en-keyword= insulin secretion
kn-keyword= insulin secretion
en-keyword= glucose metabolism markers
kn-keyword= glucose metabolism markers
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=1434800
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241127
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of extracting and preventively intervening late-stage older adults who are at high risk for spending high medical costs by using the health check-up system in Japan: a pilot study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: In Japan, the seven diseases (femur fracture, cerebral infarction, chronic renal failure, heart failure, dementia, pneumonia, and chronic obstructive pulmonary disease) are the top causes of inpatient medical costs among the late-stage older adults aged 75 years and over. This pilot study was conducted with the following two objectives; (1) to examine the proportion of risks of onset and severity of seven diseases among the late-stage older adults, and (2) to examine the efficacy of interventions focusing on the prevention of unplanned hospitalization. <br>
Methods: Participants were 45,233 older adults aged 75 and over living in Kure City, Japan. In addition to the government-mandated health checkup items, the Intervention group underwent additional risk screening tests included questionnaires, physical examinations, blood tests, and educational guidance by nurses. The efficacy of the intervention was examined whether there were differences in the number of hospitalizations, the use of emergency and critical care, and the incidence of hemodialysis induction between the Intervention and control groups (Usual Health Checkup group and No Health Checkup group) for the 2 years. <br>
Results: There were 485 participants in the Intervention group, 1,067 in the Usual Health Checkup group, and 43,712 in the No Health Checkup group. As the risks of seven diseases in the Intervention group, the largest proportion of deviations occurred for systolic blood pressure (63.3%), estimated salt intake (60.3%), and low-density lipoprotein cholesterol (51.5%). Estimated glomerular filtration rate deviated in 41.0%, N-terminal pro b-type natriuretic peptide in 37.9%. 7.5% scored <2 points on the Mini-Cog (c), and 9.1% performed the Timed Up and Go test in >12 s. The incidence of hospitalization due to any of the seven diseases was significantly higher in the No Health Checkup group (p < 0.001). There were no differences among the three groups in the use of emergency and critical care or the introduction of hemodialysis. <br>
Conclusion: This study revealed that additional health checkup tests and intervention methods could be prevented hospitalization among the adults of 75 years and older. It is necessary to make health checkups and follow-ups more accessible those are already available within the existing health system in Japan.
en-copyright=
kn-copyright=

en-aut-name=KazawaKana
en-aut-sei=Kazawa
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaiMadoka
en-aut-sei=Kawai
en-aut-mei=Madoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriyamaMichiko
en-aut-sei=Moriyama
en-aut-mei=Michiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Nursing Science, Graduate School of Biomedical and Health Sciences, Hiroshima University
kn-affil=

affil-num=3
en-affil=Division of Nursing Science, Graduate School of Biomedical and Health Sciences, Hiroshima University
kn-affil=
en-keyword=older adults
kn-keyword=older adults
en-keyword=health checkups
kn-keyword=health checkups
en-keyword=health risk
kn-keyword=health risk
en-keyword=hospitalization
kn-keyword=hospitalization
en-keyword=education
kn-keyword=education
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=がん細胞へのsiRNA送達のためのペプチドナノミセルの開発
kn-title=Development of Peptide Nanomicelle for siRNA Delivery into Cancer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAUFIK FATWA NUR HAKIM
en-aut-sei=TAUFIK FATWA NUR HAKIM
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=岡山大学大学院ヘルスシステム統合科学研究科
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=腫瘍ホーミングペプチド修飾磁性ナノ粒子の磁気温熱療法および腫瘍検出への応用
kn-title=Application of novel tumor-homing peptide-modified magnetic nanoparticles for magnetic hyperthermia and tumor cell detection
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ZHOUSHENGLI
en-aut-sei=ZHOU
en-aut-mei=SHENGLI
kn-aut-name=周聖力
kn-aut-sei=周
kn-aut-mei=聖力
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=岡山大学大学院ヘルスシステム統合科学研究科
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=モンゴルの伝統的発酵乳アイラグから分離した乳酸菌2菌株Leuconostoc mesenteroides subsp. mesenteroides 406 と213M0が産生する抗菌ペプチドのバクテリオシンに関する比較研究
kn-title=Comparative research on antibacterial peptides, bacteriocins, produced by two strains of lactic acid bacteria, Leuconostoc mesenteroides subsp. mesenteroides 406 and 213M0, isolated from Mongolian traditional fermented milk, airag
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HASIQIMUGE
en-aut-sei=HASIQIMUGE
en-aut-mei=
kn-aut-name=哈斯其木格
kn-aut-sei=哈斯其木格
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
END

start-ver=1.4
cd-journal=joma
no-vol=300
cd-vols=
no-issue=6
article-no=
start-page=107360
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nonspecific N-terminal tetrapeptide insertions disrupt the translation arrest induced by ribosome-arresting peptide sequences
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The nascent polypeptide chains passing through the ribosome tunnel not only serve as an intermediate of protein synthesis but also, in some cases, act as dynamic genetic information, controlling translation through interaction with the ribosome. One notable example is Escherichia coli SecM, in which translation of the ribosome arresting peptide (RAP) sequence in SecM leads to robust elongation arrest. Translation regulations, including the SecM-induced translation arrest, play regulatory roles such as gene expression control. Recent investigations have indicated that the insertion of a peptide sequence, SKIK (or MSKIK), into the adjacent N-terminus of the RAP sequence of SecM behaves as an "arrest canceler". As the study did not provide a direct assessment of the strength of translation arrest, we conducted detailed biochemical analyses. The results revealed that the effect of SKIK insertion on weakening SecM-induced translation arrest was not specific to the SKIK sequence, that is, other tetrapeptide sequences inserted just before the RAP sequence also attenuated the arrest. Our data suggest that SKIK or other tetrapeptide insertions disrupt the context of the RAP sequence rather than canceling or preventing the translation arrest.
en-copyright=
kn-copyright=

en-aut-name=KoboAkinao
en-aut-sei=Kobo
en-aut-mei=Akinao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TaguchiHideki
en-aut-sei=Taguchi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=2
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=3
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=387
end-page=399
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Radon Inhalation on Murine Brain Proteins: Investigation Using Proteomic and Multivariate Analyses
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Radon is a known risk factor for lung cancer; however, it can be used beneficially, such as in radon therapy. We have previously reported the enhancement of antioxidant effects associated with trace amounts of oxidative stress as one of the positive biological effects of radon inhalation. However, the biological effects of radon inhalation are incompletely understood, and more detailed and comprehensive studies are required. Although several studies have used proteomics to investigate the effects of radon inhalation on body proteins, none has focused on brain proteins. In this study, we evaluated the expression status of proteins in murine brains using proteomic and multivariate analyses to identify those whose expressions changed following two days of radon inhalation at a concentration of 1,500 Bq/m3. We found associations of radon inhalation with the expressions of seven proteins related to neurotransmission and heat shock. These proteins may be proposed as biomarkers indicative of radon inhalation. Although further studies are required to obtain the detailed biological significance of these protein alterations, this study contributes to the elucidation of the biological effects of radon
inhalation as a low-dose radiation.
en-copyright=
kn-copyright=

en-aut-name=NaoeShota
en-aut-sei=Naoe
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaAyumi
en-aut-sei=Tanaka
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KanzakiNorie
en-aut-sei=Kanzaki
en-aut-mei=Norie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakenakaReiju
en-aut-sei=Takenaka
en-aut-mei=Reiju
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakodaAkihiro
en-aut-sei=Sakoda
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamaokaKiyonori
en-aut-sei=Yamaoka
en-aut-mei=Kiyonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KataokaTakahiro
en-aut-sei=Kataoka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=4
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=6
en-affil=Advanced Science Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=
en-keyword=radon inhalation
kn-keyword=radon inhalation
en-keyword=proteomics
kn-keyword=proteomics
en-keyword=multivariate analysis
kn-keyword=multivariate analysis
en-keyword=brain
kn-keyword=brain
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=9
article-no=
start-page=1781
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240828
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel C-Terminal Truncated Bacteriocin Found by Comparison between Leuconostoc mesenteroides 406 and 213M0 Isolated from Mongolian Traditional Fermented Milk, Airag
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bacteriocins produced by lactic acid bacteria are known to be useful tools for food biopreservation and fermentation control. Leuconostoc mesenteroides subsp. mesenteroides 406 and 213M0 isolated from different samples of Mongolian traditional fermented milk, airag, had been reported to produce listericidal bacteriocin-like inhibitory substances with similar but slightly different properties. In this study, the antibacterial properties and the related gene sequences of both strains were compared, and then their bacteriocins were purified and identified. Strain 406 was superior to strain 213M0 in cell growth and antibacterial activity against many strains. However, the activity of 213M0 was stronger than that of 406 against a few strains. DNA sequencing revealed two and three plasmids in 406 and 213M0, respectively, and each one of them harbored an almost identical mesentericin Y105-B105 gene cluster. Removal of these plasmids resulted in a complete loss of activity, indicating that the antibacterial activity of both strains was generated by bacteriocins encoded on the plasmids. Mesentericins Y105 and B105 were purified from both cultures, and another novel bacteriocin, named mesentericin M, was identified from the 213M0 culture only. Its structural gene was coded on a 213M0 plasmid and, surprisingly, its C-terminal three amino acid residues were post-translationally cleaved. To our knowledge, this is the first report of a C-terminal truncated bacteriocin. In conclusion, the novel bacteriocin should be mainly responsible for the difference in antibacterial properties between the two strains.
en-copyright=
kn-copyright=

en-aut-name=HasiqimugeChihiro
en-aut-sei=Hasiqimuge
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HanoChihiro
en-aut-sei=Hano
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ArakawaKensuke
en-aut-sei=Arakawa
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaSaki
en-aut-sei=Yoshida
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZhaoJunliang
en-aut-sei=Zhao
en-aut-mei=Junliang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TohHidehiro
en-aut-sei=Toh
en-aut-mei=Hidehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritaHidetoshi
en-aut-sei=Morita
en-aut-mei=Hidetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyamotoTaku
en-aut-sei=Miyamoto
en-aut-mei=Taku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Advanced Genomics Center, National Institute of Genetics
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Leuconostoc mesenteroides
kn-keyword=Leuconostoc mesenteroides
en-keyword=antimicrobial peptide
kn-keyword=antimicrobial peptide
en-keyword=bacteriocin
kn-keyword=bacteriocin
en-keyword=Listeria monocytogenes
kn-keyword=Listeria monocytogenes
en-keyword=fermented milk
kn-keyword=fermented milk
en-keyword=biopreservation
kn-keyword=biopreservation
en-keyword=fermentation control
kn-keyword=fermentation control
en-keyword=post-translational modification
kn-keyword=post-translational modification
en-keyword=C-terminal cleavage
kn-keyword=C-terminal cleavage
END

start-ver=1.4
cd-journal=joma
no-vol=149
cd-vols=
no-issue=
article-no=
start-page=13
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=201809
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Functional analysis of N-terminal propeptide in the precursor of Vibrio vulnificus metalloprotease by using cell-free translational system
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Vibrio vulnificus is a human pathogen causing fatal septicemia with edematous and hemorrhagic skin damage. Among multiple virulence factors, an extracellular metalloprotease termed as V. vulnificus protease (VVP) is known to play a crucial role in eliciting the skin damage. The mature VVP (413 aa) is composed of two domains, the N-terminal core domain with proteolytic activity and the C-terminal domain mediates efficient attachment to protein substrates. However, VVP is produced as an inactive precursor (609 aa) with a signal peptide (24 aa) and propeptide (172 aa). In order to clarify the function of propeptide, a series of DNA fragments encoding the VVP precursor and its various domains were designed and the proteins were expressed in vitro by using cell-free translational system. The results indicated that the propeptide might function as an intramolecular chaperon to promote the proper folding of both N-terminal and C-terminal domains. The obtained results also suggest that the propeptide, itself was unstable and thus digested easily by the enzymes present in cell lysate used for cell-free system. Additionally, the C-terminal domain in VVP found to inhibit the folding of the N-terminal domain in absence of propeptide.
en-copyright=
kn-copyright=

en-aut-name=KawaseTomoka
en-aut-sei=Kawase
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiuraFumi
en-aut-sei=Miura
en-aut-mei=Fumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DebnathAnusuya
en-aut-sei=Debnath
en-aut-mei=Anusuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImakuraKinuyo
en-aut-sei=Imakura
en-aut-mei=Kinuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiShin-ichi
en-aut-sei=Miyoshi
en-aut-mei=Shin-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Vibrio vulnificus
kn-keyword=Vibrio vulnificus
en-keyword=Protease
kn-keyword=Protease
en-keyword=Propeptide
kn-keyword=Propeptide
en-keyword=Domain
kn-keyword=Domain
en-keyword=Cell-free translational system
kn-keyword=Cell-free translational system
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=15
article-no=
start-page=4384
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240726
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of Serum Indoxyl Sulfate on One-Year Adverse Events in Chronic Kidney Disease Patients with Heart Failure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: Indoxyl sulfate, a uremic toxin, is associated with mortality and cardiovascular events in patients with chronic kidney disease (CKD). This study aimed to evaluate the prognostic implications of serum indoxyl sulfate levels in patients with heart failure and CKD. Methods and Results: This was a prospective multicenter observational study. Overall, 300 patients with chronic heart failure with a previous history of hospitalization and an estimated glomerular filtration rate (eGFR) of 45 mL/min/1.73 m2 or less (CKD stage G3b to G5) without dialysis were analyzed. The primary outcome assessed in a time-to-event analysis from the measurement of indoxyl sulfate was a composite of all-cause death, hospitalization for heart failure, nonfatal myocardial infarction, and nonfatal stroke. Clinical events were followed-up to one year after indoxyl sulfate measurement. The median patient age was 75 years, and 57% of the patients were men. We divided the cohort into low and high indoxyl sulfate categories according to a median value of 9.63 mg/mL. The primary outcome occurred in 27 of 150 patients (18.0%) in the low indoxyl sulfate group and 27 of 150 patients (18.0%) in the high indoxyl sulfate group (hazard ratio, 1.00; 95% confidence interval, 0.58 to 1.70, p = 0.99). In the post hoc exploratory analyses, the results were consistent across age, sex, body mass index, left ventricular ejection fraction, eGFR, and N-terminal pro b-type natriuretic peptide. Conclusions: Among heart failure patients with CKD stages G3b to 5G, serum indoxyl sulfate concentrations were not significantly associated with the subsequent occurrence of cardiovascular events.
en-copyright=
kn-copyright=

en-aut-name=IwasakiKeiichiro
en-aut-sei=Iwasaki
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UrabeChikara
en-aut-sei=Urabe
en-aut-mei=Chikara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FukeSoichiro
en-aut-sei=Fuke
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DoiMasayuki
en-aut-sei=Doi
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkaTakefumi
en-aut-sei=Oka
en-aut-mei=Takefumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TokunagaNaoto
en-aut-sei=Tokunaga
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Institute of Academic and Research, Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Institute of Academic and Research, Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Institute of Academic and Research, Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Iwakuni Clinical Center
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=7
en-affil=Department of Cardiology, Kagawa Prefectural Central Hospital
kn-affil=

affil-num=8
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=9
en-affil=Department of Cardiology, Tsuyama Chuo Hospital
kn-affil=

affil-num=10
en-affil=Department of Cardiology, Ibara City Hospital
kn-affil=

affil-num=11
en-affil=Department of General Internal Medicine 3, Kawasaki Medical School
kn-affil=
en-keyword=heart failure
kn-keyword=heart failure
en-keyword=chronic kidney disease
kn-keyword=chronic kidney disease
en-keyword=indoxyl sulfate
kn-keyword=indoxyl sulfate
END

start-ver=1.4
cd-journal=joma
no-vol=100
cd-vols=
no-issue=1
article-no=
start-page=219
end-page=228
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel Peptidome Technology for the Diagnosis of Mild Cognitive Impairment and Alzheimer’s Disease by Selected Reaction Monitoring
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:With the aging of populations worldwide, Alzheimer’s disease (AD) has become a concern due to its high prevalence and the continued lack of established treatments. Early diagnosis is required as a preventive intervention to modify the disease’s progression. In our previous study, we performed peptidomic analysis of serum samples obtained from AD patients and age-matched healthy subjects to seek peptide biomarker candidates for AD by using BLOTCHIP-MS analysis, and identified four peptides as AD biomarker candidates. <br>
Objective:The objective was to validate the serum biomarker peptides to distinguish mild cognitive impairment (MCI) and AD in comparison to cognitively healthy controls using a new peptidome technology, the Dementia Risk Test. <br>
Methods:We enrolled 195 subjects with normal cognitive function (NC; n = 70), MCI (n = 55), and AD (n = 70), The concentrations of cognitive impairment marker peptides (Fibrinogen α chain (FAC), Fibrinogen β chain (FBC), Plasma protease C1 inhibitor (PPC1I), α2-HS-glycoprotein (AHSG)) were quantified by using a selected reaction monitoring assay based on liquid chromatography-MS/MS. <br>
Results:The present study confirmed that three peptides, FAC, FBC, and PPC1I, were significantly upregulated during the onset of AD. This three-peptide set was both highly sensitive in determining AD (sensitivity: 85.7%, specificity: 95.7%, AUC: 0.900) and useful in distinguishing MCI (sensitivity: 61.8%, specificity: 98.6%, AUC: 0.824) from NC. <br>
Conclusions:In this validation study, we confirmed the high diagnostic potential of the three peptides identified in our previous study as candidate serum biomarkers for AD. The Dementia Risk Test may be a powerful tool for detecting AD-related pathological changes.
en-copyright=
kn-copyright=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HamadaMinaki
en-aut-sei=Hamada
en-aut-mei=Minaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AsadaKyoichi
en-aut-sei=Asada
en-aut-mei=Kyoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LeeLyang-Ja
en-aut-sei=Lee
en-aut-mei=Lyang-Ja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TachikiHidehisa
en-aut-sei=Tachiki
en-aut-mei=Hidehisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Protosera, Inc.
kn-affil=

affil-num=4
en-affil=Protosera, Inc.
kn-affil=

affil-num=5
en-affil=Protosera, Inc.
kn-affil=

affil-num=6
en-affil=Protosera, Inc.
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurology, National Center of Neurology and Psychiatry
kn-affil=

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=biochemical marker
kn-keyword=biochemical marker
en-keyword=dementia risk test
kn-keyword=dementia risk test
en-keyword=liquid chromatography-MS/MS
kn-keyword=liquid chromatography-MS/MS
en-keyword=mild cognitive impairment
kn-keyword=mild cognitive impairment
en-keyword=peptidome
kn-keyword=peptidome
en-keyword=selected reaction monitoring
kn-keyword=selected reaction monitoring
END

start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=11
article-no=
start-page=2632
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In Vitro Study of Tumor-Homing Peptide-Modified Magnetic Nanoparticles for Magnetic Hyperthermia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer cells have higher heat sensitivity compared to normal cells; therefore, hyperthermia is a promising approach for cancer therapy because of its ability to selectively kill cancer cells by heating them. However, the specific and rapid heating of tumor tissues remains challenging. This study investigated the potential of magnetic nanoparticles (MNPs) modified with tumor-homing peptides (THPs), specifically PL1 and PL3, for tumor-specific magnetic hyperthermia therapy. The synthesis of THP-modified MNPs involved the attachment of PL1 and PL3 peptides to the surface of the MNPs, which facilitated enhanced tumor cell binding and internalization. Cell specificity studies revealed an increased uptake of PL1- and PL3-MNPs by tumor cells compared to unmodified MNPs, indicating their potential for targeted delivery. In vitro hyperthermia experiments demonstrated the efficacy of PL3-MNPs in inducing tumor cell death when exposed to an alternating magnetic field (AMF). Even without exposure to an AMF, an additional ferroptotic pathway was suggested to be mediated by the nanoparticles. Thus, this study suggests that THP-modified MNPs, particularly PL3-MNPs, hold promise as a targeted approach for tumor-specific magnetic hyperthermia therapy.
en-copyright=
kn-copyright=

en-aut-name=ZhouShengli
en-aut-sei=Zhou
en-aut-mei=Shengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsutsumiuchiKaname
en-aut-sei=Tsutsumiuchi
en-aut-mei=Kaname
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaiRitsuko
en-aut-sei=Imai
en-aut-mei=Ritsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikiYukiko
en-aut-sei=Miki
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KondoAnna
en-aut-sei=Kondo
en-aut-mei=Anna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagawaHiroshi
en-aut-sei=Nakagawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=3
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=4
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=5
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=6
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=7
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=tumor-homing peptide
kn-keyword=tumor-homing peptide
en-keyword=magnetic hyperthermia
kn-keyword=magnetic hyperthermia
en-keyword=magnetic nanoparticles
kn-keyword=magnetic nanoparticles
en-keyword=ferroptosis
kn-keyword=ferroptosis
en-keyword=tumor-specific delivery
kn-keyword=tumor-specific delivery
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=271
end-page=279
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Humidified High-Flow Nasal Cannula Oxygen Therapy with a Pulmonary Infection Control Window as a Ventilation Switching Indication in Combination with Atomizing Inhalation of Terbutaline on the Lung Function of Patients with Acute Exacerbation of COPD
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated how humidified high-flow nasal cannula oxygen therapy (HFNC) with a pulmonary infection control (PIC) window as a ventilation switching indication in combination with atomizing inhalation of terbutaline affects the lung function of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). We examined 140 hospitalized AECOPD patients randomized to control and observation groups. Conventional supportive therapy and invasive mechanical ventilation with tracheal intubation were conducted in both groups, with a PIC window as the indication for ventilation switching. Noninvasive positive pressure ventilation (NIPPV) plus atomizing inhalation of terbutaline was used in the control group. In the observation group, HFNC combined with atomizing inhalation of terbutaline was used. Compared to the control group, after 48-hr treatment and treatment completion, the observation group had significantly increased levels of lung function indicators (maximal voluntary ventilation [MVV] plus forced vital capacity [FVC], p<0.05) and oxygen metabolism indicators (arterial oxygen partial pressure [PaO2], arterial oxygen content [CaO2], and oxygenation index, p<0.05). The comparison of the groups revealed that the levels of airway remodeling indicators (matrix metalloproteinase-2 [MMP-2], tissue inhibitor of metalloproteinase 2 [TIMP-2] plus MMP-9) and inflammatory indicators (interferon gamma [IFN-γ] together with interleukin-17 [IL-17], IL-10 and IL-4) were significantly lower after 48 h of treatment as well as after treatment completion (both p<0.05). These results demonstrate that HFNC with a PIC window as the indication for ventilation switching combined with atomizing inhalation of terbutaline can relieve the disorder of oxygen metabolism and correct airway hyper-reactivity.
en-copyright=
kn-copyright=

en-aut-name=YeMengjiao
en-aut-sei=Ye
en-aut-mei=Mengjiao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ZhangRenwei
en-aut-sei=Zhang
en-aut-mei=Renwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Respiratory and Critical Care Medicine, Tiantai Hospital of Traditional Chinese Medicine
kn-affil=

affil-num=2
en-affil=Department of Respiratory and Critical Care Medicine, Tiantai Hospital of Traditional Chinese Medicine
kn-affil=
en-keyword=chronic obstructive pulmonary disease
kn-keyword=chronic obstructive pulmonary disease
en-keyword=inhalation
kn-keyword=inhalation
en-keyword=oxygen therapy
kn-keyword=oxygen therapy
en-keyword=pulmonary function
kn-keyword=pulmonary function
en-keyword=ventilation
kn-keyword=ventilation
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=4
article-no=
start-page=746
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240407
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pyrene-Modified Cyclic Peptides Detect Cu2+ Ions by Fluorescence in Water
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The detection of metal ions is an option for maintaining water quality and diagnosing metal ion-related diseases. In this study, we successfully detected metal ions using fluorescent peptides in water. First, we prepared seven linear (L1-L7) and seven cyclic (C1-C7) peptides containing two pyrenyl (Pyr) units and assessed the response to various metal ions by fluorescence. The results indicated that C1, which contains a hexameric cyclic peptide moiety consisting of Pyr and Gly units, did not show a fluorescent response to metal ions, while the linear L1 corresponding to C1 showed a response to Cu2+, but its selectivity was found to be poor through a competition assay for each metal ion. We then assessed C2-C7 and L2-L7, in which Gly was replaced by His units at various positions in the same manner. The results showed that C2-C7 responded to Cu2+ in a manner dependent on the His position. Additionally, superior selectivity was observed in C7 through a competition assay. These results demonstrate that the structural restriction of peptides and the sequence affect the selective detection of Cu2+ and reveal that peptides with an appropriate structure can accomplish the fluorescent detection of Cu2+ specifically.
en-copyright=
kn-copyright=

en-aut-name=MaekawaYuhi
en-aut-sei=Maekawa
en-aut-mei=Yuhi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakuraSora
en-aut-sei=Sakura
en-aut-mei=Sora
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FurutaniYuji
en-aut-sei=Furutani
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujiharaRento
en-aut-sei=Fujihara
en-aut-mei=Rento
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SugimeHisashi
en-aut-sei=Sugime
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Applied Chemistry, Faculty of Science and Engineering, Kindai University
kn-affil=

affil-num=2
en-affil=Department of Applied Chemistry, Faculty of Science and Engineering, Kindai University
kn-affil=

affil-num=3
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Applied Chemistry, Faculty of Science and Engineering, Kindai University
kn-affil=

affil-num=5
en-affil=Department of Applied Chemistry, Faculty of Science and Engineering, Kindai University
kn-affil=

affil-num=6
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Applied Chemistry, Faculty of Science and Engineering, Kindai University
kn-affil=
en-keyword=peptide
kn-keyword=peptide
en-keyword=pyrene
kn-keyword=pyrene
en-keyword=metal ion
kn-keyword=metal ion
en-keyword=fluorescence
kn-keyword=fluorescence
END

start-ver=1.4
cd-journal=joma
no-vol=52
cd-vols=
no-issue=10
article-no=
start-page=5825
end-page=5840
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240425
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The ABCF proteins in Escherichia coli individually cope with 'hard-to-translate' nascent peptide sequences
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Organisms possess a wide variety of proteins with diverse amino acid sequences, and their synthesis relies on the ribosome. Empirical observations have led to the misconception that ribosomes are robust protein factories, but in reality, they have several weaknesses. For instance, ribosomes stall during the translation of the proline-rich sequences, but the elongation factor EF-P assists in synthesizing proteins containing the poly-proline sequences. Thus, living organisms have evolved to expand the translation capability of ribosomes through the acquisition of translation elongation factors. In this study, we have revealed that Escherichia coli ATP-Binding Cassette family-F (ABCF) proteins, YheS, YbiT, EttA and Uup, individually cope with various problematic nascent peptide sequences within the exit tunnel. The correspondence between noncanonical translations and ABCFs was YheS for the translational arrest by nascent SecM, YbiT for poly-basic sequence-dependent stalling and poly-acidic sequence-dependent intrinsic ribosome destabilization (IRD), EttA for IRD at the early stage of elongation, and Uup for poly-proline-dependent stalling. Our results suggest that ATP hydrolysis-coupled structural rearrangement and the interdomain linker sequence are pivotal for handling 'hard-to-translate' nascent peptides. Our study highlights a new aspect of ABCF proteins to reduce the potential risks that are encoded within the nascent peptide sequences. Graphical Abstract
en-copyright=
kn-copyright=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamanouchiShun
en-aut-sei=Yamanouchi
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UemuraEri
en-aut-sei=Uemura
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamasakiKohei
en-aut-sei=Yamasaki
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NiwaTatsuya
en-aut-sei=Niwa
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaToma
en-aut-sei=Ikeda
en-aut-mei=Toma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KuriharaMiku
en-aut-sei=Kurihara
en-aut-mei=Miku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwasakiWataru
en-aut-sei=Iwasaki
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TaguchiHideki
en-aut-sei=Taguchi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biological Sciences, Graduate School of Science, the University of Tokyo
kn-affil=

affil-num=3
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=

affil-num=4
en-affil=Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=

affil-num=6
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=7
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=8
en-affil=Department of Biological Sciences, Graduate School of Science, the University of Tokyo
kn-affil=

affil-num=9
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=2
article-no=
start-page=95
end-page=106
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Roles of Neuropeptide Y in Respiratory Disease Pathogenesis via the Airway Immune Response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The lungs are very complex organs, and the respiratory system performs the dual roles of repairing tissue while protecting against infection from various environmental stimuli. Persistent external irritation disrupts the immune responses of tissues and cells in the respiratory system, ultimately leading to respiratory disease. Neuropeptide Y (NPY) is a 36-amino-acid polypeptide and a neurotransmitter that regulates homeostasis. The NPY receptor is a seven-transmembrane-domain G-protein-coupled receptor with six subtypes (Y1, Y2, Y3, Y4, Y5, and Y6). Of these receptors, Y1, Y2, Y4, and Y5 are functional in humans, and Y1 plays important roles in the immune responses of many organs, including the respiratory system. NPY and the Y1 receptor have critical roles in the pathogenesis of asthma, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis. The effects of NPY on the airway immune response and pathogenesis differ among respiratory diseases. This review focuses on the involvement of NPY in the airway immune response and pathogenesis of various respiratory diseases.
en-copyright=
kn-copyright=

en-aut-name=ItanoJunko
en-aut-sei=Itano
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=
en-keyword=neuropeptide y
kn-keyword=neuropeptide y
en-keyword=Y1 receptor
kn-keyword=Y1 receptor
en-keyword=airway immune response
kn-keyword=airway immune response
en-keyword=bronchial epithelial cells
kn-keyword=bronchial epithelial cells
en-keyword=respiratory disease
kn-keyword=respiratory disease
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=3
article-no=
start-page=164
end-page=165
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Idiopathic ventricular tachycardia detected after coronavirus disease 2019
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We present a 23-year-old woman with depression and long COVID in whom a diagnosis of idiopathic ventricular tachycardia (VT) was made. Although the relationship between idiopathic VT and long COVID remains unknown, this is the first report of idiopathic VT detected in a patient with long COVID.
en-copyright=
kn-copyright=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakagawaKoji
en-aut-sei=Nakagawa
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=radiofrequency ablation
kn-keyword=radiofrequency ablation
en-keyword=brain natriuretic peptide
kn-keyword=brain natriuretic peptide
en-keyword=idiopathic ventricular tachycardia
kn-keyword=idiopathic ventricular tachycardia
END

start-ver=1.4
cd-journal=joma
no-vol=371
cd-vols=
no-issue=
article-no=
start-page=fnae007
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Knockout of adenylosuccinate synthase purA increases susceptibility to colistin in Escherichia coli
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Colistin is a cationic cyclic antimicrobial peptide used as a last resort against multidrug-resistant gram-negative bacteria. To understand the factors involved in colistin susceptibility, we screened colistin-sensitive mutants from an E. coli gene-knockout library (Keio collection). The knockout of purA, whose product catalyzes the synthesis of adenylosuccinate from IMP in the de novo purine synthesis pathway, resulted in increased sensitivity to colistin. Adenylosuccinate is subsequently converted to AMP, which is phosphorylated to produce ADP, a substrate for ATP synthesis. The amount of ATP was lower in the purA-knockout mutant than that in the wild-type strain. ATP synthesis is coupled with proton transfer, and it contributes to the membrane potential. Using the membrane potential probe, 3,3′-diethyloxacarbocyanine iodide [DiOC2(3)], we found that the membrane was hyperpolarized in the purA-knockout mutant compared to that in the wild-type strain. Treatment with the proton uncoupler, carbonyl cyanide m-chlorophenyl hydrazone (CCCP), abolished the hyperpolarization and colistin sensitivity in the mutant. The purA-knockout mutant exhibited increased sensitivity to aminoglycosides, kanamycin, and gentamicin; their uptake requires a membrane potential. Therefore, the knockout of purA, an adenylosuccinate synthase, decreases ATP synthesis concurrently with membrane hyperpolarization, resulting in increased sensitivity to colistin.
en-copyright=
kn-copyright=

en-aut-name=KanoTomonori
en-aut-sei=Kano
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IshikawaKazuya
en-aut-sei=Ishikawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FurutaKazuyuki
en-aut-sei=Furuta
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaitoChikara
en-aut-sei=Kaito
en-aut-mei=Chikara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=colistin
kn-keyword=colistin
en-keyword=adenylosuccinate synthase
kn-keyword=adenylosuccinate synthase
en-keyword=de novo purine synthesis
kn-keyword=de novo purine synthesis
en-keyword=membrane potential
kn-keyword=membrane potential
en-keyword=ATP synthesis
kn-keyword=ATP synthesis
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=3
article-no=
start-page=1585
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240127
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mutual Effects of Orexin and Bone Morphogenetic Proteins on Catecholamine Regulation Using Adrenomedullary Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Orexins are neuronal peptides that play a prominent role in sleep behavior and feeding behavior in the central nervous system, though their receptors also exist in peripheral organs, including the adrenal gland. In this study, the effects of orexins on catecholamine synthesis in the rat adrenomedullary cell line PC12 were investigated by focusing on their interaction with the adrenomedullary bone morphogenetic protein (BMP)-4. Orexin A treatment reduced the mRNA levels of key enzymes for catecholamine synthesis, including tyrosine hydroxylase (Th), 3,4-dihydroxyphenylalanie decarboxylase (Ddc) and dopamine beta-hydroxylase (Dbh), in a concentration-dependent manner. On the other hand, treatment with BMP-4 suppressed the expression of Th and Ddc but enhanced that of Dbh with or without co-treatment with orexin A. Of note, orexin A augmented BMP-receptor signaling detected by the phosphorylation of Smad1/5/9 through the suppression of inhibitory Smad6/7 and the upregulation of BMP type-II receptor (BMPRII). Furthermore, treatment with BMP-4 upregulated the mRNA levels of OX1R in PC12 cells. Collectively, the results indicate that orexin and BMP-4 suppress adrenomedullary catecholamine synthesis by mutually upregulating the pathway of each other in adrenomedullary cells.
en-copyright=
kn-copyright=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwataNahoko
en-aut-sei=Iwata
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuyamaAtsuhito
en-aut-sei=Suyama
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=bone morphogenetic protein (BMP)
kn-keyword=bone morphogenetic protein (BMP)
en-keyword=orexin
kn-keyword=orexin
en-keyword=catecholamine and adrenal
kn-keyword=catecholamine and adrenal
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=2
article-no=
start-page=532
end-page=542
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231229
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=pSPICA Force Field Extended for Proteins and Peptides
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Many coarse-grained (CG) molecular dynamics (MD) studies have been performed to investigate biological processes involving proteins and lipids. CG force fields (FFs) in these MD studies often use implicit or nonpolar water models to reduce computational costs. CG-MD using water models cannot properly describe electrostatic screening effects owing to the hydration of ionic segments and thus cannot appropriately describe molecular events involving water channels and pores through lipid membranes. To overcome this issue, we developed a protein model in the pSPICA FF, in which a polar CG water model showing the proper dielectric response was adopted. The developed CG model greatly improved the transfer free energy profiles of charged side chain analogues across the lipid membrane. Application studies on melittin-induced membrane pores and mechanosensitive channels in lipid membranes demonstrated that CG-MDs using the pSPICA FF correctly reproduced the structure and stability of the pores and channels. Furthermore, the adsorption behavior of the highly charged nona-arginine peptides on lipid membranes changed with salt concentration, indicating the pSPICA FF is also useful for simulating protein adsorption on membrane surfaces.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiYusuke
en-aut-sei=Miyazaki
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShinodaWataru
en-aut-sei=Shinoda
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=12
article-no=
start-page=113569
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231226
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanistic dissection of premature translation termination induced by acidic residues-enriched nascent peptide
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ribosomes polymerize nascent peptides through repeated inter-subunit rearrangements between the classic and hybrid states. The peptidyl-tRNA, the intermediate species during translation elongation, stabi-lizes the translating ribosome to ensure robust continuity of elongation. However, the translation of acidic residue-rich sequences destabilizes the ribosome, leading to a stochastic premature translation cessation termed intrinsic ribosome destabilization (IRD), which is still ill-defined. Here, we dissect the molecular mechanisms underlying IRD in Escherichia coli. Reconstitution of the IRD event reveals that (1) the prolonged ribosome stalling enhances IRD-mediated translation discontinuation, (2) IRD depends on temperature, (3) the destabilized 70S ribosome complex is not necessarily split, and (4) the destabilized ribosome is subjected to peptidyl-tRNA hydrolase-mediated hydrolysis of the peptidyl-tRNA without subunit splitting or recycling factors-mediated subunit splitting. Collectively, our data indicate that the translation of acidic-rich sequences alters the conformation of the 70S ribosome to an aberrant state that allows the noncanonical pre-mature termination.
en-copyright=
kn-copyright=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KanamoriTakashi
en-aut-sei=Kanamori
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NiwaTatsuya
en-aut-sei=Niwa
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IchiharaKazuya
en-aut-sei=Ichihara
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakayamaKeiichi I.
en-aut-sei=Nakayama
en-aut-mei=Keiichi I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoAkinobu
en-aut-sei=Matsumoto
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TaguchiHideki
en-aut-sei=Taguchi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=GeneFrontier Corporation
kn-affil=

affil-num=3
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=

affil-num=4
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=5
en-affil=Anticancer Strategies Laboratory, TMDU Advanced Research Institute, Tokyo Medical and Dental University
kn-affil=

affil-num=6
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=7
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=
article-no=
start-page=1239598
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=“Input/output cytokines” in epidermal keratinocytes and the involvement in inflammatory skin diseases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Considering the role of epidermal keratinocytes, they occupy more than 90% of the epidermis, form a physical barrier, and also function as innate immune barrier. For example, epidermal keratinocytes are capable of recognizing various cytokines and pathogen-associated molecular pattern, and producing a wide variety of inflammatory cytokines, chemokines, and antimicrobial peptides. Previous basic studies have shown that the immune response of epidermal keratinocytes has a significant impact on inflammatory skin diseases. The purpose of this review is to provide foundation of knowledge on the cytokines which are recognized or produced by epidermal keratinocytes. Since a number of biologics for skin diseases have appeared, it is necessary to fully understand the relationship between epidermal keratinocytes and the cytokines. In this review, the cytokines recognized by epidermal keratinocytes are specifically introduced as "input cytokines", and the produced cytokines as "output cytokines". Furthermore, we also refer to the existence of biologics against those input and output cytokines, and the target skin diseases. These use results demonstrate how important targeted cytokines are in real skin diseases, and enhance our understanding of the cytokines.
en-copyright=
kn-copyright=

en-aut-name=MorizaneShin
en-aut-sei=Morizane
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MukaiTomoyuki
en-aut-sei=Mukai
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SunagawaKo
en-aut-sei=Sunagawa
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TachibanaKota
en-aut-sei=Tachibana
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawakamiYoshio
en-aut-sei=Kawakami
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Immunology and Molecular Genetics, Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Molecular Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=epidermal keratinocytes
kn-keyword=epidermal keratinocytes
en-keyword=input cytokines
kn-keyword=input cytokines
en-keyword=output cytokines
kn-keyword=output cytokines
en-keyword=biologics
kn-keyword=biologics
en-keyword=inflammatory skin diseases
kn-keyword=inflammatory skin diseases
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=5
article-no=
start-page=382
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220913
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Investigation of bone invasion and underlying mechanisms of oral cancer using a cell line‑derived xenograft model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The cancer stroma regulates bone invasion in oral squamous cell carcinoma (OSCC). However, data on normal stroma are limited. In the present study, the effects of gingival and periodontal ligament tissue‑derived stromal cells (G‑SCs and P‑SCs, respectively) and human dermal fibroblasts (HDFs) on bone resorption and osteoclast activation were assessed using hematoxylin and eosin and tartrate‑resistant acid phosphatase staining in a cell line‑derived xenograft model. The results demonstrated that G‑SCs promoted bone invasion and osteoclast activation and inhibited osteoclast proliferation following crosstalk with the human OSCC HSC‑3 cell line, whereas P‑SCs inhibited bone resorption and promoted osteoclast proliferation in vitro but had a minimal effect on osteoclast activation both in vitro and in vivo following crosstalk with HSC‑3 cells. Furthermore, the effects of G‑SCs, P‑SCs and HDFs on protein expression levels of matrix metalloproteinase (MMP)‑9, membrane type 1 MMP (MT1‑MMP), Snail, parathyroid hormone‑related peptide (PTHrP) and receptor activator of NF‑κB ligand (RANKL) in HSC‑3 cells in OSCC bone invasion regions were assessed using immunohistochemistry. The results demonstrated that G‑SCs had a more prominent effect on the expression of MMP‑9, MT1‑MMP, Snail, PTHrP, and RANKL, whereas P‑SCs only promoted RANKL and PTHrP expression and exerted a minimal effect on MMP‑9, MT1‑MMP and Snail expression. The potential genes underlying the differential effects of G‑SCs and P‑SCs on bone invasion in OSCC were evaluated using a microarray, which indicated that cyclin‑dependent kinase 1, insulin, aurora kinase A, cyclin B1 and DNA topoisomerase II alpha underlaid these differential effects. Therefore, these results demonstrated that G‑SCs promoted bone invasion in OSCC by activating osteoclasts on the bone surface, whereas P‑SCs exerted an inhibitory effect. These findings could indicate a potential regulatory mechanism for bone invasion in OSCC.
en-copyright=
kn-copyright=

en-aut-name=ShanQiusheng
en-aut-sei=Shan
en-aut-mei=Qiusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakabatakeKiyofumi
en-aut-sei=Takabatake
en-aut-mei=Kiyofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OmoriHaruka
en-aut-sei=Omori
en-aut-mei=Haruka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OoMay Wathone
en-aut-sei=Oo
en-aut-mei=May Wathone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SukegawaShintaro
en-aut-sei=Sukegawa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujiiMasae
en-aut-sei=Fujii
en-aut-mei=Masae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=InadaYasunori
en-aut-sei=Inada
en-aut-mei=Yasunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SanoSho
en-aut-sei=Sano
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakanoKeisuke
en-aut-sei=Nakano
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NagatsukaHitoshi
en-aut-sei=Nagatsuka
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=oral squamous cell carcinoma
kn-keyword=oral squamous cell carcinoma
en-keyword=bone invasion
kn-keyword=bone invasion
en-keyword=gingival ligament tissue‑derived stromal cell
kn-keyword=gingival ligament tissue‑derived stromal cell
en-keyword=periodontal ligament tissue‑derived stromal cell
kn-keyword=periodontal ligament tissue‑derived stromal cell
en-keyword=xenograft model
kn-keyword=xenograft model
en-keyword=microarray
kn-keyword=microarray
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=4
article-no=
start-page=81
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220224
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Significance of cancer stroma for bone destruction in oral squamous cell carcinoma using different cancer stroma subtypes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Stromal cells in the tumor microenvironment (TME) can regulate the progression of numerous types of cancer; however, the bone invasion of oral squamous cell carcinoma (OSCC) has been poorly investigated. In the present study, the effect of verrucous SCC‑associated stromal cells (VSCC‑SCs), SCC‑associated stromal cells (SCC‑SCs) and human dermal fibroblasts on bone resorption and the activation of HSC‑3 osteoclasts in vivo were examined by hematoxylin and eosin, AE1/3 (pan‑cytokeratin) and tartrate‑resistant acid phosphatase staining. In addition, the expression levels of matrix metalloproteinase (MMP)9, membrane‑type 1 MMP (MT1‑MMP), Snail, receptor activator of NF‑κB ligand (RANKL) and parathyroid hormone‑related peptide (PTHrP) in the bone invasion regions of HSC‑3 cells were examined by immunohistochemistry. The results suggested that both SCC‑SCs and VSCC‑SCs promoted bone resorption, the activation of osteoclasts, and the expression levels of MMP9, MT1‑MMP, Snail, RANKL and PTHrP. However, SCC‑SCs had a more prominent effect compared with VSCC‑SCs. Finally, microarray data were used to predict potential genes underlying the differential effects of VSCC‑SCs and SCC‑SCs on bone invasion in OSCC. The results revealed that IL1B, ICAM1, FOS, CXCL12, INS and NGF may underlie these differential effects. In conclusion, both VSCC‑SCs and SCC‑SCs may promote bone invasion in OSCC by enhancing the expression levels of RANKL in cancer and stromal cells mediated by PTHrP; however, SCC‑SCs had a more prominent effect. These findings may represent a potential regulatory mechanism underlying the bone invasion of OSCC.
en-copyright=
kn-copyright=

en-aut-name=ShanQiusheng
en-aut-sei=Shan
en-aut-mei=Qiusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakabatakeKiyofumi
en-aut-sei=Takabatake
en-aut-mei=Kiyofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OoMay Wathone
en-aut-sei=Oo
en-aut-mei=May Wathone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InadaYasunori
en-aut-sei=Inada
en-aut-mei=Yasunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SukegawaShintaro
en-aut-sei=Sukegawa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FushimiShigeko
en-aut-sei=Fushimi
en-aut-mei=Shigeko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakanoKeisuke
en-aut-sei=Nakano
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NagatsukaHitoshi
en-aut-sei=Nagatsuka
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Surgery, Kagawa Prefectural Central Hospital
kn-affil=

affil-num=7
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Oral Pathology and Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=oral squamous cell carcinoma
kn-keyword=oral squamous cell carcinoma
en-keyword=bone invasion
kn-keyword=bone invasion
en-keyword=osteoclast
kn-keyword=osteoclast
en-keyword=receptor activator of NF‑κB ligand
kn-keyword=receptor activator of NF‑κB ligand
en-keyword=parathyroid hormone‑related peptide
kn-keyword=parathyroid hormone‑related peptide
en-keyword=microarray
kn-keyword=microarray
en-keyword=cancer‑associated stromal cells
kn-keyword=cancer‑associated stromal cells
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20050930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ピロリジン環を主鎖に含むコンホメーション的に制約されたペプチド核酸
kn-title=Conformationally-restricted peptide nucleic acids with pyrrolidine rings in the main chains
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=北松瑞生
kn-aut-sei=北松
kn-aut-mei=瑞生
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=334
cd-vols=
no-issue=
article-no=
start-page=199155
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202309
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exploration of the yadokari/yadonushi nature of YkV3 and RnMBV3 in the original host and a model filamentous fungus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The yadokari/yadonushi nature is a recently discovered virus lifestyle; “yadokari” refers to the ability of capsidless positive-sense (+) RNA viruses (yadokariviruses) to utilize the capsids of phylogenetically distant double-stranded RNA (dsRNA) viruses possibly as the replication site, while “yadonushi” refers to the ability of dsRNA viruses to provide capsids to yadokariviruses. This virus–virus interaction, however, has been only studied with limited pathosystems. Here, we established a new study model with a capsidless (+)RNA yadokarivirus YkV3 (family Yadokariviridae) and its capsid donor RnMBV3 (family Megabirnaviridae) in the original host fungus Rosellinia necatrix and a model filamentous fungal host Cryphonectria parasitica. YkV3 has a simple genome structure with one open reading frame of 4305 nucleotides encoding a single polyprotein with an RNA-dependent RNA polymerase and a 2A-like self-cleavage peptide domain. Reverse genetics of YkV3 in R. necatrix showed that YkV3 tolerates a nucleotide substitution in the extreme 5′-terminus. The insertion of two termination codons immediately downstream of the 2A-like cleavage site abolished YkV3 viability, suggesting the importance of the C-terminal portion of the polyprotein of unknown function. Transfection of RnMBV3 and YkV3 into an RNA silencing-deficient mutant Δdcl2 of C. parasitica showed the replication competency of both viruses. Comparison between the wild-type and Δdcl2 strains of C. parasitica in virus accumulation suggested that RnMBV3 and YkV3 are susceptible to RNA silencing in C. parasitica. Taken together, we have established a platform to further explore the yadokari/yadonushi nature using genetically manipulable host fungal and virus strains.
en-copyright=
kn-copyright=

en-aut-name=SatoYukiyo
en-aut-sei=Sato
en-aut-mei=Yukiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HisanoSakae
en-aut-sei=Hisano
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Virus-virus interaction
kn-keyword=Virus-virus interaction
en-keyword=RNA viruses
kn-keyword=RNA viruses
en-keyword=Capsidless
kn-keyword=Capsidless
en-keyword=Fungal viruses
kn-keyword=Fungal viruses
en-keyword=Plant pathogenic fungi
kn-keyword=Plant pathogenic fungi
en-keyword=Yadokarivirus
kn-keyword=Yadokarivirus
en-keyword=Megabirnavirus
kn-keyword=Megabirnavirus
en-keyword=Reverse genetics
kn-keyword=Reverse genetics
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=4
article-no=
start-page=395
end-page=405
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association of Tumor Necrosis Factor-Alpha with Psychopathology in Patients with Schizophrenia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated the relationship between serum tumor necrosis factor-alpha (TNF-α) levels and psychopathological symptoms, clinical and socio-demographic characteristics and antipsychotic therapy in individuals with schizophrenia. TNF-α levels were measured in 90 patients with schizophrenia and 90 healthy controls matched by age, gender, smoking status, and body mass index. The Positive and Negative Syndrome Scale (PANSS) was used to assess the severity of psychopathology in patients. No significant differences in TNF-α levels were detected between the patients and controls (p=0.736). TNF-α levels were not correlated with total, positive, negative, general, or composite PANSS scores (all p>0.05). A significant negative correlation was observed between TNF-α levels and the PANSS cognitive factor (ρ=−0.222, p=0.035). A hierarchical regression analysis identified the cognitive factor as a significant predictor of the TNF-α level (beta=−0.258, t=−2.257, p=0.027). There were no significant differences in TNF-α levels among patients treated with different types of antipsychotics (p=0.596). TNF-α levels correlated positively with the age of onset (ρ=0.233, p=0.027) and negatively with illness duration (ρ=−0.247, p=0.019) and antipsychotic treatment duration (ρ=−0.256, p=0.015). These results indicate that TNF-α may be involved in cognitive impairment in schizophrenia, and would be a potential clinical-state marker in schizophrenia.
en-copyright=
kn-copyright=

en-aut-name=PavlovicMarko
en-aut-sei=Pavlovic
en-aut-mei=Marko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BabicDragan
en-aut-sei=Babic
en-aut-mei=Dragan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=RastovicPejana
en-aut-sei=Rastovic
en-aut-mei=Pejana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArapovicJurica
en-aut-sei=Arapovic
en-aut-mei=Jurica
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MartinacMarko
en-aut-sei=Martinac
en-aut-mei=Marko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JakovacSanja
en-aut-sei=Jakovac
en-aut-mei=Sanja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BarbaricRomana
en-aut-sei=Barbaric
en-aut-mei=Romana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=2
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=3
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=4
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=5
en-affil=Health Care Center Mostar, University of Mostar
kn-affil=

affil-num=6
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=

affil-num=7
en-affil=University Hospital Center Mostar, University of Mostar
kn-affil=
en-keyword=tumor necrosis factor-alpha
kn-keyword=tumor necrosis factor-alpha
en-keyword=schizophrenia
kn-keyword=schizophrenia
en-keyword=psychopathology
kn-keyword=psychopathology
en-keyword=immune system
kn-keyword=immune system
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=4
article-no=
start-page=359
end-page=364
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Changes in TRPV1 Receptor, CGRP, and BDNF Expression in Rat Dorsal Root Ganglion with Resiniferatoxin-Induced Neuropathic Pain: Modulation by Pulsed Radiofrequency Applied to the Sciatic Nerve
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulsed radiofrequency (PRF) is a safe method of treating neuropathic pain by generating intermittent electric fields at the needle tip. Resiniferatoxin (RTX) is an ultrapotent agonist of transient receptor potential vanilloid subtype-1 (TRPV1) receptors. We investigated the mechanism of PRF using a rat model of RTX-induced neuropathic pain. After administering RTX intraperitoneally, PRF was applied to the right sciatic nerve. We observed the changes in TRPV1, calcitonin gene-related peptide (CGRP), and brain-derived neurotrophic factor (BDNF) in the dorsal root ganglia by western blotting. Expressions of TRPV1 and CGRP were significantly lower in the contralateral (RTX-treated, PRF-untreated) tissue than in control rats (p<0.0001 and p<0.0001, respectively) and the ipsilateral tissues (p<0.0001 and p<0.0001, respectively). BDNF levels were significantly higher in the contralateral tissues than in the control rats (p<0.0001) and the ipsilateral tissues (p<0.0001). These results suggest that, while TRPV1 and CGRP are decreased by RTX-induced neuronal damage, increased BDNF levels result in pain development. PRF may promote recovery from neuronal damage with concomitant restoration of TRPV1 and CGRP, and exert its analgesic effect by reversing BDNF increase. Further research is required to understand the role of TRPV1 and CGRP restoration in improving mechanical allodynia.
en-copyright=
kn-copyright=

en-aut-name=KoshidaTomohiro
en-aut-sei=Koshida
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MarutaToyoaki
en-aut-sei=Maruta
en-aut-mei=Toyoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TanakaNobuhiko
en-aut-sei=Tanaka
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HidakaKotaro
en-aut-sei=Hidaka
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KurogiMio
en-aut-sei=Kurogi
en-aut-mei=Mio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NemotoTakayuki
en-aut-sei=Nemoto
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YanagitaToshihiko
en-aut-sei=Yanagita
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakeyaRyu
en-aut-sei=Takeya
en-aut-mei=Ryu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsuneyoshiIsao
en-aut-sei=Tsuneyoshi
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=2
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=3
en-affil=Tanaka homecare clinic
kn-affil=

affil-num=4
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=5
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=6
en-affil=Department of Pharmacology, Faculty of Medicine, Fukuoka University
kn-affil=

affil-num=7
en-affil=Department of Clinical Pharmacology, School of Nursing, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=8
en-affil=Department of Pharmacology, Faculty of Medicine, University of Miyazaki
kn-affil=

affil-num=9
en-affil=Department of Anesthesiology and Pain Clinic, Faculty of Medicine, University of Miyazaki
kn-affil=
en-keyword=pulsed radiofrequency
kn-keyword=pulsed radiofrequency
en-keyword=resiniferatoxin
kn-keyword=resiniferatoxin
en-keyword=transient receptor potential vanilloid subtype-1 (TRPV1)
kn-keyword=transient receptor potential vanilloid subtype-1 (TRPV1)
en-keyword=calcitonin gene-related peptide (CGRP)
kn-keyword=calcitonin gene-related peptide (CGRP)
en-keyword=brain-derived neurotrophic factor (BDNF)
kn-keyword=brain-derived neurotrophic factor (BDNF)
END

start-ver=1.4
cd-journal=joma
no-vol=35
cd-vols=
no-issue=9
article-no=
start-page=e13324
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230716
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neuropeptidergic control circuits in the spinal cord for male sexual behaviour: Oxytocin–gastrin‐releasing peptide systems
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The neuropeptidergic mechanisms controlling socio-sexual behaviours consist of complex neuronal circuitry systems in widely distributed areas of the brain and spinal cord. At the organismal level, it is now becoming clear that “hormonal regulations” play an important role, in addition to the activation of neuronal circuits. The gastrin-releasing peptide (GRP) system in the lumbosacral spinal cord is an important component of the neural circuits that control penile reflexes in rats, circuits that are commonly referred to as the “spinal ejaculation generator (SEG).” Oxytocin, long known as a neurohypophyseal hormone, is now known to be involved in the regulation of socio-sexual behaviors in mammals, ranging from social bonding to empathy. However, the functional interaction between the SEG neurons and the hypothalamo-spinal oxytocin system remains unclear. Oxytocin is known to be synthesised mainly in hypothalamic neurons and released from the posterior pituitary into the circulation. Oxytocin is also released from the dendrites of the neurons into the hypothalamus where they have important roles in social behaviours via non-synaptic volume transmission. Because the most familiar functions of oxytocin are to regulate female reproductive functions including parturition, milk ejection, and maternal behaviour, oxytocin is often thought of as a “feminine” hormone. However, there is evidence that a group of parvocellular oxytocin neurons project to the lower spinal cord and control male sexual function in rats. In this report, we review the functional interaction between the SEG neurons and the hypothalamo-spinal oxytocin system and effects of these neuropeptides on male sexual behaviour. Furthermore, we discuss the finding of a recently identified, localised “volume transmission” role of oxytocin in the spinal cord. Findings from our studies suggest that the newly discovered “oxytocin-mediated spinal control of male sexual function” may be useful in the treatment of erectile and ejaculatory dysfunction.
en-copyright=
kn-copyright=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=gastrin-releasing peptide
kn-keyword=gastrin-releasing peptide
en-keyword=male sexual function
kn-keyword=male sexual function
en-keyword=non-synaptic volume transmission
kn-keyword=non-synaptic volume transmission
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=spinal cord
kn-keyword=spinal cord
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=14
article-no=
start-page=11768
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230721
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of Hydrophobic Cell-Penetrating Stapled Peptides as Drug Carriers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cell-penetrating peptides (CPPs) are widely used for the intracellular delivery of a variety of cargo molecules, including small molecules, peptides, nucleic acids, and proteins. Many cationic and amphiphilic CPPs have been developed; however, there have been few reports regarding hydrophobic CPPs. Herein, we have developed stapled hydrophobic CPPs based on the hydrophobic CPP, TP10, by introducing an aliphatic carbon side chain on the hydrophobic face of TP10. This side chain maintained the hydrophobicity of TP10 and enhanced the helicity and cell penetrating efficiency. We evaluated the preferred secondary structures, and the ability to deliver 5(6)-carboxyfluorescein (CF) as a model small molecule and plasmid DNA (pDNA) as a model nucleotide. The stapled peptide F-3 with CF, in which the stapling structure was introduced at Gly residues, formed a stable & alpha;-helical structure and the highest cell-membrane permeability via an endocytosis process. Meanwhile, peptide F-4 demonstrated remarkable stability when forming a complex with pDNA, making it the optimal choice for the efficient intracellular delivery of pDNA. The results showed that stapled hydrophobic CPPs were able to deliver small molecules and pDNA into cells, and that different stapling positions in hydrophobic CPPs can control the efficiency of the cargo delivery.
en-copyright=
kn-copyright=

en-aut-name=TsuchiyaKeisuke
en-aut-sei=Tsuchiya
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HorikoshiKanako
en-aut-sei=Horikoshi
en-aut-mei=Kanako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujitaMinami
en-aut-sei=Fujita
en-aut-mei=Minami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HiranoMotoharu
en-aut-sei=Hirano
en-aut-mei=Motoharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyamotoMaho
en-aut-sei=Miyamoto
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YokooHidetomo
en-aut-sei=Yokoo
en-aut-mei=Hidetomo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DemizuYosuke
en-aut-sei=Demizu
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=2
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=3
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=4
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=5
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=6
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=7
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cell-penetrating peptide
kn-keyword=cell-penetrating peptide
en-keyword=stapled peptide
kn-keyword=stapled peptide
en-keyword=hydrophobic peptide
kn-keyword=hydrophobic peptide
en-keyword=helical structure
kn-keyword=helical structure
en-keyword=plasmid DNA delivery
kn-keyword=plasmid DNA delivery
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=13
article-no=
start-page=2941
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230628
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Adrenomedullin Enhances Mouse Gustatory Nerve Responses to Sugars via T1R-Independent Sweet Taste Pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=On the tongue, the T1R-independent pathway (comprising glucose transporters, including sodium-glucose cotransporter (SGLT1) and the K-ATP channel) detects only sugars, whereas the T1R-dependent (T1R2/T1R3) pathway can broadly sense various sweeteners. Cephalic-phase insulin release, a rapid release of insulin induced by sensory signals in the head after food-related stimuli, reportedly depends on the T1R-independent pathway, and the competitive sweet taste modulators leptin and endocannabinoids may function on these two different sweet taste pathways independently, suggesting independent roles of two oral sugar-detecting pathways in food intake. Here, we examined the effect of adrenomedullin (ADM), a multifunctional regulatory peptide, on sugar sensing in mice since it affects the expression of SGLT1 in rat enterocytes. We found that ADM receptor components were expressed in T1R3-positive taste cells. Analyses of chorda tympani (CT) nerve responses revealed that ADM enhanced responses to sugars but not to artificial sweeteners and other tastants. Moreover, ADM increased the apical uptake of a fluorescent D-glucose derivative into taste cells and SGLT1 mRNA expression in taste buds. These results suggest that the T1R-independent sweet taste pathway in mouse taste cells is a peripheral target of ADM, and the specific enhancement of gustatory nerve responses to sugars by ADM may contribute to caloric sensing and food intake.
en-copyright=
kn-copyright=

en-aut-name=IwataShusuke
en-aut-sei=Iwata
en-aut-mei=Shusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakaiShingo
en-aut-sei=Takai
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SanematsuKeisuke
en-aut-sei=Sanematsu
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShigemuraNoriatsu
en-aut-sei=Shigemura
en-aut-mei=Noriatsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=

affil-num=4
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=

affil-num=5
en-affil=Section of Oral Neuroscience, Graduate School of Dental Science, Kyushu University
kn-affil=

affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=taste
kn-keyword=taste
en-keyword=sweet taste
kn-keyword=sweet taste
en-keyword=taste receptor family 1 members 2 and 3
kn-keyword=taste receptor family 1 members 2 and 3
en-keyword=sodium-glucose cotransporter 1
kn-keyword=sodium-glucose cotransporter 1
en-keyword=adrenomedullin
kn-keyword=adrenomedullin
en-keyword=caloric sensing
kn-keyword=caloric sensing
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230327
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prevalence of transthyretin amyloidosis among heart failure patients with preserved ejection fraction in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims Heart failure with preserved ejection fraction (HFpEF), which is caused by wide various conditions, has become a major public health problem. Transthyretin amyloid cardiomyopathy (ATTR-CM), which is thought to be an underdiagnosed disease, can cause HFpEF. Non-invasive diagnosis using 99mTechnetium (Tc)-pyrophosphate (PYP) scintigraphy enables accurate diagnosis of ATTR-CM. The aim of this study was to clarify the prevalence and characteristics of ATTR-CM among Japanese patients with HFpEF.<br>
Methods and results This study was a multicentre, prospective, observational study conducted in Japan. We enrolled 373 patients with HFpEF [left ventricular (LV) ejection fraction ≥50%] aged ≥65 years who were admitted to the department of cardiology from September 2018 to January 2022. A 99mTc-PYP scintigraphy scan was performed during admission in all eligible patients. Cardiac 99mTc-PYP retention was graded according to a previously reported visual scale ranging from 0 to 3 points. The scan was considered positive when it revealed moderate-to-severe 99mTc-PYP uptake (Grade 2–3) in both ventricles. Patients were divided into ATTR-CM and non-ATTR-CM patients according to positive (Grade 2–3) or negative (Grade 0–1) 99mTc-PYP scintigraphy, respectively. Medical history, blood tests, electrocardiogram, echocardiography, and magnetic resonance imaging in the two groups of patients were compared. Among the 373 patients with HFpEF, 53 patients (14.2%; 95% confidence interval: 10.7–17.7) showed positive uptake on 99mTc-PYP scintigraphy. An endomyocardial biopsy was performed in 32 patients and confirmed amyloidosis in all cases. There were no significant differences between the two groups in age, severity of heart failure as assessed by the New York Heart Association (NYHA) functional classification, renal function values, left ventricular ejection fraction, and tricuspid regurgitant pressure gradient (ATTR-CM, n = 53 vs. non-ATTR-CM, n = 320). Patients in the ATTR-CM group had a higher N-terminal pro-brain natriuretic peptide level [2314 (1081–3398) vs. 900 (415–1828), P < 0.001], higher sensitive troponin T level (0.074 ± 0.049 vs. 0.035 ± 0.038, P < 0.001), and higher mean LV maximal wall thickness [12.5 (11–14) vs. 10.5 (9.5–11.5), P < 0.001].<br>
Conclusions ATTR-CM is an underdiagnosed disease with a significant prevalence in Japanese patients with HFpEF. This study showed that results of examinations for ATTR-CM patients appear to be worse than those for non-ATTR-CM patients, but clinical severities of heart failure as assessed by the NYHA functional classification are similar in ATTR-CM and non-ATTR-CM patients, and the clinical overlap between ATTR-CM and non-ATTR-CM is high.
en-copyright=
kn-copyright=

en-aut-name=NaitoTakanori
en-aut-sei=Naito
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AbeYukio
en-aut-sei=Abe
en-aut-mei=Yukio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeHiroyuki
en-aut-sei=Watanabe
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatayamaYusuke
en-aut-sei=Katayama
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkizakiAtsutaka
en-aut-sei=Okizaki
en-aut-mei=Atsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FujioHideki
en-aut-sei=Fujio
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OtsukaHiroaki
en-aut-sei=Otsuka
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OguraSoichiro
en-aut-sei=Ogura
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ATTR HFpEF Registry Investigators
en-aut-sei=ATTR HFpEF Registry Investigators
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiology, Osaka City General Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Tokyo Bay Urayasu Ichikawa Medical Center
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, National Hospital Organization Iwakuni Clinical Center
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, National Hospital Organization Iwakuni Clinical Center
kn-affil=

affil-num=7
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=8
en-affil=Department of Radiology, Asahikawa Medical University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Fukuyama City Hospital
kn-affil=

affil-num=11
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Society Himeji Hospital
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, National Hospital Organization Iwakuni Clinical Center
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=
kn-affil=
en-keyword=Transthyretin amyloidosis
kn-keyword=Transthyretin amyloidosis
en-keyword=Heart failure
kn-keyword=Heart failure
en-keyword=Scintigraphy
kn-keyword=Scintigraphy
en-keyword=Left ventricular hypertrophy
kn-keyword=Left ventricular hypertrophy
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=3
article-no=
start-page=454
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230131
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Pursuit of the "Inside" of the Amyloid Hypothesis-Is C99 a Promising Therapeutic Target for Alzheimer's Disease?
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aducanumab, co-developed by Eisai (Japan) and Biogen (U.S.), has received Food and Drug Administration approval for treating Alzheimer's disease (AD). In addition, its successor antibody, lecanemab, has been approved. These antibodies target the aggregated form of the small peptide, amyloid-beta (A beta), which accumulates in the patient brain. The "amyloid hypothesis " based therapy that places the aggregation and toxicity of A beta at the center of the etiology is about to be realized. However, the effects of immunotherapy are still limited, suggesting the need to reconsider this hypothesis. A beta is produced from a type-I transmembrane protein, A beta precursor protein (APP). One of the APP metabolites, the 99-amino acids C-terminal fragment (C99, also called beta CTF), is a direct precursor of A beta and accumulates in the AD patient's brain to demonstrate toxicity independent of A beta. Conventional drug discovery strategies have focused on A beta toxicity on the "outside " of the neuron, but C99 accumulation might explain the toxicity on the "inside " of the neuron, which was overlooked in the hypothesis. Furthermore, the common region of C99 and A beta is a promising target for multifunctional AD drugs. This review aimed to outline the nature, metabolism, and impact of C99 on AD pathogenesis and discuss whether it could be a therapeutic target complementing the amyloid hypothesis.
en-copyright=
kn-copyright=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KomaiMasato
en-aut-sei=Komai
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KaneshiroNanaka
en-aut-sei=Kaneshiro
en-aut-mei=Nanaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaAtsuya
en-aut-sei=Ikeda
en-aut-mei=Atsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KamikuboYuji
en-aut-sei=Kamikubo
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Biomedical Sciences, School of Medicine, University of California
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer's disease
kn-keyword=Alzheimer's disease
en-keyword=amyloid-beta
kn-keyword=amyloid-beta
en-keyword=amyloid beta precursor protein
kn-keyword=amyloid beta precursor protein
en-keyword=BACE1
kn-keyword=BACE1
en-keyword=C99
kn-keyword=C99
en-keyword=endolysosome
kn-keyword=endolysosome
en-keyword=autolysosome
kn-keyword=autolysosome
en-keyword=vesicular trafficking
kn-keyword=vesicular trafficking
END

start-ver=1.4
cd-journal=joma
no-vol=112
cd-vols=
no-issue=
article-no=
start-page=19
end-page=22
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Sexual Dimorphism of Arginine Vasotocin Neuron in Birds
kn-title=鳥類におけるアルギニンバソトシン神経の性差
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Arginine vasotocin (AVT) is one of neurohypophysial peptides in birds and is well known both as an antidiuretic and oxytocic hormone. AVT is produced in the hypothalamus and mainly synthesized in magnocellular neurons, supraoptic nucleus (SON) and paraventricular nucleus (PVN). Recent, immunocytochemistry and in situ hybridization results indicate that AVT is also synthesized in parvocellular neurons corresponding to mammalian stria terminalis (nST). The AVT neurons in nST in the male are more numerous than those in the female. Therefore, these data suggest that there is sexual dimorphism in the distribution of AVT neurons. Several experiments involving electrical lesion, testosterone implantation, and the detection of the immediately-early gene expression in birds expressing copulatory behavior suggested that nST and nucleus praeopticus medialis (POM) were related to the reproductive behavior. When male embryo was treated with estradiol, the distribution of AVT neurons assumes the same distribution as found in the female, and reproductive behavior was abolished, suggesting that AVT in the brain has an important role in reproductive behavior.
en-copyright=
kn-copyright=

en-aut-name=SaitoNoboru
en-aut-sei=Saito
en-aut-mei=Noboru
kn-aut-name=齋藤昇
kn-aut-sei=齋藤
kn-aut-mei=昇
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Course of Applied Animal Science
kn-affil=応用動物科学コース
en-keyword=arginine vasotocin
kn-keyword=arginine vasotocin
en-keyword=sexual dimorphism
kn-keyword=sexual dimorphism
en-keyword=reproductive behavior
kn-keyword=reproductive behavior
en-keyword=parvocellular neurons
kn-keyword=parvocellular neurons
en-keyword=bird
kn-keyword=bird
END

start-ver=1.4
cd-journal=joma
no-vol=261
cd-vols=
no-issue=
article-no=
start-page=114087
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oxytocin increased intragastric pressure in the forestomach of rats via the dorsal vagal complex
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously reported that appetite enhancing peptides facilitated phasic contractions of the distal stomach and relaxed the forestomach via the dorsal vagal complex (DVC). The present study investigated the effects of anorectic substances on gastric reservoir function. The effects of oxytocin on the motility of the forestomach were examined in rats anesthetized with urethane chloralose. Gastric motor responses were measured using an intragastric balloon. The fourth ventricular administration of oxytocin (0.1 1.0 nmol) increased intragastric pressure (IGP) in the forestomach in a dose dependent manner. Conversely, the administration of oxytocin (0.3 nmol) suppressed phasic contractions of the distal stomach. These responses were opposite to those of appetite enhancing peptides in previous studies. The oxytocin response in the forestomach was not observed after bilateral cervical vagotomy. The effects of oxytocin on forestomach motility were examined in animals that underwent ablation of the area postrema (AP) to clarify its involvement. Although the magnitude of the response to the fourth ventricular administration of oxytocin decreased, a significant response was still observed. A microinjection of oxytocin (3 pmol) into the AP, the left medial nucleus of the nucleus tractus solitarius (mNTS), the left commissural part of the NTS, or the left dorsal motor nucleus of the vagus was performed. The oxytocin injection into the AP and/or mNTS induced a rapid and large increase in IGP in the forestomach. Prior injection of L-368,899, an oxytocin receptor antagonist, into both the AP and mNTS attenuated the oxytocin response of the forestomach induced by fourth ventricular administration of oxytocin. These results indicate that oxytocin acts on the AP and/or mNTS to increase IGP in the forestomach via vagal preganglionic neurons.
en-copyright=
kn-copyright=

en-aut-name=KobashiMotoi
en-aut-sei=Kobashi
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShimataniYuichi
en-aut-sei=Shimatani
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujitaMasako
en-aut-sei=Fujita
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medical Engineering, Faculty of Engineering, Tokyo City University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=motility
kn-keyword=motility
en-keyword=area postrema
kn-keyword=area postrema
en-keyword=forestomach
kn-keyword=forestomach
en-keyword=nucleus tractus solitarius
kn-keyword=nucleus tractus solitarius
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=50
article-no=
start-page=46573
end-page=46582
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221220
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oligoarginine-Conjugated Peptide Foldamers Inhibiting Vitamin D Receptor-Mediated Transcription
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The vitamin D receptor (VDR) is a nuclear receptor, which is involved in several physiological processes, including differentiation and bone homeostasis. The VDR is a promising target for the development of drugs against cancer and bone-related diseases. To date, several VDR antagonists, which bind to the ligand binding domain of the VDR and compete with the endogenous agonist 1 alpha,25(OH)D3, have been reported. However, these ligands contain a secosteroidal skeleton, which is chemically unstable and complicated to synthesize. A few VDR antagonists with a nonsecosteroidal skeleton have been reported. Alternative inhibitors against VDR transactivation that act via different mechanisms are desirable. Here, we developed peptide-based VDR inhibitors capable of disrupting the VDR-coactivator interaction. It was reported that helical SRC2-3 peptides strongly bound to the VDR and competed with the coactivator in vitro. Therefore, we designed and synthesized a series of SRC2-3 derivatives by the introduction of nonproteinogenic amino acids, such as beta-amino acids, and by side-chain stapling to stabilize helical structures and provide resistance against digestive enzymes. In addition, conjugation with a cell-penetrating peptide increased the cell membrane permeability and was a promising strategy for intracellular VDR inhibition. The nona-arginine-conjugated peptides 24 with side-chain stapling and 25 with cyclic beta-amino acids showed strong intracellular VDR inhibitory activity, resulting in suppression of the target gene expression and inhibition of the cell differentiation of HL-60 cells. Herein, the peptide design, structure-activity relationship (SAR) study, and biological evaluation of the peptides are described.
en-copyright=
kn-copyright=

en-aut-name=TakyoMami
en-aut-sei=Takyo
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SatoYumi
en-aut-sei=Sato
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HirataNaoya
en-aut-sei=Hirata
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsuchiyaKeisuke
en-aut-sei=Tsuchiya
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IshidaHiroaki
en-aut-sei=Ishida
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KuroharaTakashi
en-aut-sei=Kurohara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YanaseYuta
en-aut-sei=Yanase
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ItoTakahito
en-aut-sei=Ito
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KandaYasunari
en-aut-sei=Kanda
en-aut-mei=Yasunari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamamotoKeiko
en-aut-sei=Yamamoto
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MisawaTakashi
en-aut-sei=Misawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=DemizuYosuke
en-aut-sei=Demizu
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=2
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=3
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=4
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=5
en-affil=Laboratory of Drug Design and Medicinal Chemistry, Showa Pharmaceutical University
kn-affil=

affil-num=6
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=7
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=8
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=9
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=10
en-affil=Laboratory of Drug Design and Medicinal Chemistry, Showa Pharmaceutical University
kn-affil=

affil-num=11
en-affil=National Institute of Health Sciences
kn-affil=

affil-num=12
en-affil=National Institute of Health Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=3
article-no=
start-page=1059
end-page=1073
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221116
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The secreted immune response peptide 1 functions as a phytocytokine in rice immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Small signalling peptides play important roles in various plant processes, but information regarding their involvement in plant immunity is limited. We previously identified a novel small secreted protein in rice, called immune response peptide 1 (IRP1). Here, we studied the function of IRP1 in rice immunity. Rice plants overexpressing IRP1 enhanced resistance to the virulent rice blast fungus. Application of synthetic IRP1 to rice suspension cells triggered the expression of IRP1 itself and the defence gene phenylalanine ammonia-lyase 1 (PAL1). RNA-seq results revealed that 84% of genes up-regulated by IRP1, including 13 OsWRKY transcription factors, were also induced by a microbe-associated molecular pattern (MAMP), chitin, indicating that IRP1 and chitin share a similar signalling pathway. Co-treatment with chitin and IRP1 elevated the expression level of PAL1 and OsWRKYs in an additive manner. The increased chitin concentration arrested the induction of IRP1 and PAL1 expression by IRP1, but did not affect IRP1-triggered mitogen-activated protein kinases (MAPKs) activation. Collectively, our findings indicate that IRP1 functions as a phytocytokine in rice immunity regulating MAPKs and OsWRKYs that can amplify chitin and other signalling pathways, and provide new insights into how MAMPs and phytocytokines cooperatively regulate rice immunity.
en-copyright=
kn-copyright=

en-aut-name=WangPingyu
en-aut-sei=Wang
en-aut-mei=Pingyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=JiaHuimin
en-aut-sei=Jia
en-aut-mei=Huimin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GuoTing
en-aut-sei=Guo
en-aut-mei=Ting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZhangYuanyuan
en-aut-sei=Zhang
en-aut-mei=Yuanyuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangWanqing
en-aut-sei=Wang
en-aut-mei=Wanqing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NishimuraHideki
en-aut-sei=Nishimura
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=LiZhengguo
en-aut-sei=Li
en-aut-mei=Zhengguo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawanoYoji
en-aut-sei=Kawano
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Key Laboratory of Plant Hormones and Development Regulation of Chongqing, School of Life Sciences, Chongqing University
kn-affil=

affil-num=2
en-affil=Shanghai Center for Plant Stress Biology and Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=3
en-affil=Shanghai Center for Plant Stress Biology and Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=4
en-affil=Shanghai Center for Plant Stress Biology and Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=7
en-affil=Key Laboratory of Plant Hormones and Development Regulation of Chongqing, School of Life Sciences, Chongqing University
kn-affil=

affil-num=8
en-affil=Shanghai Center for Plant Stress Biology and Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=
en-keyword=Immunity
kn-keyword=Immunity
en-keyword=IRP1
kn-keyword=IRP1
en-keyword=pattern-triggered immunity
kn-keyword=pattern-triggered immunity
en-keyword=phytocytokine
kn-keyword=phytocytokine
en-keyword=Pyricularia oryzae
kn-keyword=Pyricularia oryzae
en-keyword=rice
kn-keyword=rice
END

start-ver=1.4
cd-journal=joma
no-vol=289
cd-vols=
no-issue=1985
article-no=
start-page=20221126
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221019
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Footedness for scratching itchy eyes in rodents
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The neural bases of itchy eye transmission remain unclear compared with those involved in body itch. Here, we show in rodents that the gastrin-releasing peptide receptor (GRPR) of the trigeminal sensory system is involved in the transmission of itchy eyes. Interestingly, we further demonstrate a difference in scratching behaviour between the left and right hindfeet in rodents; histamine instillation into the conjunctival sac of both eyes revealed right-foot biased laterality in the scratching movements. Unilateral histamine instillation specifically induced neural activation in the ipsilateral sensory pathway, with no significant difference between the activations following left- and right-eye instillations. Thus, the behavioural laterality is presumably due to right-foot preference in rodents. Genetically modified rats with specific depletion of Grpr-expressing neurons in the trigeminal sensory nucleus caudalis of the medulla oblongata exhibited fewer and shorter histamine-induced scratching movements than controls and eliminated the footedness. These results taken together indicate that the Grp-expressing neurons are required for the transmission of itch sensation from the eyes, but that foot preference is generated centrally. These findings could open up a new field of research on the mechanisms of the laterality in vertebrates and also offer new potential therapeutic approaches to refractory pruritic eye disorders.
en-copyright=
kn-copyright=

en-aut-name=KatayamaYukitoshi
en-aut-sei=Katayama
en-aut-mei=Yukitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiuraAyane
en-aut-sei=Miura
en-aut-mei=Ayane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakanamiKeiko
en-aut-sei=Takanami
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University, Ushimado, Setouchi
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University, Ushimado, Setouchi
kn-affil=

affil-num=3
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University, Ushimado, Setouchi
kn-affil=

affil-num=4
en-affil=Mouse Genomics Resources Laboratory, National Institute of Genetics, Yata, Mishima
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University, Ushimado, Setouchi
kn-affil=
en-keyword=itchy eyes
kn-keyword=itchy eyes
en-keyword=histamine
kn-keyword=histamine
en-keyword=gastrin-releasing peptide receptor
kn-keyword=gastrin-releasing peptide receptor
en-keyword=footedness
kn-keyword=footedness
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=6
article-no=
start-page=705
end-page=713
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Impact of Tofogliflozin on Physiological and Hormonal Function, Serum Electrolytes, and Cardiac Diastolic Function in Elderly Japanese Patients with Type 2 Diabetes Mellitus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The sodium glucose transporter 2 (SGLT2) inhibitor tofogliflozin is a glucose-lowering drug that causes the excretion of surplus glucose by inhibiting SGLT2. Because of tofogliflozin’s osmotic diuresis mechanism, patients’ serum electrolytes, body fluid levels, and cardiac function must be monitored. We retrospectively analyzed the cases of 64 elderly Japanese patients with type 2 diabetes mellitus (T2DM) who received tofogliflozin for 3 months. Their HbA1c, serum electrolytes (sodium, potassium, chloride), hematocrit, brain natriuretic peptide (cardiac volume load marker) and renin and aldosterone (RAA; an index of regulatory hormones involved in body fluid retention) were continuously monitored during the investigation period. Renal function and cardiac function (by echocardiography) were assessed throughout the period. HbA1c significantly decreased (β1=−0.341, p<0.0001, linear regression analysis [LRA]). Most of the hormonal, electrolyte, and physiological parameters were maintained throughout the study period. In these circumstances, E/e’ tended to decrease (β1=−0.382, p=0.13, LRA). Compared to the baseline, E/e’ was significantly decreased at 1 and 3 months (p<0.01, p<0.05). In the higher E/e’ group (E/e’≥10, n=34), E/e’ decreased significantly (β1=−0.63, p<0.05, LRA). ΔE/e’ was correlated with body-weight change during treatment (r=0.64, p<0.01). The 3-month tofogliflozin treatment improved glycemic control and diastolic function represented by E/e’ in T2DM patients, without affecting serum electrolytes, renal function, or RAA. No negative impacts on the patients were observed. Three-month tofogliflozin treatment lowered glucose and improved cardiac diastolic function.
en-copyright=
kn-copyright=

en-aut-name=HigashikawaToshihiro
en-aut-sei=Higashikawa
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ItoTomohiko
en-aut-sei=Ito
en-aut-mei=Tomohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MizunoTakurou
en-aut-sei=Mizuno
en-aut-mei=Takurou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshigamiKeiichiro
en-aut-sei=Ishigami
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KurokiKengo
en-aut-sei=Kuroki
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MaekawaNaoto
en-aut-sei=Maekawa
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UsudaDaisuke
en-aut-sei=Usuda
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IzumidaToshihide
en-aut-sei=Izumida
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamadaShinya
en-aut-sei=Yamada
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SangenRyusho
en-aut-sei=Sangen
en-aut-mei=Ryusho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HamadaKazu
en-aut-sei=Hamada
en-aut-mei=Kazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KiyosawaJun
en-aut-sei=Kiyosawa
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SaitoAtsushi
en-aut-sei=Saito
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=IguchiMasaharu
en-aut-sei=Iguchi
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KasamakiYuji
en-aut-sei=Kasamaki
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=NakahashiTakeshi
en-aut-sei=Nakahashi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=FukudaAkihiro
en-aut-sei=Fukuda
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SaitoHitoshi
en-aut-sei=Saito
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KandaTsugiyasu
en-aut-sei=Kanda
en-aut-mei=Tsugiyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=OkuroMasashi
en-aut-sei=Okuro
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=2
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=3
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=4
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=5
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=6
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=7
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=8
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=9
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=10
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=11
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=12
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=13
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=14
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=15
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=16
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=17
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=18
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=19
en-affil=Kanazawa Medical University Himi Municipal Hospital
kn-affil=

affil-num=20
en-affil=Department of Geriatric Medicine, Kanazawa Medical University
kn-affil=
en-keyword=tofogliflozin
kn-keyword=tofogliflozin
en-keyword=SGLT2 inhibitor
kn-keyword=SGLT2 inhibitor
en-keyword=elderly patient
kn-keyword=elderly patient
en-keyword=HbA1c
kn-keyword=HbA1c
en-keyword=cardiac diastolic function
kn-keyword=cardiac diastolic function
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=6
article-no=
start-page=625
end-page=633
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Knockdown of LncRNA SBF2-AS1 Inhibited Gastric Cancer Tumorigenesis via the Wnt/LRP5 Signaling Pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This investigation aimed to uncover the impact of a long noncoding RNA, SET-binding factor 2 antisense RNA1 (SBF2-AS1) on the malignant progression of gastric cancer (GC) and to further explore its underlying mechanism. SBF2-AS1 expression was quantified by qRT-PCR in GC cell lines and GC tissues. In vitro loss-of-function studies of SBF2-AS1, accompanied by flow cytometry, CCK-8, and cell invasion tests, were applied to elucidate the impact of SBF2-AS1 on the tumor progression of GC cells. Finally, Western blotting and a luciferase assay were used to detect WNT/LRP5 signaling pathway activation. SBF2-AS1 was aberrantly expressed in GC cell lines (p<0.05) and GC tissues (p<0.05). Cell invasive and proliferative capabilities were inhibited via SBF2-AS1 knockdown, resulting in apoptosis of NCI-N87 and MKN74 cells. Additionally, online database analysis uncovered a positive correlation between SBF2-AS1 and the Wnt/LRP5 signaling pathway (p<0.05). SBF2-AS1 knockdown blocked the Wnt/LRP5 signaling pathway, whereas the effects of SBF2-AS1 knockdown on the malignant genotype of MKN74 as well as NCI-N87 cells were partially restored by triggering the Wnt/ LRP5 signaling pathway. High expression of SBF2-AS1 was found in GC, the malignant progression of which was repressed via SBF2-AS1 knockdown by inhibiting the Wnt/LRP5 signaling pathway.
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=LiuZhisheng
kn-aut-sei=Liu
kn-aut-mei=Zhisheng
aut-affil-num=1
ORCID=

en-aut-name=LiQingmei
en-aut-sei=Li
en-aut-mei=Qingmei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangYe
en-aut-sei=Wang
en-aut-mei=Ye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=GeYunjie
en-aut-sei=Ge
en-aut-mei=Yunjie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of General surgery, Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine)
kn-affil=

affil-num=2
en-affil=Department of General surgery, Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine)
kn-affil=

affil-num=3
en-affil=Department of General surgery, Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine)
kn-affil=

affil-num=4
en-affil=Department of Healthcare Internal Medicine, Affiliated Qingdao Municipal Hospital of Qingdao University
kn-affil=
en-keyword=gastric cancer (GC)
kn-keyword=gastric cancer (GC)
en-keyword=SET-binding factor 2 antisense RNA1 (SBF2-AS1)
kn-keyword=SET-binding factor 2 antisense RNA1 (SBF2-AS1)
en-keyword=invasion
kn-keyword=invasion
en-keyword=proliferation
kn-keyword=proliferation
en-keyword=signaling
kn-keyword=signaling
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=5
article-no=
start-page=503
end-page=510
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202210
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Viral Sequences Are Repurposed for Controlling Antiviral Responses as Non-Retroviral Endogenous Viral Elements
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Eukaryotic genomes contain numerous copies of endogenous viral elements (EVEs), most of which are considered endogenous retrovirus (ERV) sequences. Over the past decade, non-retroviral endogenous viral elements (nrEVEs) derived from ancient RNA viruses have been discovered. Several functions have been proposed for these elements, including antiviral defense. This review summarizes the current understanding of nrEVEs derived from RNA viruses, particularly endogenous bornavirus-like elements (EBLs) and endogenous filovirus-like elements (EFLs). EBLs are one of the most extensively studied nrEVEs. The EBL derived from bornavirus nucleoprotein (EBLN) is thought to function as a non-coding RNA or protein that regulates host gene expression or inhibits virus propagation. Ebolavirus and marburgvirus, which are filoviruses, induce severe hemorrhagic fever in humans and nonhuman primates. Although the ecology of filoviruses remains unclear, bats are believed to be potential reservoirs. Based on the knowledge from EBLs, it is postulated that EFLs in the bat genome help to maintain the balance between filovirus infection and the bat’s defense system, which may partially explain why bats act as potential reservoirs. Further research into the functions of nrEVEs could reveal novel antiviral systems and inspire novel antiviral approaches.
en-copyright=
kn-copyright=

en-aut-name=OgawaHirohito
en-aut-sei=Ogawa
en-aut-mei=Hirohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HondaTomoyuki
en-aut-sei=Honda
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=EVE
kn-keyword=EVE
en-keyword=nrEVE
kn-keyword=nrEVE
en-keyword=bornavirus
kn-keyword=bornavirus
en-keyword=filovirus
kn-keyword=filovirus
en-keyword=antiviral
kn-keyword=antiviral
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=12
article-no=
start-page=241
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221022
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Second extracellular protease mediating maturation of Vibrio mimicus hemolysin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Vibrio mimicus is a bacterium that causes gastroenteritis in humans. This pathogen produces an enterotoxic hemolysin called V. mimicus hemolysin (VMH), which is secreted extracellularly as an inactive 80-kDa protoxin and converted to a 66-kDa mature toxin through cleavage between Arg(151) and Ser(152). The 56-kDa serine protease termed V. mimicus trypsin-like protease (VmtA) is known to mediate this maturating process. However, some strains including strain ES-20 does not possess the vmtA gene. In the present study, the vmtA-negative strains were found to have a replaced gene that encodes a 43-kDa (403 aa) precursor of a serine protease designated by VmtX (V. mimicus trypsin-like protease X). To examine whether VmtX is also involved in the maturation of VMH, VmtX was isolated from the culture supernatant of V. mimicus strain NRE-20, a metalloprotease-negative mutant constructed from strain ES-20. Concretely, the culture supernatant was fractionated with 70% saturated ammonium sulfate and subjected to affinity column chromatography using a HiTrap Benzamidine FF column. The analysis of the N-terminal amino acid sequences of the proteins in the obtained VmtX preparation indicated that the 39-kDa protein was active VmtX consisting of 371 aa (Ile(33)-Ser(403)). The VmtX preparation was found to activate pro-VMH through generation of the 66-kDa protein. Additionally, treatment of the VmtX preparation with serine protease inhibitors, such as leupeptin and phenylmethylsulfonyl fluoride, significantly suppressed the activities to hydrolyze the specific peptide substrate and to synthesize the 66-kDa toxin. These findings indicate that VmtX is the second protease that mediats the maturation of VMH.
en-copyright=
kn-copyright=

en-aut-name=MiyoshiShin-ichi
en-aut-sei=Miyoshi
en-aut-mei=Shin-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TokoNorie
en-aut-sei=Toko
en-aut-mei=Norie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DodoTetsuya
en-aut-sei=Dodo
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NankoAyako
en-aut-sei=Nanko
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MizunoTamaki
en-aut-sei=Mizuno
en-aut-mei=Tamaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Vibrio mimicus
kn-keyword=Vibrio mimicus
en-keyword=Serine protease
kn-keyword=Serine protease
en-keyword=Hemolysin
kn-keyword=Hemolysin
en-keyword=Maturation
kn-keyword=Maturation
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=1004184
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220915
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Time-series transcriptome of Brachypodium distachyon during bacterial flagellin-induced pattern-triggered immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plants protect themselves from microorganisms by inducing pattern-triggered immunity (PTI) via recognizing microbe-associated molecular patterns (MAMPs), conserved across many microbes. Although the MAMP perception mechanism and initial events during PTI have been well-characterized, knowledge of the transcriptomic changes in plants, especially monocots, is limited during the intermediate and terminal stages of PTI. Here, we report a time-series high-resolution RNA-sequencing (RNA-seq) analysis during PTI in the leaf disks of Brachypodium distachyon. We identified 6,039 differentially expressed genes (DEGs) in leaves sampled at 0, 0.5, 1, 3, 6, and 12 hours after treatment (hat) with the bacterial flagellin peptide flg22. The k-means clustering method classified these DEGs into 10 clusters (6 upregulated and 4 downregulated). Based on the results, we selected 10 PTI marker genes in B. distachyon. Gene ontology (GO) analysis suggested a tradeoff between defense responses and photosynthesis during PTI. The data indicated the recovery of photosynthesis started at least at 12 hat. Over-representation analysis of transcription factor genes and cis-regulatory elements in DEG promoters implied the contribution of 12 WRKY transcription factors in plant defense at the early stage of PTI induction.
en-copyright=
kn-copyright=

en-aut-name=OgasaharaTsubasa
en-aut-sei=Ogasahara
en-aut-mei=Tsubasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KouzaiYusuke
en-aut-sei=Kouzai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WatanabeMegumi
en-aut-sei=Watanabe
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakahashiAkihiro
en-aut-sei=Takahashi
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakahagiKotaro
en-aut-sei=Takahagi
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KimJune-Sik
en-aut-sei=Kim
en-aut-mei=June-Sik
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuiHidenori
en-aut-sei=Matsui
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoMikihiro
en-aut-sei=Yamamoto
en-aut-mei=Mikihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ToyodaKazuhiro
en-aut-sei=Toyoda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IchinoseYuki
en-aut-sei=Ichinose
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MochidaKeiichi
en-aut-sei=Mochida
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NoutoshiYoshiteru
en-aut-sei=Noutoshi
en-aut-mei=Yoshiteru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Kihara Institute for Biological Research, Yokohama City University
kn-affil=

affil-num=6
en-affil=Bioproductivity Informatics Research Team, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=11
en-affil=Bioproductivity Informatics Research Team, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=12
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Brachypodium distachyon
kn-keyword=Brachypodium distachyon
en-keyword=monocotyledonous plant
kn-keyword=monocotyledonous plant
en-keyword=microbe-associated molecular pattern
kn-keyword=microbe-associated molecular pattern
en-keyword=time-series transcriptome analysis
kn-keyword=time-series transcriptome analysis
en-keyword=reactive oxygen species
kn-keyword=reactive oxygen species
en-keyword=pattern-triggered immunity
kn-keyword=pattern-triggered immunity
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=11
article-no=
start-page=3322
end-page=3337
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220907
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=FE UPTAKE‐INDUCING PEPTIDE1 maintains Fe translocation by controlling Fe deficiency response genes in the vascular tissue of Arabidopsis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=FE UPTAKE-INDUCING PEPTIDE1 (FEP1), also named IRON MAN3 (IMA3) is a short peptide involved in the iron deficiency response in Arabidopsis thaliana. Recent studies uncovered its molecular function, but its physiological function in the systemic Fe response is not fully understood. To explore the physiological function of FEP1 in iron homoeostasis, we performed a transcriptome analysis using the FEP1 loss-of-function mutant fep1-1 and a transgenic line with oestrogen-inducible expression of FEP1. We determined that FEP1 specifically regulates several iron deficiency-responsive genes, indicating that FEP1 participates in iron translocation rather than iron uptake in roots. The iron concentration in xylem sap under iron-deficient conditions was lower in the fep1-1 mutant and higher in FEP1-induced transgenic plants compared with the wild type (WT). Perls staining revealed a greater accumulation of iron in the cortex of fep1-1 roots than in the WT root cortex, although total iron levels in roots were comparable in the two genotypes. Moreover, the fep1-1 mutation partially suppressed the iron overaccumulation phenotype in the leaves of the oligopeptide transporter3-2 (opt3-2) mutant. These data suggest that FEP1 plays a pivotal role in iron movement and in maintaining the iron quota in vascular tissues in Arabidopsis.
en-copyright=
kn-copyright=

en-aut-name=OkadaSatoshi
en-aut-sei=Okada
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LeiGui J.
en-aut-sei=Lei
en-aut-mei=Gui J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamajiNaoki
en-aut-sei=Yamaji
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HuangSheng
en-aut-sei=Huang
en-aut-mei=Sheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MaJian F.
en-aut-sei=Ma
en-aut-mei=Jian F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MochidaKeiichi
en-aut-sei=Mochida
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HirayamaTakashi
en-aut-sei=Hirayama
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Group of Environmental Stress Response Systems, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Group of Plant Stress Physiology, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Group of Plant Stress Physiology, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=4
en-affil=Group of Plant Stress Physiology, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=5
en-affil=Group of Plant Stress Physiology, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Crop Design Research Team, Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=7
en-affil=Group of Environmental Stress Response Systems, Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=oestrogen induction system
kn-keyword=oestrogen induction system
en-keyword=fep1-1
kn-keyword=fep1-1
en-keyword=iron-deficiency response
kn-keyword=iron-deficiency response
en-keyword=transcriptome
kn-keyword=transcriptome
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=8
article-no=
start-page=1722
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220804
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Transfectable Fusagravirus from a Japanese Strain of Cryphonectria carpinicola with Spherical Particles
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A novel dsRNA virus (Cryphonectria carpinicola fusagravirus 1, CcFGV1), isolated from a Japanese strain (JS13) of Cryphonectria carpinicola, was thoroughly characterized. The biological comparison of a set of isogenic CcFGV1-infected and -free (JS13VF) strains indicated asymptomatic infection by CcFGV1. The sequence analysis showed that the virus has a two open reading frame (ORF) genome of 9.6 kbp with the RNA-directed RNA polymerase domain encoded by ORF2. The N-terminal sequencing and peptide mass fingerprinting showed an N-terminally processed or degraded product (150 kDa) of the 5'-proximal ORF1-encoded protein (1462 amino acids) to make up the CcFGV1 spherical particles of similar to 40 nm in diameter. Interestingly, a portion of CcFGV1 dsRNA co-fractionated with a host protein of 70 kDa. The purified CcFGV1 particles were used to transfect protoplasts of JS13VF as well as the standard strain of an experimental model filamentous fungal host Cryphonectria parasitica. CcFGV1 was confirmed to be associated with asymptomatic infection of both fungi. RNA silencing was shown to target the virus in C. parasitica, resulting in reduced CcFGV1 accumulation by comparing the CcFGV1 content between RNA silencing-competent and -deficient strains. These results indicate the transfectability of spherical particles of a fusagravirus associated with asymptomatic infection.
en-copyright=
kn-copyright=

en-aut-name=DasSubha
en-aut-sei=Das
en-aut-mei=Subha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HisanoSakae
en-aut-sei=Hisano
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Eusebio-CopeAna
en-aut-sei=Eusebio-Cope
en-aut-mei=Ana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoHideki
en-aut-sei=Kondo
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Cryphonectria carpinicola
kn-keyword=Cryphonectria carpinicola
en-keyword=Cryphonectria parasitica
kn-keyword=Cryphonectria parasitica
en-keyword=fusagravirus
kn-keyword=fusagravirus
en-keyword=fungal virus
kn-keyword=fungal virus
en-keyword=dsRNA
kn-keyword=dsRNA
en-keyword=spherical virion
kn-keyword=spherical virion
en-keyword=transfection
kn-keyword=transfection
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=12353
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220719
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Treatment resistance of rheumatoid arthritis relates to infection of periodontal pathogenic bacteria: a case-control cross-sectional study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent studies have shown that periodontitis is associated with rheumatoid arthritis (RA) and periodontal bacteria, such as Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) are involved in the pathogenesis of RA via citrullinated proteins. Smoking has also been shown to be involved in the pathogenesis of RA; however, the extent of this involvement is still poorly understood. In addition, RA and polymyalgia rheumatica (PMR) are sometimes difficult to differentiate; however, the relationship between PMR and the factors from smoking and periodontal bacteria is unclear. The aim of this study was to clarify the relationship between periodontal pathogenic bacterial infections and smoking in patients with RA or PMR. This case-control study included 142 patients with untreated RA or PMR. This study evaluated the serum antibody titers against periodontal pathogenic bacterial antigens and an anti-citrullinated peptide antibody (ACPA). In patients with RA, the relationship between antibody titers and disease activity of RA and response after 3 months of treatment was also investigated. Additionally, the effects of smoking were evaluated. Although there was no significant difference in serum antibody titer against periodontal pathogenic bacteria between the ACPA-positive RA group and the ACPA-negative PMR group, we found an association between the elevated antibody titer against Pg and the degree of ACPA value, especially between negative group and high-value positive group (>= 100 U/mL). The antibody titers against Aa and Pg did not differ depending on disease activity score 28 (DAS28) at baseline; however, patients with high antibody titers had poor RA therapeutic response as judged by DAS28 after 3 months. We could not find any association between smoking and any of these parameters. Periodontal pathogenic bacteria, especially Pg, are associated with elevated ACPA levels. Our findings suggest that Pg and Aa infections interfere with the therapeutic response of RA.
en-copyright=
kn-copyright=

en-aut-name=Takeuchi-HatanakaKazu
en-aut-sei=Takeuchi-Hatanaka
en-aut-mei=Kazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KoyamaYoshinobu
en-aut-sei=Koyama
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkamotoKentaro
en-aut-sei=Okamoto
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakaidaKyosuke
en-aut-sei=Sakaida
en-aut-mei=Kyosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoTadashi
en-aut-sei=Yamamoto
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Center for Autoimmune Diseases, Division of Rheumatology, Japan Red Cross Okayama Hospital
kn-affil=

affil-num=3
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Periodontics and Endodontics, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Pathophysiology‑Periodontal Science, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Pathophysiology‑Periodontal Science, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220713
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Differences in extracellular fluid volume between acute heart failure patients with and without high systolic blood pressure
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims Some reports have suggested that hypertensive acute heart failure (AHF) is caused by intravascular congestion, not interstitial congestion. We evaluated the differences in extracellular fluid volume assessed by bioelectrical impedance analysis (BIA) between AHF patients with and without high systolic blood pressure (sBP). <br>
Methods This prospective single-centre study (UMIN000030266) included 178 patients hospitalized due to AHF between September 2017 and August 2018. We calculated extracellular water (ECW), intracellular water (ICW), total body water (TBW), and ECW-to-TBW ratio (oedema index: EI) by BIA and evaluated conventional parameters as follows: weight, N-terminal pro brain natriuretic peptide values, and echocardiography parameters on admission and before discharge. One-year outcomes included all-cause death and re-admission due to heart failure. We compared patients with sBP > 140 mmHg on admission [clinical scenario 1 (CS1) group] and with sBP of <= 140 mmHg on admission (non-CS1 group). <br>
Results The mean age of the patients was 79.5 +/- 11.1 years, and 48.9% of the patients were female. EI on admission of 83 patients in the CS1 group was lower than that of 95 patients in the non-CS1 group. The change in EI from admission to before discharge was no significant in the CS1 group but was significant in the non-CS1 group. Comparing the changes from admission to before discharge between the CS1 and the non-CS1 group, delta ECW, delta ICW, delta TBW, and delta EI of the CS1 group were significantly smaller than those of the non-CS1 group. During the 1-year follow-up period after discharge of the 178 patients, the numbers of deaths and re-admissions due to acute HF were 26 (15%) and 49 (28%), respectively. Patients with high EI before discharge [> 0.408 (median)] had significantly more cardiac events than patients with low EI [hazard ratio (HR): 2.15, 95% confidence interval (CI): 1.30-3.55]. Cox regression analysis revealed that higher EI as a continuous variable was significantly associated with worse outcome in non-CS1 group (HR: 1.46, 95% CI: 1.13-1.87), but not significantly associated with worse outcome in CS1 group (HR: 1.29, 95% CI: 0.98-1.69). <br>
Conclusions EI on admission in patients with high sBP was not elevated, and changes in ECW, ICW, TBW, and EI in patients with high sBP were smaller than those in patients without high sBP. EI measured by BIA could distinguish AHF with interstitial or intravascular congestion.
en-copyright=
kn-copyright=

en-aut-name=NambaYusuke
en-aut-sei=Namba
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YunokiKei
en-aut-sei=Yunoki
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkaTakefumi
en-aut-sei=Oka
en-aut-mei=Takefumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Tsuyama Chuo Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Tsuyama Chuo Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Acute heart failure
kn-keyword=Acute heart failure
en-keyword=High systolic blood pressure
kn-keyword=High systolic blood pressure
en-keyword=Fluid volume
kn-keyword=Fluid volume
en-keyword=Oedema index
kn-keyword=Oedema index
END

start-ver=1.4
cd-journal=joma
no-vol=27
cd-vols=
no-issue=12
article-no=
start-page=3917
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220618
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rational Design of Peptides Derived from Odorant-Binding Proteins for SARS-CoV-2-Related Volatile Organic Compounds Recognition
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Peptides are promising molecular-binding elements and have attracted great interest in novel biosensor development. In this study, a series of peptides derived from odorant-binding proteins (OBPs) were rationally designed for recognition of SARS-CoV-2-related volatile organic compounds (VOCs). Ethanol, nonanal, benzaldehyde, acetic acid, and acetone were selected as representative VOCs in the exhaled breath during the COVID-19 infection. Computational docking and prediction tools were utilized for OBPs peptide characterization and analysis. Multiple parameters, including the docking model, binding affinity, sequence specification, and structural folding, were investigated. The results demonstrated a rational, rapid, and efficient approach for designing breath-borne VOC-recognition peptides, which could further improve the biosensor performance for pioneering COVID-19 screening and many other applications.
en-copyright=
kn-copyright=

en-aut-name=WangJin
en-aut-sei=Wang
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakaiKenji
en-aut-sei=Sakai
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KiwaToshihiko
en-aut-sei=Kiwa
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Faculty of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Faculty of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=rational design
kn-keyword=rational design
en-keyword=odorant-binding protein
kn-keyword=odorant-binding protein
en-keyword=peptide
kn-keyword=peptide
en-keyword=SARS-CoV-2
kn-keyword=SARS-CoV-2
en-keyword=volatile organic compounds
kn-keyword=volatile organic compounds
en-keyword=computational tools
kn-keyword=computational tools
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=
article-no=
start-page=128767
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202207
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ultrasound-dependent RNAi using TatU1A-rose bengal conjugate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tat-U1A-rose bengal conjugate (TatU1A-RB) was prepared as an ultrasound-sensitive RNA carrier molecule. This molecule consists of Tat cell-penetrating peptide, U1A RNA-binding protein, and rose bengal as a sonosensitizer. We demonstrated that TatU1A-RB delivered RNA via the endocytosis pathway, which was followed by ultrasound-dependent endosomal escape and cytosolic dispersion of the RNA. A short hairpin RNA (shRNA) delivered by TatU1A-RB mediated RNA interference (RNAi) ultrasound-dependently. Even by ultrasound irradiation through blood cells, RNAi could be induced with TatU1A-RB and the shRNA. This ultrasound-dependent cytosolic RNA delivery method will serve as the basis for a new approach to nucleic acid therapeutics.
en-copyright=
kn-copyright=

en-aut-name=SumiNanako
en-aut-sei=Sumi
en-aut-mei=Nanako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagahiroShota
en-aut-sei=Nagahiro
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakataEiji
en-aut-sei=Nakata
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Advanced Energy, Kyoto University
kn-affil=

affil-num=4
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=Ultrasound
kn-keyword=Ultrasound
en-keyword=Sonosensitizer
kn-keyword=Sonosensitizer
en-keyword=Rose Bengal
kn-keyword=Rose Bengal
en-keyword=RNAi
kn-keyword=RNAi
en-keyword=RNA delivery
kn-keyword=RNA delivery
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=5
article-no=
start-page=924
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Helical Foldamers and Stapled Peptides as New Modalities in Drug Discovery: Modulators of Protein-Protein Interactions
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A "foldamer" is an artificial oligomeric molecule with a regular secondary or tertiary structure consisting of various building blocks. A "stapled peptide" is a peptide with stabilized secondary structures, in particular, helical structures by intramolecular covalent side-chain cross-linking. Helical foldamers and stapled peptides are potential drug candidates that can target protein-protein interactions because they enable multipoint molecular recognition, which is difficult to achieve with low-molecular-weight compounds. This mini-review describes a variety of peptide-based foldamers and stapled peptides with a view to their applications in drug discovery, including our recent progress.
en-copyright=
kn-copyright=

en-aut-name=TsuchiyaKeisuke
en-aut-sei=Tsuchiya
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KuroharaTakashi
en-aut-sei=Kurohara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukuharaKiyoshi
en-aut-sei=Fukuhara
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MisawaTakashi
en-aut-sei=Misawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DemizuYosuke
en-aut-sei=Demizu
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=2
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=3
en-affil=Graduate School of Pharmacy, Showa University
kn-affil=

affil-num=4
en-affil=Division of Organic Chemistry, National Institute of Health Sciences
kn-affil=

affil-num=5
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=foldamers
kn-keyword=foldamers
en-keyword=protein-protein interaction
kn-keyword=protein-protein interaction
en-keyword=helical structure
kn-keyword=helical structure
en-keyword=building blocks
kn-keyword=building blocks
en-keyword=drug discovery
kn-keyword=drug discovery
en-keyword=modality
kn-keyword=modality
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=シロイヌナズナの内生サプレッサーとしての CEP ペプチドの作用機序に関する研究
kn-title=Study on the mode of action of CEP peptide as an endogenous suppressor in Arabidopsis thaliana
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=APRILIA NUR FITRIANTI
en-aut-sei=APRILIA NUR FITRIANTI
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=9
article-no=
start-page=eabk0331
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=202234
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vasopressin-oxytocin–type signaling is ancient and has a conserved water homeostasis role in euryhaline marine planarians
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Vasopressin/oxytocin (VP/OT)–related peptides are essential for mammalian antidiuresis, sociosexual behavior, and reproduction. However, the evolutionary origin of this peptide system is still uncertain. Here, we identify orthologous genes to those for VP/OT in Platyhelminthes, intertidal planarians that have a simple bilaterian body structure but lack a coelom and body-fluid circulatory system. We report a comprehensive characterization of the neuropeptide derived from this VP/OT-type gene, identifying its functional receptor, and name it the “platytocin” system. Our experiments with these euryhaline planarians, living where environmental salinities fluctuate due to evaporation and rainfall, suggest that platytocin functions as an “antidiuretic hormone” and also organizes diverse actions including reproduction and chemosensory-associated behavior. We propose that bilaterians acquired physiological adaptations to amphibious lives by such regulation of the body fluids. This neuropeptide-secreting system clearly became indispensable for life even without the development of a vascular circulatory system or relevant synapses.
en-copyright=
kn-copyright=

en-aut-name=KobayashiAoshi
en-aut-sei=Kobayashi
en-aut-mei=Aoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HamadaMayuko
en-aut-sei=Hamada
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaMasa-aki
en-aut-sei=Yoshida
en-aut-mei=Masa-aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobayashiYasuhisa
en-aut-sei=Kobayashi
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsutsuiNaoaki
en-aut-sei=Tsutsui
en-aut-mei=Naoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SekiguchiToshio
en-aut-sei=Sekiguchi
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsukawaYuta
en-aut-sei=Matsukawa
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaejimaSho
en-aut-sei=Maejima
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=GingellJoseph J.
en-aut-sei=Gingell
en-aut-mei=Joseph J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SekiguchiShoko
en-aut-sei=Sekiguchi
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HamamotoAyumu
en-aut-sei=Hamamoto
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HayDebbie L.
en-aut-sei=Hay
en-aut-mei=Debbie L.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MorrisJohn F.
en-aut-sei=Morris
en-aut-mei=John F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Oki Marine Biological Station, Shimane University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Noto Marine Laboratory, Institute of Nature and Environmental Technology, Division of Marine Environmental Studies, Kanazawa University
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=9
en-affil=Vertex Pharmaceuticals (Europe) Ltd.
kn-affil=

affil-num=10
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=12
en-affil=School of Biological Sciences and Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland
kn-affil=

affil-num=13
en-affil=Department of Physiology, Anatomy, and Genetic, Le Gros Clark Building, University of Oxford
kn-affil=

affil-num=14
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=15
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University, Ushimado
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=3
article-no=
start-page=103869
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220318
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lipid flippase dysfunction as a therapeutic target for endosomal anomalies in Alzheimer's disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Endosomal anomalies because of vesicular traffic impairment have been indicated as an early pathology of Alzheimer'vertical bar disease (AD). However, the mechanisms and therapeutic targets remain unclear. We previously reported thatbCTF, one of the pathogenic metabolites of APP, interacts with TMEM30A. TMEM30A constitutes a lipid flippase with P4-ATPase and regulates vesicular trafficking through the asymmetric distribution of phospholipids. Therefore, the alteration of lipid flippase activity in AD pathology has got attention. Herein, we showed that the interaction between beta CTF and TMEM30A suppresses the physiological formation and activity of lipid flippase in AD model cells, A7, and App(NLG-F/NLG-F) model mice. Furthermore, the T-RAP peptide derived from the beta CTF binding site of TMEM30A improved endosomal anomalies, which could be a result of the restored lipid flippase activity. Our results provide insights into the mechanisms of vesicular traffic impairment and suggest a therapeutic target for AD.
en-copyright=
kn-copyright=

en-aut-name=KaneshiroNanaka
en-aut-sei=Kaneshiro
en-aut-mei=Nanaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KomaiMasato
en-aut-sei=Komai
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaokaRyosuke
en-aut-sei=Imaoka
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaAtsuya
en-aut-sei=Ikeda
en-aut-mei=Atsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KamikuboYuji
en-aut-sei=Kamikubo
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaitoTakashi
en-aut-sei=Saito
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaidoTakaomi C.
en-aut-sei=Saido
en-aut-mei=Takaomi C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TomitaTaisuke
en-aut-sei=Tomita
en-aut-mei=Taisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HashimotoTadafumi
en-aut-sei=Hashimoto
en-aut-mei=Tadafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IwatsuboTakeshi
en-aut-sei=Iwatsubo
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakuraiTakashi
en-aut-sei=Sakurai
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Neurocognitive Science, Nagoya City University Graduate School of Medical Sciences
kn-affil=

affil-num=7
en-affil=Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science
kn-affil=

affil-num=8
en-affil=Laboratory of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Neuropathology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Neuropathology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=
kn-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University

affil-num=13
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=19
article-no=
start-page=10362
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210926
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Sexual Experience Induces the Expression of Gastrin-Releasing Peptide and Oxytocin Receptors in the Spinal Ejaculation Generator in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Male sexual function in mammals is controlled by the brain neural circuits and the spinal cord centers located in the lamina X of the lumbar spinal cord (L3-L4). Recently, we reported that hypothalamic oxytocin neurons project to the lumbar spinal cord to activate the neurons located in the dorsal lamina X of the lumbar spinal cord (dXL) via oxytocin receptors, thereby facilitating male sexual activity. Sexual experiences can influence male sexual activity in rats. However, how this experience affects the brain-spinal cord neural circuits underlying male sexual activity remains unknown. Focusing on dXL neurons that are innervated by hypothalamic oxytocinergic neurons controlling male sexual function, we examined whether sexual experience affects such neural circuits. We found that >50% of dXL neurons were activated in the first ejaculation group and similar to 30% in the control and intromission groups in sexually naive males. In contrast, in sexually experienced males, similar to 50% of dXL neurons were activated in both the intromission and ejaculation groups, compared to similar to 30% in the control group. Furthermore, sexual experience induced expressions of gastrin-releasing peptide and oxytocin receptors in the lumbar spinal cord. This is the first demonstration of the effects of sexual experience on molecular expressions in the neural circuits controlling male sexual activity in the spinal cord.
en-copyright=
kn-copyright=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UedaRyota
en-aut-sei=Ueda
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KumagaiRyoko
en-aut-sei=Kumagai
en-aut-mei=Ryoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NagafuchiJunta
en-aut-sei=Nagafuchi
en-aut-mei=Junta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoTakashi
en-aut-sei=Ito
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KondoYasuhiko
en-aut-sei=Kondo
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Animal Sciences, Teikyo University of Science
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Animal Sciences, Teikyo University of Science
kn-affil=

affil-num=8
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=sexual experience
kn-keyword=sexual experience
en-keyword=lumbosacral spinal cord
kn-keyword=lumbosacral spinal cord
en-keyword=spinal ejaculation generator
kn-keyword=spinal ejaculation generator
en-keyword=brain-spinal cord neural circuits
kn-keyword=brain-spinal cord neural circuits
en-keyword=gastrin-releasing peptide
kn-keyword=gastrin-releasing peptide
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=male sexual activity
kn-keyword=male sexual activity
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211103
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of luseogliflozin on estimated plasma volume in patients with heart failure with preserved ejection fraction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aims<br>
Sodium glucose co-transporter 2 inhibitors have diuretic effects in both patients with glycosuria and with natriuresis. We sought to assess the effect of luseogliflozin on estimated plasma volume (ePV) in patients with type 2 diabetes and heart failure with preserved ejection fraction (HFpEF). <br>
Methods and results<br>
This study was a post-hoc analysis of the MUSCAT-HF trial (UMIN000018395), a multicentre, prospective, open-label, randomized controlled trial that assessed the effect of 12 weeks of luseogliflozin (2.5 mg, once daily, n = 83) as compared with voglibose (0.2 mg, three times daily, n = 82) on the reduction in brain natriuretic peptide (BNP) in patients with type 2 diabetes and HFpEF. The analysis compared the change in ePV calculated by the Straus formula from baseline to Weeks 4, 12, and 24, using a mixed-effects model for repeated measures. We also estimated the association between changes in ePV and changes in other clinical parameters, including BNP levels. Luseogliflozin significantly reduced ePV as compared to voglibose at Week 4 {adjusted mean group-difference -6.43% [95% confidence interval (CI): -9.11 to -3.74]}, at Week 12 [-8.73% (95%CI: -11.40 to -6.05)], and at Week 24 [-11.02% (95%CI: -13.71 to -8.33)]. The effect of luseogliflozin on these parameters was mostly consistent across various patient clinical characteristics. The change in ePV at Week 12 was significantly associated with log-transformed BNP (r = 0.197, P = 0.015) and left atrial volume index (r = 0.283, P = 0.019). <br>
Conclusions<br>
Luseogliflozin significantly reduced ePV in patients with type 2 diabetes and HFpEF, as compared with voglibose. The reduction of intravascular volume by luseogliflozin may provide clinical benefits to patients with type 2 diabetes and HFpEF.
en-copyright=
kn-copyright=

en-aut-name=NakashimaMitsutaka
en-aut-sei=Nakashima
en-aut-mei=Mitsutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HataYoshiki
en-aut-sei=Hata
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaganoToshihiko
en-aut-sei=Nagano
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NanbaSeiji
en-aut-sei=Nanba
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakamuraYoichi
en-aut-sei=Nakamura
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MinagawaTaro
en-aut-sei=Minagawa
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FukeSoichiro
en-aut-sei=Fuke
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MUSCAT-HF Study Investigators
en-aut-sei=MUSCAT-HF Study Investigators
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=5
en-affil=Department of Cardiology, Minamino Cardiovascular Hospital
kn-affil=

affil-num=6
en-affil=Department of Internal Medicine, Iwasa Hospital,
kn-affil=

affil-num=7
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cardiology, Okayama Rosai Hospital
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Specified Clinic of Soyokaze CardioVascular Medicine and Diabetes Care, Matsuyama
kn-affil=

affil-num=11
en-affil=Department of Internal Medicine, Akaiwa Medical Association Hospital
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Iwakuni Clinical Center
kn-affil=

affil-num=13
en-affil=Department of Internal Medicine, Minagawa Cardiovascular Clinic
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=17
en-affil=Department of Cardiology, Fukuyama City Hospital
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=
kn-affil=
en-keyword=Estimated plasma volume
kn-keyword=Estimated plasma volume
en-keyword=Heart failure with preserved ejection fraction
kn-keyword=Heart failure with preserved ejection fraction
en-keyword=Luseogliflozin
kn-keyword=Luseogliflozin
en-keyword=Sodium glucose co-transporter 2 inhibitors
kn-keyword=Sodium glucose co-transporter 2 inhibitors
en-keyword=Voglibose
kn-keyword=Voglibose
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=10
article-no=
start-page=e244861
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202110
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Idiopathic combined adrenocorticotropin and growth hormone deficiency mimicking chronic fatigue syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 42-year-old man who had suffered from severe fatigue for 5 years was diagnosed as having chronic fatigue syndrome (CFS) and fibromyalgia. Endocrinological workup using combined anterior pituitary function tests showed that the patient had adrenocorticotropin hormone (ACTH) deficiency, with a normal pituitary MRI. Treatment with a physiologic dose of oral hydrocortisone replacement physically ameliorated his general fatigue. A secondary workup using a growth hormone-releasing peptide-2 test revealed that he also had growth hormone (GH) deficiency, and GH replacement therapy was started. His muscle pain and depression were improved by the therapy. Here, we present a rare case of combined deficiency of ACTH and GH in a middle-aged man with severe general fatigue. This case report aims to raise awareness of combined deficiency of ACTH and GH as a differential diagnosis of CFS and its mimics.
en-copyright=
kn-copyright=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OchiKanako
en-aut-sei=Ochi
en-aut-mei=Kanako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Center for Education in Medicine and Health Sciences, Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=6
article-no=
start-page=671
end-page=675
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202112
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multiple Roles of Histidine-Rich Glycoprotein in Vascular Homeostasis and Angiogenesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Histidine-rich glycoprotein (HRG) is a 75 kDa plasma protein that is synthesized in the liver of many verte-brates and present in their plasma at relatively high concentrations of 100-150 μg/mL. HRG is an abundant and well-characterized protein having a multidomain structure that enable it to interact with many ligands, func-tion as an adaptor molecule, and participate in numerous physiological and pathological processes. As a plasma protein, HRG has been reported to regulate vascular biology, including coagulation, fibrinolysis and angiogenesis, through its binding with several ligands (heparin, FXII, fibrinogen, thrombospondin, and plas-minogen) and interaction with many types of cells (endothelial cells, erythrocytes, neutrophils and platelets). This review aims to summarize the roles of HRG in maintaining vascular homeostasis and regulating angiogen-esis in various pathological conditions.
en-copyright=
kn-copyright=

en-aut-name=GaoShangze
en-aut-sei=Gao
en-aut-mei=Shangze
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=histidine-rich glycoprotein
kn-keyword=histidine-rich glycoprotein
en-keyword=vascular biology
kn-keyword=vascular biology
en-keyword=coagulation
kn-keyword=coagulation
en-keyword=angiogenesis
kn-keyword=angiogenesis
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=9
article-no=
start-page=e04574
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210907
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Longitudinal observation of insulin secretory ability before and after the onset of immune checkpoint inhibitor-induced diabetes mellitus: A report of two cases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitor-induced diabetes mellitus is a rare immune-related adverse event. This report illustrates clinical data and insulin secretory ability before and after the onset of immune checkpoint inhibitor-induced diabetes.
en-copyright=
kn-copyright=

en-aut-name=FujiwaraNoriko
en-aut-sei=Fujiwara
en-aut-mei=Noriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WatanabeMayu
en-aut-sei=Watanabe
en-aut-mei=Mayu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatayamaAkihiro
en-aut-sei=Katayama
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NodaYohei
en-aut-sei=Noda
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KataokaHitomi
en-aut-sei=Kataoka
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KagawaShunsuke
en-aut-sei=Kagawa
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Primary Care and Medical Education, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Diabetes Center, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Otolaryngology-Head and Neck Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Primary Care and Medical Education, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Minimally Invasive Therapy Center, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=C-peptide
kn-keyword=C-peptide
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
en-keyword=immune checkpoint inhibitor
kn-keyword=immune checkpoint inhibitor
en-keyword=insulin secretion
kn-keyword=insulin secretion
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=647684
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210810
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Purification, Characterization, and Gene Expression of Rice Endo-beta-N-Acetylglucosaminidase, Endo-Os
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the endoplasmic reticulum-associated degradation system of plant and animal cells, high-mannose type free N-glycans (HMT-FNGs) are produced from misfolded glycoproteins prior to proteasomal degradation, and two enzymes, cytosolic peptide:N-glycanase (cPNGase) and endo-beta-N-acetylglucosaminidase (endo-beta-GlcNAc-ase), are involved in the deglycosylation. Although the physiological functions of these FNGs in plant growth and development remain to be elucidated, detailed characterization of cPNGase and endo-beta-GlcNAc-ase is required. In our previous work, we described the purification, characterization, and subcellular distribution of some plant endo-beta-GlcNAc-ases and preliminarily reported the gene information of rice endo-beta-GlcNAc-ase (Endo-Os). Furthermore, we analyzed the changes in gene expression of endo-beta-GlcNAc-ase during tomato fruit maturation and constructed a mutant line of Arabidopsis thaliana, in which the two endo-beta-GlcNAc-ase genes were knocked-out based on the Endo-Os gene. In this report, we describe the purification, characterization, amino acid sequence, and gene cloning of Endo-Os in detail. Purified Endo-Os, with an optimal pH of 6.5, showed high activity for high-mannose type N-glycans bearing the Man alpha 1-2Man alpha 1-3Man beta 1 unit; this substrate specificity was almost the same as that of other plant endo-beta-GlcNAc-ases, suggesting that Endo-Os plays a critical role in the production of HTM-FNGs in the cytosol. Electrospray ionization-mass spectrometry analysis of the tryptic peptides revealed 17 internal amino acid sequences, including the C terminus; the N-terminal sequence could not be identified due to chemical modification. These internal amino acid sequences were consistent with the amino acid sequence (UniProt ID: Q5W6R1) deduced from the Oryza sativa cDNA clone AK112067 (gene ID: Os05g0346500). Recombinant Endo-Os expressed in Escherichia coli using cDNA showed the same enzymatic properties as those of native Endo-Os.
en-copyright=
kn-copyright=

en-aut-name=MaedaMegumi
en-aut-sei=Maeda
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkamotoNaoko
en-aut-sei=Okamoto
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ArakiNode
en-aut-sei=Araki
en-aut-mei=Node
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KimuraYoshinobu
en-aut-sei=Kimura
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Tumor Genetics and Biology, Graduate School of Medical Sciences, Kumamoto University
kn-affil=

affil-num=4
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=endo-beta-N-acetylglucosaminidase
kn-keyword=endo-beta-N-acetylglucosaminidase
en-keyword=free N-glycans
kn-keyword=free N-glycans
en-keyword=Oryza sativa
kn-keyword=Oryza sativa
en-keyword=ER associated degradation
kn-keyword=ER associated degradation
en-keyword=peptide:N-glycanase
kn-keyword=peptide:N-glycanase
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=1
article-no=
start-page=13315
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The gastrin-releasing peptide/bombesin system revisited by a reverse-evolutionary study considering Xenopus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bombesin is a putative antibacterial peptide isolated from the skin of the frog, Bombina bombina. Two related (bombesin-like) peptides, gastrin-releasing peptide (GRP) and neuromedin B (NMB) have been found in mammals. The history of GRP/bombesin discovery has caused little attention to be paid to the evolutionary relationship of GRP/bombesin and their receptors in vertebrates. We have classified the peptides and their receptors from the phylogenetic viewpoint using a newly established genetic database and bioinformatics. Here we show, by using a clawed frog (Xenopus tropicalis), that GRP is not a mammalian counterpart of bombesin and also that, whereas the GRP system is widely conserved among vertebrates, the NMB/bombesin system has diversified in certain lineages, in particular in frog species. To understand the derivation of GRP system in the ancestor of mammals, we have focused on the GRP system in Xenopus. Gene expression analyses combined with immunohistochemistry and Western blotting experiments demonstrated that GRP peptides and their receptors are distributed in the brain and stomach of Xenopus. We conclude that GRP peptides and their receptors have evolved from ancestral (GRP-like peptide) homologues to play multiple roles in both the gut and the brain as one of the 'gut-brain peptide' systems.
en-copyright=
kn-copyright=

en-aut-name=HirookaAsuka
en-aut-sei=Hirooka
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HamadaMayuko
en-aut-sei=Hamada
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujiyamaDaiki
en-aut-sei=Fujiyama
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakanamiKeiko
en-aut-sei=Takanami
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobayashiYasuhisa
en-aut-sei=Kobayashi
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatayamaYukitoshi
en-aut-sei=Katayama
en-aut-mei=Yukitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=9
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=10
article-no=
start-page=4408
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210513
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fibril Growth Behavior of Amyloid beta on Polymer-Based Planar Membranes: Implications for the Entanglement and Hydration of Polymers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The design of biosensors and artificial organs using biocompatible materials with a low affinity for amyloid beta peptide (A beta) would contribute to the inhibition of fibril growth causing Alzheimer's disease. We systematically studied the amyloidogenicity of A beta on various planar membranes. The planar membranes were prepared using biocompatible polymers, viz., poly(methyl methacrylate) (PMMA), polysulfone (PSf), poly(L-lactic acid) (PLLA), and polyvinylpyrrolidone (PVP). Phospholipids from biomembranes, viz., 1,2-dioleoyl-phosphatidylcholine (DOPC), 1,2-dipalmitoyl-phosphatidylcholine (DPPC), and polyethylene glycol-graft-phosphatidyl ethanolamine (PEG-PE) were used as controls. Phospholipid- and polymer-based membranes were prepared to determine the kinetics of A beta fibril formation. Rates of A beta nucleation on the PSf- and DPPC-based membranes were significantly higher than those on the other membranes. A beta accumulation, calculated by the change in frequency of a quartz crystal microbalance (QCM), followed the order: PSf > PLLA > DOPC > PMMA, PVP, DPPC, and PEG-PE. Nucleation rates exhibited a positive correlation with the corresponding accumulation (except for the DPPC-based membrane) and a negative correlation with the molecular weight of the polymers. Strong hydration along the polymer backbone and polymer-A beta entanglement might contribute to the accumulation of A beta and subsequent fibrillation.
en-copyright=
kn-copyright=

en-aut-name=ShimanouchiToshinori
en-aut-sei=Shimanouchi
en-aut-mei=Toshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwamuraMiki
en-aut-sei=Iwamura
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DeguchiShintaro
en-aut-sei=Deguchi
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KimuraYukitaka
en-aut-sei=Kimura
en-aut-mei=Yukitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environment and Life Science, Okayama University
kn-affil=
en-keyword=biocompatible polymer
kn-keyword=biocompatible polymer
en-keyword=amyloid fibril
kn-keyword=amyloid fibril
en-keyword=amyloid beta
kn-keyword=amyloid beta
en-keyword=nucleation
kn-keyword=nucleation
en-keyword=quartz crystal microbalance
kn-keyword=quartz crystal microbalance
en-keyword=hydration
kn-keyword=hydration
en-keyword=entanglement
kn-keyword=entanglement
en-keyword=hydration
kn-keyword=hydration
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=4
article-no=
start-page=330
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Theranostics in Boron Neutron Capture Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Boron neutron capture therapy (BNCT) has the potential to specifically destroy tumor cells without damaging the tissues infiltrated by the tumor. BNCT is a binary treatment method based on the combination of two agents that have no effect when applied individually: B-10 and thermal neutrons. Exclusively, the combination of both produces an effect, whose extent depends on the amount of B-10 in the tumor but also on the organs at risk. It is not yet possible to determine the B-10 concentration in a specific tissue using non-invasive methods. At present, it is only possible to measure the B-10 concentration in blood and to estimate the boron concentration in tissues based on the assumption that there is a fixed uptake of B-10 from the blood into tissues. On this imprecise assumption, BNCT can hardly be developed further. A therapeutic approach, combining the boron carrier for therapeutic purposes with an imaging tool, might allow us to determine the B-10 concentration in a specific tissue using a non-invasive method. This review provides an overview of the current clinical protocols and preclinical experiments and results on how innovative drug development for boron delivery systems can also incorporate concurrent imaging. The last section focuses on the importance of proteomics for further optimization of BNCT, a highly precise and personalized therapeutic approach.
en-copyright=
kn-copyright=

en-aut-name=SauerweinWolfgang A. G.
en-aut-sei=Sauerwein
en-aut-mei=Wolfgang A. G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SanceyLucie
en-aut-sei=Sancey
en-aut-mei=Lucie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Hey-HawkinsEvamarie
en-aut-sei=Hey-Hawkins
en-aut-mei=Evamarie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KellertMartin
en-aut-sei=Kellert
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=PanzaLuigi
en-aut-sei=Panza
en-aut-mei=Luigi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ImperioDaniela
en-aut-sei=Imperio
en-aut-mei=Daniela
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BalcerzykMarcin
en-aut-sei=Balcerzyk
en-aut-mei=Marcin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=RizzoGiovanna
en-aut-sei=Rizzo
en-aut-mei=Giovanna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ScalcoElisa
en-aut-sei=Scalco
en-aut-mei=Elisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HerrmannKen
en-aut-sei=Herrmann
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MauriPierluigi
en-aut-sei=Mauri
en-aut-mei=Pierluigi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=De PalmaAntonella
en-aut-sei=De Palma
en-aut-mei=Antonella
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=WittigAndrea
en-aut-sei=Wittig
en-aut-mei=Andrea
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=2
en-affil=UGA/Inserm U 1209/CNRS UMR 5309 Joint Research Center, Institute for Advanced Biosciences
kn-affil=

affil-num=3
en-affil=Deutsche Gesellschaft für Bor-Neutroneneinfangtherapie DGBNCT e.V.
kn-affil=

affil-num=4
en-affil=Institute of Inorganic Chemistry, Department of Chemistry and Mineralogy, University Leipzig
kn-affil=

affil-num=5
en-affil=Deutsche Gesellschaft für Bor-Neutroneneinfangtherapie DGBNCT e.V.
kn-affil=

affil-num=6
en-affil=Deutsche Gesellschaft für Bor-Neutroneneinfangtherapie DGBNCT e.V.
kn-affil=

affil-num=7
en-affil=Departamento de Fisiología Medica y Biofísica, Universidad de Sevilla
kn-affil=

affil-num=8
en-affil=Institute for Biomedical Technologies (ITB-CNR)
kn-affil=

affil-num=9
en-affil=Institute for Biomedical Technologies (ITB-CNR)
kn-affil=

affil-num=10
en-affil=Department for Nuclear Medicine, University Hospital Essen
kn-affil=

affil-num=11
en-affil=Deutsche Gesellschaft für Bor-Neutroneneinfangtherapie DGBNCT e.V.
kn-affil=

affil-num=12
en-affil=Proteomics and Metabolomics Laboratory, ELIXIR Infrastructure, National Research Council (ITB-CNR)
kn-affil=

affil-num=13
en-affil=Deutsche Gesellschaft für Bor-Neutroneneinfangtherapie DGBNCT e.V.
kn-affil=
en-keyword=BNCT
kn-keyword=BNCT
en-keyword=radiation oncology
kn-keyword=radiation oncology
en-keyword=small molecules
kn-keyword=small molecules
en-keyword=BSH
kn-keyword=BSH
en-keyword=BPA
kn-keyword=BPA
en-keyword=PET
kn-keyword=PET
en-keyword=quantitative MRI
kn-keyword=quantitative MRI
en-keyword=image registration
kn-keyword=image registration
en-keyword=cell-penetrating peptides CPP
kn-keyword=cell-penetrating peptides CPP
en-keyword=proteomics
kn-keyword=proteomics
END

start-ver=1.4
cd-journal=joma
no-vol=22
cd-vols=
no-issue=7
article-no=
start-page=3400
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210326
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In Vivo Electrophysiology of Peptidergic Neurons in Deep Layers of the Lumbar Spinal Cord after Optogenetic Stimulation of Hypothalamic Paraventricular Oxytocin Neurons in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The spinal ejaculation generator (SEG) is located in the central gray (lamina X) of the rat lumbar spinal cord and plays a pivotal role in the ejaculatory reflex. We recently reported that SEG neurons express the oxytocin receptor and are activated by oxytocin projections from the paraventricular nucleus of hypothalamus (PVH). However, it is unknown whether the SEG responds to oxytocin in vivo. In this study, we analyzed the characteristics of the brain-spinal cord neural circuit that controls male sexual function using a newly developed in vivo electrophysiological technique. Optogenetic stimulation of the PVH of rats expressing channel rhodopsin under the oxytocin receptor promoter increased the spontaneous firing of most lamina X SEG neurons. This is the first demonstration of the in vivo electrical response from the deeper (lamina X) neurons in the spinal cord. Furthermore, we succeeded in the in vivo whole-cell recordings of lamina X neurons. In vivo whole-cell recordings may reveal the features of lamina X SEG neurons, including differences in neurotransmitters and response to stimulation. Taken together, these results suggest that in vivo electrophysiological stimulation can elucidate the neurophysiological response of a variety of spinal neurons during male sexual behavior.
en-copyright=
kn-copyright=

en-aut-name=UtaDaisuke
en-aut-sei=Uta
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=in vivo extracellular recording
kn-keyword=in vivo extracellular recording
en-keyword=in vivo whole-cell patch-clamp recording
kn-keyword=in vivo whole-cell patch-clamp recording
en-keyword=optogenetics
kn-keyword=optogenetics
en-keyword=spinal cord
kn-keyword=spinal cord
en-keyword=lamina X
kn-keyword=lamina X
en-keyword=spinal ejaculation generator
kn-keyword=spinal ejaculation generator
en-keyword=gastrin-releasing peptide neurons
kn-keyword=gastrin-releasing peptide neurons
en-keyword=oxytocin
kn-keyword=oxytocin
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=10
article-no=
start-page=5760
end-page=5772
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Two different regimes in alcohol-induced coil–helix transition: effects of 2,2,2-trifluoroethanol on proteins being either independent of or enhanced by solvent structural fluctuations
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Inhomogeneous distribution of constituent molecules in a mixed solvent has been known to give remarkable effects on the solute, e.g., conformational changes of biomolecules in an alcohol-water mixture. We investigated the general effects of 2,2,2-trifiuoroethanoE (TFE) on proteins/peptides in a mixture of water and TFE using melittin as a model protein. Fluctuations and Kirkwood-Buff integrals (KBIs) in the TFE-H2O mixture, quantitative descriptions of inhomogeneity, were determined by smallangle X-ray scattering investigation and compared with those in the aqueous solutions of other alcohols. The concentration fluctuation for the mixtures ranks as methanol < ethanol << TFE < tert-butanol < 1-propanol, indicating that the inhomogeneity of molecular distribution in the TFE-H2O mixture is unexpectedly comparable to those in the series of mono-ok. On the basis of the concentration dependence of KBIs between the TFE molecules, it was found that a strong attraction between the TFE molecules is not necessarily important to induce helix conformation, which is inconsistent with the previously proposed mechanism. To address this issue, by combining the KBIs and the helix contents reported by the experimental spectroscopic studies, we quantitatively evaluated the change in the preferential binding parameter of TFE to melittin attributed to the coil-helix transition. As a result, we found two different regimes on TFE-induced helix formation. In the dilute concentration region of TFE below similar to 2 M, where the TFE molecules are not aggregated among themselves, the excess preferential binding of TFE to the helix occurs due to the direct interaction between them, namely independent of the solvent fluctuation. In the higher concentration region above similar to 2 M, in addition to the former effect, the excess preferential binding is significantly enhanced by the solvent fluctuation. This scheme should be held as general cosoEvent effects of TFE on proteins/peptides.
en-copyright=
kn-copyright=

en-aut-name=OhgiHiroyo
en-aut-sei=Ohgi
en-aut-mei=Hiroyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ImamuraHiroshi
en-aut-sei=Imamura
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SumiTomonari
en-aut-sei=Sumi
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishikawaKeiko
en-aut-sei=Nishikawa
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KogaYoshikata
en-aut-sei=Koga
en-aut-mei=Yoshikata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WesthPeter
en-aut-sei=Westh
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritaTakeshi
en-aut-sei=Morita
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Chemistry, Graduate School of Science, Chiba University
kn-affil=

affil-num=2
en-affil=Department of Applied Chemistry, College of Life Sciences, Ritsumeikan University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Chemistry, Graduate School of Science, Chiba University
kn-affil=

affil-num=5
en-affil=Department of Chemistry, The University of British Columbia
kn-affil=

affil-num=6
en-affil=Department of Biotechnology and Biomedicine, Technical University of Denmark
kn-affil=

affil-num=7
en-affil=Department of Chemistry, Graduate School of Science, Chiba University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=110
cd-vols=
no-issue=
article-no=
start-page=1788
end-page=1798
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lactosome-Conjugated siRNA Nanoparticles for Photo-Enhanced Gene Silencing in Cancer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The A3B-type Lactosome comprised of poly(sarcosine)3-block-poly(l-lactic acid), a biocompatible and biodegradable polymeric nanomicelle, was reported to accumulate in tumors in vivo via the enhanced permeability and retention (EPR) effect. Recently, the cellular uptake of Lactosome particles was enhanced through the incorporation of a cell-penetrating peptide (CPP), L7EB1. However, the ability of Lactosome as a drug delivery carrier has not been established. Herein, we have developed a method to conjugate the A3B-type Lactosome with ATP-binding cassette transporter G2 (ABCG2) siRNA for inducing in vitro apoptosis in the cancer cell lines PANC-1 and NCI-H226. The L7EB1 peptide facilitates the cellular uptake efficiency of Lactosome but does not deliver siRNA into cytosol. To establish the photoinduced cytosolic dispersion of siRNA, a photosensitizer loaded L7EB1-Lactosome was prepared, and the photosensitizer 5,10,15,20-tetra-kis(pentafluorophenyl)porphyrin (TPFPP) showed superiority in photoinduced cytosolic dispersion. We exploited the combined effects of enhanced cellular uptake by L7EB1 and photoinduced endosomal escape by TPFPP to efficiently deliver ABCG2 siRNA into the cytosol for gene silencing. Moreover, the silencing of ABCG2, a protoporphyrin IX (PpIX) transporter, also mediated photoinduced cell death via 5-aminolevulinic acid (ALA)-mediated PpIX accumulated photodynamic therapy (PDT). The synergistic capability of the L7EB1/TPFPP/siRNA-Lactosome complex enabled both gene silencing and PDT.
en-copyright=
kn-copyright=

en-aut-name=LimMelissa Siaw Han
en-aut-sei=Lim
en-aut-mei=Melissa Siaw Han
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyamaYuki
en-aut-sei=Nishiyama
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KobuchiHirotsugu
en-aut-sei=Kobuchi
en-aut-mei=Hirotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiKazuko
en-aut-sei=Kobayashi
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuuraEiji
en-aut-sei=Matsuura
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=

affil-num=2
en-affil=
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=
kn-affil=

affil-num=6
en-affil=Collaborative Research Center (OMIC), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=
kn-affil=
en-keyword=Lactosome
kn-keyword=Lactosome
en-keyword=ABCG2
kn-keyword=ABCG2
en-keyword=siRNA
kn-keyword=siRNA
en-keyword=Cancer
kn-keyword=Cancer
en-keyword=siRNA delivery
kn-keyword=siRNA delivery
en-keyword=Photodynamic therapy
kn-keyword=Photodynamic therapy
en-keyword=Polymeric micelle
kn-keyword=Polymeric micelle
en-keyword=Photosensitizer
kn-keyword=Photosensitizer
en-keyword=Photochemical internalization
kn-keyword=Photochemical internalization
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=2
article-no=
start-page=158
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210218
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel 89Zr-labeled DDS Device Utilizing Human IgG Variant (scFv): “Lactosome” Nanoparticle-Based Theranostics for PET Imaging and Targeted Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=“Theranostics,” a new concept of medical advances featuring a fusion of therapeutic and diagnostic systems, provides promising prospects in personalized medicine, especially cancer. The theranostics system comprises a novel 89Zr-labeled drug delivery system (DDS), derived from the novel biodegradable polymeric micelle, “Lactosome” nanoparticles conjugated with specific shortened IgG variant, and aims to successfully deliver therapeutically effective molecules, such as the apoptosis-inducing small interfering RNA (siRNA) intracellularly while offering simultaneous tumor visualization via PET imaging. A 27 kDa-human single chain variable fragment (scFv) of IgG to establish clinically applicable PET imaging and theranostics in cancer medicine was fabricated to target mesothelin (MSLN), a 40 kDa-differentiation-related cell surface glycoprotein antigen, which is frequently and highly expressed by malignant tumors. This system coupled with the cell penetrating peptide (CPP)-modified and photosensitizer (e.g., 5, 10, 15, 20-tetrakis (4-aminophenyl) porphyrin (TPP))-loaded Lactosome particles for photochemical internalized (PCI) driven intracellular siRNA delivery and the combination of 5-aminolevulinic acid (ALA) photodynamic therapy (PDT) offers a promising nano-theranostic-based cancer therapy via its targeted apoptosis-inducing feature. This review focuses on the combined advances in nanotechnology and material sciences utilizing the “89Zr-labeled CPP and TPP-loaded Lactosome particles” and future directions based on important milestones and recent developments in this platform. 
en-copyright=
kn-copyright=

en-aut-name=LimMelissa Siaw Han
en-aut-sei=Lim
en-aut-mei=Melissa Siaw Han
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakenakaFumiaki
en-aut-sei=Takenaka
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobayashiKazuko
en-aut-sei=Kobayashi
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkehiMasaru
en-aut-sei=Akehi
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UjiHirotaka
en-aut-sei=Uji
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KobuchiHirotsugu
en-aut-sei=Kobuchi
en-aut-mei=Hirotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SasakiTakanori
en-aut-sei=Sasaki
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OzekiEiichi
en-aut-sei=Ozeki
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MatsuuraEiji
en-aut-sei=Matsuura
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cell Chemistry, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Collaborative Research Centre for OMIC, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Collaborative Research Centre for OMIC, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Collaborative Research Centre for OMIC, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Material Chemistry, Graduate School of Engineering, Kyoto University
kn-affil=

affil-num=7
en-affil=Department of Cell Chemistry, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Collaborative Research Centre for OMIC, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Technology Research Laboratory, Shimadzu Corporation
kn-affil=

affil-num=10
en-affil=Department of Cell Chemistry, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=theranostics
kn-keyword=theranostics
en-keyword=single chain variable fragment of IgG (scFv)
kn-keyword=single chain variable fragment of IgG (scFv)
en-keyword=drug delivery system (DDS)
kn-keyword=drug delivery system (DDS)
en-keyword=photodynamic therapy (PDT)
kn-keyword=photodynamic therapy (PDT)
en-keyword=PET imaging
kn-keyword=PET imaging
en-keyword=accelerated blood clearance (ABC)
kn-keyword=accelerated blood clearance (ABC)
en-keyword=cell penetrating peptide (CPP)
kn-keyword=cell penetrating peptide (CPP)
en-keyword=siRNA
kn-keyword=siRNA
en-keyword=ATP-binding cassette subfamily G member 2 (ABCG2)
kn-keyword=ATP-binding cassette subfamily G member 2 (ABCG2)
END

start-ver=1.4
cd-journal=joma
no-vol=384
cd-vols=
no-issue=
article-no=
start-page=1028
end-page=1037
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210318
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pegcetacoplan versus Eculizumab in Paroxysmal Nocturnal Hemoglobinuria
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background</br>
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired disease characterized by chronic complement-mediated hemolysis. C5 inhibition controls intravascular hemolysis in untreated PNH but cannot address extravascular hemolysis. Pegcetacoplan, a pegylated peptide targeting proximal complement protein C3, potentially inhibits both intravascular and extravascular hemolysis.</br>
Methods</br>
We conducted a phase 3 open-label, controlled trial to assess the efficacy and safety of pegcetacoplan as compared with eculizumab in adults with PNH and hemoglobin levels lower than 10.5 g per deciliter despite eculizumab therapy. After a 4-week run-in phase in which all patients received pegcetacoplan plus eculizumab, we randomly assigned patients to subcutaneous pegcetacoplan monotherapy (41 patients) or intravenous eculizumab (39 patients). The primary end point was the mean change in hemoglobin level from baseline to week 16. Additional clinical and hematologic markers of hemolysis and safety were assessed.</br>
Results</br>
Pegcetacoplan was superior to eculizumab with respect to the change in hemoglobin level from baseline to week 16, with an adjusted (least squares) mean difference of 3.84 g per deciliter (P<0.001). A total of 35 patients (85%) receiving pegcetacoplan as compared with 6 patients (15%) receiving eculizumab no longer required transfusions. Noninferiority of pegcetacoplan to eculizumab was shown for the change in absolute reticulocyte count but not for the change in lactate dehydrogenase level. Functional Assessment of Chronic Illness Therapy–Fatigue scores improved from baseline in the pegcetacoplan group. The most common adverse events that occurred during treatment in the pegcetacoplan and eculizumab groups were injection site reactions (37% vs. 3%), diarrhea (22% vs. 3%), breakthrough hemolysis (10% vs. 23%), headache (7% vs. 23%), and fatigue (5% vs. 15%). There were no cases of meningitis in either group.</br>
Conclusions</br>
Pegcetacoplan was superior to eculizumab in improving hemoglobin and clinical and hematologic outcomes in patients with PNH by providing broad hemolysis control, including control of intravascular and extravascular hemolysis. (Funded by Apellis Pharmaceuticals; PEGASUS ClinicalTrials.gov, NCT03500549. opens in new tab.)
en-copyright=
kn-copyright=

en-aut-name=HillmenPeter
en-aut-sei=Hillmen
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SzerJeff
en-aut-sei=Szer
en-aut-mei=Jeff
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WeitzIlene
en-aut-sei=Weitz
en-aut-mei=Ilene
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=RöthAlexander
en-aut-sei=Röth
en-aut-mei=Alexander
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HöchsmannBritta
en-aut-sei=Höchsmann
en-aut-mei=Britta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=PanseJens
en-aut-sei=Panse
en-aut-mei=Jens
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UsukiKensuke
en-aut-sei=Usuki
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GriffinMorag
en-aut-sei=Griffin
en-aut-mei=Morag
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KiladjianJean-Jacques
en-aut-sei=Kiladjian
en-aut-mei=Jean-Jacques
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=de CastroCarlos
en-aut-sei=de Castro
en-aut-mei=Carlos
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TanLisa
en-aut-sei=Tan
en-aut-mei=Lisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HamdaniMohamed
en-aut-sei=Hamdani
en-aut-mei=Mohamed
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=DeschateletsPascal
en-aut-sei=Deschatelets
en-aut-mei=Pascal
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FrancoisCedric
en-aut-sei=Francois
en-aut-mei=Cedric
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=GrossiFederico
en-aut-sei=Grossi
en-aut-mei=Federico
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=AjayiTemitayo
en-aut-sei=Ajayi
en-aut-mei=Temitayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=RisitanoAntonio
en-aut-sei=Risitano
en-aut-mei=Antonio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=Peffault de la TourRégis
en-aut-sei=Peffault de la Tour
en-aut-mei=Régis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

affil-num=1
en-affil=the Department of Haematology, St. James’s University Hospital
kn-affil=

affil-num=2
en-affil=the Department of Clinical Haematology, Peter MacCallum Cancer Center and Royal Melbourne Hospital
kn-affil=

affil-num=3
en-affil=Jane Anne Nohl Division of Hematology, Keck School of Medicine of USC
kn-affil=

affil-num=4
en-affil=the Department of Hematology, West German Cancer Center University Hospital Essen, University of Duisburg-Essen
kn-affil=

affil-num=5
en-affil=the Institute of Transfusion Medicine, University of Ulm and Institute of Clinical Transfusion Medicine and Immunogenetics, German Red Cross Blood Transfusion Service and University Hospital Ulm
kn-affil=

affil-num=6
en-affil=the Department of Oncology, Hematology, Hemostaseology and Stem Cell Transplantation, University Hospital RWTH Aachen
kn-affil=

affil-num=7
en-affil= the Department of Hematology, NTT Medical Center Tokyo
kn-affil=

affil-num=8
en-affil=the Department of Haematology, St. James’s University Hospital
kn-affil=

affil-num=9
en-affil=Centre d’Investigations Cliniques, Hôpital Saint-Louis, Assistance Publique–Hôpitaux de Paris, Université de Paris
kn-affil=

affil-num=10
en-affil=the Department of Medicine, Division of Hematologic Malignancies and Cellular Therapy, Duke University
kn-affil=

affil-num=11
en-affil=the Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Lisa Tan Pharma Consulting
kn-affil=

affil-num=13
en-affil=Apellis Pharmaceuticals
kn-affil=

affil-num=14
en-affil=Apellis Pharmaceuticals
kn-affil=

affil-num=15
en-affil=Apellis Pharmaceuticals
kn-affil=

affil-num=16
en-affil=Apellis Pharmaceuticals
kn-affil=

affil-num=17
en-affil=Apellis Pharmaceuticals
kn-affil=

affil-num=18
en-affil=the Hematology and BMT Unit, AORN San Giuseppe Moscati
kn-affil=

affil-num=19
en-affil=the French Reference Center for Aplastic Anemia and Paroxysmal Nocturnal Hemoglobinuria, Hôpital Saint-Louis, Assistance Publique–Hôpitaux de Paris, Université de Paris
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=2
article-no=
start-page=100
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210131
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of an RNA Silencing Suppressor Encoded by a Symptomless Fungal Hypovirus, Cryphonectria Hypovirus 4
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Previously, we have reported the ability of a symptomless hypovirus Cryphonectria hypovirus 4 (CHV4) of the chestnut blight fungus to facilitate stable infection by a co-infecting mycoreovirus 2 (MyRV2)—likely through the inhibitory effect of CHV4 on RNA silencing (Aulia et al., Virology, 2019). In this study, the N-terminal portion of the CHV4 polyprotein, termed p24, is identified as an autocatalytic protease capable of suppressing host antiviral RNA silencing. Using a bacterial expression system, CHV4 p24 is shown to cleave autocatalytically at the di-glycine peptide (Gly214-Gly215) of the polyprotein through its protease activity. Transgenic expression of CHV4 p24 in Cryphonectria parasitica suppresses the induction of one of the key genes of the antiviral RNA silencing, dicer-like 2, and stabilizes the infection of RNA silencing-susceptible virus MyRV2. This study shows functional similarity between CHV4 p24 and its homolog p29, encoded by the symptomatic prototype hypovirus CHV1.
en-copyright=
kn-copyright=

en-aut-name=AuliaAnnisa
en-aut-sei=Aulia
en-aut-mei=Annisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HyodoKiwamu
en-aut-sei=Hyodo
en-aut-mei=Kiwamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisanoSakae
en-aut-sei=Hisano
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoHideki
en-aut-sei=Kondo
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HillmanBradley I.
en-aut-sei=Hillman
en-aut-mei=Bradley I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=5
en-affil=Plant Biology and Pathology, Rutgers University
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=
en-keyword=mycovirus
kn-keyword=mycovirus
en-keyword=reovirus
kn-keyword=reovirus
en-keyword=hypovirus
kn-keyword=hypovirus
en-keyword=Cryphonectria parasitica
kn-keyword=Cryphonectria parasitica
en-keyword=co-infection
kn-keyword=co-infection
en-keyword=RNA silencing
kn-keyword=RNA silencing
en-keyword=RNAi suppressor
kn-keyword=RNAi suppressor
en-keyword=chestnut blight fungus
kn-keyword=chestnut blight fungus
en-keyword=Dicer
kn-keyword=Dicer
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=
article-no=
start-page=610124
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cytosolic Free N-Glycans Are Retro-Transported Into the Endoplasmic Reticulum in Plant Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=During endoplasmic reticulum (ER)-associated degradation, free N-glycans (FNGs) are produced from misfolded nascent glycoproteins via the combination of the cytosolic peptide N-glycanase (cPNGase) and endo-beta-N-acetylglucosaminidase (ENGase) in the plant cytosol. The resulting high-mannose type (HMT)-FNGs, which carry one GlcNAc residue at the reducing end (GN1-FNGs), are ubiquitously found in developing plant cells. In a previous study, we found that HMT-FNGs assisted in protein folding and inhibited beta-amyloid fibril formation, suggesting a possible biofunction of FNGs involved in the protein folding system. However, whether these HMT-FNGs occur in the ER, an organelle involved in protein folding, remained unclear. On the contrary, we also reported the presence of plant complex type (PCT)-GN1-FNGs, which carry the Lewis(a) epitope at the non-reducing end, indicating that these FNGs had been fully processed in the Golgi apparatus. Since plant ENGase was active toward HMT-N-glycans but not PCT-N-glycans that carry beta 1-2xylosyl and/or alpha 1-3 fucosyl residue(s), these PCT-GN1-FNGs did not appear to be produced from fully processed glycoproteins that harbored PCT-N-glycans via ENGase activity. Interestingly, PCT-GN1-FNGs were found in the extracellular space, suggesting that HMT-GN1-FNGs formed in the cytosol might be transported back to the ER and processed in the Golgi apparatus through the protein secretion pathway. As the first step in elucidating the production mechanism of PCT-GN1-FNGs, we analyzed the structures of free oligosaccharides in plant microsomes and proved that HMT-FNGs (Man(9-7)GlcNAc(1) and Man(9-8)GlcNAc(2)) could be found in microsomes, which almost consist of the ER compartments.
en-copyright=
kn-copyright=

en-aut-name=KatsubeMakoto
en-aut-sei=Katsube
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EbaraNatsuki
en-aut-sei=Ebara
en-aut-mei=Natsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaedaMegumi
en-aut-sei=Maeda
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KimuraYoshinobu
en-aut-sei=Kimura
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biofunctional Chemistry, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=free N-glycans
kn-keyword=free N-glycans
en-keyword=ER-associated degradation
kn-keyword=ER-associated degradation
en-keyword=peptide:N-glycanase
kn-keyword=peptide:N-glycanase
en-keyword=endo-beta-N-acetylglucosaminidase
kn-keyword=endo-beta-N-acetylglucosaminidase
en-keyword=plant glycoproteins
kn-keyword=plant glycoproteins
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=1
article-no=
start-page=103
end-page=107
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202102
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Marked Hypertriglyceridemia in a Patient with type 2 Diabetes Receiving SGLT2 Inhibitors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 43-year-old male with type 2 diabetes, under treatment with 5 mg/day of dapagliflozin, was referred to our hospital with upper left abdominal pain and marked hypertriglyceridemia (triglycerides [TGs], 5,960 mg/dl). He was also on a low-carbohydrate diet that promoted ketosis under sodium glucose cotransporter 2 (SGLT2) inhibitor administration. Polyacrylamide gel electrophoresis revealed a remarkable increase in very-low-den-sity lipoprotein, a TG-rich lipoprotein particle synthesized in the liver using free fatty acids derived from adi-pose tissue. Although SGLT2 inhibitors generally improve the lipid profile, under certain conditions such as a low-carbohydrate diet, they may adversely exacerbate the lipid profile via ketosis.
en-copyright=
kn-copyright=

en-aut-name=SenooMayumi
en-aut-sei=Senoo
en-aut-mei=Mayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ToneAtsuhito
en-aut-sei=Tone
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaiYusuke
en-aut-sei=Imai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeSatoko
en-aut-sei=Watanabe
en-aut-mei=Satoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KanetoMitsuhiro
en-aut-sei=Kaneto
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShimomuraYasuyuki
en-aut-sei=Shimomura
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakatouTatsuaki
en-aut-sei=Nakatou
en-aut-mei=Tatsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=2
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=4
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=6
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=7
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=8
en-affil=Department of Internal Medicine, Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=
en-keyword=sodium glucose cotransporter 2 inhibitor
kn-keyword=sodium glucose cotransporter 2 inhibitor
en-keyword=dyslipidemia
kn-keyword=dyslipidemia
en-keyword=hypertriglyceridemia
kn-keyword=hypertriglyceridemia
en-keyword=type 2 diabetes mellitus
kn-keyword=type 2 diabetes mellitus
END

start-ver=1.4
cd-journal=joma
no-vol=110
cd-vols=
no-issue=
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20210201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A comparative gene analysis reveals a diatom-specific SET domain protein family
kn-title=遺伝子比較解析による珪藻類特異的なSET ドメインタンパク質ファミリーの同定
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=　The silica cell walls of diatoms, which exhibit species-spe-cific micro- and nano- patterned structures are promising candidates for applications in nanotechnology. Previous studies revealed a number of silica cell wall-associated proteins involved in silica formation. However, molecular biological analyses toward understanding of diatom cell wall formation have been mostly limited to model diatom species and general silica formation process in diatoms is still incompletely understood. In this study, to gain a compre-hensive insight into diatom silica biomineralization, tran-scriptome data of three diatom species, Nitzschia palea, Achnanthes kuwaitensis and Pseudoleyanella lunata, were newly developed. The reads obtained from RNA sequencing were assembled into 31,946, 60,767 and 38,314 unique transcripts for N. palea, A. kuwaitensis and P. lunata, respectively. In order to identify the diatom-specific genes, three transcriptome data sets developed in this study and the protein-coding gene sets of five genome-sequenced diatoms were compared. The proteins shared only by eight diatom species that are predicted to possess an endoplasmic reticulum (ER)-targeting signal peptide were selected for further analyses. These include proteins showing homology to silicanin-1, a recently reported diatom-specific protein involved in silica formation, as well as a number of SET domain proteins. The SET domain proteins might be novel diatom-specific family of methyltransferases that may reg-ulate the function of silica formation related proteins or long chain polyamines. The genes encoding the diatom-specific SET domain proteins identified in this study, which were shown to respond to silicon were suggested to be implicated in silica biomineralization.  
en-copyright=
kn-copyright=

en-aut-name=NemotoMichiko
en-aut-sei=Nemoto
en-aut-mei=Michiko
kn-aut-name=根本理子
kn-aut-sei=根本
kn-aut-mei=理子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
en-keyword=Biomineralization
kn-keyword=Biomineralization
en-keyword=Diatom
kn-keyword=Diatom
en-keyword=Silica
kn-keyword=Silica
en-keyword=Protein
kn-keyword=Protein
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=1
article-no=
start-page=36
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201223
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Photoinduced Endosomal Escape Mechanism: A View from Photochemical Internalization Mediated by CPP-Photosensitizer Conjugates
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Endosomal escape in cell-penetrating peptide (CPP)-based drug/macromolecule delivery systems is frequently insufficient. The CPP-fused molecules tend to remain trapped inside endosomes and end up being degraded rather than delivered into the cytosol. One of the methods for endosomal escape of CPP-fused molecules is photochemical internalization (PCI), which is based on the use of light and a photosensitizer and relies on photoinduced endosomal membrane destabilization to release the cargo molecule. Currently, it remains unclear how this delivery strategy behaves after photostimulation. Recent findings, including our studies using CPP-cargo-photosensitizer conjugates, have shed light on the photoinduced endosomal escape mechanism. In this review, we discuss the structural design of CPP-photosensitizer and CPP-cargo-photosensitizer conjugates, and the PCI mechanism underlying their application.
en-copyright=
kn-copyright=

en-aut-name=SoeTet Htut
en-aut-sei=Soe
en-aut-mei=Tet Htut
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Biotechnology, Mandalay Technological University
kn-affil=

affil-num=2
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=photochemical internalization
kn-keyword=photochemical internalization
en-keyword=photosensitizer
kn-keyword=photosensitizer
en-keyword=cell-penetrating peptide
kn-keyword=cell-penetrating peptide
en-keyword=endosome
kn-keyword=endosome
en-keyword=membrane
kn-keyword=membrane
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=8
article-no=
start-page=e12875
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200523
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vasopressin gene products are colocalised with corticotrophin‐releasing factor within neurosecretory vesicles in the external zone of the median eminence of the Japanese macaque monkey (Macaca fuscata)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Arginine vasopressin (AVP), when released into portal capillaries with corticotrophin‐releasing factor (CRF) from terminals of parvocellular neurones of the hypothalamic paraventricular nucleus (PVH), facilitates the secretion of adrenocorticotrophic hormone (ACTH) in stressed rodents. The AVP gene encodes a propeptide precursor containing AVP, AVP‐associated neurophysin II (NPII), and a glycopeptide copeptin, although it is currently unclear whether copeptin is always cleaved from the neurophysin and whether the NPII and/or copeptin have any functional role in the pituitary. Furthermore, for primates, it is unknown whether CRF, AVP, NPII and copeptin are all colocalised in neurosecretory vesicles in the terminal region of the paraventricular CRF neurone axons. Therefore, we investigated, by fluorescence and immunogold immunocytochemistry, the cellular and subcellular relationships of these peptides in the CRF‐ and AVP‐producing cells in unstressed Japanese macaque monkeys (Macaca fuscata). Reverse transcription‐polymerase chain reaction analysis showed the expression of both CRF and AVP mRNAs in the monkey PVH. As expected, in the magnocellular neurones of the PVH and supraoptic nucleus, essentially no CRF immunoreactivity could be detected in NPII‐immunoreactive (AVP‐producing) neurones. Immunofluorescence showed that, in the parvocellular part of the PVH, NPII was detectable in a subpopulation (approximately 39%) of the numerous CRF‐immunoreactive neuronal perikarya, whereas, in the outer median eminence, NPII was more prominent (approximately 52%) in the CRF varicosities. Triple immunoelectron microscopy in the median eminence demonstrated the presence of both NPII and copeptin immunoreactivity in dense‐cored vesicles of CRF‐containing axons. The results are consistent with an idea that the AVP propeptide is processed and NPII and copeptin are colocalised in hypothalamic‐pituitary CRF axons in the median eminence of a primate. The CRF, AVP and copeptin are all co‐packaged in neurosecretory vesicles in monkeys and are thus likely to be co‐released into the portal capillary blood to amplify ACTH release from the primate anterior pituitary.
en-copyright=
kn-copyright=

en-aut-name=OtuboAkito
en-aut-sei=Otubo
en-aut-mei=Akito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawakamiNatsuko
en-aut-sei=Kawakami
en-aut-mei=Natsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaejimaSho
en-aut-sei=Maejima
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UedaYasumasa
en-aut-sei=Ueda
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MorrisJohn F.
en-aut-sei=Morris
en-aut-mei=John F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Physiology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=5
en-affil=Department of Physiology, Anatomy & Genetics, University of Oxford
kn-affil=

affil-num=6
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=corticotrophin‐releasing factor
kn-keyword=corticotrophin‐releasing factor
en-keyword=Japanese macaque monkey (Macaca fuscata)
kn-keyword=Japanese macaque monkey (Macaca fuscata)
en-keyword=median eminence
kn-keyword=median eminence
en-keyword=paraventricular nucleus of the hypothalamus
kn-keyword=paraventricular nucleus of the hypothalamus
en-keyword=vasopressin
kn-keyword=vasopressin
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=217
end-page=227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A New Serum Biomarker Set to Detect Mild Cognitive Impairment and Alzheimer’s Disease by Peptidome Technology 
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:</br>
Because dementia is an emerging problem in the world, biochemical markers of cerebrospinal fluid (CSF) and radio-isotopic analyses are helpful for diagnosing Alzheimer’s disease (AD). Although blood sample is more feasible and plausible than CSF or radiological biomarkers for screening potential AD, measurements of serum amyloid- β (Aβ), plasma tau, and serum antibodies for Aβ1 - 42 are not yet well established.</br>
Objective:</br>
We aimed to identify a new serum biomarker to detect mild cognitive impairment (MCI) and AD in comparison to cognitively healthy control by a new peptidome technology.</br>
Methods:</br>
With only 1.5μl of serum, we examined a new target plate “BLOTCHIP®” plus a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF/MS) to discriminate control (n = 100), MCI (n = 60), and AD (n = 99). In some subjects, cognitive Mini-Mental State Examination (MMSE) were compared to positron emission tomography (PET) with Pittsburgh compound B (PiB) and the serum probability of dementia (SPD). The mother proteins of candidate serum peptides were examined in autopsied AD brains.</br>
Results:</br>
Apart from Aβ or tau, the present study discovered a new diagnostic 4-peptides-set biomarker for discriminating control, MCI, and AD with 87% of sensitivity and 65% of specificity between control and AD (***p < 0.001). MMSE score was well correlated to brain Aβ deposition and to SPD of AD. The mother proteins of the four peptides were upregulated for coagulation, complement, and plasticity (three proteins), and was downregulated for anti-inflammation (one protein) in AD brains.</br>
Conclusion:</br>
The present serum biomarker set provides a new, rapid, non-invasive, highly quantitative and low-cost clinical application for dementia screening, and also suggests an alternative pathomechanism of AD for neuroinflammation and neurovascular unit damage.
en-copyright=
kn-copyright=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShangJingwei
en-aut-sei=Shang
en-aut-mei=Jingwei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShiXiaowen
en-aut-sei=Shi
en-aut-mei=Xiaowen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HishikawaNozomi
en-aut-sei=Hishikawa
en-aut-mei=Nozomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OhtaYasuyuki
en-aut-sei=Ohta
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=DeguchiKentaro
en-aut-sei=Deguchi
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IkedaMasaki
en-aut-sei=Ikeda
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IkedaYoshio
en-aut-sei=Ikeda
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OkamotoKoichi
en-aut-sei=Okamoto
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ShojiMikio
en-aut-sei=Shoji
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TakatamaMasamitsu
en-aut-sei=Takatama
en-aut-mei=Masamitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=KojoMotohisa
en-aut-sei=Kojo
en-aut-mei=Motohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=KurodaTakeshi
en-aut-sei=Kuroda
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=OnoKenjiro
en-aut-sei=Ono
en-aut-mei=Kenjiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KimuraNoriyuki
en-aut-sei=Kimura
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MatsubaraEtsuro
en-aut-sei=Matsubara
en-aut-mei=Etsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=OsakadaYosuke
en-aut-sei=Osakada
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=WakutaniYosuke
en-aut-sei=Wakutani
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=TakaoYoshiki
en-aut-sei=Takao
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=HigashiYasuto
en-aut-sei=Higashi
en-aut-mei=Yasuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=AsadaKyoichi
en-aut-sei=Asada
en-aut-mei=Kyoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=SengaTakehito
en-aut-sei=Senga
en-aut-mei=Takehito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name= LeeLyang-Ja
en-aut-sei= Lee
en-aut-mei=Lyang-Ja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=TanakaKenji
en-aut-sei=Tanaka
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Neurology, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Okayama City Hospital, Okayama
kn-affil=

affil-num=11
en-affil=Department of Neurology, Gunma University, Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Neurology, Gunma University, Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Neurology, Geriatrics Research Institute and Hospital
kn-affil=

affil-num=14
en-affil=Department of Neurology, Geriatrics Research Institute and Hospital
kn-affil=

affil-num=15
en-affil=Department of Neurology, Geriatrics Research Institute and Hospital
kn-affil=

affil-num=16
en-affil=Department of Neurology, Ako Chuo Hospital
kn-affil=

affil-num=17
en-affil=Division of Neurology, Department of Medicine, Showa University, School of Medicine
kn-affil=

affil-num=18
en-affil=Division of Neurology, Department of Medicine, Showa University, School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Neurology, Faculty of Medicine, Oita University
kn-affil=

affil-num=20
en-affil=Department of Neurology, Faculty of Medicine, Oita University
kn-affil=

affil-num=21
en-affil=Department of Neurology, Kurashiki Heisei Hospital
kn-affil=

affil-num=22
en-affil=Department of Neurology, Kurashiki Heisei Hospital
kn-affil=

affil-num=23
en-affil=Department of Neurology, Kurashiki Heisei Hospital
kn-affil=

affil-num=24
en-affil=Department of Neurology, Himeji Central Hospital
kn-affil=

affil-num=25
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=

affil-num=26
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=

affil-num=27
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=

affil-num=28
en-affil=Membrane Protein and Ligand Analysis Center, Protosera Inc.,
kn-affil=
en-keyword=Alzheimer’s disease
kn-keyword=Alzheimer’s disease
en-keyword=biomarker
kn-keyword=biomarker
en-keyword=coagulation
kn-keyword=coagulation
en-keyword=complement
kn-keyword=complement
en-keyword=MALDI-TOF
kn-keyword=MALDI-TOF
en-keyword=mild cognitive impairment
kn-keyword=mild cognitive impairment
en-keyword=neuroinflammation
kn-keyword=neuroinflammation
en-keyword=peptidome
kn-keyword=peptidome
en-keyword=plasticity
kn-keyword=plasticity
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=1
article-no=
start-page=103
end-page=114.e5
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201029
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oxytocin Influences Male Sexual Activity via Non-synaptic Axonal Release in the Spinal Cord
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Oxytocinergic neurons in the paraventricular nucleus of the hypothalamus that project to extrahypothalamic brain areas and the lumbar spinal cord play an important role in the control of erectile function and male sexual behavior in mammals. The gastrin-releasing peptide (GRP) system in the lumbosacral spinal cord is an important component of the neural circuits that control penile reflexes in rats, circuits that are commonly referred to as the “spinal ejaculation generator (SEG).” We have examined the functional interaction between the SEG neurons and the hypothalamo-spinal oxytocin system in rats. Here, we show that SEG/GRP neurons express oxytocin receptors and are activated by oxytocin during male sexual behavior. Intrathecal injection of oxytocin receptor antagonist not only attenuates ejaculation but also affects pre-ejaculatory behavior during normal sexual activity. Electron microscopy of potassium-stimulated acute slices of the lumbar cord showed that oxytocin-neurophysin-immunoreactivity was detected in large numbers of neurosecretory dense-cored vesicles, many of which are located close to the plasmalemma of axonal varicosities in which no electron-lucent microvesicles or synaptic membrane thickenings were visible. These results suggested that, in rats, release of oxytocin in the lumbar spinal cord is not limited to conventional synapses but occurs by exocytosis of the dense-cored vesicles from axonal varicosities and acts by diffusion—a localized volume transmission—to reach oxytocin receptors on GRP neurons and facilitate male sexual function.
en-copyright=
kn-copyright=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SatohKeita
en-aut-sei=Satoh
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UtaDaisuke
en-aut-sei=Uta
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NagafuchiJunta
en-aut-sei=Nagafuchi
en-aut-mei=Junta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TateishiSayaka
en-aut-sei=Tateishi
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UedaRyota
en-aut-sei=Ueda
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakanamiKeiko
en-aut-sei=Takanami
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoungLarry J.
en-aut-sei=Young
en-aut-mei=Larry J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=GalioneAntony
en-aut-sei=Galione
en-aut-mei=Antony
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MorrisJohn F.
en-aut-sei=Morris
en-aut-mei=John F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Applied Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Center for Translational Social Neuroscience, Silvio O. Conte Center for Oxytocin and Social Cognition, Department of Psychiatry and Behavioral Sciences, Yerkes National Primate Research Center, Emory University
kn-affil=

affil-num=9
en-affil=Department of Pharmacology, University of Oxford
kn-affil=

affil-num=10
en-affil=Department of Physiology, Anatomy & Genetics, University of Oxford
kn-affil=

affil-num=11
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=12
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=localized volume transmission
kn-keyword=localized volume transmission
en-keyword=spinal cord
kn-keyword=spinal cord
en-keyword=male sexual activity
kn-keyword=male sexual activity
en-keyword=gastrin-releasing peptide
kn-keyword=gastrin-releasing peptide
en-keyword=spinal ejaculation generator
kn-keyword=spinal ejaculation generator
END

start-ver=1.4
cd-journal=joma
no-vol=330
cd-vols=
no-issue=
article-no=
start-page=788
end-page=196
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201111
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Self-assembling A6K peptide nanotubes as a mercaptoundecahydrododecaborate (BSH) delivery system for boron neutron capture t (BNCT)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Boron neutron capture therapy (BNCT) is a tumor selective therapy, the effectiveness of which depends on sufficient 10B delivery to and accumulation in tumors. In this study, we used self-assembling A6K peptide nanotubes as boron carriers and prepared new boron agents by simple mixing of A6K and BSH. BSH has been used to treat malignant glioma patients in clinical trials and its drug safety and availability have been confirmed; however, its contribution to BNCT efficacy is low. A6K nanotube delivery improved two major limitations of BSH, including absence of intracellular transduction and non-specific drug delivery to tumor tissue. Varying the A6K peptide and BSH mixture ratio produced materials with different morphologies—determined by electron microscopy—and intracellular transduction efficiencies. We investigated the A6K/BSH 1:10 mixture ratio and found high intracellular boron uptake with no toxicity. Microscopy observation showed intracellular localization of A6K/BSH in the perinuclear region and endosome in human glioma cells. The intracellular boron concentration using A6K/BSH was almost 10 times higher than that of BSH. The systematic administration of A6K/BSH via mouse tail vein showed tumor specific accumulation in a mouse brain tumor model with immunohistochemistry and pharmacokinetic study. Neutron irradiation of glioma cells treated with A6K/BSH showed the inhibition of cell proliferation in a colony formation assay. Boron delivery using A6K peptide provides a unique and simple strategy for next generation BNCT drugs.
en-copyright=
kn-copyright=

en-aut-name=MichiueHiroyuki
en-aut-sei=Michiue
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukunagaAsami
en-aut-sei=Fukunaga
en-aut-mei=Asami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsuboiNobushige
en-aut-sei=Tsuboi
en-aut-mei=Nobushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsushitaHiroaki
en-aut-sei=Matsushita
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IgawaKazuyo
en-aut-sei=Igawa
en-aut-mei=Kazuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KasaiTomonari
en-aut-sei=Kasai
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KondoNatsuko
en-aut-sei=Kondo
en-aut-mei=Natsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MatsuiHideki
en-aut-sei=Matsui
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FuruyaShuichi
en-aut-sei=Furuya
en-aut-mei=Shuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Applied Chemistry, Kindai University
kn-affil=

affil-num=3
en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=8
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=9
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=10
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=11
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=
en-keyword=Malignant brain tumor
kn-keyword=Malignant brain tumor
en-keyword=Boron neutron capture therapy (BNCT)
kn-keyword=Boron neutron capture therapy (BNCT)
en-keyword=Peptide nanotube
kn-keyword=Peptide nanotube
en-keyword=Boron drug
kn-keyword=Boron drug
en-keyword=Drug delivery system (DDS)
kn-keyword=Drug delivery system (DDS)
en-keyword=A6K peptide
kn-keyword=A6K peptide
END

start-ver=1.4
cd-journal=joma
no-vol=95
cd-vols=
no-issue=3
article-no=
start-page=119
end-page=131
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200601
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ribosome rescue activity of an Arabidopsis thaliana ArfB homolog
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A homolog of the bacterial ribosome rescue factor ArfB was identified in Arabidopsis thaliana. The factor, named AtArfB for Arabidopsis thaliana ArfB, showed ribosome rescue activity in both in vivo and in vitro assays based on the bacterial translation system. As has been shown for ArfB, the ribosome rescue activity of AtArfB was dependent on the GGQ motif, the crucial motif for the function of class I release factors and ArfB. The C-terminal region of AtArfB was also important for its function. The N-terminal region of AtArfB, which is absent in bacterial ArfB, functioned as a transit peptide for chloroplast targeting in tobacco cells. These results strongly suggest that AtArfB is a ribosome rescue factor that functions in chloroplasts.
en-copyright=
kn-copyright=

en-aut-name=NagaoMichiaki
en-aut-sei=Nagao
en-aut-mei=Michiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsuchiyaFumina
en-aut-sei=Tsuchiya
en-aut-mei=Fumina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MotohashiReiko
en-aut-sei=Motohashi
en-aut-mei=Reiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AboTatsuhiko
en-aut-sei=Abo
en-aut-mei=Tatsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University 
kn-affil=

affil-num=2
en-affil=Graduate School of Integrated Science and Technology, Shizuoka University 
kn-affil=

affil-num=3
en-affil=Graduate School of Integrated Science and Technology, Shizuoka University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University 
kn-affil=
en-keyword=Arabidopsis thaliana
kn-keyword=Arabidopsis thaliana
en-keyword=ArfB
kn-keyword=ArfB
en-keyword=chloroplast
kn-keyword=chloroplast
en-keyword=ribosome rescue
kn-keyword=ribosome rescue
en-keyword=translation
kn-keyword=translation
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=19087
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20201105
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cell cycle dependence of apoptosis photo-triggered using peptide-photosensitizer conjugate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Investigation of the relevance between cell cycle status and the bioactivity of exogenously delivered biomacromolecules is hindered by their time-consuming cell internalization and the cytotoxicity of transfection methods. In this study, we addressed these problems by utilizing the photochemical internalization (PCI) method using a peptide/protein-photosensitizer conjugate, which enables immediate cytoplasmic internalization of the bioactive peptides/proteins in a light-dependent manner with low cytotoxicity. To identify the cell-cycle dependent apoptosis, a TatBim peptide-photosensitizer conjugate (TatBim-PS) with apoptotic activity was photo-dependently internalized into HeLa cells expressing a fluorescent ubiquitination-based cell cycle indicator (Fucci2). Upon irradiation, cytoplasmic TatBim-PS internalization exceeded 95% for all cells classified in the G(1), S, and G(2)/M cell cycle phases with no significant differences between groups. TatBim-PS-mediated apoptosis was more efficiently triggered by photoirradiation in the G(1)/S transition than in the G(1) and S/G(2)/M phases, suggesting high sensitivity of the former phase to Bim-induced apoptosis. Thus, the cell cycle dependence of Bim peptide-induced apoptosis was successfully investigated using Fucci2 indicator and the PCI method. Since PCI-mediated cytoplasmic internalization of peptides is rapid and does not span multiple cell cycle phases, the Fucci-PCI method constitutes a promising tool for analyzing the cell cycle dependence of peptides/protein functions.
en-copyright=
kn-copyright=

en-aut-name=KimHyungjin
en-aut-sei=Kim
en-aut-mei=Hyungjin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WatanabeSho
en-aut-sei=Watanabe
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Applied Chemistry, Kindai University
kn-affil=

affil-num=4
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=Biological techniques
kn-keyword=Biological techniques
en-keyword=Biotechnology
kn-keyword=Biotechnology
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=16
article-no=
start-page=e015103
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200818
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Luseogliflozin on Heart Failure With Preserved Ejection Fraction in Patients With Diabetes Mellitus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background</br>
Effects of sodium‐glucose cotransporter 2 inhibitors on reducing hospitalization for heart failure have been reported in randomized controlled trials, but their effects on patients with heart failure with preserved ejection fraction (HFpEF) are unknown. This study aimed to evaluate the drug efficacy of luseogliflozin, a sodium‐glucose cotransporter 2 inhibitor, in patients with type 2 diabetes mellitus and HFpEF.</br>
Methods and Results</br>
We performed a multicenter, open‐label, randomized, controlled trial for comparing luseogliflozin 2.5 mg once daily with voglibose 0.2 mg 3 times daily in patients with type 2 diabetes mellitus suffering from HFpEF (left ventricular ejection fraction >45% and BNP [B‐type natriuretic peptide] concentrations ≥35 pg/mL) in a 1:1 randomization fashion. The primary outcome was the difference from baseline in BNP levels after 12 weeks of treatment between the 2 drugs. A total of 173 patients with diabetes mellitus and HFpEF were included. Of these, 83 patients were assigned to receive luseogliflozin and 82 to receive voglibose. There was no significant difference in the reduction in BNP concentrations after 12 weeks from baseline between the 2 groups. The ratio of the mean BNP value at week 12 to the baseline value was 0.79 in the luseogliflozin group and 0.87 in the voglibose group (percent change, −9.0% versus −1.9%; ratio of change with luseogliflozin versus voglibose, 0.93; 95% CI, 0.78–1.10; P=0.26).</br>
Conclusion</br>
In patients with type 2 diabetes mellitus and HFpEF, there is no significant difference in the degree of reduction in BNP concentrations after 12 weeks between luseogliflozin and voglibose.
en-copyright=
kn-copyright=

en-aut-name=EjiriKentaro
en-aut-sei=Ejiri
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KiharaHajime
en-aut-sei=Kihara
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HataYoshiki
en-aut-sei=Hata
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaganoToshihiko
en-aut-sei=Nagano
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakaishiAtsushi
en-aut-sei=Takaishi
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TodaHironobu
en-aut-sei=Toda
en-aut-mei=Hironobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NanbaSeiji
en-aut-sei=Nanba
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraYoichi
en-aut-sei=Nakamura
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakuragiSatoru
en-aut-sei=Sakuragi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MinagawaTaro
en-aut-sei=Minagawa
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NishiiNobuhiro
en-aut-sei=Nishii
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FukeSoichiro
en-aut-sei=Fuke
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YoshikawaMasaki
en-aut-sei=Yoshikawa
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine, Kihara Cardiovascular Clinic
kn-affil=

affil-num=4
en-affil=Department of Cardiology, Minamino Cardiovascular Hospital
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Iwasa Hospital
kn-affil=

affil-num=6
en-affil=Department of Cardiology, Mitoyo General Hospital
kn-affil=

affil-num=7
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cardiology, Okayama Rosai Hospital
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, Specified Clinic of Soyokaze Cardiovascular Medicine and Diabetes Care
kn-affil=

affil-num=10
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cardiovascular Medicine, Iwakuni Clinical Center
kn-affil=

affil-num=12
en-affil=Department of Internal Medicine, Minagawa Cardiovascular Clinic
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Okayama City Hospital
kn-affil=

affil-num=14
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=16
en-affil=Department of Cardiology, Fukuyama City Hospital
kn-affil=

affil-num=17
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=
en-keyword=B-type natriuretic peptide
kn-keyword=B-type natriuretic peptide
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
en-keyword=heart failure
kn-keyword=heart failure
en-keyword=sodium-glucose cotransporter 2 inhibitor
kn-keyword=sodium-glucose cotransporter 2 inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=10
article-no=
start-page=2149
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200923
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In Vitro Studies to Define the Cell-Surface and Intracellular Targets of Polyarginine-Conjugated Sodium Borocaptate as a Potential Delivery Agent for Boron Neutron Capture Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Boron neutron capture therapy (BNCT) requires pharmaceutical innovations and molecular-based evidence of effectiveness to become a standard cancer therapeutic in the future. Recently, in Japan, 4-borono-L-phenylalanine (BPA) was approved as a boron agent for BNCT against head and neck (H&N) cancers. H&N cancer appears to be a suitable target for BPA-BNCT, because the expression levels of L-type amino acid transporter 1 (LAT1), one of the amino acid transporters responsible for BPA uptake, are elevated in most cases of H&N cancer. However, in other types of cancer including malignant brain tumors, LAT1 is not always highly expressed. To expand the possibility of BNCT for these cases, we previously developed poly-arginine peptide (polyR)-conjugated mercaptoundecahydrododecaborate (BSH). PolyR confers the cell membrane permeability and tumor selectivity of BSH. However, the molecular determinants for the properties are not fully understood. In this present study, we have identified the cluster of differentiation 44 (CD44) protein and translational machinery proteins as a major cell surface target and intracellular targets of BSH-polyR, respectively. CD44, also known as a stem cell-associated maker in various types of cancer, is required for the cellular uptake of polyR-conjugated molecules. We showed that BSH-polyR was predominantly delivered to a CD44(High) cell population of cancer cells. Once delivered, BSH-polyR interacted with the translational machinery components, including the initiation factors, termination factors, and poly(A)-biding protein (PABP). As a proof of principle, we performed BSH-polyR-based BNCT against glioma stem-like cells and revealed that BSH-polyR successfully induced BNCT-dependent cell death specifically in CD44(High) cells. Bioinformatics analysis indicated that BSH-polyR would be suitable for certain types of malignant tumors. Our results shed light on the biochemical properties of BSH-polyR, which may further contribute to the therapeutic optimization of BSH-BNCT in the future.
en-copyright=
kn-copyright=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuiSeiji
en-aut-sei=Yasui
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IgawaKazuyo
en-aut-sei=Igawa
en-aut-mei=Kazuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UedaAi
en-aut-sei=Ueda
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeKaori
en-aut-sei=Watanabe
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HanafusaTadashi
en-aut-sei=Hanafusa
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IchikawaYasuaki
en-aut-sei=Ichikawa
en-aut-mei=Yasuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshihashiSachiko
en-aut-sei=Yoshihashi
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsuchidaKazuki
en-aut-sei=Tsuchida
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KamiyaAtsunori
en-aut-sei=Kamiya
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FuruyaShuichi
en-aut-sei=Furuya
en-aut-mei=Shuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=3
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=4
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=5
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=6
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Engineering, Nagoya University
kn-affil=

affil-num=9
en-affil=Graduate School of Engineering, Nagoya University
kn-affil=

affil-num=10
en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=
en-keyword=boron neutron capture therapy (BNCT)
kn-keyword=boron neutron capture therapy (BNCT)
en-keyword=BSH-polyR
kn-keyword=BSH-polyR
en-keyword=CD44
kn-keyword=CD44
en-keyword=translational machinery
kn-keyword=translational machinery
en-keyword=bioinformatics
kn-keyword=bioinformatics
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=5
article-no=
start-page=449
end-page=453
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Seronegative Oligoarthritis Preceding Psoriasis by 9.5 Years
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We report a case of psoriatic arthritis where oligoarthritis preceded the skin lesions. A 57-year-old man complained of left third-finger pain. Laboratory examinations were negative for anti-cyclic citrullinated peptide antibodies and rheumatoid factor; he was treated for suspected rheumatoid arthritis. Six years later, X-ray revealed enthesitis of his fingers and wrist joint. At 9.5 years after the initial visit, skin lesions appeared in the left auricular region and buttock and dermatopathology findings indicated psoriasis vulgaris. The final diagnosis was psoriatic arthritis. In cases of seronegative oligoarthritis, psoriatic arthritis must be considered because some patients demonstrate osteoarticular lesions preceding skin lesions.
en-copyright=
kn-copyright=

en-aut-name=TsuchiyaJunpei
en-aut-sei=Tsuchiya
en-aut-mei=Junpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KondoNaoki
en-aut-sei=Kondo
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujimotoAtsushi
en-aut-sei=Fujimoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoRie
en-aut-sei=Kondo
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamadaMasahiko
en-aut-sei=Yamada
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KuraishiTatsuya
en-aut-sei=Kuraishi
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YodaTakuya
en-aut-sei=Yoda
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AbeRiichiro
en-aut-sei=Abe
en-aut-mei=Riichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EndoNaoto
en-aut-sei=Endo
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=2
en-affil=Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=3
en-affil=Division of Dermatology, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=4
en-affil=Division of Respiratory Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=5
en-affil=Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=6
en-affil=Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=7
en-affil=Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=8
en-affil=Division of Dermatology, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=

affil-num=9
en-affil=Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences
kn-affil=
en-keyword=enthesitis
kn-keyword=enthesitis
en-keyword=psoriatic arthritis
kn-keyword=psoriatic arthritis
en-keyword=seronegative oligoarthritis
kn-keyword=seronegative oligoarthritis
en-keyword=classification criteria for psoriatic arthritis
kn-keyword=classification criteria for psoriatic arthritis
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=5
article-no=
start-page=381
end-page=389
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical Relevance of Serum Prolactin Levels to Inflammatory Reaction in Male Patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To clarify the relevance of prolactin (PRL) to clinical parameters in patients who visited our general medicine department, medical records of 353 patients in whom serum PRL levels were measured during the period from 2016 to 2018 were retrospectively reviewed. Data for 140 patients (M/F: 42/98) were analyzed after excluding patients lacking detailed records and patients taking dopaminergic agents. Median serum PRL levels were significantly lower in males than females: 6.5 ng/ml (IQR: 4.2-10.3) versus 8.1 ng/ml (5.9-12.9), respectively. Pain and general fatigue were the major symptoms at the first visit, and past histories of hypertension and dyslipidemia were frequent. Male patients with relatively high PRL levels (≥ 10 ng/ml) had significantly lower levels of serum albumin and significantly higher levels of serum LDH than those with low PRL (< 10 ng/ml). There were significant correlations of male PRL level with the erythrocyte sedimentation rate (R=0.62), serum LDH level (R=0.39) and serum albumin level (R=−0.52), while the level of serum CRP (R=0.33) showed an insignificant but weak positive correlation with PRL level. Collectively, these results show that PRL levels had gender-specific relevance to various clinical factors, with PRL levels in males being significantly related to inflammatory status.
en-copyright=
kn-copyright=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HanayamaYoshihisa
en-aut-sei=Hanayama
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HasegawaKou
en-aut-sei=Hasegawa
en-aut-mei=Kou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiTomoko
en-aut-sei=Miyoshi
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OgawaHiroko
en-aut-sei=Ogawa
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ObikaMikako
en-aut-sei=Obika
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoshimaKoichi
en-aut-sei=Itoshima
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Laboratory Medicine, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=hormones
kn-keyword=hormones
en-keyword=hyperprolactinemia
kn-keyword=hyperprolactinemia
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=pituitary
kn-keyword=pituitary
en-keyword=prolactin
kn-keyword=prolactin
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=1
article-no=
start-page=14928
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dysfunction of CD8+PD-1+T cells in type 2 diabetes caused by the impairment of metabolism-immune axis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The metabolic changes and dysfunction in CD8+T cells may be involved in tumor progression and susceptibility to virus infection in type 2 diabetes (T2D). In C57BL/6JJcl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8+splenic and tumor-infiltrating lymphocytes (TILs) was impaired and associated with enhanced tumor growth, which were inhibited by metformin. In CD8+splenic T cells from the HFS mice, glycolysis/basal respiration ratio was significantly reduced and reversed by metformin. In the patients with T2D (DM), multifunctionality of circulating CD8+PD-1+T cells stimulated with PMA/ionomycin as well as with HLA-A*24:02 CMV peptide was dampened, while metformin recovered multifunctionality. Both glycolysis and basal respiration were reduced in DM, and glycolysis was increased by metformin. The disturbance of the link between metabolism and immune function in CD8+PD-1+T cells in T2D was proved by recovery of antigen-specific and non-specific cytokine production via metformin-mediated increase in glycolytic activity.
en-copyright=
kn-copyright=

en-aut-name=NojimaIchiro
en-aut-sei=Nojima
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EikawaShingo
en-aut-sei=Eikawa
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HadaYoshiko
en-aut-sei=Hada
en-aut-mei=Yoshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KajitaniNobuo
en-aut-sei=Kajitani
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TeshigawaraSanae
en-aut-sei=Teshigawara
en-aut-mei=Sanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ToneAtsuhito
en-aut-sei=Tone
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UchidaHaruhito A.
en-aut-sei=Uchida
en-aut-mei=Haruhito A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=EguchiJun
en-aut-sei=Eguchi
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=UdonoHeiichiro
en-aut-sei=Udono
en-aut-mei=Heiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Hematology/Oncology, Hess Cancer Institute, Icahn School of Medicine At Mount Sinai
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Diabetes Center, Okayama City Hospital
kn-affil=

affil-num=6
en-affil=Diabetes Center, Okayama S
kn-affil=italama Univ, Dept Med & Clin Sci, Grad Sch Med Dent & Pharmaceut Sci

affil-num=7
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Diabetes Center, Okayama Saiseikai General Hospital
kn-affil=

affil-num=9
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=13
en-affil=Department of Immunology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cytokines
kn-keyword=Cytokines
en-keyword=Diabetes
kn-keyword=Diabetes
en-keyword=Endocrine system and metabolic diseases
kn-keyword=Endocrine system and metabolic diseases
en-keyword=Immunology
kn-keyword=Immunology
en-keyword=Tumour immunology
kn-keyword=Tumour immunology
END

start-ver=1.4
cd-journal=joma
no-vol=529
cd-vols=
no-issue=7
article-no=
start-page=1372
end-page=1390
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200906
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Variation of pro‐vasopressin processing in parvocellular and magnocellular neurons in the paraventricular nucleus of the hypothalamus: Evidence from the vasopressin‐related glycopeptide copeptin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Arginine vasopressin (AVP) is synthesized in parvocellular‐ and magnocellular neuroendocrine neurons in the paraventricular nucleus (PVN) of the hypothalamus. Whereas magnocellular AVP neurons project primarily to the posterior pituitary, parvocellular AVP neurons project to the median eminence (ME) and to extrahypothalamic areas. The AVP gene encodes pre‐pro‐AVP that comprises the signal peptide, AVP, neurophysin (NPII), and a copeptin glycopeptide. In the present study, we used an N‐terminal copeptin antiserum to examine copeptin expression in magnocellular and parvocellular neurons in the hypothalamus in the mouse, rat, and macaque monkey. Although magnocellular NPII‐expressing neurons exhibited strong N‐terminal copeptin immunoreactivity in all three species, a great majority (~90%) of parvocellular neurons that expressed NPII was devoid of copeptin immunoreactivity in the mouse, and in approximately half (~53%) of them in the rat, whereas in monkey hypothalamus, virtually all NPII‐immunoreactive parvocellular neurons contained strong copeptin immunoreactivity. Immunoelectron microscopy in the mouse clearly showed copeptin‐immunoreactivity co‐localized with NPII‐immunoreactivity in neurosecretory vesicles in the internal layer of the ME and posterior pituitary, but not in the external layer of the ME. Intracerebroventricular administration of a prohormone convertase inhibitor, hexa‐d‐arginine amide resulted in a marked reduction of copeptin‐immunoreactivity in the NPII‐immunoreactive magnocellular PVN neurons in the mouse, suggesting that low protease activity and incomplete processing of pro‐AVP could explain the disproportionally low levels of N‐terminal copeptin expression in rodent AVP (NPII)‐expressing parvocellular neurons. Physiologic and phylogenetic aspects of copeptin expression among neuroendocrine neurons require further exploration.
en-copyright=
kn-copyright=

en-aut-name=KawakamiNatsuko
en-aut-sei=Kawakami
en-aut-mei=Natsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtuboAkito
en-aut-sei=Otubo
en-aut-mei=Akito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaejimaSho
en-aut-sei=Maejima
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TalukderAshraf H.
en-aut-sei=Talukder
en-aut-mei=Ashraf H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatohKeita
en-aut-sei=Satoh
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakanamiKeiko
en-aut-sei=Takanami
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UedaYasumasa
en-aut-sei=Ueda
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ItoiKeiichi
en-aut-sei=Itoi
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MorrisJohn F.
en-aut-sei=Morris
en-aut-mei=John F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Laboratory of Information Biology, Graduate School of Information Sciences, Tohoku University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Physiology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=9
en-affil=Laboratory of Information Biology, Graduate School of Information Sciences, Tohoku University
kn-affil=

affil-num=10
en-affil=Department of Physiology, Anatomy and Genetics, University of Oxford
kn-affil=

affil-num=11
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=12
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=copeptin
kn-keyword=copeptin
en-keyword=hypothalamo‐pituitary–adrenal system
kn-keyword=hypothalamo‐pituitary–adrenal system
en-keyword=immunohistochemistry
kn-keyword=immunohistochemistry
en-keyword=paraventricular nucleus of the hypothalamus
kn-keyword=paraventricular nucleus of the hypothalamus
en-keyword=processing
kn-keyword=processing
en-keyword=vasopressin
kn-keyword=vasopressin
en-keyword=RRID: AB_2722604
kn-keyword=RRID: AB_2722604
en-keyword=RRID: AB_2061966
kn-keyword=RRID: AB_2061966
en-keyword=RRID: AB_2314234
kn-keyword=RRID: AB_2314234
en-keyword=RRID: AB_10013361
kn-keyword=RRID: AB_10013361
en-keyword=RRID: AB_2313960
kn-keyword=RRID: AB_2313960
en-keyword=RRID: AB_2722605
kn-keyword=RRID: AB_2722605
en-keyword=RRID: AB_90782
kn-keyword=RRID: AB_90782
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=
article-no=
start-page=541
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200819
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Transcriptomic Analysis of the Kuruma PrawnMarsupenaeus japonicusReveals Possible Peripheral Regulation of the Ovary
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Crustacean reproduction has been hypothesized to be under complex endocrinological regulation by peptide hormones. To further improve our understanding of the mechanisms underlying this complex regulation, knowledge is needed regarding the hormones not only of the central nervous system (CNS) such as the X-organ/sinus gland (XOSG), brain, and thoracic ganglia, but also the peripheral gonadal tissues. For example, in vertebrates, some gonadal peptide hormones including activin, inhibin, follistatin, and relaxin are known to be involved in the reproductive physiology. Therefore, it is highly likely that some peptide factors from the ovary are serving as the signals among peripheral tissues and central nervous tissues in crustaceans. In this work, we sought to find gonadal peptide hormones and peptide hormone receptors by analyzing the transcriptome of the ovary of the kuruma prawnMarsupenaeus japonicus. The generated ovarian transcriptome data led to the identification of five possible peptide hormones, including bursicon-alpha and -beta, the crustacean hyperglycemic hormone (CHH)-like peptide, insulin-like peptide (ILP), and neuroparsin-like peptide (NPLP). Dominant gene expressions for the bursicons were observed in the thoracic ganglia and the ovary, in the CNS for the CHH-like peptide, in the heart for NPLP, and in the ovary for ILP. Since the gene expressions of CHH-like peptide and NPLP were affected by a CHH (Penaeus japonicussinus gland peptide-I) from XOSG, we produced recombinant peptides for CHH-like peptide and NPLP usingEscherichia coliexpression system to examine their possible peripheral regulation. As a result, we found that the recombinant NPLP increased vitellogenin gene expression in incubated ovarian tissue fragments. Moreover, contigs encoding putative receptors for insulin-like androgenic gland factor, insulin, neuroparsin, and neuropeptide Y/F, as well as several contigs encoding orphan G-protein coupled receptors and receptor-type guanylyl cyclases were also identified in the ovarian transcriptome. These results suggest that reproductive physiology in crustaceans is regulated by various gonadal peptide hormones, akin to vertebrates.
en-copyright=
kn-copyright=

en-aut-name=TsutsuiNaoaki
en-aut-sei=Tsutsui
en-aut-mei=Naoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KobayashiYasuhisa
en-aut-sei=Kobayashi
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IzumikawaKouichi
en-aut-sei=Izumikawa
en-aut-mei=Kouichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Faculty of Science, Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Science, Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=3
en-affil=Research Institute for Fisheries Science, Okayama Prefectural Technology Center for Agriculture, Forestry, and Fisheries
kn-affil=

affil-num=4
en-affil=Faculty of Science, Ushimado Marine Institute, Okayama University
kn-affil=
en-keyword=peptide hormone
kn-keyword=peptide hormone
en-keyword=Marsupenaeus japonicus
kn-keyword=Marsupenaeus japonicus
en-keyword=ovary
kn-keyword=ovary
en-keyword=reproduction
kn-keyword=reproduction
en-keyword=transcriptome
kn-keyword=transcriptome
en-keyword=vitellogenesis
kn-keyword=vitellogenesis
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=12
article-no=
start-page=4422
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200622
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Effects of Mutual Interaction of Orexin-A and Glucagon-Like Peptide-1 on Reflex Swallowing Induced by SLN Afferents in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=(1) Background: Our previous studies revealed that orexin-A, an appetite-increasing peptide, suppressed reflex swallowing via the commissural part of the nucleus tractus solitarius (cNTS), and that glucagon-like peptide-1 (GLP-1), an appetite-reducing peptide, also suppressed reflex swallowing via the medial nucleus of the NTS (mNTS). In this study, we examined the mutual interaction between orexin-A and GLP-1 in reflex swallowing. (2) Methods: Sprague-Dawley rats under urethane-chloralose anesthesia were used. Swallowing was induced by electrical stimulation of the superior laryngeal nerve (SLN) and was identified by the electromyographic (EMG) signals obtained from the mylohyoid muscle. (3) Results: The injection of GLP-1 (20 pmol) into the mNTS reduced the swallowing frequency and extended the latency of the first swallow. These suppressive effects of GLP-1 were not observed after the fourth ventricular administration of orexin-A. After the injection of an orexin-1 receptor antagonist (SB334867) into the cNTS, an ineffective dose of GLP-1 (6 pmol) into the mNTS suppressed reflex swallowing. Similarly, the suppressive effects of orexin-A (1 nmol) were not observed after the injection of GLP-1 (6 pmol) into the mNTS. After the administration of a GLP-1 receptor antagonist (exendin-4(5-39)), an ineffective dose of orexin-A (0.3 nmol) suppressed reflex swallowing. (4) Conclusions: The presence of reciprocal inhibitory connections between GLP-1 receptive neurons and orexin-A receptive neurons in the NTS was strongly suggested.
en-copyright=
kn-copyright=

en-aut-name=KobashiMotoi
en-aut-sei=Kobashi
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShimataniYuichi
en-aut-sei=Shimatani
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujitaMasako
en-aut-sei=Fujita
en-aut-mei=Masako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsuoRyuji
en-aut-sei=Matsuo
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Engineering, Faculty of Science and Engineering, Tokyo City University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Oral Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=GLP-1
kn-keyword=GLP-1
en-keyword=orexin
kn-keyword=orexin
en-keyword=SB334867
kn-keyword=SB334867
en-keyword=swallowing
kn-keyword=swallowing
en-keyword=NTS
kn-keyword=NTS
en-keyword=rats
kn-keyword=rats
END

start-ver=1.4
cd-journal=joma
no-vol=34
cd-vols=
no-issue=
article-no=
start-page=575
end-page=582
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200608
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improvement of biodistribution profile of a radiogallium-labeled, αvβ6 integrin-targeting peptide probe by incorporation of negatively charged amino acids
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective</br>
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers. Since αvβ6 integrin has been reported as a promising target for PDAC diagnosis, we previously developed H-Cys(mal-NOTA-67Ga)-(Gly)6-A20FMDV2-NH2 ([67Ga]CG6) as an αvβ6 integrin-targeting probe. Although [67Ga]CG6 specifically binds to αvβ6 integrin-positive xenografts, the uptake of [67Ga]CG6 in the organs surrounding the pancreas, such as the liver and spleen, was comparable to that in the αvβ6 integrin-positive xenografts. We hypothesized that the undesirable accumulation of [67Ga]CG6 in those organs was caused by the positive charges of [67Ga]CG6 (+ 3). In this study, we aimed to decrease [67Ga]CG6 uptake in the liver and spleen by reducing the electric charges of the probe.</br>
Methods</br>
We synthesized H-Cys(mal-NOTA-67Ga)-(Asp)6-A20FMDV2-NH2 ([67Ga]CD6) and evaluated its affinity to αvβ6 integrin via in vitro competitive binding assay. Isoelectric points of the probes were determined by electrophoresis. Biodistribution study, autoradiography, and immunostaining for β6 integrin were conducted using αvβ6 integrin-positive and negative tumor-bearing mice.</br>
Results</br>
In vitro competitive binding assay showed that the alteration of the linker had a negligible impact on the affinity of [67Ga]CG6 to αvβ6 integrin. The results of electrophoresis revealed that [67Ga]CG6 was positively charged whereas [67Ga]CD6 was negatively charged. In the biodistribution study, the uptake of [67Ga]CD6 in the αvβ6 integrin-positive xenografts was significantly higher than that in the αvβ6 integrin-negative ones at 60 and 120 min. The uptake of [67Ga]CD6 in the liver and spleen was more than two-fold lower than that of [67Ga]CG6 at both time points. In the immunohistochemistry study, the radioactivity accumulated areas in the autoradiogram of the αvβ6 integrin-positive xenograft roughly coincided with β6 integrin-expressing areas.</br>
Conclusion</br>
We have successfully reduced the nonspecific uptake in the liver and spleen by altering the linker amino acid from G6 to D6. [67Ga]CD6 overcame the drawbacks of [67Ga]CG6 in its biodistribution.
en-copyright=
kn-copyright=

en-aut-name=NakamuraShunsuke
en-aut-sei=Nakamura
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsunoAya
en-aut-sei=Matsuno
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UedaMasashi
en-aut-sei=Ueda
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil= Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=αvβ6 integrin
kn-keyword=αvβ6 integrin
en-keyword=Pancreatic ductal adenocarcinoma (PDAC)
kn-keyword=Pancreatic ductal adenocarcinoma (PDAC)
en-keyword=A20FMDV2
kn-keyword=A20FMDV2
en-keyword=Aspartic acids
kn-keyword=Aspartic acids
en-keyword=Electric charge
kn-keyword=Electric charge
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=4
article-no=
start-page=e1008469
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200423
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Non-pathogenic Escherichia coli acquires virulence by mutating a growth-essential LPS transporter
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The molecular mechanisms that allow pathogenic bacteria to infect animals have been intensively studied. On the other hand, the molecular mechanisms by which bacteria acquire virulence functions are not fully understood. In the present study, we experimentally evaluated the evolution of a non-pathogenic strain of Escherichia coli in a silkworm infection model and obtained pathogenic mutant strains. As one cause of the high virulence properties of E. coli mutants, we identified amino acid substitutions in LptD (G580S) and LptE (T95I) constituting the lipopolysaccharide (LPS) transporter, which translocates LPS from the inner to the outer membrane and is essential for E. coli growth. The growth of the LptD and LptE mutants obtained in this study was indistinguishable from that of the parent strain. The LptD and LptE mutants exhibited increased secretion of outer membrane vesicles containing LPS and resistance against various antibiotics, antimicrobial peptides, and host complement. In vivo cross-linking studies revealed that the conformation of the LptD-LptE complex was altered in the LptD and LptE mutants. Furthermore, several clinical isolates of E. coli carried amino acid substitutions of LptD and LptE that conferred resistance against antimicrobial substances. This study demonstrated an experimental evolution of bacterial virulence properties in an animal infection model and identified functional alterations of the growth-essential LPS transporter that led to high bacterial virulence by conferring resistance against antimicrobial substances. These findings suggest that non-pathogenic bacteria can gain virulence traits by changing the functions of essential genes, and provide new insight to bacterial evolution in a host environment. 

Author summary 

Pathogenic bacteria developed their virulence properties by changing the functions of various genes after the emergence of the host animals on earth. The types of gene function alterations that confer bacterial virulence properties, however, have remained unclear. We utilized a silkworm infection model to perform an experimental evolution of bacterial virulence activity. From a non-pathogenic strain of Escherichia coli, we obtained a mutant strain that exhibited 500-fold higher virulence than the original strain and identified mutations of the lipopolysaccharide (LPS) transporter, which translocates LPS onto the bacterial surface, as one cause of the high virulence. The mutations changed the structure of the LPS transporter, increased the secretion of outer membrane vesicles, and enabled bacterial survival in the presence of host antimicrobial substances. This mechanism to gain high virulence occurs naturally, as several E. coli clinical isolates carried mutations of the LPS transporter that confer resistance against antimicrobial substances. Our study unveiled a novel mechanism by which bacteria increase their virulence through modifying their gene function.
en-copyright=
kn-copyright=

en-aut-name=KaitoChikara
en-aut-sei=Kaito
en-aut-mei=Chikara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshikaiHirono
en-aut-sei=Yoshikai
en-aut-mei=Hirono
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WakamatsuAi
en-aut-sei=Wakamatsu
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyashitaAtsushi
en-aut-sei=Miyashita
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsumotoYasuhiko
en-aut-sei=Matsumoto
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiyukiTomoko
en-aut-sei=Fujiyuki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatoMasaru
en-aut-sei=Kato
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OguraYoshitoshi
en-aut-sei=Ogura
en-aut-mei=Yoshitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HayashiTetsuya
en-aut-sei=Hayashi
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IsogaiTakao
en-aut-sei=Isogai
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SekimizuKazuhisa
en-aut-sei=Sekimizu
en-aut-mei=Kazuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Pharmaceutical Sciences, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Japan Biological Informatics Consortium (JBIC)
kn-affil=

affil-num=4
en-affil=Graduate School of Pharmaceutical Sciences, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Microbiology, Meiji Pharmaceutical University
kn-affil=

affil-num=6
en-affil=The Institute of Medical Science, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Devision of Bioanalytical Chemistry, School of Pharmacy,Showa University
kn-affil=

affil-num=8
en-affil=Department of Bacteriology, Faculty of Medical Sciences,Kyushu University
kn-affil=

affil-num=9
en-affil=Department of Bacteriology, Faculty of Medical Sciences,Kyushu University
kn-affil=

affil-num=10
en-affil=Translational Research Center, Fukushima Medical University
kn-affil=

affil-num=11
en-affil=Institute of Medical Mycology, Teikyo University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=1
article-no=
start-page=115189
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development and characterization of a 68Ga-labeled A20FMDV2 peptide probe for the PET imaging of αvβ6 integrin-positive pancreatic ductal adenocarcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pancreatic ductal adenocarcinoma (PDAC) is known to be one of the most lethal cancers. Since the majority of patients are diagnosed at an advanced stage, development of a detection method for PDAC at an earlier stage of disease progression is strongly desirable. Integrin αVβ6 is a promising target for early PDAC detection because its expression increases during precancerous changes. The present study aimed to develop an imaging probe for positron emission tomography (PET) which targets αVβ6 integrin-positive PDAC. We selected A20FMDV2 peptide, which binds specifically to αvβ6 integrin, as a probe scaffold, and 68Ga as a radioisotope. A20FMDV2 peptide has not been previously labeled with 68Ga. A cysteine residue was introduced to the N-terminus of the probe at a site-specific conjugation of maleimide-NOTA (mal-NOTA) chelate. Different numbers of glycine residues were also introduced between cysteine and the A20FMDV2 sequence as a spacer in order to reduce the steric hindrance of the mal-NOTA on the binding probe to αVβ6 integrin. In vitro, the competitive binding assay revealed that probes containing a 6-glycine linker ([natGa]CG6 and [natGa]Ac-CG6) showed high affinity to αVβ6 integrin. Both probes could be labeled by 67/68Ga with high radiochemical yield (>50%) and purity (>98%). On biodistribution analysis, [67Ga]Ac-CG6 showed higher tumor accumulation, faster blood clearance, and lower accumulation in the surrounding organs of pancreas than did [67Ga]CG6. The αVβ6 integrin-positive xenografts were clearly visualized by PET imaging with [68Ga]Ac-CG6. The intratumoral distribution of [68Ga]Ac-CG6 coincided with the αVβ6 integrin-positive regions detected by immunohistochemistry. Thus, [68Ga]Ac-CG6 is a useful peptide probe for the imaging of αVβ6 integrin in PDAC.
en-copyright=
kn-copyright=

en-aut-name=UiTakashi
en-aut-sei=Ui
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UedaMasashi
en-aut-sei=Ueda
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HigakiYusuke
en-aut-sei=Higaki
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaminoShinichiro
en-aut-sei=Kamino
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SanoKohei
en-aut-sei=Sano
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KimuraHiroyuki
en-aut-sei=Kimura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SajiHideo
en-aut-sei=Saji
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=EnomotoShuichi
en-aut-sei=Enomoto
en-aut-mei=Shuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama Universit
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Pharmaceutical Sciences, Kyoto University
kn-affil=

affil-num=6
en-affil=Graduate School of Pharmaceutical Sciences, Kyoto University
kn-affil=

affil-num=7
en-affil=Graduate School of Pharmaceutical Sciences, Kyoto University
kn-affil=

affil-num=8
en-affil=RIKEN Center for Life Science Technologies
kn-affil=
en-keyword=αvβ6 integrin
kn-keyword=αvβ6 integrin
en-keyword=Pancreatic ductal adenocarcinoma
kn-keyword=Pancreatic ductal adenocarcinoma
en-keyword=Gallium-68
kn-keyword=Gallium-68
en-keyword=A20FMDV2 peptide
kn-keyword=A20FMDV2 peptide
en-keyword=Positron emission tomography
kn-keyword=Positron emission tomography
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=2
article-no=
start-page=115
end-page=122
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202004
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Increased Plasma Levels of Platelet Factor 4 and β-thromboglobulin in Women with Recurrent Pregnancy Loss
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Thrombosis in decidual vessels is one of the mechanisms of pregnancy loss. However, few studies have assessed the relation between platelet activation, which is known to cause of thrombosis, and recurrent pregnancy loss (RPL). We investigated platelet activation in women with RPL compared to controls by measuring plasma levels of platelet factor 4 (PF4) and β-thromboglobulin (βTG), and assessed correlations between PF4/βTG and coagulative risk factors associated with RPL. The study group included 135 women who had experienced two or more consecutive pregnancy losses. The control group included 28 age-matched healthy women who had never experienced pregnancy loss. PF4 and βTG plasma levels were significantly higher in the women with RPL than controls (PF4: 14.0 [8.0-20.0] vs. 9.0 [6.0-12.0] ng/ml, p=0.043; βTG: 42.0 [24.3-59.8] vs. 31.5 [26.6-36.4] ng/ml, p=0.002). There was a significant association between βTG and anti-phosphatidylethanolamine antibody immunoglobulin M (aPE IgM) (p=0.048). Among the women with RPL, 18 of those who were positive for PF4 (45%) and 18 of those who were positive for βTG (37%) were negative for all known coagulative risk factors associated with RPL. Measurements of PF4 and βTG may be important because they help identify women who are at risk of RPL.
en-copyright=
kn-copyright=

en-aut-name=KotaniSayoko
en-aut-sei=Kotani
en-aut-mei=Sayoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KamadaYasuhiko
en-aut-sei=Kamada
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShimizuKeiko
en-aut-sei=Shimizu
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakamotoAi
en-aut-sei=Sakamoto
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakatsukaMikiya
en-aut-sei=Nakatsuka
en-aut-mei=Mikiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HiramatsuYuji
en-aut-sei=Hiramatsu
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MasuyamaHisashi
en-aut-sei=Masuyama
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Okayama Rosai Hospital
kn-affil=

affil-num=4
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Okayama City Hospital
kn-affil=

affil-num=7
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=recurrent pregnancy loss
kn-keyword=recurrent pregnancy loss
en-keyword=platelet factor 4
kn-keyword=platelet factor 4
en-keyword=β-thromboglobulin
kn-keyword=β-thromboglobulin
en-keyword=platelet activation
kn-keyword=platelet activation
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=415
end-page=428
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190713
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of endogenous small peptides involved in rice immunity through transcriptomics- and proteomics-based screening
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Small signalling peptides, generated from larger protein precursors, are important components to orchestrate various plant processes such as development and immune responses. However, small signalling peptides involved in plant immunity remain largely unknown. Here, we developed a pipeline using transcriptomics- and proteomics-based screening to identify putative precursors of small signalling peptides: small secreted proteins (SSPs) in rice, induced by rice blast fungus Magnaporthe oryzae and its elicitor, chitin. We identified 236 SSPs including members of two known small signalling peptide families, namely rapid alkalinization factors and phytosulfokines, as well as many other protein families that are known to be involved in immunity, such as proteinase inhibitors and pathogenesis-related protein families. We also isolated 52 unannotated SSPs and among them, we found one gene which we named immune response peptide (IRP) that appeared to encode the precursor of a small signalling peptide regulating rice immunity. In rice suspension cells, the expression of IRP was induced by bacterial peptidoglycan and fungal chitin. Overexpression of IRP enhanced the expression of a defence gene, PAL1 and induced the activation of the MAPKs in rice suspension cells. Moreover, the IRP protein level increased in suspension cell medium after chitin treatment. Collectively, we established a simple and efficient pipeline to discover SSP candidates that probably play important roles in rice immunity and identified 52 unannotated SSPs that may be useful for further elucidation of rice immunity. Our method can be applied to identify SSPs that are involved not only in immunity but also in other plant functions.
en-copyright=
kn-copyright=

en-aut-name=WangPingyu
en-aut-sei=Wang
en-aut-mei=Pingyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YaoShaolun
en-aut-sei=Yao
en-aut-mei=Shaolun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KosamiKen-ichi
en-aut-sei=Kosami
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=GuoTing
en-aut-sei=Guo
en-aut-mei=Ting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiJing
en-aut-sei=Li
en-aut-mei=Jing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ZhangYuanyuan
en-aut-sei=Zhang
en-aut-mei=Yuanyuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FukaoYoichiro
en-aut-sei=Fukao
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Kaneko-KawanoTakako
en-aut-sei=Kaneko-Kawano
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ZhangHeng
en-aut-sei=Zhang
en-aut-mei=Heng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SheYi-Min
en-aut-sei=She
en-aut-mei=Yi-Min
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=WangPengcheng
en-aut-sei=Wang
en-aut-mei=Pengcheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=XingWeiman
en-aut-sei=Xing
en-aut-mei=Weiman
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HanadaKousuke
en-aut-sei=Hanada
en-aut-mei=Kousuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=LiuRenyi
en-aut-sei=Liu
en-aut-mei=Renyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KawanoYoji
en-aut-sei=Kawano
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=2
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=3
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=4
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=5
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=6
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=7
en-affil=Department of Bioinformatics, Ritsumeikan University
kn-affil=

affil-num=8
en-affil=College of Pharmaceutical Sciences, Ritsumeikan University
kn-affil=

affil-num=9
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=10
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=11
en-affil=Shanghai Center for Plant Stress Biology, Center of Excellence for Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=12
en-affil=Biomolecular Structure and Design, Shanghai Center for Plant Stress Biology
kn-affil=

affil-num=13
en-affil=Department of Bioscience and Bioinformatics, Kyushu Institute of Technology
kn-affil=

affil-num=14
en-affil=Center for Agroforestry Mega Data Science and FAFU-UCR Joint Center for Horticultural Biology and Metabolomics, Haixia Institute of Science and Technology,Fujian Agriculture and Forestry University
kn-affil=

affil-num=15
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=immunity
kn-keyword=immunity
en-keyword=Magnaporthe oryzae
kn-keyword=Magnaporthe oryzae
en-keyword=proteomics
kn-keyword=proteomics
en-keyword=transcriptomics
kn-keyword=transcriptomics
en-keyword=rice
kn-keyword=rice
en-keyword=signalling peptide
kn-keyword=signalling peptide
en-keyword=small secreted protein
kn-keyword=small secreted protein
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=8
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190416
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Melittin Exerts Beneficial Effects on Paraquat-Induced Lung Injuries in Mice by Modifying Oxidative Stress and Apoptosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Melittin (MEL) is a 26-amino acid peptide with numerous biological activities. Paraquat (PQ) is one of the most widely used herbicides, although it is extremely toxic to humans. To date, PQ poisoning has no effective treatment, and therefore the current study aimed to assess for the first time the possible effects of MEL on PQ-induced lung injuries in mice. Mice received a single intraperitoneal (IP) injection of PQ (30 mg/kg), followed by IP treatment with MEL (0.1 and 0.5 mg/kg) twice per week for four consecutive weeks. Histological alterations, oxidative stress, and apoptosis in the lungs were studied. Hematoxylin and eosin (H&E) staining indicated that MEL markedly reduced lung injuries induced by PQ. Furthermore, treatment with MEL increased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity, and decreased malonaldehyde (MDA) and nitric oxide (NO) levels in lung tissue homogenates. Moreover, immunohistochemical staining showed that B-cell lymphoma-2 (Bcl-2) and survivin expressions were upregulated after MEL treatment, while Ki-67 expression was downregulated. The high dose of MEL was more effective than the low dose in all experiments. In summary, MEL efficiently reduced PQ-induced lung injuries in mice. Specific pharmacological examinations are required to determine the effectiveness of MEL in cases of human PQ poisoning.
en-copyright=
kn-copyright=

en-aut-name=El-AaragBishoy
en-aut-sei=El-Aarag
en-aut-mei=Bishoy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MagdyMohamed
en-aut-sei=Magdy
en-aut-mei=Mohamed
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AlAjmiMohamed F.
en-aut-sei=AlAjmi
en-aut-mei=Mohamed F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KhalifaShaden A. M.
en-aut-sei=Khalifa
en-aut-mei=Shaden A. M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=El-SeediHesham R.
en-aut-sei=El-Seedi
en-aut-mei=Hesham R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Chemistry, Faculty of Science, Menoufia University
kn-affil=

affil-num=3
en-affil=Department of Pharmacognosy, College of Pharmacy, King Saud University
kn-affil=

affil-num=4
en-affil=Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University
kn-affil=

affil-num=5
en-affil=Department of Chemistry, Faculty of Science, Menoufia University
kn-affil=
en-keyword=paraquat
kn-keyword=paraquat
en-keyword=lung injury
kn-keyword=lung injury
en-keyword=melittin
kn-keyword=melittin
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=apoptosis
kn-keyword=apoptosis
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=
article-no=
start-page=3745
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201936
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Imaging Amyloplasts in the Developing Endosperm of Barley and Rice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyloplasts are plant-specific organelles responsible for starch biosynthesis and storage. Inside amyloplasts, starch forms insoluble particles, referred to as starch grains (SGs). SG morphology differs between species and SG morphology is particularly diverse in the endosperm of Poaceae plants, such as rice (Oryza sativa) and barley (Hordeum vulgare), which form compound SGs and simple SGs, respectively. SG morphology has been extensively imaged, but the comparative imaging of amyloplast morphology has been limited. In this study, SG-containing amyloplasts in the developing endosperm were visualized using stable transgenic barley and rice lines expressing amyloplast stroma-targeted green fluorescent protein fused to the transit peptide (TP) of granule-bound starch synthase I (TP-GFP). The TP-GFP barley and rice plants had elongated amyloplasts containing multiple SGs, with constrictions between the SGs. In barley, some amyloplasts were connected by narrow protrusions extending from their surfaces. Transgenic rice lines producing amyloplast membrane-localized SUBSTANDARD STARCH GRAIN6 (SSG6)-GFP were used to demonstrate that the developing amyloplasts contained multiple compound SGs. TP-GFP barley can be used to visualize the chloroplasts in leaves and other plastids in pollen and root in addition to the endosperm, therefore it provides as a useful tool to observe diverse plastids.
en-copyright=
kn-copyright=

en-aut-name=MatsushimaRyo
en-aut-sei=Matsushima
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HisanoHiroshi
en-aut-sei=Hisano
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil= Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil= Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=5
article-no=
start-page=433
end-page=440
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Relationship between Intracellular Signaling of the (Pro)renin Receptor and the Pathogenesis of Preeclampsia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= An association between preeclampsia and (pro)renin was recently reported. Intracellular signaling of the (pro) renin receptor [(P)RR] increases the expressions of TGF-β and PAI-1. In this study we sought to clarify the involvement of (pro)renin in the pathogenesis of preeclampsia via the intracellular signaling of (P)RR on preeclampsia placentas. Activated (pro)renin plasma concentrations were compared between pregnant women with (n=15) and without (n=28) preeclampsia. The placentas were immunohistochemically evaluated with anti-HIF-1α and anti-(P)RR antibodies. HTR-8/SVneo cells were cultured under hypoxic conditions and treated with human recombinant (pro)renin. The mRNA expressions of HIF-1α, (P)RR, PAI-1, TGF-β, and ET-1 were also examined by real-time RCR. The activated (pro)renin plasma concentration was significantly higher in the third vs. the second trimester in the preeclampsia patients. HIF-1α and (P)RR expressions were significantly increased in the preeclampsia placentas. The mRNA expressions of PAI-1, TGF-β, and ET-1 were significantly increased in the experiments using recombinant (pro)renin vs. hypoxic conditions. (P)RR expression in preeclampsia placentas is increased by persistent hypoxia through the second and third trimesters, and PAI-1, TGF-β, and ET-1 production is increased via (P)RR. Our results suggest that ET-1 production via the intracellular signaling of (P)RR is important in the pathogenesis of preeclampsia.
en-copyright=
kn-copyright=

en-aut-name=TamadaShoko
en-aut-sei=Tamada
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MitsuiTakashi
en-aut-sei=Mitsui
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhiraAkiko
en-aut-sei=Ohira
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TaniKazumasa
en-aut-sei=Tani
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MakiJota
en-aut-sei=Maki
en-aut-mei=Jota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=EguchiTakeshi
en-aut-sei=Eguchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EtoEriko
en-aut-sei=Eto
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HayataKei
en-aut-sei=Hayata
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MasuyamaHisashi
en-aut-sei=Masuyama
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=preeclampsia
kn-keyword=preeclampsia
en-keyword=(pro)renin
kn-keyword=(pro)renin
en-keyword=(pro)renin receptor
kn-keyword=(pro)renin receptor
en-keyword=endothelin-1
kn-keyword=endothelin-1
en-keyword=HTR-8/SVneo
kn-keyword=HTR-8/SVneo
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=5
article-no=
start-page=379
end-page=382
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Histidine-rich Glycoprotein Modulates the Blood-vascular System in Septic Condition
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Histidine-rich glycoprotein (HRG) is a 75 kDa glycoprotein synthesized in the liver whose plasma concentration is 100-150 μg/ml. HRG has been shown to modulate sepsis-related biological reactions by binding to several substances and cells, including heparin, factor XII, fibrinogen, thrombospondin, plasminogen, C1q, IgG, heme, LPS, dead cells, bacteria, and fungi. Therefore, reduction of plasma HRG levels in sepsis leads to dysregulation of coagulation, fibrinolysis, and immune response, resulting in disseminated intravascular coagulation and multiple organ failure. This review summarizes the binding and functional properties of HRG in sepsis.
en-copyright=
kn-copyright=

en-aut-name=WakeHidenori
en-aut-sei=Wake
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=htidine-rich glycoprotein
kn-keyword=htidine-rich glycoprotein
en-keyword=septic pathogenesis
kn-keyword=septic pathogenesis
en-keyword=immunothrombosis
kn-keyword=immunothrombosis
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=オレキシンAのプロラクチン分泌への影響とBMP-4の関与：ラット下垂体細胞を用いた検討
kn-title=Orexin A modulates prolactin production by regulating BMP-4 activity in rat pituitary lactotorope cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=FujisawaSatoshi
en-aut-sei=Fujisawa
en-aut-mei=Satoshi
kn-aut-name=藤澤諭
kn-aut-sei=藤澤
kn-aut-mei=諭
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=11
article-no=
start-page=e50082
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20121126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mitochondrial localization of ABC transporter ABCG2 and its function in 5-aminolevulinic acid-mediated protoporphyrin IX accumulation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Accumulation of protoporphyrin IX (PpIX) in malignant cells is the basis of 5-aminolevulinic acid (ALA)-mediated photodynamic therapy. We studied the expression of proteins that possibly affect ALA-mediated PpIX accumulation, namely oligopeptide transporter-1 and -2, ferrochelatase and ATP-binding cassette transporter G2 (ABCG2), in several tumor cell lines. Among these proteins, only ABCG2 correlated negatively with ALA-mediated PpIX accumulation. Both a subcellular fractionation study and confocal laser microscopic analysis revealed that ABCG2 was distributed not only in the plasma membrane but also intracellular organelles, including mitochondria. In addition, mitochondrial ABCG2 regulated the content of ALA-mediated PpIX in mitochondria, and Ko143, a specific inhibitor of ABCG2, enhanced mitochondrial PpIX accumulation. To clarify the possible roles of mitochondrial ABCG2, we characterized stably transfected-HEK (ST-HEK) cells overexpressing ABCG2. In these ST-HEK cells, functionally active ABCG2 was detected in mitochondria, and treatment with Ko143 increased ALA-mediated mitochondrial PpIX accumulation. Moreover, the mitochondria isolated from ST-HEK cells exported doxorubicin probably through ABCG2, because the export of doxorubicin was inhibited by Ko143. The susceptibility of ABCG2 distributed in mitochondria to proteinase K, endoglycosidase H and peptide-N-glycosidase F suggested that ABCG2 in mitochondrial fraction is modified by N-glycans and trafficked through the endoplasmic reticulum and Golgi apparatus and finally localizes within the mitochondria. Thus, it was found that ABCG2 distributed in mitochondria is a functional transporter and that the mitochondrial ABCG2 regulates ALA-mediated PpIX level through PpIX export from mitochondria to the cytosol.
en-copyright=
kn-copyright=

en-aut-name=KobuchiHirotsugu
en-aut-sei=Kobuchi
en-aut-mei=Hirotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriyaKoko
en-aut-sei=Moriya
en-aut-mei=Koko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OginoTetsuya
en-aut-sei=Ogino
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujitaHirofumi
en-aut-sei=Fujita
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InoueKeiji
en-aut-sei=Inoue
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShuinTaro
en-aut-sei=Shuin
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasudaTatsuji
en-aut-sei=Yasuda
en-aut-mei=Tatsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UtsumiKozo
en-aut-sei=Utsumi
en-aut-mei=Kozo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UtsumiToshihiko
en-aut-sei=Utsumi
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=1 Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Applied Molecular Bioscience, Graduate School of Medicine, Yamaguchi University
kn-affil=

affil-num=3
en-affil=Department of Nursing Science, Faculty of Health and Welfare Science, Okayama Prefectural University
kn-affil=

affil-num=4
en-affil=Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=5
en-affil=Department of Urology, Kochi Medical School
kn-affil=

affil-num=6
en-affil=Department of Urology, Kochi Medical School
kn-affil=

affil-num=7
en-affil=1 Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=9
en-affil=Applied Molecular Bioscience, Graduate School of Medicine, Yamaguchi University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=4
article-no=
start-page=285
end-page=297
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dynamic Reorganization of Microtubule and Glioma Invasion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Gliomas are characterized as highly diffuse infiltrating tumors, and currently available treatments such as surgery, radiation and chemotherapy are unfeasible or show limited efficacy against these tumors. Recent genetic and epigenetic analyses of glioma have revealed increasing evidence of the role of driver genetic alterations in glioma development and led to the identification of prognostic factors. Despite these findings, the survival rates of glioma patients remain low, and alternative treatments and novel targets are needed. Recent studies identified neural stem cells as the possible origin of gliomas, and some evidence has revealed shared functions and mechanisms between glioma cells and neurons, also supporting their similarity. The cytoskeleton plays important roles in the migration of normal cells as well as cancer cells. Recent reports have described a role for microtubules, a component of the cytoskeleton, in glioma invasion. Notably, several factors that regulate microtubule functions, such as microtubule-associated proteins, plus-end tracking proteins, or motor proteins, are upregulated in glioma tissues compared with normal tissue, and upregulation of these factors is associated with high invasiveness of glioma cells. In this review, we describe the mechanism of microtubules in glioma invasion and discuss the possibility of microtubule-targeted therapy to inhibit glioma invasion.
en-copyright=
kn-copyright=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IchikawaTomotsugu
en-aut-sei=Ichikawa
en-aut-mei=Tomotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurozumiKazuhiko
en-aut-sei=Kurozumi
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Neurosurgery, The University of Texas Health Science Center at Houston
kn-affil=

affil-num=2
en-affil=Department of Neurosurgery, Kagawa Prefectural Central Hospital
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=glioma
kn-keyword=glioma
en-keyword=cytoskeletons
kn-keyword=cytoskeletons
en-keyword=invasion
kn-keyword=invasion
en-keyword=microtubules
kn-keyword=microtubules
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=2
article-no=
start-page=135
end-page=146
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Collagen XVIII Deposition in the Basement Membrane Zone beneath the Newly Forming Epidermis during Wound Healing in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The basement membrane (BM) is composed of various extracellular molecules and regulates tissue regeneration and maintenance. Here, we demonstrate that collagen XVIII was spatiotemporally expressed in the BM during skin wound healing in a mouse excisional wound-splinting model. Re-epithelialization was detected at days 3 and 6 post-wounding. The ultrastructure of epidermal BM was discontinuous at day 3, whereas on day 6 a continuous BM was observed in the region proximal to the wound edge. Immunohistochemistry demonstrated that collagen XVIII was deposited in the BM zone beneath newly forming epidermis in day 3 and 6 wounds. Laminin-332, known to be the earliest BM component appearing in wounds, was colocalized with collagen XVIII in the epidermal BM zone at days 3 and 6. The deposition of α1(IV) collagen and nidogen-1 in the epidermal BM zone occurred later than that of collagen XVIII. We also observed the short isoform of collagen XVIII in the epidermal BM zone at day 3 post-wounding. Collectively, our results suggested that collagen XVIII plays a role in the formation of the dermal-epidermal junction during re-epithelialization, and that it is the short isoform that is involved in the early phase of re-epithelialization.
en-copyright=
kn-copyright=

en-aut-name=MaebaTakahiro
en-aut-sei=Maeba
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonoYasuko
en-aut-sei=Tomono
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HeljasvaaraRitva
en-aut-sei=Heljasvaara
en-aut-mei=Ritva
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=PihlajaniemiTaina
en-aut-sei=Pihlajaniemi
en-aut-mei=Taina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=InagawaKiichi
en-aut-sei=Inagawa
en-aut-mei=Kiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=

affil-num=4
en-affil=Shigei Medical Research Institute
kn-affil=

affil-num=5
en-affil=Center for Cancer Biomarkers CCBIO, Department of Biomedicine, University of Bergen
kn-affil=

affil-num=6
en-affil=Oulu Center for Cell-Matrix Research, Biocenter Oulu, Faculty of Biochemistry and Molecular Medicine, University of Oulu
kn-affil=

affil-num=7
en-affil=Department of Plastic and Reconstructive Surgery, Kawasaki Medical School, Kurashiki
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Science
kn-affil=
en-keyword=collagen XVIII
kn-keyword=collagen XVIII
en-keyword=basement membrane
kn-keyword=basement membrane
en-keyword=wound healing
kn-keyword=wound healing
en-keyword=re-epithelialization
kn-keyword=re-epithelialization
en-keyword=skin
kn-keyword=skin
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=29
end-page=39
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Histidine-rich Glycoprotein Could Be an Early Predictor of Vasospasm after Aneurysmal Subarachnoid Hemorrhage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Cerebral vasospasm (CVS) is a major contributor to the high morbidity and mortality of aneurysmal subarachnoid hemorrhage (aSAH) patients. We measured histidine-rich glycoprotein (HRG), a new biomarker of aSAH, in cerebrospinal fluid (CSF) to investigate whether HRG might be an early predictor of CVS. A total of seven controls and 14 aSAH patients (8 males, 6 females aged 53.4±15.4 years) were enrolled, and serial CSF and serum samples were taken. We allocated these samples to three phases (T1-T3) and measured HRG, interleukin (IL)-6, fibrinopeptide A (FpA), and 8-hydroxy-2’-deoxyguanosine (8OHdG) in the CSF, and the HRG in serum. We also examined the release of HRG in rat blood incubated in artificial CSF. In contrast to the other biomarkers examined, the change in the CSF HRG concentration was significantly different between the nonspasm and spasm groups (p<0.01). The rat blood/CSF model revealed a time course similar to that of the human CSF samples in the non-spasm group. HRG thus appears to have the potential to become an early predictor of CVS. In addition, the interaction of HRG with IL-6, FpA, and 8OHdG may form the pathology of CVS.
en-copyright=
kn-copyright=

en-aut-name=MatsumotoAtsushi
en-aut-sei=Matsumoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraTakehiro
en-aut-sei=Nakamura
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShinomiyaAya
en-aut-sei=Shinomiya
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawakitaKenya
en-aut-sei=Kawakita
en-aut-mei=Kenya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawanishiMasahiko
en-aut-sei=Kawanishi
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyakeKeisuke
en-aut-sei=Miyake
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaYasuhiro
en-aut-sei=Kuroda
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KeepRichard F.
en-aut-sei=Keep
en-aut-mei=Richard F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TamiyaTakashi
en-aut-sei=Tamiya
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=2
en-affil=Department of Medical Technology, Kagawa Prefectural University of Health Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=4
en-affil=Emergency Medical Center, Kagawa University Hospital
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=7
en-affil=Emergency Medical Center, Kagawa University Hospital
kn-affil=

affil-num=8
en-affil=Department of Neurosurgery, University of Michigan
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=
en-keyword=biomarker
kn-keyword=biomarker
en-keyword=histidine-rich glycoprotein
kn-keyword=histidine-rich glycoprotein
en-keyword=predictor
kn-keyword=predictor
en-keyword=subarachnoid hemorrhage
kn-keyword=subarachnoid hemorrhage
en-keyword=vasospasm
kn-keyword=vasospasm
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=201902
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Role of Kallikrein-Related Peptidases in Atopic Dermatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Excessive protease activity is a characteristic abnormality that affects the epidermal barrier in patients with atopic dermatitis (AD). Kallikrein-related peptidases (KLKs) are excessively expressed in AD lesions, and it is suggested that the abnormal action of KLKs is involved in the skin barrier dysfunction in AD. In other words, overexpressed KLKs disrupt the normal barrier function, and due to that breakdown, external substances that can become antigens of AD easily invade the epidermis, resulting in dermatitis, coupled with the induction of Th2 cytokines. Further investigations are required to elucidate the role of KLKs in AD; this knowledge could contribute to the design of new therapeutic and prophylactic drugs for AD.
en-copyright=
kn-copyright=

en-aut-name=MorizaneShin
en-aut-sei=Morizane
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=atopic dermatitis
kn-keyword=atopic dermatitis
en-keyword=kallikrein-related peptidases
kn-keyword=kallikrein-related peptidases
en-keyword=epidermal barrier dysfunction
kn-keyword=epidermal barrier dysfunction
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=機能性ペプチドKP24が顎下腺組織成長に及ぼす影響の検討
kn-title=Functional peptide KP24 enhances submandibular gland tissue growth in vitro
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IkedaAtsushi
en-aut-sei=Ikeda
en-aut-mei=Atsushi
kn-aut-name=池田篤司
kn-aut-sei=池田
kn-aut-mei=篤司
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Okayama University
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20171227
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=メラトニンによる下垂体プロラクチン分泌調節メカニズムの研究
kn-title=Regulatory role of melatonin and BMP-4 in prolactin production by rat pituitary lactotrope GH3 cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OchiKanako
en-aut-sei=Ochi
en-aut-mei=Kanako
kn-aut-name=越智可奈子
kn-aut-sei=越智
kn-aut-mei=可奈子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=71
cd-vols=
no-issue=6
article-no=
start-page=459
end-page=465
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=201712
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Signal Diversity of Receptor for Advanced Glycation End Products
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= The receptor for advanced glycation end products (RAGE) is involved in inflammatory pathogenesis. It functions as a receptor to multiple ligands such as AGEs, HMGB1 and S100 proteins, activating multiple intracellular signaling pathways with each ligand binding. The molecular events by which ligand-activated RAGE controls diverse signaling are not well understood, but some progress was made recently. Accumulating evidence revealed that RAGE has multiple binding partners within the cytoplasm and on the plasma membrane. It was first pointed out in 2008 that RAGE’s cytoplasmic tail is able to recruit Diaphanous-1 (Dia-1), resulting in the acquisition of increased cellular motility through Rac1/Cdc42 activation. We also observed that within the cytosol, RAGE’s cytoplasmic tail behaves similarly to a Toll-like receptor (TLR4)-TIR domain, interacting with TIRAP and MyD88 adaptor molecules that in turn activate multiple downstream signals. Subsequent studies demonstrated the presence of an alternative adaptor molecule, DAP10, on the plasma membrane. The coupling of RAGE with DAP10 is critical for enhancing the RAGE-mediated survival signal. Interestingly, RAGE interaction on the membrane was not restricted to DAP10 alone. The chemotactic G-protein-coupled receptors (GPCRs) formyl peptide receptors1 and 2 (FPR1 and FPR2) also interacted with RAGE on the plasma membrane. Binding interaction between leukotriene B4 receptor 1 (BLT1) and RAGE was also demonstrated. All of the interactions affected the RAGE signal polarity. These findings indicate that functional interactions between RAGE and various molecules within the cytoplasmic area or on the membrane area coordinately regulate multiple ligand-mediated RAGE responses, leading to typical cellular phenotypes in several pathological settings. Here we review RAGE’s signaling diversity, to contribute to the understanding of the elaborate functions of RAGE in physiological and pathological contexts.
en-copyright=
kn-copyright=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Endy Widya Putranto
en-aut-sei=Endy Widya Putranto
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=I Made Winarsa Ruma
en-aut-sei=I Made Winarsa Ruma
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=I Wayan Sumardika
en-aut-sei=I Wayan Sumardika
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YouyiChen
en-aut-sei=Youyi
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TomonobuNaoko
en-aut-sei=Tomonobu
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Faculty of Medicine, Universitas Gadjah Mada
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=5
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=receptor for advanced glycation end products
kn-keyword=receptor for advanced glycation end products
en-keyword=RAGE
kn-keyword=RAGE
en-keyword=adaptor protein
kn-keyword=adaptor protein
en-keyword=signal transduction
kn-keyword=signal transduction
en-keyword=inflammatory pathogenesis
kn-keyword=inflammatory pathogenesis
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=10
article-no=
start-page=1479
end-page=1486
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multiple roles of hypoxia in ovarian function: roles of hypoxia-inducible factor-related and -unrelated signals during the luteal phase
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= There is increasing interest in the role of oxygen conditions in the microenvironment of organs because of the discovery of a hypoxia-specific transcription factor, namely hypoxia-inducible factor (HIF) 1. Ovarian function has several phases that change day by day, including ovulation, follicular growth and corpus luteum formation and regression. These phases are regulated by many factors, including pituitary hormones and local hormones, such as steroids, peptides and cytokines, as well as oxygen conditions. Hypoxia strongly induces angiogenesis because transcription of the potent angiogenic factor vascular endothelial growth factor (VEGF) is regulated by HIF1. Follicular development and luteal formation are accompanied by a marked increase in angiogenesis assisted by HIF1-VEGF signalling. Hypoxia is also one of the factors that induces luteolysis by suppressing progesterone synthesis and by promoting apoptosis of luteal cells. The present review focuses on recent studies of hypoxic conditions, as well as HIF1-regulated genes and proteins, in the regulation of ovarian function.
en-copyright=
kn-copyright=

en-aut-name=NishimuraRyo
en-aut-sei=Nishimura
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkudaKiyoshi
en-aut-sei=Okuda
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=angiogenesis
kn-keyword=angiogenesis
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=corpus luteum
kn-keyword=corpus luteum
en-keyword=follicular development
kn-keyword=follicular development
en-keyword=luteal formation
kn-keyword=luteal formation
en-keyword=luteal regression
kn-keyword=luteal regression
en-keyword=steroidogenesis
kn-keyword=steroidogenesis
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=11
article-no=
start-page=e50082
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20121126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mitochondrial localization of ABC transporter ABCG2 and its function in 5-aminolevulinic acid-mediated protoporphyrin IX accumulation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Accumulation of protoporphyrin IX (PpIX) in malignant cells is the basis of 5-aminolevulinic acid (ALA)-mediated photodynamic therapy. We studied the expression of proteins that possibly affect ALA-mediated PpIX accumulation, namely oligopeptide transporter-1 and -2, ferrochelatase and ATP-binding cassette transporter G2 (ABCG2), in several tumor cell lines. Among these proteins, only ABCG2 correlated negatively with ALA-mediated PpIX accumulation. Both a subcellular fractionation study and confocal laser microscopic analysis revealed that ABCG2 was distributed not only in the plasma membrane but also intracellular organelles, including mitochondria. In addition, mitochondrial ABCG2 regulated the content of ALA-mediated PpIX in mitochondria, and Ko143, a specific inhibitor of ABCG2, enhanced mitochondrial PpIX accumulation. To clarify the possible roles of mitochondrial ABCG2, we characterized stably transfected-HEK (ST-HEK) cells overexpressing ABCG2. In these ST-HEK cells, functionally active ABCG2 was detected in mitochondria, and treatment with Ko143 increased ALA-mediated mitochondrial PpIX accumulation. Moreover, the mitochondria isolated from ST-HEK cells exported doxorubicin probably through ABCG2, because the export of doxorubicin was inhibited by Ko143. The susceptibility of ABCG2 distributed in mitochondria to proteinase K, endoglycosidase H and peptide-N-glycosidase F suggested that ABCG2 in mitochondrial fraction is modified by N-glycans and trafficked through the endoplasmic reticulum and Golgi apparatus and finally localizes within the mitochondria. Thus, it was found that ABCG2 distributed in mitochondria is a functional transporter and that the mitochondrial ABCG2 regulates ALA-mediated PpIX level through PpIX export from mitochondria to the cytosol.
en-copyright=
kn-copyright=

en-aut-name=KobuchiHirotsugu
en-aut-sei=Kobuchi
en-aut-mei=Hirotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriyaKoko
en-aut-sei=Moriya
en-aut-mei=Koko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OginoTetsuya
en-aut-sei=Ogino
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujitaHirofumi
en-aut-sei=Fujita
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InoueKeiji
en-aut-sei=Inoue
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShuinTaro
en-aut-sei=Shuin
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasudaTatsuji
en-aut-sei=Yasuda
en-aut-mei=Tatsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UtsumiKozo
en-aut-sei=Utsumi
en-aut-mei=Kozo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UtsumiToshihiko
en-aut-sei=Utsumi
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=525
cd-vols=
no-issue=7
article-no=
start-page=1586
end-page=1598
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20170501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of the sexually dimorphic gastrin-releasing peptide system in the lumbosacral spinal cord that controls male reproductive function in the mouse and Asian house musk shrew (Suncus murinus)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Several regions of the brain and spinal cord control male reproductive function. We previously demonstrated that the gastrin-releasing peptide (GRP) system, located in the lumbosacral spinal cord of rats, controls spinal centers to promote penile reflexes during male copulatory behavior. However, little information exists on the male-specific spinal GRP system in animals other than rats. The objective of this study was to examine the functional generality of the spinal GRP system in mammals using the Asian house musk shrew (Suncus murinus; suncus named as the laboratory strain), a specialized placental mammal model. Mice are also used for a representative model of small laboratory animals. We first isolated complementary DNA encoding GRP in suncus. Phylogenetic analysis revealed that suncus preproGRP was clustered to an independent branch. Reverse transcription-PCR showed that GRP and its receptor mRNAs were both expressed in the lumbar spinal cord of suncus and mice. Immunohistochemistry for GRP demonstrated that the sexually dimorphic GRP system and male-specific expression/distribution patterns of GRP in the lumbosacral spinal cord in suncus are similar to those of mice. In suncus, we further found that most GRP-expressing neurons in males also express androgen receptors, suggesting that this male-dominant system in suncus is also androgen-dependent. Taken together, these results indicate that the sexually dimorphic spinal GRP system exists not only in mice but also in suncus, suggesting that this system is a conserved property in mammals.
en-copyright=
kn-copyright=

en-aut-name=TamuraKei
en-aut-sei=Tamura
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KobayashiYasuhisa
en-aut-sei=Kobayashi
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HirookaAsuka
en-aut-sei=Hirooka
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakanamiKeiko
en-aut-sei=Takanami
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JogaharaTakamichi
en-aut-sei=Jogahara
en-aut-mei=Takamichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OdaSen-ichi
en-aut-sei=Oda
en-aut-mei=Sen-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil= Laboratory of Animal Management and Resources, Department of Zoology, Okayama University of Science
kn-affil=

affil-num=7
en-affil= Laboratory of Animal Management and Resources, Department of Zoology, Okayama University of Science
kn-affil=

affil-num=8
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=9
en-affil=Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=RRID
kn-keyword=RRID
en-keyword=AB_2060157
kn-keyword=AB_2060157
en-keyword=RRID: AB_2571636
kn-keyword=RRID: AB_2571636
en-keyword=RRID: AB_626757
kn-keyword=RRID: AB_626757
en-keyword=Suncus murinus (suncus)
kn-keyword=Suncus murinus (suncus)
en-keyword=gastrin-releasing peptide
kn-keyword=gastrin-releasing peptide
en-keyword=male reproductive function
kn-keyword=male reproductive function
en-keyword=sexual dimorphism
kn-keyword=sexual dimorphism
en-keyword=spinal cord
kn-keyword=spinal cord
END

start-ver=1.4
cd-journal=joma
no-vol=129
cd-vols=
no-issue=1
article-no=
start-page=53
end-page=57
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20170403
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Drug interaction (38. Combination with novel hypnotic drugs : ramelteon and suvorexant)
kn-title=薬物相互作用 （ 38 - 新規睡眠薬 : ラメルテオン, スボレキサントの相互作用）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KuboKazuko
en-aut-sei=Kubo
en-aut-mei=Kazuko
kn-aut-name=久保和子
kn-aut-sei=久保
kn-aut-mei=和子
aut-affil-num=1
ORCID=

en-aut-name=EsumiSatoru
en-aut-sei=Esumi
en-aut-mei=Satoru
kn-aut-name=江角悟
kn-aut-sei=江角
kn-aut-mei=悟
aut-affil-num=2
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=北村佳久
kn-aut-sei=北村
kn-aut-mei=佳久
aut-affil-num=3
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=千堂年昭
kn-aut-sei=千堂
kn-aut-mei=年昭
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部

affil-num=2
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部

affil-num=3
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部

affil-num=4
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=下垂体ゴナドトロピン分泌に対するソマトスタチン作用とBMP-6の影響
kn-title=BMP-6 modulates somatostatin effects on luteinizing hormone production by gonadrotrope cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TomaKishio
en-aut-sei=Toma
en-aut-mei=Kishio
kn-aut-name=当真貴志雄
kn-aut-sei=当真
kn-aut-mei=貴志雄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=18577
end-page=18577
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201512
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The molecular mechanism of photochemical internalization of cell penetrating peptide-cargo-photosensitizer conjugates.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In many drug delivery strategies, an inefficient transfer of macromolecules such as proteins and nucleic acids to the cytosol often occurs because of their endosomal entrapment. One of the methods to overcome this problem is photochemical internalization, which is achieved using a photosensitizer and light to facilitate the endosomal escape of the macromolecule. In this study, we examined the molecular mechanism of photochemical internalization of cell penetrating peptide-cargo (macromolecule)-photosensitizer conjugates. We measured the photophysical properties of eight dyes (photosensitizer candidates) and determined the respective endosomal escape efficiencies using these dyes. Correlation plots between these factors indicated that the photogenerated (1)O2 molecules from photosensitizers were highly related to the endosomal escape efficiencies. The contribution of (1)O2 was confirmed using (1)O2 quenchers. In addition, time-lapse fluorescence imaging showed that the photoinduced endosomal escape occurred at a few seconds to a few minutes after irradiation (much longer than (1)O2 lifetime), and that the pH increased in the endosome prior to the endosomal escape of the macromolecule. 
en-copyright=
kn-copyright=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiShunya
en-aut-sei=Miki
en-aut-mei=Shunya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KobayashiShouhei
en-aut-sei=Kobayashi
en-aut-mei=Shouhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HaraguchiTokuko
en-aut-sei=Haraguchi
en-aut-mei=Tokuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakataEiji
en-aut-sei=Nakata
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HirakawaKazutaka
en-aut-sei=Hirakawa
en-aut-mei=Kazutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SumitaKensuke
en-aut-sei=Sumita
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkazakiShigetoshi
en-aut-sei=Okazaki
en-aut-mei=Shigetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medical Bioengineering, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medical Bioengineering, Okayama University
kn-affil=

affil-num=3
en-affil=Advanced ICT Research Institute Kobe, NICT
kn-affil=

affil-num=4
en-affil=Advanced ICT Research Institute Kobe, NICT
kn-affil=

affil-num=5
en-affil=Institute of Advanced Energy, Kyoto University
kn-affil=

affil-num=6
en-affil=Department of Applied Chemistry and Biochemical Engineering, Graduate School of Engineering, Shizuoka University
kn-affil=

affil-num=7
en-affil=Department of Medical Bioengineering, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Medical Bioengineering, Okayama University
kn-affil=岡山大学大学院自然科学研究科

affil-num=9
en-affil=Department of Medical Spectroscopy, Hamamatsu University School of Medicine
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=2
article-no=
start-page=91
end-page=94
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2015 Incentive Award of the Okayama Medical Association in General Medical Science (2015 Yuuki Prize)
kn-title=平成27年度岡山医学会賞 総合研究奨励賞（結城賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KajitaAi
en-aut-sei=Kajita
en-aut-mei=Ai
kn-aut-name=梶田藍
kn-aut-sei=梶田
kn-aut-mei=藍
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Dermatology, Okayama University Hospital
kn-affil=岡山大学病院　皮膚科
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=雄の性機能を調節する脊髄ガストリン放出ペプチド系の神経ネットワークとその性差構築機構に関する研究
kn-title=Studies on the sexually dimorphic gastrin-releasing peptide system in the lumbosacral spinal cord that controls male reproductive function
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OchiTakumi
en-aut-sei=Ochi
en-aut-mei=Takumi
kn-aut-name=越智拓海
kn-aut-sei=越智
kn-aut-mei=拓海
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=BMP-2による骨芽細胞分化に対するFGF-8とTNF-αの制御機序の解析
kn-title=Regulatory effects of fibroblast growth factor-8 and tumor necrosis factor-α on osteoblast marker expression induced by bone morphogenetic protein-2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KatsuyamaTakayuki
en-aut-sei=Katsuyama
en-aut-mei=Takayuki
kn-aut-name=勝山隆行
kn-aut-sei=勝山
kn-aut-mei=隆行
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20151231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=頻回インスリン治療の必要な非肥満2型糖尿病患者を見分ける最適な指標は食後血中C-ペプチド値である：短期強化インスリン治療前後のC-ペプチド分析
kn-title=Postprandial serum C-peptide value is the optimal index to identify patients with non-obese type 2 diabetes who require multiple daily insulin injection: Analysis of C-peptide values before and after short-term intensive insulin therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=FujiwaraDaisuke
en-aut-sei=Fujiwara
en-aut-mei=Daisuke
kn-aut-name=藤原大介
kn-aut-sei=藤原
kn-aut-mei=大介
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=11468
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=2015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Peptide-modified Substrate for Modulating Gland Tissue Growth and Morphology In Vitro
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In vitro fabricated biological tissue would be a valuable tool to screen newly synthesized drugs or understand the tissue development process. Several studies have attempted to fabricate biological tissue in vitro. However, controlling the growth and morphology of the fabricated tissue remains a challenge. Therefore, new techniques are required to modulate tissue growth. RGD (arginine-glycine-aspartic acid), which is an integrin-binding domain of fibronectin, has been found to enhance cell adhesion and survival; it has been used to modify substrates for in vitro cell culture studies or used as tissue engineering scaffolds. In addition, this study shows novel functions of the RGD peptide, which enhances tissue growth and modulates tissue morphology in vitro. When an isolated submandibular gland (SMG) was cultured on an RGD-modified alginate hydrogel sheet, SMG growth including bud expansion and cleft formation was dramatically enhanced. Furthermore, we prepared small RGD-modified alginate beads and placed them on the growing SMG tissue. These RGD-modified beads successfully induced cleft formation at the bead position, guiding the desired SMG morphology. Thus, this RGD-modified material might be a promising tool to modulate tissue growth and morphology in vitro for biological tissue fabrication.
en-copyright=
kn-copyright=

en-aut-name=TaketaHiroaki
en-aut-sei=Taketa
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GulsanAra Sathi
en-aut-sei=Gulsan
en-aut-mei=Ara Sathi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MahmoudFarahat
en-aut-sei=Mahmoud
en-aut-mei=Farahat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaziAnisur Rahman
en-aut-sei=Kazi
en-aut-mei=Anisur Rahman
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaiTakayoshi
en-aut-sei=Sakai
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HiranoYoshiaki
en-aut-sei=Hirano
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KubokiTakuo
en-aut-sei=Kuboki
en-aut-mei=Takuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ToriiYasuhiro
en-aut-sei=Torii
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsumotoTakuya
en-aut-sei=Matsumoto
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Biomaterials, Okayama University

affil-num=2
en-affil=
kn-affil=Department of Biomaterials, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Biomaterials, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Biomaterials, Okayama University

affil-num=5
en-affil=
kn-affil=Department of Oral-Facial Disorders, Osaka University

affil-num=6
en-affil=
kn-affil=Department of Chemical Engineering, Kansai University

affil-num=7
en-affil=
kn-affil=Department of Biomaterials, Okayama University

affil-num=8
en-affil=
kn-affil=Department of Biomaterials, Okayama University

affil-num=9
en-affil=
kn-affil=Department of Biomaterials, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Peptide directs artificial tissue growth
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MatsumotoTakuya
en-aut-sei=Matsumoto
en-aut-mei=Takuya
kn-aut-name=松本卓也
kn-aut-sei=松本
kn-aut-mei=卓也
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Biomaterials, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=4
article-no=
start-page=271
end-page=276
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cytokine expression in human dermal fibroblasts stimulated with eosinophil cationic protein measured by protein array
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=[Background] : Eosinophil cationic protein (ECP) was reported previously to be involved in allergic inflammation with cytotoxic activity. On the other hand, recent studies showed that ECP did not induce cell death but inhibited the growth of cancer-derived cells. Our previous study indicated that human ECP enhanced differentiation of rat neonatal cardiomyocytes and stress fiber formation in Balb/c 3T3 mouse fibroblasts, while the effects of human ECP on human fibroblasts are unknown.

[Objective] : The present study was performed to determine the effects of human ECP on cytokine expression in human fibroblasts by protein array.

[Methods] : The effects of recombinant human ECP (rhECP) on normal human dermal fibroblasts (NHDF) were examined by assaying cell growth. Furthermore, cytokine expression of NHDF stimulated by ECP, which could influence cell growth, was evaluated by protein array.

[Results] : ECP was not cytotoxic but enhanced the growth of NHDF. The peak rhECP concentration that enhanced the cell counts by 1.56-fold was 100 ng/mL, which was significantly different from cultures without ECP stimulation (ANOVA/Scheffe’s test, P < 0.05). Array analyses indicated that ciliary neurotrophic factor (CNTF), neutrophilactivating peptide (NAP)-2, and neurotrophin (NT)-3 were significantly upregulated in NHDF stimulated with 100 ng/mL ECP compared to those without stimulation.

[Conclusion] : ECP is not cytotoxic but enhances the growth of NHDF. CNTF, NAP-2, and NT-3 were suggested to be involved in enhancing the growth of NHDF. These findings will contribute to determination of the role of ECP in allergic inflammation. (Asian Pac J Allergy Immunol 2013;31:271-6)
en-copyright=
kn-copyright=

en-aut-name=SatoTakamaro
en-aut-sei=Sato
en-aut-mei=Takamaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SogaYoshihiko
en-aut-sei=Soga
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamaguchiTomoko
en-aut-sei=Yamaguchi
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MeguroMichio
en-aut-sei=Meguro
en-aut-mei=Michio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MaedaHiroshi
en-aut-sei=Maeda
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TadaJoji
en-aut-sei=Tada
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OtaniTakayuki
en-aut-sei=Otani
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SenoMasaharu
en-aut-sei=Seno
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Division of Hospital Dentistry, Central Clinical Department, Okayama University Hospital

affil-num=3
en-affil=
kn-affil=Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Division of Dermatology, National Sanatorium Nagashima-Aiseien

affil-num=7
en-affil=
kn-affil=Department of Medical and Bioengineering Science, Okayama University Graduate School of Natural Science and Technology

affil-num=8
en-affil=
kn-affil=Department of Medical and Bioengineering Science, Okayama University Graduate School of Natural Science and Technology

affil-num=9
en-affil=
kn-affil=Department of Pathophysiology - Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=cytokine
kn-keyword=cytokine
en-keyword=eosinophil cationic protein
kn-keyword=eosinophil cationic protein
en-keyword=fibroblast
kn-keyword=fibroblast
en-keyword=growth
kn-keyword=growth
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=3
article-no=
start-page=203
end-page=207
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20151201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Non-high-output cardiac failure in patients undergoing hemodialysis through an arteriovenous shunt
kn-title=透析シャント心不全―非過大シャント心不全 “Non-High-Output Cardiac Failure”の病態―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Hemodialysis-related heart failure has been considered to be associated with excessive blood flow through the arteriovenous (AV) shunt used for vascular access. However, some patients undergoing dialysis have heart failure in the absence of an increase in cardiac output (CO) related to shunt blood-flow loading because the loading cannot be compensated for by increasing CO. This condition may be challenging to manage ; thus, early diagnosis is important.
 Methods and Results: Twelve patients (mean age, 71 years ; 9 men) with end-stage renal disease, dialysis-related heart failure, a high brain natriuretic peptide (BNP) level, and a mean New York Heart Association (NYHA) class of II underwent AV shunt closure. Their cardiac index (CI), pre- and post-dialysis BNP levels, and several cardiac variables were assessed pre- and postoperatively. All patients achieved relief of heart failure symptoms and a reduction in NYHA class after AV closure, but six patients had a postoperative increase in CI (the "non-high-output" cardiac failure group), whereas the other six had a decrease in CI (the "high-output" cardiac failure group). The high-output patients had greater improvements in BNP levels and most cardiac variables compared to the non-high-output group ;
therefore, the heart failure in the non-high-output patients was considered more serious than that in the high-output group.
 Conclusions: The selection of effective strategies for treating dialysis-related heart failure may depend partly on identifying which patients have non-high-output failure. Such identification requires serial measurements of BNP levels and evaluations of cardiac variables other than the ejection fraction.
en-copyright=
kn-copyright=

en-aut-name=UgawaToyomu
en-aut-sei=Ugawa
en-aut-mei=Toyomu
kn-aut-name=鵜川豊世武
kn-aut-sei=鵜川
kn-aut-mei=豊世武
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科
en-keyword=心拍出量（cardiac output）
kn-keyword=心拍出量（cardiac output）
en-keyword=心不全（heart failure）
kn-keyword=心不全（heart failure）
en-keyword=脳性ナトリウム利尿ペプチド（brain natriuretic peptide）
kn-keyword=脳性ナトリウム利尿ペプチド（brain natriuretic peptide）
en-keyword=非過大シャント心不全（non-high-output cardiac failure）
kn-keyword=非過大シャント心不全（non-high-output cardiac failure）
en-keyword=腎臓（kidney）
kn-keyword=腎臓（kidney）
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=2
article-no=
start-page=111
end-page=115
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Peritoneal dialysis update
kn-title=腹膜透析Update
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=杉山斉
kn-aut-sei=杉山
kn-aut-mei=斉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科
en-keyword=持続携行式腹膜透析（CAPD）
kn-keyword=持続携行式腹膜透析（CAPD）
en-keyword=自動腹膜透析（APD）
kn-keyword=自動腹膜透析（APD）
en-keyword=SMAP法
kn-keyword=SMAP法
en-keyword=尿素Kt/V
kn-keyword=尿素Kt/V
en-keyword=腹膜平衡試験（peritoneal equilibration test:PET）
kn-keyword=腹膜平衡試験（peritoneal equilibration test:PET）
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=2
article-no=
start-page=87
end-page=90
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2014 Incentive Award of the Okayama Medical Association in General Medical Science (2014 Yuuki Prize)
kn-title=平成26年度岡山医学会賞 総合研究奨励賞（結城賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OokuboNanako
en-aut-sei=Ookubo
en-aut-mei=Nanako
kn-aut-name=大久保奈々子
kn-aut-sei=大久保
kn-aut-mei=奈々子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=11
article-no=
start-page=2103
end-page=2107
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20081101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Royal jelly ameliorates insulin resistance in fructose-drinking rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Royal jelly (RJ) is known to contain excellent nutrition and a variety of biological activities. The present study was designed to investigate the effects of RJ on insulin resistance (hyperinsulinemia) in fructose-drinking rats (FDR; insulin resistance animal model). Male Wistar rats (6 weeks old) received 15% fructose solution in drinking water for 8 weeks. FDR showed significant increases in plasma levels of insulin and triglyceride, Homeostasis Model Assessment ratio (HOMA-R, an index of insulin resistance), and systolic blood pressure, but not blood glucose levels, when compared with control rats. RJ (100, 300mg/kg, p.o.) treatment for 8 weeks significantly decreased the plasma levels of insulin and triglyceride, HOMA-R, without affecting blood glucose or total cholesterol levels and tended to lower systolic blood pressure. In isolated and perfused mesenteric vascular beds of FDR, RJ treatment resulted in a significant reduction in sympathetic nerve-mediated vasoconstrictor response to periarterial nerve stimulation (PNS) and tended to increase the calcitonin gene-related peptide (CGRP) nervemediated vasodilator response to PNS, compared with those in untreated FDR. However, RJ treatment did not significantly affect norepinephrine-induced vasoconstriction or CGRP-induced vasodilation. These results suggest that RJ could be an effective functional food to prevent insulin resistance associated with the development of hypertension.
en-copyright=
kn-copyright=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=座間味義人
kn-aut-sei=座間味
kn-aut-mei=義人
aut-affil-num=1
ORCID=

en-aut-name=TakatoriShingo
en-aut-sei=Takatori
en-aut-mei=Shingo
kn-aut-name=高取真吾
kn-aut-sei=高取
kn-aut-mei=真吾
aut-affil-num=2
ORCID=

en-aut-name=GodaMitsuhiro
en-aut-sei=Goda
en-aut-mei=Mitsuhiro
kn-aut-name=合田光寛
kn-aut-sei=合田
kn-aut-mei=光寛
aut-affil-num=3
ORCID=

en-aut-name=KoyamaToshihiro
en-aut-sei=Koyama
en-aut-mei=Toshihiro
kn-aut-name=小山敏広
kn-aut-sei=小山
kn-aut-mei=敏広
aut-affil-num=4
ORCID=

en-aut-name=IwataniYukiko
en-aut-sei=Iwatani
en-aut-mei=Yukiko
kn-aut-name=岩谷有希子
kn-aut-sei=岩谷
kn-aut-mei=有希子
aut-affil-num=5
ORCID=

en-aut-name=JinXin
en-aut-sei=Jin
en-aut-mei=Xin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=Takada-DoiShima
en-aut-sei=Takada-Doi
en-aut-mei=Shima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawasakiHiromu
en-aut-sei=Kawasaki
en-aut-mei=Hiromu
kn-aut-name=川﨑博己
kn-aut-sei=川﨑
kn-aut-mei=博己
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=2
en-affil=
kn-affil=日本新薬創薬研究所

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=7
en-affil=
kn-affil=山田養蜂場本社研究開発部

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野
en-keyword=royal jelly
kn-keyword=royal jelly
en-keyword=fructose-drinking rat
kn-keyword=fructose-drinking rat
en-keyword=insulin resistance
kn-keyword=insulin resistance
en-keyword=periarterial nerve function
kn-keyword=periarterial nerve function
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=12
article-no=
start-page=2065
end-page=2073
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20071201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effect of propolis on insulin resistance in fructose-drinking rats
kn-title=フルクトース負荷インスリン抵抗性モデル(ラット)におけるPropolisによるインスリン抵抗性改善作用
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Propolis, a honeybee product, contains a variety of biologically active substances. The present study was designed to investigate the effects of propolis on insulin resistance induced by fructose-drinking rats (FDR; type 2 diabetic animal model). Male Wistar rats (6 weeks old) received 15% fructose solution in drinking water for 8 weeks. FDR showed significant increases in plasma levels of insulin, Homeostasis Model Assessment ratio (HOMA-R, an index of insulin resistance), body weight, and systolic blood pressure but not blood glucose levels, when compared with control rats. Brazilian propolis extract (100 and 300mg/kg, p. o.) treatment for 8 weeks significantly decreased the plasma level of insulin, HOMA-R, and body weight, increased plasma triglyceride levels without affecting blood glucose and total cholesterol levels, and tended to decrease systolic blood pressure. In isolated and perfused mesenteric vascular beds of FDR, propolis treatment resulted in a significant reduction of sympathetic nerve-mediated vasoconstrictor response to periarterial nerve stimulation (PNS; 8Hz) and tended to increase the calcitonin gene-related peptide (CGRP) nerve-mediated vasodilator response to PNS, compared with those in untreated FDR. However, propolis treatment did not significantly affect norepinephrine-induced vasoconstriction and CGRP-induced vasodilation. These results suggest that propolis could be an effective functional food to prevent the development of insulin resistance.
en-copyright=
kn-copyright=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=座間味義人
kn-aut-sei=座間味
kn-aut-mei=義人
aut-affil-num=1
ORCID=

en-aut-name=TakatoriShingo
en-aut-sei=Takatori
en-aut-mei=Shingo
kn-aut-name=高取真吾
kn-aut-sei=高取
kn-aut-mei=真吾
aut-affil-num=2
ORCID=

en-aut-name=KoayamaToshihiro
en-aut-sei=Koayama
en-aut-mei=Toshihiro
kn-aut-name=小山敏広
kn-aut-sei=小山
kn-aut-mei=敏広
aut-affil-num=3
ORCID=

en-aut-name=GodaMitsuhiro
en-aut-sei=Goda
en-aut-mei=Mitsuhiro
kn-aut-name=合田光寛
kn-aut-sei=合田
kn-aut-mei=光寛
aut-affil-num=4
ORCID=

en-aut-name=IwataniYukiko
en-aut-sei=Iwatani
en-aut-mei=Yukiko
kn-aut-name=岩谷有希子
kn-aut-sei=岩谷
kn-aut-mei=有希子
aut-affil-num=5
ORCID=

en-aut-name=DoiShima
en-aut-sei=Doi
en-aut-mei=Shima
kn-aut-name=土井志真
kn-aut-sei=土井
kn-aut-mei=志真
aut-affil-num=6
ORCID=

en-aut-name=KawasakiHiromu
en-aut-sei=Kawasaki
en-aut-mei=Hiromu
kn-aut-name=川﨑博己
kn-aut-sei=川﨑
kn-aut-mei=博己
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=2
en-affil=
kn-affil=日本新薬創薬研究所

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=6
en-affil=
kn-affil=山田養蜂場本社研究開発部

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野
en-keyword=propolis
kn-keyword=propolis
en-keyword=fructose-drinking rat
kn-keyword=fructose-drinking rat
en-keyword=insulin resistance
kn-keyword=insulin resistance
en-keyword=periarterial nerve function
kn-keyword=periarterial nerve function
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=3
article-no=
start-page=419
end-page=424
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness
kn-title=食後高血糖が血管反応性に及ぼす影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin generelated peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented adrenergic nerve-mediated pressor responses to SCS without affecting injection of pressor responses to noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of adrenergic nervemediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemic, significantly augmented adrenergic nerve-mediated pressor responses and attenuated CGRPergic nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases adrenergic nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.
en-copyright=
kn-copyright=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=座間味義人
kn-aut-sei=座間味
kn-aut-mei=義人
aut-affil-num=1
ORCID=

en-aut-name=TakatoriShingo
en-aut-sei=Takatori
en-aut-mei=Shingo
kn-aut-name=高取真吾
kn-aut-sei=高取
kn-aut-mei=真吾
aut-affil-num=2
ORCID=

en-aut-name=IwataniYukiko
en-aut-sei=Iwatani
en-aut-mei=Yukiko
kn-aut-name=岩谷有希子
kn-aut-sei=岩谷
kn-aut-mei=有希子
aut-affil-num=3
ORCID=

en-aut-name=YamawakiKosuke
en-aut-sei=Yamawaki
en-aut-mei=Kosuke
kn-aut-name=山脇康佑
kn-aut-sei=山脇
kn-aut-mei=康佑
aut-affil-num=4
ORCID=

en-aut-name=MiyashitaSatoko
en-aut-sei=Miyashita
en-aut-mei=Satoko
kn-aut-name=宮下智子
kn-aut-sei=宮下
kn-aut-mei=智子
aut-affil-num=5
ORCID=

en-aut-name=YabumaeNana
en-aut-sei=Yabumae
en-aut-mei=Nana
kn-aut-name=藪前奈々
kn-aut-sei=藪前
kn-aut-mei=奈々
aut-affil-num=6
ORCID=

en-aut-name=TakayamaFusako
en-aut-sei=Takayama
en-aut-mei=Fusako
kn-aut-name=高山房子
kn-aut-sei=高山
kn-aut-mei=房子
aut-affil-num=7
ORCID=

en-aut-name=MioMitsunobu
en-aut-sei=Mio
en-aut-mei=Mitsunobu
kn-aut-name=見尾光庸
kn-aut-sei=見尾
kn-aut-mei=光庸
aut-affil-num=8
ORCID=

en-aut-name=KawasakiHiromu
en-aut-sei=Kawasaki
en-aut-mei=Hiromu
kn-aut-name=川﨑博己
kn-aut-sei=川﨑
kn-aut-mei=博己
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=2
en-affil=
kn-affil=日本新薬(株)創薬研究所

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=8
en-affil=
kn-affil=就実大学薬学部薬効解析学分野

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野
en-keyword=hyperglycemia
kn-keyword=hyperglycemia
en-keyword=hyperinsulinemia
kn-keyword=hyperinsulinemia
en-keyword=Calcitonin gene-related peptide nerve
kn-keyword=Calcitonin gene-related peptide nerve
END

start-ver=1.4
cd-journal=joma
no-vol=130
cd-vols=
no-issue=6
article-no=
start-page=833
end-page=840
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100601
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Ameliorative effect of propolis on insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats
kn-title=Propolis 長期投与による Otsuka Long-Evans Tokushima Fatty (OLETF) ラットの インスリン抵抗性改善作用
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Propolis is known to have abundant bioactive constituents and a variety of biological activities. To investigate the effect of Brazilian propolis on insulin resistance, 10-week-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a non-insulin-dependent type 2 diabetic model, were treated for 4 weeks with propolis (100 and 300 mg/kg, p.o.) or vehicle (control). Propolis treatment significantly decreased the plasma levels of insulin and insulin resistance index (Homeostasis Model Assessment-Insulin Resistance; HOM-IR), without affecting blood glucose levels and tended to lower systolic blood pressure compared with the control. In isolated and perfused mesenteric vascular beds of OLETF rats, propolis treatment resulted in significant reduction of sympathetic nerve-mediated vasoconstrictor response to periarterial nerve stimulation (PNS) and tended to increase calcitonin gene-related peptide (CGRP) nerve-mediated vasodilator response to PNS compared with in vehicle-treated OLETF rats. However, propolis treatment did not significantly affect the vasoconstrictor and vasodilator response to noradrenaline, CGRP, acetylcholine, and sodium nitroprusside. These results suggest that propolis could be an effective and functional food to prevent development of insulin resistance.
en-copyright=
kn-copyright=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=座間味義人
kn-aut-sei=座間味
kn-aut-mei=義人
aut-affil-num=1
ORCID=

en-aut-name=FujiwaraHiroki
en-aut-sei=Fujiwara
en-aut-mei=Hiroki
kn-aut-name=藤原弘喜
kn-aut-sei=藤原
kn-aut-mei=弘喜
aut-affil-num=2
ORCID=

en-aut-name=HosodaMiho
en-aut-sei=Hosoda
en-aut-mei=Miho
kn-aut-name=細田美穂
kn-aut-sei=細田
kn-aut-mei=美穂
aut-affil-num=3
ORCID=

en-aut-name=HinoHayato
en-aut-sei=Hino
en-aut-mei=Hayato
kn-aut-name=日野隼人
kn-aut-sei=日野
kn-aut-mei=隼人
aut-affil-num=4
ORCID=

en-aut-name=HiraiKazuhiro
en-aut-sei=Hirai
en-aut-mei=Kazuhiro
kn-aut-name=平井和浩
kn-aut-sei=平井
kn-aut-mei=和浩
aut-affil-num=5
ORCID=

en-aut-name=OkamotoKazuaki
en-aut-sei=Okamoto
en-aut-mei=Kazuaki
kn-aut-name=岡本和明
kn-aut-sei=岡本
kn-aut-mei=和明
aut-affil-num=6
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=金鑫
kn-aut-sei=金
kn-aut-mei=鑫
aut-affil-num=7
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=高取真吾
kn-aut-sei=高取
kn-aut-mei=真吾
aut-affil-num=8
ORCID=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=高木志真
kn-aut-sei=高木
kn-aut-mei=志真
aut-affil-num=9
ORCID=

en-aut-name=KawasakiHiromu
en-aut-sei=Kawasaki
en-aut-mei=Hiromu
kn-aut-name=川﨑博己
kn-aut-sei=川﨑
kn-aut-mei=博己
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野

affil-num=8
en-affil=
kn-affil=日本新薬株式会社創薬研究所

affil-num=9
en-affil=
kn-affil=山田養蜂場本社研究開発部

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科臨床薬学分野
en-keyword=propolis
kn-keyword=propolis
en-keyword=insulin resistance
kn-keyword=insulin resistance
en-keyword=Otsuka Long-Evans Tokushima Fatty rat
kn-keyword=Otsuka Long-Evans Tokushima Fatty rat
en-keyword=periarterial nerve function
kn-keyword=periarterial nerve function
en-keyword=mesenteric vascular bed
kn-keyword=mesenteric vascular bed
END

start-ver=1.4
cd-journal=joma
no-vol=61
cd-vols=
no-issue=130
article-no=
start-page=349
end-page=353
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201403
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Management Of Peritoneal Effusion by Sealing with a Self-Assembling Nanofiber Polypeptide Following Pelvic Surgery
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Aims: PuraMatrix is a synthetic material consisting of 16-amino acid peptides that self-assemble into nanofibers, previously used as a scaffold for functional cell cultures. We conducted a clinical study to determine the safety and sealing properties of PuraMatrix in post-operative lymphorrhea following pelvic surgery in humans. Methodology: A total of 20 patients who underwent rectal cancer resection were analyzed. The study group (n = 10) consisted of patients who received PuraMatrix, matched with a control group (n = 10) of patients operated on conventionally. Results: During the 2 to 3 month follow-up period, there were no abnormal findings or adverse events in any the patients who received PuraMatrix. We found that the patients who received PuraMatrix had significantly reduced post-operative drainage volumes compared with the patients in the control group. Conclusions: PuraMatrix is a safe and effective bio-compatible sealing material for the management of post-operative peritoneal effusion following pelvic surgery.
en-copyright=
kn-copyright=

en-aut-name=KondoYoshitaka
en-aut-sei=Kondo
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagasakaTakeshi
en-aut-sei=Nagasaka
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KobayashiSatoru
en-aut-sei=Kobayashi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobayashiNaoya
en-aut-sei=Kobayashi
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Surg Gastroenterol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Surg Gastroenterol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=3D Matrix Ltd

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Surg Gastroenterol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Surg Gastroenterol, Grad Sch Med Dent & Pharmaceut Sci
en-keyword=Peritoneal effusion
kn-keyword=Peritoneal effusion
en-keyword=Nanofiber polypeptide
kn-keyword=Nanofiber polypeptide
en-keyword=Lymphorrhea
kn-keyword=Lymphorrhea
en-keyword=Pelvic surgery
kn-keyword=Pelvic surgery
END

start-ver=1.4
cd-journal=joma
no-vol=171
cd-vols=
no-issue=3
article-no=
start-page=492
end-page=498
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201409
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cathelicidin antimicrobial peptide LL-37 augments interferon-beta expression and antiviral activity induced by double-stranded RNA in keratinocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Cathelicidin antimicrobial peptide LL-37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL-37 and DNA greatly increases interferon (IFN)-beta through Toll-like receptor (TLR) 9. However, the effect of LL-37 on the induction of IFN-beta through TLR3, a sensor of double-stranded (ds) RNA, in keratinocytes is not well known. 

Objectives To investigate whether LL-37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs). 

Methods We investigated the production of IFN-beta in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL-37. To examine the effect of LL-37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type-1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL-37. Immunostaining for TLR3 and LL-37 was performed using skin samples from HS. 

Results LL-37 and poly (I:C) synergistically induced the expression of IFN-beta in NHEKs. Furthermore, co-stimulation with LL-37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL-37 alone. LL-37 enhanced the uptake of FITC-conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL-37 is up-regulated in HS lesions. 

Conclusions Our findings suggest that LL-37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
en-copyright=
kn-copyright=

en-aut-name=TakiguchiT
en-aut-sei=Takiguchi
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MorizaneS
en-aut-sei=Morizane
en-aut-mei=S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoT
en-aut-sei=Yamamoto
en-aut-mei=T
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KajitaA
en-aut-sei=Kajita
en-aut-mei=A
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IkedaK
en-aut-sei=Ikeda
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwatsukiK
en-aut-sei=Iwatsuki
en-aut-mei=K
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Kawasaki Med Univ, Dept Dermatol

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=抗菌ペプチド、Cathelicidin/LL-37は表皮角化細胞において2本鎖RNAによるIFN-βの発現ならびに抗ウィルス作用を増強する
kn-title=Cathelicidin antimicrobial peptide LL-37 augments IFN-β expression and anti-viral activity induced by double-stranded RNA in keratinocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TakiguchiTetsuya
en-aut-sei=Takiguchi
en-aut-mei=Tetsuya
kn-aut-name=瀧口徹也
kn-aut-sei=瀧口
kn-aut-mei=徹也
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=高度救命救急センターにおける外傷患者評価－BNP値にeGFRを併用した新たな外傷患者評価分類－
kn-title=A New Classification System for Evaluating Patients with Severe Trauma Using B-type Natriuretic Peptide Levels and Estimated Glomerular Filtration Rate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MorisadaSunao
en-aut-sei=Morisada
en-aut-mei=Sunao
kn-aut-name=森定淳
kn-aut-sei=森定
kn-aut-mei=淳
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=5
article-no=
start-page=307
end-page=311
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prompt Resolution of Hypoglycemia by Hepatic Transarterial Embolization for Malignant Insulinoma with Multiple Liver Metastases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A 45-year-old female who presented with loss of consciousness and a cold sweat was found to have a pancreatic tumor and multiple liver metastases. Laboratory studies showed marked hypoglycemia and inappropriately elevated serum insulin, C-peptide, and serum tumor markers. Fine needle aspiration revealed Grade 3 small-cell type primary pancreatic neuroendocrine carcinoma. Consequently, the diagnosis of malignant insulinoma was made. Transarterial embolization (TAE) for hepatic metastases resulted in the reduction of tumor volume and prompt resolution of hypoglycemic attacks, whereas diazoxide and systemic chemotherapy had been ineffective for controlling blood glucose levels, and octreotide was unavailable due to the allergic effect. This case report highlights the potential usefulness of TAE for malignant insulinomas in the management of hypoglycemia.
en-copyright=
kn-copyright=

en-aut-name=MuroShinichiro
en-aut-sei=Muro
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NasuJunichiro
en-aut-sei=Nasu
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HaradaRyo
en-aut-sei=Harada
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsubaraMinoru
en-aut-sei=Matsubara
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakaraiAsuka
en-aut-sei=Nakarai
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KanzakiHiromitsu
en-aut-sei=Kanzaki
en-aut-mei=Hiromitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsutsumiKouichiro
en-aut-sei=Tsutsumi
en-aut-mei=Kouichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatoHironari
en-aut-sei=Kato
en-aut-mei=Hironari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujiwaraHiroyasu
en-aut-sei=Fujiwara
en-aut-mei=Hiroyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=UnoMasatoshi
en-aut-sei=Uno
en-aut-mei=Masatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OkadaHiroyuki
en-aut-sei=Okada
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamamotoKazuhide
en-aut-sei=Yamamoto
en-aut-mei=Kazuhide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=8
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Pathology, Okayama University Hospital

affil-num=10
en-affil=
kn-affil=Department of Radiology, Okayama University Hospital

affil-num=11
en-affil=
kn-affil=Kaneda Hospital

affil-num=12
en-affil=
kn-affil=Department of Endoscopy, Okayama University Hospital

affil-num=13
en-affil=
kn-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=malignant insulinoma
kn-keyword=malignant insulinoma
en-keyword=hypoglycemia
kn-keyword=hypoglycemia
en-keyword=liver metastases
kn-keyword=liver metastases
en-keyword=transarterial embolization
kn-keyword=transarterial embolization
en-keyword=neuroendocrinetumor
kn-keyword=neuroendocrinetumor
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=5
article-no=
start-page=285
end-page=290
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=201410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A New Classification System for Evaluating Patients with Severe Trauma Using B-type Natriuretic Peptide Levels and Estimated Glomerular Filtration Rate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Current systems for the evaluation of trauma severity are tedious and difficult to apply in an actual emergency setting. We aimed to develop and assess the accuracy of a more efficient severity evaluation system, termed the Ugawa classification, using brain-type natriuretic peptide (BNP) measurement and the estimated glomerular filtration rate (eGFR). Two-hundred trauma patients were divided into 2 groups using an eGFR cut-off value of 90ml/min/1.73m2 as an indicator of normal renal function and 2 additional groups according to whether the BNP values were greater or less than the age in years. This resulted in 4 subject groups with different combinations of eGFR and BNP. The mean SOFA score, injury severity scores (ISS), trauma and injury severity scores (TRISS), and Acute Physiology and Chronic Health Evaluation II (APACHE II) scores of the groups were compared by Kruskal-Wallis test, and the mortality rate after 90 days was calculated. Significant intergroup differences were found in SOFA scores, ISS scores, and APACHE II-predicted mortality rates. Although no significant differences were found in the mortality rate after 90 days or TRISS-predicted mortality rate among the 4 groups, there was a trend toward increasing trauma severity from group 1 to 4. Thus, the Ugawa classification is as accurate as existing systems, has greater efficiency, and is user-friendly.
en-copyright=
kn-copyright=

en-aut-name=MorisadaSunao
en-aut-sei=Morisada
en-aut-mei=Sunao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UgawaToyomu
en-aut-sei=Ugawa
en-aut-mei=Toyomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NosakaNobuyuki
en-aut-sei=Nosaka
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UjikeYoshihito
en-aut-sei=Ujike
en-aut-mei=Yoshihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Advanced Emergency and Critical Care Center of Okayama University Hospital

affil-num=2
en-affil=
kn-affil=Advanced Emergency and Critical Care Center of Okayama University Hospital

affil-num=3
en-affil=
kn-affil=Advanced Emergency and Critical Care Center of Okayama University Hospital

affil-num=4
en-affil=
kn-affil=Advanced Emergency and Critical Care Center of Okayama University Hospital
en-keyword=acute injury
kn-keyword=acute injury
en-keyword=Acute Physiology and Chronic Health Evaluation II
kn-keyword=Acute Physiology and Chronic Health Evaluation II
en-keyword=injury severity score
kn-keyword=injury severity score
en-keyword=sequential organ failure assessment
kn-keyword=sequential organ failure assessment
en-keyword=trauma and injury severity score
kn-keyword=trauma and injury severity score
END

start-ver=1.4
cd-journal=joma
no-vol=381
cd-vols=
no-issue=1-2
article-no=
start-page=8
end-page=15
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20131205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mutual interaction of kisspeptin, estrogen and bone morphogenetic protein-4 activity in GnRH regulation by GT1-7 cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Reproduction is integrated by interaction of neural and hormonal signals converging on hypothalamic neurons for controlling gonadotropin-releasing hormone (GnRH). Kisspeptin, the peptide product of the kiss1 gene and the endogenous agonist for the GRP54 receptor, plays a key role in the regulation of GnRH secretion. In the present study, we investigated the interaction between kisspeptin, estrogen and BMPs in the regulation of GnRH production by using mouse hypothalamic GT1-7 cells. Treatment with kisspeptin increased GnRH mRNA expression and GnRH protein production in a concentration-dependent manner. The expression levels of kiss1 and GPR54 were not changed by kisspeptin stimulation. Kisspeptin induction of GnRH was suppressed by co-treatment with BMPs, with BMP-4 action being the most potent for suppressing the kisspeptin effect. The expression of kisspeptin receptor, GPR54, was suppressed by BMPs, and this effect was reversed in the presence of kisspeptin. It was also revealed that BMP-induced Smad1/5/8 phosphorylation and Id-1 expression were suppressed and inhibitory Smad6/7 was induced by kisspeptin. In addition, estrogen induced GPR54 expression, while kisspeptin increased the expression levels of ER alpha. and ER beta, suggesting that the actions of estrogen and kisspeptin are mutually enhanced in GT1-7 cells. Moreover, kisspeptin stimulated MAPKs and AKT signaling, and ERK signaling was functionally involved in the kisspeptin-induced GnRH expression. BMP-4 was found to suppress kisspeptin-induced GnRH expression by reducing ERK signaling activity. Collectively, the results indicate that the axis of kisspeptin-induced GnRH production is bi-directionally controlled, being augmented by an interaction between ER alpha/beta and GPR54 signaling and suppressed by BMP-4 action in GT1-7 neuron cells.
en-copyright=
kn-copyright=

en-aut-name=TerasakaTomohiro
en-aut-sei=Terasaka
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsukamotoNaoko
en-aut-sei=Tsukamoto
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraEri
en-aut-sei=Nakamura
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InagakiKenichi
en-aut-sei=Inagaki
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TomaKishio
en-aut-sei=Toma
en-aut-mei=Kishio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=Ogura-OchiKanako
en-aut-sei=Ogura-Ochi
en-aut-mei=Kanako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Glidewell-KenneyChristine
en-aut-sei=Glidewell-Kenney
en-aut-mei=Christine
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=LawsonMark A.
en-aut-sei=Lawson
en-aut-mei=Mark A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Gen Med

affil-num=3
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci

affil-num=8
en-affil=
kn-affil=Univ Calif San Diego, Dept Reprod Med

affil-num=9
en-affil=
kn-affil=Univ Calif San Diego, Dept Reprod Med

affil-num=10
en-affil=
kn-affil=Okayama Univ Grad Sch Med Dent & Pharmaceut Sci, Dept Med & Clin Sci
en-keyword=BMP
kn-keyword=BMP
en-keyword=Estradiol
kn-keyword=Estradiol
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=GPR54
kn-keyword=GPR54
en-keyword=Kisspeptin
kn-keyword=Kisspeptin
en-keyword=MAPK
kn-keyword=MAPK
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=7
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140721
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Neutral Self-Assembling Peptide Hydrogel SPG-178 as a Topical Hemostatic Agent
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Conventional self-assembling peptide hydrogels are effective as topical hemostatic agents. However, there is a possibility to harm living tissues due to their low pH. The aim of the present study was to demonstrate the efficacy of SPG-178, a neutral self-assembling peptide hydrogel, as a topical hemostatic agent. First, we measured the bleeding duration of incisions made on rat livers after application of SPG-178 (1.0% w/v), SPG-178 (1.5% w/v), RADA16 (1.0% w/v), and saline (n = 12/group). Second, we observed the bleeding surfaces by transmission electron microscopy immediately after hemostasis. Third, we measured the elastic and viscous responses (G′ and G″, respectively) of the hydrogels using a rheometer. Our results showed that bleeding duration was significantly shorter in the SPG-178 group than in the RADA16 group and that there were no significant differences in transmission electron microscopy findings between the groups. The greater the G′ value of a hydrogel, the shorter was the bleeding duration. We concluded that SPG-178 is more effective and has several advantages: it is non-biological, transparent, nonadherent, and neutral and can be sterilized by autoclaving.
en-copyright=
kn-copyright=

en-aut-name=KomatsuSeiji
en-aut-sei=Komatsu
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KimataYoshihiro
en-aut-sei=Kimata
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Plastic and Reconstructive Surgery, Okayama Saiseikai General Hospital

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Plastic and Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=2
article-no=
start-page=95
end-page=98
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 2013 Incentive Award of the Okayama Medical Association in Cardiovascular and Pulmonary Research (2013 Sunada Prize)
kn-title=平成25年度岡山医学会賞 胸部・循環研究奨励賞（砂田賞）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=中司敦子
kn-aut-sei=中司
kn-aut-mei=敦子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　腎臓・糖尿病・内分泌内科
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=938
end-page=944
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201310
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inhibition of RAGE signaling through the intracellular delivery of inhibitor peptides by PEI cationization
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The receptor for advanced glycation end products (RAGE) is a multi-ligand cell surface receptor and a member of the immunoglobulin superfamily. RAGE is involved in a wide range of inflammatory, degenerative and hyper-proliferative disorders which span over different organs by engaging diverse ligands, including advanced glycation end products, S100 family proteins, high-mobility group protein B1 (HMGB1) and amyloid beta. We previously demonstrated that the cytoplasmic domain of RAGE is phosphorylated upon the binding of ligands, enabling the recruitment of two distinct pairs of adaptor proteins, Toll-interleukin 1 receptor domain-containing adaptor protein (TIRAP) and myeloid differentiation protein 88 (MyD88). This engagement allows the activation of downstream effector molecules, and thereby mediates a wide variety of cellular processes, such as inflammatory responses, apoptotic cell death, migration and cell growth. Therefore, inhibition of the binding of TIRAP to RAGE may abrogate intracellular signaling from ligand-activated RAGE. In the present study, we developed inhibitor peptides for RAGE signaling (RAGE-I) by mimicking the phosphorylatable cytosolic domain of RAGE. RAGE-I was efficiently delivered into the cells by polyethylenimine (PEI) cationization. We demonstrated that RAGE-I specifically bound to TIRAP and abrogated the activation of Cdc42 induced by ligand-activated RAGE. Furthermore, we were able to reduce neuronal cell death induced by an excess amount of S100B and to inhibit the migration and invasion of glioma cells in vitro. Our results indicate that RAGE-I provides a powerful tool for therapeutics to block RAGE-mediated multiple signaling.
en-copyright=
kn-copyright=

en-aut-name=PutrantoEndy Widya
en-aut-sei=Putranto
en-aut-mei=Endy Widya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoKen-Ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KataokaKen
en-aut-sei=Kataoka
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamadaHidenori
en-aut-sei=Yamada
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FutamiJun-Ichiro
en-aut-sei=Futami
en-aut-mei=Jun-Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HuhNam-Ho
en-aut-sei=Huh
en-aut-mei=Nam-Ho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol

affil-num=4
en-affil=
kn-affil=Okayama Univ Sci, Fac Sci, Dept Life Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Biotechnol, Dept Med Bioengn Sci

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Biotechnol, Dept Med Bioengn Sci

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Biol
en-keyword=receptor for advanced glycation end products
kn-keyword=receptor for advanced glycation end products
en-keyword=Toll-interleukin 1 receptor domain-containing adaptor protein
kn-keyword=Toll-interleukin 1 receptor domain-containing adaptor protein
en-keyword=cationization
kn-keyword=cationization
en-keyword=S100B
kn-keyword=S100B
en-keyword=cell death
kn-keyword=cell death
en-keyword=cell migration
kn-keyword=cell migration
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=1
article-no=
start-page=7
end-page=10
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The mechanical stimulation of cells in 3D culture within a self-assembling peptide hydrogel
kn-title=自己集合性ペプチドハイドロゲル内で三次元培養された細胞への機械刺激
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=永井祐介
kn-aut-sei=永井
kn-aut-mei=祐介
aut-affil-num=1
ORCID=

en-aut-name=YokoiHidenori
en-aut-sei=Yokoi
en-aut-mei=Hidenori
kn-aut-name=横井秀典
kn-aut-sei=横井
kn-aut-mei=秀典
aut-affil-num=2
ORCID=

en-aut-name=KaiharaKeiko
en-aut-sei=Kaihara
en-aut-mei=Keiko
kn-aut-name=貝原恵子
kn-aut-sei=貝原
kn-aut-mei=恵子
aut-affil-num=3
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=成瀬恵治
kn-aut-sei=成瀬
kn-aut-mei=恵治
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学

affil-num=2
en-affil=
kn-affil=株式会社メニコン

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　システム生理学
en-keyword=機械刺激
kn-keyword=機械刺激
en-keyword=メカノバイオロジー
kn-keyword=メカノバイオロジー
en-keyword=自己集合性ペプチド
kn-keyword=自己集合性ペプチド
en-keyword=３次元培養
kn-keyword=３次元培養
en-keyword=スキャフォールド
kn-keyword=スキャフォールド
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Cholecystokinin plays a novel protective role in diabetic kidney through anti-inflammatory actions on macrophages
kn-title=糖尿病の腎臓においてcholecystokininはマクロファージに対する抗炎症作用を介した新規の保護効果を発揮する
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MiyamotoSatoshi
en-aut-sei=Miyamoto
en-aut-mei=Satoshi
kn-aut-name=宮本聡
kn-aut-sei=宮本
kn-aut-mei=聡
aut-affil-num=1
ORCID=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=2
ORCID=

en-aut-name=MiyasakaKyoko
en-aut-sei=Miyasaka
en-aut-mei=Kyoko
kn-aut-name=宮坂京子
kn-aut-sei=宮坂
kn-aut-mei=京子
aut-affil-num=3
ORCID=

en-aut-name=OkadaShinichi
en-aut-sei=Okada
en-aut-mei=Shinichi
kn-aut-name=岡田震一
kn-aut-sei=岡田
kn-aut-mei=震一
aut-affil-num=4
ORCID=

en-aut-name=SasakiMotofumi
en-aut-sei=Sasaki
en-aut-mei=Motofumi
kn-aut-name=佐々木基史
kn-aut-sei=佐々木
kn-aut-mei=基史
aut-affil-num=5
ORCID=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=小寺亮
kn-aut-sei=小寺
kn-aut-mei=亮
aut-affil-num=6
ORCID=

en-aut-name=HirotaDaisho
en-aut-sei=Hirota
en-aut-mei=Daisho
kn-aut-name=廣田大昌
kn-aut-sei=廣田
kn-aut-mei=大昌
aut-affil-num=7
ORCID=

en-aut-name=KajitaniNobuo
en-aut-sei=Kajitani
en-aut-mei=Nobuo
kn-aut-name=梶谷展生
kn-aut-sei=梶谷
kn-aut-mei=展生
aut-affil-num=8
ORCID=

en-aut-name=TakatsukaTetsuharu
en-aut-sei=Takatsuka
en-aut-mei=Tetsuharu
kn-aut-name=高塚哲全
kn-aut-sei=高塚
kn-aut-mei=哲全
aut-affil-num=9
ORCID=

en-aut-name=Kataoka UsuiHitomi
en-aut-sei=Kataoka Usui
en-aut-mei=Hitomi
kn-aut-name=片岡仁美
kn-aut-sei=片岡
kn-aut-mei=仁美
aut-affil-num=10
ORCID=

en-aut-name=NishishitaShingo
en-aut-sei=Nishishita
en-aut-mei=Shingo
kn-aut-name=西下伸吾
kn-aut-sei=西下
kn-aut-mei=伸吾
aut-affil-num=11
ORCID=

en-aut-name=Horiguchi SatoChikage
en-aut-sei=Horiguchi Sato
en-aut-mei=Chikage
kn-aut-name=堀口千景
kn-aut-sei=堀口
kn-aut-mei=千景
aut-affil-num=12
ORCID=

en-aut-name=FunakoshiAkihiro
en-aut-sei=Funakoshi
en-aut-mei=Akihiro
kn-aut-name=船越顕博
kn-aut-sei=船越
kn-aut-mei=顕博
aut-affil-num=13
ORCID=

en-aut-name=NishimoriHisakazu
en-aut-sei=Nishimori
en-aut-mei=Hisakazu
kn-aut-name=西森久和
kn-aut-sei=西森
kn-aut-mei=久和
aut-affil-num=14
ORCID=

en-aut-name=UchidaHaruhito Adam
en-aut-sei=Uchida
en-aut-mei=Haruhito Adam
kn-aut-name=内田治仁
kn-aut-sei=内田
kn-aut-mei=治仁
aut-affil-num=15
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=小川大輔
kn-aut-sei=小川
kn-aut-mei=大輔
aut-affil-num=16
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=17
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=東京家政大学　栄養学科

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=10
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=11
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=12
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=13
en-affil=
kn-affil=国立病院機構九州がんセンター　消化器肝胆膵内科

affil-num=14
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　血液・腫瘍・呼吸器内科学

affil-num=15
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=16
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=17
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=cholecystokinin
kn-keyword=cholecystokinin
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=抗炎症作用
kn-keyword=抗炎症作用
en-keyword=腎保護効果
kn-keyword=腎保護効果
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20131231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=細胞内導入型RAGE阻害ペプチドの開発
kn-title=Inhibition of RAGE signaling through the intracellular delivery of inhibitor peptides by PEI cationization
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=PutrantoEndy Widya
en-aut-sei=Putranto
en-aut-mei=Endy Widya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=
article-no=
start-page=1
end-page=4
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=大豆発芽時期におけるグリシニン分解酵素の活性変動
kn-title=Changes in Glycinin‒Digesting Protease Activity During Soybean Germination.
en-subtitle=
kn-subtitle=
en-abstract=　大豆発芽期におけるグリシニン分解酵素 (98 kDa SBP) の活性変動を解析した．大豆種子を４時間水で膨潤後， 25
℃ 暗黒下で発芽させた．経時的にサンプリングを行い，2M NaCl を含むトリス緩衝液 (㏗ 7.0) により粗酵素を抽出
後，グリシニン由来のトリプシン分解ペプチドを基質としてグリシニン分解酵素の活性変動を逆相 HPLC により追
跡した．その結果，種子膨潤後４日間比活性はほぼ一定の値を保ち，以後徐々に低下することが分かった．次いで，
粗酵素溶液からイオン交換 HPLC により98 kDa SBP を部分精製するとともに，発芽期における 98 kDa SBP の消長
を解析したところ，98 kDa SBP は乾燥種子及び各発芽段階の種子中全てに認められ，かつグリシン分解活性もグリ
シニン由来のトリプシン分解ペプチド基質に対する活性と同様に認められた．以上の結果から，98 kDa SBP は種子
発芽に伴い誘導されるプロテアーゼではなく，種子貯蔵型のプロテアーゼであることが明らかになった．
kn-abstract=　Changes in glycinin-digesting protease activity during soybean germination have been investigated.
The glycinin-digesting protease activities of imbibed or germinated soybean seed were assayed by
RP‒HPLC using a tryptic peptide from CM‒glycinin or by SDS‒PAGE using CM‒glycinin as the endogenous
substrate. Proteolytic activities of the germinated soybean seeds were found through the whole
period of germination, the activities were maintained significantly unchanged during germination for 4
days, and then those specific activities declined slowly. AE‒HPLC analysis of the glycinin-digesting
protease in the imbibed or germinated soybean seeds showed unchanged peaks corresponding to glycinin-
digesting activity, suggesting that the glycinin-digesting protease was not induced during germination
but had already been synthesized during seed maturation.
en-copyright=
kn-copyright=

en-aut-name=Md. Akhtaruzzaman
en-aut-sei=Md. Akhtaruzzaman
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaedaMegumi
en-aut-sei=Maeda
en-aut-mei=Megumi
kn-aut-name=前田恵
kn-aut-sei=前田
kn-aut-mei=恵
aut-affil-num=2
ORCID=

en-aut-name=KitagawaKeiko
en-aut-sei=Kitagawa
en-aut-mei=Keiko
kn-aut-name=北川恵子
kn-aut-sei=北川
kn-aut-mei=恵子
aut-affil-num=3
ORCID=

en-aut-name=TakagiShigeaki
en-aut-sei=Takagi
en-aut-mei=Shigeaki
kn-aut-name=高木茂明
kn-aut-sei=高木
kn-aut-mei=茂明
aut-affil-num=4
ORCID=

en-aut-name=KimuraYoshinobu
en-aut-sei=Kimura
en-aut-mei=Yoshinobu
kn-aut-name=木村吉伸
kn-aut-sei=木村
kn-aut-mei=吉伸
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学

affil-num=2
en-affil=
kn-affil=岡山大学

affil-num=3
en-affil=
kn-affil=岡山大学

affil-num=4
en-affil=
kn-affil=岡山大学

affil-num=5
en-affil=
kn-affil=岡山大学
en-keyword=Plant protease
kn-keyword=Plant protease
en-keyword=glycinin
kn-keyword=glycinin
en-keyword=germination
kn-keyword=germination
en-keyword=Glycine max
kn-keyword=Glycine max
END

start-ver=1.4
cd-journal=joma
no-vol=37
cd-vols=
no-issue=11
article-no=
start-page=1003
end-page=1008
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130704
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of atrial natriuretic Peptide after prolonged hypothermic storage of the isolated rat heart
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Primary graft failure (PGF) caused by ischemia-reperfusion injury (IRI) is the strongest determinant of perioperative mortality after heart transplantation. Atrial natriuretic peptide (ANP) has been found to reduce the IRI of cardiomyocytes and may be beneficial in alleviating PGF after heart transplantation, although there is a lack of evidence to support this issue. The purpose of this study was to investigate the cardioprotective effects of ANP after prolonged hypothermic storage. For this purpose, an isolated working-heart rat model was used. After the preparation, the hearts were arrested with and stored in an extracellular-based cardioplegic solution at 3-4°C for 6 h and followed by 25 min of reperfusion. The hearts were divided into four groups (n = 7 in each group) according to the timing of ANP administration: Group 1 (in perfusate before storage), Group 2 (in cardioplegia), Group 3 (in reperfusate), and control (no administration of ANP). Left ventricular functional recovery and the incidence of ventricular fibrillation (VF) were compared. ANP administration at the time of reperfusion improved the percent recovery of left ventricular developed pressure (control, 45.5 ± 10.2; Group 1, 47.4 ± 8.8; Group 2, 45.3 ± 12 vs. Group 3, 76.3 ± 7; P < 0.05) and maximum first derivative of the left ventricular pressure (control, 47.9 ± 8.7; Group 1, 46.7 ± 8.8; Group 2, 49.6 ± 10.8 vs. Group 3, 76.6 ± 7.5; P < 0.05). The incidence of VF after reperfusion did not differ significantly among these four groups (71.4, 85.7, 57.1, and 85.7% in Groups 1, 2, 3, and control, respectively). This result suggests that the administration of ANP at the time of reperfusion may have the potential to decrease the incidence of PGF after heart transplantation.
en-copyright=
kn-copyright=

en-aut-name=KanamitsuHitoshi
en-aut-sei=Kanamitsu
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiiYasuhiro
en-aut-sei=Fujii
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsuiHideya
en-aut-sei=Mitsui
en-aut-mei=Hideya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SanoShunji
en-aut-sei=Sano
en-aut-mei=Shunji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=Atrial natriuretic peptide
kn-keyword=Atrial natriuretic peptide
en-keyword=Hypothermic storage
kn-keyword=Hypothermic storage
en-keyword=Myocardial reperfusion injury
kn-keyword=Myocardial reperfusion injury
en-keyword=Primary graft failure
kn-keyword=Primary graft failure
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=長時間低温保存ラット心における心房性ナトリウムペプチドの心保護効果の検討
kn-title=Effects of Atrial Natriuretic Peptide After Prolonged Hypothermic Storage of the Isolated Rat Heart
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KanemitsuHitoshi
en-aut-sei=Kanemitsu
en-aut-mei=Hitoshi
kn-aut-name=金光仁志
kn-aut-sei=金光
kn-aut-mei=仁志
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=11
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20121126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mitochondrial Localization of ABC Transporter ABCG2 and Its Function in 5-Aminolevulinic Acid-Mediated Protoporphyrin IX Accumulation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Accumulation of protoporphyrin IX (PpIX) in malignant cells is the basis of 5-aminolevulinic acid (ALA)-mediated photodynamic therapy. We studied the expression of proteins that possibly affect ALA-mediated PpIX accumulation, namely oligopeptide transporter-1 and -2, ferrochelatase and ATP-binding cassette transporter G2 (ABCG2), in several tumor cell lines. Among these proteins, only ABCG2 correlated negatively with ALA-mediated PpIX accumulation. Both a subcellular fractionation study and confocal laser microscopic analysis revealed that ABCG2 was distributed not only in the plasma membrane but also intracellular organelles, including mitochondria. In addition, mitochondrial ABCG2 regulated the content of ALA-mediated PpIX in mitochondria, and Ko143, a specific inhibitor of ABCG2, enhanced mitochondrial PpIX accumulation. To clarify the possible roles of mitochondrial ABCG2, we characterized stably transfected-HEK (ST-HEK) cells overexpressing ABCG2. In these ST-HEK cells, functionally active ABCG2 was detected in mitochondria, and treatment with Ko143 increased ALA-mediated mitochondrial PpIX accumulation. Moreover, the mitochondria isolated from ST-HEK cells exported doxorubicin probably through ABCG2, because the export of doxorubicin was inhibited by Ko143. The susceptibility of ABCG2 distributed in mitochondria to proteinase K, endoglycosidase H and peptide-N-glycosidase F suggested that ABCG2 in mitochondrial fraction is modified by N-glycans and trafficked through the endoplasmic reticulum and Golgi apparatus and finally localizes within the mitochondria. Thus, it was found that ABCG2 distributed in mitochondria is a functional transporter and that the mitochondrial ABCG2 regulates ALA-mediated PpIX level through PpIX export from mitochondria to the cytosol.
en-copyright=
kn-copyright=

en-aut-name=KobuchiHirotsugu
en-aut-sei=Kobuchi
en-aut-mei=Hirotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriyaKoko
en-aut-sei=Moriya
en-aut-mei=Koko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OginoTetsuya
en-aut-sei=Ogino
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FujitaHirofumi
en-aut-sei=Fujita
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=InoueKeiji
en-aut-sei=Inoue
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShuinTaro
en-aut-sei=Shuin
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasudaTatsuji
en-aut-sei=Yasuda
en-aut-mei=Tatsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UtsumiKozo
en-aut-sei=Utsumi
en-aut-mei=Kozo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UtsumiToshihiko
en-aut-sei=Utsumi
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Cell Chem, Grad Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Yamaguchi Univ, Grad Sch Med

affil-num=3
en-affil=
kn-affil=Okayama Prefectural Univ, Dept Nursing Sci, Fac Hlth & Welf Sci

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Cytol & Histol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Kochi Med Sch, Dept Urol

affil-num=6
en-affil=
kn-affil=Kochi Med Sch, Dept Urol

affil-num=7
en-affil=
kn-affil=Okayama Univ, Dept Cell Chem, Grad Sch Med Dent & Pharmaceut Sci

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Cytol & Histol, Grad Sch Med Dent & Pharmaceut Sci

affil-num=9
en-affil=
kn-affil=Yamaguchi Univ, Grad Sch Med
END

start-ver=1.4
cd-journal=joma
no-vol=62
cd-vols=
no-issue=4
article-no=
start-page=639
end-page=652
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201304
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Intratumoral peptide injection enhances tumor cell antigenicity recognized by cytotoxic T lymphocytes: a potential option for improvement in antigen-specific cancer immunotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Antigen-specific cancer immunotherapy is a promising strategy for improving cancer treatment. Recently, many tumor-associated antigens and their epitopes recognized by cytotoxic T lymphocytes (CTLs) have been identified. However, the density of endogenously presented antigen-derived peptides on tumor cells is generally sparse, resulting in the inability of antigen-specific CTLs to work effectively. We hypothesize that increasing the density of an antigen-derived peptide would enhance antigen-specific cancer immunotherapy. Here, we demonstrated that intratumoral peptide injection leads to additional peptide loading onto major histocompatibility complex class I molecules of tumor cells, enhancing tumor cell recognition by antigen-specific CTLs. In in vitro studies, human leukocyte antigen (HLA)-A*02:01-restricted glypican-3(144-152) (FVGEFFTDV) and cytomegalovirus(495-503) (NLVPMVATV) peptide-specific CTLs showed strong activity against all peptide-pulsed cell lines, regardless of whether the tumor cells expressed the antigen. In in vivo studies using immunodeficient mice, glypican-3(144-152) and cytomegalovirus(495-503) peptides injected into a solid mass were loaded onto HLA class I molecules of tumor cells. In a peptide vaccine model and an adoptive cell transfer model using C57BL/6 mice, intratumoral injection of ovalbumin(257-264) peptide (SIINFEKL) was effective for tumor growth inhibition and survival against ovalbumin-negative tumors without adverse reactions. Moreover, we demonstrated an antigen-spreading effect that occurred after intratumoral peptide injection. Intratumoral peptide injection enhances tumor cell antigenicity and may be a useful option for improvement in antigen-specific cancer immunotherapy against solid tumors.
en-copyright=
kn-copyright=

en-aut-name=NobuokaDaisuke
en-aut-sei=Nobuoka
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshikawaToshiaki
en-aut-sei=Yoshikawa
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiMari
en-aut-sei=Takahashi
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IwamaTatsuaki
en-aut-sei=Iwama
en-aut-mei=Tatsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HorieKazutaka
en-aut-sei=Horie
en-aut-mei=Kazutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShimomuraManami
en-aut-sei=Shimomura
en-aut-mei=Manami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SuzukiShiro
en-aut-sei=Suzuki
en-aut-mei=Shiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakemuraNoriko
en-aut-sei=Sakemura
en-aut-mei=Noriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakatsugawaMunehide
en-aut-sei=Nakatsugawa
en-aut-mei=Munehide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SadamoriHiroshi
en-aut-sei=Sadamori
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YagiTakahito
en-aut-sei=Yagi
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NakatsuraTetsuya
en-aut-sei=Nakatsura
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=2
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=3
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=4
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=5
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=6
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=7
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=8
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=9
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy

affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol

affil-num=11
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol

affil-num=12
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Surg Gastroenterol

affil-num=13
en-affil=
kn-affil=Natl Canc Ctr Hosp East, Res Ctr Innovat Oncol, Div Canc Immunotherapy
en-keyword=Intratumoral peptide injection
kn-keyword=Intratumoral peptide injection
en-keyword=Antigen
kn-keyword=Antigen
en-keyword=Immunotherapy
kn-keyword=Immunotherapy
en-keyword=Cytotoxic T lymphocyte
kn-keyword=Cytotoxic T lymphocyte
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=腫瘍内ペプチド注入は細胞傷害性T細胞により認識される腫瘍細胞の抗原性を増強する：抗原特異的がん免疫療法の効果を増強する治療オプションとしての可能性
kn-title=Intratumoral peptide injection enhances tumor cell antigenicity recognized by cytotoxic T lymphocytes: a potential option for improvement in antigen-specific cancer immunotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NobuokaDaisuke
en-aut-sei=Nobuoka
en-aut-mei=Daisuke
kn-aut-name=信岡大輔
kn-aut-sei=信岡
kn-aut-mei=大輔
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=32
article-no=
start-page=5338
end-page=5346
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100719
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Three novel NY-ESO-1 epitopes bound to DRB1*0803, DQB1*0401 and DRB1*0901 recognized by CD4 T cells from CHP-NY-ESO-1-vaccinated patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Three novel NY-ESO-1 CD4 T cell epitopes were identified using PBMC obtained from patients who were vaccinated with a complex of cholesterol-bearing hydrophobized pullulan (CHP) and NY-ESO-1 protein (CHP-NY-ESO-1). The restriction molecules were determined by antibody blocking and using various EBV-B cells with different HLA alleles as APC to present peptides to CD4 T cells. The minimal epitope peptides were determined using various N- and C-termini truncated peptides deduced from 18-mer overlapping peptides originally identified for recognition. Those epitopes were DRB1*0901-restricted NY-ESO-1 87-100. DQB1*0401-restricted NY-ESO-1 95-107 and DRB1*0803-restricted NY-ESO-1 124-134. CD4 T cells used to determine those epitope peptides recognized EBV-B cells or DC that were treated with recombinant NY-ESO-1 protein or NY-ESO-1-expressing tumor cell lysate, suggesting that the epitope peptides are naturally processed. These CD4 T cells showed a cytokine profile with Th1 characteristics. Furthermore, NY-ESO-1 87-100 peptide/HLA-DRB1*0901 tetramer staining was observed. Multiple Th1-type CD4 T cell responses are beneficial for inducing effective anti-tumor responses after NY-ESO-1 protein vaccination.
en-copyright=
kn-copyright=

en-aut-name=MizoteYu
en-aut-sei=Mizote
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TaniguchiTaku
en-aut-sei=Taniguchi
en-aut-mei=Taku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TanakaKei
en-aut-sei=Tanaka
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IsobeMidori
en-aut-sei=Isobe
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WadaHisashi
en-aut-sei=Wada
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaikaTakashi
en-aut-sei=Saika
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KitaShoichi
en-aut-sei=Kita
en-aut-mei=Shoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KoideYukari
en-aut-sei=Koide
en-aut-mei=Yukari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UenakaAkiko
en-aut-sei=Uenaka
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakayamaEiichi
en-aut-sei=Nakayama
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Immunol

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Immunol

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Immunol

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Immunol

affil-num=5
en-affil=
kn-affil=Osaka Univ, Grad Sch Med, Dept Surg, Suita

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Urol

affil-num=7
en-affil=
kn-affil=Med & Biol Labs Ltd

affil-num=8
en-affil=
kn-affil=Med & Biol Labs Ltd

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Immunol

affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Immunol
END

start-ver=1.4
cd-journal=joma
no-vol=131
cd-vols=
no-issue=11
article-no=
start-page=2537
end-page=2546
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20121201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Runt-related transcription factor 3 reverses epithelial-mesenchymal transition in hepatocellular carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Loss or decreased expression of runt-related transcription factor 3 (RUNX3), a tumor suppressor gene involved in gastric and other cancers, has been frequently observed in hepatocellular carcinoma (HCC). The objective of this study was to identify the regulatory mechanism of the epithelialmesenchymal transition (EMT) by RUNX3 in HCC. Human HCC cell lines, Hep3B, Huh7, HLF and SK-Hep1, were divided into low- and high-EMT lines, based on their expression of TWIST1 and SNAI2, and were used in this in vitro study. Ectopic RUNX3 expression had an anti-EMT effect in low-EMT HCC cell lines characterized by increased E-cadherin expression and decreased N-cadherin and vimentin expression. RUNX3 expression has previously been reported to reduce jagged-1 (JAG1) expression; therefore, JAG1 ligand peptide was used to reinduce EMT in RUNX3-expressing low-EMT HCC cells. Immunohistochemical analyses were performed for RUNX3, E-cadherin, N-cadherin and TWIST1 in 33 human HCC tissues, also divided into low- and high-EMT HCC, based on TWIST1 expression. E-cadherin expression was correlated positively and N-cadherin expression was correlated negatively with RUNX3 expression in low-EMT HCC tissues. Correlations between EMT markers and RUNX3 mRNA expression were analyzed using Oncomine datasets. Similarly, mRNA expression of E-cadherin was also significantly correlated with that of RUNX3 in low-EMT HCC, while mRNA expression of JAG1 was negatively correlated with that of RUNX3. These results suggest a novel mechanism by which loss or decreased expression of RUNX3 induces EMT via induction of JAG1 expression in low-EMT HCC.
en-copyright=
kn-copyright=

en-aut-name=TanakaShigetomi
en-aut-sei=Tanaka
en-aut-mei=Shigetomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShirahaHidenori
en-aut-sei=Shiraha
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakanishiYutaka
en-aut-sei=Nakanishi
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishinaShin-Ichi
en-aut-sei=Nishina
en-aut-mei=Shin-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsubaraMinoru
en-aut-sei=Matsubara
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HoriguchiShigeru
en-aut-sei=Horiguchi
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakaokaNobuyuki
en-aut-sei=Takaoka
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwamuroMasaya
en-aut-sei=Iwamuro
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KataokaJunro
en-aut-sei=Kataoka
en-aut-mei=Junro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KuwakiKenji
en-aut-sei=Kuwaki
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HagiharaHiroaki
en-aut-sei=Hagihara
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ToshimoriJunichi
en-aut-sei=Toshimori
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OhnishiHideki
en-aut-sei=Ohnishi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TakakiAkinobu
en-aut-sei=Takaki
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NakamuraShinichiro
en-aut-sei=Nakamura
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=NousoKazuhiro
en-aut-sei=Nouso
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YagiTakahito
en-aut-sei=Yagi
en-aut-mei=Takahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=YamamotoKazuhide
en-aut-sei=Yamamoto
en-aut-mei=Kazuhide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=4
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=7
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=8
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=9
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=10
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=11
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=12
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=13
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=14
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=15
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=16
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol

affil-num=17
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol Surg Transplant & Surg Oncol

affil-num=18
en-affil=
kn-affil=Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol & Hepatol
en-keyword=cell migration
kn-keyword=cell migration
en-keyword=tumor invasion
kn-keyword=tumor invasion
en-keyword=jagged-1
kn-keyword=jagged-1
en-keyword=E-cadherin
kn-keyword=E-cadherin
en-keyword=N-cadherin
kn-keyword=N-cadherin
END

start-ver=1.4
cd-journal=joma
no-vol=67
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=18
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201302
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phospholipase C Produced by Clostridium botulinum Types C and D:Comparison of Gene, Enzymatic, and Biological Activities with Those of Clostridium perfringens Alpha-toxin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Clostridium botulinum type C and D strains recently have been found to produce PLC on egg yolk agar plates. To characterize the gene, enzymatic and biological activities of C. botulinum PLCs (Cb-PLCs), the cb-plc genes from 8 strains were sequenced, and 1 representative gene was cloned and expressed as a recombinant protein. The enzymatic and hemolytic activities of the recombinant Cb-PLC were measured and compared with those of the Clostridium perfringens alpha-toxin. Each of the eight cb-plc genes encoded a 399 amino acid residue protein preceded by a 27 residue signal peptide. The protein consists of 2 domains, the N- and C-domains, and the overall amino acid sequence identity between Cb-PLC and alpha-toxin was greater than 50%, suggesting that Cb-PLC is homologous to the alpha-toxin. The key residues in the N-domain were conserved, whereas those in the C-domain which are important in membrane interaction were different than in the alpha-toxin. As expected, Cb-PLC could hydrolyze egg yolk phospholipid, p-nitrophenylphosphorylcholine, and sphingomyelin, and also exhibited hemolytic activity;however, its activities were about 4- to over 200-fold lower than those of alpha-toxin. Although Cb-PLC showed weak enzymatic and biological activities, it is speculated that Cb-PLC might play a role in the pathogenicity of botulism or for bacterial survival.
en-copyright=
kn-copyright=

en-aut-name=FatmawatiNi Nengah Dwi
en-aut-sei=Fatmawati
en-aut-mei=Ni Nengah Dwi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuzukiTomonori
en-aut-sei=Suzuki
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OdaMasataka
en-aut-sei=Oda
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShimizuKenta
en-aut-sei=Shimizu
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoYumiko
en-aut-sei=Yamamoto
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuraiJun
en-aut-sei=Sakurai
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsushitaOsamu
en-aut-sei=Matsushita
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OgumaKeiji
en-aut-sei=Oguma
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Interdisciplinary Research Organization, Miyazaki University

affil-num=3
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University

affil-num=5
en-affil=
kn-affil=Shin-Nakamura Chemical Co., Ltd

affil-num=6
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University

affil-num=8
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=9
en-affil=
kn-affil=Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=botulinum phospholipase C
kn-keyword=botulinum phospholipase C
en-keyword=botulinum toxin
kn-keyword=botulinum toxin
en-keyword=phospholipase C activity
kn-keyword=phospholipase C activity
en-keyword=sphingomyelinase activity
kn-keyword=sphingomyelinase activity
en-keyword=hemolytic activity
kn-keyword=hemolytic activity
END

start-ver=1.4
cd-journal=joma
no-vol=124
cd-vols=
no-issue=2
article-no=
start-page=175
end-page=177
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Heat shock protein and anti-tumor immunity
kn-title=熱ショックタンパク質と抗腫瘍免疫
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MizukamiShusaku
en-aut-sei=Mizukami
en-aut-mei=Shusaku
kn-aut-name=水上修作
kn-aut-sei=水上
kn-aut-mei=修作
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　免疫学
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=4
article-no=
start-page=1044
end-page=1051
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201202
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The mechanical stimulation of cells in 3D culture within a self-assembling peptide hydrogel
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of this present study was to provide a scaffold as a tool for the investigation of the effect of mechanical stimulation on three-dimensionally cultured cells. For this purpose, we developed an artificial self-assembling peptide (SPG-178) hydrogel scaffold. The structural properties of the SPG-178 peptide were confirmed by attenuated total reflection-Fourier transform infrared spectroscopy (ATR-FTIR) and transmission electron microscopy (TEM). The mechanical properties of the SPG-178 hydrogel were studied using rheology measurements. The SPG-178 peptide was able to form a stable, transparent hydrogel in a neutral pH environment In the SPG-178 hydrogel, mouse skeletal muscle cells proliferated successfully (increased by 12.4 +/- 1.5 times during 8 days of incubation; mean +/- SEM). When the scaffold was statically stretched, a rapid phosphorylation of ERK was observed (increased by 2.8 +/- 0.2 times; mean +/- SEM). These results demonstrated that the developed self-assembling peptide gel is non-cytotoxic and is a suitable tool for the investigation of the effect of mechanical stimulation on three-dimensional cell culture.
en-copyright=
kn-copyright=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
en-keyword=Cell proliferation
kn-keyword=Cell proliferation
en-keyword=Self-assembly
kn-keyword=Self-assembly
en-keyword=Hydrogel
kn-keyword=Hydrogel
en-keyword=Scaffold
kn-keyword=Scaffold
en-keyword=Mechanical strain
kn-keyword=Mechanical strain
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=自己集合性ペプチドハイドロゲル内で三次元培養された細胞への機械刺激
kn-title=The mechanical stimulation of cells in 3D culture within a self-assembling peptide hydrogel
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NagaiYusuke
en-aut-sei=Nagai
en-aut-mei=Yusuke
kn-aut-name=永井祐介
kn-aut-sei=永井
kn-aut-mei=祐介
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=124
cd-vols=
no-issue=1
article-no=
start-page=15
end-page=26
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Hypoglycemic activity of Momordica charantia (bitter melon)
kn-title=ニガウリ抽出物の血糖降下作用に関する文献的考察
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetes mellitus (DM) represents a global health and economical problem. Many patients with DM in Asia, South America, India and East Africa have traditionally used the water extract of unripe fruits of Momordica charantia (bitter melon) as some form of complementary and alternative medicine. Studies of laboratory animals have shown the beneficial blood-glucose lowering and anti-diabetic effects of this remedy. Some oral components that bring lower blood glucose level have been isolated : charantin (sterol glycosides), charantin (polypeptide) and cucurbine-type triterpenes. Part of their actions are related to AMP-activated kinase and repression of the oxidative stress that is increased in DM. Most clinical reports are not fully convincing due to the lack of randomized control studies. The present article reviews the pharmacological and clinical effects of bitter melon with special emphasis on the anti-diabetic effects, and some effects that would require caution in the context of human trials.
en-copyright=
kn-copyright=

en-aut-name=MankuraMitsumasa
en-aut-sei=Mankura
en-aut-mei=Mitsumasa
kn-aut-name=万倉三正
kn-aut-sei=万倉
kn-aut-mei=三正
aut-affil-num=1
ORCID=

en-aut-name=NodaYasuko
en-aut-sei=Noda
en-aut-mei=Yasuko
kn-aut-name=野田泰子
kn-aut-sei=野田
kn-aut-mei=泰子
aut-affil-num=2
ORCID=

en-aut-name=MoriAkitane
en-aut-sei=Mori
en-aut-mei=Akitane
kn-aut-name=森昭胤
kn-aut-sei=森
kn-aut-mei=昭胤
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　医療薬学・先端薬物療法開発学

affil-num=2
en-affil=
kn-affil=岡山大学医学部　病原細菌学

affil-num=3
en-affil=
kn-affil=岡山大学
en-keyword=ニガウリ (bitter melon)
kn-keyword=ニガウリ (bitter melon)
en-keyword=Momordica charantia
kn-keyword=Momordica charantia
en-keyword=糖尿病 (diabetes mellitus)
kn-keyword=糖尿病 (diabetes mellitus)
en-keyword=酸化ストレス (oxidative stress)
kn-keyword=酸化ストレス (oxidative stress)
END

start-ver=1.4
cd-journal=joma
no-vol=66
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=201202
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Heat Shock Protein Magic in Antigen Trafficking within Dendritic Cells:Implications in Antigen Cross-presentation in Immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dendritic cells (DCs) take up soluble- or cell-associated antigens and digest them, delivering fragments to the MHC class I pathway to display antigenic peptides to CD8＋ T cells, a process known as cross-presentation. The pathway requires that, in order to be degraded by proteosomes, the extracellular antigens must have access to the cytosol across the endosomal membranes. Although the cross-presentation phenomena was first identified in the 1970s, the molecular mechanism responsible for the translocation is still not fully understood. In this context, we have recently found that cytosolic heat shock protein (HSP)90 translocates internalized antigen to the cytosol in DCs. Our results revealed the important role that cytosolic HSP90 plays in cross-presentation by pulling out endosomal antigen to the cytosol.
en-copyright=
kn-copyright=

en-aut-name=UdonoHeiichiro
en-aut-sei=Udono
en-aut-mei=Heiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Immunology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
en-keyword=heat shock protein 90
kn-keyword=heat shock protein 90
en-keyword=dendritic cells
kn-keyword=dendritic cells
en-keyword=cross-presentation
kn-keyword=cross-presentation
en-keyword=proteasome
kn-keyword=proteasome
en-keyword=cytotoxic T cell immunity
kn-keyword=cytotoxic T cell immunity
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=
article-no=
start-page=65
end-page=70
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Research into food preservation using a bacteriocin produced by Lactobacillus gasseri
kn-title=Lactobacillus gasseri の生産するバクテリオシンの食品利用へ向けた検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bacteriocins are natural antibacterial peptides ribosomally biosynthesized by bacteria. Gassericin T which is a bacteriocin produced by many strains of Lactobacillus gasseri has a broad antibacterial spectrum against food spoilage and pathogenic Gram-positive bacteria; therefore, the bacteriocin and its producers are predicted for use as safe food preservatives. However, probiotic Lb. gasseri strains show poor growth and minimally produce gassericin T in food-grade
natural media such as reconstituted cheese whey, unlike in MRS broth. The growth of Lb. gasseri in reconstituted cheese whey was improved by adding proteose peptone as a nutrient factor. The production of gassericin T in MRS broth was specifically inhibited by adding divalent metal cations, and then the inhibition was removed using a chelator of divalent cations, trisodium citrate dihydrate. The production of gassericin T in reconstituted cheese whey was also restored by adding trisodium citrate dihydrate, and the activity was enhanced by a surfactant, Tween 80. In addition, trisodium citrate dihydrate led to over-production of and synergistic antibacterial effect with gassericin T. In this study, we developed a cheese whey-based medium containing proteose peptone, trisodium citrate dihydrate and Tween 80 for gassericin T production. The developed food-grade medium may contribute to the effective use of some bacteriocins from probiotic lactic acid bacteria for biopreservation of foods.
en-copyright=
kn-copyright=

en-aut-name=ArakawaKensuke
en-aut-sei=Arakawa
en-aut-mei=Kensuke
kn-aut-name=荒川健佑
kn-aut-sei=荒川
kn-aut-mei=健佑
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=
en-keyword=Bacteriocin
kn-keyword=Bacteriocin
en-keyword=Lactobacillus gasseri
kn-keyword=Lactobacillus gasseri
en-keyword=Gassericin T
kn-keyword=Gassericin T
en-keyword=Biopreservation
kn-keyword=Biopreservation
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=11
article-no=
start-page=1347
end-page=1354
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2003
dt-pub=200311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phase Shifts of the Circadian Locomotor Rhythm Induced by Pigment-Dispersing Factor in the Cricket Gryllus bimaculatus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pigment-dispersing factors (PDFs) are octadeca-peptides widely distributed in insect optic lobes and brain. In this study, we have purified PDF and determined its amino acid sequence in the cricket Gryllus bimaculatus. Its primary structure was NSEIINSLLGLPKVLNDA-NH2, homologous to other PDH family members so far reported. When injected into the optic lobe of experimentally blinded adult male crickets, Gryllus-PDF induced phase shifts in their activity rhythms in a phase dependent and dose dependent manner. The resulted phase response curve (PRC) showed delays during the late subjective night to early subjective day and advances during the mid subjective day to mid subjective night. The PRC was different in shape from those for light, serotonin and temperature. These results suggest that PDF plays a role in phase regulation of the circadian clock through a separate pathway from those of other known phase regulating agents.
en-copyright=
kn-copyright=

en-aut-name=SingaravelMuniyandi
en-aut-sei=Singaravel
en-aut-mei=Muniyandi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujisawaYuko
en-aut-sei=Fujisawa
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisadaMiki
en-aut-sei=Hisada
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaifullahASM
en-aut-sei=Saifullah
en-aut-mei=ASM
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomiokaKenji
en-aut-sei=Tomioka
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Physics, Biology and Informatics, Faculty of Science, Research Institute of Time Studies, Yamaguchi University

affil-num=2
en-affil=
kn-affil=Suntory Institute for Bioorganic Research

affil-num=3
en-affil=
kn-affil=Suntory Institute for Bioorganic Research

affil-num=4
en-affil=
kn-affil=Department of Physics, Biology and Informatics, Faculty of Science, Research Institute of Time Studies, Yamaguchi University

affil-num=5
en-affil=
kn-affil=Department of Physics, Biology and Informatics, Faculty of Science, Research Institute of Time Studies, Yamaguchi University
en-keyword=pigment-dispersing factor
kn-keyword=pigment-dispersing factor
en-keyword=circadian rhythm
kn-keyword=circadian rhythm
en-keyword=crickets
kn-keyword=crickets
en-keyword=phase shifts
kn-keyword=phase shifts
en-keyword=phase response curve
kn-keyword=phase response curve
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=3
article-no=
start-page=197
end-page=206
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20111201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A new paradigm for the treatment of lifestyle-related diseases : Microinflammation as a novel therapeutic target
kn-title=生活習慣病治療のパラダイムシフト―慢性炎症を標的とした治療戦略―
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ShikataKenichi
en-aut-sei=Shikata
en-aut-mei=Kenichi
kn-aut-name=四方賢一
kn-aut-sei=四方
kn-aut-mei=賢一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　新医療研究開発センター
en-keyword=生活習慣病
kn-keyword=生活習慣病
en-keyword=メタボリック症候群
kn-keyword=メタボリック症候群
en-keyword=糖尿病
kn-keyword=糖尿病
en-keyword=炎症
kn-keyword=炎症
en-keyword=心血管疾患
kn-keyword=心血管疾患
END

start-ver=1.4
cd-journal=joma
no-vol=66
cd-vols=
no-issue=51
article-no=
start-page=9659
end-page=9666
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20101218
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synthesis of pyrrolidine-based oxy-peptide nucleic acids carrying four types of nucleobases and their transport into cytoplasm
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We synthesized 16 pyrrolidine-based oxy-peptide nucleic acid (POPNA) monomers carrying four different nucleobases onto four different stereoisomers of pyrrolidine rings. Using these monomers, we prepared POPNA oligomers, which formed sequence-specific hybrids with DNAs. The oligomer configurations influenced the hybrid stability. The oligomers were not taken into CHO cells. However, they could enter the cell cytoplasm when mixed with the influenza virus hemagglutinin peptide-arginine heptamer conjugate.
en-copyright=
kn-copyright=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiAkiko
en-aut-sei=Takahashi
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SisidoMasahiko
en-aut-sei=Sisido
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Okayama University

affil-num=2
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Okayama University
en-keyword=Peptide nucleic acid
kn-keyword=Peptide nucleic acid
en-keyword=Solid-phase peptide synthesis
kn-keyword=Solid-phase peptide synthesis
en-keyword=Cell-penetrating peptide
kn-keyword=Cell-penetrating peptide
en-keyword=Confocal laser scanning microscopy
kn-keyword=Confocal laser scanning microscopy
END

start-ver=1.4
cd-journal=joma
no-vol=46
cd-vols=
no-issue=5
article-no=
start-page=761
end-page=763
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=2010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A novel method for screening peptides that bind to proteins by using multiple fluorescent amino acids as fluorescent tags
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We describe a new screening method for simultaneously detecting peptides that bind to a target protein by fluorescence obtained from fluorescent amino acid-modified peptides.
en-copyright=
kn-copyright=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FutamiMidori
en-aut-sei=Futami
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SisidoMasahiko
en-aut-sei=Sisido
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=20
article-no=
start-page=5976
end-page=5978
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20101015
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Quantitative screening of EGF receptor-binding peptides by using a peptide library with multiple fluorescent amino acids as fluorescent tags
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=EGF receptor-binding peptides could be found by a peptide screening method using fifteen fluorescent amino acids as fluorescent tags. Of 225 peptides, we found an 8-mer peptide containing a dipeptide unit, Y-F, which was the strongest binding peptide to the EGF receptor.
en-copyright=
kn-copyright=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamotoTakahiro
en-aut-sei=Yamamoto
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FutamiMidori
en-aut-sei=Futami
en-aut-mei=Midori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SisidoMasahiko
en-aut-sei=Sisido
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=3
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology, Okayama University
en-keyword=Peptide
kn-keyword=Peptide
en-keyword=Peptide library
kn-keyword=Peptide library
en-keyword=Peptide screening
kn-keyword=Peptide screening
en-keyword=EGFR
kn-keyword=EGFR
en-keyword=Fluorescent amino acid
kn-keyword=Fluorescent amino acid
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=13
article-no=
start-page=3410
end-page=3413
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090701
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Carrier PNA for shRNA delivery into cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A peptide nucleic acid (PNA)-cell-penetrating peptide (CPP) conjugate (carrier PNA) was used as 'bridgebuilder' to connect a CPP with an shRNA. The carrier PNA successfully formed a hybrid with an shRNA bearing complementary dangling bases and the shRNA was introduced into cells by the carrier PNA, and RNAi was induced by the shRNA.
en-copyright=
kn-copyright=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KuboTakanori
en-aut-sei=Kubo
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsuzakiRino
en-aut-sei=Matsuzaki
en-aut-mei=Rino
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EndohTamaki
en-aut-sei=Endoh
en-aut-mei=Tamaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SisidoMasahiko
en-aut-sei=Sisido
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University

affil-num=2
en-affil=
kn-affil=Faculty of Pharmacy, Yasuda Women’s University

affil-num=3
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University

affil-num=4
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University

affil-num=5
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University

affil-num=6
en-affil=
kn-affil=Department of Bioscience and Biotechnology, Faculty of Engineering, Okayama University
en-keyword=Peptide nucleic acid
kn-keyword=Peptide nucleic acid
en-keyword=Cell-penetrating peptide
kn-keyword=Cell-penetrating peptide
en-keyword=RNA interference
kn-keyword=RNA interference
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=1
article-no=
start-page=225
end-page=227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Antisense effect of pyrrolidine-based oxy-peptide nucleic acids in Escherichia coli
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To investigate the antisense effect of a pyrrolidine-based oxy-peptide nucleic acid (POPNA), we carried out the LacZ reporter assay using a 12-mer trans-l-POPNA conjugated with a cell-penetrating peptide (antisense reagent). The antisense effect of the conjugated POPNA (inhibition of LacZ activity) was comparable to that shown by a Nielsen-type peptide nucleic acid. Furthermore, the conjugated POPNA could switch the LacZ activity over a wide range of ambient temperatures.
en-copyright=
kn-copyright=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KuramiShunsuke
en-aut-sei=Kurami
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SisidoMasahiko
en-aut-sei=Sisido
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology

affil-num=2
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology

affil-num=3
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology

affil-num=4
en-affil=
kn-affil=Department of Medical and Bioengineering, Graduate School of Natural Science and Technology
en-keyword=Peptide nucleic acid
kn-keyword=Peptide nucleic acid
en-keyword=Cell-penetrating peptide
kn-keyword=Cell-penetrating peptide
en-keyword=Antisense effect
kn-keyword=Antisense effect
END

start-ver=1.4
cd-journal=joma
no-vol=1808
cd-vols=
no-issue=1
article-no=
start-page=490
end-page=497
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201101
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Comparative study of the membrane-permeabilizing activities of mastoparans and related histamine-releasing agents in bacteria, erythrocytes, and mast cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The membrane-permeabilizing activities of mastoparans and related histamine-releasing agents were compared through measurements of K(+) efflux from bacteria, erythrocytes, and mast cells. Changes in bacterial cell viability, hemolysis, and histamine release, as well as in the shape of erythrocytes were also investigated. The compounds tested were mastoparans (HR1, a mastoparan from Polistes jadwagae, and a mastoparan from Vespula lewisii), granuliberin R, mast cell-degranulating peptide, and compound 48/80, as well as antimicrobial peptides, such as magainin I, magainin II, gramicidin S. and melittin. We used a K(+)-selective electrode to determine changes in the permeability to K(+) of the cytoplasmic membranes of cells. Consistent with the surface of mast cells becoming negatively charged during histamine release, due to the translocation of phosphatidylserine to the outer leaflet of the cytoplasmic membrane, histamine-releasing agents induced K(+) efflux from mast cells, dependent on their ability to increase the permeability of bacterial cytoplasmic membranes rich in negatively charged phospholipids. The present results demonstrated that amphiphilic peptides, possessing both histamine-releasing and antimicrobial capabilities, induced the permeabilization of the cytoplasmic membranes of not only bacteria but mast cells. Mastoparans increased the permeability of membranes in human erythrocytes at higher concentrations, and changed the normal discoid shape to a crenated form. The structural requirement for making the crenated form was determined using compound 48/80 and its constituents (monomer, dimer, and trimer), changing systematically the number of cationic charges of the molecules.
en-copyright=
kn-copyright=

en-aut-name=NakaoSatoshi
en-aut-sei=Nakao
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KomagoeKeiko
en-aut-sei=Komagoe
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InoueTsuyoshi
en-aut-sei=Inoue
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatsuTakashi
en-aut-sei=Katsu
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
en-keyword=Mastoparan
kn-keyword=Mastoparan
en-keyword=Compound 48/80
kn-keyword=Compound 48/80
en-keyword=Antimicrobial peptide
kn-keyword=Antimicrobial peptide
en-keyword=Histamine-releasing agent
kn-keyword=Histamine-releasing agent
en-keyword=Membrane permeability
kn-keyword=Membrane permeability
en-keyword=Cell shape
kn-keyword=Cell shape
END

start-ver=1.4
cd-journal=joma
no-vol=402
cd-vols=
no-issue=2
article-no=
start-page=329
end-page=334
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20101112
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Combined use of bFGF and GDF-5 enhances the healing of medial collateral ligament injury
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Basic fibroblast growth factor (bFGF) and growth and differentiation factor (GDF)-5 stimulate the healing of medial collateral ligament (MCL) injury. However, the effect of isolated and combined use of bFGF/GDF-5 remains still unclear. We investigated cellular proliferation and migration responding to bFGF/GDF-5 using rabbit MCL fibroblasts. Rabbit MCL injury was treated by bFGF and/or GDF-5 with peptide hydrogels. Gene expression and deposition of collagens in healing tissues were evaluated. bFGF/GDF-5 treatment additively enhanced cell proliferation and migration. bFGF/GDF-5 hydrogels stimulated Col1a1 expression without increasing Col3a1 expression. Combined use of bFGF/GDF-5 stimulated type I collagen deposition and the reorganization of fiber alignment, and induced better morphology of fibroblasts in healing MCLs. Our study indicates that combined use of bFGF/GDF-5 might enhance MCL healing by increasing proliferation and migration of MCL fibroblasts, and by regulating collagen synthesis and connective fiber alignment.
en-copyright=
kn-copyright=

en-aut-name=SaigaKenta
en-aut-sei=Saiga
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FurumatsuTakayuki
en-aut-sei=Furumatsu
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaAki
en-aut-sei=Yoshida
en-aut-mei=Aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MasudaShin
en-aut-sei=Masuda
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakihiraShota
en-aut-sei=Takihira
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AbeNobuhiro
en-aut-sei=Abe
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=6
en-affil=
kn-affil=Department of Intelligent Orthopaedic System Development, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=7
en-affil=
kn-affil=Department of Orthopaedic Surgery, Science of Functional Recovery and Reconstruction, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
en-keyword=Medial collateral ligament
kn-keyword=Medial collateral ligament
en-keyword=bFGF
kn-keyword=bFGF
en-keyword=GDF-5
kn-keyword=GDF-5
en-keyword=Hydrogel scaffold
kn-keyword=Hydrogel scaffold
en-keyword=Ligament healing
kn-keyword=Ligament healing
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=3
article-no=
start-page=403
end-page=410
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=201105
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characterization of an OmpA-like outer membrane protein of the acidophilic iron-oxidizing bacterium, Acidithiobacillus ferrooxidans
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=An OmpA family protein (FopA) previously reported as one of the major outer membrane proteins of an acidophilic iron-oxidizing bacterium Acidithiobacillus ferrooxidans was characterized with emphasis on the modification by heat and the interaction with peptidoglycan. A 30-kDa band corresponding to the FopA protein was detected in outer membrane proteins extracted at 75A degrees C or heated to 100A degrees C for 10 min prior to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). However, the band was not detected in outer membrane proteins extracted at a parts per thousand currency sign40A degrees C and without boiling prior to electrophoresis. By Western blot analysis using the polyclonal antibody against the recombinant FopA, FopA was detected as bands with apparent molecular masses of 30 and 90 kDa, suggesting that FopA existed as an oligomeric form in the outer membrane of A. ferrooxidans. Although the fopA gene with a sequence encoding the signal peptide was successfully expressed in the outer membrane of Escherichia coli, the recombinant FopA existed as a monomer in the outer membrane of E. coli. FopA was detected in peptidoglycan-associated proteins from A. ferrooxidans. The recombinant FopA also showed the peptidoglycan-binding activity.
en-copyright=
kn-copyright=

en-aut-name=ManchurMohammed Abul
en-aut-sei=Manchur
en-aut-mei=Mohammed Abul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KikumotoMei
en-aut-sei=Kikumoto
en-aut-mei=Mei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KanaoTadayoshi
en-aut-sei=Kanao
en-aut-mei=Tadayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakadaJun
en-aut-sei=Takada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KamimuraKazuo
en-aut-sei=Kamimura
en-aut-mei=Kazuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University

affil-num=3
en-affil=
kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University

affil-num=4
en-affil=
kn-affil=Division of Chemical and Biological Technology, Graduate School of Natural Science and Technology, Okayama University

affil-num=5
en-affil=
kn-affil=Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University
en-keyword=Acidithiobacillus ferrooxidans
kn-keyword=Acidithiobacillus ferrooxidans
en-keyword=Iron-oxidizing bacterium
kn-keyword=Iron-oxidizing bacterium
en-keyword=Acidophile
kn-keyword=Acidophile
en-keyword=Outer membrane protein
kn-keyword=Outer membrane protein
en-keyword=OmpA
kn-keyword=OmpA
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=グルカゴン様ペプチド１受容体作動薬は1型糖尿病モデルラットにおいて血糖値を低下させることなしに抗炎症作用を介して腎障害を改善させる
kn-title=Glucagon-like peptide-1 receptor agonist ameliorates renal injury through its anti-inflammatory action without lowering blood glucose level in a rat model of type 1 diabetes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KoderaRyo
en-aut-sei=Kodera
en-aut-mei=Ryo
kn-aut-name=小寺亮
kn-aut-sei=小寺
kn-aut-mei=亮
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=25
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Vasohibin-1, a negative feedback regulator of angiogenesis, ameliorates renal alterations in a mouse model of diabetic nephropathy
kn-title=血管新生negative feedback制御因子Vasohibin-1によるマウス糖尿病性腎症進展制御効果の検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NasuTatsuyo
en-aut-sei=Nasu
en-aut-mei=Tatsuyo
kn-aut-name=那須達世
kn-aut-sei=那須
kn-aut-mei=達世
aut-affil-num=1
ORCID=

en-aut-name=MaeshimaYohei
en-aut-sei=Maeshima
en-aut-mei=Yohei
kn-aut-name=前島洋平
kn-aut-sei=前島
kn-aut-mei=洋平
aut-affil-num=2
ORCID=

en-aut-name=KinomuraMasaru
en-aut-sei=Kinomura
en-aut-mei=Masaru
kn-aut-name=木野村賢
kn-aut-sei=木野村
kn-aut-mei=賢
aut-affil-num=3
ORCID=

en-aut-name=Hirokoshi-KawaharaKumiko
en-aut-sei=Hirokoshi-Kawahara
en-aut-mei=Kumiko
kn-aut-name=川原（広越）久美子
kn-aut-sei=川原（広越）
kn-aut-mei=久美子
aut-affil-num=4
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=田邊克幸
kn-aut-sei=田邊
kn-aut-mei=克幸
aut-affil-num=5
ORCID=

en-aut-name=SugiyamaHitoshi
en-aut-sei=Sugiyama
en-aut-mei=Hitoshi
kn-aut-name=杉山斉
kn-aut-sei=杉山
kn-aut-mei=斉
aut-affil-num=6
ORCID=

en-aut-name=SonodaHikaru
en-aut-sei=Sonoda
en-aut-mei=Hikaru
kn-aut-name=園田光
kn-aut-sei=園田
kn-aut-mei=光
aut-affil-num=7
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=佐藤靖史
kn-aut-sei=佐藤
kn-aut-mei=靖史
aut-affil-num=8
ORCID=

en-aut-name=MakinoHirofumi
en-aut-sei=Makino
en-aut-mei=Hirofumi
kn-aut-name=槇野博史
kn-aut-sei=槇野
kn-aut-mei=博史
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学

affil-num=7
en-affil=
kn-affil=塩野義製薬

affil-num=8
en-affil=
kn-affil=東北大学加齢医学研究所　腫瘍循環研究分野

affil-num=9
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腎・免疫・内分泌代謝内科学
en-keyword=糖尿病性腎症
kn-keyword=糖尿病性腎症
en-keyword=血管新生
kn-keyword=血管新生
en-keyword=vasohibin-1
kn-keyword=vasohibin-1
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=トマト果実由来のα-マンノシダーゼ及びペプチド:N-グリカナーゼの分子生物学的解析：果実熟成期におけるN型糖タンパク質分解に関与する２種の糖鎖関連酵素
kn-title=Molecular identification and characterization of α-mannosidase and peptide :N-glycanase from tomato: two glycoenzymes involved in N-glycoprotein degradation during fruit ripening
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=Md. AnowarHossain
en-aut-sei=Md. Anowar
en-aut-mei=Hossain
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=71
cd-vols=
no-issue=4-1
article-no=
start-page=1635
end-page=1639
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1959
dt-pub=19590325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the Free Amino Acids in the Brains IX The Influence of Hypophysectomy on the Free Amino Acids and Related Compounds in the Brain of Rat
kn-title=脳の遊離アミノ酸について(IX) 下垂体剔除の脳遊離アミノ酸およびその関連物質におよぼす影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=With the aid of the chromatography on the 150 x 0.9 cm column of Dowex 50-x4 the author estimated 20 kinds of free amino acids and their related compounds isolated from the brain of the hypophysectomized Rattus; and obtained the following results: 1. A marked decrease has been observed in the metabolically active amino acid groups such as aspartic acid, glutamic acid, γ-aminobutyric acid, alanine and serine. 2. Likewise a decrease can clearly be noticed in the content of N-acetylaspartic acid that exists specifically in the brain and in the content of phosphor containing amine, glycerophosphoethanolamine as well as in the glutathione content, the only peptide which has been successfully estimated. 3. In the sutdy of 6 indispensable amino acids such as threonine, isoleucine, leucine, lysine, histidine, and arginine no noteworthy changes can be recognized.
en-copyright=
kn-copyright=

en-aut-name=NishiokaHirosuke
en-aut-sei=Nishioka
en-aut-mei=Hirosuke
kn-aut-name=西岡博輔
kn-aut-sei=西岡
kn-aut-mei=博輔
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=5-6
article-no=
start-page=593
end-page=601
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199006
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Establishment of a new cell line derived from hepatocellular carcinoma exhibiting non-epithelial morphology
kn-title=非上皮細胞様形態を呈するヒト肝細胞癌由来細胞株の樹立
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A cell line, HuH-33, was established in vitro from a patient with hepatocellular carcinoma (HCC), who had been treated with some chemotherapeutic agents. The chromosome number was widely distributed in 6888. This cell line has grown slowly, exhibiting a doubling time of approximately 150h, was intransplantable into nude mice, and secreted alpha-fetoprotein, albumin, β2-microglobulin, ferritin, tissue peptide antigen and extracellular matrix materials. HuH-33 was polygonal or spindle shaped, but it was keratin-positive and desmosome-like structures were observed with transmission electron microscopy, suggesting an epithelial origin of HuH-33.
en-copyright=
kn-copyright=

en-aut-name=EndoAkira
en-aut-sei=Endo
en-aut-mei=Akira
kn-aut-name=遠藤彰
kn-aut-sei=遠藤
kn-aut-mei=彰
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部癌源研究施設病理部門
en-keyword=Hepatoma cell line
kn-keyword=Hepatoma cell line
en-keyword=cytokeratin
kn-keyword=cytokeratin
en-keyword=non-epithelial
kn-keyword=non-epithelial
END

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=2
article-no=
start-page=101
end-page=106
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Intravenous administration of nicorandil immediately before percutaneous coronary intervention can prevent slow coronary flow phenomenon
kn-title=経皮的冠動脈形成術直前のニコランジル経静脈的投与による冠動脈slow flowの抑制効果
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KawaiYusuke
en-aut-sei=Kawai
en-aut-mei=Yusuke
kn-aut-name=河合勇介
kn-aut-sei=河合
kn-aut-mei=勇介
aut-affil-num=1
ORCID=

en-aut-name=HisamatsuKenichi
en-aut-sei=Hisamatsu
en-aut-mei=Kenichi
kn-aut-name=久松研一
kn-aut-sei=久松
kn-aut-mei=研一
aut-affil-num=2
ORCID=

en-aut-name=MatsubaraHiromi
en-aut-sei=Matsubara
en-aut-mei=Hiromi
kn-aut-name=松原広己
kn-aut-sei=松原
kn-aut-mei=広己
aut-affil-num=3
ORCID=

en-aut-name=FujimotoYoshihisa
en-aut-sei=Fujimoto
en-aut-mei=Yoshihisa
kn-aut-name=藤本良久
kn-aut-sei=藤本
kn-aut-mei=良久
aut-affil-num=4
ORCID=

en-aut-name=MiyajiKatsumasa
en-aut-sei=Miyaji
en-aut-mei=Katsumasa
kn-aut-name=宮地克維
kn-aut-sei=宮地
kn-aut-mei=克維
aut-affil-num=5
ORCID=

en-aut-name=MunemasaMitsuru
en-aut-sei=Munemasa
en-aut-mei=Mitsuru
kn-aut-name=宗政充
kn-aut-sei=宗政
kn-aut-mei=充
aut-affil-num=6
ORCID=

en-aut-name=KusanoKengo F
en-aut-sei=Kusano
en-aut-mei=Kengo F
kn-aut-name=草野研吾
kn-aut-sei=草野
kn-aut-mei=研吾
aut-affil-num=7
ORCID=

en-aut-name=OheTohru
en-aut-sei=Ohe
en-aut-mei=Tohru
kn-aut-name=大江透
kn-aut-sei=大江
kn-aut-mei=透
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=国立病院機構岡山医療センター　循環器科

affil-num=2
en-affil=
kn-affil=国立病院機構岡山医療センター　循環器科

affil-num=3
en-affil=
kn-affil=国立病院機構岡山医療センター　循環器科

affil-num=4
en-affil=
kn-affil=国立病院機構岡山医療センター　循環器科

affil-num=5
en-affil=
kn-affil=国立病院機構岡山医療センター　循環器科

affil-num=6
en-affil=
kn-affil=国立病院機構岡山医療センター　循環器科

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　循環器内科学

affil-num=8
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　循環器内科学
en-keyword=冠動脈slow flow現象
kn-keyword=冠動脈slow flow現象
en-keyword=ニコランジル経静脈的投与
kn-keyword=ニコランジル経静脈的投与
en-keyword=急性冠症候群
kn-keyword=急性冠症候群
END

start-ver=1.4
cd-journal=joma
no-vol=41
cd-vols=
no-issue=3
article-no=
start-page=134
end-page=139
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=200802
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association of elevated plasma B-type natriuretic peptide levels with paroxysmal atrial fibrillation in patients with nonobstructive hypertrophic cardiomyopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Objectives: To investigate the relationship between the plasma B-type natriuretic peptide (BNP) level and the occurrence of atrial fibrillation (AF) in nonobstructive hypertrophic cardiomyopathy (HCM) patients.<br />
Methods: Patients (n=97) were classified into chronic AF (CAF; n=14), paroxysmal AF (PAF; n=18) and normal sinus rhythm (NSR; n=65) groups. The plasma BNP values were analyzed with logarithmic transformation.<br />
Results: The PAF group showed significantly higher plasma BNP levels than the NSR group [mean (range; -1 SD and +1 SD); 248.3 (143.5, 429.5) vs. 78.2 (27.9, 218.8 ng/L), p<0.0001]. The CAF group also showed significantly higher plasma BNP levels than the NSR group [291.1 (161.4, 524.8 ng/L), p<0.0001]. Multivariate analysis with other clinical factors selected association of PAF as one of the factors that increased the plasma BNP level.<br />
Conclusions: The present study indicated that plasma BNP level is clinically useful for identification of nonobstructive HCM patients who have a risk of PAF.</p>
en-copyright=
kn-copyright=

en-aut-name=MatsuuraHiroko
en-aut-sei=Matsuura
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MurakamiTakashi
en-aut-sei=Murakami
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HinaKazuyoshi
en-aut-sei=Hina
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamamotoKeizo
en-aut-sei=Yamamoto
en-aut-mei=Keizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawamuraHiroshi
en-aut-sei=Kawamura
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SogoTaiji
en-aut-sei=Sogo
en-aut-mei=Taiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShinohataRyoko
en-aut-sei=Shinohata
en-aut-mei=Ryoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UsuiShinichi
en-aut-sei=Usui
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NinomiyaYoshifumi
en-aut-sei=Ninomiya
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KusachiShozo
en-aut-sei=Kusachi
en-aut-mei=Shozo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital

affil-num=3
en-affil=
kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital

affil-num=4
en-affil=
kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital

affil-num=5
en-affil=
kn-affil=Department of Cardiology, Cardiovascular Center, Sakakibara Hospital

affil-num=6
en-affil=
kn-affil=Department of Cardiovascular Medicine, Takamatsu Red Cross Hospital

affil-num=7
en-affil=
kn-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences

affil-num=8
en-affil=
kn-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences

affil-num=9
en-affil=
kn-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=10
en-affil=
kn-affil=Department of Medical Technology, Okayama University Graduate School of Health Sciences
en-keyword=clinical study
kn-keyword=clinical study
en-keyword=cardiomyopathy
kn-keyword=cardiomyopathy
en-keyword=tachyarrhythmia
kn-keyword=tachyarrhythmia
en-keyword=enzyme immunoassay
kn-keyword=enzyme immunoassay
en-keyword=peptide
kn-keyword=peptide
en-keyword=sensitivity and specificity
kn-keyword=sensitivity and specificity
END

start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=8
article-no=
start-page=887
end-page=893
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=200412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Generation of active fragments from human zymogens in the bradykinin-generating cascade by extracellular proteases from Vibrio vulnificus and V. parahaemolyticus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Vibrio vulnificus is an opportunistic human pathogen causing septicemia, and the infection is
characterized by formation of the edematous skin lesions on limbs. This pathogenic species
secretes a thermolysin-like metalloprotease as a virulence determinant. The metalloprotease
was confirmed to activate human factor XII-plasma kallikrein-kinin cascade that results in
liberation of bradykinin, a chemical mediator enhancing the vascular permeability, from
high-molecular weight kininogen. Namely, the metalloprotease showed to generate active
fragments by cleavage of Arg-Ile, Arg-Val or Gly-Leu peptide bond in human zymogens
(plasma prekallikrein and factor XII). In spite of induction of the sufficient vascular
permeability-enhancing and edema-forming reaction in the guinea pig model, a serine
protease from V. parahaemolyticus, a human pathogen causing primarily watery diarrhea,
showed far less ability to activate and to cleave the human zymogens. These results in part
may explain why only V. vulnificus often causes serious edematous skin damages in humans.</p>
en-copyright=
kn-copyright=

en-aut-name=MiyoshiShin-ichi
en-aut-sei=Miyoshi
en-aut-mei=Shin-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WatanabeHirofumi
en-aut-sei=Watanabe
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaseTomoka
en-aut-sei=Kawase
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamadaHidenori
en-aut-sei=Yamada
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShinodaSumio
en-aut-sei=Shinoda
en-aut-mei=Sumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=vibrio vulnificus
kn-keyword=vibrio vulnificus
en-keyword=vibrio parahaemolyticus
kn-keyword=vibrio parahaemolyticus
en-keyword=protease
kn-keyword=protease
en-keyword=factor XII
kn-keyword=factor XII
en-keyword=plasma prekallikrein
kn-keyword=plasma prekallikrein
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=4
article-no=
start-page=281
end-page=285
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070705
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=N-terminal domain including conserved flg22 is required for flagellin-induced hypersensitive cell death in Arabidopsis thaliana
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Flagellin in Pseudomonas syringae is a potent elicitor of defense responses including hypersensitive cell death in dicot plants. The oligopeptides flg22 consisting of 22 conserved amino acids near the N-terminus of flagellins is reported to induce plant defense responses. Because glycosylation of the central domain of flagellin affects its elicitor activity, we investigated whether any peptide sequence in addition to flg22 is required for flagellin-induced hypersensitive reaction. A study of recombinant flagellin polypeptides indicated that the N-terminal domain including the conserved flg22 is required for flagellin-induced hypersensitive cell death in Arabidopsis thaliana.</p>

en-copyright=
kn-copyright=

en-aut-name=KanaNaito
en-aut-sei=Kana
en-aut-mei=Naito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuhiroIshiga
en-aut-sei=Yasuhiro
en-aut-mei=Ishiga
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KazuhiroToyoda
en-aut-sei=Kazuhiro
en-aut-mei=Toyoda
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonoriShiraishi
en-aut-sei=Tomonori
en-aut-mei=Shiraishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YukiIchinose
en-aut-sei=Yuki
en-aut-mei=Ichinose
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Laboratory of Plant Pathology and Genetic Engineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=2
en-affil=
kn-affil=Laboratory of Plant Pathology and Genetic Engineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=3
en-affil=
kn-affil=Laboratory of Plant Pathology and Genetic Engineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=4
en-affil=
kn-affil=Laboratory of Plant Pathology and Genetic Engineering, Graduate School of Natural Science and Technology, Okayama University

affil-num=5
en-affil=
kn-affil=Laboratory of Plant Pathology and Genetic Engineering, Graduate School of Natural Science and Technology, Okayama University
en-keyword=Arabidopsis  thaliana
kn-keyword=Arabidopsis  thaliana
en-keyword=Flagellin
kn-keyword=Flagellin
en-keyword=Flg22
kn-keyword=Flg22
en-keyword=FLS2
kn-keyword=FLS2
en-keyword=HR cell death
kn-keyword=HR cell death
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=5
article-no=
start-page=517
end-page=522
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Simultaneous measurements of K+ and calcein release from liposomes and the determination of pore size formed in a membrane
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The changes induced by biologically active substances in the permeability to K+ and calcein of liposomes composed of egg phosphatidylcholine and cholesterol were measured simultaneously in order to rapidly screen the sizes of pores formed in a membrane, using different sized markers. The substances examined in the present study were classified into three types based on differences in the rates at which K+ and calcein were released. The first type released only K+, and included gramicidin A. The second type predominantly released K+, preceding the release of calcein, and included amphotericin B and nystatin. The third type, including antimicrobial peptides, such as gramicidin S, alamethicin, and melittin, and several membrane-active drugs, like celecoxib (non-steroidal anti-inflammatory drug), 1-dodecylazacycloheptan-2-one (named azone; skin permeation enhancer), and chlorpromazine (tranquilizer), caused the release of K+ and calcein simultaneously. Thus, the sizes of pores formed in a liposomal membrane increased in the following order: types one, two, and three. We determined the size more precisely by conducting an osmotic protection experiment, measuring the release of calcein in the presence of osmotic protectants of different sizes. The radii of pores formed by the second type, amphotericin B and nystatin, were 0.36 - 0.46 nm, while the radii of pores formed by the third type were much larger, 0.63 - 0.67 nm or more. The permeability changes induced by substances of the third type are discussed in connection with a transient pore formed in a lipid packing mismatch taking place during the phase transition of dipalmitoylphosphatidylcholine liposomes.</p>

en-copyright=
kn-copyright=

en-aut-name=KatsuTakashi
en-aut-sei=Katsu
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ImamuraTomonori
en-aut-sei=Imamura
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KomagoeKeiko
en-aut-sei=Komagoe
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MasudaKazufumi
en-aut-sei=Masuda
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MizushimaTohru
en-aut-sei=Mizushima
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=5
en-affil=
kn-affil=Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University
END

start-ver=1.4
cd-journal=joma
no-vol=203
cd-vols=
no-issue=2
article-no=
start-page=447
end-page=456
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=200412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Connective Tissue Growth Factor Causes Persistent Proα2(I) Collagen Gene Expression Induced by Transforming Growth Factor-β in a Mouse Fibrosis Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Skin fibrotic disorders such as systemic sclerosis (SSc) are characterized by an excessive production of extracellular matrix (ECM) and understood to develop under the influence of certain growth factors. Connective tissue growth factor (CTGF) is a cysteine-rich mitogenic peptide that is implicated in various fibrotic disorders and induced in fibroblasts after activation with transforming growth factor-beta (TGF-beta). To better understand the mechanisms of persistent fibrosis seen in SSc, we previously established an animal model of skin fibrosis induced by exogenous application of growth factors. In this model, TGF-beta transiently induced subcutaneous fibrosis and serial injections of CTGF after TGF-beta caused persistent fibrosis. To further define the mechanisms of skin fibrosis induced by TGF-beta and CTGF in vivo, we investigated in this study, the effects of growth factors on the promoter activity of the pro alpha 2 (1) collagen (COL1A2) gene in skin fibrosis. For this purpose, we utilized transgenic reporter mice harboring the -17 kb promoter sequence of the mouse COL1A2 linked to either a firefly luciferase gene or a bacterial P-galactosidase gene. Serial injections of CTGF after TGF-beta resulted in a sustained elevation of COL1A2 mRNA expression and promoter activity compared with consecutive injection of TGF-beta alone on day 8. We also demonstrated that the number of fibroblasts with activated COL1A2 transcription was increased by serial injections of CTGF after TGF-beta in comparison with the injection of TGF-beta alone. Furthermore, the serial injections recruited mast cells and macrophages. The number of mast cells reached a maximum on day 4 and remained relatively high up to day 8. In contrast to the kinetics of mast cells, the number of macrophages was increased on day 4 and continued to rise during the subsequent consecutive CTGF injections until day 8. These results suggested that CTGF maintains TGF-beta-induced skin fibrosis by sustaining COL1A2 promoter activation and increasing the number of activated fibroblasts. The infiltrated mast cells and macrophages may also contribute to the maintenance of fibrosis.
en-copyright=
kn-copyright=

en-aut-name=ChujoSonoko
en-aut-sei=Chujo
en-aut-mei=Sonoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShirasakiFumiaki
en-aut-sei=Shirasaki
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaraShigeru
en-aut-sei=Kawara
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InagakiYutaka
en-aut-sei=Inagaki
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KinbaraTakuro
en-aut-sei=Kinbara
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=InaokiMakoto
en-aut-sei=Inaoki
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakigawaMasaharu
en-aut-sei=Takigawa
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakeharaKazuhiko
en-aut-sei=Takehara
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science

affil-num=2
en-affil=
kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science

affil-num=3
en-affil=
kn-affil=Department of Dermatology, National Kanazawa Hospital

affil-num=4
en-affil=
kn-affil=Department of Community Health, Tokai University School of Medicine

affil-num=5
en-affil=
kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science

affil-num=6
en-affil=
kn-affil=Department of Dermatology, Kawasaki Medical School

affil-num=7
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry

affil-num=8
en-affil=
kn-affil=Department of Dermatology, Kanazawa University Graduate School of Medical Science
en-keyword=systemic sclerosis
kn-keyword=systemic sclerosis
en-keyword=fibrosis
kn-keyword=fibrosis
en-keyword=transforming growth factor-?
kn-keyword=transforming growth factor-?
en-keyword=connective tissue growth factor
kn-keyword=connective tissue growth factor
END

start-ver=1.4
cd-journal=joma
no-vol=111
cd-vols=
no-issue=14
article-no=
start-page=1929
end-page=1940
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1998
dt-pub=19987
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Initiation of skin basement membrane formation at the epidermo-dermal interface involves assembly of laminins through binding to cell membrane receptors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>To study the mechanism of basement membrane formation, we determined by immunochemistry temporal and spatial expression of laminin-5 (Ln-5), laminin-1 (Ln-1) and their integrin receptors during early skin morphogenesis. A 3-dimensional skin culture was used that allows the study of the sequential molecular events of basement membrane formation at the epidermodermal interface. During early anchorage of keratinocytes to the extracellular matrix there is expression of Ln-5, BP-230 antigen and &#945;3, &#946;1 integrin subunits. During epidermal stratification and prior to the formation of the lamina densa there is assembly of Ln-5, Ln-1, collagen IV and nidogen accompanied by keratinocyte basal clustering of &#945;2, &#945;3, &#945;6, &#946;1, and &#946;4 integrin subunits. The assembly pattern of Ln-1 and Ln-5 can be disturbed with functional antibodies against the &#946;1 (AIIB2) and &#945;6 (GoH3) integrin subunits. Ln-1 assembly can also be disturbed with antibodies against its E8 domain and by competitive inhibition with a synthetic peptide (AG-73) derived from its G-4 domain. Quantitative RT-PCR showed that the dermis contributes about 80% of the laminin &#947;1 chain mRNA while 20% is produced by the epidermis which emphasizes its dual tissue origin and the major contribution of the mesenchyma in laminin production. The laminin &#947;2 chain mRNA, present in Ln-5, was mostly of epidermal origin. This study presents evidence that during the initiation of basement membrane formation, laminins bind to keratinocyte plasma membrane receptors and thus may serve as nucleation sites for further polymerization of these compounds by a self-assembly process.</p>

en-copyright=
kn-copyright=

en-aut-name=FleischmajerRaul
en-aut-sei=Fleischmajer
en-aut-mei=Raul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UtaniAtsushi
en-aut-sei=Utani
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Douglas MacDonald IIE.
en-aut-sei=Douglas MacDonald II
en-aut-mei=E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=PerlishJerome S
en-aut-sei=Perlish
en-aut-mei=Jerome S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=PanTe-Cheng
en-aut-sei=Pan
en-aut-mei=Te-Cheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ChuMon-Li
en-aut-sei=Chu
en-aut-mei=Mon-Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NomizuMotoyoshi
en-aut-sei=Nomizu
en-aut-mei=Motoyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NinomiyaYoshifumi
en-aut-sei=Ninomiya
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamadaYoshihiko
en-aut-sei=Yamada
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Mount Sinai School of Medicine, New York

affil-num=2
en-affil=
kn-affil=National Institute of Dental Research, National Institutes of Health

affil-num=3
en-affil=
kn-affil=Mount Sinai School of Medicine, New York

affil-num=4
en-affil=
kn-affil=Mount Sinai School of Medicine, New York

affil-num=5
en-affil=
kn-affil=Thomas Jefferson University

affil-num=6
en-affil=
kn-affil=Thomas Jefferson University

affil-num=7
en-affil=
kn-affil=National Institute of Dental Research, National Institutes of Health

affil-num=8
en-affil=
kn-affil=Okayama University

affil-num=9
en-affil=
kn-affil=National Institute of Dental Research, National Institutes of Health
en-keyword=Basement membrane
kn-keyword=Basement membrane
en-keyword=Laminin
kn-keyword=Laminin
en-keyword=Integrin
kn-keyword=Integrin
END

start-ver=1.4
cd-journal=joma
no-vol=150
cd-vols=
no-issue=3
article-no=
start-page=730
end-page=741
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080528
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Angiotensin II type 2 receptors facilitate reinnervation of phenol-lesioned vascular calcitonin gene-related peptide (CGRP)-containing nerves in rat mesenteric arteries
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>The present study was designed to investigate involvement of angiotensin (Ang) II type 2 receptors (AT2 receptors) in restoration of perivascular nerve innervation injured by topical phenol treatment. Male Wistar rats underwent in vivo topical application of 10% phenol around the superior mesenteric artery. After phenol treatment, animals were subjected to immunohistochemistry of the third branch of small arteries, Western blot analysis of AT2 receptor protein expression in dorsal root ganglia (DRG) and studies of mesenteric neurogenic vasoresponsiveness. Ang II (750 ng/kg/day), nerve growth factor (NGF; 20 μg/kg/day) and PD123,319 (AT2 receptor antagonist; 10 mg/kg/day) were intraperitoneally administered for 7 days using osmotic mini-pumps immediately after topical phenol treatment. Losartan (AT1 receptor antagonist) was administered in
drinking water (0.025%). Phenol treatment markedly reduced densities of both calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI)- and neuropeptide Y (NPY)-LI-containing fibers. NGF restored densities of both nerve fibers to the Sham control level. Coadministration of Ang II and losartan significantly increased the density of CGRP-LI-fibers but not
NPY-LI-fibers compared with saline control. The increase of the density of CGRP-LI-fibers by coadministration of Ang II and losartan was suppressed by adding PD123,319. Coadministration of Ang II and losartan ameliorated reduction of CGRP nerve-mediated vasodilation of perfused mesenteric arteries caused by phenol treatment. The AT2 receptor protein expression detected in DRG was markedly increased by NGF. These results suggest that selective stimulation of AT2 receptors by Ang II facilitates reinnervation of mesenteric perivascular CGRP-containing nerves injured by topical phenol application in the rat.</p>
en-copyright=
kn-copyright=

en-aut-name=HobaraNarumi
en-aut-sei=Hobara
en-aut-mei=Narumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GodaMitsuhiro
en-aut-sei=Goda
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshidaNamika
en-aut-sei=Yoshida
en-aut-mei=Namika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakatoriShingo
en-aut-sei=Takatori
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MioMitsunobu
en-aut-sei=Mio
en-aut-mei=Mitsunobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawasakiHiromu
en-aut-sei=Kawasaki
en-aut-mei=Hiromu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=2
en-affil=
kn-affil=Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=3
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=4
en-affil=
kn-affil=Shujitsu University School of Pharmacy

affil-num=5
en-affil=
kn-affil=Department of Pharmaceutical Care and Health Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University

affil-num=6
en-affil=
kn-affil=Shujitsu University School of Pharmacy

affil-num=7
en-affil=
kn-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
en-keyword=Angiotensin II type 2 receptors
kn-keyword=Angiotensin II type 2 receptors
en-keyword=Phenol-induced perivascular nerve injury
kn-keyword=Phenol-induced perivascular nerve injury
en-keyword=Calcitonin gene-related peptide-containing nerves
kn-keyword=Calcitonin gene-related peptide-containing nerves
en-keyword=Neuropeptide Y-containing nerves
kn-keyword=Neuropeptide Y-containing nerves
en-keyword=Neurotrophic
kn-keyword=Neurotrophic
en-keyword=Rat mesenteric artery
kn-keyword=Rat mesenteric artery
END

start-ver=1.4
cd-journal=joma
no-vol=57
cd-vols=
no-issue=4
article-no=
start-page=191
end-page=197
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2003
dt-pub=200308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Plasma brain natriuretic peptide and the evaluation of volume overload in infants and children with congenital heart disease.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>This study was designed to explore whether it was possible to evaluate the severity of VSD, PDA, and ASD by measuring brain natriuretic peptide (BNP) levels. We also investigated normal BNP levels in children to provide a baseline for our study. We measured BNP levels in 253 normal children, including 11 normal neonates, and in 91 VSD patients, 29 PDA patients, and 34 ASD patients. BNP levels showed no age-related differences in normal children (the mean value: 5.3 +/- 3.8 pg/ml). In the healthy neonates, BNP levels rose from 10.4 +/- 11.9 pg/ml in cord blood to 118.8 +/- 83.2 pg/ml on day 0, then fell to 15.3 +/- 7.8 pg/ml by day 7. In VSD and PDA patients, BNP levels correlated significantly with Qp/Qs, LVEDV, and peak RVP/LVP. In ASD patients, BNP levels correlated with Qp/Qs and RVEDV. Especially, in VSD patients, as an index corresponding to 1.5-2.0 of the Qp/Qs ratio, BNP levels of 20-35 pg/ml were found to be best with regard to both sensitivity and specificity. In the healthy neonates, BNP levels changed rapidly after birth. In VSD, PDA, and ASD patients, BNP levels were well-correlated with the severity of the disease. Especially, in VSD patients, it that appears BNP levels may be useful in evaluating surgical indications, with 20-35 pg/ml levels being the appropriate cut-off value.</p>

en-copyright=
kn-copyright=

en-aut-name=KuniiYuko
en-aut-sei=Kunii
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KamadaMasahiro
en-aut-sei=Kamada
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhtsukiShinichi
en-aut-sei=Ohtsuki
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ArakiTohru
en-aut-sei=Araki
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KataokaKohichi
en-aut-sei=Kataoka
en-aut-mei=Kohichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KageyamaMisao
en-aut-sei=Kageyama
en-aut-mei=Misao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakagawaNaomi
en-aut-sei=Nakagawa
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SeinoYoshiki
en-aut-sei=Seino
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University

affil-num=4
en-affil=
kn-affil=Okayama University

affil-num=5
en-affil=
kn-affil=Okayama University

affil-num=6
en-affil=
kn-affil=Okayama University

affil-num=7
en-affil=
kn-affil=Okayama University

affil-num=8
en-affil=
kn-affil=Okayama University
en-keyword=brain natriuretic peptide
kn-keyword=brain natriuretic peptide
en-keyword=congenital heart disease
kn-keyword=congenital heart disease
en-keyword=ventricular volume overload
kn-keyword=ventricular volume overload
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=5
article-no=
start-page=537
end-page=547
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1970
dt-pub=197010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Antibody formation for malignant tumor. &#8546;. Antigenicity of peptide of ribosomal digest in Ehrlich ascites tumor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>Antigenicity of the peptide of ribosomal digest in Ehrlich ascites tumor was studied. The peptide was purified by DEAE Sephadex A-50 column chromatography. The peptide was electrophoretically basic, single, and 1.32 S20w sedimentation coefficient with poor content of tyrosine and phenylalanine. The maximum absorbancy was at 267 m&#956;. Mice and rabbits were immunized with the mixture of the purified peptide with Freund's complete adjuvant. The inhibitory effect of immune &#947;-globulin
on the tumor growth was demonstrated in vitro cultured JTC-11 cells. A single precipitin line was observed between rabbit antiserum and tumor cell extract of Ehrlich ascites cells in ouchterlony double diffusion chamber and immunoelectrophoresis. The sedimentation coefficient of the effective fraction in immune-serum was 17 S20w. The precipitin line was observed at &#946;2-&#947; region in immunoelectrophoresis.</p>

en-copyright=
kn-copyright=

en-aut-name=YamamotoYasuhisa
en-aut-sei=Yamamoto
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=JituikiDairoku
en-aut-sei=Jituiki
en-aut-mei=Dairoku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YabukiYasuo
en-aut-sei=Yabuki
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama University

affil-num=2
en-affil=
kn-affil=Okayama University

affil-num=3
en-affil=
kn-affil=Okayama University
END

start-ver=1.4
cd-journal=joma
no-vol=46
cd-vols=
no-issue=2
article-no=
start-page=83
end-page=86
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Changes in plasma human atrial natriuretic peptide (hANP) level in normal pregnancy and pregnancy induced hypertension.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=<p>We determined plasma human atrial natriuretic peptide (hANP) levels in normal pregnancy and pregnancy induced hypertension (PIH). The plasma hANP levels slightly decreased in the first trimester of normal pregnancy and tended to recover as pregnancy advanced, although these changes were slight. However, the plasma hANP level in puerperium was higher than that in the third trimester of normal pregnancy. The plasma hANP level in mild PIH was not significantly higher than that in the third trimester of normal pregnancy. In contrast, the plasma hANP level in three cases of severe PIH was approximately 200% higher than those in the normal third trimester and mild PIH.</p>

en-copyright=
kn-copyright=

en-aut-name=OguniNobutsugu
en-aut-sei=Oguni
en-aut-mei=Nobutsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MitsuiYukiteru
en-aut-sei=Mitsui
en-aut-mei=Yukiteru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KamimuraShigehito
en-aut-sei=Kamimura
en-aut-mei=Shigehito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EguchiKatsuto
en-aut-sei=Eguchi
en-aut-mei=Katsuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SekibaKaoru
en-aut-sei=Sekiba
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama  University

affil-num=2
en-affil=
kn-affil=Okayama  University

affil-num=3
en-affil=
kn-affil=Okayama Univeristy

affil-num=4
en-affil=
kn-affil=Okayama  University

affil-num=5
en-affil=
kn-affil=Okayama University
en-keyword=human atrial natriuretic peptide(hANP)
kn-keyword=human atrial natriuretic peptide(hANP)
en-keyword=preload
kn-keyword=preload
en-keyword= pregnancy induced hypertesion(PIH)
kn-keyword= pregnancy induced hypertesion(PIH)
END