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JaLCDOI 10.18926/AMO/56649
FullText URL 73_2_135.pdf
Author Maeba, Takahiro| Yonezawa, Tomoko| Ono, Mitsuaki| Tomono, Yasuko| Heljasvaara, Ritva| Pihlajaniemi, Taina| Inagawa, Kiichi| Oohashi, Toshitaka|
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.
Keywords collagen XVIII basement membrane wound healing re-epithelialization skin
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2019-04
Volume volume73
Issue issue2
Publisher Okayama University Medical School
Start Page 135
End Page 146
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2019 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 31015748
JaLCDOI 10.18926/AMO/56456
FullText URL 73_1_29.pdf
Author Matsumoto, Atsushi| Nakamura, Takehiro| Shinomiya, Aya| Kawakita, Kenya| Kawanishi, Masahiko| Miyake, Keisuke| Kuroda, Yasuhiro| Keep, Richard F.| Tamiya, Takashi|
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.
Keywords biomarker histidine-rich glycoprotein predictor subarachnoid hemorrhage vasospasm
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2019-02
Volume volume73
Issue issue1
Publisher Okayama University Medical School
Start Page 29
End Page 39
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2019 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 30820052
JaLCDOI 10.18926/AMO/56452
FullText URL 73_1_1.pdf
Author Morizane, Shin|
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.
Keywords atopic dermatitis kallikrein-related peptidases epidermal barrier dysfunction
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2019-02
Volume volume73
Issue issue1
Publisher Okayama University Medical School
Start Page 1
End Page 6
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2019 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 30820048
FullText URL O0004485_abstract_review.pdf O0004485_summary.pdf O0004485_fulltext.pdf
Author Ikeda, Atsushi|
Published Date 2018-03-23
Content Type Thesis or Dissertation
Grant Number 乙第4485号
Granted Date 2018-03-23
Thesis Type Doctor of Philosophy in Dental Science
Grantor 岡山大学
language English
FullText URL K0005639_abstract_review.pdf K0005639_summary.pdf K0005639_fulltext.pdf K0005639_other.pdf
Author Ochi, Kanako|
Published Date 2017-12-27
Content Type Thesis or Dissertation
Grant Number 甲第5639号
Granted Date 2017-12-27
Thesis Type Doctor of Philosophy in Medical Science
Grantor 岡山大学
language English
JaLCDOI 10.18926/AMO/55582
FullText URL 71_6_459.pdf
Author Sakaguchi, Masakiyo| Kinoshita, Rie| Endy Widya Putranto| I Made Winarsa Ruma| I Wayan Sumardika| Youyi, Chen| Tomonobu, Naoko| Yamamoto, Ken-ichi| Murata, Hitoshi|
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.
Keywords receptor for advanced glycation end products RAGE adaptor protein signal transduction inflammatory pathogenesis
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2017-12
Volume volume71
Issue issue6
Publisher Okayama University Medical School
Start Page 459
End Page 465
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2017 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 29276218
FullText URL Reprod_Fertil_Dev_28_10_1479.pdf fig.pdf
Author Nishimura, Ryo| Okuda, Kiyoshi|
Keywords angiogenesis apoptosis corpus luteum follicular development luteal formation luteal regression steroidogenesis
Note This is an Accepted Manuscript of an article published by CSIRO Publishing|
Published Date 2015-05
Publication Title Reproduction, Fertility and Development
Volume volume28
Issue issue10
Publisher CSIRO Publishing
Start Page 1479
End Page 1486
ISSN 1031-3613
NCID AA10718189
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version author
PubMed ID 25940685
DOI 10.1071/RD15010
Web of Science KeyUT 000383600500002
Related Url isVersionOf https://doi.org/10.1071/RD15010
FullText URL plosone_7_11_e50082.PDF
Author Kobuchi, Hirotsugu| Moriya, Koko| Ogino, Tetsuya| Fujita, Hirofumi| Inoue, Keiji| Shuin, Taro| Yasuda, Tatsuji| Utsumi, Kozo| Utsumi, Toshihiko|
Published Date 2012-11-26
Publication Title PLoS ONE
Volume volume7
Issue issue11
Publisher Public Library of Science
Start Page e50082
ISSN 1932-6203
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
Copyright Holders https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
File Version publisher
PubMed ID 23189181
DOI 10.1371/journal.pone.0050082
Web of Science KeyUT 000311929800058
Related Url https://doi.org/10.1371/journal.pone.0050082
FullText URL J_Comp_Neurol_525_7_1586.pdf
Author Tamura, Kei| Kobayashi, Yasuhisa| Hirooka, Asuka| Takanami, Keiko| Oti, Takumi| Jogahara, Takamichi| Oda, Sen-ichi| Sakamoto, Tatsuya| Sakamoto, Hirotaka|
Keywords RRID AB_2060157 RRID: AB_2571636 RRID: AB_626757 Suncus murinus (suncus) gastrin-releasing peptide male reproductive function sexual dimorphism spinal cord
Note This is the peer reviewed version of the following article: Tamura K. Kobayashi Y. Hirooka A. et al. 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). J Comp Neurol. 2017;525:1601–1613. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.| 2018年5月公開予定|
Published Date 2017-05-01
Publication Title Journal of Comparative Neurology
Volume volume525
Issue issue7
Publisher Wistar Institute of Anatomy and Biology
Start Page 1586
End Page 1598
ISSN 0021-9967
NCID AA00695917
Content Type Journal Article
language English
OAI-PMH Set 岡山大学
File Version author
PubMed ID 27804131
DOI 10.1002/cne.24138
Web of Science KeyUT 000397559700004
Related Url https://doi.org/10.1002/cne.24138
Title Alternative Drug interaction (38. Combination with novel hypnotic drugs : ramelteon and suvorexant)
FullText URL 129_53.pdf
Author Kubo, Kazuko| Esumi, Satoru| Kitamura, Yoshihisa| Sendo, Toshiaki|
Publication Title Journal of Okayama Medical Association
Published Date 2017-04-03
Volume volume129
Issue issue1
Start Page 53
End Page 57
ISSN 0030-1558
language Japanese
Copyright Holders Copyright (c) 2017 岡山医学会
File Version publisher
DOI 10.4044/joma.129.53
NAID 130005632075
FullText URL K0005391_abstract_review.pdf K0005391_fulltext.pdf
Author Toma, Kishio|
Published Date 2016-06-30
Content Type Thesis or Dissertation
Grant Number 甲第5391号
Granted Date 2016-06-30
Thesis Type Doctor of Philosophy in Medical Science
Grantor 岡山大学
language English
Author Ohtsuki, Takashi| Miki, Shunya| Kobayashi, Shouhei| Haraguchi, Tokuko| Nakata, Eiji| Hirakawa, Kazutaka| Sumita, Kensuke| Watanabe, Kazunori| Okazaki, Shigetoshi|
Published Date 2015-12
Publication Title Scientific Reports
Volume volume5
Content Type Journal Article
Title Alternative The 2015 Incentive Award of the Okayama Medical Association in General Medical Science (2015 Yuuki Prize)
FullText URL 128_91.pdf
Author Kajita, Ai|
Publication Title Journal of Okayama Medical Association
Published Date 2016-08-01
Volume volume128
Issue issue2
Start Page 91
End Page 94
ISSN 0030-1558
Related Url isVersionOf https://doi.org/10.4044/joma.128.91
language Japanese
Copyright Holders Copyright (c) 2016 岡山医学会
File Version publisher
DOI 10.4044/joma.128.91
NAID 130005262638
FullText URL K0005343_abstract_review.pdf K0005343_fulltext.pdf
Author Ochi, Takumi|
Published Date 2016-03-25
Content Type Thesis or Dissertation
Grant Number 甲第5343号
Granted Date 2016-03-25
Thesis Type Doctor of Philosophy in Science
Grantor 岡山大学
language English
FullText URL K0005275_abstract_review.pdf K0005275_fulltext.pdf
Author Katsuyama, Takayuki|
Published Date 2016-03-25
Content Type Thesis or Dissertation
Grant Number 甲第5275号
Granted Date 2016-03-25
Thesis Type Doctor of Philosophy in Medical Science
Grantor 岡山大学
language English
FullText URL O0004451_abstract_review.pdf O0004451_fulltext.pdf
Author Fujiwara, Daisuke|
Published Date 2015-12-31
Content Type Thesis or Dissertation
Grant Number 乙第4451号
Granted Date 2015-12-31
Thesis Type Doctor of Philosophy in Medical Science
Grantor 岡山大学
language English
Author Taketa, Hiroaki| Gulsan, Ara Sathi| Mahmoud, Farahat| Kazi, Anisur Rahman| Sakai, Takayoshi| Hirano, Yoshiaki| Kuboki, Takuo| Torii, Yasuhiro| Matsumoto, Takuya|
Published Date 2015
Publication Title Scientific reports
Volume volume5
Content Type Journal Article
Author Matsumoto, Takuya|
Published Date 2015-08
Publication Title Okayama University Medical Research Updates
Volume volume13
Content Type Others
Author Sato, Takamaro| Soga, Yoshihiko| Yamaguchi, Tomoko| Meguro, Michio| Maeda, Hiroshi| Tada, Joji| Otani, Takayuki| Seno, Masaharu| Takashiba, Shogo|
Published Date 2013-12
Publication Title Asian Pacific Journal of Allergy And Immunology
Volume volume31
Issue issue4
Content Type Journal Article
Title Alternative Non-high-output cardiac failure in patients undergoing hemodialysis through an arteriovenous shunt
FullText URL 127_203.pdf
Author Ugawa, Toyomu|
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.
Keywords 心拍出量(cardiac output) 心不全(heart failure) 脳性ナトリウム利尿ペプチド(brain natriuretic peptide) 非過大シャント心不全(non-high-output cardiac failure) 腎臓(kidney)
Publication Title 岡山医学会雑誌
Published Date 2015-12-01
Volume volume127
Issue issue3
Start Page 203
End Page 207
ISSN 0030-1558
Related Url isVersionOf https://doi.org/10.4044/joma.127.203
language Japanese
Copyright Holders Copyright (c) 2015 岡山医学会
File Version publisher
DOI 10.4044/joma.127.203
NAID 130005116810