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JaLCDOI 10.18926/AMO/56649
フルテキストURL 73_2_135.pdf
著者 Maeba, Takahiro| Yonezawa, Tomoko| Ono, Mitsuaki| Tomono, Yasuko| Heljasvaara, Ritva| Pihlajaniemi, Taina| Inagawa, Kiichi| Oohashi, Toshitaka|
抄録 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.
キーワード collagen XVIII basement membrane wound healing re-epithelialization skin
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2019-04
73巻
2号
出版者 Okayama University Medical School
開始ページ 135
終了ページ 146
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2019 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 31015748
JaLCDOI 10.18926/AMO/56456
フルテキストURL 73_1_29.pdf
著者 Matsumoto, Atsushi| Nakamura, Takehiro| Shinomiya, Aya| Kawakita, Kenya| Kawanishi, Masahiko| Miyake, Keisuke| Kuroda, Yasuhiro| Keep, Richard F.| Tamiya, Takashi|
抄録 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.
キーワード biomarker histidine-rich glycoprotein predictor subarachnoid hemorrhage vasospasm
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2019-02
73巻
1号
出版者 Okayama University Medical School
開始ページ 29
終了ページ 39
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2019 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 30820052
JaLCDOI 10.18926/AMO/56452
フルテキストURL 73_1_1.pdf
著者 Morizane, Shin|
抄録 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.
キーワード atopic dermatitis kallikrein-related peptidases epidermal barrier dysfunction
Amo Type Review
出版物タイトル Acta Medica Okayama
発行日 2019-02
73巻
1号
出版者 Okayama University Medical School
開始ページ 1
終了ページ 6
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2019 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 30820048
フルテキストURL O0004485_abstract_review.pdf O0004485_summary.pdf O0004485_fulltext.pdf
著者 池田 篤司|
発行日 2018-03-23
資料タイプ 学位論文
学位授与番号 乙第4485号
学位授与年月日 2018-03-23
学位・専攻分野 博士(歯学)
授与大学 岡山大学
言語 英語
フルテキストURL K0005639_abstract_review.pdf K0005639_summary.pdf K0005639_fulltext.pdf K0005639_other.pdf
著者 越智 可奈子|
発行日 2017-12-27
資料タイプ 学位論文
学位授与番号 甲第5639号
学位授与年月日 2017-12-27
学位・専攻分野 博士(医学)
授与大学 岡山大学
言語 英語
JaLCDOI 10.18926/AMO/55582
フルテキストURL 71_6_459.pdf
著者 Sakaguchi, Masakiyo| Kinoshita, Rie| Endy Widya Putranto| I Made Winarsa Ruma| I Wayan Sumardika| Youyi, Chen| Tomonobu, Naoko| Yamamoto, Ken-ichi| Murata, Hitoshi|
抄録 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.
キーワード receptor for advanced glycation end products RAGE adaptor protein signal transduction inflammatory pathogenesis
Amo Type Review
出版物タイトル Acta Medica Okayama
発行日 2017-12
71巻
6号
出版者 Okayama University Medical School
開始ページ 459
終了ページ 465
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 英語
著作権者 CopyrightⒸ 2017 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 29276218
フルテキストURL Reprod_Fertil_Dev_28_10_1479.pdf fig.pdf
著者 Nishimura, Ryo| Okuda, Kiyoshi|
キーワード angiogenesis apoptosis corpus luteum follicular development luteal formation luteal regression steroidogenesis
備考 This is an Accepted Manuscript of an article published by CSIRO Publishing|
発行日 2015-05
出版物タイトル Reproduction, Fertility and Development
28巻
10号
出版者 CSIRO Publishing
開始ページ 1479
終了ページ 1486
ISSN 1031-3613
NCID AA10718189
資料タイプ 学術雑誌論文
言語 英語
OAI-PMH Set 岡山大学
著作権者 https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
論文のバージョン author
PubMed ID 25940685
DOI 10.1071/RD15010
Web of Science KeyUT 000383600500002
関連URL isVersionOf https://doi.org/10.1071/RD15010
フルテキストURL plosone_7_11_e50082.PDF
著者 Kobuchi, Hirotsugu| Moriya, Koko| Ogino, Tetsuya| Fujita, Hirofumi| Inoue, Keiji| Shuin, Taro| Yasuda, Tatsuji| Utsumi, Kozo| Utsumi, Toshihiko|
発行日 2012-11-26
出版物タイトル PLoS ONE
7巻
11号
出版者 Public Library of Science
開始ページ e50082
ISSN 1932-6203
資料タイプ 学術雑誌論文
言語 英語
OAI-PMH Set 岡山大学
著作権者 https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
論文のバージョン publisher
PubMed ID 23189181
DOI 10.1371/journal.pone.0050082
Web of Science KeyUT 000311929800058
関連URL https://doi.org/10.1371/journal.pone.0050082
フルテキストURL J_Comp_Neurol_525_7_1586.pdf
著者 Tamura, Kei| Kobayashi, Yasuhisa| Hirooka, Asuka| Takanami, Keiko| Oti, Takumi| Jogahara, Takamichi| Oda, Sen-ichi| Sakamoto, Tatsuya| Sakamoto, Hirotaka|
キーワード RRID AB_2060157 RRID: AB_2571636 RRID: AB_626757 Suncus murinus (suncus) gastrin-releasing peptide male reproductive function sexual dimorphism spinal cord
備考 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|
発行日 2017-05-01
出版物タイトル Journal of Comparative Neurology
525巻
7号
出版者 Wistar Institute of Anatomy and Biology
開始ページ 1586
終了ページ 1598
ISSN 0021-9967
NCID AA00695917
資料タイプ 学術雑誌論文
言語 英語
OAI-PMH Set 岡山大学
論文のバージョン author
PubMed ID 27804131
DOI 10.1002/cne.24138
Web of Science KeyUT 000397559700004
関連URL https://doi.org/10.1002/cne.24138
タイトル(別表記) Drug interaction (38. Combination with novel hypnotic drugs : ramelteon and suvorexant)
フルテキストURL 129_53.pdf
著者 久保 和子| 江角 悟| 北村 佳久| 千堂 年昭|
出版物タイトル 岡山医学会雑誌
発行日 2017-04-03
129巻
1号
開始ページ 53
終了ページ 57
ISSN 0030-1558
言語 日本語
著作権者 Copyright (c) 2017 岡山医学会
論文のバージョン publisher
DOI 10.4044/joma.129.53
NAID 130005632075
フルテキストURL K0005391_abstract_review.pdf K0005391_fulltext.pdf
著者 当真 貴志雄|
発行日 2016-06-30
資料タイプ 学位論文
学位授与番号 甲第5391号
学位授与年月日 2016-06-30
学位・専攻分野 博士(医学)
授与大学 岡山大学
言語 英語
著者 Ohtsuki, Takashi| Miki, Shunya| Kobayashi, Shouhei| Haraguchi, Tokuko| Nakata, Eiji| Hirakawa, Kazutaka| Sumita, Kensuke| Watanabe, Kazunori| Okazaki, Shigetoshi|
発行日 2015-12
出版物タイトル Scientific Reports
5巻
資料タイプ 学術雑誌論文
タイトル(別表記) The 2015 Incentive Award of the Okayama Medical Association in General Medical Science (2015 Yuuki Prize)
フルテキストURL 128_91.pdf
著者 梶田 藍|
出版物タイトル 岡山医学会雑誌
発行日 2016-08-01
128巻
2号
開始ページ 91
終了ページ 94
ISSN 0030-1558
関連URL isVersionOf https://doi.org/10.4044/joma.128.91
言語 日本語
著作権者 Copyright (c) 2016 岡山医学会
論文のバージョン publisher
DOI 10.4044/joma.128.91
NAID 130005262638
フルテキストURL K0005343_abstract_review.pdf K0005343_fulltext.pdf
著者 越智 拓海|
発行日 2016-03-25
資料タイプ 学位論文
学位授与番号 甲第5343号
学位授与年月日 2016-03-25
学位・専攻分野 博士(理学)
授与大学 岡山大学
言語 英語
フルテキストURL K0005275_abstract_review.pdf K0005275_fulltext.pdf
著者 勝山 隆行|
発行日 2016-03-25
資料タイプ 学位論文
学位授与番号 甲第5275号
学位授与年月日 2016-03-25
学位・専攻分野 博士(医学)
授与大学 岡山大学
言語 英語
フルテキストURL O0004451_abstract_review.pdf O0004451_fulltext.pdf
著者 藤原 大介|
発行日 2015-12-31
資料タイプ 学位論文
学位授与番号 乙第4451号
学位授与年月日 2015-12-31
学位・専攻分野 博士(医学)
授与大学 岡山大学
言語 英語
著者 Taketa, Hiroaki| Gulsan, Ara Sathi| Mahmoud, Farahat| Kazi, Anisur Rahman| Sakai, Takayoshi| Hirano, Yoshiaki| Kuboki, Takuo| Torii, Yasuhiro| Matsumoto, Takuya|
発行日 2015
出版物タイトル Scientific reports
5巻
資料タイプ 学術雑誌論文
著者 松本 卓也|
発行日 2015-08
出版物タイトル Okayama University Medical Research Updates
13巻
資料タイプ その他
著者 Sato, Takamaro| Soga, Yoshihiko| Yamaguchi, Tomoko| Meguro, Michio| Maeda, Hiroshi| Tada, Joji| Otani, Takayuki| Seno, Masaharu| Takashiba, Shogo|
発行日 2013-12
出版物タイトル Asian Pacific Journal of Allergy And Immunology
31巻
4号
資料タイプ 学術雑誌論文
タイトル(別表記) Non-high-output cardiac failure in patients undergoing hemodialysis through an arteriovenous shunt
フルテキストURL 127_203.pdf
著者 鵜川 豊世武|
抄録 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.
キーワード 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)
出版物タイトル 岡山医学会雑誌
発行日 2015-12-01
127巻
3号
開始ページ 203
終了ページ 207
ISSN 0030-1558
関連URL isVersionOf https://doi.org/10.4044/joma.127.203
言語 日本語
著作権者 Copyright (c) 2015 岡山医学会
論文のバージョン publisher
DOI 10.4044/joma.127.203
NAID 130005116810