start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=4
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20040615
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Addition of granulocyte-colony stimulating factor (G-CSF) may further increase chemosensitive state in premenopausal node-positive breast cancer patients with induced angiogenesis after surgery
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
en-aut-name=AltundagKadri
en-aut-sei=Altundag
en-aut-mei=Kadri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=AltundagOzden
en-aut-sei=Altundag
en-aut-mei=Ozden
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=GunduzMehmet
en-aut-sei=Gunduz
en-aut-mei=Mehmet
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Medical Oncology, Hacettepe University Faculty of Medicine
affil-num=2
en-affil=
kn-affil=Department of Medical Oncology, Hacettepe University Faculty of Medicine
affil-num=3
en-affil=
kn-affil=Department of Oral Pathology and Medicine, Graduate School of Medicine and Dentistry, Okayama University
END
start-ver=1.4
cd-journal=joma
no-vol=3
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20050415
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Comparable response of ccn1 with ccn2 genes upon arthritis: An in vitro evaluation with a human chondrocytic cell line stimulated by a set of cytokines
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
Background: The chondrosarcoma-derived HCS-2/8 has been known to be an excellent model of human articular chondrocytes. By mimicking the arthritic conditions through the treatment of HCS-2/8 cells with cytokines, we estimated the gene expression response of ccn1 and ccn2 during the course of joint inflammation in vitro.
Results: In order to mimic the initiation of inflammation, HCS-2/8 cells were treated with tumor necrosis factor (TNF)-ƒ¿. To induce pro-inflammatory or reparative responses, TGF-ƒÀ was employed. Effects of an anti-inflammatory glucocorticoid were also evaluated. After stimulation, expression levels of ccn1 and ccn2 were quantitatively analyzed. Surprisingly, not only ccn2, but also ccn1 expression was repressed upon TNF-ƒ¿ stimulation, whereas both mRNAs were uniformly induced by transforming growth factor (TGF)-ƒÀ and a glucocorticoid.
Conclusion: These results describing the same response during the course of inflammation suggest similar and co-operative roles of these 2 ccn family members in the course of arthritis.
en-copyright=
kn-copyright=
en-aut-name=MoritaniNorifumi H
en-aut-sei=Moritani
en-aut-mei=Norifumi H
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KubotaSatoshi
en-aut-sei=Kubota
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SugaharaToshio
en-aut-sei=Sugahara
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry
affil-num=2
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry
affil-num=3
en-affil=
kn-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine and Dentistry
affil-num=4
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine and Dentistry
END
start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=4
article-no=
start-page=R291
end-page=R299
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20040426
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Conjugated docosahexaenoic acid suppresses KPL-1 human breast cancer cell growth in vitro and in vivo: potential mechanisms of action
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction The present study was conducted to examine the effect of conjugated docosahexaenoic acid (CDHA) on cell growth, cell cycle progression, mode of cell death, and expression of cell cycle regulatory and/or apoptosis-related proteins in KPL-1 human breast cancer cell line. This effect of CDHA was compared with that of docosahexaenoic acid (DHA).
Methods KPL-1 cell growth was assessed by colorimetric 3- (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay; cell cycle progression and mode of cell death were examined by flow cytometry; and levels of expression of p53, p21Cip1/Waf1, cyclin D1, Bax, and Bcl-2 proteins were examined by Western blotting analysis. In vivo tumor growth was examined by injecting KPL-1 cells subcutaneously into the area of the right thoracic mammary fat pad of female athymic mice fed a CDHA diet.
Results CDHA inhibited KPL-1 cells more effectively than did DHA (50% inhibitory concentration for 72 hours: 97 ƒÊmol/l and 270 ƒÊmol/l, respectively). With both CDHA and DHA growth inhibition was due to apoptosis, as indicated by the appearance of a sub-G1 fraction. The apoptosis cascade involved downregulation of Bcl-2 protein; Bax expression was unchanged. Cell cycle progression was due to G0/G1 arrest, which involved increased expression of p53 and p21Cip1/Waf1, and decreased expression of cyclin D1. CDHA modulated cell cycle regulatory proteins and apoptosis-related proteins in a manner similar to that of parent DHA. In the athymic mouse system 1.0% dietary CDHA, but not 0.2%, significantly suppressed growth of KPL-1 tumor cells; CDHA tended to decrease regional lymph node metastasis in a dose dependent manner.
Conclusion CDHA inhibited growth of KPL-1 human breast cancer cells in vitro more effectively than did DHA. The mechanisms of action involved modulation of apoptosis cascade and cell cycle progression. Dietary CDHA at 1.0% suppressed KPL-1 cell growth in the athymic mouse system.
en-copyright=
kn-copyright=
en-aut-name=Tsujita-KyutokuMiki
en-aut-sei=Tsujita-Kyutoku
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=YuriTakashi
en-aut-sei=Yuri
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=DanbaraNaoyuki
en-aut-sei=Danbara
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=SenzakiHideto
en-aut-sei=Senzaki
en-aut-mei=Hideto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=KiyozukaYasuhiko
en-aut-sei=Kiyozuka
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=UeharaNorihisa
en-aut-sei=Uehara
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=TakadaHideho
en-aut-sei=Takada
en-aut-mei=Hideho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=HadaTakahiko
en-aut-sei=Hada
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MiyazawaTeruo
en-aut-sei=Miyazawa
en-aut-mei=Teruo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=OgawaYutaka
en-aut-sei=Ogawa
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=TsuburaAiro
en-aut-sei=Tsubura
en-aut-mei=Airo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
affil-num=2
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
affil-num=3
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
affil-num=4
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
affil-num=5
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
affil-num=6
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
affil-num=7
en-affil=
kn-affil=Division of Surgery, Kansai Medical University Kori Hospital
affil-num=8
en-affil=
kn-affil=R&D Division, Bizen Chemical Co., Ltd
affil-num=9
en-affil=
kn-affil=Laboratory of Biodynamic Chemistry, Tohoku University Graduate School of Life Science and Agriculture
affil-num=10
en-affil=
kn-affil=Department of Plastic and Reconstructive Surgery, Kansai Medical University
affil-num=11
en-affil=
kn-affil=Department of Pathology II, Kansai Medical University
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=conjugated docosahexaenoic acid
kn-keyword=conjugated docosahexaenoic acid
en-keyword=docosahexaenoic acid
kn-keyword=docosahexaenoic acid
en-keyword=human
kn-keyword=human
END
start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=
article-no=
start-page=81
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130515
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=De novo CD5-positive diffuse large B-cell lymphomas show high specificity for cyclin D2 expression
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=@D cyclins positively regulate the cell cycle and mediate the pathogenesis of some lymphomas. Cyclin D1 overexpression is the hallmark of mantle cell lymphoma, whereas cyclins D2 and D3 are reportedly not as specific to certain lymphomas as cyclin D1. In this study, cyclin D2 was found to be overexpressed in 98% of de novo CD5-positive diffuse large B-cell lymphomas (DLBCLs) (50/51) and in 28% of CD5-negative DLBCLs (14/51). A statistically significant difference was observed between these two groups (p<0.0001). In contrast, no statistical difference was found in the cyclin D3 expression between CD5-positive (18/51) and CD5-negative (24/51) DLBCLs (p=0.23). Based on these findings, cyclin D2 is therefore considered to be closely associated with de novo CD5-positive DLBCLs. This insight may be useful for overcoming the inferior survival of this aggressive lymphoma.
en-copyright=
kn-copyright=
en-aut-name=IgawaTakuro
en-aut-sei=Igawa
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TakataKatsuyoshi
en-aut-sei=Takata
en-aut-mei=Katsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=IwakiNoriko
en-aut-sei=Iwaki
en-aut-mei=Noriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=
en-aut-name=AsanoNaoko
en-aut-sei=Asano
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=
en-aut-name=OritaYorihisa
en-aut-sei=Orita
en-aut-mei=Yorihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=NakamuraNaoya
en-aut-sei=Nakamura
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=NakamuraShigeo
en-aut-sei=Nakamura
en-aut-mei=Shigeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=YoshinoTadashi
en-aut-sei=Yoshino
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
affil-num=1
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=2
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=3
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=4
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=5
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=6
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=7
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=8
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=9
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=10
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
affil-num=11
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cyclin D2
kn-keyword=Cyclin D2
en-keyword=CD5
kn-keyword=CD5
en-keyword=Diffuse large B-cell lymphoma
kn-keyword=Diffuse large B-cell lymphoma
END
start-ver=1.4
cd-journal=joma
no-vol=3
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20051005
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of connective tissue growth factor (CCN2/CTGF) on proliferation and differentiation of mouse periodontal ligament-derived cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: CCN2/CTGF is known to be involved in tooth germ development and periodontal tissue remodeling, as well as in mesenchymal tissue development and regeneration. In this present study, we investigated the roles of CCN2/CTGF in the proliferation and differentiation of periodontal ligament cells (murine periodontal ligament-derived cell line: MPL) in vitro.
Results: In cell cultures of MPL, the mRNA expression of the CCN2/CTGF gene was stronger in sparse cultures than in confluent ones and was significantly enhanced by TGF-ƒÀ. The addition of Recombinant CCN2/CTGF (rCCN2) to MPL cultures stimulated DNA synthesis and cell growth in a dose-dependent manner. Moreover, rCCN2 addition also enhanced the mRNA expression of alkaline phosphatase (ALPase), type I collagen, and periostin, the latter of which is considered to be a specific marker of the periosteum and periodontium; whereas it showed little effect on the mRNA expression of typical osteoblastic markers, e.g., osteopontin and osteocalcin. Finally, rCCN2/CTGF also stimulated ALPase activity and collagen synthesis.
Conclusion: These results taken together suggest important roles of CCN2/CTGF in the development and regeneration of periodontal tissue including the periodontal ligament.
en-copyright=
kn-copyright=
en-aut-name=AsanoMasahiro
en-aut-sei=Asano
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=KubotaSatoshi
en-aut-sei=Kubota
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NakanishiTohru
en-aut-sei=Nakanishi
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=NishidaTakashi
en-aut-sei=Nishida
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=YamaaiTomoichiro
en-aut-sei=Yamaai
en-aut-mei=Tomoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YosimichiGen
en-aut-sei=Yosimichi
en-aut-mei=Gen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=OhyamaKazumi
en-aut-sei=Ohyama
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SugimotoTomosada
en-aut-sei=Sugimoto
en-aut-mei=Tomosada
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=MurayamaYoji
en-aut-sei=Murayama
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=2
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=3
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=4
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=5
en-affil=
kn-affil=Department of Oral Functional Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=6
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=7
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=8
en-affil=
kn-affil=Department of Oral Functional Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=9
en-affil=
kn-affil=Department of Periodontal Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=10
en-affil=
kn-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END
start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=1
article-no=
start-page=314
end-page=322
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2017
dt-pub=20170505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy and safety of rebamipide liquid for chemoradiotherapy-induced oral mucositis in patients with head and neck cancer: a multicenter, randomized, double-blind, placebo-controlled, parallel-group phase II study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=BACKGROUND:
Recent preclinical and phase I studies have reported that rebamipide decreased the severity of chemoradiotherapy-induced oral mucositis in patients with oral cancer. This placebo-controlled randomized phase II study assessed the clinical benefit of rebamipide in reducing the incidence of severe chemoradiotherapy-induced oral mucositis in patients with head and neck cancer (HNC).
METHODS:
Patients aged 20-75 years with HNC who were scheduled to receive chemoradiotherapy were enrolled. Patients were randomized to receive rebamipide 2% liquid, rebamipide 4% liquid, or placebo. The primary endpoint was the incidence of grade ? 3 oral mucositis determined by clinical examination and assessed by central review according to the Common Terminology Criteria of Adverse Events version 3.0. Secondary endpoints were the time to onset of grade ? 3 oral mucositis and the incidence of functional impairment (grade ? 3) based on the evaluation by the Oral Mucositis Evaluation Committee.
RESULTS:
From April 2014 to August 2015, 97 patients with HNC were enrolled, of whom 94 received treatment. The incidence of grade ? 3 oral mucositis was 29% and 25% in the rebamipide 2% and 4% groups, respectively, compared with 39% in the placebo group. The proportion of patients who did not develop grade ? 3 oral mucositis by day 50 of treatment was 57.9% in the placebo group, whereas the proportion was 68.0% in the rebamipide 2% group and 71.3% in the rebamipide 4% group. The incidences of adverse events potentially related to the study drug were 16%, 26%, and 13% in the placebo, rebamipide 2%, and rebamipide 4% groups, respectively. There was no significant difference in treatment compliance among the groups.
CONCLUSIONS:
The present phase II study suggests that mouth washing with rebamipide may be effective and safe for patients with HNC receiving chemoradiotherapy, and 4% liquid is the optimal dose of rebamipide.
TRIAL REGISTRATION:
ClinicalTrials.gov under the identifier NCT02085460 (the date of trial registration: March 11, 2014).
en-copyright=
kn-copyright=
en-aut-name=YokotaT.
en-aut-sei=Yokota
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=OgawaT.
en-aut-sei=Ogawa
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=TakahashiS.
en-aut-sei=Takahashi
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=OkamiK.
en-aut-sei=Okami
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=FujiiT.
en-aut-sei=Fujii
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=TanakaK.
en-aut-sei=Tanaka
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=IwaeS.
en-aut-sei=Iwae
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=OtaI.
en-aut-sei=Ota
en-aut-mei=I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=UedaT.
en-aut-sei=Ueda
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=MondenN.
en-aut-sei=Monden
en-aut-mei=N.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=MatsuuraK.
en-aut-sei=Matsuura
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=KojimaH.
en-aut-sei=Kojima
en-aut-mei=H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=UedaS.
en-aut-sei=Ueda
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=SasakiK.
en-aut-sei=Sasaki
en-aut-mei=K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=FujimotoY.
en-aut-sei=Fujimoto
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
en-aut-name=HasegawaY.
en-aut-sei=Hasegawa
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=
en-aut-name=BeppuT.
en-aut-sei=Beppu
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
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=18
ORCID=
en-aut-name=HiranoS.
en-aut-sei=Hirano
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=
en-aut-name=NakaY.
en-aut-sei=Naka
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=
en-aut-name=MatsushimaY.
en-aut-sei=Matsushima
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=
en-aut-name=FujiiM.
en-aut-sei=Fujii
en-aut-mei=M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=
en-aut-name=TaharaM.
en-aut-sei=Tahara
en-aut-mei=M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=
affil-num=1
en-affil=Division of Gastrointestinal Oncology, Shizuoka Cancer Center
kn-affil=
affil-num=2
en-affil=Department of Otolaryngology-Head and Neck Surgery, Tohoku University Graduate School of Medicine
kn-affil=
affil-num=3
en-affil=Department of Medical Oncology, The Cancer Institute Hospital of JFCR
kn-affil=
affil-num=4
en-affil=Department of Otolaryngology, Center of Head and Neck Surgery, Tokai University
kn-affil=
affil-num=5
en-affil=Department of Otolaryngology, Head and Neck Surgery, Osaka Medical Center for Cancer and Cardiovascular Diseases
kn-affil=
affil-num=6
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=
affil-num=7
en-affil=Department of Head and Neck Cancer, Hyogo Cancer Center
kn-affil=
affil-num=8
en-affil=Department of Otolaryngology-Head and Neck Surgery, Nara Medical University
kn-affil=
affil-num=9
en-affil=Department of Otorhinolaryngology-Head and Neck Surgery, Hiroshima University Hospital
kn-affil=
affil-num=10
en-affil=Department of Head and Neck Surgery, Shikoku Cancer Center
kn-affil=
affil-num=11
en-affil=Department of Head and Neck Surgery, Miyagi Cancer Center
kn-affil=
affil-num=12
en-affil=Department of Otorhinolaryngology, Jikei University School of Medicine
kn-affil=
affil-num=13
en-affil= Medical Oncology, Nara Hospital, Kindai University School of Medicine
kn-affil=
affil-num=14
en-affil=Head and Neck, Chiba Cancer Center
kn-affil=
affil-num=15
en-affil=Department of Otorhinolaryngology, Nagoya University, Graduate School of Medicine
kn-affil=
affil-num=16
en-affil=Department of Head and Neck Surgery, Aichi Cancer Center Hospital and Research Institute
kn-affil=
affil-num=17
en-affil=Division of Head and Neck Surgery, Saitama Cancer Center
kn-affil=
affil-num=18
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=
affil-num=19
en-affil=Department of Otolaryngology-Head and Neck Surgery, Kyoto University Hospital
kn-affil=
affil-num=20
en-affil= Headquarters of New Product Evaluation and Development, Otsuka Pharmaceutical Co., Ltd.
kn-affil=
affil-num=21
en-affil= Headquarters of New Product Evaluation and Development, Otsuka Pharmaceutical Co., Ltd.
kn-affil=
affil-num=22
en-affil=Department of Otolaryngology, Eiju General Hospital
kn-affil=
affil-num=23
en-affil=Department of Head and Neck Medical Oncology, National Cancer Center Hospital East
kn-affil=
en-keyword=Chemoradiotherapy
kn-keyword=Chemoradiotherapy
en-keyword=Head and neck cancer
kn-keyword=Head and neck cancer
en-keyword=Oral mucositis
kn-keyword=Oral mucositis
en-keyword=Placebo-controlled
kn-keyword=Placebo-controlled
en-keyword=Randomized
kn-keyword=Randomized
en-keyword=Rebamipide liquid
kn-keyword=Rebamipide liquid
END
start-ver=1.4
cd-journal=joma
no-vol=3
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20040114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Elevated levels of tissue inhibitor of metalloproteinases (TIMPS) in human hepatocellular carcinomas
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
en-aut-name=MatsumotoEiji
en-aut-sei=Matsumoto
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=NakatsukaHarushige
en-aut-sei=Nakatsuka
en-aut-mei=Harushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NousoKazuhi‚’o
en-aut-sei=Nouso
en-aut-mei=Kazuhi‚’o
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=NakamuraShin-ichiro
en-aut-sei=Nakamura
en-aut-mei=Shin-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=SuzukiMayumi
en-aut-sei=Suzuki
en-aut-mei=Mayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=KobayashiYoshiyuki
en-aut-sei=Kobayashi
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=UemuraMasayuki
en-aut-sei=Uemura
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=SatoSyuichiro
en-aut-sei=Sato
en-aut-mei=Syuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=SatoEi-ichiro
en-aut-sei=Sato
en-aut-mei=Ei-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=YokoyamaJunko
en-aut-sei=Yokoyama
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
en-aut-name=TsuboiSou
en-aut-sei=Tsuboi
en-aut-mei=Sou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=
en-aut-name=TanakaHironori
en-aut-sei=Tanaka
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=
en-aut-name=TakumaYoshitake
en-aut-sei=Takuma
en-aut-mei=Yoshitake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=
en-aut-name=FujikawaTatsuya
en-aut-sei=Fujikawa
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=
en-aut-name=ShiratoriYasushi
en-aut-sei=Shiratori
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=2
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=3
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=4
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=5
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=6
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=7
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=8
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=9
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=10
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=11
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=12
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=13
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=14
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
affil-num=15
en-affil=
kn-affil=Department of Medicine and Medical Science, Okayama University Graduate School of Medicine and Dentistry
END
start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=2005823
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of the Total Design Method in a survey of Japanese dentists
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: This study assessed the application of the Total Design Method (TDM) in a mail survey of Japanese dentists. The TDM was chosen because survey response rates in Japan are
unacceptably low and the TDM had previously been used in a general population survey.
Methods: Four hundred and seventy eight dentist members of the Okayama Medical and Dental Practitioner's Association were surveyed. The nine-page, 27-item questionnaire covered dentist
job satisfaction, physical practice, and dentist and patient characteristics. Respondents to the first mailing or the one-week follow-up postcard were defined as early responders; others who responded were late responders. Responder bias was assessed by examining age, gender and training.
Results: The overall response rate was 46.7% (223/478). The response rates by follow-up mailing were, 18% after the first mailing, 35.4% after the follow-up postcard, 42.3% after the second mailing, and 46.7% after the third mailing. Respondents did not differ from non-respondents in age or gender, nor were there differences between early and late responders.
Conclusion: The application of TDM in this survey of Japanese dentists produced lower rates of response than expected from previous Japanese and US studies.
en-copyright=
kn-copyright=
en-aut-name=NakaiYukie
en-aut-sei=Nakai
en-aut-mei=Yukie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=MilgromPeter
en-aut-sei=Milgrom
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=YoshidaToshiko
en-aut-sei=Yoshida
en-aut-mei=Toshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=IshiharaChikako
en-aut-sei=Ishihara
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=ShimonoTsutomu
en-aut-sei=Shimono
en-aut-mei=Tsutomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=2
en-affil=
kn-affil=Department of Dental Public Heath Sciences, University of Washington
affil-num=3
en-affil=
kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=4
en-affil=
kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=5
en-affil=
kn-affil=Department of Behavioral Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END
start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20050120
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Functional promoter upstream p53 regulatory sequence of IGFBP3 that is silenced by tumor specific methylation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Insulin-like growth factor binding protein (IGFBP)-3 functions as a carrier of insulinlike
growth factors (IGFs) in circulation and a mediator of the growth suppression signal in cells. There are two reported p53 regulatory regions in the IGFBP3 gene; one upstream of the promoter and one intronic. We previously reported a hot spot of promoter hypermethylation of IGFBP-3 in
human hepatocellular carcinomas and derivative cell lines. As the hot spot locates at the putative upstream p53 consensus sequences, these p53 consensus sequences are really functional is a question to be answered.
Methods: In this study, we examined the p53 consensus sequences upstream of the IGFBP-3 promoter for the p53 induced expression of IGFBP-3. Deletion, mutagenesis, and methylation
constructs of IGFBP-3 promoter were assessed in the human hepatoblastoma cell line HepG2 for promoter activity.
Results: Deletions and mutations of these sequences completely abolished the expression of IGFBP-3 in the presence of p53 overexpression. In vitro methylation of these p53 consensus
sequences also suppressed IGFBP-3 expression. In contrast, the expression of IGFBP-3 was not affected in the absence of p53 overexpression. Further, we observed by electrophoresis mobility
shift assay that p53 binding to the promoter region was diminished when methylated.
Conclusion: From these observations, we conclude that four out of eleven p53 consensus sequences upstream of the IGFBP-3 promoter are essential for the p53 induced expression of
IGFBP-3, and hypermethylation of these sequences selectively suppresses p53 induced IGFBP-3 expression in HepG2 cells.
en-copyright=
kn-copyright=
en-aut-name=HanafusaTadashi
en-aut-sei=Hanafusa
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=ShinjiToshiyuki
en-aut-sei=Shinji
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=
en-aut-name=IwasakiYoshiaki
en-aut-sei=Iwasaki
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YumotoEichiro
en-aut-sei=Yumoto
en-aut-mei=Eichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=OnoToshiro
en-aut-sei=Ono
en-aut-mei=Toshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=KoideNorio
en-aut-sei=Koide
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
affil-num=1
en-affil=
kn-affil=Okayama University Advanced Science Research Center, Department of Radiation Research, Shikata Laboratory
affil-num=2
en-affil=
kn-affil=Department of Laboratory Medicine, Okayama University Graduate School of Medicine and Dentistry
affil-num=3
en-affil=
kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry
affil-num=4
en-affil=
kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry
affil-num=5
en-affil=
kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry
affil-num=6
en-affil=
kn-affil=First Department of Internal Medicine, Okayama University Graduate School of Medicine and Dentistry
affil-num=7
en-affil=
kn-affil=Okayama University Advanced Science Research Center, Department of Radiation Research, Shikata Laboratory
affil-num=8
en-affil=
kn-affil=Department of Laboratory Medicine, Okayama University Graduate School of Medicine and Dentistry
END
start-ver=1.4
cd-journal=joma
no-vol=2
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2002
dt-pub=20020402
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=High-susceptibility of photosynthesis to photoinhibition in the tropical plant Ficus microcarpa L. f. cv. Golden Leaves
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The tropical plant Ficus microcarpa L. f. cv. Golden Leaves (GL) is a high-light sensitive tropical fig tree in which sun-leaves are yellow and shade-leaves are green. We compared the response of photosynthetic activities to strong light between GL and its wild-type (WT, Ficus microcarpa L. f.).
Results: Field measurements of maximum photosystem II (PSII) efficiency (Fv/Fm) of intact sunleaves in GL showed that photo synthetic activity was severely photoinhibited during the daytime (Fv/Fm = 0.46) and subsequently recovered in the evening (Fv/Fm = 0.76). In contrast, WT did not show any substantial changes of Fv/Fm values throughout the day (between 0.82 and 0.78). Light dependency of the CO2 assimilation rate in detached shade-leaves of GL showed a response similar
to that in WT, suggesting no substantial difference in photosynthetic performance between them.Several indicators of photoinhibition, including declines in PSII reaction center protein (D1)content, Fv/Fm value, and O2 evolution and CO2 assimilation rates, all indicated that GL is much
more susceptible to photoinhibition than WT. Kinetics of PAM chlorophyll a fluorescence revealed
that nonphotochemical quenching (NPQ) capacity of GL was lower than that of WT.
Conclusion: We conclude that the photosynthetic apparatus of GL is more highly susceptible to
photoinhibition than that of WT.
en-copyright=
kn-copyright=
en-aut-name=TakahashiShunichi
en-aut-sei=Takahashi
en-aut-mei=Shunichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=TamashiroAyumu
en-aut-sei=Tamashiro
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=SakihamaYasuko
en-aut-sei=Sakihama
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=YamamotoYasusi
en-aut-sei=Yamamoto
en-aut-mei=Yasusi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=KawamitsuYoshinobu
en-aut-sei=Kawamitsu
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=YamasakiHideo
en-aut-sei=Yamasaki
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
affil-num=1
en-affil=
kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus
affil-num=2
en-affil=
kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus
affil-num=3
en-affil=
kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus
affil-num=4
en-affil=
kn-affil=Department of Biology, Faculty of Science, Okayama University
affil-num=5
en-affil=
kn-affil=Laboratory of Crop Science, Faculty of Agriculture, University of the Ryukyus
affil-num=6
en-affil=
kn-affil=Laboratory of Cell and Functional Biology, Faculty of Science, University of the Ryukyus
en-keyword=Carbon dioxide
kn-keyword=Carbon dioxide
en-keyword=Chlorophyll
kn-keyword=Chlorophyll
en-keyword=Ficus
kn-keyword=Ficus
en-keyword=Genotype
kn-keyword=Genotype
en-keyword=Oxygen
kn-keyword=Oxygen
en-keyword=Photosynthesis
kn-keyword=Photosynthesis
en-keyword=Photosystem II protein complex
kn-keyword=Photosystem II protein complex
en-keyword=Plant leaves
kn-keyword=Plant leaves
END
start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=1
article-no=
start-page=36
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20131203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inflammatory diarrhea due to enteroaggregative Escherichia coli: evidence from clinical and mice model studies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background@
This study was conducted to determine the role of enteroaggregative Escherichia coli (EAEC) in inflammatory diarrhea among hospitalized patients in Kolkata. The inflammatory pathogenesis of EAEC was established in mice model and histopathological studies. Presence of fecal leucocytes (FLCs) can be suspected for EAEC infection solely or as a mixed with other enteric pathogens.@
Methods@
Active surveillance was conducted for 2 years on 2 random days per week with every 5th patient admitted to the Infectious Diseases Hospital (IDH). Diarrheal samples were processed by conventional culture, microscopy, ELISA and molecular methods. Two EAEC isolated as sole pathogens were examined in mice after induced intestinal infection. The intestinal tissue samples were processed to analyze the histological changes.@
Results@
Of the 2519 samples screened, fecal leucocytes, erythrocytes and occult blood were detected in 1629 samples. Most of the patients had acute watery diarrhea (75%) and vomiting (78%). Vibrio cholerae O1 was the main pathogen in patients of 5?10 years age group (33%). Shigellosis was more in children from 2?5 years of age (19%), whereas children <2 years appeared to be susceptible for infection caused by EAEC (16%). When tested for the pathogenicity, the EAEC strains colonized well and caused inflammatory infection in the gut mucosa of BALB/C mice.@
Conclusion@
This hospital-based surveillance revealed prevalence of large number of inflammatory diarrhea. EAEC was the suspected pathogen and <2 years children appeared to be the most susceptible age group. BALB/C mice may be a suitable animal model to study the EAEC-mediated pathogenesis.
en-copyright=
kn-copyright=
en-aut-name=Dhira Rani Saha
en-aut-sei=Dhira Rani Saha
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=GuinSucharita
en-aut-sei=Guin
en-aut-mei=Sucharita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=KrishnanRajendran
en-aut-sei=Krishnan
en-aut-mei=Rajendran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=NagDhrubajyoti
en-aut-sei=Nag
en-aut-mei=Dhrubajyoti
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=KoleyHemanta
en-aut-sei=Koley
en-aut-mei=Hemanta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=
en-aut-name=RamamurthyThandavarayan
en-aut-sei=Ramamurthy
en-aut-mei=Thandavarayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
affil-num=1
en-affil=Division of Histology & Electron microscopy, National Institute of Cholera and Enteric Diseases
kn-affil=
affil-num=2
en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol
kn-affil=
affil-num=3
en-affil=Natl Inst Cholera & Enter Dis, Div Data Management
kn-affil=
affil-num=4
en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol
kn-affil=
affil-num=5
en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol
kn-affil=
affil-num=6
en-affil=Okayama Univ Infect Dis India, Collaborat Res Ctr
kn-affil=
affil-num=7
en-affil=Natl Inst Cholera & Enter Dis, Div Bacteriol
kn-affil=
END
start-ver=1.4
cd-journal=joma
no-vol=3
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2003
dt-pub=20031021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=No association between the sigma receptor type 1 gene and schizophrenia: results of analysis and meta-analysis of case-control studies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Several lines of evidence have supported possible roles of the sigma receptors in the etiology of schizophrenia and mechanisms of antipsychotic efficacy. An association study provided genetic evidence that the sigma receptor type 1 gene (SIGMAR1) was a possible susceptibility factor for schizophrenia, however, it was not replicated by a subsequent study. It is necessary to evaluate further the possibility that the SIGMAR1 gene is associated with susceptibility to schizophrenia.
Methods: A case-control association study between two polymorphisms of the SIGMAR1 gene, G-241T/C-240T and Gln2Pro, and schizophrenia in Japanese population, and meta-analysis including present and previous studies.
Results:There was no significant association of any allele or genotype of the polymorphisms with schizophrenia. Neither significant association was observed with hebephrenic or paranoid subtype of schizophrenia. Furthermore, a meta-analysis including the present and previous studies comprising 779 controls and 636 schizophrenics also revealed no significant association between the SIGMAR1 gene and schizophrenia.
Conclusion: In view of this evidence, it is likely that the SIGMAR1 gene does not confersusceptibility to schizophrenia.
en-copyright=
kn-copyright=
en-aut-name=UchidaNaohiko
en-aut-sei=Uchida
en-aut-mei=Naohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=UjikeHiroshi
en-aut-sei=Ujike
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=NakataKenji
en-aut-sei=Nakata
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=NomuraAkira
en-aut-sei=Nomura
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
en-aut-name=KatsuTakeshi
en-aut-sei=Katsu
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=
en-aut-name=TanakaYuji
en-aut-sei=Tanaka
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=
en-aut-name=ImamuraTakaki
en-aut-sei=Imamura
en-aut-mei=Takaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=
en-aut-name=SakaiAyumu
en-aut-sei=Sakai
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=
en-aut-name=KurodaShigetoshi
en-aut-sei=Kuroda
en-aut-mei=Shigetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=2
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=3
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=4
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=5
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=6
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=7
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=8
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=9
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
affil-num=10
en-affil=
kn-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry
END
start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2006
dt-pub=20060803
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Simultaneous gene transfer of bone morphogenetic protein (BMP)-2 and BMP-7 by in vivo electroporation induces rapid bone formation and BMP-4 expression
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Transcutaneous in vivo electroporation is expected to be an effective gene-transfer method for promoting bone regeneration using the BMP-2 plasmid vector. To promote enhanced osteoinduction using this method, we simultaneously transferred cDNAs for BMP-2 and BMP-7, as inserts in the non-viral vector pCAGGS.
Methods: First, an in vitro study was carried out to confirm the expression of BMP-2 and BMP-7 following the double-gene transfer. Next, the individual BMP-2 and BMP-7 plasmids or both
together were injected into rat calf muscles, and transcutaneous electroporation was applied 8 times at 100 V, 50 msec.
Results: In the culture system, the simultaneous transfer of the BMP-2 and BMP-7 genes led to a much higher ALP activity in C2C12 cells than did the transfer of either gene alone. In vivo, ten days after the treatment, soft X-ray analysis showed that muscles that received both pCAGGS-BMP-2 and pCAGGS-BMP-7 had better-defined opacities than those receiving a single gene. Histological examination showed advanced ossification in calf muscles that received the double-gene transfer.
BMP-4 mRNA was also expressed, and RT-PCR showed that its level increased for 3 days in a timedependent manner in the double-gene transfer group. Immunohistochemistry confirmed that BMP-
4-expressing cells resided in the matrix between muscle fibers.
Conclusion: The simultaneous transfer of BMP-2 and BMP-7 genes using in vivo electroporation induces more rapid bone formation than the transfer of either gene alone, and the increased
expression of endogenous BMP-4 suggests that the rapid ossification is related to the induction of
BMP-4.
en-copyright=
kn-copyright=
en-aut-name=KawaiMariko
en-aut-sei=Kawai
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=
en-aut-name=BesshoKazuhisa
en-aut-sei=Bessho
en-aut-mei=Kazuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=
en-aut-name=MaruyamaHiroki
en-aut-sei=Maruyama
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=
en-aut-name=MiyazakiJun-ichi
en-aut-sei=Miyazaki
en-aut-mei=Jun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=
en-aut-name=YamamotoToshio
en-aut-sei=Yamamoto
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=
affil-num=1
en-affil=
kn-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
affil-num=2
en-affil=
kn-affil=Department of Oral and Maxillofacial Surgery, Graduate School of Medicine, Kyoto University
affil-num=3
en-affil=
kn-affil=Division of Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences
affil-num=4
en-affil=
kn-affil=Division of Stem Cell Regulation Research, Osaka University Medical School
affil-num=5
en-affil=
kn-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
END