Tokushima University / Educator and Researcher Directory --- Tsuchiya, Koichiro

Personal Web Page

https://researchmap.jp/tsuchiyak (researchmap)

Field of Study

○	Clinical Pharmacology

Subject of Study

○	Detection of ROS and RNS in in vivo (reactive oxygen species, reactive nitrogen species, electron paramagnetic resonance) (Our main study is development of new detection method available to identify target sites and molecule of reactive species of oxygen and nitrogen, which can be expected to clarify the relation between these reactive molecules and disease and to establish early diagnostic method and pharmacotherapy.)

Book / Paper

Book:

1.	Koichiro Tsuchiya : ウェアラブル医療・ヘルスケア機器の技術と市場, Tokyo, 2020. (Keyword) シーエムシー出版
2.	Kirino Yutaka, Koichiro Tsuchiya, Youichi Sato, Shinji Abe and Chiemi Sato : 世界薬学探訪記四国の全薬学部による海外薬学視察団最新報告: 日本の薬学，薬剤師はどう変わるべきか?, Apr. 2019.
3.	香川県TDM委員会 and Koichiro Tsuchiya : スタートアップTDM, NANZANDO Co.,Ltd., Tokyo, Feb. 2019.
4.	Licht Miyamoto and Koichiro Tsuchiya : 土屋浩一郎，生活習慣病治療を指向したエネルギーセンサー分子AMPKの新たな活性調節機構の解明, Oct. 2018.
5.	渡辺和彦 and Koichiro Tsuchiya : 肥料の夜明け, 化学工業日報社, Tokyo, Sep. 2018.
6.	Licht Miyamoto and Koichiro Tsuchiya : 生活習慣病治療を指向したエネルギーセンサー分子AMPKの新たな活性調節機構の解明, 住友電工グループ社会貢献基金研究報告書, 2018.
7.	Licht Miyamoto, 山根萌, 冨田洋輔, Keisuke Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞における亜硝酸塩によるAMPK-eNOS活性化経路の検討, TOKYO IGAKUSHA, Oct. 2014.
8.	Koichiro Tsuchiya, Keisuke Ishizawa, 智子中西 and 山口巧 : 臨床思考プロセス薬物治療学 -最適治療への論理スパイラル-, 京都廣川書店, Tokyo, Mar. 2013.
9.	Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
10.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Shoko Fujii, Jumpei Taniguchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
11.	Koichiro Tsuchiya, Keisuke Ishizawa, Licht Miyamoto, Yuya Horinouchi, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
12.	Satoru GOTO, Kentaro Kogure, Koichiro Tsuchiya and 尾関哲也 : エピソード物理化学, Mar. 2011.
13.	田島壮一郎, Koichiro Tsuchiya, 濱本磨以, 久住祥子, Yuya Horinouchi, 八木祐子, 櫻田巧, Keisuke Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第10集, TOKYO IGAKUSHA, Tokyo, Jun. 2010.
14.	大西秀樹, Koichiro Tsuchiya, 田島壮一郎, Yuya Horinouchi, 福原弥生, Kunihisa Yamaguchi, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第9集, TOKYO IGAKUSHA, Tokyo, Sep. 2008.
15.	Keisuke Ishizawa, 三木恵里加, Yuki Izawa-Ishizawa, 大西秀樹, Narantungalag Dorjsuren, 元林有紀, Kunihisa Yamaguchi, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 腎とフリーラジカル第9集, TOKYO IGAKUSHA, Tokyo, Sep. 2008.
16.	Masanori Miyata, Koichiro Tsuchiya, Toshiki Takeuchi and Tetsushi Ueta : テスト問題·レポート課題作成ハンドブック, Center for University Extension, Tokushima, Jan. 2004. (Summary) 大学の授業で成績評価をする際のテスト問題やレポート課題を作成するためのハンドブックです． (Keyword) テスト問題 / レポート課題

Academic Paper (Judged Full Paper):

1.	Yoshino Yuki, Masaki Imanishi, Licht Miyamoto, Daisuke Tsuji, Akagi Reiko, Koichiro Tsuchiya, Yoshiki Kashiwada and Naonobu Tanaka : Dauferulins A-L, daucane-type sesquiterpenes from the roots of Ferula communis: Their structures and biological activities, Fitoterapia, Vol.174, 105877, 2024. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.fitote.2024.105877 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.fitote.2024.105877 (DOI: 10.1016/j.fitote.2024.105877)
2.	Honoka Tsunematsu, Masaki Imanishi, Yuka Uemura, Yoshiya Higaki, Miyu Morisaki, Akari Katsura, Licht Miyamoto, Masafumi Funamoto, Mayuko Ichimura-Shimizu, Yuya Horinouchi, Yasumasa Ikeda, Koichi Tsuneyama and Koichiro Tsuchiya : Indigo Leaves-Induced Pulmonary Arterial Remodeling without Right Ventricular Hypertrophy in Rats., Biological & Pharmaceutical Bulletin, Vol.47, No.7, 1350-1359, 2024. (Summary) Indigo naturalis (IN), derived from the leaves of the indigo plant, is a traditional Chinese medicine that has historically been used for its anti-inflammatory properties in the treatment of various diseases, including ulcerative colitis (UC). However, long-term use of IN in UC patients is incontrovertibly associated with the onset of pulmonary arterial hypertension (PAH). To investigate the mechanisms by which IN induces PAH, we focused on the raw material of IN, indigo leaves (IL). Only the condition of long-term chronic (6 months) and high-dose (containing 5% IL in the control diet) administration of IL induced medial thickening in the pulmonary arteries without right ventricular hypertrophy in our rat model. IL administration for a month did not induce pulmonary arterial remodeling but increased endothelin-1 (ET-1) expression levels within endothelial cell (EC) layers in the lungs. Gene Expression Omnibus analysis showed that ET-1 is a key regulator of PAH and that the IL component indican and its metabolite IS induced ET-1 mRNA expression via reactive oxygen species-dependent mechanism. We identified the roles of indican and IS in ET-1 expression in ECs, which were linked to pulmonary arterial remodeling in an animal model. (Keyword) Animals / Plant Leaves / Pulmonary Artery / Male / Endothelin-1 / Vascular Remodeling / Hypertrophy, Right Ventricular / Rats, Sprague-Dawley / Hypertension, Pulmonary / Rats / Endothelial Cells / Lung (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b24-00289 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39085074 ● CiNii @ National Institute of Informatics (CRID): 1390863937794660096 ● Summary page in Scopus @ Elsevier: 2-s2.0-85199865455 (DOI: 10.1248/bpb.b24-00289, PubMed: 39085074, CiNii: 1390863937794660096, Elsevier: Scopus)
3.	Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, Ryosuke Yamashita, Ryo Nakayama, Masataka Nojima, Kosuke Kondo, Yoshiki Gomi, Honoka Tsunematsu, Kohei Goto, Licht Miyamoto, Masafumi Funamoto, Masaya Denda, Keisuke Ishizawa, Akira Otaka, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : CA9 and PRELID2; hypoxia-responsive potential therapeutic targets for pancreatic ductal adenocarcinoma as per bioinformatics analyses., Journal of Pharmacological Sciences, Vol.153, No.4, 232-242, 2023. (Summary) A strong hypoxic environment has been observed in pancreatic ductal adenocarcinoma (PDAC) cells, which contributes to drug resistance, tumor progression, and metastasis. Therefore, we performed bioinformatics analyses to investigate potential targets for the treatment of PDAC. To identify potential genes as effective PDAC treatment targets, we selected all genes whose expression level was related to worse overall survival (OS) in The Cancer Genome Atlas (TCGA) database and selected only the genes that matched with the genes upregulated due to hypoxia in pancreatic cancer cells in the dataset obtained from the Gene Expression Omnibus (GEO) database. Although the extracted 107 hypoxia-responsive genes included the genes that were slightly enriched in angiogenic factors, TCGA data analysis revealed that the expression level of endothelial cell (EC) markers did not affect OS. Finally, we selected CA9 and PRELID2 as potential targets for PDAC treatment and elucidated that a CA9 inhibitor, U-104, suppressed pancreatic cancer cell growth more effectively than 5-fluorouracil (5-FU) and PRELID2 siRNA treatment suppressed the cell growth stronger than CA9 siRNA treatment. Thus, we elucidated that specific inhibition of PRELID2 as well as CA9, extracted via exhaustive bioinformatic analyses of clinical datasets, could be a more effective strategy for PDAC treatment. (Keyword) Humans / Carbonic Anhydrase IX / Antigens, Neoplasm / Carcinoma, Pancreatic Ductal / Pancreatic Neoplasms / Hypoxia / RNA, Small Interfering / Computational Biology / Pancreatic Neoplasms (Tokushima University Institutional Repository) ● Metadata: 119176 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2023.10.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37973221 ● CiNii @ National Institute of Informatics (CRID): 1872553967456110848 ● Search Scopus @ Elsevier (PMID): 37973221 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2023.10.003 (Tokushima University Institutional Repository: 119176, DOI: 10.1016/j.jphs.2023.10.003, PubMed: 37973221, CiNii: 1872553967456110848)
4.	Takashi Tsuji, Honoka Tsunematsu, Masaki Imanishi, Masaya Denda, Koichiro Tsuchiya and Akira Otaka : Enhanced tumor specific drug release by hypoxia sensitive dual-prodrugs based on 2-nitroimidazole, Bioorganic & Medicinal Chemistry Letters, 129484, 2023. (Summary) Hypoxia in cancer is important in the development of cancer-selective medicines. Here, a novel hypoxia-responsible dual-prodrug is described. We designed and synthesized 2-nitroimidazole derivatives which spontaneously release both a PYG inhibitor and gemcitabine under hypoxic conditions. One such derivative, a prodrug 9 was found to be stable against chemical and enzymatic hydrolysis, and upon chemical reduction of the nitro group on imidazole, successfully releases both drugs. In an in vitro proliferation assay using human pancreatic cells, compound 9 exhibited significant anti-proliferative effects in hypoxia but fewer effects in normoxia. Consequently, prodrug 9 should be useful for cancer treatment due to its improved cancer selectivity and potential to overcome drug resistance. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmcl.2023.129484 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37716415 ● Search Scopus @ Elsevier (PMID): 37716415 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmcl.2023.129484 (DOI: 10.1016/j.bmcl.2023.129484, PubMed: 37716415)
5.	Aoi Suenaga, Yasuyuki Seto, Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : TJ-17 (Goreisan) mitigates renal fibrosis in a mouse model of folic acid-induced chronic kidney disease., Journal of Pharmacological Sciences, Vol.153, No.1, 31-37, 2023. (Summary) TJ-17 may have a novel preventive effect against inflammation, oxidative stress, and fibrosis, contributing to innovation in the treatment of CKD. (Tokushima University Institutional Repository) ● Metadata: 118452 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2023.07.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37524452 ● Search Scopus @ Elsevier (PMID): 37524452 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2023.07.001 (Tokushima University Institutional Repository: 118452, DOI: 10.1016/j.jphs.2023.07.001, PubMed: 37524452)
6.	Chiemi Sato, Koichiro Tsuchiya and Shinji Abe : Evaluation of the Influence of Non-face-to-face Teaching in Case Study Exercise Module Education Outcome Evaluation using a Rubric for Comprehension of Clinical Laboratory Data, Journal of University Education Research, No.20, 45-51, 2023. (Summary) 2020年，新型コロナウイルス感染症(COVID-19)拡大により，大学では対面授業に替わる新たな授業形態が必要となった．本学でも，臨床実習後に行う模擬症例演習科目で非対面授業を取り入れた．そこで本研究では，この非対面授業の教育成果を確認するため，従来の対面授業との比較を行った．臨床検査値に対する学生の理解度を指標とした考察の結果，非対面授業においても教育成果は得られていたものの，対面授業と比べると十分とは言えないことが示唆された．要因の一つとして，今回行った非対面授業はグループ討論を含まなかったため，学生間で知識や意見交換ができなかったことが考えられる．様々な授業形態が可能となった時代を迎え，今後も教育成果の評価とそれに基づく授業改善を継続して行い，それぞれの利点を活かした教育プログラムを開発していく必要がある． (Keyword) pharmacy education / non-face-to-face teaching / education outcome evaluation / clinical laboratory data (Tokushima University Institutional Repository) ● Metadata: 118124 (Tokushima University Institutional Repository: 118124)
7.	Yuya Horinouchi, Yuka Murashima, Yuto Yamada, Shun Yoshioka, Keijo Fukushima, Takumi Kure, Naofumi Sasaki, Masaki Imanishi, Hiromichi Fujino, Koichiro Tsuchiya, Kazuaki Shinomiya and Yasumasa Ikeda : Pemafibrate inhibited renal dysfunction and fibrosis in a mouse model of adenine-induced chronic kidney disease., Life Sciences, Vol.321, 121590, 2023. (Summary) These results demonstrated the renoprotective effects of pemafibrate in CKD mice, confirming its potential as a therapeutic agent for renal disorders. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2023.121590 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36940907 ● CiNii @ National Institute of Informatics (CRID): 1360017282221457024 ● Summary page in Scopus @ Elsevier: 2-s2.0-85151399970 (DOI: 10.1016/j.lfs.2023.121590, PubMed: 36940907, CiNii: 1360017282221457024, Elsevier: Scopus)
8.	Hanif Ali, Miyu Kobayashi, Katsuya Morito, Rumana Yesmin, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Koichiro Tsuchiya, Kazunori Sango and Tamotsu Tanaka : Peroxisomes attenuate cytotoxicity of very long-chain fatty acids, Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1868, No.2, 159259, 2023. (Summary) One of the major functions of peroxisomes in mammals is oxidation of very long-chain fatty acids (VLCFAs). Genetic defects in peroxisomal β-oxidation result in the accumulation of VLCFAs and lead to a variety of health problems, such as demyelination of nervous tissues. However, the mechanisms by which VLCFAs cause tissue degeneration have not been fully elucidated. Recently, we found that the addition of small amounts of isopropanol can enhance the solubility of saturated VLCFAs in an aqueous medium. In this study, we characterized the biological effect of extracellular VLCFAs in peroxisome-deficient Chinese hamster ovary (CHO) cells, neural crest-derived pheochromocytoma cells (PC12), and immortalized adult Fischer rat Schwann cells (IFRS1) using this solubilizing technique. C20:0 FA was the most toxic of the C16-C26 FAs tested in all cells. The basis of the toxicity of C20:0 FA was apoptosis and was observed at 5 μM and 30 μM in peroxisome-deficient and wild-type CHO cells, respectively. The sensitivity of wild-type CHO cells to cytotoxic C20:0 FA was enhanced in the presence of a peroxisomal β-oxidation inhibitor. Further, a positive correlation was evident between cell toxicity and the extent of intracellular accumulation of toxic FA. These results suggest that peroxisomes are pivotal in the detoxification of apoptotic VLCFAs by preventing their accumulation. (Keyword) Cricetinae / Animals / Peroxisomes / Fatty Acids / CHO Cells / Cricetulus / Oxidation-Reduction (Tokushima University Institutional Repository) ● Metadata: 117825 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2022.159259 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36460260 ● Search Scopus @ Elsevier (PMID): 36460260 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2022.159259 (Tokushima University Institutional Repository: 117825, DOI: 10.1016/j.bbalip.2022.159259, PubMed: 36460260)
9.	Yasumasa Ikeda, Masafumi Funamoto, Seiji Kishi, Masaki Imanishi, Ken-ichi Aihara, Yoshiki Kashiwada and Koichiro Tsuchiya : The novel preventive effect of a Japanese ethical Kampo extract formulation TJ-90 (Seihaito) against cisplatin-induced nephrotoxicity, Phytomedicine, Vol.103, No.8, 154213, 2022. (Tokushima University Institutional Repository) ● Metadata: 117134 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.phymed.2022.154213 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.phymed.2022.154213 (Tokushima University Institutional Repository: 117134, DOI: 10.1016/j.phymed.2022.154213)
10.	Akihiro Shirai, Kaito Kawasaka and Koichiro Tsuchiya : Antimicrobial action of phenolic acids combined with violet 405-nm light for disinfecting pathogenic and spoilage fungi, Journal of Photochemistry and Photobiology B: Biology, Vol.229, 112411, 2022. (Summary) The aim of this study is to investigate the fungicidal spectrum of six phenolic-cinnamic and -benzoic acid derivatives using four fungi, Aspergillus niger, Cladosporium cladosporioides, Trichophyton mentagrophytes and Candida albicans, in a photocombination system with violet 405-nm light. This is the first study to examine the fungicidal mechanism involving oxidative damage using the conidium of A. niger, as well as an assessment of cellular function and chemical characteristics. The results of the screening assay indicated that ferulic acid (FA) and vanillic acid (VA), which possess 4-hydroxyl and 3-methoxy groups in their phenolic acid structures, produced synergistic activity with 405-nm light irradiation. FA and VA (5.0 mM) significantly decreased the viability of A. niger by 2.4 to 2.6-logs under 90-min irradiation. The synergistic effects were attenuated by the addition of the radical scavenger dimethyl sulfoxide. Generation of reactive oxygen species (ROS), such as hydrogen peroxide and hydroxyl radicals, were confirmed in the phenolic acid solutions tested after irradiation with colorimetric and electron spin resonance analyses. Adsorption of FA and VA to conidia was greater than other tested phenolic acids, and produced 1.55- and 1.85-fold elevation of intracellular ROS levels, as determined using an oxidant-sensitive probe with flow cytometry analysis. However, cell wall or membrane damage was not the main mechanism by which the combination-induced fungal death was mediated. Intracellular ATP was drastically diminished (5% of control levels) following combined treatment with FA and light exposure, even under a condition that produced negligible decreases in viability, thereby resulting in pronounced growth delay. These results suggest that the first stage in the photofungicidal mechanism is oxidative damage to mitochondria or the cellular catabolism system associated with ATP synthesis, which is a result of the photoreaction of phenolic acids adsorbed and internalized by conidia. This photo-technology in combination with food-grade phenolic acids can aid in developing alternative approaches for disinfection of pathogenic and spoilage fungi in the fields of agriculture, food processing and medical care. (Keyword) Synergistic antifungal activity / Fungicidal action / Phenolic acid / Violet 405-nm light / Oxidative stress / Growth delay (Tokushima University Institutional Repository) ● Metadata: 116754 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphotobiol.2022.112411 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35219030 ● Summary page in Scopus @ Elsevier: 2-s2.0-85125124978 (Tokushima University Institutional Repository: 116754, DOI: 10.1016/j.jphotobiol.2022.112411, PubMed: 35219030, Elsevier: Scopus)
11.	Akihiro Shirai, Haruka Kunimi and Koichiro Tsuchiya : Antifungal action of the combination of ferulic acid and ultraviolet-A irradiation against Saccharomyces cerevisiae, Journal of Applied Microbiology, Vol.132, No.4, 2957-2967, 2022. (Summary) Aims To examine the antifungal action of photocombination treatment with ferulic acid (FA) and ultraviolet-A (UV-A) light (wavelength, 365 nm) by investigating associated changes in cellular functions of Saccharomyces cerevisiae. Methods and Results When pre-incubation of yeast cells with FA was extended from 0.5 to 10 min, its photofungicidal activity increased. Flow cytometry analysis of stained live and dead cells revealed that 10-min UV-A exposure combined with FA (1 mg ml-1) induced a ~ 99.9% decrease in cell viability although maintaining cell membrane integrity when compared with pre-exposure samples. When morphological and biochemical analysis were performed, treated cells exhibited an intact cell surface and oxidative DNA damage similar to control cells. Photocombination treatment induced cellular proteins oxidation, as shown by 2.3-fold increasing in immunostaining levels of ~49-kDa carbonylated proteins compared with pre-irradiation samples. Pyruvate kinase 1 (PK1) was identified by proteomics analysis as a candidate protein whose levels was affected by photocombination treatment. Moreover, intracellular ATP levels decreased following FA treatment both in darkness and with UV-A irradiation, thus suggesting a possible FA-induced delay in cell growth. Conclusions FA functions within the cytoplasmic membrane; addition of UV-A exposure induces increased oxidative modifications of cytosolic proteins such as PK1, which functions in ATP generation, without causing detectable genotoxicity, thus triggering inactivation of yeast cells. Significance and Impact of Study Microbial contamination is a serious problem that diminishes the quality of fruits and vegetables. Combining light exposure with food-grade phenolic acids such as FA is a promising disinfection technology for applications in agriculture and food processing. However, the mode of photofungicidal action of FA with UV-A light remains unclear. This study is the first to elucidate the mechanism using S. cerevisiae. Moreover, proteomics analyses identified a specific cytosolic protein, PK1, which is oxidatively modified by photocombination treatment. (Keyword) Antifungal action / Ferulic acid / Ultraviolet-A / Synergism / Oxidative stress / Pyruvate kinase 1 (Tokushima University Institutional Repository) ● Metadata: 116597 (Link to Publication Site) ● Publication site (DOI): 10.1111/jam.15407 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34894031 ● Search Scopus @ Elsevier (PMID): 34894031 ● Search Scopus @ Elsevier (DOI): 10.1111/jam.15407 (Tokushima University Institutional Repository: 116597, DOI: 10.1111/jam.15407, PubMed: 34894031)
12.	Ali Hanif, Morito Katsuya, Rumana Hasi Yesmin, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Kaori Kanemaru, Koichiro Tsuchiya, Sango Kazunori and Tamotsu Tanaka : Characterization of uptake and metabolism of very long-chain fatty acids in peroxisome-deficient CHO cells, Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1867, No.2, 159088, 2022. (Summary) Fatty acids (FAs) longer than C20 are classified as very long-chain fatty acids (VLCFAs). Although biosynthesis and degradation of VLCFAs are important for the development and integrity of the myelin sheath, knowledge on the incorporation of extracellular VLCFAs into the cells is limited due to the experimental difficulty of solubilizing them. In this study, we found that a small amount of isopropanol solubilized VLCFAs in aqueous medium by facilitating the formation of the VLCFA/albumin complex. Using this solubilizing technique, we examined the role of the peroxisome in the uptake and metabolism of VLCFAs in Chinese hamster ovary (CHO) cells. When wild-type CHO cells were incubated with saturated VLCFAs (S-VLCFAs), such as C23:0 FA, C24:0 FA, and C26:0 FA, extensive uptake was observed. Most of the incorporated S-VLCFAs were oxidatively degraded without acylation into cellular lipids. In contrast, in peroxisome-deficient CHO cells uptake of S-VLCFAs was marginal and oxidative metabolism was not observed. Extensive uptake and acylation of monounsaturated (MU)-VLCFAs, such as C24:1 FA and C22:1 FA, were observed in both types of CHO cells. However, oxidative metabolism was evident only in wild-type cells. Similar manners of uptake and metabolism of S-VLCFAs and MU-VLCFAs were observed in IFRS1, a Schwan cell-derived cell line. These results indicate that peroxisome-deficient cells limit intracellular S-VLCFAs at a low level by halting uptake, and as a result, peroxisome-deficient cells almost completely lose the clearance ability of S-VLCFAs accumulated outside of the cells. (Tokushima University Institutional Repository) ● Metadata: 116579 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2021.159088 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34848380 ● CiNii @ National Institute of Informatics (CRID): 1360013168847983360 ● Search Scopus @ Elsevier (PMID): 34848380 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2021.159088 (Tokushima University Institutional Repository: 116579, DOI: 10.1016/j.bbalip.2021.159088, PubMed: 34848380, CiNii: 1360013168847983360)
13.	Daishiroh Kobayashi, Yutaka Kohmura, Junya Hayashi, Masaya Denda, Koichiro Tsuchiya and Akira Otaka : Copper (II)-mediated C-H sulphenylation or selenylation of tryptophan enabling macrocyclization of peptides, Chemical Communications, Vol.57, 10763-10766, 2021. (Tokushima University Institutional Repository) ● Metadata: 116325 (Link to Publication Site) ● Publication site (DOI): 10.1039/D1CC04856B (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34585682 ● Search Scopus @ Elsevier (PMID): 34585682 ● Search Scopus @ Elsevier (DOI): 10.1039/D1CC04856B (Tokushima University Institutional Repository: 116325, DOI: 10.1039/D1CC04856B, PubMed: 34585682)
14.	Hanif Ali, Ryouhei Yamashita, Jun-ichi Morishige, Katsuya Morito, Naoya Kakiuchi, Junji Hayashi, Mutsumi Aihara, Ryushi Kawakami, Koichiro Tsuchiya and Tamotsu Tanaka : Massspectrometric analysis of sphingomyelin with N-alfa-hydroxy fatty acyl residue in mouse tissues, Lipids, Vol.56, No.2, 181-188, 2021. (Tokushima University Institutional Repository) ● Metadata: 117826 (Link to Publication Site) ● Publication site (DOI): 10.1002/lipd.12285 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1002/lipd.12285 (Tokushima University Institutional Repository: 117826, DOI: 10.1002/lipd.12285)
15.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Licht Miyamoto, Hitayama Tasuku, Hideko Nagasawa, Toshiaki Tamaki and Koichiro Tsuchiya : Role of ferroptosis in cisplatin-induced acute nephrotoxicity in mice, Journal of Trace Elements in Medicine and Biology, Vol.67, 126798, 2021. (Tokushima University Institutional Repository) ● Metadata: 116131 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtemb.2021.126798 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtemb.2021.126798 (Tokushima University Institutional Repository: 116131, DOI: 10.1016/j.jtemb.2021.126798)
16.	Shimon Takahashi, Kenshi Takechi, Natsumi Jozukuri, Takahiro Niimura, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya, Hiroaki Yanagawa and Keisuke Ishizawa : Examination of the antiepileptic effects of valacyclovir using kindling mice- search for novel antiepileptic agents by drug repositioning using a large medical information database., European Journal of Pharmacology, Vol.902, 2021. (Summary) Despite the availability of more than 20 clinical antiepileptic drugs, approximately 30% of patients with epilepsy do not respond to antiepileptic drug treatment. Therefore, it is important to develop antiepileptic products that function via novel mechanisms. In the present study, we evaluated data from one of the largest global databases to identify drugs with antiepileptic effects, and subsequently attempted to understand the effect of the combination of antiepileptic drugs and valacyclovir in epileptic seizures using a kindling model. To induce kindling in mice, pentylenetetrazol at a dose of 40 mg/kg was administered once every 48 h. Valacyclovir was orally administered 30 min before antiepileptic drug injection in kindled mice, and behavioral seizures were monitored for 20 min following pentylenetetrazol administration. Additionally, c-Fos expression in the hippocampal dentate gyrus was measured in kindled mice. Valacyclovir showed inhibitory effects on pentylenetetrazol-induced kindled seizures. In addition, simultaneous use of levetiracetam and valacyclovir caused more potent inhibition of seizure activity, and neither valproic acid nor diazepam augmented the anti-seizure effect in kindled mice. Furthermore, kindled mice showed increased c-Fos levels in the dentate gyrus. The increase in c-Fos expression was significantly inhibited by the simultaneous use of levetiracetam and valacyclovir. The findings of the present study indicate that a combination of levetiracetam and valacyclovir had possible anticonvulsive effects on pentylenetetrazol-induced kindled epileptic seizures. These results suggest that valacyclovir may have an antiseizure effect in patients with epilepsy. (Tokushima University Institutional Repository) ● Metadata: 116301 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2021.174099 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33910036 ● Search Scopus @ Elsevier (PMID): 33910036 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2021.174099 (Tokushima University Institutional Repository: 116301, DOI: 10.1016/j.ejphar.2021.174099, PubMed: 33910036)
17.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Michiko Yamashita, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Izawa-Ishizawa Yuki, Licht Miyamoto, Ishizawa Keisuke, Hiromichi Fujino, Toshiaki Tamaki, Ken-ichi Aihara and Koichiro Tsuchiya : Diphenhydramine may be a preventive medicine against cisplatin-induced kidney toxicity, Kidney International, Vol.99, No.4, 885-889, 2021. (Summary) Cisplatin is widely used as an anti-tumor drug for the treatment of solid tumors. Unfortunately, it causes kidney toxicity as a critical side effect, limiting its use, given that no preventive drug against cisplatin-induced kidney toxicity is currently available. Here, based on a repositioning analysis of the Food and Drug Administration Adverse Events Reporting System, we found that a previously developed drug, diphenhydramine, may provide a novel treatment for cisplatin-induced kidney toxicity. To confirm this, the actual efficacy of diphenhydramine was evaluated in in vitro and in vivo experiments. Diphenhydramine inhibited cisplatin-induced cell death in kidney proximal tubular cells. Mice administered cisplatin developed kidney injury with significant dysfunction (mean plasma creatinine: 0.43 vs 0.15 mg/dl) and showed augmented oxidative stress, increased apoptosis, elevated inflammatory cytokines, and MAPKs activation. However, most of these symptoms were suppressed by treatment with diphenhydramine. Furthermore, the concentration of cisplatin in the kidney was significantly attenuated in diphenhydramine-treated mice (mean platinum content: 70.0 vs 53.4 μg/g dry kidney weight). Importantly, diphenhydramine did not influence or interfere with the anti-tumor effect of cisplatin in any of the in vitro or in vivo experiments. In a selected cohort of 98 1:1 matched patients from a retrospective database of 1467 patients showed that patients with malignant cancer who had used diphenhydramine before cisplatin treatment exhibited significantly less acute kidney injury compared to ones who did not (6.1 % vs 22.4 %, respectively). Thus, diphenhydramine demonstrated efficacy as a novel preventive medicine against cisplatin-induced kidney toxicity. (Tokushima University Institutional Repository) ● Metadata: 115399 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.kint.2020.10.041 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33307103 ● Search Scopus @ Elsevier (PMID): 33307103 ● Search Scopus @ Elsevier (DOI): 10.1016/j.kint.2020.10.041 (Tokushima University Institutional Repository: 115399, DOI: 10.1016/j.kint.2020.10.041, PubMed: 33307103)
18.	Takeo Minamikawa, Takaaki Koma, Akihiro Suzuki, Takahiko Mizuno, Kentaro Nagamatsu, Hideki Arimochi, Koichiro Tsuchiya, Kaoru Matsuoka, Takeshi Yasui, Koji Yasutomo and Masako Nomaguchi : Quantitative evaluation of SARS-CoV-2 inactivation using a deep ultraviolet light-emitting diode., Scientific Reports, Vol.11, 5070, 2021. (Summary) for 300 nm are required to inactivate 99.9% of SARS-CoV-2. Our results provide quantitative antiviral effects of DUV irradiation on SARS-CoV-2, serving as basic knowledge of inactivation technologies against SARS-CoV-2. (Tokushima University Institutional Repository) ● Metadata: 117265 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-021-84592-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33658595 ● Search Scopus @ Elsevier (PMID): 33658595 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-021-84592-0 (Tokushima University Institutional Repository: 117265, DOI: 10.1038/s41598-021-84592-0, PubMed: 33658595)
19.	Yasumasa Ikeda, Hiroaki Watanabe, Tetsuya Shiuchi, Hirofumi Hamano, Yuya Horinouchi, Masaki Imanishi, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Deletion of H-ferritin in macrophages alleviates obesity and diabetes induced by high-fat diet in mice, Diabetologia, Vol.63, No.8, 1588-1602, 2020. (Summary) Iron accumulation affects obesity and diabetes, both of which are ameliorated by iron reduction. Ferritin, an iron-storage protein, plays a crucial role in iron metabolism. H-ferritin exerts its cytoprotective action by reducing toxicity via its ferroxidase activity. We investigated the role of macrophage H-ferritin in obesity and diabetes. Conditional macrophage-specific H-ferritin (Fth, also known as Fth1) knockout (LysM-Cre Fth KO) mice were used and divided into four groups: wild-type (WT) and LysM-Cre Fth KO mice with normal diet (ND), and WT and LysM-Cre Fth KO mice with high-fat diet (HFD). These mice were analysed for characteristics of obesity and diabetes, tissue iron content, inflammation, oxidative stress, insulin sensitivity and metabolic measurements. RAW264.7 macrophage cells were used for in vitro experiments. Iron concentration reduced, and mRNA expression of ferroportin increased, in macrophages from LysM-Cre Fth KO mice. HFD-induced obesity was lower in LysM-Cre Fth KO mice than in WT mice at 12 weeks (body weight: KO 34.6 ± 5.6 g vs WT 40.1 ± 5.2 g). mRNA expression of inflammatory cytokines and infiltrated macrophages and oxidative stress increased in the adipose tissue of HFD-fed WT mice, but was not elevated in HFD-fed LysM-Cre Fth KO mice. However, WT mice fed an HFD had elevated iron concentration in adipose tissue and spleen, which was not observed in LysM-Cre Fth KO mice fed an HFD (adipose tissue [μmol Fe/g protein]: KO 1496 ± 479 vs WT 2316 ± 866; spleen [μmol Fe/g protein]: KO 218 ± 54 vs WT 334 ± 83). Moreover, HFD administration impaired both glucose tolerance and insulin sensitivity in WT mice, which was ameliorated in LysM-Cre Fth KO mice. In addition, energy expenditure, mRNA expression of thermogenic genes, and body temperature were higher in KO mice with HFD than WT mice with HFD. In vitro experiments showed that iron content was reduced, and lipopolysaccharide-induced Tnf-α (also known as Tnf) mRNA upregulation was inhibited in a macrophage cell line transfected with Fth siRNA. Deletion of macrophage H-ferritin suppresses the inflammatory response by reducing intracellular iron levels, resulting in the prevention of HFD-induced obesity and diabetes. The findings from this study highlight macrophage iron levels as a potential therapeutic target for obesity and diabetes. (Tokushima University Institutional Repository) ● Metadata: 114409 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00125-020-05153-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32430665 ● Summary page in Scopus @ Elsevier: 2-s2.0-85085484596 (Tokushima University Institutional Repository: 114409, DOI: 10.1007/s00125-020-05153-0, PubMed: 32430665, Elsevier: Scopus)
20.	Masaki Imanishi, Yusuke Yamakawa, Keijo Fukushima, Raiki Ikuto, Akiko Maegawa, Yuki Izawa-Ishizawa, Yuya Horinouchi, Masateru Kondo, Masatoshi Kishuku, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Koichiro Tsuchiya, Hiromichi Fujino, Koichi Tsuneyama and Keisuke Ishizawa : Fibroblast-specific ERK5 deficiency changes tumor vasculature and exacerbates tumor progression in a mouse model., Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.393, No.7, 1239-1250, 2020. (Summary) The roles of cancer-associated fibroblasts (CAFs) have been studied in the tumor progression, and CAFs are expected to become the new targets for cancer pharmacotherapies. CAFs contribute to tumor cell survival and proliferation, tumor angiogenesis, immune suppression, tumor inflammation, tumor cell invasion and metastasis, and extracellular matrix remodeling. However, detailed mechanisms of how CAFs function in the living system remain unclear. CAFs include α-smooth muscle actin, expressing activated fibroblasts similar to myofibroblasts, and are highly capable of producing collagen. Several reports have demonstrated the contributions of extracellular-signal-regulated kinase 5 (ERK5) in fibroblasts to the fibrotic processes; however, the roles of CAF-derived ERK5 remain unclear. To investigate the roles of CAF-derived ERK5 in the tumor progression, we created mice lacking the ERK5 gene specifically in fibroblasts. Colon-26 mouse colon cancer cells were implanted into the mice subcutaneously, and the histological analyses of the tumor tissue were performed after 2 weeks. Immunofluorescence analyses showed that recipient-derived fibroblasts existed within the tumor tissue. The present study demonstrated that fibroblast-specific ERK5 deficiency exacerbated tumor progression and it was accompanied with thicker tumor vessel formation and the increase in the number of activated fibroblasts. We combined the results of The Cancer Genome Atlas (TCGA) database analysis with our animal studies, and indicated that regulating ERK5 activity in CAFs or CAF invasion into the tumor tissue can be important strategies for the development of new targets in cancer pharmacotherapies. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-020-01859-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32307577 ● Search Scopus @ Elsevier (PMID): 32307577 ● Search Scopus @ Elsevier (DOI): 10.1007/s00210-020-01859-5 (DOI: 10.1007/s00210-020-01859-5, PubMed: 32307577)
21.	Yuki Tsuchihashi, Shinji Abe, Licht Miyamoto, Honoka Tsunematsu, Toshihiro Izumi, Aya Hatano, Hiroko Okuno, Megumi Yamane, Takashi Yasuoka, Yasumasa Ikeda and Koichiro Tsuchiya : Novel Hydrophilic Camptothecin Derivatives Conjugated to Branched Glycerol Trimer Suppress Tumor Growth without Causing Diarrhea in Murine Xenograft Models of Human Lung Cancer., Molecular Pharmaceutics, Vol.17, No.4, 1049-1058, 2020. (Summary) Camptothecin possesses broad antitumor spectra on various cancers. In spite of its marked tumor-suppressing potency, camptothecin is too hydrophobic to be solved in water and therefore not currently in clinical use. CPT-11 (irinotecan) is one of the hydrophilic analogues of camptothecin and widely prescribed. However, its water solubility is still low and furthermore evokes severe diarrhea. Therefore, we designed and synthesized novel highly hydrophilic camptothecin derivatives by conjugating SN38 with branched glycerol trimer (SN38-BGL), which we have been developing as a unique strategy to endow hydrophobic molecule with much hydrophilicity, to maximize the benefit of CPT-11 and minimize the adverse effects. The SN38-BGLs exhibited equivalent or slightly stronger tumor-suppressing effects in murine xenograft human lung cancer models compared to CPT-11. However, neither early- nor late-onset diarrhea was observed when SN38-BGL was administered. Heights of villi in jejunum and ileum were bigger than those from CPT-11-treated mice, indicating that SN38-BGL is less harmful than CPT-11. Ex vivo digestion by liver microsome did not yield SN38 but a couple of other molecules against our expectations, which suggests the involvement of other active metabolites than SN38 and may explain the differences. Hence, SN38-BGLs can be a novel hydrophilic camptothecin derivative without causing severe diarrhea. (Keyword) A549 Cells / Animals / Antineoplastic Agents, Phytogenic / Camptothecin / Cell Line, Tumor / Diarrhea / Disease Models, Animal / Glycerol / Heterografts / Humans / Hydrophobic and Hydrophilic Interactions / Irinotecan / Lung Neoplasms / Male / Mice / Mice, Inbred BALB C / Mice, Nude / Microsomes, Liver / Rats, Sprague-Dawley / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.1021/acs.molpharmaceut.9b00249 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32068412 ● Search Scopus @ Elsevier (PMID): 32068412 ● Search Scopus @ Elsevier (DOI): 10.1021/acs.molpharmaceut.9b00249 (DOI: 10.1021/acs.molpharmaceut.9b00249, PubMed: 32068412)
22.	Hirofumi Hamano, Takahiro Niimura, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Mitsuhiro Goda, Masaki Imanishi, Masayuki Chuma, Yuki Izawa-Ishizawa, Licht Miyamoto, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Keisuke Ishizawa, Toshiaki Tamaki and Yasumasa Ikeda : Proton pump inhibitors block iron absorption through direct regulation of hepcidin via the aryl hydrocarbon receptor-mediated pathway, Toxicology Letters, Vol.318, 86-91, 2020. (Summary) Proton pump inhibitors (PPIs) have been used worldwide to treat gastrointestinal disorders. A recent study showed that long-term use of PPIs caused iron deficiency; however, it is unclear whether PPIs affect iron metabolism directly. We investigated the effect of PPIs on the peptide hepcidin, an important iron regulatory hormone. First, we used the FDA Adverse Event Reporting System database and analyzed the influence of PPIs. We found that PPIs, as well as H2 blockers, increased the odds ratio of iron-deficient anemia. Next, HepG2 cells were used to examine the action of PPIs and H2 blockers on hepcidin. PPIs augmented hepcidin expression, while H2 blockers did not. In fact, the PPI omeprazole increased hepcidin secretion, and omeprazole-induced hepcidin upregulation was inhibited by gene silencing or the pharmacological inhibition of the aryl hydrocarbon receptor. In mouse experiments, omeprazole also increased hepatic hepcidin mRNA expression and blood hepcidin levels. In mice treated with omeprazole, protein levels of duodenal and splenic ferroportin decreased. Taken together, PPIs directly affect iron metabolism by suppressing iron absorption through the inhibition of duodenal ferroportin via hepcidin upregulation. These findings provide a new insight into the molecular mechanism of PPI-induced iron deficiency. (Tokushima University Institutional Repository) ● Metadata: 113812 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.toxlet.2019.10.016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31669099 ● Search Scopus @ Elsevier (PMID): 31669099 ● Search Scopus @ Elsevier (DOI): 10.1016/j.toxlet.2019.10.016 (Tokushima University Institutional Repository: 113812, DOI: 10.1016/j.toxlet.2019.10.016, PubMed: 31669099)
23.	Yoshito Zamami, Takahiro Niimura, Toshihiro Koyama, Yuta Shigemi, Yuki Izawa-Ishizawa, Mizuki Morita, Ayako Ohshima, Keisaku Harada, Toru Imai, Hiromi Hagiwara, Naoto Okada, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Yutaka Kondo, Koichiro Tsuchiya, Shiro Hinotsu, R Mitsunobu Kano and Keisuke Ishizawa : Search for Therapeutic Agents for Cardiac Arrest Using a Drug Discovery Tool and Large-Scale Medical Information Database., Frontiers in Pharmacology, Vol.10, 2019. (Summary) The survival rate of cardiac arrest patients is less than 10%; therefore, development of a therapeutic strategy that improves their prognosis is necessary. Herein, we searched data collected from medical facilities throughout Japan for drugs that improve the survival rate of cardiac arrest patients. Candidate drugs, which could improve the prognosis of cardiac arrest patients, were extracted using "TargetMine," a drug discovery tool. We investigated whether the candidate drugs were among the drugs administered within 1 month after cardiac arrest in data of cardiac arrest cases obtained from the Japan Medical Data Center. Logistic regression analysis was performed, with the explanatory variables being the presence or absence of the administration of those candidate drugs that were administered to 10 patients and the objective variable being the "survival discharge." Adjusted odds ratios for survival discharge were calculated using propensity scores for drugs that significantly improved the proportion of survival discharge; the influence of covariates, such as patient background, medical history, and treatment factors, was excluded by the inverse probability-of-treatment weighted method. Using the search strategy, we extracted 165 drugs with vasodilator activity as candidate drugs. Drugs not approved in Japan, oral medicines, and external medicines were excluded. Then, we investigated whether the candidate drugs were administered to the 2,227 cardiac arrest patients included in this study. The results of the logistic regression analysis showed that three (isosorbide dinitrate, nitroglycerin, and nicardipine) of seven drugs that were administered to 10 patients showed significant association with improvement in the proportion of survival discharge. Further analyses using propensity scores revealed that the adjusted odds ratios for survival discharge for patients administered isosorbide dinitrate, nitroglycerin, and nicardipine were 3.35, 5.44, and 4.58, respectively. Thus, it can be suggested that isosorbide dinitrate, nitroglycerin, and nicardipine could be novel therapeutic agents for improving the prognosis of cardiac arrest patients. (Tokushima University Institutional Repository) ● Metadata: 114461 (Link to Publication Site) ● Publication site (DOI): 10.3389/fphar.2019.01257 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31780928 ● Summary page in Scopus @ Elsevier: 2-s2.0-85075592155 (Tokushima University Institutional Repository: 114461, DOI: 10.3389/fphar.2019.01257, PubMed: 31780928, Elsevier: Scopus)
24.	Yasumasa Ikeda, Akiho Satoh, Yuya Horinouchi, Hirofumi Hamano, Hiroaki Watanabe, Mizuki Imao, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, Licht Miyamoto, Hirayama Tasuku, Hideko Nagasawa, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress, The FASEB journal, Vol.33, No.8, 9551-9564, 2019. (Summary) Skeletal muscle atrophy is caused by disruption in the homeostatic balance of muscle degeneration and regeneration under various pathophysiological conditions. We have previously reported that iron accumulation induces skeletal muscle atrophy a ubiquitin ligase-dependent pathway. However, the potential effect of iron accumulation on muscle regeneration remains unclear. To examine the effect of iron accumulation on myogenesis, we used a mouse model with cardiotoxin (CTX)-induced muscle regeneration and C2C12 mouse myoblast cells . In mice with iron overload, the skeletal muscles exhibited increased oxidative stress and decreased expression of satellite cell markers. Following CTX-induced muscle injury, these mice also displayed delayed muscle regeneration with a decrease in the size of regenerating myofibers, reduced expression of myoblast differentiation markers, and decreased phosphorylation of MAPK signaling pathways. , iron overload also suppressed the differentiation of C2C12 myoblast cells but the suppression could be reversed by superoxide scavenging using tempol. Excess iron inhibits myogenesis oxidative stress, leading to an imbalance in skeletal muscle homeostasis.-Ikeda, Y., Satoh, A., Horinouchi, Y., Hamano, H., Watanabe, H., Imao, M., Imanishi, M., Zamami, Y., Takechi, K., Izawa-Ishizawa, Y., Miyamoto, L., Hirayama, T., Nagasawa, H., Ishizawa, K., Aihara, K.-I., Tsuchiya, K., Tamaki, T. Iron accumulation causes impaired myogenesis correlated with MAPK signaling pathway inhibition by oxidative stress. (Tokushima University Institutional Repository) ● Metadata: 113746 (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.201802724RR (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31145863 ● Search Scopus @ Elsevier (PMID): 31145863 ● Search Scopus @ Elsevier (DOI): 10.1096/fj.201802724RR (Tokushima University Institutional Repository: 113746, DOI: 10.1096/fj.201802724RR, PubMed: 31145863)
25.	Masateru Kondo, Masaki Imanishi, Keijo Fukushima, Raiki Ikuto, Yoichi Murai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Xanthine Oxidase Inhibition by Febuxostat in Macrophages Suppresses Angiotensin II-induced Aortic Fibrosis., American Journal of Hypertension, Vol.32, No.3, 249-256, 2019. (Summary) Our results suggested that FEB ameliorates Ang II-induced aortic fibrosis via suppressing macrophage-derived TGF-1 expression. (Link to Publication Site) ● Publication site (DOI): 10.1093/ajh/hpy157 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30351343 ● Search Scopus @ Elsevier (PMID): 30351343 ● Search Scopus @ Elsevier (DOI): 10.1093/ajh/hpy157 (DOI: 10.1093/ajh/hpy157, PubMed: 30351343)
26.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Toya Hiroki, Nagao Tomoko, Marin Morishita, Koichi Tsuneyama, Yuya Horinouchi, Yoshitaka Kihira, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Masanori Yoshizumi, Toshiaki Tamaki and Keisuke Ishizawa : Development of a novel aortic dissection mouse model and evaluation of drug efficacy using in-vivo assays and database analyses., Journal of Hypertension, Vol.37, No.1, 73-83, 2019. (Summary) Aortic dissection is a life-threatening disease. At present, the only therapeutic strategies available are surgery and antihypertensive drugs. Moreover, the molecular mechanisms underlying the onset of aortic dissection are still unclear. We established a novel aortic dissection model in mice using pharmacologically induced endothelial dysfunction. We then used the Japanese Adverse Drug Event Report database to investigate the role of pitavastatin in preventing the onset of aortic dissection. To induce endothelial dysfunction, Nω-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, was administered to C57BL/6 mice. Three weeks later, angiotensin II (Ang II) and β-aminopropionitrile (BAPN), a lysyl oxidase inhibitor, were administered with osmotic mini-pumps. False lumen formation was used as the pathological determinant of aortic dissection. The incidences of aortic dissection and death from aneurysmal rupture were significantly higher in the Nω-nitro-L-arginine methyl ester, Ang II, and BAPN (LAB) group than they were in the Ang II and BAPN (AB) group.Pitavastatin was administered orally to LAB mice. It significantly lowered the incidences of dissection and rupture. It also decreased inflammation and medial degradation, both of which were exacerbated in the LAB group. The Japanese Adverse Drug Event Report database analysis indicated that there were 113 cases of aortic dissection out of 95 090 patients (0.12%) not receiving statins but only six cases out of 16 668 patients receiving statins (0.04%) (odds ratio: 0.30; P = 0.0043). Our results suggest that endothelial dysfunction is associated with the onset of aortic dissection and pitavastatin can help prevent this condition. (Tokushima University Institutional Repository) ● Metadata: 113264 (Link to Publication Site) ● Publication site (DOI): 10.1097/HJH.0000000000001898 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30303488 ● Search Scopus @ Elsevier (PMID): 30303488 ● Search Scopus @ Elsevier (DOI): 10.1097/HJH.0000000000001898 (Tokushima University Institutional Repository: 113264, DOI: 10.1097/HJH.0000000000001898, PubMed: 30303488)
27.	Yu Zhou, Yukio Yamamura, Masatoshi Ogawa, Ryosuke Tsuji, Koichiro Tsuchiya, Jiro Kasahara and Satoshi Goto : c-Abl inhibition exerts symptomatic antiparkinsonian effects through a striatal postsynaptic mechanism., Frontiers in Pharmacology, Vol.9, 1311, 2018. (Summary) Parkinson's disease (PD) is caused by a progressive degeneration of nigral dopaminergic cells leading to striatal dopamine deficiency. From the perspective of antiparkinsonian drug mechanisms, pharmacologic treatment of PD can be divided into symptomatic and disease-modifying (neuroprotective) therapies. An increase in the level and activity of the Abelson non-receptor tyrosine kinase (c-Abl) has been identified in both human and mouse brains under PD conditions. In the last decade, it has been observed that the inhibition of c-Abl activity holds promise for protection against the degeneration of nigral dopaminergic cells in PD and thereby exerts antiparkinsonian effects. Accordingly, c-Abl inhibitors have been applied clinically as a disease-modifying therapeutic strategy for PD treatment. Moreover, in a series of studies, including that presented here, experimental evidence suggests that in a mouse model of parkinsonism induced by -methyl-4-phenyl-1,2,3,6-tetrahydropyridine, c-Abl inhibition exerts an immediate effect improving motor impairments by normalizing altered activity in striatal postsynaptic signaling pathways mediated by Cdk5 (cyclin-dependent kinase 5) and DARPP-32 (dopamine- and cyclic AMP-regulated phosphoprotein 32 kDa). Based on this, we suggest that c-Abl inhibitors represent an ideal antiparkinsonian agent that has both disease-modifying and symptomatic effects. Future research is required to carefully evaluate the therapeutic efficacy and clinical challenges associated with applying c-Abl inhibitors to the treatment of PD. (Tokushima University Institutional Repository) ● Metadata: 114097 (Link to Publication Site) ● Publication site (DOI): 10.3389/fphar.2018.01311 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30505273 ● Search Scopus @ Elsevier (PMID): 30505273 ● Search Scopus @ Elsevier (DOI): 10.3389/fphar.2018.01311 (Tokushima University Institutional Repository: 114097, DOI: 10.3389/fphar.2018.01311, PubMed: 30505273)
28.	Masaki Imanishi, Yuki Izawa-Ishizawa, T Sakurada, Y Kohara, Yuya Horinouchi, E Sairyo, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, M Yoshizumi, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Suppresses Pharmacologically Induced Aortic Aneurysm Formation., Pharmacology, Vol.102, No.5-6, 281-286, 2018. (Summary) We have reported that nitrosonifedipine (NO-NIF), a photodegradation product of nifedipine, has strong antioxidant and endothelial protective effects, and can suppress several cardiovascular diseases in animal models. The objective of the present study was to investigate the effects of NO-NIF on aortic aneurysm formation. The mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. The oxidative stress was measured by dihydroethidium staining and nitrotyrosine staining. The expressions of inflammation-related genes were assessed by quantitative real-time PCR and immunohistochemical staining. To clarify the mechanisms of how NO-NIF suppresses vascular cell adhesion molecule (VCAM)-1, endothelial cells were used in in vitro system. NO-NIF suppressed pharmacologically induced the aortic aneurysm formation and aortic expansion without blood pressure changes. NO-NIF suppressed elastin degradation and matrix metalloproteinase-2 mRNA expression. NO-NIF suppressed the reactive oxygen species-cyclophilin A positive feedback loop. Upregulated mRNA expressions of inflammation-related genes and endothelial VCAM-1 were suppressed by NO-NIF co-treatment in aortae. NO-NIF has the potential to be a new, nifedipine-derived therapeutic drug for suppressing aortic aneurysm formation by directly improving aortic structure with its strong ability to reduce oxidative stress and inflammation. (Keyword) Aminopropionitrile / Angiotensin II / Animals / Antigens, Differentiation / Antioxidants / Aortic Aneurysm / Chemokine CCL2 / Cyclophilins / Disease Models, Animal / Elastin / Endothelial Cells / Human Umbilical Vein Endothelial Cells / Humans / Male / Matrix Metalloproteinase 2 / Mice / Nifedipine / Nitroso Compounds / Oxidative Stress / Photolysis / Reactive Oxygen Species / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1159/000492577 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30253416 ● Summary page in Scopus @ Elsevier: 2-s2.0-85054191604 (DOI: 10.1159/000492577, PubMed: 30253416, Elsevier: Scopus)
29.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Hirofumi Hamano, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Renoprotective effects of a factor Xa inhibitor: fusion of basic research and a database analysis., Scientific Reports, Vol.8, No.1, 2018. (Summary) Renal tubulointerstitial injury, an inflammation-associated condition, is a major cause of chronic kidney disease (CKD). Levels of activated factor X (FXa), a blood coagulation factor, are increased in various inflammatory diseases. Therefore, we investigated the protective effects of an FXa inhibitor against renal tubulointerstitial injury using unilateral ureteral obstruction (UUO) mice (a renal tubulointerstitial fibrosis model) and the Food and Drug Administration Adverse Events Reporting System (FAERS) database. The renal expression levels of FX and the FXa receptors protease-activated receptor (PAR)-1 and PAR-2 were significantly higher in UUO mice than in sham-operated mice. UUO-induced tubulointerstitial fibrosis and extracellular matrix expression were suppressed in UUO mice treated with the FXa inhibitor edoxaban. Additionally, edoxaban attenuated UUO-induced macrophage infiltration and inflammatory molecule upregulation. In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors. These results suggest that FXa inhibitors exert protective effects against CKD by inhibiting tubulointerstitial fibrosis. (Tokushima University Institutional Repository) ● Metadata: 112445 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-018-29008-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30022146 ● Search Scopus @ Elsevier (PMID): 30022146 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-018-29008-2 (Tokushima University Institutional Repository: 112445, DOI: 10.1038/s41598-018-29008-2, PubMed: 30022146)
30.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease, Nephrology, Dialysis, Transplantation, Vol.33, No.4, 586-597, 2018. (Tokushima University Institutional Repository) ● Metadata: 110922 (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfx252 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28992067 ● Search Scopus @ Elsevier (PMID): 28992067 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfx252 (Tokushima University Institutional Repository: 110922, DOI: 10.1093/ndt/gfx252, PubMed: 28992067)
31.	Tamiko Nagao, Haruyuki Nakayama-Imaohji, Miad Etahi, Ayano Tada, Emika Toyonaga, Hisashi Yamasaki, Katsuichiro Okazaki, Hirokazu Miyoshi, Koichiro Tsuchiya and Tomomi Kuwahara : L-histidine augments the oxidative damage against Gram-negative bacteria by hydrogen peroxide, International Journal of Molecular Medicine, Vol.41, No.5, 2847-2854, 2018. (Summary) Excessive damage to DNA and lipid membranes by reactive oxygen species reduces the viability of bacteria. In the present study, the proliferation of recA-deficient Escherichia coli strains was revealed to be inhibited by 1% L-histidine under aerobic conditions. This inhibition of proliferation was not observed under anaerobic conditions, indicating that L-histidine enhances oxidative DNA damage to E. coli cells. Reverse transcription-quantitative polymerase chain reaction analysis demonstrated that the expression of recA in E. coli MG1655 increased ~7-fold following treatment with 10 mM hydrogen peroxide (H2O2) plus 1% L-histidine, compared with that following exposure to H2O2 alone. L-histidine increased the genomic fragmentation of E. coli MG1655 following exposure to H2O2. In addition, L-histidine increased the generation of intracellular hydroxyl radicals in the presence of H2O2 in E. coli cells. Next, our group investigated the disinfection properties of the H2O2 and L-histidine combination. The combination of 100 mM H2O2 and 1.0% L-histidine significantly reduced the number of viable cells of extended-spectrum-β-lactamase-producing E. coli and multidrug-resistant Pseudomonas aeruginosa, and this treatment was more effective than 100 mM H2O2 alone, but this effect was not observed in methicillin-resistant Staphylococcus aureus or vancomycin-resistant Enterococcus faecium. The combination of L-histidine and H2O2 may be a useful strategy to selectively increase the microbicidal activity of oxidative agents against Gram-negative bacteria. (Keyword) Anti-Bacterial Agents / DNA Damage / Disinfection / Escherichia coli / Gram-Negative Bacteria / Gram-Negative Bacterial Infections / Histidine / Humans / Hydrogen Peroxide / Oxidants / Oxidative Stress / Reactive Oxygen Species (Link to Publication Site) ● Publication site (DOI): 10.3892/ijmm.2018.3473 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29436593 ● Search Scopus @ Elsevier (PMID): 29436593 ● Search Scopus @ Elsevier (DOI): 10.3892/ijmm.2018.3473 (DOI: 10.3892/ijmm.2018.3473, PubMed: 29436593)
32.	Licht Miyamoto and Koichiro Tsuchiya : SGLT as a therapeutic target for diabetes - from a view of drug discovery and pharmacotherapy, Journal of the Pharmaceutical Society of Japan, Vol.138, No.7, 933-938, 2018. (Summary) Sodium-glucose transporter (SGLT)-2 inhibitors, which are currently in clinical use in most of the world, are unique as their hypoglycemic effects are completely independent of insulin action. Potential benefits and indications for the treatment of other diseases like circulatory and renal disorders are attracting attention. SGLT2 inhibitors not only reduce blood glucose levels but also alter the whole-body energy balance to lower body weight, which should result in the amelioration of multiple metabolic disorders like metabolic syndrome. In the symposium, we briefly introduced the physiological as well as biological functions of SGLTs and discussed strategies for drug design by looking back at the history of drug discovery for SGLT2 inhibitors. We also shared our recent data on their combined usage with other hypoglycemic agents and effects on glucagon secretion, which are current clinical topics relevant to SGLT2 inhibitors. Among those topics, strategies for drug discovery of SGLT2 inhibitors are discussed in this review. (Keyword) Body Weight / Carbonates / Diabetes Mellitus / Drug Discovery / Energy Metabolism / Glucosides / Humans / Hypoglycemic Agents / Molecular Targeted Therapy / Phloretin / Phlorhizin / Sodium-Glucose Transporter 2 / Sodium-Glucose Transporter 2 Inhibitors (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.17-00223-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29962472 ● Summary page in Scopus @ Elsevier: 2-s2.0-85049485923 (DOI: 10.1248/yakushi.17-00223-1, PubMed: 29962472, Elsevier: Scopus)
33.	Wenting Xu, Licht Miyamoto, Haruna Aihara, Tomomi Yamaoka, Naonobu Tanaka, Yuki Tsuchihashi, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : Methanol extraction fraction from Citrus Sudachi peel exerts lipid reducing effects in cultured cells., The Journal of Medical Investigation : JMI, Vol.65, No.3.4, 225-230, 2018. (Summary) Ectopic fat accumulation is associated with insulin resistance and type 2 diabetes mellitus. Citrus sudachi is an evergreen tree that is found mainly in Tokushima Prefecture in Japan. Previously, it was demonstrated that Citrus sudachi could inhibit the rising trend of blood glucose and fatty acid in human subjects. In the current study, we illustrated the function of methanol extracts from sudachi peel and investigated the mechanism of this effect. We got the five kinds of methanol extracts by using diaion HP-20, and those were named by hydrophobicity from M-F1 to M-F5. Among the 5 kinds of sudachi methanol extracts, only M-F4 significantly decreased the intracellular triglyceride of C2C12 cells. It augmented the AMPK activity and increased the transcription of PPARα and its downstream targets CPT-1b and UCP2. In conclusion, M-F4 improved the lipid metabolism possibly through AMPK, PPARα and their downstream targets like CPT-1b and UCP2. Furthermore, this extract may be useful for preventing obesity and diabetes related diseases. J. Med. Invest. 65:225-230, August, 2018. (Keyword) AMP-Activated Protein Kinases / Animals / Cell Line / Citrus / Humans / Hypolipidemic Agents / Lipid Metabolism / methanol / knockout mice / Models, Biological / PPAR alpha / Phytotherapy / Plant Extracts / signal transduction / Sirtuin 1 / Triglycerides (Tokushima University Institutional Repository) ● Metadata: 112243 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.225 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30282865 ● Search Scopus @ Elsevier (PMID): 30282865 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.225 (Tokushima University Institutional Repository: 112243, DOI: 10.2152/jmi.65.225, PubMed: 30282865)
34.	Katsunori Tsuda, Licht Miyamoto, Shuichi Hamano, Yuri Morimoto, Yumi Kangawa, Chika Fukue, Yoko Kagawa, Yuya Horinouchi, Wenting Xu, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Mechanisms of the pH- and Oxygen-Dependent Oxidation Activities of Artesunate., Biological & Pharmaceutical Bulletin, Vol.41, No.4, 555-563, 2018. (Summary) Artemisinin was discovered in 1971 as a constituent of the wormwood genus plant (Artemisia annua). This plant has been used as an herbal medicine to treat malaria since ancient times. The compound artemisinin has a sesquiterpene lactone bearing a peroxide group that offers its biological activity. In addition to anti-malarial activity, artemisinin derivatives have been reported to exert antitumor activity in cancer cells, and have attracted attention as potential anti-cancer drugs. Mechanisms that might explain the antitumor activities of artemisinin derivatives reportedly induction of apoptosis, angiogenesis inhibitory effects, inhibition of hypoxia-inducible factor-1 (HIF-1) activation, and direct DNA injury. Reactive oxygen species (ROS) generation is involved in many cases. However, little is known about the mechanism of ROS formation from artemisinin derivatives and what types of ROS are produced. Therefore, we investigated the iron-induced ROS formation mechanism by using artesunate, a water-soluble artemisinin derivative, which is thought to be the underlying mechanism involved in artesunate-mediated cell death. The ROS generated by the coexistence of iron(II), artesunate, and molecular oxygen was a hydroxyl radical or hydroxyl radical-like ROS. Artesunate can reduce iron(III) to iron(II), which enables generation of ROS irrespective of the iron valence. We found that reduction from iron(III) to iron(II) was activated in the acidic rather than the neutral region and was proportional to the hydrogen ion concentration. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b17-00855 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29607928 ● Search Scopus @ Elsevier (PMID): 29607928 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b17-00855 (DOI: 10.1248/bpb.b17-00855, PubMed: 29607928)
35.	Takahiro Niimura, Yoshito Zamami, Toshihiro Koyama, Yuki Izawa-Ishizawa, Masashi Miyake, Tadashi Koga, Keisaku Harada, Ayako Ohshima, Toru Imai, Yutaka Kondo, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki, Shiro Hinotsu, R Mitsunobu Kano and Keisuke Ishizawa : Hydrocortisone administration was associated with improved survival in Japanese patients with cardiac arrest., Scientific Reports, Vol.7, No.1, 2017. (Summary) There are few reports on hydrocortisone administration after cardiac arrest, and those that have been published included few subjects. This study aimed to evaluate the effect of hydrocortisone administration on the outcomes of patients who experienced cardiac arrest. We investigated the survival discharge rates and the length of hospital stay from cardiac arrest to discharge, stratified by use of hydrocortisone, using a Japanese health-insurance claims dataset that covers approximately 2% of the Japanese population. The study included the data of 2233 subjects who experienced either in-hospital or out-of-hospital cardiac arrest between January 2005 and May 2014. These patients were divided into two groups, based on the administration of hydrocortisone. We adjusted the baseline characteristics, medical treatment, and drug administration data of the two groups using propensity scores obtained via the inverse probability of treatment weighted method. The hydrocortisone group had a significantly higher survival discharge rate (13/61 [21.1%] vs. 240/2172 [11.0%], adjusted odds ratio: 4.2, 95% CI: 1.60-10.98, p = 0.004). In addition, the administration of hydrocortisone was independent predictor of survival to discharge (hazard ratio: 4.6, p < 0.001). The results demonstrate a correlation between hydrocortisone administration and the high rates of survival to discharge. (Tokushima University Institutional Repository) ● Metadata: 112397 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-17686-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29263333 ● Search Scopus @ Elsevier (PMID): 29263333 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-17686-3 (Tokushima University Institutional Repository: 112397, DOI: 10.1038/s41598-017-17686-3, PubMed: 29263333)
36.	Yasumasa Ikeda, Yuya Horinouchi, Hamano Hirofumi, Hirayama Tasuku, Seiji Kishi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Hideko Nagasawa, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary iron restriction alleviates renal tubulointerstitial injury induced by protein overload in mice, Scientific Reports, Vol.7, No.1, 10621, 2017. (Summary) Increased proteinuria causes tubulointerstitial injury due to inflammation in chronic kidney disease (CKD). Iron restriction exhibits protective effects against renal dysfunction; however, its effects against protein overload-induced tubulointerstitial damage remain unclear. Here, we investigated dietary iron restriction effect on tubulointerstitial damage in mice with protein-overload tubulointerstitial injury. Renal tubulointerstitial injury in animal model was induced by intraperitoneal injection of an overdose of bovine serum albumin (BSA). We divided mice into three groups: normal saline + normal diet (ND), BSA + ND, and BSA + iron-restricted diet (IRD). BSA overload induced renal tubulointerstitial injury in the ND mice, which was ameliorated in the IRD mice. Inflammatory cytokines and extracellular matrix mRNA expression was upregulated in BSA + ND mice kidneys and was inhibited by IRD. BSA-induced increase in renal superoxide production, NADPH oxidase activity, and p22(phox) expression was diminished in the IRD mice. IRD suppression increased BSA-induced renal macrophage infiltration. Moreover, BSA mice exhibited nucleotide-binding oligomerisation domain-like receptor pyrin domain-containing protein (NLRP) inflammasome activation, which was inhibited by IRD. Ferrous iron increased in kidneys with BSA overload and was inhibited by IRD. Thus, iron restriction inhibited oxidative stress and inflammatory changes, contributing to the protective effect against BSA overload-induced tubulointerstitial injury. (Tokushima University Institutional Repository) ● Metadata: 112368 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-017-11089-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28878231 ● Search Scopus @ Elsevier (PMID): 28878231 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-017-11089-0 (Tokushima University Institutional Repository: 112368, DOI: 10.1038/s41598-017-11089-0, PubMed: 28878231)
37.	Keisuke Oshima, Yasumasa Ikeda, Yuya Horinouchi, Hiroaki Watanabe, Hirofumi Hamano, Yoshitaka Kihira, Seiji Kishi, Yuki Izawa-Ishizawa, Licht Miyamoto, Tasuku Hirayama, Hideko Nagasawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron suppresses erythropoietin expression via oxidative stress-dependent hypoxia-inducible factor-2 alpha inactivation, Laboratory Investigation; a Journal of Technical Methods and Pathology, Vol.97, No.5, 555-566, 2017. (Summary) Renal anemia is a major complication in chronic kidney disease (CKD). Iron supplementation, as well as erythropoiesis-stimulating agents, are widely used for treatment of renal anemia. However, excess iron causes oxidative stress via the Fenton reaction, and iron supplementation might damage remnant renal function including erythropoietin (EPO) production in CKD. EPO gene expression was suppressed in mice following direct iron treatment. Hypoxia-inducible factor-2 alpha (HIF-2α), a positive regulator of the EPO gene, was also diminished in the kidney of mice following iron treatment. Anemia-induced increase in renal EPO and HIF-2α expression was inhibited by iron treatment. In in vitro experiments using EPO-producing HepG2 cells, iron stimulation reduced the expression of the EPO gene, as well as HIF-2α. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound. HIF-2α interaction with the Epo promoter was inhibited by iron treatment, and was restored by tempol. These findings suggested that iron supplementation reduced EPO gene expression via an oxidative stress-HIF-2α-dependent signaling pathway. (Tokushima University Institutional Repository) ● Metadata: 113749 (Link to Publication Site) ● Publication site (DOI): 10.1038/labinvest.2017.11 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28263291 ● Search Scopus @ Elsevier (PMID): 28263291 ● Search Scopus @ Elsevier (DOI): 10.1038/labinvest.2017.11 (Tokushima University Institutional Repository: 113749, DOI: 10.1038/labinvest.2017.11, PubMed: 28263291)
38.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yuya Horinouchi, Eriko Sairyo, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Yoshiro Abe, Ichiro Hashimoto and Toshiaki Tamaki : Topical Application of Nitrosonifedipine, a Novel Radical Scavenger, Ameliorates Ischemic Skin Flap Necrosis in a Mouse Model., Wound Repair and Regeneration, Vol.25, No.2, 217-223, 2017. (Summary) Ischemic skin flap necrosis can occur in random pattern flaps. An excess amount of reactive oxygen species is generated and causes necrosis in the ischemic tissue. Nitrosonifedipine (NO-NIF) has been demonstrated to possess potent radical scavenging ability. However, there has been no study on the effects of NO-NIF on ischemic skin flap necrosis. Therefore, they evaluated the potential of NO-NIF in ameliorating ischemic skin flap necrosis in a mouse model. A random pattern skin flap (1.0 × 3.0 cm) was elevated on the dorsum of C57BL/6 mice. NO-NIF was administered by topical injection immediately after surgery and every 24 hours thereafter. Flap survival was evaluated on postoperative day 7. Tissue samples from the skin flaps were harvested on postoperative days 1 and 3 to analyze oxidative stress, apoptosis and endothelial dysfunction. The viable area of the flap in the NO-NIF group was significantly increased (78.30 ± 7.041%) compared with that of the control group (47.77 ± 6.549%, p < 0.01). NO-NIF reduced oxidative stress, apoptosis and endothelial dysfunction, which were evidenced by the decrease of malondialdehyde, p22phox protein expression, number of apoptotic cells, phosphorylated p38 MAPK protein expression, and vascular cell adhesion molecule-1 protein expression while endothelial nitric oxide synthase protein expression was increased. In conclusion, they demonstrated that NO-NIF ameliorated ischemic skin flap necrosis by reducing oxidative stress, apoptosis, and endothelial dysfunction. NO-NIF is considered to be a candidate for the treatment of ischemic flap necrosis. (Tokushima University Institutional Repository) ● Metadata: 110118 (Link to Publication Site) ● Publication site (DOI): 10.1111/wrr.12510 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28090711 ● Search Scopus @ Elsevier (PMID): 28090711 ● Search Scopus @ Elsevier (DOI): 10.1111/wrr.12510 (Tokushima University Institutional Repository: 110118, DOI: 10.1111/wrr.12510, PubMed: 28090711)
39.	Shinji Abe, Kato Mika Kaneko, Yuki Tsuchihashi, Toshihiro Izumi, Satoshi Ogasawara, Naoto Okada, Chiemi Sato, Makoto Tobiume, Kenji Otsuka, Licht Miyamoto, Koichiro Tsuchiya, Kazuyoshi Kawazoe, Yukinari Kato and Yasuhiko Nishioka : Antitumor effect of novel anti-podoplanin antibody NZ-12 against malignant pleural mesothelioma in an orthotopic xenograft model., Cancer Science, Vol.107, No.9, 1198-1205, 2016. (Keyword) cancer immunotherapy / ADCC / podoplanin (Tokushima University Institutional Repository) ● Metadata: 112378 (Link to Publication Site) ● Publication site (DOI): 10.1111/cas.12985 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27294401 ● Search Scopus @ Elsevier (PMID): 27294401 ● Search Scopus @ Elsevier (DOI): 10.1111/cas.12985 (Tokushima University Institutional Repository: 112378, DOI: 10.1111/cas.12985, PubMed: 27294401)
40.	Yasumasa Ikeda, Mizuki Imao, Akiho Satoh, Hiroaki Watanabe, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway, Journal of Trace Elements in Medicine and Biology, Vol.35, No.5, 66-76, 2016. (Summary) Skeletal muscle wasting or sarcopenia is a critical health problem. Skeletal muscle atrophy is induced by an excess of iron, which is an essential trace metal for all living organisms. Excessive amounts of iron catalyze the formation of highly toxic hydroxyl radicals via the Fenton reaction. However, the molecular mechanism of iron-induced skeletal muscle atrophy has remained unclear. In this study, 8-weeks-old C57BL6/J mice were divided into 2 groups: vehicle-treated group and the iron-injected group (10 mg iron·day-1·mouse-1) during 2 weeks. Mice in the iron-injected group showed an increase in the iron content of the skeletal muscle and serum and ferritin levels in the muscle, along with reduced skeletal muscle mass. The skeletal muscle showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1), on days 7 and 14 of iron treatment. Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. Inhibition of FOXO3a using siRNA in vitro in C2C12 myotube cells inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by reactivating the Akt-FOXO3 pathway. Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress. (Tokushima University Institutional Repository) ● Metadata: 113750 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jtemb.2016.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27049128 ● Search Scopus @ Elsevier (PMID): 27049128 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jtemb.2016.01.011 (Tokushima University Institutional Repository: 113750, DOI: 10.1016/j.jtemb.2016.01.011, PubMed: 27049128)
41.	Hirokazu Miyoshi, Fumio Kida, Kenji Yamada, Koichiro Tsuchiya and Hase Hitoshi : Optical property of CR-39 synthesized by doping with methylviologen-encapsulated SiO2 nanocapsules as a solid-state X-ray plate detector, Optical Materials, Vol.55, 109-114, 2016. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.optmat.2016.02.042 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.optmat.2016.02.042 (DOI: 10.1016/j.optmat.2016.02.042)
42.	Hirokazu Miyoshi, Fumio Kida, Hitoshi Hase and Koichiro Tsuchiya : Silica-nanocapsule-doped CR-39 for fluorescence detection of Xrays, Physics Procedia, Vol.80, 90-93, 2015. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.phpro.2015.11.100 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.phpro.2015.11.100 (DOI: 10.1016/j.phpro.2015.11.100)
43.	Yasumasa Ikeda, Hirofumi Hamano, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin exerts pro-angiogenic effects through an Akt-eNOS-dependent pathway, Hypertension Research, Vol.38, No.11, 733-740, 2015. (Summary) Low serum bilirubin levels are associated with the risk of cardiovascular diseases including peripheral artery disease. Bilirubin is known to exert its property such as antioxidant effect or the enhancement of flow-mediated vasodilation, however, bilirubin action on angiogenesis remains unclear. To investigate the molecular mechanism of bilirubin on angiogenic effect, we first employed C57BL/6J mice with unilateral hindlimb ischemia surgery and divided the mice into two groups (vehicle-treated group and bilirubin-treated group). The analysis of laser speckle blood flow demonstrated the enhancement of blood flow recovery in response to ischemia of mice with bilirubin treatment. The density of capillaries was significantly higher in ischemic-adductor muscles of bilirubin-treated mice. The phosphorylated levels of endothelial nitric oxide synthase (eNOS) and Akt were increased in ischemic skeletal muscles of mice with bilirubin treatment compared with vehicle treatment. In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation. These bilirubin actions on endothelial cell activation were inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. In conclusion, bilirubin promotes angiogenesis through endothelial cells activation via Akt-eNOS-dependent manner. (Tokushima University Institutional Repository) ● Metadata: 113751 (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2015.74 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26134126 ● Summary page in Scopus @ Elsevier: 2-s2.0-84946558014 (Tokushima University Institutional Repository: 113751, DOI: 10.1038/hr.2015.74, PubMed: 26134126, Elsevier: Scopus)
44.	Soichiro Tajima, Yasumasa Ikeda, Hideaki Enomoto, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II alters the expression of duodenal iron transporters, hepatic hepcidin, and body iron distribution in mice, European Journal of Nutrition, Vol.54, No.5, 709-719, 2015. (Summary) Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear. The C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into three groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups. Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 and CCAAT/enhancer-binding protein alpha, which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by the administration of an ARB. Angiotensin II (ANG II) altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution. (Tokushima University Institutional Repository) ● Metadata: 113753 (Link to Publication Site) ● Publication site (DOI): 10.1007/s00394-014-0749-1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25096756 ● Summary page in Scopus @ Elsevier: 2-s2.0-84937513465 (Tokushima University Institutional Repository: 113753, DOI: 10.1007/s00394-014-0749-1, PubMed: 25096756, Elsevier: Scopus)
45.	Miku Kita, Jun Yamamoto, Takuya Morisaki, Chiaki Komiya, Tsubasa Inokuma, Licht Miyamoto, Koichiro Tsuchiya, Akira Shigenaga and Akira Otaka : Design and synthesis of a hydrogen peroxide-responsive amino acid that induces peptide bond cleavage after exposure to hydrogen peroxide, Tetrahedron Letters, Vol.56, No.28, 4228-4231, 2015. (Tokushima University Institutional Repository) ● Metadata: 111909 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.tetlet.2015.05.060 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84930930016 (Tokushima University Institutional Repository: 111909, DOI: 10.1016/j.tetlet.2015.05.060, Elsevier: Scopus)
46.	Toshitaka Ikehara, Mutsumi Nakahashi, Zehong Su, Masatake Akutagawa, Koichiro Tsuchiya, Mitsuo Kitamura, Akira Takahashi and Yohsuke Kinouchi : Effects of UV-A LED light irradiation on growth of cultured RAW 264.7 cells, Toxicological and Environmental Chemistry, Vol.97, No.2, 243-255, 2015. (Keyword) 365 nm / LED light / reactive oxygen species / Raw 264.7 cells / scavenger (Link to Publication Site) ● Publication site (DOI): 10.1080/02772248.2015.1039771 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-84931571408 (DOI: 10.1080/02772248.2015.1039771, Elsevier: Scopus)
47.	Yoshitaka Kihira, Ariunzaya Burentogtokh, Mari Itoh, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia decreases glucagon-like peptide-1 secretion from GLUTag cell line, Biological & Pharmaceutical Bulletin, Vol.38, No.4, 514-521, 2015. (Summary) Glucagon-like peptide-1 (GLP-1), an incretin hormone, is secreted from L cells located in the intestinal epithelium. It is known that intestinal oxygen tension is decreased postprandially. In addition, we found that the expression of hypoxia-inducible factor-1α (HIF-1α), which accumulates in cells under hypoxic conditions, was significantly increased in the colons of mice with food intake, indicating that the oxygen concentration is likely reduced in the colon after eating. Therefore, we hypothesized that GLP-1 secretion is affected by oxygen tension. We found that forskolin-stimulated GLP-1 secretion from GLUTag cells, a model of intestinal L cells, is suppressed in hypoxia (1% O2). Forskolin-stimulated elevations of preproglucagon (ppGCG) and proprotein convertase 1/3 (PC1/3) mRNA expression were decreased under hypoxic conditions. The finding that H89, a protein kinase A (PKA) inhibitor, inhibited the forskolin-stimulated increase of ppGCG and PC1/3 indicated that the cAMP-PKA pathway is involved in the hypoxia-induced suppression of the genes. Hypoxia decreased hexokinase 2 mRNA and protein expression and increased lactate dehydrogenase A mRNA and protein expression. Concomitantly, lactate production was increased and ATP production was decreased. Together, the results indicate that hypoxia decreases glucose utilization for ATP production, which probably causes a decrease in cAMP production and in subsequent GLP-1 production. Our findings suggest that the postprandial decrease in oxygen tension in the intestine attenuates GLP-1 secretion. (Tokushima University Institutional Repository) ● Metadata: 109948 (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b14-00612 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25832631 ● CiNii @ National Institute of Informatics (CRID): 1390001204631777920 ● Summary page in Scopus @ Elsevier: 2-s2.0-84928951796 (Tokushima University Institutional Repository: 109948, DOI: 10.1248/bpb.b14-00612, PubMed: 25832631, CiNii: 1390001204631777920, Elsevier: Scopus)
48.	Licht Miyamoto, Yuko Yagi, Aya Hatano, Kazuyoshi Kawazoe, Keisuke Ishizawa, Kazuo Minakuchi, Shuhei Tomita and Koichiro Tsuchiya : Spontaneously hyperactive MEK-Erk pathway mediates paradoxical facilitation of cell proliferation in mild hypoxia, Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1850, No.4, 640-646, 2015. (Summary) Oxygen is important for common eukaryotic cells to generate ATP. Pathophysiological conditions such as ischemic diseases cause tissue hypoxia. In addition, oxygen availability in deep tissues is supposed to be far lower than surrounding atmosphere even in healthy animals, and the oxygen partial pressures in most normal tissues are estimated to be around 40-50mmHg, so-called mild hypoxia. Recent studies have demonstrated that mild hypoxia has distinct effects on living cells from severe hypoxia. For instance, mild hypoxia was reported to promote cell reprogramming. Although severe hypoxia is known to inhibit cell proliferation, mild hypoxia has been paradoxically demonstrated to increase cell proliferation. However, it has not been clarified by which molecular mechanisms mild hypoxia evokes the discontinuous increment of cell proliferation. We established experimental conditions showing the opposite influences of mild and severe hypoxia on cell proliferation using undifferentiated Caco2 human colon carcinoma cells in order to clarify the underlying molecular mechanism. The basal activity of Erk, which is a typical mediator of mitogenic signals, is spontaneously increased specifically in cells exposed to mild hypoxia, and inhibition of MEK, an upstream kinase of the Erk, completely inhibited the mild hypoxia-induced enhancement of cell proliferation. Spontaneous hyperactivation of the MEK-Erk pathway by mild hypoxia should be the plausible molecular mechanism of the paradoxical promotion of cell proliferation. Our findings will provide clues to the molecular basis of mild hypoxia-evoked phenomena such as cell reprogramming. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2014.12.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25497211 ● Summary page in Scopus @ Elsevier: 2-s2.0-84921044624 (DOI: 10.1016/j.bbagen.2014.12.006, PubMed: 25497211, Elsevier: Scopus)
49.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Licht Miyamoto, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : A Long-Term High-Fat Diet Changes Iron Distribution in Body, Increasing Iron Accumulation Specifically in the Mouse Spleen, Journal of Nutritional Science and Vitaminology, Vol.61, No.1, 20-27, 2015. (Summary) Although iron is an essential trace metal, its presence in excess causes oxidative stress in the human body. Recent studies have indicated that iron storage is a risk factor for type 2 diabetes mellitus. Dietary iron restriction or iron chelation ameliorates symptoms of type 2 diabetes in mouse models. However, whether iron content in the body changes with the development of diabetes is unknown. Here, we investigated the dynamics of iron accumulation and changes in iron absorption-related genes in mice that developed obesity and diabetes by consuming a high-fat diet (HFD-fed mice). HFD-fed mice (18-20 wk) were compared with control mice for hematologic features, serum ferritin levels, and iron contents in the gastrocnemius muscle, heart, epididymal fat, testis, liver, duodenum, and spleen. In addition, the spleen was examined histologically. Iron absorption-related gene expression in the liver and duodenum was also examined. Hemoglobin and serum ferritin levels were increased in HFD-fed mice. The HFD-fed mice showed iron accumulation in the spleen, but not in the heart or liver. Increased percentages of the splenic red pulp and macrophages were observed in HFD-fed mice and iron accumulation in the spleen was found mainly in the splenic red pulp. The HFD-fed mice also showed decreased iron content in the duodenum. The mRNA expression of divalent metal transporter-1 (DMT-1), an iron absorption-related gene, was elevated in the duodenum of HFD-fed mice. These results indicate that iron accumulation (specifically accumulation in the spleen) is enhanced by the development of type 2 diabetes induced by HFD. (Keyword) iron/spleen/diet / high fat/diabetes mellitus / type 2/DMT1 protein (iron transporter) (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.61.20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25994136 ● CiNii @ National Institute of Informatics (CRID): 1390282681302013696 ● Summary page in Scopus @ Elsevier: 2-s2.0-84929747372 (DOI: 10.3177/jnsv.61.20, PubMed: 25994136, CiNii: 1390282681302013696, Elsevier: Scopus)
50.	Masashi Akaike, Ken-ichi Aihara, Hiroaki Yanagawa, Takashi Iwase, Sumiko Yoshida, Sato Chiho, Saijo Tomoka, Hiroaki Mikasa, Kashiwada Yoshizaki, Yoshihisa Takaishi, Koichiro Tsuchiya, Toshiaki Tamaki, Toshio Matsumoto and Masataka Sata : Efficacy and safety of Citrus sudachi peel in obese adults:A randomized, double-blind, pilot study, Functional Foods in Health and Disease, Vol.4, No.6, 276-284, 2014. (Link to Publication Site) ● Publication site (DOI): 10.31989/ffhd.v4i7.5 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85054855286 (DOI: 10.31989/ffhd.v4i7.5, Elsevier: Scopus)
51.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Masaki Ueno, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : Smooth muscle cell specific Hif-1 deficiency suppresses angiotensin II-induced vascular remodeling in mice, Cardiovascular Research, Vol.102, No.3, 460-468, 2014. (Summary) Vascular remodelling is mediated by vascular smooth muscle cell (VSMC) proliferation and hypertrophy, both processes of which are linked to medial thickening and fibrosis. Here, we show that hypoxia-inducible factor-1α (Hif-1α) expressed in smooth muscle cells (SMCs) is involved in angiotensin II (Ang II)-induced vascular remodelling in an in vivo model. To clarify the role of Hif-1α in vascular remodelling, we created mice lacking the Hif-1α gene in SMCs (SMKO mice). Ang II infusion induced medial thickening and vascular fibrosis, accompanied by Hif-1α up-regulation, in the aortae of control mice, but not in those of SMKO mice. In accordance with those results, our in vitro studies showed that the deletion of SMC-derived Hif-1α suppressed the Ang II-induced hypertrophy of VSMCs, and our in vivo studies showed that the Ang II-induced expression of fibrosis-related genes in aortae was suppressed by SMC-specific Hif-1α deficiency. In addition, the SMC-specific Hif-1α deficiency suppressed Ang II-induced macrophage infiltration and Ang II-induced expression of inflammation-related genes in aortae. The superoxide production observed in the aortae of control mice with Ang II was suppressed in those of SMKO mice with Ang II, and this finding was consistent with the results of little Ang II-induced c-Src phosphorylation in SMKO mouse aortae. Loss- and gain-of-function analysis in in vitro experiments confirmed that VSMC-derived Hif-1α functions as an intrinsic modulator of vascular remodelling-related gene expression. Our results revealed that SMC-derived Hif-1α is a crucial mediator of Ang II-induced vascular remodelling. (Keyword) Angiotensin II / Animals / Fibrosis / Gene Expression Regulation / Hemodynamics / Hypoxia-Inducible Factor 1, alpha Subunit / Mice / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / phosphorylation / Superoxides / Vascular Remodeling (Tokushima University Institutional Repository) ● Metadata: 106145 (Link to Publication Site) ● Publication site (DOI): 10.1093/cvr/cvu061 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24623277 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901457818 (Tokushima University Institutional Repository: 106145, DOI: 10.1093/cvr/cvu061, PubMed: 24623277, Elsevier: Scopus)
52.	Yuko Imamura, Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : HIF-2α/ARNT complex regulates hair development via induction of p21Waf1/Cip1 and p27Kip1, The FASEB journal, Vol.28, No.6, 2517-2524, 2014. (Summary) The hypoxia-inducible factors HIF-1α or HIF-2α form heterodimeric complexes with the aryl hydrocarbon receptor nuclear translocator (ARNT). HIF-1α/ARNT and HIF-2α/ARNT complexes activate hypoxia-inducible genes that play critical roles in angiogenesis, anaerobic metabolism, and other processes in response to O2 deprivation. HIF-2α is known to regulate the function and/or differentiation of stem cells by activating the POU domain transcription factor Oct4; however, the precise underlying mechanism is unknown. This study examined the role of HIF-2α/ARNT in hair development using conditional-knockout mice, in which Arnt was specifically deleted in keratinocytes. In wild-type mice, HIF-2α and ARNT were highly expressed in the precortex above the hair matrix, an area containing differentiating stem cells. An analysis of hair size and type in these mice showed that loss of ARNT decreased the production of zigzag hairs, corresponding to reduced expression of HIF-2α and induction of the mammalian cyclin-dependent kinase inhibitors p21(Waf1/Cip1) and p27 (Kip1). The results suggest that the HIF-2α/ARNT complex regulates hair follicle differentiation via induction of p21(Waf1/Cip1) and possibly p27(Kip1), as p27(Kip1) expression was not altered in ARNT knockout mice. The findings provide insight into a possible mechanism underlying hair growth disorders and can be useful for future studies on hair follicle response to insults, such as chemotherapy and ionizing radiation.-Imamura, Y., Tomita, S., Imanishi, M., Kihira, Y., Ikeda, Y., Ishizawa, K., Tsuchiya, K., Tamaki, T. HIF-2α/ARNT complex regulates hair development via induction of p21(Waf1/Cip1) and p27(Kip1). (Keyword) Animals / Aryl Hydrocarbon Receptor Nuclear Translocator / Basic Helix-Loop-Helix Transcription Factors / cell differentiation / Cells, Cultured / Cyclin-Dependent Kinase Inhibitor p21 / Cyclin-Dependent Kinase Inhibitor p27 / Hair / Hair Follicle / Hypoxia-Inducible Factor 1, alpha Subunit / Keratinocytes / Mice / knockout mice (Link to Publication Site) ● Publication site (DOI): 10.1096/fj.13-244079 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24599965 ● Summary page in Scopus @ Elsevier: 2-s2.0-84901845393 (DOI: 10.1096/fj.13-244079, PubMed: 24599965, Elsevier: Scopus)
53.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yoji Hoshina, Kana Kato, Hitoshi Shirakawa, Hiroshi Sakaue, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Deletion of hypoxia-inducible factor-1α in adipocytes enhances glucagon-like peptide-1 secretion and reduces adipose tissue inflammation., PLoS ONE, Vol.9, No.4, e93856, 2014. (Summary) It is known that obese adipose tissues are hypoxic and express hypoxia-inducible factor (HIF)-1α. Although some studies have shown that the expression of HIF-1α in adipocytes induces glucose intolerance, the mechanisms are still not clear. In this study, we examined its effects on the development of type 2 diabetes by using adipocyte-specific HIF-1α knockout (ahKO) mice. ahKO mice showed improved glucose tolerance compared with wild type (WT) mice. Macrophage infiltration and mRNA levels of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor α (TNFα) were decreased in the epididymal adipose tissues of high fat diet induced obese ahKO mice. The results indicated that the obesity-induced adipose tissue inflammation was suppressed in ahKO mice. In addition, in the ahKO mice, serum insulin levels were increased under the free-feeding but not the fasting condition, indicating that postprandial insulin secretion was enhanced. Serum glucagon-like peptide-1 (GLP-1) levels were also increased in the ahKO mice. Interestingly, adiponectin, whose serum levels were increased in the obese ahKO mice compared with the obese WT mice, stimulated GLP-1 secretion from cultured intestinal L cells. Therefore, insulin secretion may have been enhanced through the adiponectin-GLP-1 pathway in the ahKO mice. Our results suggest that the deletion of HIF-1α in adipocytes improves glucose tolerance by enhancing insulin secretion through the GLP-1 pathway and by reducing macrophage infiltration and inflammation in adipose tissue. (Keyword) Adipocytes / Animals / Blotting, Western / Chemokine CCL2 / DNA Primers / Diabetes Mellitus, Type 2 / Gene Deletion / Glucagon-Like Peptide 1 / Glucose Tolerance Test / Hypoxia-Inducible Factor 1, alpha Subunit / Immunohistochemistry / Insulin / Mice / Mice, Knockout / Real-Time Polymerase Chain Reaction / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0093856 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705496 ● Summary page in Scopus @ Elsevier: 2-s2.0-84899440448 (DOI: 10.1371/journal.pone.0093856, PubMed: 24705496, Elsevier: Scopus)
54.	Yasumasa Ikeda, Iori Ozono, Soichro Tajima, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron chelation by deferoxamine prevents renal interstitial fibrosis in mice with unilateral ureteral obstruction, PLoS ONE, Vol.9, No.2, e89355, 2014. (Summary) Renal fibrosis plays an important role in the onset and progression of chronic kidney diseases (CKD). Although several mechanisms underlying renal fibrosis and candidate drugs for its treatment have been identified, the effect of iron chelator on renal fibrosis remains unclear. In the present study, we examined the effect of an iron chelator, deferoxamine (DFO), on renal fibrosis in mice with surgically induced unilateral ureter obstruction (UUO). Mice were divided into 4 groups: UUO with vehicle, UUO with DFO, sham with vehicle, and sham with DFO. One week after surgery, augmented renal tubulointerstitial fibrosis and the expression of collagen I, III, and IV increased in mice with UUO; these changes were suppressed by DFO treatment. Similarly, UUO-induced macrophage infiltration of renal interstitial tubules was reduced in UUO mice treated with DFO. UUO-induced expression of inflammatory cytokines and extracellular matrix proteins was abrogated by DFO treatment. DFO inhibited the activation of the transforming growth factor-β1 (TGF-β1)-Smad3 pathway in UUO mice. UUO-induced NADPH oxidase activity and p22(phox) expression were attenuated by DFO. In the kidneys of UUO mice, divalent metal transporter 1, ferroportin, and ferritin expression was higher and transferrin receptor expression was lower than in sham-operated mice. Increased renal iron content was observed in UUO mice, which was reduced by DFO treatment. These results suggest that iron reduction by DFO prevents renal tubulointerstitial fibrosis by regulating TGF-β-Smad signaling, oxidative stress, and inflammatory responses. (Tokushima University Institutional Repository) ● Metadata: 113752 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0089355 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24586712 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897786390 (Tokushima University Institutional Repository: 113752, DOI: 10.1371/journal.pone.0089355, PubMed: 24586712, Elsevier: Scopus)
55.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Noriko Yamano, Maki Urushihara, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Asami Nuno, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shoji Kagami, Hiroyuki Kobori, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of type 2 diabetic nephropathy by exerting antioxidative effects, PLoS ONE, Vol.9, No.1, e86335, 2014. (Summary) Diabetic nephropathy (DN) is the major cause of end-stage renal failure. Oxidative stress is implicated in the pathogenesis of DN. Nitrosonifedipine (NO-NIF) is a weak calcium channel blocker that is converted from nifedipine under light exposure. Recently, we reported that NO-NIF has potential as a novel antioxidant with radical scavenging abilities and has the capacity to treat vascular dysfunction by exerting an endothelial protective effect. In the present study, we extended these findings by evaluating the efficacy of NO-NIF against DN and by clarifying the mechanisms of its antioxidative effect. In a model of type 2 DN (established in KKAy mice), NO-NIF administration reduced albuminuria and proteinuria as well as glomerular expansion without affecting glucose metabolism or systolic blood pressure. NO-NIF also suppressed renal and systemic oxidative stress and decreased the expression of intercellular adhesion molecule (ICAM)-1, a marker of endothelial cell injury, in the glomeruli of the KKAy mice. Similarly, NO-NIF reduced albuminuria, oxidative stress, and ICAM-1 expression in endothelial nitric oxide synthase (eNOS) knockout mice. Moreover, NO-NIF suppressed urinary angiotensinogen (AGT) excretion and intrarenal AGT protein expression in proximal tubular cells in the KKAy mice. On the other hand, hyperglycemia-induced mitochondrial superoxide production was not attenuated by NO-NIF in cultured endothelial cells. These findings suggest that NO-NIF prevents the progression of type 2 DN associated with endothelial dysfunction through selective antioxidative effects. (Keyword) Animals / Antioxidants / Cell Line / Diabetic Nephropathies / Humans / Male / Mice / Mice, Inbred C57BL / knockout mice / Nifedipine / Nitric Oxide Synthase Type III / Nitroso Compounds / oxidative stress (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0086335 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24489716 ● Summary page in Scopus @ Elsevier: 2-s2.0-84900332178 (DOI: 10.1371/journal.pone.0086335, PubMed: 24489716, Elsevier: Scopus)
56.	Licht Miyamoto, Masashi Watanabe, Chiaki Taoka, Mai Kono, Yosuke Tomida, Tsuyoshi Matsushita, Masaki Kamiya, Hatsuhiko Hattori, Keisuke Ishizawa, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : A novel prodrug strategy for extremely hydrophobic agents; - Conjugation to symmetrically branched glycerol trimer improves pharmacological and pharmacokinetic properties of fenofibrate, Molecular Pharmaceutics, Vol.10, No.7, 2723-2729, 2013. (Summary) Management of a lipophilic-hydrophilic balance is a key element in drug design to achieve desirable pharmacokinetic characters. Therefore we have created unique modular molecules, symmetrically branched oligoglycerols (BGL), as an alternative way to endow hydrophobic molecules with sufficient hydrophilicity. We have successfully demonstrated amelioration of the water solubility and thermal stability of several hydrophobic agents by covalent conjugation to BGL so far. However, it has not been clarified whether the molecular modification by BGL also improves the pharmacological and/or pharmacokinetic properties indeed. Recently, we synthesized a novel BGL-prodrug derivative of fenofibrate, which is an antihyperlipidemic agent and one of the most hydrophobic medicinal compounds currently used clinically, by conjugating fenofibric acid to symmetrically branched glycerol trimer (BGL003), the simplest BGL. We have previously demonstrated that the hydrophilicity and water solubility of fenofibrate are improved more than 2000 times just by conjugation to the BGL003. To verify our hypothesis that the prodrug strategy with BGL should improve pharmacological efficacy and pharmacokinetic properties of extremely hydrophobic agents such as fenofibrate by the rise in hydrophilicity, we evaluated the BGL003-prodrug derivative of fenofibrate (FF-BGL) using rodent models. Here we demonstrate that the lipid-lowering effects of fenofibrate are much potentiated by chemical conjugation to BGL003 without exhibiting significant toxicity. Plasma concentration of fenofibric acid, an active metabolite of fenofibrate, after single oral administration of FF-BGL was more than 3 times higher than that of fenofibrate, in accordance. In fasting rats, plasma concentration of fenofibric acid after fenofibrate administration was curtailed into less than half of that in ad libitum-fed rats, while FF-BGL showed about the same plasma level even in the starving rats. This is the first report showing that BGL-prodrug improves pharmacological and pharmacokinetic properties as well as hydrophilicity of highly hydrophobic compounds. Furthermore, prodrug strategy using BGL suggests the possibility of diminishing the food-drug interaction effects, which should be advantageous for promoting drug compliance. BGL will be a suitable prodrug strategy to ameliorate physical, pharmacological, and pharmacokinetic characteristics of extremely hydrophobic compounds. (Link to Publication Site) ● Publication site (DOI): 10.1021/mp400133j (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23672178 ● Search Scopus @ Elsevier (PMID): 23672178 ● Search Scopus @ Elsevier (DOI): 10.1021/mp400133j (DOI: 10.1021/mp400133j, PubMed: 23672178)
57.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary iron restriction inhibits progression of diabetic nephropathy in db/db mice., American Journal of Physiology, Renal Physiology, Vol.304, No.7, F1028-F1036, 2013. (Summary) Excess iron causes oxidative stress through hydroxyl-radical production via Fenton/Haber-Weiss reactions. Recently, body iron reduction has been found to ameliorate diabetes. In the present study, we examined the protective effect of dietary iron restriction against diabetic nephropathy in the db/db mouse model of diabetic nephropathy using db/m mice as controls. The db/db mice were divided into 2 groups and fed a normal diet (ND) or a low iron diet (LID). Increasing urinary albumin excretion was observed in the ND db/db mice, but this was suppressed in db/db mice with LID. Histologically, the db/db mice in the ND group had increased glomerular volume and mesangial area compared to the LID group. Augmented deposition of extracellular matrices was decreased in db/db mice with LID. In terms of oxidative stress, increased superoxide production observed in the kidneys of the ND db/db mice was diminished in the LID group. NADPH oxidase activity and renal expression of NADPH oxidase components p22(phox) and NOX4 were augmented in the ND group, and this was abolished by LID. There were no differences in expression of renal iron importers, transferrin receptor, or divalent metal transporter-1 between db/m mice and db/db mice. The level of ferroportin, an iron exporter, increased in the kidneys of the db/db mice. Urinary iron excretion was significantly higher in ND db/db mice and was reduced in the LID group. These findings suggest that dietary iron restriction exerts a preventive effect on the progression of diabetic nephropathy partly due to the reduction of oxidative stress. (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00473.2012 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23389454 ● Search Scopus @ Elsevier (PMID): 23389454 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00473.2012 (DOI: 10.1152/ajprenal.00473.2012, PubMed: 23389454)
58.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Sumiko Yoshida, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine milk-derived lactoferrin exerts proangiogenic effects in an Src-Akt-eNOS-dependent manner in response to ischemia, Journal of Cardiovascular Pharmacology, Vol.61, No.5, 423-429, 2013. (Summary) Lactoferrin (LF) exerts a variety of biological effects, including the promotion of angiogenesis by increasing the expression of angiogenesis-related genes and reducing blood pressure via a nitric oxide-dependent mechanism. In this study, we investigated the effects of LF on angiogenesis using C57BL/6J mice that received daily unilateral treatment with or without bovine milk-derived LF (bLF) after unilateral hindlimb surgery. The analysis of laser speckle blood flow showed that bLF treatment promoted blood flow recovery in response to ischemic hindlimb. The capillary density of ischemic adductor muscles and the phosphorylation of Src, Akt, and endothelial nitric oxide synthase (eNOS) were also significantly higher in bLF-treated mice than in vehicle-treated mice. Furthermore, bLF increased the phosphorylation levels of Src, Akt, and eNOS in in vitro experiments using human aortic endothelial cells. The action of bLF on eNOS phosphorylation was abolished by both LY294002, a phosphatidylinositol 3-kinase inhibitor, and 4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo [3,4-d]pyrimidine (PP2), an Src inhibitor. Similarly, bLF-induced acceleration of tube formation, cell proliferation, and cell migration in human aortic endothelial cells were inhibited by LY294002 or PP2. Thus, bLF promotes vascular endothelial cell function via an Src Akt eNOS-dependent pathway, thereby contributing to revascularization in response to ischemia. (Keyword) Animals / Aorta / Cell Movement / Cell Proliferation / Cells, Cultured / Endothelial Cells / Endothelium, Vascular / Enzyme Activation / Hindlimb / Humans / Ischemia / Lactoferrin / Laser-Doppler Flowmetry / Mice / Mice, Inbred C57BL / Milk / Neovascularization, Physiologic / Nitric Oxide Synthase Type III / Phosphorylation / Proto-Oncogene Proteins c-akt / Reperfusion Injury / Signal Transduction / src-Family Kinases (Tokushima University Institutional Repository) ● Metadata: 113754 (Link to Publication Site) ● Publication site (DOI): 10.1097/FJC.0b013e318287d526 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23364610 ● Search Scopus @ Elsevier (PMID): 23364610 ● Search Scopus @ Elsevier (DOI): 10.1097/FJC.0b013e318287d526 (Tokushima University Institutional Repository: 113754, DOI: 10.1097/FJC.0b013e318287d526, PubMed: 23364610)
59.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuki Izawa-Ishizawa, Shoko Fujii, Erika Tominaga, Teppei Tsuneishi, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Ken-ichi Aihara, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects, Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.386, No.1, 29-39, 2013. (Summary) Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress. (Keyword) Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / calcium / Cell Movement / Cell Proliferation / Fibrosis / Male / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Nifedipine / Nitroso Compounds / oxidative stress / Rats / reactive oxygen species (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-012-0810-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23149861 ● Summary page in Scopus @ Elsevier: 2-s2.0-84872316103 (DOI: 10.1007/s00210-012-0810-7, PubMed: 23149861, Elsevier: Scopus)
60.	Licht Miyamoto, Masashi Watanabe, Yosuke Tomida, Mai Kono, Shoko Fujii, Tsuyoshi Matsushita, Hatsuhiko Hattori, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : Acute oral toxicity evaluation of symmetrically branched glycerol trimer in ddY mice, The Journal of Toxicological Sciences, Vol.37, No.6, 1253-1259, 2012. (Summary) Lipophilic-hydrophilic balance is a quite important determinant of pharmacokinetic properties of pharmaceuticals. Thus it is a key step to successfully manage lipophilic-hydrophilic balance in drug design. We have designed unique modular molecules, symmetrically branched oligoglycerols (BGL) as an alternative means to endow hydrophobic molecules with much hydrophilicity. We have succeeded in improving the water-solubility of several hydrophobic medicinal small molecules and thermal stability of artificial protein by covalent conjugation to BGL. We have also demonstrated that a representative BGL, symmetrically branched glycerol trimer (BGL003) does not exhibit significant cytotoxicity against human hepatocarcinoma HepG2 cells. However, there have been no reports suggesting whether BGL could be used in safety in vivo. Therefore, evaluation of acute oral toxicity of BGL003 in healthy mice was conducted. Here we demonstrate that an oral administration of BGL003 did not exhibit acute lethal toxicity up to 3,000 mg/kg. Body weight, food intake, blood glucose levels and weights of tissues were not affected by a short-term repetitive administration of increasing doses of BGL003. Biochemical indications related to hepatic disorders and tissue damage were unchanged, either. A single administration study revealed that 50% lethal dose of BGL003 should be more than 2,000 mg/kg. BGL003 will be safe and suitable approach to improve hydrophilicity of hydrophobic compounds. (Keyword) Hydrophilicity / Lipophilicity / Branched oligoglycerols / Acute oral toxicity / Mice (Link to Publication Site) ● Publication site (DOI): 10.2131/jts.37.1253 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23208440 ● CiNii @ National Institute of Informatics (CRID): 1390282679880737408 ● Search Scopus @ Elsevier (PMID): 23208440 ● Search Scopus @ Elsevier (DOI): 10.2131/jts.37.1253 (DOI: 10.2131/jts.37.1253, PubMed: 23208440, CiNii: 1390282679880737408)
61.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Licht Miyamoto, Shoko Fujii, Hironori Taira, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker improves tumor necrosis factor-α-induced cytotoxicity via antioxidative effect in human glomerular endothelial cells, Pharmacology, Vol.90, No.5-6, 324-331, 2012. (Summary) Tumor necrosis factor-α (TNF-α) is known to involve the progression of renal dysfunction through its cytotoxicity and proinflammatory effects such as the induction of intercellular adhesion molecule (ICAM)-1 expression in vascular endothelial cells (ECs). Olmesartan, one of the angiotensin II type 1 receptor blockers (ARBs), has been reported to show protective effects on injured ECs by some causal factors of renal disorder other than angiotensin II. However, the effects of olmesartan on TNF-α-induced glomerular EC damage have not been investigated. In the present study, we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Cultured HGECs were stimulated by TNF-α, and then cell viability and cytotoxicity were measured by MTT assay and lactate dehydrogenase release assay, respectively. TNF-α-induced oxidative stress was estimated by dihydroethidium assay and lucigenin chemiluminescence assay. ICAM-1 expression and the phosphorylations of mitogen-activated protein kinases were measured using Western blotting assay. RNH-6270 suppressed cell death and the increase in ICAM-1 expression induced by TNF-α via the inhibition of reactive oxygen species in HGECs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction. (Keyword) Angiotensin II Type 1 Receptor Blockers / apoptosis / Cell Survival / Cells, Cultured / Endothelial Cells / Humans / Imidazoles / Intercellular Adhesion Molecule-1 / Kidney Glomerulus / reactive oxygen species / Tetrazoles / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1159/000343244 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23052181 ● Summary page in Scopus @ Elsevier: 2-s2.0-84867214872 (DOI: 10.1159/000343244, PubMed: 23052181, Elsevier: Scopus)
62.	Licht Miyamoto, Masashi Watanabe, Mai Kono, Tsuyoshi Matsushita, Hatsuhiko Hattori, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : Cytotoxicity evaluation of symmetrically branched glycerol trimer in human hepatocellular carcinoma HepG2 cells, The Journal of Toxicological Sciences, Vol.37, No.5, 1059-1063, 2012. (Keyword) Hydrophilicity / Lipophilicity / Cytotoxicity / Branched oligoglycerols / HepG2 / Fenofibrate (Link to Publication Site) ● Publication site (DOI): 10.2131/jts.37.1059 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23038013 ● CiNii @ National Institute of Informatics (CRID): 1390282679882410752 ● Search Scopus @ Elsevier (PMID): 23038013 ● Search Scopus @ Elsevier (DOI): 10.2131/jts.37.1059 (DOI: 10.2131/jts.37.1059, PubMed: 23038013, CiNii: 1390282679882410752)
63.	Yasumasa Ikeda, Ken-ichi Aihara, Sumiko Yoshida, Takashi Iwase, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya, Masataka Sata, Masashi Akaike, Shigeaki Kato, Toshio Matsumoto and Toshiaki Tamaki : Heparin cofactor II, a serine protease inhibitor, promotes angiogenesis via activation of the AMP-activated protein kinase-endothelial nitric-oxide synthase signaling pathway, The Journal of Biological Chemistry, Vol.287, No.41, 34256-34263, 2012. (Summary) We previously clarified that heparin cofactor II (HCII), a serine proteinase inhibitor, exerts various protective actions on cardiovascular diseases in both experimental and clinical studies. In the present study, we aimed to clarify whether HCII participates in the regulation of angiogenesis. Male heterozygous HCII-deficient (HCII(+/-)) mice and male littermate wild-type (HCII(+/+)) mice at the age of 12-16 weeks were subjected to unilateral hindlimb ligation surgery. Laser speckle blood flow analysis showed that blood flow recovery in response to hindlimb ischemia was delayed in HCII(+/-) mice compared with that in HCII(+/+) mice. Capillary number, arteriole number, and endothelial nitric-oxide synthase (eNOS), AMP-activated protein kinase (AMPK), and liver kinase B1 (LKB1) phosphorylation in ischemic muscles were decreased in HCII(+/-) mice. Human purified HCII (h-HCII) administration almost restored blood flow recovery, capillary density, and arteriole number as well as phosphorylation levels of eNOS, AMPK, and LKB1 in ischemic muscles of HCII(+/-) mice. Although treatment with h-HCII increased phosphorylation levels of eNOS, AMPK, and LKB1 in human aortic endothelial cells (HAECs), the h-HCII-induced eNOS phosphorylation was abolished by compound C, an AMPK inhibitor, and by AMPK siRNA. In a similar fashion, tube formation, proliferation, and migration of HAECs were also promoted by h-HCII treatment and were abrogated by pretreatment with compound C. HCII potentiates the activation of vascular endothelial cells and the promotion of angiogenesis in response to hindlimb ischemia via an AMPK-eNOS signaling pathway. These findings suggest that HCII is a novel therapeutic target for treatment of patients with peripheral circulation insufficiency. (Keyword) Heparin cofactor II (HCII) / vascular endothelial cells / angiogenesis (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M112.353532 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22904320 ● Search Scopus @ Elsevier (PMID): 22904320 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M112.353532 (DOI: 10.1074/jbc.M112.353532, PubMed: 22904320)
64.	Hisao Nemoto, Masaki Kamiya, Aki Nakamoto, Tsuyoshi Matsushita, Kosuke Matsumura, Hatsuhiko Hattori, Tomoyuki Kawamura, Chiaki Taoka, Shinji Abe, Keisuke Ishizawa, Licht Miyamoto and Koichiro Tsuchiya : Synthesis of highly water-soluble fibrate derivatives via BGLation, Bioorganic & Medicinal Chemistry Letters, Vol.22, No.20, 6425-6428, 2012. (Summary) Three water-soluble fibrates (fenofibrate, bezafibrate and chlofibrate) conjugated with a symmetrically branched glyceryl trimer (BGL003) were synthesized, and an evaluation of the fenofibrate-BGL003 conjugate as a candidate for anti-hyperlipemia drug was carried out using rats. The water-solubility of the fenofibrate-BGL003 conjugate was several thousand times greater than that of the original fenofibrate. The lipid-lowering effects of the fenofibrate-BGL003 conjugate were as strong as those of the same grams of fenofibrate. The actual active species of fenofibrate, fenofibric acid, was detected in rats' blood, but neither the fenofibrate-BGL003 conjugate nor fenofibrate was detected, probably due to enzymatic hydrolysis of the ester bond. The plasma concentration of fenofibric acid derived from the fenofibrate-BGL003 conjugate was five times higher than that derived from fenofibrate 4h after administration. (Keyword) Animals / Bezafibrate / Clofibrate / Fenofibrate / Hypolipidemic Agents / Male / Rats / Rats, Sprague-Dawley / Solubility / Triglycerides / Water (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmcl.2012.08.057 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22975299 ● Search Scopus @ Elsevier (PMID): 22975299 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmcl.2012.08.057 (DOI: 10.1016/j.bmcl.2012.08.057, PubMed: 22975299)
65.	Hisao Nemoto, Ayato Katagiri, Masaki Kamiya, Tomoyuki Kawamura, Tsuyoshi Matsushita, Kosuke Matsumura, Tomohiro Itou, Hatsuhiko Hattori, Miho Tamaki, Keisuke Ishizawa, Licht Miyamoto, Shinji Abe and Koichiro Tsuchiya : Synthesis of paclitaxel-BGL conjugates, Bioorganic & Medicinal Chemistry, Vol.20, No.18, 5559-5567, 2012. (Summary) Four kinds of symmetrically branched oligoglyceryl trimeric (BGL003)-paclitaxel conjugates and a corresponding heptameric (BGL007) conjugate were synthesized. Molecular weights of all the compounds were less than two times that of paclitaxel. The anti-tumor activity of the most water-soluble BGL003 conjugate was examined and found to be preserved in spite of the chemical modification that is displacement of the N3'-debenzoyl residue with the BGL003 succinyl residue. (Keyword) Animals / Antineoplastic Agents, Phytogenic / Cell Line, Tumor / Dose-Response Relationship, Drug / Glycerol / Humans / Male / Mice / Mice, Inbred BALB C / Mice, Nude / Molecular Conformation / Molecular Weight / Neoplasms, Experimental / Paclitaxel / Solubility / Structure-Activity Relationship / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bmc.2012.07.031 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22892212 ● Search Scopus @ Elsevier (PMID): 22892212 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bmc.2012.07.031 (DOI: 10.1016/j.bmc.2012.07.031, PubMed: 22892212)
66.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Estrogen regulates hepcidin expression via GPR30-BMP6-dependent signaling in hepatocytes, PLoS ONE, Vol.7, No.7, e40465, 2012. (Summary) Hepcidin, a liver-derived iron regulatory protein, plays a crucial role in iron metabolism. It is known that gender differences exist with respect to iron storage in the body; however, the effects of sex steroid hormones on iron metabolism are not completely understood. We focused on the effects of the female sex hormone estrogen on hepcidin expression. First, ovariectomized (OVX) and sham-operated mice were employed to investigate the effects of estrogen on hepcidin expression in an in vivo study. Hepcidin expression was decreased in the livers of OVX mice compared to the sham-operated mice. In OVX mice, bone morphologic protein-6 (BMP6), a regulator of hepcidin, was also found to be downregulated in the liver, whereas ferroportin (FPN), an iron export protein, was upregulated in the duodenum. Both serum and liver iron concentrations were elevated in OVX mice relative to their concentrations in sham-operated mice. In in vitro studies, 17β-estradiol (E(2)) increased the mRNA expression of hepcidin in HepG2 cells in a concentration-dependent manner. E(2)-induced hepatic hepcidin upregulation was not inhibited by ICI 182720, an inhibitor of the estrogen receptor; instead, hepcidin expression was increased by ICI 182720. E(2) and ICI 182720 exhibit agonist actions with G-protein coupled receptor 30 (GPR30), the 7-transmembrane estrogen receptor. G1, a GPR30 agonist, upregulated hepcidin expression, and GPR30 siRNA treatment abolished E(2)-induced hepcidin expression. BMP6 expression induced by E(2) was abolished by GPR30 silencing. Finally, both E(2) and G1 supplementation restored reduced hepatic hepcidin and BMP6 expression and reversed the augmentation of duodenal FPN expression in the OVX mice. In contrast, serum hepcidin was elevated in OVX mice, which was reversed in these mice with E(2) and G1. Thus, estrogen is involved in hepcidin expression via a GPR30-BMP6-dependent mechanism, providing new insight into the role of estrogen in iron metabolism. (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0040465 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22792339 ● Summary page in Scopus @ Elsevier: 2-s2.0-84863827034 (DOI: 10.1371/journal.pone.0040465, PubMed: 22792339, Elsevier: Scopus)
67.	Akira Shigenaga, Keiji Ogura, Hiroko Hirakawa, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Development of a reduction-responsive amino acid that induces peptide bond cleavage in hypoxic cells, ChemBioChem, Vol.13, 968-971, 2012. (Summary) Hypoxia-responsive amino acids are indispensable in the preparation of hypoxic tumor-specific peptidyl prodrugs. In this paper, the design and synthesis of a reduction-responsive amino acid that induces peptide bond cleavage after reduction of the nitro group are described. Application to hypoxia-responsive peptide bond cleavage system is also reported. (Keyword) Amides / Amino Acids / Cell Hypoxia / Fluorescence Resonance Energy Transfer / Molecular Structure / Oxidation-Reduction / Peptides / Prodrugs (Tokushima University Institutional Repository) ● Metadata: 111913 (Link to Publication Site) ● Publication site (DOI): 10.1002/cbic.201200141 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22505188 ● Search Scopus @ Elsevier (PMID): 22505188 ● Search Scopus @ Elsevier (DOI): 10.1002/cbic.201200141 (Tokushima University Institutional Repository: 111913, DOI: 10.1002/cbic.201200141, PubMed: 22505188)
68.	Soichiro Tajima, Yasumasa Ikeda, Kaori Sawada, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice., American Journal of Physiology, Endocrinology and Metabolism, Vol.302, No.1, E77-86, 2012. (Summary) Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity. (Keyword) ferrum / oxidative stress / obesity (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00033.2011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21917632 ● Search Scopus @ Elsevier (PMID): 21917632 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00033.2011 (DOI: 10.1152/ajpendo.00033.2011, PubMed: 21917632)
69.	Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Basic fibroblast growth factor regulates glucose metabolism through glucose transporter 1 induced by hypoxia-inducible factor-1α in adipocytes, The International Journal of Biochemistry & Cell Biology, Vol.43, No.11, 1602-1611, 2011. (Summary) Hypoxia-inducible factor-1 (HIF-1), which is a transcription factor that enhances glycolysis in cells in response to hypoxia, is induced in hypertrophied adipocytes in obesity. Recent studies have shown that growth factors are able to induce HIF-1 by mechanisms independent of hypoxia. Since basic fibroblast growth factor (bFGF), an angiogenic factor, is concentrated in expanding adipose tissue, the possible effects of bFGF on regulation of HIF-1 in adipocytes were investigated. Treatment of differentiated 3T3-L1 adipocytes with bFGF induced HIF-1. Concomitantly, glucose transporter 1 (GLUT1), which is a target gene of HIF-1, was induced at both mRNA and protein levels and was translocated to the plasma membrane. A chromatin immunoprecipitation assay and an RNA interference study indicated that bFGF-induced HIF-1 directly upregulates GLUT1. In addition, it was observed that bFGF increases lactate production of adipocytes. This result indicates that bFGF reprograms the metabolism toward glycolysis. Intraperitoneal injection of bFGF into mice upregulated HIF-1 and GLUT1 in adipose tissues, suggesting that bFGF regulates the metabolism of adipocytes via HIF-1-GLUT1 regulation in vivo. We also found that bFGF inhibits insulin-induced phosphorylation of insulin receptor substrate-1 and Akt, suggesting that bFGF attenuates the insulin signal in adipocytes. Taken together, the findings suggest that bFGF has a harmful effect on the development of type 2 diabetes through metabolism reprogramming and attenuation of the insulin signal. (Keyword) 3T3-L1 Cells / Adipocytes / Animals / Anoxia / Diabetes Mellitus, Type 2 / Fibroblast Growth Factor 2 / Glucose / Glucose Transporter Type 1 / Glycolysis / Hypoxia-Inducible Factor 1, alpha Subunit / Injections, Intraperitoneal / Insulin / Insulin Receptor Substrate Proteins / Male / Mice / Obesity / Phosphorylation / Proto-Oncogene Proteins c-akt / Signal Transduction / Transcriptional Activation / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biocel.2011.07.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21810481 ● Search Scopus @ Elsevier (PMID): 21810481 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biocel.2011.07.009 (DOI: 10.1016/j.biocel.2011.07.009, PubMed: 21810481)
70.	Shuhei Tomita, Yoshitaka Kihira, Masaki Imanishi, Yayoi Fukuhara, Yuko Imamura, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Pathophysiological Response to Hypoxia From the Molecular Mechanisms of Malady to Drug Discovery: Inflammatory Responses of Hypoxia-Inducible Factor 1 (HIF-1) in T Cells Observed in Development of Vascular Remodeling, Journal of Pharmacological Sciences, Vol.115, No.4, 433-439, 2011. (Summary) Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor 1 (HIF-1). Impairment of HIF-1-dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif-1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF-1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF-1α. (Keyword) Animals / Anoxia / Drug Discovery / Humans / Hypoxia-Inducible Factor 1, alpha Subunit / Immunity, Cellular / Reperfusion Injury / T lymphocytes / Vasculitis (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R22FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21422726 ● Summary page in Scopus @ Elsevier: 2-s2.0-79955046642 (DOI: 10.1254/jphs.10R22FM, PubMed: 21422726, Elsevier: Scopus)
71.	Keisuke Ishizawa, Masanori Yoshizumi, Yoshichika Kawai, Junji Terao, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Pharmacology in health food: Metabolism of quercetin in vivo and its protective effect against arteriosclerosis, Journal of Pharmacological Sciences, Vol.115, No.4, 466-470, 2011. (Summary) Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor-induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II-induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders. (Keyword) Animals / Antioxidants / Arteriosclerosis / Cell Movement / Cell Proliferation / Drug Evaluation, Preclinical / Free Radicals / Health Food / Humans / Hypertrophy / Muscle, Smooth, Vascular / Quercetin / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R38FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21436601 ● Search Scopus @ Elsevier (PMID): 21436601 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.10R38FM (DOI: 10.1254/jphs.10R38FM, PubMed: 21436601)
72.	Yuya Horinouchi, Koichiro Tsuchiya, Chiaki Taoka, Soichiro Tajima, Yoshitaka Kihira, Yuko Matsuda, Kozo Shishido, Masahiro Yoshida, Shuichi Hamano, Kazuyoshi Kawazoe, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : Antioxidant effects of photodegradation product of nifedipine, Chemical & Pharmaceutical Bulletin, Vol.59, No.2, 208-214, 2011. (Summary) Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nifedipine is unstable under light and reportedly decomposes to a stable nitrosonifedipine (NO-NIF). NO-NIF has no antihypertensive effect, and it has been recognized as a contaminant of nifedipine. The present study for the first time demonstrated that NO-NIF changed to a NO-NIF radical in a time-dependent manner when it interacted with human umbilical vein endothelial cells (HUVECs). The electron paramagnetic resonance (EPR) signal of NO-NIF radicals in HUVECs showed an asymmetric pattern suggesting that the radicals were located in the membrane. The NO-NIF radicals had radical scavenging activity for 1,1-diphenyl-2-picrylhydrazyl, whereas neither NO-NIF nor nifedipine did. In addition, the NO-NIF radical more effectively quenched lipid peroxides than NO-NIF or nifedipine. Furthermore, NO-NIF attenuated the superoxide-derived free radicals in HUVECs stimulated with LY83583, and suppressed iron-nitrilotriacetic acid (Fe-NTA)-induced cytotoxicity in rat pheochromocytoma (PC12) cells. Our findings suggest that NO-NIF is a candidate for a new class of antioxidative drugs that protect cells against oxidative stress. (Keyword) Animals / Antioxidants / Cells, Cultured / Endothelial Cells / Humans / Nifedipine / PC12 Cells / Photolysis / Rats (Link to Publication Site) ● Publication site (DOI): 10.1248/cpb.59.208 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21297301 ● Summary page in Scopus @ Elsevier: 2-s2.0-79551489998 (DOI: 10.1248/cpb.59.208, PubMed: 21297301, Elsevier: Scopus)
73.	Yayoi Fukuhara, Koichiro Tsuchiya, Yuya Horinouchi, Soichiro Tajima, Yoshitaka Kihira, Shuichi Hamano, Kazuyoshi Kawazoe, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita and Toshiaki Tamaki : Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells, The Journal of Medical Investigation : JMI, Vol.58, No.1, 2, 118-126, 2011. (Summary) Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF has been recognized as a contaminant of nifedipine because it has no antihypertensive effect. Treatment of tumor necrosis factor-α (TNF-α) suppressed the cell viability and facilitated the expression of Inter-Cellular Adhesion Molecule 1(ICAM-1) in human glomerular endothelial cells (HGECs) though, pretreatment of NO-NIF significantly recovered the TNF-α-induced cell damage to the same extent as Trolox-C did, and suppressed the ICAM-1 expression in a concentration dependent manner. In addition, NO-NIF inhibited the cell toxicity induced by cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, as effective as Trolox-c. These data suggest that NO-NIF is a candidate for a new class of antioxidative drug that protect cells against oxidative stress in glomerular endothelial cells. (Keyword) Antioxidants / Benzene Derivatives / Cell Survival / Cells, Cultured / Endothelial Cells / Humans / Intercellular Adhesion Molecule-1 / Kidney Glomerulus / Nifedipine / Nitroso Compounds / oxidative stress / Tumor Necrosis Factor-alpha (Tokushima University Institutional Repository) ● Metadata: 72667 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.58.118 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21372496 ● CiNii @ National Institute of Informatics (CRID): 1390001204242892288 ● Search Scopus @ Elsevier (PMID): 21372496 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.118 (Tokushima University Institutional Repository: 72667, DOI: 10.2152/jmi.58.118, PubMed: 21372496, CiNii: 1390001204242892288)
74.	Yasumasa Ikeda, Soichiro Tajima, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine promotes angiogenesis via the activation of vascular endothelial cell function., Atherosclerosis, Vol.215, No.2, 339-347, 2011. (Summary) BACKGROUND: Deferoxamine (DFO), an iron chelator for disorders of excess iron, upregulates the expression of angiogenic factors, such as vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2), indicating that it affects angiogenesis. Herein, we clarify the effect and mechanism of action of DFO on angiogenesis. METHODS AND RESULTS: In an in vitro study, DFO increased endothelial nitric oxide synthesis (eNOS) phosphorylation in human aortic endothelial cells (HAECs), which were inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002. Tube formation, cell proliferation, and cell migration in HAECs were promoted by DFO, which were significantly reduced by LY294002. In an in vivo study, DFO promoted blood flow recovery in response to the hindlimb ischemia in mice with unilateral hindlimb surgery. The density of capillaries and arterioles in ischemic muscle was higher in DFO-treated mice compared to vehicle-treated mice. Endothelial cell proliferation increased and oxidative stress and apoptosis decreased in ischemic muscles of DFO-treated mice. The phosphorylation of Akt and eNOS on the ischemic side was elevated and urinary nitric oxide/nitric dioxide (NOx) excretion was higher in DFO-treated mice compared to vehicle-treated mice. The effect of DFO on angiogenesis was abolished in eNOS-deficient mice with hindlimb ischemia. CONCLUSION: These findings indicate that DFO promotes revascularization via the activation of vascular endothelial cell function by an Akt-eNOS-dependent mechanism. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2011.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21315355 ● Search Scopus @ Elsevier (PMID): 21315355 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2011.01.009 (DOI: 10.1016/j.atherosclerosis.2011.01.009, PubMed: 21315355)
75.	Hiroaki Yanagawa, Junji Terao, Eiji Takeda, Yoshihisa Takaishi, Yoshiki Kashiwada, Kazuyoshi Kawazoe, Fushitani Shuji, Koichiro Tsuchiya, Aiko Yamauchi, Sato Chiho and Minoru Irahara : Consultation clinics for complementary and alternative medicine at Japanese university hospitals: An analysis at Tokushima University Hospital, Experimental and Therapeutic Medicine, Vol.1, No.3, 481-483, 2010. (Summary) Here, we report on a Consultation Clinic for Complementary and Alternative Medicine (CAM) which we established at Tokushima University Hospital in July of 2007 with the aim of providing person-to-person information on CAM, though not CAM therapy itself. In December of 2008, we received 55 applications for consultation, 37% concerning health foods, 37% Japanese herbal medicine (Kampo), and 26% various other topics. The consultants (nutritionists and pharmacists) communicated individually with 38 applicants; malignancies (26%) and cardiovascular disease (24%) were the main underlying concerns. To promote the quality of consultation, data was collected by means of focus group interviews concerning the perspective of the consultants. Safe and effective use of CAM requires a network of communication linking individuals, consultation teams, physicians, primary care institutions and university hospitals. To advance this goal, we plan to broaden the efforts described herein. Our findings indicate that the specific role of the consultation clinic in promoting the scientific use of CAM merits further study. (Link to Publication Site) ● Publication site (DOI): 10.3892/etm_00000075 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22993564 ● Search Scopus @ Elsevier (PMID): 22993564 ● Search Scopus @ Elsevier (DOI): 10.3892/etm_00000075 (DOI: 10.3892/etm_00000075, PubMed: 22993564)
76.	Soichiro Tajima, Koichiro Tsuchiya, Yuya Horinouchi, Keisuke Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Masayuki Shono, Kazuyoshi Kawazoe, Shuhei Tomita and Toshiaki Tamaki : Effect of angiotensin II on iron-transporting protein expression and subsequent intracellular labile iron concentration in human glomerular endothelial cells, Hypertension Research, Vol.33, No.7, 713-721, 2010. (Summary) Angiotensin II (Ang II)-induced endothelial injury, which is associated with atherosclerosis, is believed to be mediated by intracellular reactive oxygen species (ROS) through stimulation of nicotinamide adenine dinucleotide phosphate oxidase (NOX). Iron is essential for the amplification of oxidative stress. In this study, we investigated whether Ang II altered iron metabolism and whether the Ang II-induced endothelial injury is attributable to changes in iron metabolism of human glomerular endothelial cells (HGECs). When 90% iron-saturated human transferrin (90% Tf) was applied to HGECs without Ang II, the labile ferrous iron level was same as the effect of control in spite of a significant increase in the total cellular iron concentration. Treatment with Ang II and 30% Tf or 90% Tf significantly (P<0.01) increased the intracellular iron concentration, as well as labile ferrous iron and protein oxidation levels, compared with the effect of separate administration of each compound. Ang II treatment facilitated the protein expression of the Tf receptor, divalent metal transporter 1, and ferroportin 1 in a dose- and time-dependent manner. It was also found that simultaneous exposure of HGECs to Ang II and 90% Tf accelerated hydroxyl radical production, as shown by using an electron paramagnetic resonance spectrometer. These results suggest that Ang II not only induces production of ROS by NOX activation but also iron incorporation followed by an increase in labile iron in HGECs. Both of these events may participate in the progression of oxidative stress because of endothelial cell dysfunction through ferrous iron-mediated ROS generation. (Keyword) Angiotensin II / Cation Transport Proteins / Endothelial Cells / Humans / Hydroxyl Radical / Iron / Kidney Glomerulus / oxidation and reduction / Receptors, Transferrin / Transferrin (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2010.63 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20431588 ● Summary page in Scopus @ Elsevier: 2-s2.0-77954369377 (DOI: 10.1038/hr.2010.63, PubMed: 20431588, Elsevier: Scopus)
77.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Narantungalag Dorjsuren, Erika Miki, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Kazuyoshi Kawazoe, Kazuo Minakuchi, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner, Nephrology, Dialysis, Transplantation, Vol.25, No.2, 364-372, 2010. (Summary) Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Cell Movement / Cells, Cultured / Imidazoles / Male / Mesangial Cells / Platelet-Derived Growth Factor / Rats / Rats, Sprague-Dawley / Signal Transduction / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfp520 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19812233 ● Search Scopus @ Elsevier (PMID): 19812233 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfp520 (DOI: 10.1093/ndt/gfp520, PubMed: 19812233)
78.	Koichiro Tsuchiya, Shuhei Tomita, Keisuke Ishizawa, Shinji Abe, Yasumasa Ikeda, Yoshitaka Kihira and Toshiaki Tamaki : Dietary nitrite ameliorates renal injury in l-NAME-induced hypertensive rats, Nitric Oxide: Biology and Chemistry, Vol.22, No.2, 98-103, 2010. (Summary) Nitric oxide (NO) has numerous important functions in the kidney, and long-term blockage of nitric oxide synthases in rats by L-NAME results in severe hypertension and progressive kidney damage. On the other hand, NO production seems to be low in patients with chronic kidney disease (CKD), and NO deficiency may play a role in CKD progression. In this review, we summarized the mechanisms of amelioration of renal injury induced by L-NAME treated rats by treatment of nitrite. First, we demonstrate whether orally-administrated nitrite-derived NO can shift to the circulation. When 3mg/kg body weight Na(15)NO(2) was orally administered to rats, an apparent EPR signal derived from Hb(15)NO (A(z)=23.4 gauss) appeared in the blood, indicating that orally ingested nitrite can be a source of NO in vivo. Next, in order to clarify the capacity of nitrite to prevent renal disease, we administered low-dose nitrite (LDN: 0.1mg of sodium nitrite in 1L of drinking water), medium-dose nitrite (MDN: 1mg sodium nitrite/L, which corresponds to the amount of nitrite ingested by vegetarians), or high-dose nitrite (HDN: 10mg sodium nitrite/L) to rats simultaneously with L-NAME (1 g l-NAME/L) for 8 weeks, then examined the blood NO level as a hemoglobin-NO adduct (iron-nitrosyl-hemoglobin) using electron paramagnetic resonance spectroscopy, urinary protein excretion, and renal histological changes at the end of the experiment. It was found that oral administration of MDN and HDN but not LDN increased the blood iron-nitrosyl-hemoglobin concentration to the normal level, ameliorated the L-NAME-induced proteinuria, and reduced renal histological damage. The findings demonstrate that chronic administration of a mid-level dietary dose of nitrite restores the circulating iron-nitrosyl-hemoglobin levels reduced by L-NAME and that maintenance of the circulating iron-nitrosyl-hemoglobin level in a controlled range protects against L-NAME-induced renal injury. Taking these findings together, we propose that dietary supplementation of nitrite is a potentially useful nonpharmacological strategy for maintaining circulating NO level in order to prevent or slow the progression of renal disease. It had been believed that nitrite could result in intragastric formation of nitrosamines, which had been linked to esophageal and other gastrointestinal cancers. However, there is no positive association between the intake of nitrate or nitrite and gastric and pancreatic cancer by recent researches. Furthermore, nitrate-derived NO formation pathway is a possible mechanism for the hypotensive effect of vegetable- and fruit-rich diets, which may explain, at least in part, the mechanism of the Dietary Approach to Stop Hypertension (DASH) diet-induced hypotensive and organ-protective effects. Further research is needed to investigate the interaction between nitrite-nitrate intakes and human health. (Keyword) Animals / Diet / Hypertension / Kidney Diseases / NG-Nitroarginine Methyl Ester / Rats / Sodium Nitrite (Link to Publication Site) ● Publication site (DOI): 10.1016/j.niox.2009.12.002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20005970 ● Search Scopus @ Elsevier (PMID): 20005970 ● Search Scopus @ Elsevier (DOI): 10.1016/j.niox.2009.12.002 (DOI: 10.1016/j.niox.2009.12.002, PubMed: 20005970)
79.	Keisuke Ishizawa, Narantungalag Dorjsuren, Yuki Izawa-Ishizawa, Rika Sugimoto, Yasumasa Ikeda, Yoshitaka Kihira, Kazuyoshi Kawazoe, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration, The Journal of Endocrinology, Vol.202, No.2, 309-316, 2009. (Summary) Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders. (Keyword) Adiponectin / Animals / Cell Movement / Cells, Cultured / Dose-Response Relationship, Drug / Enzyme Inhibitors / Glomerular Mesangium / Imidazoles / Male / Mitogen-Activated Protein Kinase 7 / Phosphorylation / Platelet-Derived Growth Factor / Pyridines / RNA, Small Interfering / Rats / Rats, Sprague-Dawley / Recombinant Proteins / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1677/JOE-08-0469 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19460854 ● Search Scopus @ Elsevier (PMID): 19460854 ● Search Scopus @ Elsevier (DOI): 10.1677/JOE-08-0469 (DOI: 10.1677/JOE-08-0469, PubMed: 19460854)
80.	Yuki Motobayashi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Orino, Kunihisa Yamaguchi, Kazuyoshi Kawazoe, Shuichi Hamano, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Adiponectin inhibits insulin-like growth factor-1-induced cell migration by the suppression of extracellular signal-regulated kinase 1/2 activation, but not Akt in vascular smooth muscle cells, Hypertension Research, Vol.32, No.3, 188-193, 2009. (Summary) Adiponectin, an adipocyte-derived hormone, has been proposed to show antiatherogenic properties through the inhibitory effects against various growth factors. Insulin-like growth factor-1 (IGF-1) is one of the potent mitogens, which has been considered to play important roles in both atherogenesis and plaque stabilization in accordance to the phase of atherosclerosis. The aim of this study is to elucidate the adiponectin effects on IGF-1-induced cell migration and its intracellular signaling pathways in vascular smooth muscle cells (VSMCs). In this study, we assessed cell migration and several kinase activities in cultured rat aortic smooth muscle cells (RASMCs). Adiponectin pretreatment suppressed IGF-1-induced cell migration and extracellular signal-regulated kinase (ERK)1/2 activation, which is one of the major mediators for IGF-1-induced cell migration. In RASMCs, adiponectin and 5-aminoimidazole-4-carboxamide riboside (AICAR), a 5'-AMP-activated protein kinase (AMPK) activator, stimulated AMPK activation. AMPK activation by AICAR inhibited IGF-1-induced ERK1/2 activation and cell migration in RASMCs. On the other hand, phosphorylation of Akt and Bad, proapoptotic molecules of the Bcl-2 family, which were increased by IGF-1 stimulation, was not diminished by the pretreatment with adiponectin. It was shown that adiponectin inhibited IGF-1-induced VSMC migration through suppression of ERK1/2 activation, which might be implicated in AMPK activation. Furthermore, adiponectin selectively inhibited ERK1/2 pathway, not Akt-Bad pathway, stimulated by IGF-1. From these findings, it was implied that adiponectin suppressed IGF-1-induced VSMC migration and its signaling selectivity. (Keyword) Adiponectin / Aminoimidazole Carboxamide / Animals / Blotting, Western / Cell Movement / Enzyme Activation / Enzyme Activators / Insulin-Like Growth Factor I / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Myocytes, Smooth Muscle / Oncogene Protein v-akt / Phosphorylation / Rats / Rats, Sprague-Dawley / Ribonucleotides / signal transduction / bcl-Associated Death Protein / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1038/hr.2008.19 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19262481 ● Search Scopus @ Elsevier (PMID): 19262481 ● Search Scopus @ Elsevier (DOI): 10.1038/hr.2008.19 (DOI: 10.1038/hr.2008.19, PubMed: 19262481)
81.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Sachiyo Ohnishi, Yuki Motobayashi, Kazuyoshi Kawazoe, Shuichi Hamano, Koichiro Tsuchiya, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells, Journal of Pharmacological Sciences, Vol.109, No.2, 257-264, 2009. (Summary) Many epidemiologic studies have reported that dietary flavonoids provide protection against cardiovascular disease. Quercetin, a member of the bioflavonoids family, has been proposed to have anti-inflammatory, anti-atherogenic, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. Recent studies demonstrated that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore, we examined the effect of chemically synthesized quercetin glucuronide on platelet-derived growth factor (PDGF)-induced cell migration and kinase activation in cultured rat aortic smooth muscle cells (RASMCs). PDGF-induced RASMC migration was inhibited by quercetin 3-O-beta-D-glucuronide (Q3GA). Q3GA also attenuated PDGF-induced cell proliferation in RASMCs. PDGF activated extracellular-signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and Akt in RASMCs. PDGF-induced JNK and Akt activations were suppressed by Q3GA, whereas ERK1/2 and p38 MAP kinase activations were not affected. We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may possess preventing effects for cardiovascular diseases relevant to vascular smooth muscle cell disorders. (Keyword) Animals / Antioxidants / Cell Movement / Cell Proliferation / Cells, Cultured / Glucuronides / MAP Kinase Kinase 4 / Male / Muscle, Smooth, Vascular / Platelet-Derived Growth Factor / Quercetin / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.08236FP (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19202317 ● Search Scopus @ Elsevier (PMID): 19202317 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.08236FP (DOI: 10.1254/jphs.08236FP, PubMed: 19202317)
82.	Keisuke Ishizawa, Kunihisa Yamaguchi, Yuya Horinouchi, Yayoi Fukuhara, Soichiro Tajima, Shuichi Hamano, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Toward drug discovery for overcoming CKD: Development of drugs on endothelial cell protection for overcoming CKD, Journal of Pharmacological Sciences, Vol.109, No.1, 14-19, 2009. (Summary) Chronic kidney disease (CKD) is becoming a major public health problem worldwide. It is important to protect endothelial function in CKD treatment because injury of the endothelium is a critical event for the generation and progression of CKD. Recently, clinical studies showed that nifedipine, an antihypertensive drug, acts as a protective agent of endothelial cells (ECs). Nifedipine is reported to partially decompose to a nitrosonifedipine that has high reactivity against lipid-derived radicals in vitro. However, it is still unclear whether nitrosonifedipine is a biologically active agent against endothelial injury. We observed that nitrosonifedipine was converted to radical form by reaction with cultured ECs. The cumene hydroperoxide mediated cytotoxity was reduced by nitrosonifedipine in cultured human glomerular ECs (HGECs). Also nitrosonifedipine suppressed the expression of TNF-alpha-induced intercellular cell adhesion molecule-1 in HGECs. Chronic administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) caused systemic arterial hypertension, endothelial injury, and renal dysfunction. In L-NAME-induced hypertensive rats, nitrosonifedipine treatment improved not only the acetylcholine-induced vasodilation of the aortic rings, but also renal dysfunction such as increasing the levels of serum creatinine and urinary protein excretion. Our preliminary data suggest that nitrosonifedipine is a new and useful drug for the treatment of CKD involving ameliorating effects on EC disorder. (Keyword) Animals / Cells, Cultured / Drug Discovery / Endothelial Cells / Humans / Kidney Failure, Chronic / Molecular Structure / Nifedipine / Nitroso Compounds / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.08R08FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19151535 ● Search Scopus @ Elsevier (PMID): 19151535 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.08R08FM (DOI: 10.1254/jphs.08R08FM, PubMed: 19151535)
83.	Hitoshi Kawazoe, kyoko Takaoka, Hirofumi Shibata, Naokatu Arakaki, Tomihiko Higuti, K Negayama, Hitoshi Houchi, Koichiro Tsuchiya and Yoshiharu Takiguchi : Comparison of antibacterial activity of fluoroquinolones with their sucralfate-complexes against clinically-isolated bacteria, Journal of Health Science, Vol.55, No.5, 790-795, 2009. (Summary) Oral fluoroquinolones are widely known to form chelate complexes with metal-containing drugs, resulting in inhibition of their intestinal absorption. However, for intestinal sterilization, the concomitant regimen may be a selective and effective strategy due to decreased absorption of fluoroquinolones result in the retainment of antibiotics at the intestine if the mixture still perpetuated antibacterial activity. Therefore, to clarify whether the mixture of fluoroquinolones and sucralfate affects their antibacterial activity or not, we conducted in vitro study. According from the checkerboard study using a microdilution method with Mueller-Hinton broth, the antibacterial activity of these fluoroquinolones-sucralfate mixtures equaled to the parent fluoroquinolones even in the presence of sucralfate at the molar ratio of [sucralfate: fluoroquinolone] was less than 166, and the minimal inhibitory concentrations for clinical isolated Escherichia coli and Pseudomonas aeruginosa strains were independent of the existence of sucralfate. These data imply that the chelated forms of each fluoroquinolone retain antibacterial activity even in the presence of the recommended therapeutic doses of sucralfate in clinical practice. (Keyword) fluoroquinolone / interaction / antibacterial activity / chelate / sucralfate (Link to Publication Site) ● Publication site (DOI): 10.1248/jhs.55.790 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679474052224 ● Search Scopus @ Elsevier (DOI): 10.1248/jhs.55.790 (DOI: 10.1248/jhs.55.790, CiNii: 1390282679474052224)
84.	Sanae Iwana, Tomoya Kawazoe, Hwan Ki Park, Koichiro Tsuchiya, Koji Ono, Kazuko YORITA, Takashi Sakai, Takenori Kusumi and Kiyoshi Fukui : Chlorpromazine oligomer is a potentially active substance that inhibits human D-amino acid oxidase, product of a susceptibility gene for schizophrenia, Journal of Enzyme Inhibition and Medicinal Chemistry, Vol.23, No.6, 901-911, 2008. (Summary) D-amino acid oxidase (DAO), a potential risk factor for schizophrenia, has been proposed to be involved in the decreased glutamatergic neurotransmission in schizophrenia. Here we show the inhibitory effect of an antipsychotic drug, chlorpromazine, on human DAO, which is consistent with previous reports using porcine DAO, although human DAO was inhibited to a lesser degree (K(i) = 0.7 mM) than porcine DAO. Since chlorpromazine is known to induce phototoxic or photoallergic reactions and also to be transformed into various metabolites, we examined the effects of white light-irradiated chlorpromazine on the enzymatic activity. Analytical methods including high-resolution mass spectrometry revealed that irradiation triggered the oligomerization of chlorpromazine molecules. The oligomerized chlorpromazine showed a mixed type inhibition with inhibition constants of low micromolar range, indicative of enhanced inhibition. Taken together, these results suggest that oligomerized chlorpromazine could act as an active substance that might contribute to the therapeutic effects of this drug. (Keyword) D-amino acid oxidase / schizophrenia / chlorpromazine / oligomer / glutamatergic neurotransmission / inhibition (Link to Publication Site) ● Publication site (DOI): 10.1080/14756360701745478 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18615285 ● Search Scopus @ Elsevier (PMID): 18615285 ● Search Scopus @ Elsevier (DOI): 10.1080/14756360701745478 (DOI: 10.1080/14756360701745478, PubMed: 18615285)
85.	Hideki Ohnishi, Satoshi Iwanaga, Kazuyoshi Kawazoe, Keisuke Ishizawa, Sakiko Orino, Shuhei Tomita, Koichiro Tsuchiya, Yasuhisa Kanematsu, Nagakatsu Harada, Kazuhiro Mori, Tomoko Tsuchihashi, Yasuko Ishikawa and Toshiaki Tamaki : Effect of iron-quercetin complex on reduction of nitrite in in vitro and in vivo systems, Journal of Agricultural and Food Chemistry, Vol.56, No.21, 10092-10098, 2008. (Summary) This study investigated whether reducing agents such as quercetin and iron(II) facilitate formation of nitric oxide (NO) gas from orally ingested nitrite in an vivo study. When 3 mg/kg Na (15)NO2 was orally administered to rats with or without iron(II) or quercetin, Hb (15)NO, which is indicative of systemic (15)NO, was detected in the blood, with the maximum blood concentration of Hb (15)NO at 15 min after nitrite or nitrite plus quercetin treatment, whereas after administration of nitrite plus iron(II) or nitrite plus iron(II) and quercetin, the time was shortened to 10 min. Interestingly, iron(II), quercetin, or iron(II) plus quercetin did not affect the total amount of Hb (15)NO generated from orally administered Na (15)NO2. However, the systemic nitrite concentration was significantly decreased in the presence of iron(II) or iron(II) plus quercetin. These results may indicate that iron(II) is critical to the generation of NO gas from nitrite, whereas quercetin contributed little under the in vivo experimental conditions. (Keyword) Animals / Antioxidants / Iron / Male / Nitrates / Nitric Oxide / Nitrites / Oxidation-Reduction / Quercetin / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1021/jf801010j (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18831560 ● Search Scopus @ Elsevier (PMID): 18831560 ● Search Scopus @ Elsevier (DOI): 10.1021/jf801010j (DOI: 10.1021/jf801010j, PubMed: 18831560)
86.	Yasuhisa Kanematsu, Kunihisa Yamaguchi, Hideki Ohnishi, Yuki Motobayashi, Keisuke Ishizawa, Yuki Izawa, Kazuyoshi Kawazoe, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Dietary doses of nitrite restore circulating nitric oxide level and improve renal injury in L-NAME-induced hypertensive rats, American Journal of Physiology, Renal Physiology, Vol.295, No.5, F1457-F1462, 2008. (Summary) We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1 g/l) or L-NAME + nitrite (low dose: 0.1 mg/l, medium dose: 1 mg/l, high dose: 10 mg/l) for 8 wk. We evaluated blood NO levels as hemoglobin-NO adducts (iron-nitrosyl-hemoglobin), using an electron paramagnetic resonance method. Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 +/- 8.9 vs. L-NAME 6.0 +/- 3.1 arbitrary units). Coadministration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAME-induced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histological changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude that dietary nitrite-derived NO generation may serve as a backup system when the nitric oxide synthase/L-arginine-dependent NO generation system is compromised. (Keyword) Administration, Oral / Animals / blood pressure / Body Weight / Diet / Hemoglobin A, Glycosylated / Hypertension / Kidney / Kidney Diseases / Kidney Glomerulus / Male / NG-Nitroarginine Methyl Ester / Nitrates / nitric oxide / Proteinuria / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00621.2007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18753302 ● Search Scopus @ Elsevier (PMID): 18753302 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00621.2007 (DOI: 10.1152/ajprenal.00621.2007, PubMed: 18753302)
87.	Masahiro Abe, Yoshiharu Takiguchi, Satoshi Ichimaru, Shinichiro Kaji, Koichiro Tsuchiya and Koichiro Wada : Different effect of acute treatment with rosiglitazone on rat myocardial ischemia/reperfusion injury by administration method., European Journal of Pharmacology, Vol.589, No.1-3, 215-219, 2008. (Summary) The present study was undertaken to examine the effect of rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma agonist, using different administration methods, on rat myocardial infarct size induced by 30 min of ischemia followed by 4 h of reperfusion. The infarct size was significantly reduced by the continuous infusion of rosiglitazone (0.5 mg/kg/h) from 30 min before occlusion for 2 h. On the other hand, limitation of the infarct size was shown by a bolus injection of 0.75 mg/kg at 5 min before reperfusion, but not by a bolus injection of 1 mg at 30 min before occlusion. The protective effect of rosiglitazone by the bolus injection before occlusion was obtained when an antioxidant, N-acetylcysteine, was concomitantly administered. The cardioprotection by rosiglitazone was associated with the inhibition of increased myeloperoxidase activity, tumor necrosis factor-alpha content and phosphorylation of inhibitor kappaB in the myocardium. The present study demonstrated that the protective effect of rosiglitazone on myocardial ischemia/reperfusion injury occurred most likely by inhibition of the nuclear factor-kappaB pathway through PPAR-gamma activation. However, acute treatment with rosiglitazone is harmful if its concentration is high during ischemia. (Keyword) Acetylcysteine / Animals / Antioxidants / Computer Simulation / Disease Models, Animal / Dose-Response Relationship, Drug / Drug Administration Schedule / I-kappa B Proteins / Infusions, Intravenous / Injections, Intravenous / Male / Models, Biological / Myocardial Infarction / Myocardial Reperfusion Injury / myocardium / NF-kappa B / PPAR gamma / Peroxidase / phosphorylation / Protective Agents / Rats / Rats, Wistar / Thiazolidinediones / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2008.05.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18571644 ● Search Scopus @ Elsevier (PMID): 18571644 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2008.05.005 (DOI: 10.1016/j.ejphar.2008.05.005, PubMed: 18571644)
88.	Masahiro Abe, Yoshiharu Takiguchi, Satoshi Ichimaru, Koichiro Tsuchiya and Koichiro Wada : Comparison of the protective effect of N-acetylcysteine by different treatments on rat myocardial ischemia-reperfusion injury., Journal of Pharmacological Sciences, Vol.106, No.4, 571-577, 2008. (Summary) Reactive oxygen species have been known as important contributors to ischemia/reperfusion (I/R) injury. Studies on the beneficial effect of N-acetylcysteine (NAC), a potent antioxidant, on limiting infarct size induced by I/R yielded contrasting results. The present study was undertaken to compare the effect of NAC by different administration methods on infarct size in a rat myocardial I/R model. Rats underwent 30 min of left coronary occlusion followed by 4 h of reperfusion. Treatment with continuous infusion of NAC (150 mg/kg per hour) from 30 min before occlusion for 2 h (until 1 h after the start of reperfusion) produced a significant limitation of the infarct size as a percentage of the ischemic area (8%) compared to the non-treated control (60%). However, bolus injection of 150 mg/kg at 30 min prior to occlusion and 5 min prior to reperfusion failed to reduce it (56%) although the total dose is the same. The decreased total glutathione content and glutathione peroxidase activity in the ischemic region were recovered in the continuous infusion group, but not in the bolus injection group. The increased myeloperoxidase activity and phosphorylation of inhibitor kappaB after I/R were inhibited by the continuous treatment. These results indicate that the protective effect of NAC on myocardial infarction induced by I/R was different depending on the administration method. It is necessary to maintain blood concentration during the early period of reperfusion to obtain the beneficial effect of NAC. (Keyword) Acetylcysteine / Animals / Antioxidants / Disease Models, Animal / Glutathione / Glutathione Peroxidase / I-kappa B Proteins / Infusions, Intravenous / Injections, Intravenous / L-Lactate Dehydrogenase / Male / Myocardial Reperfusion Injury / myocardium / Peroxidase / phosphorylation / Rats / Rats, Wistar (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0071664 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18385540 ● Search Scopus @ Elsevier (PMID): 18385540 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0071664 (DOI: 10.1254/jphs.FP0071664, PubMed: 18385540)
89.	Yuki Izawa, Masanori Yoshizumi, Keisuke Ishizawa, Yoshiko Fujita, Shuji Kondo, Shoji Kagami, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Big mitogen-activated protein kinase 1 (BMK1)/extracellular signal regulated kinase 5 (ERK5) is involved in platelet-derived growth factor (PDGF)-induced vascular smooth muscle cell migration, Hypertension Research, Vol.30, No.11, 1107-1117, 2007. (Summary) Big mitogen-activated protein kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a newly identified member of the mitogen-activated protein (MAP) kinase family. Recently, several studies have suggested that BMK1 plays an important role in the pathogenesis of cardiovascular disease. To clarify the pathophysiological significance of BMK1 in the process of vascular remodeling, we explored the molecular mechanisms of BMK1 activation in vascular smooth muscle cells (VSMCs). From the results of co-immunoprecipitation and immunoblotting analyses, it was found that platelet-derived growth factor (PDGF), a known potent mitogen, activated BMK1 and triggered the Gab1-SHP-2 interaction in rat aortic smooth muscle cells (RASMCs). The abrogation of SHP-2 phosphatase activity by transfection of the SHP-2-C/S mutant suppressed PDGF-stimulated BMK1 activation. Infection with an adenoviral vector expressing dominant-negative MEK5alpha, which can suppress PDGF-stimulated BMK1 activation to the control level, inhibited PDGF-induced RASMC migration. Moreover, we observed an increase of BMK1 activation in injured mouse femoral arteries. From these findings, it is suggested that BMK1 activation leads to VSMC migration induced by PDGF via Gab1-SHP-2 interaction, and that BMK1-mediated VSMC migration may play a role in the pathogenesis of vascular remodeling. (Keyword) Animals / Cell Movement / Humans / MAP Kinase Kinase 5 / Male / Mice / Mice, Inbred C57BL / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Phosphoproteins / Phosphorylation / Platelet-Derived Growth Factor / Protein Tyrosine Phosphatase, Non-Receptor Type 11 / Rats (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.30.1107 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18250560 ● Search Scopus @ Elsevier (PMID): 18250560 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.30.1107 (DOI: 10.1291/hypres.30.1107, PubMed: 18250560)
90.	Deliorman Didem Orhan, Fatma Ergun, Erdem Yesilada, Koichiro Tsuchiya, Yoshihisa Takaishi and Kazuyoshi Kawazoe : Antioxidant activity of two flavonol glycosides from Cirsium hypoleucum DC. through bioassay-guided fractionation, Turkish Journal of Pharmaceutical Sciences, Vol.4, No.1, 1-14, 2007. (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-34250900361 (Elsevier: Scopus)
91.	Yoshichika Kawai, Hitomi Kiyokawa, Yuki Kimura, Yoji Kato, Koichiro Tsuchiya and Junji Terao : Hypochlorous acid-derived modification of phospholipids: characterization of aminophospholipids as regulatory molecules for lipid peroxidation., Biochemistry, Vol.45, No.47, 14201-14211, 2006. (Summary) Hypochlorous acid (HOCl), an inflammatory oxidant derived from neutrophil myeloperoxidase, can chlorinate cytosolic proteins and nuclear DNA bases of target cells by passing through the cell membrane. However, little is known about the consequences of HOCl-derived modification of cell membrane components, including phospholipids. In this study, we characterize the reaction of HOCl with phospholipid molecules and found that aminophospholipids are the key molecules that chemically regulate lipid peroxidation. Upon incubation with HOCl, the peroxidation of egg yolk phosphatidylcholine was significantly enhanced in the presence of phosphatidylethanolamine (PE). In contrast, the peroxidation was significantly inhibited in the presence of phosphatidylserine (PS). On the basis of mass spectrometric and electron paramagnetic resonance characterization, the initiator of the peroxidation was identified as the nitrogen-centered radical originating from PE-derived chloramines, especially N,N-dichlorinated PE, a major product in the HOCl-modified PE. Although PS was also chlorinated upon reaction with HOCl, the formed chloramine rapidly decomposed to phosphatidylglycolaldehyde, a novel class of lipid aldehyde. Formation of phosphatidylglycolaldehyde was also confirmed in the porcine brain PS and erythrocyte cell membrane ghost exposed to HOCl. These results provide a novel mechanism for the HOCl-induced oxidative damage and its endogenous protection in the cell membrane at the site of inflammation. (Keyword) Chromatography, High Pressure Liquid / Chromatography, Thin Layer / Gas Chromatography-Mass Spectrometry / Hypochlorous Acid / Lipid Peroxidation / Mass Spectrometry / Phospholipids / Spectrophotometry, Ultraviolet (Link to Publication Site) ● Publication site (DOI): 10.1021/bi0610909 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17115715 ● Search Scopus @ Elsevier (PMID): 17115715 ● Search Scopus @ Elsevier (DOI): 10.1021/bi0610909 (DOI: 10.1021/bi0610909, PubMed: 17115715)
92.	Ali Nermin, Masanori Yoshizumi, Seiji Yano, Saburo Sone, Hideki Ohnishi, Keisuke Ishizawa, Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : The novel Src kinase inhibitor M475271 inhibits VEGF-induced vascular endothelial-cadherin and β-catenin phosphorylation but increases their association, Journal of Pharmacological Sciences, Vol.102, No.1, 112-120, 2006. (Summary) M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that displays selective inhibition of Src kinase activity and tumor growth in vivo. Vascular endothelial growth factor (VEGF)-induced angiogenesis plays a pivotal role in tumor growth and metastasis. Vascular endothelial (VE)-cadherin is an endothelial cell-specific adhesion molecule that can interact with the cytoskeleton via several anchoring molecules such as beta-catenin. Here, we examined the effect of M475271 on VE-cadherin and beta-catenin phosphorylation and association. We also examined its effect on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation, migration, and tube formation. The findings reveal pretreatment with M475271 significantly inhibits VEGF-induced VE-cadherin and beta-catenin phosphorylation. However, M475271 significantly increases VE-cadherin and beta-catenin association compared to the VEGF-treated group. Confocal laser microscopic examination confirmed the augmentation effect of M475271 on VE-cadherin and beta-catenin association. Finally, M475271 was shown to have inhibitory effects comparable to those of PP2 and Herbimycin A on VEGF-induced HUVEC proliferation, migration, and tube formation. These findings suggest that M475271 attenuates VEGF-induced angiogenesis by maintaining cell-cell junction stability. Although the involvement of other signaling molecules cannot be ruled out, M475271 has potential as a drug for the inhibition of the angiogenesis needed for tumor growth and metastasis. (Keyword) M475271 / vascular endothelial growth factor (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0060357 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16974068 ● Search Scopus @ Elsevier (PMID): 16974068 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0060357 (DOI: 10.1254/jphs.FP0060357, PubMed: 16974068)
93.	Shinji Abe, Hideki Ohnishi, Koichiro Tsuchiya, Keisuke Ishizawa, Mayumi Torii, Yasuhisa Kanematsu, Kazuyoshi Kawazoe, Kazuo Minakuchi, Masanori Yoshizumi and Toshiaki Tamaki : Calcium and reactive oxygen species mediated Zn²⁺-induced apoptosis in PC12 cells, Journal of Pharmacological Sciences, Vol.102, No.1, 103-111, 2006. (Summary) The release of excessive Zn(2+) from presynaptic boutons into extracellular regions contributes to neuronal apoptotic events, which result in neuronal cell death. However, the mechanisms of Zn(2+)-induced neuronal cell death are still unclear. Therefore, we investigated the dynamics of intracellular Zn(2+), calcium, and reactive oxygen species in PC12 cells. The addition of Zn(2+) produced cell death in a concentration- and time-dependent manner. (45)Ca(2+) influx occurred just after the treatment with Zn(2+), although subsequent hydroxyl radical (()OH) production did not begin until 3 h after Zn(2+) exposure. ()OH production was significantly attenuated in Ca(2+)-free medium or by L-type Ca(2+) channel antagonist treatment, but it was independent of the intracellular Zn(2+) content. Dantrolene treatment had no protective effects against Zn(2+)-induced cell death. Treatment with N-acetyl-L-cysteine blocked ()OH generation and subsequent cell death. These data indicate that Ca(2+) influx and subsequent ()OH production are critical events in Zn(2+)-induced toxicity in PC12 cells. (Keyword) Acetylcysteine / Animals / Apoptosis / Bisbenzimidazole / Calcium / Calcium Channel Blockers / Calcium Channels, L-Type / Calcium Radioisotopes / Cell Survival / Dantrolene / Fluorescent Dyes / Free Radical Scavengers / Hydroxyl Radical / PC12 Cells / Rats / Reactive Oxygen Species / Spectrophotometry, Atomic / Zinc (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0060342 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16990703 ● Search Scopus @ Elsevier (PMID): 16990703 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0060342 (DOI: 10.1254/jphs.FP0060342, PubMed: 16990703)
94.	Hiroyuki Nakagawa, Yoshihisa Takaishi, Naonobu Tanaka, Koichiro Tsuchiya, Hirofumi Shibata and Tomihiko Higuti : Chemical Constituents from the Peels of Citrus sudachi, Journal of Natural Products, Vol.69, No.8, 1177-1179, 2006. (Summary) A methanol extract of the peels of Citrus sudachi gave five new compounds (1-5) and 27 known compounds. The structures were elucidated on the basis of spectroscopic evidence. Several of these compounds were assayed for antimicrobial activity against methicillin-resistant Staphylococcus aureus and Helicobacter pylori, and sudachitin (6) and 3'-demethoxysudachitin (7) were the most active. (Keyword) Anti-Bacterial Agents / Citrus / Coumaric Acids / Flavonoids / Fruit / Glycosides / Helicobacter pylori / Japan / Limonins / Methicillin Resistance / Microbial Sensitivity Tests / Plants, Medicinal / Staphylococcus aureus (Link to Publication Site) ● Publication site (DOI): 10.1021/np060217s (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16933871 ● Search Scopus @ Elsevier (PMID): 16933871 ● Search Scopus @ Elsevier (DOI): 10.1021/np060217s (DOI: 10.1021/np060217s, PubMed: 16933871)
95.	F.A. Ramos, Yoshihisa Takaishi, M. Shirotori, Y. Kawaguchi, Koichiro Tsuchiya, Hirofumi Shibata, Tomihiko Higuti, T. Tadokoro and M. Takeuchi : Antibacterial and Antioxidant Activities of Quercetin Oxidation Products from Yellow Onion (Alliu cepa) Skin, Journal of Agricultural and Food Chemistry, Vol.54, No.10, 3551-3357, 2006. (Summary) Four new quercetin-derived oxidation products (1-4) and lunularin-4-O-beta-D-glucoside (5) were isolated from a water extract of onion (Allium cepa) skin, together with 17 other known compounds. Antibacterial assays for the isolated compounds showed that 2-(3,4-dihydroxyphenyl)-4,6-dihydroxy-2-methoxybenzofuran-3-one (1) presented selective activity against Helicobacter pylori strains and 3-(quercetin-8-yl)-2,3-epoxyflavanone (4) showed antibacterial activity against MRSA and H. pylori strains at the same time that it increased susceptibility of MRSA to beta-lactams. Evaluation of antioxidant activity against DPPH for the isolated compounds showed that the new derivative compounds (1-4) and 2,5,7,3',4'-pentahydroxy-3,4-flavandione (6) are more active than quercetin. (Keyword) Anti-Bacterial Agents / Antioxidants / Bibenzyls / Biphenyl Compounds / Disk Diffusion Antimicrobial Tests / Glucosides / Helicobacter pylori / Hydrazines / Methicillin-Resistant Staphylococcus aureus / Molecular Structure / Onions / Phenols / Picrates / Plant Extracts (Link to Publication Site) ● Publication site (DOI): 10.1021/jf060251c (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19127724 ● Search Scopus @ Elsevier (PMID): 19127724 ● Search Scopus @ Elsevier (DOI): 10.1021/jf060251c (DOI: 10.1021/jf060251c, PubMed: 19127724)
96.	Yasuhisa Kanematsu, Koichiro Tsuchiya, Hideki Onishi, Yuki Motobayashi, Yuki Izawa, Manabu Ishihara, Keisuke Ishizawa, Shinji Abe, Kazuyoshi Kawazoe and Toshiaki Tamaki : Effects of angiotensin II type 1 receptor blockade on the systemic blood nitric oxide dynamics in Nω-nitro-L-arginine methyl ester-treated rats, Hypertension Research, Vol.29, No.5, 369-374, 2006. (Summary) We previously succeeded in measuring the nitrosylhemoglobin (HbNO) level as an index of blood nitric oxide (NO) by the electron paramagnetic resonance (EPR) HbNO signal subtraction method. In this study, we examined the effects of olmesartan, an angiotensin II type 1 receptor blocker (ARB), on NO dynamics in N(omega)-nitro-L-arginine methyl ester (L-NAME)-treated rats by the EPR-subtraction method. Oral administration of L-NAME for 2 weeks induced serious hypertension, and the HbNO concentration was reduced to 37.6% of the level in controls. Coadministration of olmesartan improved hypertension and increased the blood HbNO concentration of L-NAME-treated rats. In contrast, coadministration of hydralazine improved hypertension but did not affect the blood HbNO concentration. In conclusion, our findings suggested that chronic administration of olmesartan ameliorated the endothelial dysfunction in L-NAME-treated rats. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Antihypertensive Agents / Blood Pressure / Body Weight / Electron Spin Resonance Spectroscopy / Endothelium, Vascular / Heart Rate / Hemodynamics / Hemoglobins / Hydralazine / Hypertension / Imidazoles / Male / NG-Nitroarginine Methyl Ester / Nitric Oxide / Rats / Rats, Sprague-Dawley / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.29.369 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16832158 ● Search Scopus @ Elsevier (PMID): 16832158 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.29.369 (DOI: 10.1291/hypres.29.369, PubMed: 16832158)
97.	Yoshiko Fujita, Masanori Yoshizumi, Yuki Izawa, Nermin Ali, Yasuhisa Kanematsu, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Transactivation of fetal liver kinase-1/kinase-insert domain-containing receptor by lysophosphatidylcholine induces vascular endothelial cell proliferation., Endocrinology, Vol.147, No.3, 1377-1385, 2006. (Summary) Lysophosphatidylcholine (LPC), a major lipid component of oxidized low-density lipoprotein, is a bioactive lipid molecule involved in numerous biological processes including the progression of atherosclerosis. Recently orphan G protein-coupled receptors were identified as high-affinity receptors for LPC. Although several G protein-coupled receptor ligands transactivate receptor tyrosine kinases, LPC-stimulated transactivation of receptor tyrosine kinase has not yet been reported. Here we observed for the first time that LPC treatment of human umbilical vein endothelial cells (HUVECs) induces tyrosyl phosphorylation of vascular endothelial growth factor receptor 2 [fetal liver kinase-1/kinase-insert domain-containing receptor, Flk-1/KDR)]. Flk-1/KDR transactivation by LPC was inhibited by vascular endothelial growth factor receptor tyrosine kinase inhibitors, SU1498 and 4-[(4'-chloro-2'-fluoro) phenylamino]6,7-dimethoxyquinazoline (VTKi) in immunoprecipitation. Furthermore, we examined the effects of the Src family kinases inhibitors, herbimycin A and 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d] pyrimidine (PP2), on LPC-induced Flk-1/KDR transactivation. Results from Western blots, c-Src is involved in LPC-induced Flk-1/KDR transactivation because herbimycin A and PP2 inhibited this transactivation. Kinase-inactive (KI) Src transfection also inhibited LPC-induced Flk-1/KDR transactivation. In addition, results from Western blots, ERK1/2 and Akt, which are downstream effectors of Flk-1/KDR, were also activated by LPC, and this was inhibited by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in HUVECs. LPC-induced stimulation of HUVEC proliferation was shown to be secondary to transactivation because it was suppressed by SU1498, VTKi, herbimycin A, PP2, and KI Src transfection in dimethylthiazoldiphenyltetra-zoliumbromide assay. These findings suggest that LPC-induced Flk-1/KDR transactivation via c-Src may have important implications for the progression of atherosclerosis. (Keyword) atherosclerosis / Benzoquinones / Blotting, Western / Cell Line / Cell Proliferation / Cell Survival / Cells, Cultured / Cinnamates / Disease Progression / Endothelial Cells / Endothelium, Vascular / Humans / Immunoblotting / Immunoprecipitation / Lactams, Macrocyclic / Ligands / Lysophosphatidylcholines / phosphorylation / Protein Structure, Tertiary / Protein-Tyrosine Kinases / Pyrimidines / Quinazolines / Quinones / Transcriptional Activation / Transfection / Vascular Endothelial Growth Factor Receptor-2 (Link to Publication Site) ● Publication site (DOI): 10.1210/en.2005-0644 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16322069 ● Summary page in Scopus @ Elsevier: 2-s2.0-32644452665 (DOI: 10.1210/en.2005-0644, PubMed: 16322069, Elsevier: Scopus)
98.	Shuji Kondo, Maki Shimizu, Maki Urushihara, Koichiro Tsuchiya, Masanori Yoshizumi, Toshiaki Tamaki, Akira Nishiyama, Hiroshi Kawachi, Fujio Shimizu, Quinn T. Mark, Lambeth J. David and Shoji Kagami : Addition of the antioxidant probucol to angiotensin II type I receptor antagonist arrests progression mesangioproliferative glomerulonephritis in the rat, Journal of the American Society of Nephrology, Vol.17, No.3, 783-794, 2006. (Summary) Angiotensin II (Ang II) and reactive oxidative species (ROS) that are produced by NADPH oxidase have been implicated in the progression of glomerulonephritis (GN). This study examined the effect of simultaneously interrupting Ang II and ROS with an Ang II receptor blocker (ARB), candesartan, and a free radical scavenger, probucol, in a model of progressive mesangioproliferative GN induced by the injection of anti-Thy-1 antibody into uninephrectomized rats. Nephritic rats were divided into four groups and given daily oral doses of the following: Vehicle, 1% probucol diet, 70 mg/L candesartan in drinking water, and probucol plus candesartan. These treatments lasted until day 56. Vehicle-treated nephritic rats developed progressively elevated proteinuria and glomerulosclerosis. Candesartan kept proteinuria significantly lower than vehicle or probucol. The addition of probucol to candesartan normalized urinary protein excretion. Increases in BP in nephritic rats were lowered by these treatments, except with probucol. It is interesting that both glomerular cell number and glomerulosclerosis were significantly decreased by candesartan and normalized by the addition of probucol. Immunohistochemical studies for TGF-beta1, collagen type I, and fibronectin revealed that the combined treatment abolished glomerular fibrotic findings compared with candesartan. In addition, glomerular expression of NADPH oxidase components and superoxide production suggested that the combined treatment completely eliminated NADPH oxidase-associated ROS production. In conclusion, our study provides the first evidence that the antioxidant probucol, when added to an Ang II receptor blockade, fully arrests proteinuria and disease progression in GN. Furthermore, the data suggest that NADPH oxidase-associated ROS production may play a pivotal role in the progression of GN. The combination of probucol and candesartan may represent a novel route of therapy for patients with progressive GN. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Antioxidants / Biopsy, Needle / Blotting, Western / Disease Models, Animal / Disease Progression / Drug Therapy, Combination / Female / Glomerulonephritis, Membranoproliferative / Immunohistochemistry / Male / Probability / Probucol / Proteinuria / Rats / Rats, Sprague-Dawley / Sensitivity and Specificity (Link to Publication Site) ● Publication site (DOI): 10.1681/ASN.2005050519 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16467449 ● Search Scopus @ Elsevier (PMID): 16467449 ● Search Scopus @ Elsevier (DOI): 10.1681/ASN.2005050519 (DOI: 10.1681/ASN.2005050519, PubMed: 16467449)
99.	Yoshiko Fujita, Yuki Izawa, Nermin Ali, Koichiro Tsuchiya, Shuichi Hamano, Toshiaki Tamaki and Masanori Yoshizumi : Pramipexole protects against H2O2-induced PC12 cell death, Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.372, No.4, 257-266, 2006. (Summary) Pramipexole, a novel non-ergot dopamine (DA) agonist, has been successfully applied to the treatment of Parkinson's disease (PD). Although the specific cause of PD remains unknown, recent studies have provided evidence that oxidative stress plays a role in the parthenogenesis of the disease. In the present study, we examined the effect of pramipexole on hydrogen peroxide (H2O2, 100 microM)-induced PC12 cell death, and the intracellular mechanism of this effect. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) assay revealed that pretreatment of PC12 cells with pramipexole (1-100 microM) resulted in significant protection against H2O2-induced cell death in a concentration-dependent manner. The protective effect of pramipexole was not affected by pretreatment with the DA receptor antagonists sulpiride, spiperone or domperidone, suggesting that the effect of pramipexole is not mediated by DA receptors. In PC12 cells, pramipexole inhibited H2O2-induced lactate dehydrogenase (LDH) leakage, as well as H2O2-induced cytochrome c release and caspase-3 activation with the resultant apoptosis. It was also observed in PC12 cells that H2O2 stimulated phosphorylation of mitogen-activated protein (MAP) kinases, i.e., extracellular signal-regulated kinase1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase. Pramipexole inhibited H2O2-induced JNK and p38 MAP kinase, but not ERK1/2 phosphorylation. Furthermore, in these cells experiments with a fluorescent probe, 2-[6-(4'-amino)phenoxy-3H-xanthen-3-on-9-yl]benzoic acid, revealed that pramipexole, the JNK inhibitor SP600125 and the p38 MAP kinase inhibitor SB203580 inhibited the generation of H2O2-induced reactive oxygen species. Caspase inhibitors Z-DEVD-FMK and Z-IETD-FMK, as well as SP600125 and SB203580, inhibited H2O2-induced PC12 cell death to a similar extent as pramipexole. These results suggest that pramipexole exerts a protective effect against oxidative stress-induced PC12 cell death in part through an inhibition of JNK and p38 MAP kinase. (Keyword) Animals / Antiparkinson Agents / apoptosis / Benzothiazoles / Caspase 3 / Caspases / cell death / Cell Survival / Cytochromes c / Dopamine Agonists / Dopamine Antagonists / hydrogen peroxide / L-Lactate Dehydrogenase / Mitogen-Activated Protein Kinases / Neuroprotective Agents / oxidative stress / PC12 Cells / Rats / Thiazoles (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-005-0025-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16362428 ● Summary page in Scopus @ Elsevier: 2-s2.0-31144433876 (DOI: 10.1007/s00210-005-0025-2, PubMed: 16362428, Elsevier: Scopus)
100.	田島壮一郎, Koichiro Tsuchiya, 大西秀樹, Yasuhisa Kanematsu, Toshiaki Tamaki, Ronald Mason and Yoshiharu Takiguchi : Detection of protein - derived radicals by the immunochemical technique, Folia Pharmacologica Japonica, Vol.126, No.4, 246-249, 2005. (Keyword) 酸化ストレス / ラジカル / ミオグロビン / チオレドキシン (Link to Publication Site) ● Publication site (DOI): 10.1254/fpj.126.246 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16327204 ● Search Scopus @ Elsevier (PMID): 16327204 ● Search Scopus @ Elsevier (DOI): 10.1254/fpj.126.246 (DOI: 10.1254/fpj.126.246, PubMed: 16327204)
101.	Koichiro Tsuchiya, Kaori Akai, Akira Tokumura, Shinji Abe, Toshiaki Tamaki, Yoshiharu Takiguchi and Kenji Fukuzawa : Oxygen radical photo-induced by ferric nitrilotriacetate complex, Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1725, No.1, 111-119, 2005. (Summary) This study examined the photo-induced generation of reactive oxygen species (ROS) by the carcinogenic iron(III)-NTA complex. Iron(III)-NTA complex (1:1) has three conformations (type (a) in acidic conditions of pH 1-6, type (n) in neutral conditions of pH 3-9, and type (b) in basic conditions of pH 7-10) with two pK(a) values (pK(a1) approximately 4, pK(a2) approximately 8). The iron(III)-NTA complex was reduced to iron(II) under cool-white fluorescent light without the presence of any reducing agent, and the reduction rates of the three conformations of iron(III)-NTA were in the order type (a)>type (n)>type (b) as reported previously (Akai K. et al., Free Radic. Res. 38, 951-962, 2004). ROS generation was investigated by electron paramagnetic resonance (EPR) spectroscopy with a spin-trapping technique. Apparent EPR signals attributed to PBN/(13)CH(3) and PBN/OCH(3) spin adducts were observed after incubation of the iron(III)-NTA complex was mixed with alpha-phenyl-tert-butylnitrone (PBN) and (13)C-DMSO in an aerobic condition. The addition of catalase effectively attenuated the PBN adducts, but superoxide dismutase enhanced them. Taken together, these results indicate that the iron(III)-NTA complex is spontaneously reduced to the iron(II)-NTA complex by light under acidic to neutral pH, and in turn transfers an electron to molecular oxygen to form ROS. (Keyword) Catalase / Cyclic N-Oxides / Electron Spin Resonance Spectroscopy / Ferric Compounds / Free Radicals / Light / Nitrilotriacetic Acid / Nitrogen Oxides / Oxygen / Photochemistry / Superoxide Dismutase / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2005.05.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15950386 ● Search Scopus @ Elsevier (PMID): 15950386 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbagen.2005.05.001 (DOI: 10.1016/j.bbagen.2005.05.001, PubMed: 15950386)
102.	Yuki Izawa, Masanori Yoshizumi, Keisuke Ishizawa, Yoshiko Fujita, Shuji Kondo, Shoji Kagami, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : ERK1/2 activation by angiotensin II inhibits insulin-induced glucose uptake in vascular smooth muscle cells, Experimental Cell Research, Vol.308, No.2, 291-299, 2005. (Summary) Clinical evidence suggests a relationship between hypertension and insulin resistance, and cross-talk between angiotensin II (Ang II) and insulin signaling pathways may take place. We now report the effect of Ang II on insulin-induced glucose uptake and its intracellular mechanisms in vascular smooth muscle cells (VSMC). We examined the translocation of glucose transporter-4 (GLUT-4) and glucose uptake in rat aortic smooth muscle cells (RASMC). Mitogen-activated protein (MAP) kinases and Akt activities, and phosphorylation of insulin receptor substrate-1 (IRS-1) at the serine and tyrosine residues were measured by immunoprecipitation and immunoblotting. As a result, Ang II inhibited insulin-induced GLUT-4 translocation from cytoplasm to the plasma membrane in RASMC. Ang II induced extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK) activation and IRS-1 phosphorylation at Ser307 and Ser616. Ang II-induced Ser307 and Ser616 phophorylation of IRS-1 was inhibited by a MEK inhibitor, PD98059, and a JNK inhibitor, SP600125. Ang II inhibition of insulin-stimulated IRS-1 tyrosyl phophorylation and Akt activation were reversed by PD98059 but not by SP600125. Ang II inhibited insulin-induced glucose uptake, which was also reversed by PD98059 but not by SP600125. It is shown that Ang II-induced ERK1/2 activation inhibits insulin-dependent glucose uptake through serine phophorylation of IRS-1 in RASMC. (Keyword) Angiotensin II / Animals / Blood Vessels / Cell Membrane / Cytoplasm / Enzyme Activation / Enzyme Inhibitors / Glucose / Glucose Transporter Type 4 / Hypertension / Insulin / Insulin Receptor Substrate Proteins / Insulin Resistance / JNK Mitogen-Activated Protein Kinases / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Monosaccharide Transport Proteins / Muscle Proteins / Myocytes, Smooth Muscle / Phosphoproteins / Phosphorylation / Protein Transport / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Rats, Sprague-Dawley / Serine / Tyrosine (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2005.04.028 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15921682 ● Search Scopus @ Elsevier (PMID): 15921682 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2005.04.028 (DOI: 10.1016/j.yexcr.2005.04.028, PubMed: 15921682)
103.	Yoshihiko Fujita, Koichiro Tsuchiya, Shinji Abe, Yohiharu Takiguchi, Shin-ichi Kubo and Hiromu Sakurai : Estimation of the age of human bloodstains by electron paramagnetic resonance spectroscopy: Long-term controlled experiment on the effects of environmental factors, Forensic Science International, Vol.152, No.1, 39-43, 2005. (Summary) In this study, we examined the efficacy and limitations of electron paramagnetic resonance (EPR) for estimating the age of human bloodstains. At 77K, human bloodstains give four striking EPR signals in the g=6.2 (g6), 4.3 (g4), 2.27 (H) and 2.005 (R) regions due to ferric high-spin, ferric non-heme, ferric low-spin and free radical species, respectively. We found that plotting double logarithms of the EPR intensity ratio of H/g4 versus days past bleeding gave a linear correlation up to 432 days with an error range within 25% of the actual number of days under controlled conditions. However, environmental factors such as differences of absorbent, light exposure and fluctuations of storage temperature affected the changes of these EPR-active compounds, which result in misestimation of the time since bleeding occurred. Therefore, one should take such factors into account in estimating the period since bleeding by this method. (Keyword) Absorption / Aging / Blood Stains / Electron Spin Resonance Spectroscopy / Ferric Compounds / Forensic Medicine / Humans / Light / Nonheme Iron Proteins / Temperature (Link to Publication Site) ● Publication site (DOI): 10.1016/j.forsciint.2005.02.029 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15939175 ● Search Scopus @ Elsevier (PMID): 15939175 ● Search Scopus @ Elsevier (DOI): 10.1016/j.forsciint.2005.02.029 (DOI: 10.1016/j.forsciint.2005.02.029, PubMed: 15939175)
104.	Keisuke Ishizawa, Yuki Izawa, Hiroyuki Ito, Chieko Miki, Kayoko Miyama, Yoshiko Fujita, Yasuhisa Kanematsu, Koichiro Tsuchiya, Toshiaki Tamaki, Akira Nishiyama and Masanori Yoshizumi : Aldosterone stimulates vascular smooth muscle cell proliferation via big mitoten-activated protein kinase 1 activation, Hypertension, Vol.46, No.4, 1046-1052, 2005. (Summary) The nongenomic effects of aldosterone have been implicated in the pathogenesis of various cardiovascular diseases. Aldosterone-induced nongenomic effects are attributable in part to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2), a classical mitogen-activated protein (MAP) kinase. Big MAP kinase 1 (BMK1), a newly identified MAP kinase, has been shown to be involved in cell proliferation, differentiation, and survival. We examined whether aldosterone stimulates BMK1-mediated proliferation of cultured rat aortic smooth muscle cells (RASMCs). Mineralocorticoid receptor (MR) expression and localization were evaluated by Western blotting analysis and fluorolabeling methods. ERK1/2 and BMK1 activities were measured by Western blotting analysis with the respective phosphospecific antibodies. Cell proliferation was determined by Alamar Blue colorimetric assay. Aldosterone (0.1 to 100 nmol/L) dose-dependently activated BMK1 in RASMCs, with a peak at 30 minutes. To clarify whether aldosterone-induced BMK1 activation is an MR-mediated phenomenon, we examined the effect of eplerenone, a selective MR antagonist, on aldosterone-induced BMK1 activation. Eplerenone (0.1 to 10 micromol/L) dose-dependently inhibited aldosterone-induced BMK1 activation in RASMCs. Aldosterone also stimulated RASMC proliferation, which was inhibited by eplerenone. Aldosterone-mediated phenomena were concluded to be attributable to a nongenomic effect because cycloheximide failed to inhibit aldosterone-induced BMK1 activation. Transfection of dominant-negative MAP kinase/ERK kinase 5 (MEK5), which is an upstream regulator of BMK1, partially inhibited aldosterone-induced RASMC proliferation, which was almost completely inhibited by MEK inhibitor PD98059. In addition to the classical steroid activity, rapid nongenomic effects induced by aldosterone may represent an alternative etiology for vascular diseases such as hypertension. (Keyword) 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt / Aldosterone / Animals / Calcium-Calmodulin-Dependent Protein Kinases / Cell Proliferation / Cells, Cultured / Cycloheximide / Enzyme Activation / flavonoids / Genes, Dominant / MAP Kinase Kinase 5 / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Protein Synthesis Inhibitors / Rats / Receptors, Mineralocorticoid / Spironolactone / Transfection (Link to Publication Site) ● Publication site (DOI): 10.1161/01.HYP.0000172622.51973.f5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16087789 ● Search Scopus @ Elsevier (PMID): 16087789 ● Search Scopus @ Elsevier (DOI): 10.1161/01.HYP.0000172622.51973.f5 (DOI: 10.1161/01.HYP.0000172622.51973.f5, PubMed: 16087789)
105.	Ali Nermin, Masanori Yoshizumi, Yoshiko Fujita, Yuki Izawa, Yasuhisa Kanematsu, Keisuke Ishizawa, Koichiro Tsuchiya, Seiji Yano, Saburo Sone and Toshiaki Tamaki : A Novel Src Kinase Inhibitor, M475271, Inhibits VEGF-Induced Human Umbilical Vein Endothelial Cell Proliferation and Migration, Journal of Pharmacological Sciences, Vol.98, No.2, 130-141, 2005. (Summary) Vascular endothelial growth factor (VEGF) was reported to be a potent proangiogenic factor that plays a pivotal role in both physiological and pathological angiogenesis. M475271, 4-quinazolinamine, N-(2-chloro-5-methoxyphenyl)-6-methoxy-7-[(1-methyl-4-piperidinyl) methoxy]-(9Cl), is a new anilinoquinazoline derivative that showed selective inhibition of Src kinase activity and tumor growth in vivo. Here, we examined the effect of M475271 on VEGF-induced human umbilical vein endothelial cell (HUVEC) proliferation and migration and their intracellular mechanisms. Our findings showed that M475271 pretreatment resulted in a significant inhibition of VEGF-induced HUVEC proliferation, [(3)H]thymidine incorporation, and migration. M475271 inhibited VEGF-induced Flk-1 and Src phosphorylation and their association. Confocal laser microscopic examination confirmed the inhibitory effect of M475271 on VEGF-induced Flk-1/Src association. M475271 inhibited VEGF-induced extracellular signal-regulated kinase1/2 (ERK1/2) and p38 but not Akt activation in a concentration-dependent manner. M475271, PI3-K inhibitor, and p38 inhibitor inhibited VEGF-induced HUVEC proliferation and migration. However, a MEK1/2 inhibitor inhibited VEGF-induced proliferation but not migration. These findings suggest that M475271 attenuates VEGF-induced HUVEC proliferation and migration through the inhibition of signaling pathways involving Src, ERK1/2, and/or p38. Taken together, these data indicate that M475271 may be a useful candidate for inhibition of endothelial cell proliferation and migration relevant to angiogenesis. (Keyword) M475271 / vascular endothelial growth factor / human umbilical vein endothelial cell proliferation and migration / angiogenesis (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0040850 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15937404 ● Search Scopus @ Elsevier (PMID): 15937404 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0040850 (DOI: 10.1254/jphs.FP0040850, PubMed: 15937404)
106.	Koichiro Tsuchiya, Yasuhisa Kanematsu, Masanori Yoshizumi, Hideki Ohnishi, Kazuyoshi Kirima, Yuki Izawa, Michiyo Shikishima, Tatsuhiro Ishida, Shuji Kondo, Shoji Kagami, Yoshiharu Takiguchi and Toshiaki Tamaki : Nitrite is an alternative source of NO in vivo, American Journal of Physiology, Heart and Circulatory Physiology, Vol.288, No.5, H2163-H2170, 2005. (Summary) In this study, we investigated whether orally administered nitrite is changed to NO and whether nitrite attenuates hypertension in a dose-dependent manner. We utilized a stable isotope of [15N]nitrite (15NO2-) as a source of nitrite to distinguish between endogenous nitrite and that exogenously administered and measured hemoglobin (Hb)-NO as an index of circulating NO in whole blood using electron paramagnetic resonance (EPR) spectroscopy. When 1 mg/kg Na15NO2 was orally administered to rats, an apparent EPR signal derived from Hb15NO (A(Z) = 23.4 gauss) appeared in the blood. The peak blood HbNO concentration occurred at the first measurement after intake (5 min) for treatment with 1 and 3 mg/kg (HbNO: 4.93 +/- 0.52 and 10.58 +/- 0.40 microM, respectively) and at 15 min with 10 mg/kg (HbNO: 38.27 +/- 9.23 microM). In addition, coadministration of nitrite (100 mg/l drinking water) with N(omega)-nitro-L-arginine methyl ester (L-NAME; 1 g/l) for 3 wk significantly attenuated the L-NAME-induced hypertension (149 +/- 10 mmHg) compared with L-NAME alone (170 +/- 13 mmHg). Furthermore, this phenomenon was associated with an increase in circulating HbNO. Our findings clearly indicate that orally ingested nitrite can be an alternative to L-arginine as a source of NO in vivo and may explain, at least in part, the mechanism of the nitrite/nitrate-rich Dietary Approaches to Stop Hypertension diet-induced hypotensive effects. (Keyword) nitric oxide / hypertension / electron paramagnetic resonance (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.00525.2004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15626692 ● Search Scopus @ Elsevier (PMID): 15626692 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.00525.2004 (DOI: 10.1152/ajpheart.00525.2004, PubMed: 15626692)
107.	生田雅子, 会田真規, Keisuke Ishizawa, Kazuo Minakuchi, Koichiro Tsuchiya, Masaru Kihara and Aiko Yamauchi : 徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良, Japanese Journal of Pharmaceutical Health Care and Sciences, Vol.31, No.4, 279-286, 2005. (Summary) Fluid therapy is a fundamental treatment for almost all inpatients, and nutritional therapy is the most important type of such therapy. Currently, total parenteral nutrition (TPN) is widely used to provide complete nutritional support but 30-40% of TPN recipients are considered to in a malnourished state due to inappropriate TPN prescriptions. Computer-assisted TPN prescription systems are thought to be useful to clinical professionals in solving this problem because they can perform complicated calculations that make it easy to draw up correct TPN prescriptions. So, we made a prototype system for aiding the preparation of TPN prescriptions based on Microsoft^[ !R] EXCEL and it was tested by physicians, pharmacists, dietitians and nurses engaged in TPN therapy at Tokushima University Hospital. We also had them fill out a questionnaire on the system in which they rated it for ease of operation and usefulness according to a scoring system in which 5 indicated full marks. Our Computer-Assisted TPN Prescription System was improved on the basis of the questionnaire results and is now being effectively used by the nutrition support team (NST) in Tokushima University Hospital. (Keyword) computer-assisted TPN prescription system / calculation software / TPN (total parenteral nutrition) / fluid therapy / questionnaire (Link to Publication Site) ● Publication site (DOI): 10.5649/jjphcs.31.279 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679753550336 ● Search Scopus @ Elsevier (DOI): 10.5649/jjphcs.31.279 (DOI: 10.5649/jjphcs.31.279, CiNii: 1390282679753550336)
108.	Masumi Okamoto, Koichiro Tsuchiya, Yasuhisa Kanematsu, Yuki Izawa, Masanori Yoshizumi, Susumu Kagawa and Toshiaki Tamaki : Nitrite-derived nitric oxide formation following ischemia-reperfusion injyury in kidney., American Journal of Physiology, Renal Physiology, Vol.288, No.1, 182-187, 2005. (Summary) Nitric oxide (NO) is synthesized from l-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are believed to be waste forms of NO. We previously reported an enzyme-independent pathway of NO generation from nitrite in acidic conditions. In this study, we show nitrite-derived NO formation in renal ischemia-reperfusion injury using electron paramagnetic resonance (EPR) spectroscopy. In this experiment, we utilized a stable isotope of [(15)N]nitrite as a source of nitrite to distinguish l-arginine-derived NO from [(15)N]nitrite-derived (15)NO. Intravenous infusion of a stable isotope of [(15)N]nitrite ((15)NO(2)(-)) facilitated the formation of Hb(15)NO during renal ischemia, which demonstrated that the origin of NO was nitrite. The EPR signal of Hb(15)NO in kidney appeared after 40 min of renal ischemia, and renal reperfusion decreased the Hb(15)NO level in the kidney and increased it in blood by contrast. In addition, the amount of HbNO was nitrite concentration dependent, and this formation was NOS independent. Our findings suggest that nitrite can be an alternative source of NO in ischemic kidney and that it binds with hemoglobin and then is spread by the circulation after reperfusion. (Keyword) Animals / Electron Spin Resonance Spectroscopy / Hemoglobins / Kidney / Male / nitric oxide / Nitric Oxide Synthase / Nitrites / Rats / Rats, Sprague-Dawley / Reperfusion Injury (Link to Publication Site) ● Publication site (DOI): 10.1152/ajprenal.00036.2004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15367387 ● Search Scopus @ Elsevier (PMID): 15367387 ● Search Scopus @ Elsevier (DOI): 10.1152/ajprenal.00036.2004 (DOI: 10.1152/ajprenal.00036.2004, PubMed: 15367387)
109.	Koichiro Tsuchiya, Yoshiharu Takiguchi, Masumi Okamoto, Yuki Izawa, Yasuhisa Kanematsu, Masanori Yoshizumi and Toshiaki Tamaki : Malfunction of vascular control in lifestyle-related diseases : formation of systemic hemoglobin-nitric oxide Complex(HbNO) From Dietary Nitrite, Journal of Pharmacological Sciences, Vol.96, No.4, 395-400, 2004. (Summary) Nitric oxide (NO) has many physiological functions. It is believed to be produced from L-arginine by nitric oxide synthase (NOS), and nitrite and nitrate are waste forms of it. By the way, nitrate and nitrite are abundant in vegetables and fruits, especially leafy vegetables and pickled vegetables. Orally-ingested nitrate is changed to nitrite by micro-organelles living in the hypopharynx area, and nitrite is expected to change to NO in the stomach due to its low pH. Indeed, some researchers reported that NO is produced in the gastric cavity, although few reports mentioned the physiological meanings of this NO formation. Therefore, we investigated whether the nitrite-derived NO can shift to the circulation and acts like NOS-derived NO does in tissues. We adopted a stable isotope of nitrite (15NO2-) in order to distinguish between the endogenous nitrite and the exogenously administered one and measured nitrosyl hemoglobin (HbNO) as an index of circulating NO using electron paramagnetic resonance spectroscopy. It appeared that the oral administration of 15N-nitrite formed the Hb15NO in rat blood and decreased the blood pressure of chronic L-NAME treated rats. Our findings suggest that the intake of nitrite (or nitrate)-rich foods such as vegetables and fruits would alter the systemic HbNO dynamism, resulting in the improvement of cardiovascular diseases. (Keyword) nitric oxide(NO) / hemoglobin-NO adduct / electron paramagnetic resonance / nitrite (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FMJ04006X3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15599101 ● Search Scopus @ Elsevier (PMID): 15599101 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FMJ04006X3 (DOI: 10.1254/jphs.FMJ04006X3, PubMed: 15599101)
110.	Kaori Akai, Koichiro Tsuchiya, Akira Tokumura, Kentaro Kogure, Satoru Ueno, Akira Shibata, Toshiaki Tamaki and Kenji Fukuzawa : Ability of ferric nitrilotriacetate complex with three pH-dependent conformations to induce lipid peroxidation., Free Radical Research, Vol.38, No.9, 951-962, 2004. (Link to Publication Site) ● Publication site (DOI): 10.1080/1071576042000261945 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15621713 ● Search Scopus @ Elsevier (PMID): 15621713 ● Search Scopus @ Elsevier (DOI): 10.1080/1071576042000261945 (DOI: 10.1080/1071576042000261945, PubMed: 15621713)
111.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Yuki Izawa, Yasuhisa Kanematsu, Yoshiko Fujita, Nermin Ali, Keisuke Ishizawa, Aiko Yamauchi and Toshiaki Tamaki : Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation, Journal of Pharmacological Sciences, Vol.95, No.4, 483-486, 2004. (Summary) We examined the effects of the stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on cellular glutathione (GSH) concentration and whether NAC-regulated cellular GSH levels are directly associated with angiotensin II (Ang II)-induced intracellular signaling events in vascular smooth muscle cells (VSMC). Both L-NAC and D-NAC similarly increased intracellular GSH concentration. We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC. Our present study indicates the comparable effects of NAC stereoisomers in regulating intracellular GSH and the redox-dependent intracellular signaling mechanisms in VSMC. (Keyword) Acetylcysteine / Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / Cell Proliferation / Enzyme Activation / Glutathione / JNK Mitogen-Activated Protein Kinases / Male / Mitogen-Activated Protein Kinases / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Rats / Rats, Sprague-Dawley / Signal Transduction / Stereoisomerism / Thymidine / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.SC0040061 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15297771 ● Search Scopus @ Elsevier (PMID): 15297771 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.SC0040061 (DOI: 10.1254/jphs.SC0040061, PubMed: 15297771)
112.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Yuki Izawa, Yasuhisa Kanematsu and Toshiaki Tamaki : Atheroprotective effects of antioxidants through inhibition of mitogen-activated protein kinases, Acta Pharmacologica Sinica, Vol.25, No.8, 977-985, 2004. (Summary) Reactive oxygen species (ROS) have been known to play an important role in the pathogenesis of atherosclerosis and several other cardiovascular diseases. It is now apparent that ROS induce endothelial cell damage and vascular smooth muscle cell (VSMC) growth and cardiac remodeling, which are associated with hypertension, atherosclerosis, heart failure, and restenosis. Several lines of evidence have indicated that ROS and mitogen-activated protein (MAP) kinases were involved in vascular remodeling under various pathological conditions. Recently, it was also reported that MAP kinases were sensitive to oxidative stress. MAP kinases play an important role in cell differentiation, growth, apoptosis, and the regulation of a variety of transcription factors and gene expressions. Bioflavonoids and polyphenolic compounds are believed to be beneficial for the prevention and treatment of atherosclerosis and cardiovascular diseases. One of the most widely distributed bioflavonoids, 3,3',4',5,7-penta-hydroxyflavone (quercetin) and its metabolite quercetin 3-O-beta-D-glucuronide (Q3GA) inhibited Angiotensin II-stimulated JNK activation and resultant hypertrophy of VSMC. Several studies have suggested that various antioxidants including probucol, N-acetyl-L-cysteine, diphenylene iodonium, Trolox C (vitamin E analogue), and vitamin C inhibit VSMC growth, which is associated with pathogenesis of cardiovascular diseases. Therefore, inhibition of MAP kinases by antioxidant treatment may prove to be a therapeutic strategy for cardiovascular diseases. In contrast, some clinical studies have reported that antioxidant vitamins did not show beneficial effects in coronary artery disease or in a number of high-risk people. Thus, further studies are needed to clarify why antioxidants showed beneficial effects in vitro, whereas less satisfactory results were obtained in some clinical conditions. (Keyword) reactive oxygen species / mitogen-activated protein kinase / antioxidant / vascular smooth muscle cell / atherosclerosis (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15301727 ● Search Scopus @ Elsevier (PMID): 15301727 (PubMed: 15301727)
113.	Keisuke Ishizawa, Masanori Yoshizumi, Koichiro Tsuchiya, Hitoshi Houchi, Kazuo Minakuchi, Yuki Izawa, Yasuhisa Kanematsu, Shoji Kagami, Masao Hirose and Toshiaki Tamaki : Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and facilitation of monocyte recruitment through monocyte chemoattractant protein-1 production by mesangial cells, Hypertension Research, Vol.27, No.6, 433-440, 2004. (Summary) We previously found that human chymase selectively cleaves big endothelin-1 (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 (1-31), without any further degradation products. In this study, we investigated the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) and on cells of the human monocytic cell line, THP-1. In addition, we examined the interaction between RMCs and THP-1 cells using conditioned media from ET-1 (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a concentration-dependent manner, and the degree of increase was similar to those by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause significant migration of THP-1 cells. However, significant recruitment of THP-1 cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was increased by treatment with ET-1 (1-31). The addition of neutralizing antibody for MCP-1 to the medium inhibited the migration of THP-1 cells induced by conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly cause the migration of mesangial cells (MCs) and may be responsible for the recruitment of mononuclear cells mediated through the activation of MCs. Since human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) may be among the mediators. (Keyword) Animals / Antibodies / Antihypertensive Agents / Cell Movement / Cells, Cultured / Chemokine CCL2 / Culture Media, Conditioned / Endothelin-1 / Glomerular Mesangium / Peptide Fragments / Peptides, Cyclic / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.27.433 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15253109 ● Search Scopus @ Elsevier (PMID): 15253109 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.27.433 (DOI: 10.1291/hypres.27.433, PubMed: 15253109)
114.	Yuki Suzaki, Masanori Yoshizumi, Shoji Kagami, Akira Nishiyama, Yuichi Ozawa, Moe Kyaw, Yuki Izawa, Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions, Kidney International, Vol.65, No.5, 1749-1760, 2004. (Summary) High glucose causes renal cell injury through various signal transduction pathways, including mitogen-activated protein (MAP) kinases cascades. Big MAP kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a recently identified MAP kinase family member and was reported to be sensitive to osmotic and oxidative stress. However, the role of BMK1 in diabetic nephropathy has not been elucidated yet. We investigated whether BMK1 is activated in the glomeruli of Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus in comparison with the control Long Evans Tokushima Otsuka (LETO) rats. We also examined the effect of high glucose on BMK1 activity in cultured rat mesangial cells. BMK1 and ERK1/2 but not p38 were activated in the glomeruli of OLETF rats, which showed diabetic nephropathy at 52 weeks of age. High glucose, in addition to a high concentration of raffinose, caused rapid and significant activation of BMK1 in rat mesangial cells. MAP kinase/ERK kinase (MEK) inhibitors, U0126 and PD98059, both inhibited BMK1 activation by high glucose in a concentration-dependent manner. Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation. Src kinase inhibitors, herbimycin A and PP2, also inhibited high glucose-induced BMK1 activation. PKC inhibitors, Src inhibitors and MEK inhibitors, all inhibited cell proliferation by high glucose. Finally, transfection of dominant-negative MEK5, which is an upstream regulator of BMK1, abolished the BMK1-mediated rat mesangial cell proliferation stimulated by high glucose. In the present study, we demonstrated that high glucose activates BMK1 both in vivo and in vitro. It was suggested that high glucose induces PKC- and c-Src-dependent BMK1 activation. It could not be denied that BMK1 activation is induced through an osmotic stress-sensitive mechanism. BMK1-mediated mesangial cell growth may be involved in the pathogenesis of diabetic nephropathy. (Keyword) Animals / Butadienes / Cells, Cultured / Diabetes Mellitus, Type 2 / Diabetic Nephropathies / Enzyme Activation / Enzyme Inhibitors / Glomerular Mesangium / glucose / MAP Kinase Kinase 5 / Male / Mitogen-Activated Protein Kinase 7 / Nitriles / Organic Chemicals / Protein Kinase C / Protein-Tyrosine Kinases / Rats / Rats, Inbred OLETF (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1523-1755.2004.00576.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15086914 ● Search Scopus @ Elsevier (PMID): 15086914 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1523-1755.2004.00576.x (DOI: 10.1111/j.1523-1755.2004.00576.x, PubMed: 15086914)
115.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Shoji Kagami, Yuki Izawa, Yoshiko Fujita, Nermin Ali, Yasuhisa Kanematsu, Kazunori Toida, Kazunori Ishimura and Toshiaki Tamaki : Src and Cas are essentially but differentially involved in angiotensin II-stimulated migration of vascular smooth muscle cell via extracellur signal-regulated kinase 1/2 and c-Jun NH2-terminal kinase activation, Molecular Pharmacology, Vol.65, No.4, 832-841, 2004. (Summary) Angiotensin II (Ang II) plays an important role in several cardiovascular diseases associated with vascular smooth muscle cell (VSMC) growth and migration. Src activity is known to be required for the migration of a number of cell types. p130Cas was reported to be essential for cell migration and actin filament reorganization. Mitogen-activated protein (MAP) kinases were also reported to be critical regulatory factors for growth and migration of VSMC. However, precise intracellular mechanisms involving c-Src, p130Cas, and MAP kinases in Ang II-stimulated migration of VSMC have not been well elucidated. Here we demonstrated that Ang II rapidly and significantly stimulated tyrosine phosphorylation of Src and Cas and their association in rat aortic smooth muscle cells (RASMC). Ang II-stimulated tyrosine phosphorylation of Src and Cas and activation of ERK1/2 and JNK, but not p38, were potently inhibited by Src family tyrosine kinase inhibitors, herbimycin A (HA) and PP2. Ang II-stimulated Src and Cas association, tyrosine phosphorylation of Cas, and activation of ERK1/2 and JNK were suppressed in kinase-inactive Src (KI Src)-overexpressed RASMC. Ang II-stimulated JNK activation but not ERK1/2 activation was blocked in substrate domain-deleted Cas (DeltaSD Cas)-overexpressed RASMC. In addition, HA, PP2, ERK1/2 inhibitor, 2'-amino-3'-methoxyflavone (PD98059) and JNK inhibitor, and anthra[1,9-cd]pyrazol-6(2H)-one (SP600125) significantly inhibited Ang II-stimulated migration of RASMC. Ang II-induced colocalization of Src and Cas and migration were inhibited in both KI Src- and DeltaSD Cas-overexpressed RASMC. These findings suggest that Src and Cas are essentially but differentially involved in Ang II-stimulated migration of VSMC through the activation of ERK1/2 and JNK. (Keyword) Angiotensin II / Animals / Cell Adhesion / Cell Movement / Cells, Cultured / Cellular Apoptosis Susceptibility Protein / Enzyme Activation / Genes, src / JNK Mitogen-Activated Protein Kinases / Male / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Muscle, Smooth, Vascular / phosphorylation / Rats / Rats, Sprague-Dawley / Tyrosine / Vinculin / src-Family Kinases (Link to Publication Site) ● Publication site (DOI): 10.1124/mol.65.4.832 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15044612 ● Search Scopus @ Elsevier (PMID): 15044612 ● Search Scopus @ Elsevier (DOI): 10.1124/mol.65.4.832 (DOI: 10.1124/mol.65.4.832, PubMed: 15044612)
116.	Masanori Yoshizumi, Yoshiko Fujita, Yuki Izawa, Yuki Suzaki, Moe Kyaw, Nermin Ali, Koichiro Tsuchiya, Shoji Kagami, Seiji Yano, Saburo Sone and Toshiaki Tamaki : Ebselen inhibits tumor necrosis factor-α-induced c-jun N-terminal kinase activation and adhesion molecule expression in endothelial cells, Experimental Cell Research, Vol.292, No.1, 1-10, 2004. (Summary) Tumor necrosis factor-alpha (TNF-alpha) stimulates expression of endothelial cell (EC) genes that may promote atherosclerosis in part by an activation of mitogen-activated protein (MAP) kinases. Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one), a selenoorganic compound, is effective for acute ischemic stroke; however, its effect on EC has not yet been elucidated. We examined the effect of ebselen on TNF-alpha-induced MAP kinase activation and adhesion molecule expression in cultured human umbilical vein endothelial cells (HUVEC). Extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 were rapidly and significantly activated by TNF-alpha in HUVEC. TNF-alpha-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 were not affected. Apoptosis signal-regulated kinase 1 (ASK1) was suggested to be involved in TNF-alpha-induced JNK activation because transfection of kinase-inactive ASK1 inhibited TNF-alpha-induced JNK activation. Ebselen inhibited TNF-alpha-induced TNF receptor-associated factor 2 (TRAF2)-ASK1 complex formation and phosphorylation of stress-activated protein kinase ERK kinase 1 (SEK1), which is an upstream signaling molecule of JNK. Finally, TNF-alpha-induced activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) activation and resultant intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions were inhibited by ebselen. Specific inhibitors for JNK and NF-kappaB also inhibited TNF-alpha-induced ICAM-1 and VCAM-1 expressions in HUVEC. These findings suggest that ebselen prevents TNF-alpha-induced EC activation through the inhibition of TRAF2-ASK1-SEK1 signaling pathway, which leads to JNK activation. Inhibition of JNK by ebselen may imply its usefulness for the prevention of atherosclerosis relevant to EC activation. (Keyword) Azoles / Cell Adhesion Molecules / Cells, Cultured / Endothelium, Vascular / Enzyme Activation / Humans / Intercellular Adhesion Molecule-1 / JNK Mitogen-Activated Protein Kinases / MAP Kinase Kinase 4 / Mitogen-Activated Protein Kinase Kinases / Mitogen-Activated Protein Kinases / NF-kappa B / Organoselenium Compounds / Phosphorylation / Time Factors / Transcription Factor AP-1 / Tumor Necrosis Factor-alpha / Umbilical Veins / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2003.08.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14720501 ● CiNii @ National Institute of Informatics (CRID): 1571980076667609856 ● Search Scopus @ Elsevier (PMID): 14720501 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2003.08.003 (DOI: 10.1016/j.yexcr.2003.08.003, PubMed: 14720501, CiNii: 1571980076667609856)
117.	Nermin Ali, Masanori Yoshizumi, Koichiro Tsuchiya, Moe Kyaw, Yoshiko Fujita, Yuki Izawa, Shinji Abe, Yasuhisa Kanematsu, Shoji Kagami and Toshiaki Tamaki : Ebsalen inhibits p38MAP kinase-mediated endothelial cell death by hydrogen peroxide., European Journal of Pharmacology, Vol.485, No.1-3, 127-135, 2004. (Summary) Ebselen (2-phenyl-1, 2-benzisoselenazol-3[2H]-one) is a seleno-organic compound exhibiting both glutathione peroxidase and antioxidant activity. Although it has been reported that ebselen is effective against hydrogen peroxide (H(2)O(2))-induced cell death in several cell types, its effect on endothelial cell damage has not yet been elucidated. In the present study, we examined the effect of ebselen on H(2)O(2)-induced human umbilical vein endothelial cells (HUVECs) death, and its intracellular mechanism. Our findings showed that pretreatment of HUVECs with ebselen resulted in a significant recovery from H(2)O(2)-induced cell death in a concentration-dependent manner. In addition to the inhibition of lactate dehydrogenase (LDH) leakage, ebselen inhibited H(2)O(2)-induced cytochrome c release and caspase-3 activation and the resultant apoptosis in HUVECs. Moreover, it was observed that H(2)O(2) significantly stimulated activation of mitogen-activated protein (MAP) kinases, i.e., p38 MAP kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK1/2). Ebselen inhibited H(2)O(2)-induced p38 MAP kinase, but not JNK or ERK1/2 activation. Furthermore, SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]-1H-imidazole), a specific p38 MAP kinase inhibitor, inhibited H(2)O(2)-induced p38 MAP kinase phosphorylation, cytochrome c release, caspase-3 activation, as well as cell death in HUVECs. These findings suggest that ebselen attenuates H(2)O(2)-induced endothelial cell death through the inhibition of signaling pathways mediated by p38 MAP kinase, caspase-3, and cytochrome c release. Thus, inhibition of p38 MAP kinase by ebselen may imply its usefulness for prevention and/or treatment of endothelial cell dysfunction, which was suggested to be the first step in the development of atherosclerosis. (Keyword) Azoles / cell death / Cell Survival / Dose-Response Relationship, Drug / Endothelial Cells / Enzyme Inhibitors / Humans / hydrogen peroxide / Mitogen-Activated Protein Kinases / Organoselenium Compounds / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2003.11.079 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14757132 ● Search Scopus @ Elsevier (PMID): 14757132 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2003.11.079 (DOI: 10.1016/j.ejphar.2003.11.079, PubMed: 14757132)
118.	Shinji Abe, Kazuyoshi Kirima, Koichiro Tsuchiya, Masumi Okamoto, Toyoshi Hasegawa, Hitoshi Houchi, Masanori Yoshizumi and Toshiaki Tamaki : The reaction rate of edaravone ( 3-methyl-1-phenyl-2-pyrazolin-5-one(MCI-186) with hydroxyl radical., Chemical & Pharmaceutical Bulletin, Vol.52, No.2, 186-191, 2004. (Summary) The pyrazoline derivative edaravone is a potent hydroxyl radical scavenger that has been approved for attenuation of brain damage caused by ischemia-reperfusion. In the present work, we first determined the rate constant, k(r), at which edaravone scavenges radicals generated by a Fenton reaction in aqueous solution in the presence of the spin trap agent, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), which competed with edaravone. We detected the edaravone radicals in the process of hydroxyl radical scavenging and found that edaravone reacts with hydroxyl radical around the diffusion limit (k(r)=3.0 x 10(10) M(-1) s(-1)). The EPR (electron paramagnetic resonance) spectrum of the edaravone radical was observed by oxidation with a horseradish peroxidase-hydrogen peroxide system using the fast-flow method. This radical species is unstable and changed to another radical species with time. In addition, it was found that edaravone consumed molecular oxygen when it was oxidized by horseradish peroxidase (HRP)-H(2)O(2) system, and that edaravone was capable of providing two electrons to the electrophiles. The possible mechanisms for oxidation of edaravone were investigated from these findings. (Keyword) Antipyrine / Cyclic N-Oxides / Electron Spin Resonance Spectroscopy / Free Radical Scavengers / Hydroxyl Radical / Oxidation-Reduction / Spin Trapping (Link to Publication Site) ● Publication site (DOI): 10.1248/cpb.52.186 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14758002 ● CiNii @ National Institute of Informatics (CRID): 1390001204168756992 ● Search Scopus @ Elsevier (PMID): 14758002 ● Search Scopus @ Elsevier (DOI): 10.1248/cpb.52.186 (DOI: 10.1248/cpb.52.186, PubMed: 14758002, CiNii: 1390001204168756992)
119.	Toyoshi Hasegawa, Atsushi Bando, Koichiro Tsuchiya, Shinji Abe, Masumi Okamoto, Kazuyoshi Kirima, Satoru Ueno, Masanori Yoshizumi, Hitoshi Houchi and Toshiaki Tamaki : Enzymatic and non-enzymatic formation of reactive oxygen species from 6-anilino-5,8-quinolineequinone, Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1670, No.1, 19-27, 2004. (Summary) The nonenzymatic and enzymatic formation of reactive oxygen species (ROS) from LY83583 (6-anilino-5,8-quinolinequinone) was investigated by electron paramagnetic resonance (EPR) spectroscopy. In the presence of thiol compounds such as glutathione and L-cysteine, LY83583 underwent a one-electron reduction due to low redox potential (-0.3+/-0.01 V vs. SCE), followed by formation of LY83583 semiquinone anion radical. This species was characterized by EPR spectroscopy under an argon atmosphere at neutral pH. Under an aerobic condition, this species interacts with molecular oxygen to form a superoxide anion radical. GSH-conjugated LY83583 was also identified by NMR and FAB-MS. When LY83583 was applied to PC12 cells, ROS formation was completely inhibited by both the flavoenzyme inhibitor DPI and the DT-diaphorase inhibitor dicumarol. On the other hand, ROS generation occurred independent of intracellular GSH level. These results indicate that LY83583 can generate ROS both enzymatically and nonenzymatically, although the enzymatic formation is dominant over the nonenzymatic system in PC12 cells. (Keyword) Aminoquinolines / Animals / Chromatography, High Pressure Liquid / Cyclic N-Oxides / Electrochemistry / Electron Spin Resonance Spectroscopy / Enzyme Inhibitors / Glutathione / Glutathione Disulfide / Magnetic Resonance Spectroscopy / Mass Spectrometry / Molecular Structure / Oxygen Consumption / PC12 Cells / Rats / Reactive Oxygen Species / Spin Trapping (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2003.10.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14729138 ● Search Scopus @ Elsevier (PMID): 14729138 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbagen.2003.10.008 (DOI: 10.1016/j.bbagen.2003.10.008, PubMed: 14729138)
120.	Mami Azuma, Hitoshi Houchi, Hirotaka Nishisako, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuhiko Teraoka, Toshitaka Ikehara, Takenori Kusumi and Kazuo Minakuchi : Inhibitory action of novel arginine derivative on catecholamine secretion evoked by acetylcholine from cultured bovine adrenal chromaffin cells, Journal of Cardiovascular Pharmacology, Vol.42, No.Suppl. 1, S15-S18, 2003. (Summary) A novel product, 4-amino-5-guanidinopentanoic acid 15-[(4-aminobutyl)-3-aminopropylcarbamoyl] pentadecyl ester (Arg-HSA-Spm), was synthesized based on ptilomycalin A, which is one of the extracts from marine sponge. Arg-HSA-Spm contains arginine in its chemical structure. The pharmacological action of Arg-HSA-Spm on catecholamine secretion from cultured bovine adrenal chromaffin cells was examined. Arg-HSA-Spm inhibited catecholamine secretion stimulated by the physiological secretagog acetylcholine. This inhibitory action of Arg-HSA-Spm on catecholamine secretion induced by 10(-4) M acetylcholine was dose-dependent from 10(-8) M to 10(-5) M. In the presence of 3 x 10(-7) M Arg-HSA-Spm, the stimulation of catecholamine secretion observed by increasing acetylcholine up to 10(-3) M did not reach the maximal level observed without Arg-HSA-Spm. Arg-HSA-Spm at 10(-5) M suppressed both the increase in intracellular free Ca2+ level and the influx of 45Ca2+ induced by 10(-4) M acetylcholine. The Arg-HSA-Spm-induced suppression of intracellular free Ca2+ level, the influx of 45Ca2+ and catecholamine secretion were not observed in the presence of extracellular K+ at 56 mM. The results presented in this study suggested that Arg-HSA-Spm may inhibit the influx of extracellular Ca2+ into the cells, probably through its blocking action related to acetylcholine receptors, resulting in the inhibition of catecholamine secretion in adrenal chromaffin cells. (Keyword) Acetylcholine / Adrenal Medulla / Alkaloids / Animals / Arginine / calcium / Calcium Radioisotopes / Carbamates / Catecholamines / Cattle / Cells, Cultured / Chromaffin Cells / Dose-Response Relationship, Drug / Guanidines / Spermidine (Link to Publication Site) ● Publication site (DOI): 10.1097/00005344-200312001-00005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14871022 ● Search Scopus @ Elsevier (PMID): 14871022 ● Search Scopus @ Elsevier (DOI): 10.1097/00005344-200312001-00005 (DOI: 10.1097/00005344-200312001-00005, PubMed: 14871022)
121.	Koichiro Tsuchiya, Kazuyoshi Kirima, Masanori Yoshizumi and Toshiaki Tamaki : New methods to evaluate endotherial function: Evaluation of endotherial function by hemoglobin-nitric oxide complex using electron paramagnetic resonance spectroscopy, Journal of Pharmacological Sciences, Vol.93, No.4, 417-422, 2003. (Summary) This minireview describes the practical use of assay systems to detect nitric oxide (NO) by electron paramagnetic resonance (EPR) spectroscopy for evaluation of endothelial functions. The iron(II)-dithiocarbamate complexes, such as iron(II)-(N-methyl-D-glucamine dithiocarbamate), are commonly used in EPR detection of NO both in vivo and in vitro. However, due to their redox activity, these complexes have some drawbacks that limit their usefulness for the detection of NO. On the other hand, the measurement of hemoglobin-NO adduct (HbNO) in whole blood by the EPR method seems relevant for the assessment of systemic NO levels. However, ceruloplasmin and an unknown radical species overlapping the same magnetic field as that of HbNO, which makes it physically impossible to measure small amounts of HbNO. Thus, to reveal the EPR spectrum of HbNO, we developed the EPR signal subtraction method, which is based on the computer-assisted subtraction of the digitized EPR spectrum of HbNO-depleted blood from that of the sample blood using software. Using this technique, we succeeded in measuring the steady blood HbNO level as an index of NO by the EPR HbNO signal subtraction method. We also demonstrated that temocapril reduces abnormalities of NO dynamics in the L-NAME (N(omega)-nitro-L-arginine-methylester)-induced endothelial dysfunction of rats using the EPR HbNO signal subtraction method. (Keyword) Animals / Electron Spin Resonance Spectroscopy / Endothelium, Vascular / Ferrous Compounds / Hemoglobin A, Glycosylated / Nitric Oxide / Rats / Spin Trapping / Thiocarbamates (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.93.417 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14737011 ● Search Scopus @ Elsevier (PMID): 14737011 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.93.417 (DOI: 10.1254/jphs.93.417, PubMed: 14737011)
122.	Kentaro Kogure, Koichiro Tsuchiya, Kazutoyo Abe, Michinori Akasu, Toshiaki Tamaki, Kenji Fukuzawa and Hiroshi Terada : Direct radical scavenging by the bisbenzylisoquinoline alkaloid cepharanthine., Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1622, No.1, 1-5, 2003. (Summary) Cepharanthine (Ceph) is known as a potent antiperoxidative agent. Recently, we characterized the antiperoxidative effects of Ceph [Biochim. Biophys. Acta 1426 (1999) 133]. However, it was not clear whether the antiperoxidative effect is really due to its direct radical scavenging activity. Therefore, we studied the interaction of Ceph with the hydroxyl radical (OH) by the electron paramagnetic resonance (EPR) technique. Results showed that Ceph actually scavenged OH derived by the Fenton reaction. We also found that Ceph radicals were generated on interaction of Ceph with *OH in neutral aqueous solution, but not in acidic solution, consistent with the pH-dependent anti-lipid peroxidation activity of Ceph. Hence, we concluded that anti-lipid peroxidation by Ceph is due to its direct radical scavenging activity. (Keyword) Alkaloids / Antioxidants / Benzylisoquinolines / Electron Spin Resonance Spectroscopy / Free Radical Scavengers / Hydrogen-Ion Concentration / Hydroxyl Radical / Lipid Peroxidation (Link to Publication Site) ● Publication site (DOI): 10.1016/S0304-4165(03)00095-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12829254 ● Search Scopus @ Elsevier (PMID): 12829254 ● Search Scopus @ Elsevier (DOI): 10.1016/S0304-4165(03)00095-3 (DOI: 10.1016/S0304-4165(03)00095-3, PubMed: 12829254)
123.	Masanori Yoshizumi, Abe Jun-ichi, Koichiro Tsuchiya, Bradford C.Berk and Toshiaki Tamaki : Stress and vascular responses: Atheroprotective effect of laminar fluid shear stress in endothelial cells: Possible role of mitogen-activated protein kinases ( Review ), Journal of Pharmacological Sciences, Vol.91, No.3, 172-176, 2003. (Summary) Atherosclerosis preferentially occurs in areas of turbulent blood flow and low fluid shear stress, whereas laminar blood flow and high shear stress are atheroprotective. Inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), stimulate expression of endothelial cell (EC) genes that may promote atherosclerosis. Recent findings suggest a steady laminar blood flow decreases EC apoptosis and inhibits TNF-mediated EC activation. EC apoptosis or activation is suggested to be involved in plaque erosion, which may lead to platelet aggregation. TNF-alpha regulates gene expression in ECs, in part, by stimulating mitogen-activated protein (MAP) kinases, which phosphorylate transcription factors. We hypothesized that steady laminar flow inhibits cytokine-mediated activation of MAP kinases in ECs. To test this hypothesis, we determined the effects of steady laminar flow (shear stress = 12 dynes/cm(2)) on TNF-alpha-stimulated activity of three MAP kinases in human umbilical vein ECs (HUVEC): extracellular signal-regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), and p38. TNF-alpha activated ERK1/2, JNK, and p38 maximally at 15 min in HUVEC. Pre-exposing HUVEC for 10 min to flow inhibited TNF-alpha activation of JNK, but showed no significant effect on ERK1/2 or p38 activation. Incubation of HUVEC with PD98059, a specific ERK1/2 inhibitor, blocked the flow-mediated inhibition of TNF activation of JNK. Transfection studies with dominant-negative constructs of the protein kinase MEK5 suggested an important role for big mitogen-activated protein kinase 1 (BMK1) in flow-mediated regulation of EC activation by TNF-alpha. Understanding the mechanisms by which steady laminar flow regulates JNK activation by cytokines may provide insight into the atheroprotective mechanisms induced by laminar blood flow. (Keyword) Animals / Arteriosclerosis / Blood Vessels / Endothelium, Vascular / Humans / JNK Mitogen-Activated Protein Kinases / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase 7 / Mitogen-Activated Protein Kinases / Stress, Mechanical / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.91.172 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12686737 ● Search Scopus @ Elsevier (PMID): 12686737 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.91.172 (DOI: 10.1254/jphs.91.172, PubMed: 12686737)
124.	Yuichi Ozawa, Toyoshi Hasegawa, Koichiro Tsuchiya, Masanori Yoshizumi and Toshiaki Tamaki : Effect of endothelin-1(1-31) on the renal resistance vessels., The Journal of Medical Investigation : JMI, Vol.50, No.1-2, 87-94, 2003. (Summary) Human chymase produces not only angiotensin II but also endothelin(ET)-1(1-31). We previously reported that ET-1(1-31) had several biological activities in vascular smooth muscle cells. In this study, we investigated the vasoconstrictor effect of ET-1(1-31) on the renal resistance vessels using in vitro microperfused rabbit afferent and efferent arterioles. ET-1(1-31) decreased the lumen diameter of the afferent and efferent arterioles dose-dependently. ET-1(1-31)-induced afferent arteriolar vasoconstriction was not affected by phosphoramidon, an ET converting enzyme inhibitor. ET-1(1-31)-induced renal arteriolar vasoconstriction was inhibited by BQ123, an ETA receptor inhibitor, but not by BQ788, an ETB receptor inhibitor. These results suggest that ET-1(1-31)-induced renal arteriolar vasoconstriction may be mediated by ETA-like receptors. (Keyword) Animals / Arterioles / Aspartic Acid Endopeptidases / Dose-Response Relationship, Drug / Endothelin-1 / Enzyme Inhibitors / Glycopeptides / Humans / Kidney / Male / Metalloendopeptidases / Muscle, Smooth, Vascular / Oligopeptides / Peptide Fragments / Peptides, Cyclic / Perfusion / Piperidines / Rabbits / Receptor, Endothelin A / Receptors, Endothelin / Vascular Resistance / Vasoconstriction / Vasoconstrictor Agents (Tokushima University Institutional Repository) ● Metadata: 110682 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12630573 ● Search Scopus @ Elsevier (PMID): 12630573 (Tokushima University Institutional Repository: 110682, PubMed: 12630573)
125.	Kazuyoshi Kirima, Koichiro Tsuchiya, Hiroyoshi Sei, Toyoshi Hasegawa, Michiyo Shikishima, Yuki Motobayashi, Kyoji Morita, Masanori Yoshizumi and Toshiaki Tamaki : Evaluatin of systemic blood NO dynamics by EPR Spectoscopy: HbNO as an endogenous index of NO, American Journal of Physiology, Heart and Circulatory Physiology, Vol.285, No.2, H589-H596, 2003. (Summary) The measurement of hemoglobin-nitric oxide (NO) adduct (HbNO) in whole blood by the electron paramagnetic resonance (EPR) method seems relevant for the assessment of systemic NO levels. However, ceruloplasmin and unknown radical species overlap the same magnetic field as that of HbNO. To reveal the EPR spectrum of HbNO, we then introduced the EPR signal subtraction method, which is based on the computer-assisted subtraction of the digitized EPR spectrum of HbNO-depleted blood from that of sample blood using the software. Rats were treated with N(omega)-nitro-L-arginine methyl ester (L-NAME; 120 mg. kg-1. day-1) for 1 wk to obtain HbNO-depleted blood. When this method was applied to the analysis of untreated fresh whole blood, the five-coordinate state of HbNO was observed. HbNO concentration in pentobarbital-anesthetized rats was augmented (change in [HbNO] = 1.6-5.5 microM) by infusion of L-arginine (0.2-0.6 g/kg) but not D-arginine. Using this method, we attempted to evaluate the effects of temocapril on HbNO dynamics in an L-NAME-induced rat endothelial dysfunction model. The oral administration of L-NAME for 2 wk induced a serious hypertension, and the HbNO concentration was reduced (change in [HbNO] = 5.7 microM). Coadministration of temocapril dose dependently improved both changes in blood pressure and the systemic HbNO concentration. In this study, we succeeded in measuring the blood HbNO level as an index of NO by the EPR HbNO signal subtraction method. We also demonstrated that temocapril improves abnormalities of NO dynamics in L-NAME-induced endothelial dysfunction rats using the EPR HbNO signal subtraction method. (Keyword) Angiotensin-Converting Enzyme Inhibitors / Animals / Arginine / Calibration / Electron Spin Resonance Spectroscopy / Enzyme Inhibitors / Hemoglobins / Hypertension / Male / NG-Nitroarginine Methyl Ester / Nitric Oxide / Rats / Rats, Sprague-Dawley / Thiazepines (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpheart.01010.2002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12663263 ● Search Scopus @ Elsevier (PMID): 12663263 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpheart.01010.2002 (DOI: 10.1152/ajpheart.01010.2002, PubMed: 12663263)
126.	Yuki Suzaki, Masanori Yoshizumi, Yukio Yamashita, Shinji Abe, Koichiro Tsuchiya, Yumiko Satoh, Yasuhiro Kuroda, Kazuya Horike, Masashi Kano, Yoshio Fukuta, Takashi Kitaichi, Takaki Hori, Yutaka Masuda, Tetsuya Kitagawa, Kazuo Minakuchi and Toshiaki Tamaki : Determination of plasma concentrations of endothelin-1(1-31) and endothelin-1 in healthy subjects and patients with atherosclerosis., Journal of Cardiovascular Pharmacology, Vol.41, No.suppl.1, S83-S87, 2003. (Summary) We previously found that human chymase cleaves big endothelins at the Tyr31-Gly32 bond and produces 31-amino-acid endothelins, endothelins(1-31). Endothelin-1(1-31) has been isolated from a number of human organs, including the heart and lungs. As endothelin-1 has been shown to play a significant role in the paracrine regulation of cardiovascular functions in humans, it is possible that endothelin-1(1-31) may also exhibit biological activity on human tissues. We previously reported that synthetic endothelin-1(1-31) exhibits a number of physiological actions on cultured cells in vitro. In the present study, we investigated the plasma concentrations of endothelin-1(1-31) and endothelin-1 in healthy subjects and compared them with those in patients with cardiovascular diseases. Endothelin-1(1-31) and endothelin-1 in human plasma was measured using a sandwich-enzyme-immunoassay system, which was recently described for measurement of endothelin-1(1-31). The plasma concentrations of endothelin-1(1-31) and endothelin-1 in healthy volunteers were 19.24 +/- 5.70 and 15.54 +/- 4.45 pg/ml (n = 5), respectively. We also measured plasma concentrations of endothelin-1(1-31) and endothelin-1 before and after surgery in patients with abdominal aortic aneurysms. Before surgery, plasma concentrations of endothelin-1(1-31) and endothelin-1 in these patients were higher than those in healthy individuals. After surgery, both endothelin-1(1-31) and endothelin-1 in plasma decreased to levels similar to those of healthy subjects. This suggests that endothelin-1(1-31) may have similar physiological significance to endothelin-1 in patients with atherosclerosis. (Keyword) Adult / Aged / Aortic Aneurysm, Abdominal / Arteriosclerosis / Endothelin-1 / Humans / Male / Middle Aged / Peptide Fragments (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12688403 ● Search Scopus @ Elsevier (PMID): 12688403 (PubMed: 12688403)
127.	Koichiro Tsuchiya, Kazuyoshi Kirima, Masanori Yoshizumi, Toshiaki Tamaki and Ronald Mason : The role of thiol and nitrosothiol compounds in the NO-forming reactions of the iron-MGD complex., The Biochemical Journal, Vol.367, No.Pt 3, 771-779, 2002. (Summary) The object of the present study is to investigate whether the physiologically dominant thiol compounds such as GSH and cysteine or their nitrosothiol compounds affect the formation of the iron- N -methyl-D-glucamine dithiocarbamate [(MGD)(2)Fe(2+)]-nitric oxide complex. The present study provided experimental evidence that physiological concentrations of GSH (approx. 5 mM) and L-cysteine (approx. 0.5 mM) accelerated the formation of the (MGD)(2)Fe(2+)-NO complex from nitrite by two and three times respectively. The rate constants for the reduction of (MGD)(3)Fe(3+) to (MGD)(2)Fe(2+) by GSH and cysteine were calculated as 1.3 and 2.0x10(2) M(-1).s(-1) respectively. Furthermore, depletion of GSH was demonstrated in PC12 cells, and thiol compounds enhanced the formation of reactive oxygen species by the (MGD)(2)Fe(2+) complex by accelerating its redox turnover. The main effect of the physiological concentration of thiols was the reduction of (MGD)(3)Fe(3+). S -nitrosoglutathione spontaneously reacted with (MGD)(2)Fe(2+) to produce the (MGD)(2)Fe(2+)-NO complex with a 1:2 stoichiometry. In fact, (MGD)(2)Fe(2+) was as good an indicator of nitrosothiols as it was of NO itself. The present study elucidates the difficulties of utilizing the (MGD)(2)Fe(2+) complex for the quantification of NO in biological samples, especially in vivo. (Keyword) Animals / Electron Spin Resonance Spectroscopy / Glutathione / Nitric Oxide / Nitroso Compounds / Oxygen / PC12 Cells / Rats / Sorbitol / Spin Labels / Sulfhydryl Compounds / Thiocarbamates (Link to Publication Site) ● Publication site (DOI): 10.1042/BJ20020310 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12141947 ● Search Scopus @ Elsevier (PMID): 12141947 ● Search Scopus @ Elsevier (DOI): 10.1042/BJ20020310 (DOI: 10.1042/BJ20020310, PubMed: 12141947)
128.	Masanori Yoshizumi, Toshiaki Kogame, Yuki Suzaki, Yoshiko Fujita, Moe Kyaw, Kazuyoshi Kirima, Keisuke Ishizawa, Koichiro Tsuchiya, Shoji Kagami and Toshiaki Tamaki : Ebselen attenuates oxidative styress-induced apoptosis via the inhibition of the c jun N-terminal kinase and activator protein-1 signaling pathway in PC12 cells., British Journal of Pharmacology, Vol.136, No.7, 1023-1032, 2002. (Summary) 1: Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one) is a selenoorganic compound exhibiting both glutathione peroxidase activity and antioxidant activity. Although it has been reported that ebselen is effective for oxidative stress-induced neuronal damage both in vivo and clinically, the precise mechanisms of the efficacy have not yet been elucidated. Thus, we hypothesized that ebselen may affect reactive oxygen species-induced mitogen-activated protein (MAP) kinase activation in cultured PC12 cells. 2: Our findings showed that hydrogen peroxide (H(2)O(2)) stimulated rapid and significant activation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK) and p38 in PC12 cells, which is a model of catecholamine-containing neurons. 3: H(2)O(2)-induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 activation by H(2)O(2) were not affected by ebselen. 4: Inhibition by ebselen of H(2)O(2)-induced hydroxyl radical generation in PC12 cells was observed using electron paramagnetic resonance measurements. Ebselen also inhibited H(2)O(2)-induced increases in DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK, composed of the c-Jun homo/heterodimer. 5: Finally, pretreatment of cells with ebselen resulted in a significant recovery from cell death including apoptosis by H(2)O(2) in PC12 cells. 6 These findings suggest that ebselen attenuates oxidative stress-induced neuronal cell death through the inhibition of the JNK and AP-1 signalling pathway. Thus, inhibition of JNK by ebselen may imply its usefulness for treatment of ischaemic cerebral diseases relevant to neuronal cell death. (Keyword) Analysis of Variance / Animals / Antioxidants / Apoptosis / Azoles / Cell Survival / DNA Fragmentation / Electron Spin Resonance Spectroscopy / Enzyme Activation / Hydrogen Peroxide / JNK Mitogen-Activated Protein Kinases / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Organoselenium Compounds / Oxidative Stress / PC12 Cells / Rats / Reactive Oxygen Species / Signal Transduction / Time Factors / Transcription Factor AP-1 / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1038/sj.bjp.0704808 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12145102 ● Search Scopus @ Elsevier (PMID): 12145102 ● Search Scopus @ Elsevier (DOI): 10.1038/sj.bjp.0704808 (DOI: 10.1038/sj.bjp.0704808, PubMed: 12145102)
129.	Masanori Yoshizumi, Koichiro Tsuchiya, Yuki Suzaki, Kazuyoshi Kirima, Moe Kyaw, Moon Jae-Hak, Junji Terao and Toshiaki Tamaki : Quercetin Glucronide prevents VSMC hypertrophy by angiotensin II via the inhibition of JNK and AP-1 signaling pathway., Biochemical and Biophysical Research Communications, Vol.293, No.5, 1458-1465, 2002. (Summary) We previously reported that quercetin, a bioflavonoid belonging to polyphenols, inhibited Angiotensin II (Ang II)-induced vascular smooth muscle cell (VSMC) hypertrophy through the inhibition of c-Jun N-terminal kinase (JNK) activation. However, we recently found that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore we examined the effect of chemically synthesized quercetin glucuronide on Ang II-induced mitogen-activated protein (MAP) kinase activation and hypertrophy of cultured rat aortic smooth muscle cells (RASMC). Ang II activated extracellular signal-regulated kinase (ERK)1/2, JNK, and p38 in RASMC. Ang II-induced JNK activation was inhibited by quercetin 3-O-beta-d-glucuronide (Q3GA) whereas ERK1/2 and p38 activations were not affected. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by a method of electron paramagnetic resonance. Q3GA also inhibited Ang II-induced increases in activator protein-1 (AP-1) DNA binding, a downstream transcription factor of JNK. Finally, Ang II-induced [3H]leucine incorporation into RASMC was abolished by Q3GA. These findings suggest that the preventing effect of Q3GA on Ang II-induced VSMC hypertrophy is attributable in part to its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA would be an active metabolite of quercetin in plasma and may possess a preventing effect for cardiovascular diseases relevant to VSMC growth. (Keyword) Angiotensin II / Animals / Dimerization / Dose-Response Relationship, Drug / Electron Spin Resonance Spectroscopy / Enzyme Activation / Free Radicals / Glucuronides / Humans / JNK Mitogen-Activated Protein Kinases / Leucine / MAP Kinase Signaling System / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Models, Chemical / Muscle, Smooth, Vascular / Protein Binding / Quercetin / Rats / Rats, Sprague-Dawley / Signal Transduction / Time Factors / Transcription Factor AP-1 / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/S0006-291X(02)00407-2 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12054679 ● Search Scopus @ Elsevier (PMID): 12054679 ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-291X(02)00407-2 (DOI: 10.1016/S0006-291X(02)00407-2, PubMed: 12054679)
130.	Yuki Suzaki, Masanori Yoshizumi, Shoji Kagami, Hajime Koyama, Yutaka Taketani, Hitoshi Houchi, Koichiro Tsuchiya, Eiji Takeda and Toshiaki Tamaki : Hydrogen Peroxide Stimulates c-Src-mediated Big Mitogen-activated Protein Kinase 1(BMK1) and the MEF2C Signaling Pathway in PC12 Cells, The Journal of Biological Chemistry, Vol.277, No.11, 9614-9621, 2002. (Summary) Reactive oxygen species, generated by reduction-oxidation (redox) reactions, have been recognized as one of the major mediators of ischemia and reperfusion injury in the brain. Reactive oxygen species-induced cerebral events are attributable, in part, to the change in intracellular signaling molecules including mitogen-activated protein (MAP) kinases. Big MAP kinase 1 (BMK1), also known as ERK5, is a newly identified member of the MAP kinase family and has been reported to be sensitive to oxidative stress. In the present study, we examined the effect of H(2)O(2) on BMK1 activity in PC12 cells, and we investigated the pathophysiological implication of BMK1. Findings showed that BMK1 was rapidly and significantly activated by H(2)O(2) in a concentration-dependent manner in PC12 cells. BMK1 activation by H(2)O(2) was inhibited by both PD98059 and U0126, which were reported to inhibit MEK5 as well as MEK1/2. c-Src was suggested to be involved in BMK1 activation from the experiments with herbimycin A and PP2, specific inhibitors of Src family kinases. Transfection of kinase-inactive Src also inhibited H(2)O(2)-induced BMK1 activation. In addition, H(2)O(2) treatment of cells induced an enhancement of DNA binding activity of MEF2C, a downstream transcription factor of BMK1 in PC12 cells. Finally, pretreatment of cells with PD98059 and U0126 resulted in an increase in cell death including apoptosis by H(2)O(2) in ERK1/2 down-regulated cells as well as in intact PC12 cells. These findings suggest that c-Src mediated BMK1 activation by H(2)O(2) may counteract ischemic cellular damage probably through the activation of MEF2C transcription factor. (Keyword) CENTRAL-NERVOUS-SYSTEM / SMOOTH-MUSCLE CELLS / PROTEIN-KINASE-1 BMK1 / TRANSDUCTION PATHWAY / NEURONAL DIFFERENTIATION / CEREBRAL-ISCHEMIA / TYROSINE KINASES / OXYGEN RADICALS / GENE-EXPRESSION / JUN PROMOTER (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.M111790200 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11782488 ● CiNii @ National Institute of Informatics (CRID): 1573950401500650880 ● Search Scopus @ Elsevier (PMID): 11782488 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.M111790200 (DOI: 10.1074/jbc.M111790200, PubMed: 11782488, CiNii: 1573950401500650880)
131.	Moe Kyaw, Masanori Yoshizumi, Koichiro Tsuchiya, Kasuyoshi Kirima, Yuki Suzaki, Shinji Abe, Toyoshi Hasegawa and Toshiaki Tamaki : Antioxidants inhibit endothelin-1(1-31)-induced proliferation of vascular smooth muscle cells via the inhibition of mitogen-activated protein (MAP) kinase and activator protein-1 (AP-1)., Biochemical Pharmacology, Vol.64, No.10, 1521-1531, 2002. (Link to Publication Site) ● Publication site (DOI): 10.1016/S0006-2952(02)01349-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12417265 ● Search Scopus @ Elsevier (PMID): 12417265 ● Search Scopus @ Elsevier (DOI): 10.1016/S0006-2952(02)01349-7 (DOI: 10.1016/S0006-2952(02)01349-7, PubMed: 12417265)
132.	Keisuke Ishizawa, Masanori Yoshizumi, Koichiro Tsuchiya, Eiko Takishita, Yutaka Nakaya, Kazuhiro Kishi, Yousuke Ebina, Hitoshi Houchi, Kazuo Minakuchi and Toshiaki Tamaki : Effects of losartan in combination with or without exercise on insulin resistance in Otsuka Long-Evans Tokushima Fatty rats., European Journal of Pharmacology, Vol.430, No.2-3, 359-367, 2001. (Summary) Hypertension often complicates type 2 diabetes mellitus, and angiotensin converting enzyme inhibitor treatment has been shown to improve insulin resistance in such cases. However, the effect of angiotensin II type-1 (AT(1)) receptor antagonists on insulin resistance is still controversial. To gain further information on this effect, we examined the effect of losartan on insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus. Losartan administration alone lowered systolic blood pressure, but did not improve oral glucose tolerance test or insulin resistance in OLETF rats. However, the administration of losartan with exercise significantly improved both systolic blood pressure and insulin resistance relative to control OLETF rats. On the other hand, losartan treatment, regardless of exercise, increased glucose uptake in excised soleus muscle and fat cells. To explore the beneficial effect of losartan on skeletal muscle glucose uptake, we examined intracellular signaling of soleus muscle. Although Akt activity and glucose transporter type 4 (GLUT4) expressions were not affected by losartan with or without exercise, extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein (MAP) kinase activities were increased by both interventions. These results indicate that angiotensin AT(1) receptor antagonist improved local insulin resistance, but not systemic insulin resistance. These findings may explain the controversy over the effect of angiotensin AT(1) receptor antagonists on insulin resistance in clinical use. The enhancing effect of angiotensin AT(1) receptor antagonist on skeletal muscle glucose uptake may be attributable to MAP kinase activation or other mechanisms rather than phosphatidylinositol 3-kinase activation. (Keyword) Adipocytes / Animals / Antihypertensive Agents / Blood Glucose / Blood Pressure / Blotting, Western / Body Weight / Deoxyglucose / Diabetes Mellitus, Type 2 / Enzyme Activation / Glucose / Glucose Tolerance Test / Glucose Transporter Type 4 / Heart Rate / Insulin / Insulin Resistance / JNK Mitogen-Activated Protein Kinases / Losartan / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Monosaccharide Transport Proteins / Muscle Proteins / Muscle, Skeletal / Phosphorylation / Physical Conditioning, Animal / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Rats, Inbred OLETF / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/S0014-2999(01)01405-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11711055 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035798388 (DOI: 10.1016/S0014-2999(01)01405-4, PubMed: 11711055, Elsevier: Scopus)
133.	Masanori Yoshizumi, Koichiro Tsuchiya, Kazuyoshi Kirima, Moe Kyaw, Yuki Suzaki and Toshiaki Tamaki : Quercetin inhibits Shc- and Phosphatidylinositol 3-kinase-mediated c-Jun N-terminal kinase activation by angiotensin II in cultured rat aortic smooth muscle cells., Molecular Pharmacology, Vol.60, No.4, 656-665, 2001. (Summary) Angiotensin II (Ang II) induces vascular smooth muscle cell (VSMC) hypertrophy, which results in various cardiovascular diseases. Ang II-induced cellular events have been implicated, in part, in the activation of mitogen-activated protein (MAP) kinases. Although it has been proposed that daily intake of bioflavonoids belonging to polyphenols reduces the incidence of ischemic heart diseases (known as "French paradox"), the precise mechanisms of efficacy have not been elucidated. Thus, we hypothesized that bioflavonoids may affect Ang II-induced MAP kinase activation in cultured rat aortic smooth muscle cells (RASMC). Our findings showed that Ang II stimulated rapid and significant activation of extracellular signal-regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), and p38 in RASMC. Ang II-induced JNK activation was inhibited by 3,3',4',5,7-pentahydroxyflavone (quercetin), a major bioflavonoid in foods of plant origin, whereas ERK1/2 and p38 activation by Ang II were not affected by quercetin. Ang II caused a rapid tyrosine phosphorylation of Src homology and collagen (Shc), which was inhibited by quercetin. Quercetin also inhibited Ang II-induced Shc.p85 association and subsequent activation of phosphatidylinositol 3-kinase (PI3-K)/Akt pathway in RASMC. Furthermore, LY294002, a PI3-K inhibitor and a quercetin derivative, inhibited Ang II-induced JNK activation as well as Akt phosphorylation. Finally, Ang II-induced [(3)H]leucine incorporation was abolished by both quercetin and LY294002. These findings suggest that the preventing effect of quercetin on Ang II-induced VSMC hypertrophy are attributable, in part, to its inhibitory effect on Shc- and PI3-K-dependent JNK activation in VSMC. Thus, inhibition of JNK by quercetin may imply its usefulness for the treatment of cardiovascular diseases relevant to VSMC growth. (Keyword) Angiotensin II / Animals / Chromones / Collagen / Dose-Response Relationship, Drug / Drug Interactions / Enzyme Activation / Enzyme Inhibitors / Humans / JNK Mitogen-Activated Protein Kinases / Leucine / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Morpholines / Muscle, Smooth, Vascular / Phosphatidylinositol 3-Kinases / Phosphorylation / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Quercetin / Rats / Rats, Sprague-Dawley / Time Factors / Tritium / Tyrosine / p38 Mitogen-Activated Protein Kinases / src Homology Domains (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11562426 ● Search Scopus @ Elsevier (PMID): 11562426 (PubMed: 11562426)
134.	Kazuyoshi Kirima, Koichiro Tsuchiya, Masanori Yoshizumi, Taisuke Kameda, Hitoshi Houchi, Mami Azuma and Toshiaki Tamaki : Electron paramagnetic resonance study on free radical scavanging and/or generating activity of dopamine-4-0-sulfate., Chemical & Pharmaceutical Bulletin, Vol.49, 576-580, 2001.
135.	Kyaw Moe, Masanori Yoshizumi, Koichiro Tsuchiya, Kazuyoshi Kirima and Toshiaki Tamaki : Antioxidants inhibit JNK and p38 MAPK activation but not ERK 1/2 activation by angiotensin II in rat aortic smooth muscle cells., Hypertension Research, Vol.24, No.3, 251-261, 2001. (Summary) Angiotensin II (Ang II) induces vascular smooth muscle cell (VSMC) hypertrophy, which results in several cardiovascular diseases. Ang II-induced cellular events have been mediated, in part, by reactive oxygen species (ROS) which also involve activation of mitogen-activated protein (MAP) kinases. Although it has been proposed that the therapeutic administration of antioxidants is useful for vascular diseases, the precise mechanisms which regulate ROS-sensitive signaling events have not been well characterized. Thus, we hypothesized that antioxidants may affect ROS-mediated MAP kinases activation induced by Ang II. The present findings showed that Ang II stimulated rapid and significant activation of ERK 1/2, JNK and p38 MAPK in cultured rat aortic smooth muscle cells (RASMC). Ang II-induced ERK 1/2 activation was not affected by all antioxidants examined, whereas JNK was sensitive to all antioxidants. In contrast, p38 MAPK activation was inhibited by DPI and ascorbic acid concentration-dependently, but by NAC only at high concentration. DETC and Trolox C had no effects on p38 MAPK activation by Ang II. We further examined the effects of antioxidants on Ang II-induced increases in oxygen consumption as an index of ROS generation in RASMC. DPI strongly inhibited Ang II-induced increases in oxygen consumption. DETC also inhibited Ang II-induced oxygen consumption, whereas ascorbic acid markedly augmented it. These findings suggest that the inhibitory effects of antioxidants on MAP kinases activation in VSMC are attributable, in part, to their modulating effects on ROS generation by Ang II in VSMC. Thus, inhibition of MAP kinases by antioxidants may imply their usefulness for relief of cardiovascular diseases. (Keyword) Acetylcysteine / Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / Ascorbic Acid / Cells, Cultured / Chelating Agents / Chromans / Ditiocarb / Dose-Response Relationship, Drug / Enzyme Inhibitors / Free Radical Scavengers / JNK Mitogen-Activated Protein Kinases / MAP Kinase Kinase 4 / MAP Kinase Signaling System / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinase Kinases / Mitogen-Activated Protein Kinases / Muscle, Smooth, Vascular / Onium Compounds / Oxygen Consumption / Rats / Rats, Sprague-Dawley / Reactive Oxygen Species / Vasoconstrictor Agents / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.24.251 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11409648 ● Search Scopus @ Elsevier (PMID): 11409648 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.24.251 (DOI: 10.1291/hypres.24.251, PubMed: 11409648)
136.	Naoko Okishima, Masanori Yoshizumi, Koichiro Tsuchiya, Ping Cui, Hiroko Kitamura, Toshiaki Tamaki and Hiroshi Kido : Determination of the levels of novel 31-amino acid endothelins and endothelins in human lungs., Life Sciences, Vol.68, No.18, 2073-2080, 2001.
137.	Masanori Yoshizumi, Koichiro Tsuchiya and Toshiaki Tamaki : Signal transduction of reactive oxygen species and mitogen-activated protein kinases in cardiovascular disease, The Journal of Medical Investigation : JMI, Vol.48, No.1,2, 11-24, 2001. (Summary) Reactive oxygen species (ROS), generated by reduction-oxidation (redox) reactions, have been recognized as important chemical mediators that regulate signal transduction. It has been reported that increase in ROS generation may relate to a risk for cardiovascular diseases such as atherosclerosis, angina pectoris, and myocardial infarction. Therefore, understanding the ROS-generating biological processes and ROS-induced intracellular signaling will be informative to gain insights into the pathogenesis of these diseases. In this review, we focus on the sources and reactions of ROS in the cardiovascular system and the role of mitogen-activated protein (MAP) kinase pathway in redox-mediated signal transduction. Clinical implications of ROS and MAP kinase are then described to provide insight into the pathogenesis of various redox-sensitive cardiovascular diseases. The pathways responsible for ROS generation in the cardiovascular system may provide novel therapeutic targets. (Keyword) reactive oxygen species / mitogen-activated protein kinase / signal transduction / cardiovascular disease (Tokushima University Institutional Repository) ● Metadata: 29055 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11286012 ● Search Scopus @ Elsevier (PMID): 11286012 (Tokushima University Institutional Repository: 29055, PubMed: 11286012)
138.	Daisuke Inui, Masanori Yoshizumi, Yuki Suzaki, Kazuyoshi Kirima, Koichiro Tsuchiya, Hitoshi Houchi, Shoji Kagami and Toshiaki Tamaki : Effect of Endothelin-1(1-31) on p38 Mitogen-Activated Protein Kinase in Cultured Human Mesangial Cells., Life Sciences, Vol.68, No.6, 635-645, 2000. (Summary) It was reported that human chymase cleaves big endothelins (ETs) at the Tyr31-Gly32 bond and produces 31-amino acid ETs(1-31). In this study, we investigated the effect of ET-1(1-31) on p38 mitogen-activated protein kinase (p38-MAPK) activity in human mesangial cells (HMCs). By measuring the kinase activity, we demonstrated that ET-1 (1-31) activated the p38-MAPK dose-dependently (10(-9) M to 10(-7) M), which was inhibited by SB203580. The p38-MAPK activation induced by ET-1(1-31) peaked at 10 minutes. BQ123 almost abolished ET-1(1-31)-induced p38-MAPK activation, whereas BQ788 failed to inhibit it. These findings suggest that the stimulatory effect of ET-1(1-31) on p38-MAPK activation is mediated through ET(A) or ET(A)-like receptor. In conclusion, ET-1(1-31) induced increase in p38-MAPK activation in cultured HMCs. (Keyword) Endothelin (Link to Publication Site) ● Publication site (DOI): 10.1016/S0024-3205(00)00976-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11205878 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034731282 (DOI: 10.1016/S0024-3205(00)00976-0, PubMed: 11205878, Elsevier: Scopus)
139.	Erdem Yesilada, Koichiro Tsuchiya, Yoshihisa Takaishi and Kazuyoshi Kawazoe : Isolation and characterization of free radical scavenging flavonoid glycosides from the flowers of Spartium junceum by activity-guided fractionation, Journal of Ethnopharmacology, Vol.73, No.3, 471-478, 2000. (Summary) Spartium junceum L. (Fabaceae) flowers are used for the treatment of peptic ulcers in Turkish folk medicine. The possible superoxide dismutase-like activity of the extracts, fractions and constituents obtained through activity-guided fractionation were studied by using in vitro electron spin resonance spectrometry, in order to explain the role of antioxidant principles in the potent antiulcerogenic activity of the extract. Despite the fact that the triterpene, spartitrioside, which was previously reported as the active antiulcerogenic constituent of the flowers was found almost inactive, the flavonoid-rich fractions showed potent antioxidant activity. Five flavonoid glycosides bearing catechol structure in ring B were isolated from the butanol extract and their structures were elucidated using 1H- and 13C-NMR techniques as isoquercitrin (quercetin 3beta-glucoside) (1,); luteolin 4'beta-glucoside (2); quercetin 3, 4'-diglucoside (3); azaleatin 3beta-glucoside (quercetin 5-methylether 3beta-glucoside) (4), quercetin 4'beta-glucoside (5). Flavonoids (2) and (4) showed the highest in vitro antioxidant activity with 22.59 and 19.08 U/ml, respectively. (Keyword) Electron spin resonance / Spartium junceum / Antioxidant activity / Superoxide dismutase-like activity / Spin trapping / Superoxide radical (Link to Publication Site) ● Publication site (DOI): 10.1016/S0378-8741(00)00327-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11091001 ● Search Scopus @ Elsevier (PMID): 11091001 ● Search Scopus @ Elsevier (DOI): 10.1016/S0378-8741(00)00327-5 (DOI: 10.1016/S0378-8741(00)00327-5, PubMed: 11091001)
140.	Yuichi Ozawa, Hitoshi Houchi, Kazuhiko Teraoka, Mami Azuma, Takehiro Kamimura, Masanori Yoshizumi, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : Long-term regulation of catecholamine formation by ouabain in cultured bovine adrenal cromaffin cells., Journal of Cardiovascular Pharmacology, Vol.36, No.suppl.2, S15-S18, 2000. (Summary) The long-term effects of ouabain, an inhibitor of Na+/K+ -ATPase, on catecholamine formation in cultured bovine adrenal chromaffin cells were examined. The increase in [14C]catecholamine formation from [14C]tyrosine induced by ouabain was dependent on incubation time, and its maximal effect was observed after incubation for 8 h. The stimulatory effect of ouabain was concentration dependent (10-300 nM), causing maximal stimulation at 300 nM. The formation of [14C]catecholamines induced by ouabain was not increased by incubation with [14C]DOPA instead of [14C]tyrosine. Ouabain-induced [14C]catecholamine formation was influenced by decreases in extracellular Ca2+ concentration, but not by the presence of cycloheximide or actinomycin D. These results suggested that ouabain stimulates continuous activation of hydroxylation of tyrosine through a Ca2+ -dependent mechanism in cultured bovine adrenal chromaffin cells. (Keyword) Animals / Calcium / Catecholamines / Cattle / Cells, Cultured / Chromaffin Cells / Enzyme Inhibitors / Ouabain / Sodium-Potassium-Exchanging ATPase / Tyrosine / Tyrosine 3-Monooxygenase (Link to Publication Site) ● Publication site (DOI): 10.1097/00005344-200000006-00005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11206714 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034480287 (DOI: 10.1097/00005344-200000006-00005, PubMed: 11206714, Elsevier: Scopus)
141.	Masanori Yoshizumi, Shoji Kagami, Yuki Suzaki, Koichiro Tsuchiya, Hitoshi Houchi, Tetsuhiro Hisayama, Hiroyuki Fukui and Toshiaki Tamaki : Effect of endothelin-1(1-31) on human mesangial cell proliferation, The Japanese Journal of Pharmacology, Vol.84, No.2, 146-155, 2000. (Keyword) Endothelin-1(1-31) / Human chymase / Extracellular signal-regulated kinase / Protein kinase C
142.	Ozawa Yuichi, Masanori Yoshizumi, Yasushi Fukuta, Daisuke Inui, Koichiro Tsuchiya, Hitoshi Houchi, Toshiaki Tamaki and Kazuo Minakuchi : Dopamine Clearance During Dopamine Infusion in Infants and Children After Cardiac Surgery, Journal of Cardiovascular Pharmacology, Vol.34, No.Supplement 4, S85-S89, 1999.
143.	Masanori Yoshizumi, Daisuke Inui, Kazuyoshi Kirima, Koichiro Tsuchiya, Hitoshi Houchi, Mami Azuma, Hiroaki Yasuoka, Hiroshi Kido and Toshiaki Tamaki : Comparison of the effects of endothelin-1,-2 and -3(1-31) on changes in [Ca²⁺]i in human coronary artery smooth muscle cells., The Japanese Journal of Pharmacology, Vol.81, 298-304, 1999.
144.	Daisuke Inui, Masanori Yoshizumi, Okishima Naoko, Hitoshi Houchi, Koichiro Tsuchiya and Toshiaki Tamaki : Mechanism of endothelin-1-(1-31)-induced calcium signaling in human coronary artery smooth muscle cells., American Journal of Physiology, Endocrinology and Metabolism, Vol.276, No.39, E1067-E1072, 1999. (Summary) We have found that human chymase produces a 31-amino acid endothelin [ET-1-(1-31)] from the 38-amino acid precursor (Big ET-1). We examined the mechanism of synthetic ET-1-(1-31)-induced intracellular Ca2+ signaling in cultured human coronary artery smooth muscle cells. ET-1-(1-31) increased the intracellular free Ca2+ concentration ([Ca2+]i) in a concentration-dependent manner (10(-14)-10(-10) M). This ET-1-(1-31)-induced [Ca2+]i increase was not affected by phosphoramidon, Bowman-Birk inhibitor, and thiorphan. The ET-1-(1-31)-induced [Ca2+]i increase was not influenced by removal of extracellular Ca2+ but was inhibited by thapsigargin. ET-1-(1-31) at 10(-12) M did not cause Ca2+ influx, whereas 10(-7) M ET-1-(1-31) evoked marked Ca2+ influx, which was inhibited by nifedipine. ET-1-(1-31) also increased inositol trisphosphate formation. These results suggest that the ET-1-(1-31)-induced [Ca2+]i increase at relatively low concentrations is attributable to the release of Ca2+ from inositol trisphosphate-sensitive intracellular stores, whereas Ca2+ influx into the cells evoked by high concentration of ET-1-(1-31) probably occurs through voltage-dependent Ca2+ channels. We concluded that the physiological activity of ET-1-(1-31) may be attributable to Ca2+ mobilization from intracellular stores rather than influx of Ca2+ from extracellular space. (Keyword) endothelin (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.1999.276.6.E1067 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10362619 ● Search Scopus @ Elsevier (PMID): 10362619 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.1999.276.6.E1067 (DOI: 10.1152/ajpendo.1999.276.6.E1067, PubMed: 10362619)
145.	Kazuhiro Mori, Yasunobu Hayabuchi, Yasuhiro Kuroda, Yutaka Nakaya, Koichiro Tsuchiya and Hiroyuki Morimoto : Age-related endothelium-dependent vascular relazation in rat thoracic aorta in response to colforsin, Pediatrics International, Vol.41, No.6, 673-681, 1999. (Summary) Colforsin, a novel water-soluble forskolin derivative, increases intracellular cyclic AMP by direct stimulation of adenylate cyclase and has strong positive inotropic and vasodilative effects. However, it is not known whether colforsin causes nitric oxide (NO) release and enhances endothelium-dependent vascular relaxation. We studied NO production and relaxation on exposure to colforsin in thoracic aorta from rats aged 4, 12 and 60 weeks. When a low concentration of colforsin was added to a solution bathing ring segments of aorta from 12-week-old rats, relaxation was greater in the ring segments with intact endothelium than in those from which the endothelium had been removed. A high concentration of colforsin induced the same degree of relaxation of ring segments with or without endothelium, probably by a direct effect on vascular smooth muscle cells. Production of NO in response to colforsin by cultured endothelial cells from 12-week-old rat aorta was demonstrated by the electron paramagnetic resonance spin trapping method. A low concentration of colforsin relaxed aortic segments with intact endothelium from 4-week-old rats more than those from 12-week-old or 60-week-old rats. Reversal of relaxation by NG-nitro L-arginine, an NO synthesis inhibitor, was most significant in arteries from 4-week-old rats. Production of NO after exposure to colforsin was greater in aortic segments from 4-week-old rats than older rats, as detected by an NO-selective electrode. Colforsin induces vasodilation in part by releasing NO from the endothelium in rat thoracic aorta. In addition to a direct vasodilative effect on the vascular smooth muscle cells, an endothelium-dependent vasodilative effect is also important in younger arteries. (Keyword) Aging / Animals / Aorta, Thoracic / Dose-Response Relationship, Drug / Electron Spin Resonance Spectroscopy / Endothelium, Vascular / Forskolin / Male / nitric oxide / Rats / Rats, Wistar / Vasodilation / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1442-200x.1999.01138.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10618889 ● CiNii @ National Institute of Informatics (CRID): 1570009749819091584 ● Search Scopus @ Elsevier (PMID): 10618889 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1442-200x.1999.01138.x (DOI: 10.1046/j.1442-200x.1999.01138.x, PubMed: 10618889, CiNii: 1570009749819091584)
146.	Koichiro Tsuchiya, Jiang Jin-Jie, Masanori Yoshizumi, Toshiaki Tamaki, Hitoshi Houchi, Kazuo Minakuchi, Kenji Fukuzawa and P.Mason Ronald : Nitric oxide-forming reactions of the water-soluble nitric oxide spin-trapping agent, MGD., Free Rad. Biol. Med., Vol.27, 347-355, 1999.
147.	Yuichi Ozawa, Masanori Yoshizumi, Daisuke Inui, Koichiro Tsuchiya, Hitoshi Houchi, Toshiaki Tamaki and Kazuo Minakuchi : Plasma levels of free and sulfoconjugated catecholamines in patients with atherosclerosis., Biological & Pharmaceutical Bulletin, Vol.22, 657-659, 1999.
148.	Hitoshi Houchi, Masanori Yoshizumi, Koichiro Tsuchiya, Masao Hirose, Tetsuya Kitagawa, Toshihida Kujime, Eiji Shimizu, Yasuharu Niwa, Kazuo Minakuchi and Toshiaki Tamaki : Endothelin-1 stimulates sodium-dependent calcium efflux from bovine adrenal chromaffin cells in culture., British Journal of Pharmacology, Vol.125, No.1, 55-60, 1998.
149.	Masanori Yoshizumi, Daisuke Inui, Naoko Okishima, Hitoshi Houchi, Koichiro Tsuchiya, Hideki Wakabayashi, Hiroshi Kido and Toshiaki Tamaki : Endothelin-1(1-31), a novel vasoactive peptide, increases [Ca²⁺]i in humen coronary artery smooth muscle cells., European Journal of Pharmacology, Vol.348, No.2-3, 305-309, 1998.
150.	Akira Tokumura, Masaaki Okuno, Kenji Fukuzawa, Hitoshi Houchi, Koichiro Tsuchiya and Motoo Oka : Positive and negative controls by protein kinases of sodium-dependent Ca²⁺ efflux from cultured bovine adrenal chromaffin cells stimulated by lysophosphatidic acid, Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol.1389, No.1, 67-75, 1998. (Summary) We previously found that lysophosphatidic acid (LPA), a bioactive phospholipid, induced Na+-dependent Ca2+ efflux from cultured bovine adrenal chromaffin cells, possibly by activating a Na+/Ca2+ exchanger. The present study on the structure-activity relationship of its action revealed that 1-acyl type LPAs were stronger stimulants than the corresponding 1-O-alkyl type LPAs having a long alkyl moiety with the same chain length. Lysophosphatidylglycerol, suramin and N-palmitoyl-tyrosine phosphoric acid have all been reported to inhibit the action of LPA in some animal cells and platelets, but only lysophosphatidylglycerol was found to inhibit selectively LPA-induced Ca2+ efflux from chromaffin cells. LPA-induced Ca2+ extrusion was suggested to be involved in both acceleration of return of intracellular Ca2+ in Fura 2-loaded bovine chromaffin cells after addition of carbachol, and inhibition of carbachol-induced catecholamine release when the cells were co-incubated with LPA. The Ca2+ efflux from chromaffin cells stimulated by LPA was augmented by their pretreatment with staurosporine or calphostin C, inhibitors of protein kinase C, but reduced by their preincubation with phorbol 12-myristate 13-acetate. Furthermore, the response to LPA was potentiated by sodium vanadate, a protein tyrosine phosphatase inhibitor, but inhibited by genistein, an inhibitor of protein tyrosine kinase. These results suggest that protein kinase C and protein tyrosine kinase are involved negatively and positively, respectively, in the signal transduction triggered by LPA, leading to activation of the Na+/Ca2+ exchanger. (Keyword) Adrenal Glands / Animals / Calcium / Carbachol / Catecholamines / Cattle / Chromaffin Cells / Cyclic AMP / Cyclic GMP / Enzyme Inhibitors / Genistein / Lysophospholipids / Naphthalenes / Protein Kinase Inhibitors / Protein Kinases / Signal Transduction / Sodium / Sodium-Calcium Exchanger / Staurosporine / Structure-Activity Relationship / Suramin / Tetradecanoylphorbol Acetate / Vanadates (Link to Publication Site) ● Publication site (DOI): 10.1016/S0005-2760(97)00130-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9443605 ● Search Scopus @ Elsevier (PMID): 9443605 ● Search Scopus @ Elsevier (DOI): 10.1016/S0005-2760(97)00130-6 (DOI: 10.1016/S0005-2760(97)00130-6, PubMed: 9443605)
151.	Masanori Yoshizumi, Shokei Kim, Shoji Kagami, Akinori Hamaguchi, Koichiro Tsuchiya, Hitoshi Houchi, Hiroshi Iwao, Hiroshi Kido and Toshiaki Tamaki : Effect of endothelin-1(1-31)on extracellular signal-regulated kinase and proliferation of human coronary artery smooth muscle cells., British Journal of Pharmacology, Vol.125, No.5, 1019-1027, 1998.
152.	Masanori Yoshizumi, Tetsuya Kitagawa, Yuichi Ozawa, Kasutoshi Tano, Koichiro Tsuchiya, Hitoshi Houchi, Kazuo Minakuchi and Toshiaki Tamaki : Changes in plasma free and sulfoconjugated catecholamines during the perioperative period of cardiac surgery:Effect of continuous infusion of dopamine., Biological & Pharmaceutical Bulletin, Vol.21, 787-791, 1998.
153.	Kazuhiro Mori, 松岡優, Yasunobu Hayabuchi, Yasuhiro Kuroda, Yutaka Nakaya and Koichiro Tsuchiya : 摘出ブタ大動脈でのアムリノンによる一酸化窒素(NO)産生の測定, 日本小児循環器学会雑誌, Vol.11, No.4, 545-550, 1995.
154.	松木洋子, 赤沢美保, Koichiro Tsuchiya, 桜井弘, Hiroshi Kiwada and 五郎丸毅 : [Effects of ascorbic acid on the free radical formations of isoniazid and its metabolites]., Journal of the Pharmaceutical Society of Japan, Vol.111, No.10, 600-605, 1991. (Summary) By the use of electron spin resonance (ESR) spectroscopy and of spin-trapping technique, the effects of ascorbic acid on the formation of the free radical intermediates due to isoniazid (INAH) and its metabolites were investigated with a microsomal system. When alpha-(4-pyridyl 1-oxide)-N-tert butylnitrone (4-POBN) was used as a spin trapping agent, the ESR signal due to hydrazine (Hy) was formed to be most intensive among others. Therefore, it was presumed that Hy is a potent intermediate to cause an INAH-induced hepatic injury. In the presence of ascorbic acid (AA), the free radical formation of Hy, INAH and acetyl hydrazine was significantly inhibited, suggesting that AA may affect the INAH-hepatitis. By the addition of inhibitors of cytochrome P-450 like metyrapone and CO, the generation of the radical from Hy decreased, confirming that the radical is formed by the cytochrome P-450 dependent microsome systems. The 4-POBN-trapped radical species generated from Hy was presumed to be the hydrazyl radical by the results of mass spectrometry. (Keyword) Animals / Ascorbic Acid / Chemical and Drug Induced Liver Injury / Free Radical Scavengers / Free Radicals / Hydrazines / In Vitro Techniques / Isoniazid / Microsomes, Liver / Rats / Rats, Inbred Strains (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi1947.111.10_600 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 1812280 ● Summary page in Scopus @ Elsevier: 2-s2.0-0026091912 (DOI: 10.1248/yakushi1947.111.10_600, PubMed: 1812280, Elsevier: Scopus)

Academic Paper (Unrefereed Paper):

1.	Akihiro Shirai and Koichiro Tsuchiya : フェルラ酸とUV-Aの併用殺菌力における酸素の影響, LED総合フォーラム 2022 in 徳島論文集, Vol.P-8, 143-144, 2022.
2.	Miku Kita, Jun Yamamoto, Koji Ebisuno, Chiaki Komiya, Akira Shigenaga, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Development of hydrogen peroxide-responsive amide bond cleavage device, Peptide Science 2013, 203-204, 2014.
3.	Akira Shigenaga, Keiji Ogura, Hiroko Hirakawa, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Design and synthesis of hypoxia-responsive amino acid which causes peptide bond cleavage in hypoxic cells, Peptide Science 2012, 135-136, 2013. (Keyword) hypoxia-responsive / peptide bond cleavage / prodrug / stimulus-responsive / trimethyl lock (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570854176180146304 (CiNii: 1570854176180146304)
4.	Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : 生体内における亜硝酸由来のNO産生と，その循環動態への作用検討, Japanese Journal of Circulation Research, Vol.28, No.2, 39-45, 2005. (Keyword) 亜硝酸 / NO / EPR / 循環動態 / 虚血 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570291225308796032 (CiNii: 1570291225308796032)
5.	吉栖正典, Koichiro Tsuchiya, Yasuhisa Kanematsu and Toshiaki Tamaki : Endothelin in cardiac injury, Nihon Rinsho. Japanese Journal of Clinical Medicine, Vol.62, No.9, 622-625, 2004. (Keyword) エンドセリン / エンドセリン(1ー31) / 心筋障害 / MAP kinase / apoptosis
6.	Koichiro Tsuchiya, 吉栖正典 and Toshiaki Tamaki : 亜硝酸と一酸化窒素(NO), Japanese Journal of Circulation Research, Vol.25, No.2, 63-71, 2002. (Keyword) EPR / 亜硝酸 / NO / ジチオカルバメート錯体 / ニトロチロシン (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1570572700148397056 (CiNii: 1570572700148397056)
7.	Masanori Yoshizumi, 沖嶋直子, Daisuke Inui, Koichiro Tsuchiya and Toshiaki Tamaki : エンドセリン1(1-31)の腎作用, 腎と透析, Vol.49, No.4, 739-743, 2000. (Keyword) エンドセリン
8.	Daisuke Inui, Kazuyoshi Kirima, Yuichi Ozawa, Yuki Suzaki, Toyoshi Hasegwa, Koichiro Tsuchiya, Masanori Yoshizumi and Toshiaki Tamaki : 単離ウサギ輸入及び輸出細動脈におけるアデノシン受容体, Shikoku Acta Medica, Vol.55, No.3, 124-130, 1999. (Tokushima University Institutional Repository) ● Metadata: 112145 (Tokushima University Institutional Repository: 112145)

Review, Commentary:

1.	Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : Roles of histone acetylation sites in cardiac hypertrophy and heart failure., Frontiers in Cardiovascular Medicine, Vol.10, Mar. 2023. (Summary) Heart failure results from various physiological and pathological stimuli that lead to cardiac hypertrophy. This pathological process is common in several cardiovascular diseases and ultimately leads to heart failure. The development of cardiac hypertrophy and heart failure involves reprogramming of gene expression, a process that is highly dependent on epigenetic regulation. Histone acetylation is dynamically regulated by cardiac stress. Histone acetyltransferases play an important role in epigenetic remodeling in cardiac hypertrophy and heart failure. The regulation of histone acetyltransferases serves as a bridge between signal transduction and downstream gene reprogramming. Investigating the changes in histone acetyltransferases and histone modification sites in cardiac hypertrophy and heart failure will provide new therapeutic strategies to treat these diseases. This review summarizes the association of histone acetylation sites and histone acetylases with cardiac hypertrophy and heart failure, with emphasis on histone acetylation sites. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2023.1133611 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37008337 ● Search Scopus @ Elsevier (PMID): 37008337 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2023.1133611 (DOI: 10.3389/fcvm.2023.1133611, PubMed: 37008337)
2.	Yasumasa Ikeda, Masafumi Funamoto and Koichiro Tsuchiya : The role of iron in obesity and diabetes., The Journal of Medical Investigation : JMI, Vol.69, No.1.2, 1-7, Apr. 2022. (Summary) Iron is an essential trace metal for all life, but excess iron causes oxidative stress through catalyzing the toxic hydroxy-radical production via the Fenton reaction. The number of patients with obesity and diabetes has been increasing worldwide, and their onset and development are affected by diet. In both clinical and experimental studies, a high body iron content was associated with obesity and diabetes, and the reduction of body iron content to an appropriate level can ameliorate the status and development of obesity and diabetes. Macrophages play an essential role in the pathophysiology of obesity and diabetes, and in the metabolism and homeostasis of iron in the body. Recent studies demonstrated that macrophage polarization is related to adipocyte hypertrophy and insulin resistance through their capabilities of iron handling. Control of iron in macrophages is a potential therapeutic strategy for obesity and diabetes. J. Med. Invest. 69 : 1-7, February, 2022. (Keyword) Adipose Tissue / Diabetes Mellitus / Humans / Insulin Resistance / Iron / Macrophages / obesity (Tokushima University Institutional Repository) ● Metadata: 116403 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.1 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35466128 ● Search Scopus @ Elsevier (PMID): 35466128 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.69.1 (Tokushima University Institutional Repository: 116403, DOI: 10.2152/jmi.69.1, PubMed: 35466128)
3.	Yoshiharu Takiguchi, Chiemi Sato and Koichiro Tsuchiya : 効果的な実務実習に向けたアクティブ・ラーニングの取り組み, Medicine and Drug Journal, Vol.51, No.11, 133-137, Nov. 2015.
4.	Masaki Imanishi, Keisuke Ishizawa, TAKUMI SAKURADA, Yuki Izawa-Ishizawa, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Drug development for cardiorenal disease based on oxidative stress control, Journal of the Pharmaceutical Society of Japan, Vol.134, No.6, 715-719, Jun. 2014. (Summary) Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review. (Keyword) oxidative stress / chronic kidney disease / cardiovascular disease / nitrosonifedipine (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.13-00255-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24882646 ● Search Scopus @ Elsevier (PMID): 24882646 ● Search Scopus @ Elsevier (DOI): 10.1248/yakushi.13-00255-4 (DOI: 10.1248/yakushi.13-00255-4, PubMed: 24882646)
5.	Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 抗酸化薬, 腎・高血圧の最新治療, Vol.3, No.2, 93-99, Apr. 2014.
6.	Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Role of Dietary Essential Trace Metals in the Pathogenesis of Diabetes Mellitus, Journal of the The Japan Diabetes Society, Vol.56, No.12, 919-921, Dec. 2013. (Keyword) 金属元素 / 糖尿病 / 酸化ストレス (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1520290882774966784 ● Summary page in Scopus @ Elsevier: 2-s2.0-84892762387 (CiNii: 1520290882774966784, Elsevier: Scopus)
7.	櫻田巧, Keisuke Ishizawa, Masaki Imanishi, 藤井聖子, 谷口順平, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する, 腎とフリーラジカル, Vol.11, 78-81, Jan. 2013.
8.	Yasumasa Ikeda, Soichiro Tajima, Koichiro Tsuchiya and Toshiaki Tamaki : Iron metabolism in the progression of adipocyte hypertrophy, The Cell, Vol.44, No.6, 282-286, Jun. 2012.
9.	Yasumasa Ikeda, 田島壮一郎, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : The role of iron on cardiovascular disease and diabetes mellitus, Japanese Journal of Circulation Research, Vol.34, No.2, 75-85, Jul. 2011. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1572543024868677632 (CiNii: 1572543024868677632)

Proceeding of International Conference:

1.	Amiho Muramatsu, Masafumi Funamoto, Miyako Ueno, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : Kampo medicine, orengedokuto, suppresses Doxorubicin-induced cardiotoxicity, 28th International Society of Cardiovascular Pharmacotherapy Annual Scientific Meeting, Nov. 2023.
2.	Kaito Kawasaka, Hideaki Nagamune, Koichiro Tsuchiya and Akihiro Shirai : Investigation of photoinactivation mechanism of fungal conidia using blue light in combination with phenolic acids, 2021 International Chemical Congress of Pacific Basin Societies (PACIFICHEM 2021), Vol.3417683, Honolulu, Dec. 2021.
3.	Licht Miyamoto, Riko Suetsugu, Tsubasa Sone and Koichiro Tsuchiya : Pregnancy in a cramped filed leads to increase in anxiety of offsprings, 第10回武田科学振興財団薬科学シンポジウム, Jan. 2020.
4.	Licht Miyamoto, Suguru Nakayama, Honoka Endoh, Mana Hattori, Haruka Inoue and Koichiro Tsuchiya : Relevance of SGLT2 and glucose metabolism in the regulation of glucagon secretion in murine glucagonoma, alpha-TC cells, 欧州糖尿病学会, Sep. 2019.
5.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda, Naoto Okada, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Development of therapeutic agents using drug discovery tools and large-scale medical information, FIP2019, Abu Dhabi, Sep. 2019.
6.	Niimura Takahiro, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Nicorandil improve prognosis of cardiac arrest patient: A large-scale medical information analysis, FIP2019, Abu Dhabi, Sep. 2019.
7.	Toshitaka Ikehara, Mutsumi Nakahashi, Takahiro Emoto, Masatake Akutagawa, Koichiro Tsuchiya, Akira Takahashi and Yohsuke Kinouchi : Effects of reactive oxygen species induced by 405 nm light irradiation on Hela S3 cells, The Joint Annual Meeting of the Bioelectromagnetics Society and the European BioElectromagnetics Association, Montpellier, Jun. 2019.
8.	保岡尭, Licht Miyamoto, 土橋有紀, 曽根翼, 増田栞 and Koichiro Tsuchiya : Disruption of Light-dark Cycle in Late Gestation Does Not Affect Offspring Birth Weight in Mice, 2018AASD, クアラルンプール, Nov. 2018.
9.	土橋有希, Licht Miyamoto, Masayuki Shono and Koichiro Tsuchiya : Pressurized culture suppress adipocytes differentiation on 3T3-L1 cells, 2018AASD, クアラルンプール, Nov. 2018.
10.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Utilizing Real-World Big Data in the Search for New Renoprotective Drugs, Joint Hypertension 2018 Scientific Sessions, Sep. 2018.
11.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Drug repositioning for post cardiopulmonary resuscitation syndrome using large-scale medical claims, FIP2018, グラスゴー, Sep. 2018.
12.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Renoprotective effects of edoxaban, a factor Xa inhibitor, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
13.	Yuki Izawa-Ishizawa, Masaki Imanishi, kotoko suzuki, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Koichiro Tsuchiya, Toshiaki Tamaki, Keisuke Ishizawa and Yasumasa Ikeda : The effect of quercetin on aortic aneurysms in mice, WCP2018, Jul. 2018.
14.	濱野裕章, Yasumasa Ikeda, Yuya Horinouchi, Yoshito Zamami, Masaki Imanishi, Yuki Izawa-Ishizawa, Licht Miyamoto, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : Proton Pump Inhibitor Involves Abnormality of Iron Metabolism through Hepcidin Regulation, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
15.	Licht Miyamoto, Aihara Haruna, Xu Wenting, Jin Meina, Tomida Yosuke, Yamaoka Tomomi, Tanaka Naonobu, Ikeda Yasumasa, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : A limonene-derivative purified from peels of Citrus Sudachi ameliorates lipid and glucose metabolism through upregulating sirt1, World Congress of Pharmacology, Kyoto, Jul. 2018.
16.	中山卓, Licht Miyamoto and Koichiro Tsuchiya : Effect of SGLT2 inhibitors on glucagon secretion in pancreatic α cells, WCP2018 KYOTO, Kyoto, Jul. 2018.
17.	保岡尭, Licht Miyamoto, 土橋有希, 曽根翼, 増田栞 and Koichiro Tsuchiya : Circadian disruption during the late gestation period does not affect offspring birth weight, WCP2018 KYOTO, Kyoto, Jul. 2018.
18.	土橋有希, Licht Miyamoto, Masayuki Shono and Koichiro Tsuchiya : Effect of culture gas pressure on 3T3-L1 preadipocytes differentiation, WCP2018 KYOTO, Kyoto, Jul. 2018.
19.	Licht Miyamoto, Tomokawa Goki, Yamane Megumi, Oonishi Reina, Takenokuma Kazuya and Koichiro Tsuchiya : Hypothalamic pathways mediate physical exercise-induced AMPK activation in skeletal muscles, Keystone symposia-Bioenergetics, Keystone, Jan. 2018.
20.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The effect of iron on skeletal muscle atrophy in chronic kidney disease., Free Radical Biology and Medicine, Vol.112, No.1, 204-205, Dec. 2017. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.freeradbiomed.2017.10.323 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2017.10.323 (DOI: 10.1016/j.freeradbiomed.2017.10.323)
21.	hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Indoxyl Sulfate Disturbs Normal Iron Metabolism via Hepcidin Upregulation in Chronic Kidney Disease, ASN Kidney Week 2017 Annual Meeting, Nov. 2017.
22.	Kazunori Yamaguchi, Takeyoshi Abe, Toshiki Takeuchi, Masahiro Watanabe, Koichiro Tsuchiya, Kazuro Ikawa, Noriyasu Fukuoka, Masato Kaji, Hiroaki Tanaka, Masato Asakura, Shinji Kosaka and Hitoshi Houchi : Estimation of the duration to reach peak arbekacin concentration by Monte Carlo simulation, 15th International Congress of Therapeutic Drug Monitoring & Clinical Toxicology, 26-4, Kyoto, Sep. 2017.
23.	Takeyoshi Abe, Masahiro Watanabe, Toshiki Takeuchi, Noriyasu Fukuoka, Yasuko Tomono, Akari Katsura, Hiroki Watanabe, Takayuki Kamada, Kazunori Abe, Katsunori Tsuda, Licht Miyamoto and Koichiro Tsuchiya : Development of an immunoassay-based point-of-care testing(POCT) device for therapeutic drug monitoring of vancomycin, 15th International Congress of Therapeutic Drug Monitoring & Clinical Toxicology, 25-5, Kyoto, Sep. 2017.
24.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Direct activated factor X inhibitor attenuates renal fibrosis on unilateral ureteral obstruction-induced nephrotoxicity., 53rd Congress of the European Societies of Toxicology (eurotox2017), Sep. 2017.
25.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FACTOR XA INHIBITOR ATTENUATES RENAL INTERSTITIAL FIBROSIS IN MICE WITH UNILATERAL URETERAL OBSTRUCTION, THE 13TH CONGRESS OF THE EUROPEAN ASSOCIATION FOR CLINICAL PHARMACOLOGY AND THERAPEUTICS(EACPT2017), Jun. 2017.
26.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 田淵正樹, Masaki Imanishi, Mai Takata, Eriko Sairyo, Yoshito Zamami, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : NITROSONIFEDIPINE, A NOVEL ANTIOXIDANT, AMELIORATES NEUROLOGICALSYMPTOMS AND PROLONGS THE SURVIVAL IN A MALIGNANT STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS, 27th European Meeting on Hypertension and Cardiovascular Protection, Jun. 2017.
27.	Masaki Imanishi, Kyohei Tanaka, Raiki Ikutoh, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : THE EFFECTS OF FEBUXOSTAT ON ANGIOTENSIN II-INDUCED VASCULAR REMODELING, 27th European Meeting on Hypertension and Cardiovascular Protection, Jun. 2017.
28.	Licht Miyamoto, Fukuta Keisuke, Takahashi Rie, Umemoto Kana, Okuno Hiroko, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Fragrance of aromatic oil from peels of Citrus sudachi causes adipose browning and ameliorates glucose and lipid metabolism, EMBO workshop, Sitges, Spain, May 2017.
29.	Licht Miyamoto, Tomokawa Goki, Matsuda Yuki, Yamane Megumi, Hattori Mana, Oonishi Reina and Koichiro Tsuchiya : Hypothalamic pathways regulate physical exercise-caused AMPK activation in skeletal muscles., Sweden, May 2017.
30.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Indoxyl Sulfate Involves Abnormality of Iron Metabolism through Hepcidin Regulation, Experimental Bioogy 2017, Chicago, Apr. 2017.
31.	Koichiro Tsuchiya, Aihara Haruna, Xu Wenting, Jin Meina, Tomida Yosuke, Yamaoka Tomomi, Naonobu Tanaka, Yasumasa Ikeda, Akira Shigenaga, Akira Otaka, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : A limonene-derivative from Sudachi peel activates sirt1 and improves lipid and glucose metabolism in high fat diet-fed mice., 欧州糖尿病学会, Dec. 2016.
32.	Koichiro Tsuchiya, Tomokawa Goki, Matsuda Yuki, Yamane Megumi, Hattori Mana, Oonishi Reina and Koichiro Tsuchiya : Significance of hypothalamic regulation on AMPK activation in skeletal muscles during physical exercise, Keystone symposium, Keystone, Nov. 2016.
33.	UMEMOTO Kana, Licht Miyamoto, UESHIMA Sayaka, HOSOI Mayu, TOMOKAWA Gouki and Koichiro Tsuchiya : 11th IDF-WPR Congress 2016 & 8th AASD Scientific Meeting2016/10/27-30Taipei International Convention Center( )Poster"Mechanismsofpostprandial suppression of hepatic AMPK activity through insulin - PI 3-kinasepathway", Taipei, Oct. 2016.
34.	TAKAHASHI Rie, Licht Miyamoto, FUKUTA Keisuke and Koichiro Tsuchiya : PosterInhibition of central GSK3 regulates body weight and glucose metabolism, 11th IDF-WPR Congress 2016 & 8th AASD Scientific Meeting, Taipei, Oct. 2016.
35.	Yoshito Zamami, Mitsui Marin, Moriguchi Hiroshi, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Kawasaki Hiromu, Toshiaki Tamaki and Keisuke Ishizawa : Search for a preventative therapy for Bevacizumab-induced hypertension using the drug repositioning approach, 7th Scientific Meeting of Asian Society for Vascular Biology, Oct. 2016.
36.	Tsuchihashi Yuki, Licht Miyamoto and Koichiro Tsuchiya : A hydrophilic derivative of probucol (ProBGL2) improves glucose tolerance andinsulin sensitivity, Hypertension, Seoul, Sep. 2016.
37.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Ichiro Hashimoto : Topical Application of Nitrosonifedipine, a Novel Free Radical Scavenger, Ameliorate the Ischemic Skin Flap Necrosis, Plastic Surgery THE MEETING 2016, Los Angeles, Sep. 2016.
38.	Licht Miyamoto and Koichiro Tsuchiya : Prolonged exposure to hypoxia causes downregulation of p-glycoprotein/MDR1, sensitizing Caco2 cells to anti-cancer drugs., Naito conference 2016, Sapporo, Jul. 2016.
39.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : The effects of pitavastatin, a lipid-lowering agent, against aortic dissection model mice induced by L-NAME, a nitric oxide synthase inhibitor., The 9th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide/16th Annual Scientific Meeting of the Nitric Oxide Society of Japan., May 2016.
40.	Koichiro Tsuchiya, Licht Miyamoto, Tomida Yosuke, Yamane Megumi, Tsuda Katsunori, Yasumasa Ikeda and Toshiaki Tamaki : Dietary nitrite ameliorates glucose tolerance and hyperlipidemia in diet-induced obesity rats., The 16th Annual Scientific Meeting of the Nitric Oxide Society of Japan / The 9th Internatinal Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide. (Seindai, Japan) 2016.5, May 2016.
41.	Yasumasa Ikeda, Keisuke Oshima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Involvement of Iron Supplementation on Erythropoietin Expression, Experimental Biology 2016, Apr. 2016.
42.	Licht Miyamoto, 粟飯原遥奈, 許文てい, ジン美娜, 冨田洋介, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : スダチ果皮からの抗メタボリックシンドローム活性を有する物質の同定, Journal of the The Japan Diabetes Society, No.59, Kyoto, 2016.
43.	FUKUTA Keisuke, Licht Miyamoto, TAKAHASHI Rie, Toshiaki Tamaki, Yasumasa Ikeda and Koichiro Tsuchiya : 11th IDF-WPR Congress 2016 & 8th AASD Scientific MeetingPosterEessentialoil fromsudachipealimprovesglucoseandlipidmetabolism, 2016.
44.	OKUNO Hiroko, Licht Miyamoto, TAKAHASHI Rie and Koichiro Tsuchiya : PosterElucidatingpharmacological beneficial functions of soybean extract on metabolism, 11th IDF-WPR Congress 2016 & 8th AASD Scientific Meeting, Taipei, 2016.
45.	Licht Miyamoto, Tatsuro Egawa, Rieko Oshima, Eriko Kurogi, Koichiro Tsuchiya and Tatsuya Hayashi : Impact of AMPK activation on the metabolomic alterations in contracting skeletal muscles, The 6th International Conference on Food Factors, Seoul, Nov. 2015.
46.	Licht Miyamoto, Yuki Tsuchihashi, Yosuke Tomida, Megumi Yamane, Kazuya Takenokuma, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Dietary nitrite ameliorates glucose tolerance and hyperlipidemia in diet-induced obese rats, The 6th International Conference on Food Factors, Seoul, Nov. 2015.
47.	Yasumasa Ikeda, Hamano Hirofumi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin Enhances Ischimia-induced Angiogenesis Through Akt-eNOS-Dependent Signaling Pathway, American Heart Association Scientific Sessions 2015, Orlando, Nov. 2015.
48.	Aya Hatano, Licht Miyamoto, Kazuya Takenokuma, Yuki Tsuchihashi, Tomoaki Yano and Koichiro Tsuchiya : The efficacy of combination therapy of nateglinide and canagliflozin, 2015.10.19-22 The 10th IAGG Asia / Oceania Congress of Gerontology and Geriatrics 2015, Chiang Mai, Oct. 2015.
49.	Wenting Xu, Licht Miyamoto, Haruna Aihara, Tomomi Yamaoka, Keisuke Ishizawa, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : The Mechanism of Citrus sudachi Peel Extract Exerts Lipid Reducing Effect in Cells, 2015.10.19-22 The 10th IAGG Asia / Oceania Congress of Gerontology and Geriatrics 2015, Chiang Mai, Oct. 2015.
50.	Licht Miyamoto, Tatsuro Egawa, Rieko Oshima, Eriko Kurogi, Koichiro Tsuchiya and Tatsuya Hayashi : AICAR, an AMPK activator, as a metabolomic mimetic of muscle contraction, The 10th IAGG Asia / Oceania Congress of Gerontology and Geriatrics 2015, Chiang Mai, Oct. 2015.
51.	秦野彩, Licht Miyamoto, 竹之熊和也, 友川剛己, 松田裕樹, 服部真奈 and Koichiro Tsuchiya : 速効型インスリン分泌促進薬，ナテグリニドとSGLT2 阻害薬，カナグリフロジンの併用による効果の検討, 日本肥満学会，アジアオセアニア糖尿病学会, Nagoya, Oct. 2015.
52.	Licht Miyamoto, 粟飯原遥奈, Wenting Xu, Meina Jin, 冨田洋介, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Akira Shigenaga, Akira Otaka, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : リモネン誘導体によるsirt1活性化を介した脂質低下作用, 日本肥満学会，アジアオセアニア糖尿病学会, Nagoya, Oct. 2015.
53.	Licht Miyamoto, Haruna Aihara, Wenting Xu, Meina Jin, Yosuke Tomida, Tomomi Yamaoka, Naonobu Tanaka, Yasumasa Ikeda, Akira Shigenaga, Akira Otaka, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : Limonene-derivative Ameliorates Lipid Profiles by Upregulation of Sirt1 Activity and Expression in Cultured Cells and High Fat Diet-Fed Mice, American diabetes association, Boston, Jun. 2015.
54.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Toya Hiroki, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Novel aortic dissection model by pharmacologically-induced endothelial dysfunction, 17th International Congress on Atherosclerosis 2015, Amsterdam, May 2015.
55.	Yasumasa Ikeda, Yusuke Kanai, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Effects of Bilirubin on Angiogenesis in Mice with Hindlimb Ischemia, Experimental Biology 2015, Boston, Mar. 2015.
56.	Yuya Horinouchi, A Fiona Summers, Marilyn Ehrenshaft, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and P Ronald Mason : Investigating free radical generation in HepG2 cells using immuno-spin trapping., Free Radical Biology and Medicine, Vol.75 Suppl 1, Dec. 2014. (Summary) Oxidative stress can induce the generation of free radicals, which are believed to play an important role in both physiological and pathological processes and a number of diseases such as cancer. Therefore, it is important to identify chemicals which are capable of inducing oxidative stress. In this study, we evaluated the ability of four environmental chemicals, aniline, nitrosobenzene (NB), N,N-dimethylaniline (DMA) and N,N-dimethyl-4-nitrosoaniline (DMNA), to induce free radicals and cellular damage in the hepatoma cell line HepG2. Cytotoxicity was assessed using lactate dehydrogenase (LDH) assays and morphological changes were observed using phase contrast microscopy. Free radicals were detected by immuno-spin trapping (IST) in in-cell western experiments or in confocal microscopy experiments to determine the subcellular localization of free radical generation. DMNA induced free radical generation, LDH release and morphological changes in HepG2 cells whereas aniline, NB and DMA did not. Confocal microscopy showed that DMNA induced free radical generation mainly in the cytosol. Preincubation of HepG2 cells with N-acetylcysteine and 2,2'-dipyridyl significantly prevented free radical generation upon subsequent incubation with DMNA, whereas preincubation with apocynin and dimethyl sulfoxide did not. These results suggest that DMNA induces oxidative stress and that reactive oxygen species, metals and free radical generation play a critical role in DMNA-induced cytotoxicity. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.freeradbiomed.2014.10.768 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26461344 ● Search Scopus @ Elsevier (PMID): 26461344 ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2014.10.768 (DOI: 10.1016/j.freeradbiomed.2014.10.768, PubMed: 26461344)
57.	Licht Miyamoto, Egawa Tatsuro, Oshima Rieko, Kurogi Eriko, Koichiro Tsuchiya and Hayashi Tatsuya : AICAR stimulation mimics metabolomic effects of electrical contraction in isolated rat epitrochlearis muscle., 10th IDF-WPR congress & 6th AASD scientific meeting, Singapore, Nov. 2014.
58.	Tsuchihashi Yuki, Licht Miyamoto, Tomida Yosuke, Takenokuma Kazuya, Hattori Hatsuhiko, Hisao Nemoto and Koichiro Tsuchiya : A Hydrophilic Derivative of Probucol, Ameliorates Glucose Tolerance and Insulin Sensitivity in HFD-fed mice., ASMRM 2014, Taipei, Nov. 2014.
59.	Hatano Aya, Licht Miyamoto, Yamane Megumi, Takenokuma Kazuya, Kono Mai, Keisuke Ishizawa and Koichiro Tsuchiya : Dietary nitrite ameliorates glucose tolerance and hyperlipidemia in diet-induced obesity rats., ASMRM 2014, Taipei, Nov. 2014.
60.	Licht Miyamoto, Egawa Tatsuro, Oshima Rieko, Kurogi Eriko, Koichiro Tsuchiya and Hayashi Tatsuya : AICAR stimulation mimics metabolomic effects of electrical contraction in isolated rat epitrochlearis muscle., ASMRM 2014, Taipei, Nov. 2014.
61.	Licht Miyamoto, Egawa Tatsuro, Oshima Rieko, Kurogi Eriko, Koichiro Tsuchiya and Hayashi Tatsuya : AICAR stimulation metabolome-widely mimics electrical contraction in isolated rat epitrochlearis muscle., AMPK meeting 2014, Castelvecchio, Barga, Italy, Sep. 2014.
62.	Hirokazu Miyoshi, Fumio Kida, Hitoshi Hase and Koichiro Tsuchiya : Silica-Nanocapsule-Doped CR-39 Fluorescent Detector for X-rays, 26th International Conference on Nuclear Tracks in Solids(ICNT-26), Kobe, Sep. 2014.
63.	Keisuke Ishizawa, Kohara Yusuke, Sakurada Takumi, Toya Hiroki, Iki Yutaka, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of aortic aneurysms by exerting antioxidative effects, ESC Congress 2014, Barcelona, Sep. 2014.
64.	Yasumasa Ikeda, Soichiro Tajima, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Ferritin induces IL-1 production through inflammasome activation via NF-B-dependent manner in macrophages, Experimental Biology 2014, San Diego, Apr. 2014.
65.	Licht Miyamoto, Yamane Megumi, Tomida Yosuke, Takenokuma Kazuya, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Significance of AMPK in renal protective and metabolic actions of nitrite, international conference of food science, Kyoto, Mar. 2014.
66.	Licht Miyamoto, Tomida Y, Takenokuma K, Yamane M, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Dietary nitrite ameliorates glucose and lipid metabolism in high fat diet-fed rats., 2014 Keystone Symposia Conference, Jan. 2014.
67.	Miku Kita, Jun Yamamoto, Koji Ebisuno, Chiaki Komiya, Akira Shigenaga, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Development of hydrogen peroxide-responsive amide bond cleavage device, 4th Asia-Pacific International Peptide Symposium, 50th Japanese Peptide Symposium, Suita, Nov. 2013.
68.	Keisuke Ishizawa, Noriko Yamano, Hiroyuki Kobori, Maki Urushihara, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine prevents the progression of diabetic nephropathy via attenuating the expression of intrarenal angiotensinogen and oxidative stress, High Blood Pressure Research 2013 Scientific Sessions, Sep. 2013.
69.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Doi, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Rho-kinase is involved in inorganic phosphate-induced ERK1/2 activation in vascular smooth muscle cells, World Biotechnology Congress 2013, Jun. 2013.
70.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The effect of dietary iron restriction against diabetic nephropathy in db/db mice, Experimental Biology 2013, Apr. 2013.
71.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Hirotsugu Kurobe, Masaki Imanishi, Yasushi Yoshida, Yoichiro Hirata, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Tetsuya Kitagawa, Masataka Sata and Toshiaki Tamaki : Deficiency of Hypoxia Inducible Factor-1a in SM-22a-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Formation, American Heart Association Scientific Sessions 2012, Nov. 2012.
72.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron Restriction Prevents the Progression of Diabetic Nephropathy in db/db Mice, American Heart Association Scientific Sessions 2012, Nov. 2012.
73.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible Factor-1a in Vascular Smooth Muscle Cells Regulates Angiotensin -induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media, American Heart Association Scientific Sessions 2012, Nov. 2012.
74.	Licht Miyamoto, Kono Mai, Nakagawa Takeo, Hattori Hatsuhiko, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : A Novel Hydrophilic Derivative of Probucol Ameliorates Glucose Tolerance and Insulin Sensitivity Independently of the Canonical Potency of Probucol., 48th Annual Meeting of the European Association for the Study of Diabetes, Oct. 2012.
75.	Hideaki Enomoto, Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Protective Effects of Iron-Restricted Food against Diabetic Nephropathy in db/db Mice, American Heart Association High Blood Pressure Research 2012, Sep. 2012.
76.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice, American Heart Association High Blood Pressure Research 2012, Sep. 2012.
77.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1a deficiency in smooth muscle cell attenuates angiotensin -induced vascular remodeling in mice, ISOTT (International Society on Oxygen Transport to Tissue) 2012, Aug. 2012.
78.	Takumi Sakurada, Keisuke Ishizawa, Shoko Fujii, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice, Experimental Biology 2012, Apr. 2012.
79.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron restriction prevents progression of diabetic nephropathy, KEYSTONE SYMPOSIA 40th ANNIVERSARY 1972-2012 Complications of Diabetes: Mechanisms of Injury and Failure of Repair, Mar. 2012.
80.	Licht Miyamoto, Mai Kono, Takeo Nakagawa, Hatsuhiko Hattori, Hisao Nemoto, Keisuke Ishizawa, Yoshiyuki Yoshimura and Koichiro Tsuchiya : A Hydrophilic Derivative of Probucol, Probucol-(glutaric branched-triglycerol)2 (ProBGL2) Ameliorates Glucose Tolerance and Insulin Sensitivity by Independent Mechanism of the Canonical Potency of Probucol in HFD-fed mice, Keystone symposiaon Molecular and Cellular Biology, Jan. 2012.
81.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Hirotsugu Kurobe, Masaki Imanishi, Yasushi Yoshida, Yoichiro Hirata, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Tetsuya Kitagawa, Masataka Sata and Toshiaki Tamaki : Deficiency of Hypoxia Inducible Factor-1 in SM-22-Expressing Bone Marrow-Derived Cells Alleviates Neointimal Formation Following Wire-induced Vascular Formation, AHA SCIENTIFIC SESSIONS 2012, 2012.
82.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible Factor-1 in Vascular Smooth Muscle Cells Regulates Angiotensin -induced Vascular Remodeling and AT1 Receptor Expression in Mouse Aortic Media, AHA SCIENTIFIC SESSIONS 2012, 2012.
83.	Fujii Shoko, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a Photodegradation Product of Nifedipine, Prevents the Progression of Diabetic Nephropathy in Type II Diabetic Mice, HIGH BLOOD PRESSURE RESEARCH 2012 SCIENTIFIC SESSIONS, 2012.
84.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1 deficiency in smooth muscle cell attenuates angiotensin II-induced vascular remodeling in mice, The International Society on Oxygen Transport to Tissue 2012, 2012.
85.	Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II-induced vascular remodeling is mediated by hypoxia-inducible factor-1 signaling pathway in vascular smooth muscle cells, The 33rd Naito Conference, 2012.
86.	Takumi Sakurada, Keisuke Ishizawa, Shoko Fujii, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine, a photodegradation product of nifedipine, on diabetic nephropathy in type II diabetic mice, Experimental Biology 2012, 2012.
87.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Smooth Muscle Cell-Specific Hypoxia-Inducible Factor-1a Deficiency Attenuates Angiotensin II-Induced Vascular Remodeling in Mice, AHA scientific sessions 2011, Orlando, Nov. 2011.
88.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Inhibition of Adipocyte Hypertrophy by Deferoxiamine Diabetic KKAy mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
89.	Kazuyuki Yamaguchi, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Glucose Metabolism of Adipocytes is Regulated by Basic Fibroblast Growth Factor via Hypoxia-inducible Factor-1a, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
90.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible Factor-1a Deficiency in Smooth Muscle Cells Suppresses Angiotensin -induced Vascular Remodeling in Mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
91.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin -induced Vascular Remodeling is Improved by Nitrosonifedipine, a Possible New Class Drug Against Oxidative Stress, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
92.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitorosonifedipine is a new class drug to improves angiotensin II-induced vascular remodeling, European Society of Cardiology Congress 2011, Aug. 2011.
93.	Shuhei Tomita, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Characterization on mice lacking HIF1a gene in renal ischemia-reperfusion injury, ISOTT (International Society on Oxygen Transport to Tissue) 2011, Washington, D.C., Jul. 2011.
94.	Yasumasa Ikeda, Soichiro Tajima, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Estrogen action on iron metabolism, ENDO 2011: The 93rd Annual Meeting & Expo, Boston, Jun. 2011.
95.	Masaki Imanishi, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Increment intracellular labile iron enhances Angiotensin-induced intracellular adhesion molecule-1 (ICAM-1) expression in human glomerular endothelial cells, World congress of Nephrology 2011, Vancouver, Apr. 2011.
96.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Smooth Muscle Cell-specific Hypoxia-inducible Factor-1a Deficiency Attenuates Angiotensin II-induced Vascular Remodeling In Mice, AHA SCIENTIFIC SESSIONS 2011, 2011.
97.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakurada Takumi, Masaki Imanishi, Fujii Shoko, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II-induced Vascular Remodeling Is Improved By Nitrosonifedipine, A Possible New Class Drug, HIGH BLOOD PRESSURE RESEARCH 2011 SCIENTIFIC SESSIONS, 2011.
98.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible Factor-1 Deficiency In Smooth Muscle Cells Suppresses Angiotensin II-induced Vascular Remodeling In Mice, HIGH BLOOD PRESSURE RESEARCH 2011 SCIENTIFIC SESSIONS, 2011.
99.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitorosonifedipine is a new class drug to improve angiotensin II-induced vascular remodeling, ESC Congress 2011, 2011.
100.	Masaki Imanishi, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuji Kondo, Shoji Kagami, Shuhei Tomita, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : INCREMENT INTRACELLULAR LABILE IRON ENHANCES ANGIOTENSIN II-INDUCED INTRACELLULAR ADHESION MOLECULE-1 (ICAM-1) EXPRESSION IN HUMAN GLOMERULAR ENDOTHELIAL CELLS, World Congress of Nephrology 2011, 2011.
101.	Ayato Katagiri, Hatsuhiko Hattori, Kohsuke Yoshitoimi, Keisuke Ishizawa, Koichiro Tsuchiya and Hisao Nemoto : Modification of Medicines by using Branched Oligo-Glycerols (BGL), Pachifichem 2010, Honolulu, Dec. 2010.
102.	Kohsuke Yoshitomi, Hatsuhiko Hattori, Ayato Katagiri, Keisuke Ishizawa, Koichiro Tsuchiya and Hisao Nemoto : Water-solubilization of Highly Hydrophobic Medicines by using Branched Oligo-Glycerols (BGL), Pachifichem 2010, Honolulu, Dec. 2010.
103.	Toshiaki Tamaki, Kunihisa Yamaguchi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Shuji Kondo, Shoji Kagami and Shuhei Tomita : Global gene expression analyses in renal ischemia-reperfusion injury (IRI) from mice lucking Hif-1a gene, ASN RENAL WEEK 2010 EXHIBIT, Nov. 2010.
104.	Koichiro Tsuchiya, Yuya Horinouchi, Soichiro Tajima, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Yoshiyuki Yoshimura, Shuhei Tomita, Shuichi Hamano and Toshiaki Tamaki : Antioxidant effects of photodegradation product of nifedipine, 17th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2010), Nov. 2010.
105.	Shuhei Tomita, Masahisa Urata, Yayoi Fukuhara, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Tetsuya Kitagawa and Toshiaki Tamaki : Endothelial-targeted hypoxia-inducible factor-1b (HIF-1b) loss-of function alleviates the monocrotaline-induced pulmonary hypertension in mice, American Heart Association Scientific Sessions 2010, Chicago, Nov. 2010.
106.	Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, Yayoi Fukuhara, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Yoshitaka Kihira, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitroso-nifedipine is a new class drug to protect endothelial function for overcoming organ damage, International Society of Hypertension 2010, Vancouver, Sep. 2010.
107.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : IRON DERIVATION AMELIORATES GLUCOSE TOLERANCE THROUGH REDUCTION OF OXIDATIVE STRESS AND INFLAMMATION IN DIABETIC KKAY MICE, 2010 American Physiological Society Conference Inflammation, Immunity and Cardiovascular Disease, Aug. 2010.
108.	Yoshitaka Kihira, Shuhei Tomita, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Basic fibroblast growth factor upregulates hypoxia inducible factor 1 and glucose transporter 1 in adipose cells, The 16th World Congress of Basic and Clinical Pharmacology (WorldPharma 2010), Copenhagen, Jul. 2010.
109.	Soichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Jun. 2010.
110.	Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : Metabolism of quercetin in vivo and its protective effect against cardiovascular diseases, 2nd International On-Board Symposium: Human Health, Energy and Environment, May 2010.
111.	Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, XX World Congress ISHR 2010 KYOTO, May 2010.
112.	Toshiaki Tamaki, Kunihisa Yamaguchi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Shuhei Tomita : Amelioration of acute tubular necrosis in ischemic acute renal failure was impaired in mice lucking hypoxia inducible factor-1 gene, ISN (International Society of Nephrology) nexus sympojium 2010, Apr. 2010.
113.	Souichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Kyoto, Apr. 2010.
114.	Koichiro Tsuchiya, Soichiro Tajima, Keisuke Ishizawa, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Yoshiyuki Yoshimura, Shuichi Hamano and Toshiaki Tamaki : Effect of Angiotensin II on the intracellular labile iron concentration in HGECs, 16th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2009), Nov. 2009.
115.	Yoshihisa Takaishi, Yoshiki Kashiwada, Hashida Waka, Mikuchi Kousuke and Koichiro Tsuchiya : FERULOYL MUCIC ACID DERIVATIVES AS SIRT1 STUMULATOR FROM CITRUS SUDACHI HORT. EX SHIRAI., 50th Annual Meeting of the American Society of Pharmacognosy, Honolulu, Jun. 2009.
116.	田島壮一郎, Koichiro Tsuchiya, Yuya Horinouchi, 石澤啓介, 寺岡和彦, 冨田修平, 川添和義, 芳地一, Toshiaki Tamaki and 水口和生 : ANGIOTENSIN II INCREASED INTRACELLULAR LABILE IRON IN THE PRESENCE OF TRANSFERRIN IN HGEC, Basic & Clinical Pharmacology & Toxicology, Vol.105, 127, 2009.
117.	Kunihisa Yamaguchi, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya, Shuji Kondo, Shoji Kagami and Toshiaki Tamaki : Hypoxia-Inducible Factor-1α ameliorates ischemic acute renal failure and has a relation with a recovery from acute tubular necrosis, 41th ASN annual meeting, Philadelphia, Nov. 2008.
118.	Toshiaki Tamaki, Keisuke Ishizawa, Kunihisa Yamaguchi, Shuji Kondo, Shoji Kagami, Fukuhara Yayoi, Yuya Horinouchi and Koichiro Tsuchiya : Nitoroso-nifedipine is a new class drug to protect kidney against oxidative stress, 41th ASN annual meeting, Philadelphia, Nov. 2008.
119.	Yuya Horinouchi, Koichiro Tsuchiya, 石澤啓介, 田島壮一郎, 元林有紀, 山口邦久, 川添和義, Kazuo Minakuchi and Toshiaki Tamaki : Endothelial cell protective activity of nitorosonifedipine, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
120.	Koichiro Tsuchiya, Soichiro Tajima, Mai Hamamoto, Hideki Ohnishi, Yuki Motobayashi, Yuya Horinouchi, Kunihisa Yamaguchi, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : Effect of angiotensin II on iron (II) turnover in HGEC, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
121.	Yuya Horinouchi, Koichiro Tsuchiya, Keisuke Ishizawa, Soichiro Tajima, Yuki Motobayashi, Kunihisa Yamaguchi, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : Endotherial cell protective activity of nitrosonifedipine, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
122.	Toshiaki Tamaki, Kunihisa Yamaguchi, Narantungalag Dorjsuren, Yayoi Fukuhara, Yuya Horinouchi, Yuki Motobayashi, Koichiro Tsuchiya and Keisuke Ishizawa : Olmesartan inhibits the TNF-α-induced cytotoxicity in human glomerular endothelial cells, ISN Nexus Symposium on Diabetes & the Kidney, Dublin, Jun. 2008.
123.	Keisuke Ishizawa, Narantungalag Dorjsuren, Yuki Izawa-Ishizawa, Teppei Tsuneishi, Yuki Motobayashi, Hideki Ohnishi, Kunihisa Yamaguchi, Koichiro Tsuchiya and Toshiaki Tamaki : Inhibitory effects of olmesartan on TNF-α-induced cytotoxicity in human glomerular endothelial cells, 40th ASN annual meeting, San Francisco, Nov. 2007.
124.	Koichiro Tsuchiya, Satoshi Iwanaga, Hideki Ohnishi, Yayoi Fukuhara, Chiaki Taoka, Soichiro Tajima, Yuya Horinouchi and Toshiaki Tamaki : In vivo and in vitro studies on NO formation from iron-quercetin-nitrite complexes, Second International Role of Nitrite in Physiology, Pathophysiology and Therapeutics Meeting, Bethesda, Maryland, Sep. 2007.
125.	Keisuke Ishizawa, Erika Miki, Arisa Hironaga, Koichiro Tsuchiya, Maki Urushihara, Shoji Kagami and Toshiaki Tamaki : Angiotensin II receptor blocker inhibits PDGF-induced cell migration in rat mesangial cells, 39th ASN annual meeting 2006, San Diego, Nov. 2006.
126.	Koichiro Tsuchiya, Yuya Horinouchi, Yasuhisa Kanematsu, Shinji Abe, Hideki Ohnishi, Soichiro Tajima, Keisuke Ishizawa, Toshiaki Tamaki and Yoshiharu Takiguchi : Production of nitrosonifedipine radical from nifedipine and its antioxidative activity in cultured cells, 13th annual meeting of society of free radical and biology of medicine, Denver, Nov. 2006.
127.	Hideki Ohnishi, Koichiro Tsuchiya, Yasuhisa Kanematsu, Shinji Abe, Soichiro Tajima and Toshiaki Tamaki : Effects of quercetin on NO production from nitrite at physiological conditions, 20th Scientific Meeting of the International Soiciety of Hypertension, Fukuoka, Japan, Oct. 2006.
128.	Koichiro Tsuchiya, Yasuhisa Kanematsu, Keisuke Ishizawa, Shinji Abe, Hideki Ohnishi, Soichiro Tajima, Kazuyoshi Kawazoe, Yoshiharu Takiguchi and Toshiaki Tamaki : Dietary nitrite is an alternative source of NO in vivo, International Society for Radical Research 13th Biennial Congress, Davos, Switzerland, Aug. 2006.
129.	Kenji Fukuzawa, Akira Shibata, Koichiro Tsuchiya, Akira Tokumura, H. Ichikawa and Jansuz M. Gebicki : Colored complex of ferric-xylenol orange/phosphatidylcholine vesicle in the Fox assay, XIII the Biennial Meeting of the Society for Free Radical Research International, Davos, Aug. 2006.
130.	Toshiaki Tamaki, Yasuhisa Kanematsu, Yuki Izawa, Hideki Ohnishi, Yuki Motobayashi, Shoji Kagami and Koichiro Tsuchiya : Chronic oral administration of nitrite restores circulating NO level and improves renal injury in L-NAME treated rats, 38th ASN annual meeting, Philadelphia, Nov. 2005.
131.	Keisuke Ishizawa, Rika Sugimoto, Yuki Izawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : The inhibitory effect of adiponectin on migration and proliferation induced by PDGF in rat mesangial cells, 38th ASN annual meeting, Philadelphia, Nov. 2005.
132.	Soichiro Tajima, Koichiro Tsuchiya, Hideki Ohnishi, Yasuhisa Kanematsu, Masanori Yoshizumi, Toshiaki Tamaki, Mason P. Ronald and Yoshiharu Takiguchi : Immunochemical Dection of Thioredoxin-Derived Radicals Formed by Reaction with Hydrogen Peroxide, EPR 2005, Columbus, OH, Sep. 2005.
133.	Koichiro Tsuchiya, Kaori Akai, Akira Tokumura, Shinji Abe, Toshiaki Tamaki, Yoshiharu Takiguchi and Kenji Fukuzawa : Oxygen Radicals Photo-induced by Ferric Nitrilotriacetate(FE-NTA) Complex, EPR 2005, Columbus, OH, Sep. 2005.
134.	Keisuke Ishizawa, Rika Sugimoto, Yuki Izawa, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Adiponectin inhibits PDGF-induced migration and proliferation in rat mesangial cells, 第10回アディポサイエンス研究会シンポジウム(第10回記念国際シンポジウム), Osaka, Aug. 2005.
135.	Toshiaki Tamaki, Masumi Okamoto, Yasuhisa Kanematsu, Yuki Izawa, Shoji Kagami, Shuji Kondo, Masanori Yoshizumi and Koichiro Tsuchiya : Dietary dose of nitrite attenuates L-NAME-induced renal injury in rats, 3rd World Congress of Nephrology, Singapore, Jun. 2005.
136.	Masanori Yoshizumi, Keisuke Ishizawa, Yuki Izawa, Chieko Miki, Yoshiko Fujita, Yasuhisa Kanematsu, Koichiro Tsuchiya and Toshiaki Tamaki : Aldosterone stimulates vascular smooth muscle cell proliferation through big mitogen-activated protein kinase1 activation, 16th scientific meeting of the interamerican society of hypertension, Cancun, Mexico, Apr. 2005.
137.	Toshiaki Tamaki, Masumi Okamoto, Yasuhisa Kanematsu, Yuki Izawa, Shoji Kagami, Shuji Kondo, Maki Shimizu, Masanori Yoshizumi and Koichiro Tsuchiya : Nitrite-derived nitric oxide formation following ischemia-reperfusion injury in rat kidney, 37th ASN annual meeting, St. Louis, MO, Oct. 2004.
138.	Shuji Kondo, Maki Shimizu, Koichiro Tsuchiya, Masanori Yoshizumi, Toshiaki Tamaki, Hiroshi Kawachi, Fujio Shimizu, Quinn T Mark, Lambeth J David, Yasuhiro Kuroda and Shoji Kagami : Add-on the antioxidant, probucol to angiotensin II type I receptor antagonist (ARB) arrests the progressive, St. Louis, MO, Oct. 2004.
139.	Shuji Kondo, M Shimizu, Koichiro Tsuchiya, Masanori Yoshizumi, Toshiaki Tamaki, H Kawachi, F Shimizu, Quinn MT, Lambeth DJ, Yasuhiro Kuroda and Shoji Kagami : Add-On the antioxidant,probucol to angiotensin 2 Type I receptor antagonist (ARB) arrests the progressive glomerulonephritis (GN) in the rat, 37th Annual meeting of American Society of Nephrology, St. Louis, 2004.
140.	M Hattori, Y Kobayashi, H Chikamoto, Koichiro Tsuchiya, S Gao, N Kobayashi, Shoji Kagami, P Mundel and K Ito : Induction of integrin-linked kinase (ILK) in mouse cultured podocytes after stimulation with plasma from recurrent-focal degmental glomerulosclerosis patients, 36th Annual meeting of American Society of Nephrology, San Diego, 2003.
141.	Toshiaki Tamaki, K Kirima, Masato Okamoto, S. Kondo, Shoji Kagami, Masanori Yoshizumi and Koichiro Tsuchiya : Oral nitrite increases the blood oxide and protects L-NAME-induced renal injury in rats, 36th Annual meeting of American Society of Nephrology, San Diego, 2003.

Proceeding of Domestic Conference:

1.	Masafumi Funamoto, Amiho Muramatsu, YAMAMOTO Mizuho, Shunji Hirose, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 黄連解毒湯によるドキソルビシン誘導性心毒性に対する効果検討, 第8回黒潮カンファレンス, Sep. 2024.
2.	Shunji Hirose, Masafumi Funamoto, YAMAMOTO Mizuho, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 糖尿病性心筋症に対する漢方薬五苓散の抑制効果, 第8回黒潮カンファレンス, Sep. 2024.
3.	矢崎夕奈, Koichiro Tsuchiya and Akihiro Shirai : 酸素由来の活性種に因らない近紫外線下でのフェルラ酸の殺菌機構の検討, 日本防菌防黴学会第51回年次大会要旨集, No.2P-Cp09, 186, Sep. 2024.
4.	Masafumi Funamoto, Amiho Muramatsu, Masaki Imanishi, Hidenori Yasuda, Koichiro Tsuchiya and Yasumasa Ikeda : アントラサイクリン系抗がん剤による心毒性に対する黄連解毒湯の検討, 第9回日本心血管協会(JCVA)学術集会, 72, May 2024.
5.	Shunji Hirose, Masafumi Funamoto, Hidenori Yasuda, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 糖尿病合併心不全に対する漢方薬五苓散の抑制効果, 第144回日本薬理学会近畿部会, Mar. 2024.
6.	Yasumasa Ikeda, Masafumi Funamoto, Hidenori Yasuda, Masaki Imanishi and Koichiro Tsuchiya : 低重力下における消化管と骨髄における鉄動態の検討, 第144回日本薬理学会近畿部会, Mar. 2024.
7.	Masafumi Funamoto, Amiho Muramatsu, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : ドキソルビシン誘導性心毒性を抑制する漢方薬と作用機序の解明, 第53回日本心脈管作動物質学会, Feb. 2024.
8.	Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, GOMI Yoshiki, HIGAKI Yoshiya, Masataka Nojima, Kohsuke Kondoh, SAWAMURA Takaya, Ryosuke Yamashita, Ryo Nakayama, Honoka Tsunematsu, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : TCGAがんゲノムビッグデータによる膵がん悪性化因子の網羅的探索と腫瘍血管新生の寄与についての検討, 第53回日本心脈管作動物質学会年会, Feb. 2024.
9.	Masafumi Funamoto, Amiho Muramatsu, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : ドキソルビシン心毒性を抑制する漢方薬と作用機序の解明, 第33回日本循環薬理学会, Jan. 2024.
10.	Licht Miyamoto, Yuki Tsuchihashi, Shinji Abe, Toshihiro Izumi, Aya Hatano, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 新規水溶性カンプトテシン誘導体，SN38-BGLによる，ヒト肺がん細胞移植モデルマウスにおける抗腫瘍効果と副作用の解析, 第97回日本薬理学会年会(神戸), Dec. 2023.
11.	Yasumasa Ikeda, SUENAGA Aoi, SETO Yasuyuki, Masafumi Funamoto, Masaki Imanishi and Koichiro Tsuchiya : 慢性腎臓病に対する漢方薬五苓散の効果の検討, 第97回日本薬理学会年会(神戸), Dec. 2023.
12.	Masafumi Funamoto, Amiho Muramatsu, Miyako Ueno, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 漢方薬のドキソルビシン心毒性に対する効果の検討, 第97回日本薬理学会年会(神戸)2023年12月16日, Dec. 2023.
13.	Shunji Hirose, Masafumi Funamoto, Amiho Muramatsu, Miyako Ueno, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 糖尿病性心筋症におけるエピジェネティック制御機構, 第97回日本薬理学会年会(神戸), Dec. 2023.
14.	Honoka Tsunematsu, Masaki Imanishi, Yuka Uemura, HIGAKI Yoshiya, Keijo Fukushima, Miyu Morisaki, Akari Katsura, Licht Miyamoto, Masafumi Funamoto, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichi Tsuneyama and Koichiro Tsuchiya : 藍含有成分はendothelin-1発現を制御して肺動脈血管リモデリングを形成させる, 次世代を担う若手のための創薬・医療薬理シンポジウム2023, Aug. 2023.
15.	SAWAMURA Takaya, Masaki Imanishi, Keijo Fukushima, Ryosuke Yamashita, Kohsuke Kondoh, Ryo Nakayama, GOMI Yoshiki, Honoka Tsunematsu, Takahisa Inoue, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : PARP阻害剤は低酸素環境下において生じる5-FU治療効果の減弱を回復させる, 生体機能と創薬シンポジウム2023, Aug. 2023.
16.	Natsuki Toyota, Masaki Imanishi, Takahisa Inoue, Honoka Tsunematsu, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Yasumasa Ikeda and Koichiro Tsuchiya : 亜硝酸塩が有するヒドロキシルラジカル消去活性の検討, 生体機能と創薬シンポジウム2023, Aug. 2023.
17.	GOMI Yoshiki, Masaki Imanishi, Takahisa Inoue, Keijo Fukushima, Ryosuke Yamashita, Ryo Nakayama, Masataka Nojima, Kohsuke Kondoh, SAWAMURA Takaya, Honoka Tsunematsu, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : TCGAがんゲノムビッグデータとGEOトランスクリプトームデータとの統合解析による膵がん治療標的候補遺伝子の探索, 生体機能と創薬シンポジウム2023, Aug. 2023.
18.	Amiho Muramatsu, Masafumi Funamoto, Miyako Ueno, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : ドキソルビシン心毒性に対する漢方薬効果の検討, 第7回黒潮カンファレンス(宮崎), Jul. 2023.
19.	Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 病的心肥大と老化におけるマクロファージ鉄ストレスの役割の検討, ,第7回黒潮カンファレンス(宮崎), Jul. 2023.
20.	Honoka Tsunematsu, Yuka Uemura, HIGAKI Yoshiya, Miyu Morisaki, Akari Katsura, Licht Miyamoto, Yuya Horinouchi, Koichi Tsuneyama, Masaki Imanishi and Koichiro Tsuchiya : 藍含有成分による肺動脈血管リモデリング形成作用の検討, 第143回日本薬理学会近畿部会, Jun. 2023.
21.	Amiho Muramatsu, Masafumi Funamoto, 上野実弥子, Masaki Imanishi, Yasumasa Ikeda and Koichiro Tsuchiya : 黄連解毒湯を用いたcGAS/STING/IRF3経路を介したドキソルビシン誘導性心毒性に対する検討, 第8回日本心血管協会(JCVA)学術集会(大分) 2023年6月10日, Jun. 2023.
22.	Masafumi Funamoto, Shunji Hirose, Amiho Muramatsu, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 糖尿病性心筋症におけるエピジェネティックな老化制御機構の解明, 第8回日本心血管協会(JCVA)学術集会(大分), Jun. 2023.
23.	常松保乃加, 植村宥香, 檜垣良也, 森崎実友, 桂明里, Licht Miyamoto, Koichi Tsuneyama, Masaki Imanishi and Koichiro Tsuchiya : 肺動脈性肺高血圧症発症に対する藍葉含有成分の役割, 日本薬学会第143年会, Mar. 2023.
24.	Kohsuke Kondoh, Masaki Imanishi, Ryosuke Yamashita, Keijo Fukushima, Ryo Nakayama, Honoka Tsunematsu, Takahisa Inoue, GOTOH Kohei, Licht Miyamoto, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : 5-FUの膵がん細胞増殖抑制効果に対する低酸素―PARP活性化シグナルの役割, 第262回徳島医学会学術集会(徳島), Feb. 2023.
25.	Shunji Hirose, Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 2型糖尿病による心筋症モデルマウスの検討, 第262回徳島医学会学術集会, Feb. 2023.
26.	Masaki Imanishi, 山下竜介, Keijo Fukushima, 近藤宏祐, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : 5-FU膵がん細胞増殖抑制効果に対する低酸素-PARPシグナルの役割, 第52回心脈管作動物質学会, Feb. 2023.
27.	辻哲平, Licht Miyamoto, 中山涼, Masaki Imanishi and Koichiro Tsuchiya : 身体運動による肝脂質代謝改善効果における交感神経系の関連, 第142回日本薬理学会近畿部会, Nov. 2022.
28.	山下竜介, Masaki Imanishi, Keijo Fukushima, 近藤宏祐, 中山涼, 常松保乃加, 井上貴久, 後藤廣平, Masafumi Funamoto, Hiromichi Fujino, Yasumasa Ikeda and Koichiro Tsuchiya : 低酸素がん微小環境におけるPARP活性化は5-FUによる膵がん細胞増殖抑制効果の減弱に寄与する, 第142回日本薬理学会近畿部会, Nov. 2022.
29.	Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : ドキソルビシン誘導性心毒性に対するオウゴン成分オウゴニンの効果検討, 第141回日本薬理学会近畿部会, Jul. 2022.
30.	山田佑人, Yuya Horinouchi, 吉岡駿, 村嶋優香, 久禮匠, 佐々木尚史, Masaki Imanishi, Koichiro Tsuchiya, 四宮一昭 and Yasumasa Ikeda : 慢性腎臓病に対するSPPARMαペマフィブラートの腎保護効果, 第141回日本薬理学会近畿部会, Jul. 2022.
31.	Tatsuki Itoh, Masafumi Funamoto, Masaki Imanishi, Koichiro Tsuchiya and Yasumasa Ikeda : 急性腎障害におけるマクロファージ鉄ストレスの役割の検討, 第141回日本薬理学会近畿部会, Jul. 2022.
32.	Hanif Ali, Miyu Kobayashi, Katsuya Morito, Rumana Yesmin Hasi, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Kaori Kanemaru, Koichiro Tsuchiya, Kazunori Sango and Tamotsu Tanaka : Peroxisomes attenuate lipotoxicity of very-long-chain fatty acids, 第64回日本脂質生化学会, Vol.64, 43-46, Jun. 2022.
33.	Hanif Ali, Miyu Kobayashi, Katsuya Morito, Rumana Yesmin Hasi, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Kaori Kanemaru, Koichiro Tsuchiya, Kazunori Sango and Tamotsu Tanaka : Metabolism and biological effect of very-long-chain fatty acid in peroxisome-deficient cells, 第63回日本生化学中国・四国支部例会, May 2022.
34.	Yasumasa Ikeda, Masafumi Funamoto, Masaki Imanishi and Koichiro Tsuchiya : 漢方薬の新規腎保護作用の検討, 第95回日本薬理学会年会, Mar. 2022.
35.	Chiemi Sato, Koichiro Tsuchiya and Shinji Abe : 臨床実習後模擬症例演習科目における遠隔授業導入の影響評価∼学生の臨床検査値理解度の分析より∼, 日本薬学会第142年会(名古屋online), Mar. 2022.
36.	Toshitaka Ikehara, Mutsumi Aihara, Koichiro Tsuchiya, Takahiro Emoto, Masatake Akutagawa, Akira Takahashi and Yohsuke Kinouchi : Studies of reactive oxygen species scavenging system of cultured cells by using LED light irradiation, LED総合フォーラム2022 in 徳島, 193-198, Jan. 2022.
37.	Hanif Ali, Katsuya Morito, Rumana Yesmin Hasi, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Kaori Kanemaru, Koichiro Tsuchiya, Kazunori Sango and Tamotsu Tanaka : Characterization of uptake and metabolism of very-long-chain fatty acid in peroxisome-deficient CHO cells, 第94回日本生化学大会, Nov. 2021.
38.	常松保乃加, 森崎実友, 桂明里, Koichi Tsuneyama, Licht Miyamoto and Koichiro Tsuchiya : 藍含有成分による肺動脈性肺高血圧症の発症メカニズムの解明, 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2021.
39.	Hanif Ali, Katsuya Morito, Rumana Yesmin Hasi, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Kaori Kanemaru, Koichiro Tsuchiya, Kazunori Sango and Tamotsu Tanaka : Characterization of uptake and metabolism of very-long-chain fatty acid in peroxisome-deficient CHO cells, 第62回日本生化学中国・四国支部例会, Sep. 2021.
40.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Licht Miyamoto, Toshiaki Tamaki and Koichiro Tsuchiya : シスプラチン誘発性腎毒性における鉄依存性細胞死の役割の検討, 第64回日本腎臓学会学術集会, Jun. 2021.
41.	Hanif Ali, Katsuya Morito, Rumana Yesmin Hasi, Mutsumi Aihara, Junji Hayashi, Ryushi Kawakami, Kaori Kanemaru, Koichiro Tsuchiya and Tamotsu Tanaka : Uptake and metabolism of very-long-chain fatty acid in animal cells, 第63回日本脂質生化学会, Jun. 2021.
42.	Kawasaka Kaito, Koichiro Tsuchiya, Hideaki Nagamune and Akihiro Shirai : フェノール酸とブルーライトを併用した真菌の光不活性化, 日本農芸化学会2021年度仙台大会, Vol.3G01-06, 829, Mar. 2021.
43.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Yoshito Zamami, Licht Miyamoto, 石澤啓介, Hiromichi Fujino, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Identification of a candidate drug for the prevention of cisplatin-induced nephrotoxicity by a database analysis -basic research-clinical study, 第94回日本薬理学会年会, Mar. 2021.
44.	Chiemi Sato, Koichiro Tsuchiya and Shinji Abe : 検査値理解度に対するルーブリックの作成と臨床実習後模擬症例演習の有用性評価, Rubric for lab. data comprehension and evaluation of usefulness of clinical case-study program, Mar. 2021.
45.	Rina Murata, Keiji Murakami, Yuka Hiroshima, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加によるスーパーオキシドの発生について, 第73回日本細菌学中国・四国支部総会, 22, Oct. 2020.
46.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, 石澤啓介, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン起因性腎障害を予防する既存薬の同定, 第63回日本腎臓学会学術総会, Aug. 2020.
47.	Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Mitsuhiro Goda, Yoshito Zamami, Licht Miyamoto, Keisuke Ishizawa and Koichiro Tsuchiya : The involvement of ferroptosis on cisplatin-induced nephrotoxicity, 第93回日本薬理学会年会, Mar. 2020.
48.	Licht Miyamoto, Yuko Yagi, Aya Hatano, Yasumasa Ikeda, Shinji Abe, Toshiaki Tamaki and Koichiro Tsuchiya : Chronic exposure to hypoxia facilitates chemotherapy sensitivity with downregulation of MDR1, 日本薬理学会, Mar. 2020.
49.	Keiji Murakami, 村田梨菜, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加による酸化ストレスについて, 第54回緑膿菌感染症研究会, Feb. 2020.
50.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Kenshi Takechi, Masayuki Chuma, Yoshito Zamami, Yuya Horinouchi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン誘発性腎障害を予防する既存薬物の同定, 第260回徳島医学会学術集会(令和元年度冬期), Feb. 2020.
51.	Yasumasa Ikeda, Yuya Horinouchi, Hirofumi Hamano, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン腎障害における鉄依存性細胞死の検討, 第29回日本循環薬理学会/第55回高血圧関連疾患モデル学会合同学会, Nov. 2019.
52.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連サルコペニアにおける鉄代謝異常, 第6回日本サルコペニア・フレイル学会大会, Nov. 2019.
53.	高橋千明, Licht Miyamoto, 高橋梨恵, 曽根翼, 武智研志, 宮武由実子, 阪上浩 and Koichiro Tsuchiya : 脳内グリコーゲンによる代謝調節効果の検討, 第58回中国四国支部学術大会, Nov. 2019.
54.	近藤友宏, Licht Miyamoto, 福田恵介, 高橋梨恵, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : スダチ果皮香気成分由来物質による糖脂質代謝の影響, 第58回中国四国支部学術大会, Nov. 2019.
55.	曽根翼, Licht Miyamoto, 土橋有希, 保岡尭, 増田栞, 末次璃子 and Koichiro Tsuchiya : 妊娠期概日リズム障害時の育児行動と仔の表現型, 第58回中国四国支部学術大会, Nov. 2019.
56.	Licht Miyamoto, Suguru Nakayama, Aya Hatano, Mana Hattori, Haruka Inoue and Koichiro Tsuchiya : α-TC細胞における糖輸送を介したグルカゴン分泌の調節機構とSGLT2, 日本肥満学会, Nov. 2019.
57.	定作奈津美, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : ビッグデータを活用した新規抗てんかん薬の検討, 第29回日本医療薬学会年会, Nov. 2019.
58.	Masayuki Chuma, Mitsuhiro Goda, Takahiro Niimura, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, 濱野裕章, 石田俊介, Takahiro Niimura, Masateru Kondoh, Takashi Bandoh, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討, 第13回日本腎臓病薬物療法学会学術集会・総会, Nov. 2019.
59.	Licht Miyamoto, Keisuke Fukuta, Kondo Tomohiro and Koichiro Tsuchiya : Fragrance of aromatic oil from peels of Citrus sudachi evokes browning of adipose tissue, improving glucose and lipid metabolism, 内藤カンファレンス, Oct. 2019.
60.	髙橋千明, Licht Miyamoto and Koichiro Tsuchiya : 脳内グリコーゲンによる代謝調節効果の検討, 第 26 回市大フォーラム, Aug. 2019.
61.	友成奈央実, Licht Miyamoto and Koichiro Tsuchiya : 肝臓における食後 AMPK 活性制御メカニズムの解明, 第 26 回市大フォーラム, Aug. 2019.
62.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を用いたニコランジルの心肺停止後予後改善効果の検討, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
63.	JOHZUKURI Natsumi, Shimon Takahashi, Kenshi Takechi, Masayuki Chuma, Mitsuhiro Goda, Yoshito Zamami, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報データベースを活用した新規抗てんかん薬の探索研究, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
64.	Mitsuhiro Goda, 斉家和仁, Akiko Maegawa, Masaya Kanda, Ami Yoshida, Yoichi Murai, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : 医療ビッグデータを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 第4回中四国臨床薬理学会, Jul. 2019.
65.	Licht Miyamoto, Suguru Nakayama, Aya Hatano, Mana Hattori, Haruka Inoue and Koichiro Tsuchiya : α-TC細胞におけるグルカゴン分泌調節の分子機構とSGLT2, 日本糖尿病学会, May 2019.
66.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した薬剤性副作用の機序解明および治療薬の開発, 第29回日本医療薬学会年会シンポジウム13, Mar. 2019.
67.	近藤正輝, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : キサンチンオキシダーゼ阻害剤による新規血管線維化抑制機構の検討, 日本薬学会第139年会大学院生シンポジウムGS03, Mar. 2019.
68.	Licht Miyamoto, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロールを用いた難水溶性化合物の親水化技術と医薬品への応用, 日本薬学会第139年会シンポジウム「薬学に革新をもたらす最先端技術の世界 ∼基礎研究から臨床まで∼」, Mar. 2019.
69.	Licht Miyamoto, Nakayama Suguru, Hatano Aya, Hattori Mana, Inoue Haruka and Koichiro Tsuchiya : α-TC細胞におけるグルカゴン分泌の分子制御機構とSGLT2の意義, 日本薬学会年会, Mar. 2019.
70.	土橋有紀, Licht Miyamoto, Masayuki Shono and Koichiro Tsuchiya : 加圧培養環境下における 3T3-L1細胞分化誘導への影響, 日本薬学会第139年会, Mar. 2019.
71.	Licht Miyamoto and Koichiro Tsuchiya : 「徳島特有の香酸柑橘，スダチによる代謝改善作用の分子機構」第92回日本薬理学会年会シンポジウム「ユニークな天然物資源を活かした，地域産業，国際化，医療に貢献する薬理学研究」, 第92回日本薬理学会年会シンポジウム「ユニークな天然物資源を活かした，地域産業，国際化，医療に貢献する薬理学研究」, Mar. 2019.
72.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Keijo Fukushima, Mitsuhiro Goda, Kenshi Takechi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連骨格筋萎縮における鉄代謝異常, 第92回日本薬理学会年会, Mar. 2019.
73.	Yasumasa Ikeda, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron accumulation negatively regulates skeletal muscle myogenesis, 第92回日本薬理学会年会, Mar. 2019.
74.	Licht Miyamoto, Nakayama Suguru, Hatano Aya, Hattori Mana, Inoue Haruka, Yasumasa Ikeda and Koichiro Tsuchiya : Significance of SGLT2 in glucagon secretion from α-TC cells, 日本薬理学会, Mar. 2019.
75.	土橋有紀, Licht Miyamoto, Masayuki Shono and Koichiro Tsuchiya : The effect of pressure culture on the differentiation of 3T3-L1 preadipocyte, 第92回日本薬理学会年会, Mar. 2019.
76.	Koichiro Tsuchiya : 徳島県の後発医薬品普及に向けた課題と取り組み, 平成30年度日本社会薬学会四国支部例会, Mar. 2019.
77.	Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Watanabe, Hirofumi Hamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : マクロファージフェリチン欠損は肥満・糖尿病における脂肪炎症を抑制する, 第48回日本心脈管作動物質学会, Feb. 2019.
78.	藤本望, 村田梨菜, Keiji Murakami, Hideki Fujii, Licht Miyamoto, 井上貴久, Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa and Shuichi Hamano : 唾液中の硝酸イオンが口腔細菌に与える影響について·, 第42回徳島県医学検査学会, Dec. 2018.
79.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Hiroumi Saito, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報データベースおよび遺伝子発現データベースを活用した薬剤性心筋炎に対する予防薬の探索, 第28回日本医療薬学会年会シンポジウム, Nov. 2018.
80.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Kenshi Takechi, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : リアルワールドビッグデータを活用した新規腎保護薬の探索, 第28回日本医療薬学会年会, Nov. 2018.
81.	大西伶奈, Licht Miyamoto, 友川剛己, 竹之熊和也 and Koichiro Tsuchiya : CaffeineによるAMPK活性調節メカニズムの検討, 第134回日本薬理学会近畿部会, Nov. 2018.
82.	桂明里, Licht Miyamoto, 服部真奈, 津田勝範, 森崎実友, Yuki Izawa-Ishizawa and Koichiro Tsuchiya : 青黛含有成分による細胞増殖活性の検討, 第134回日本薬理学会近畿部会, Nov. 2018.
83.	井上陽加, Licht Miyamoto, 服部真奈, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による脂肪組織への抗肥満的な影響, 第134回日本薬理学会近畿部会, Nov. 2018.
84.	Yuya Horinouchi, Yasumasa Ikeda, Hirofumi Hamano, Masaki Imanishi, Keijo Fukushima, Mitsuhiro Goda, Kenshi Takechi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全関連サルコペニアにおける鉄の関与, 第134回日本薬理学会近畿部会, Nov. 2018.
85.	保岡尭, Licht Miyamoto, 曽根翼, 増田栞, 土橋有希 and Koichiro Tsuchiya : 妊娠期概日リズムと仔の表現型の関係の検討, 第57回中国四国支部学術大会, Nov. 2018.
86.	中山卓, Licht Miyamoto, 服部真奈, 井上陽加 and Koichiro Tsuchiya : α-TCのグルカゴン分泌におけるSGLT2阻害薬の影響, 第57回中国四国支部学術大会, Nov. 2018.
87.	斉家和仁, Mitsuhiro Goda, 伊勢諒, 新村貴博, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Naoto Okada, Kenshi Takechi, Masaki Imanishi, Yasumasa Ikeda, 演野裕章, Yuya Horinouchi, Koichiro Tsuchiya and Keisuke Ishizawa : シスプラチン誘発腎障害に対する脂質異常症治療薬の影響, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
88.	中山卓, Licht Miyamoto, 服部真奈, 井上陽加 and Koichiro Tsuchiya : α-TCのグルカゴン分泌におけるSGLT2阻害剤の影響, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
89.	生藤来希, Masaki Imanishi, 山川祐介, Keijo Fukushima, 前川晃子, Yuya Horinouchi, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda, Hiromichi Fujino and Koichiro Tsuchiya : 大腸がん増大におけるがん関連線維芽細胞由来ERKSの役割, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
90.	保岡尭, Licht Miyamoto, 土橋有紀, 曽根翼, 増田栞 and Koichiro Tsuchiya : 妊娠期概日リズムと仔の表現型の関係性, 第57回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2018.
91.	Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Watanabe, Hirofumi Hamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Yoshito Zamami, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : マクロファージ鉄の肥満・糖尿病における役割第42回日本鉄バイオサイエンス学会学術集会 2018/9/2 石川県金沢医科大学病院北辰講堂, 第42回日本鉄バイオサイエンス学会学術集会, Sep. 2018.
92.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を活用した新規心肺蘇生後脳症治療薬の探索, 第29回霧島神経薬理フォーラム, Aug. 2018.
93.	井上陽加, Licht Miyamoto and Koichiro Tsuchiya : マウスにおける亜硝酸塩の脂肪組織への影響, 第25回市大フォーラム, Aug. 2018.
94.	Yoshito Zamami, 新村貴博, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : 医療情報データベースを活用した抗がん剤誘発副作用に対する予防薬の探索研究, 第21回日本医薬品情報学会総会・学術大会, Jul. 2018.
95.	Masaki Imanishi, Masateru Kondoh, 山川裕介, 生藤来希, 村井陽一, Yoshito Zamami, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Keijo Fukushima, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Angiotensin II誘発性心臓線維化は線維芽細胞特異的ERK5欠損マウスにおいて亢進される, 第133回日本薬理学会近畿部会, Jun. 2018.
96.	Licht Miyamoto, 梅本果奈, 上島沙弥香, 友成奈央実, 池田康将, 玉置俊晃 and Koichiro Tsuchiya : 食後の末梢組織における代謝調節を担う新たなAMPKの活性調節機構, 日本糖尿病学会, May 2018.
97.	Koichiro Tsuchiya, Licht Miyamoto, Shuichi Hamano, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and 津田勝範 : 抗マラリア薬artesunateからの鉄依存活性酸素生成メカニズムの検討, 第71回日本酸化ストレス学会，第18回日本NO学会合同学術集会, May 2018.
98.	Yoshihiro Uto, Hanayo Katsura, Yuki Kusuhashi, Hisatsugu Yamada, Koichiro Tsuchiya, 大崎智弘, 中島元夫, 石塚昌宏, 田中徹, 山中信康 and 倉橋司 : ESR法を用いたALA-SDTの抗腫瘍作用機序の解析, 第8回ポルフィリン‐ALA学会年会, Apr. 2018.
99.	Yoshito Zamami, Marin Mitsui, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Keijo Fukushima, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを活用したベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本薬学会第138年会, Mar. 2018.
100.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニング手法を用いた心肺蘇生後脳症治療薬の探索, 日本薬学会第138年会, Mar. 2018.
101.	Licht Miyamoto, 梅本果奈, 上島沙弥香, 友成奈央実, 保岡尭, 中山卓, 桂明里, 大西怜奈, 井上陽加, 土橋有希 and Koichiro Tsuchiya : 食事と身体運動による代謝制御のクロストークの場としてのAMPK, 第138回日本薬学会, Mar. 2018.
102.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Hirofumi Hamano, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 大規模医療情報データベース解析と基礎研究の融合による新規腎保護薬の探索, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
103.	Masaki Imanishi, Masateru Kondoh, Kyohei Tanaka, Raiki Ikutoh, Yoichi Murai, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Febuxostatの尿酸合成抑制作用とは独立した血管線維化抑制機構の解明, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
104.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用した心肺停止患者に対するニコランジルの有効性に関する検討, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
105.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害剤の腎保護効果, 第47回日本心脈管作動物質学会, Feb. 2018.
106.	Licht Miyamoto, 梅本果奈, 上島沙弥香, 友成奈央実, 土橋有希, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食後生じるAMPKの新たな翻訳後修飾を介した代謝制御機構, 心脈管作動物質学会, Feb. 2018.
107.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害薬の腎保護効果, 第10回心・血管クラスター・ミニリトリート, 2017.
108.	Masahiro Betsushiyo, 村上圭史, 藤猪英樹, Katsunori Tsuda, Licht Miyamoto, Koichiro Tsuchiya, Yasumasa Ikeda, Toshiaki Tamaki and Shuichi Hamano : Actinomyces spp. による硝酸イオンの還元と生理作用の検討, 第41回徳島県医学検査学会, Dec. 2017.
109.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を用いて新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究, 第38回日本臨床薬理学会学術総会, Dec. 2017.
110.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 臨床薬理学集中講座修了後の研究活動∼大規模医療情報を活用したドラッグリポジショニング研究を中心に∼, 第38回日本臨床薬理学会学術総会臨床薬理学集中講座フォローアップ・セミナー, Dec. 2017.
111.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 肥満・糖尿病におけるマクロファージ鉄制御機構の検討, 第132回日本薬理学会近畿部会, Nov. 2017.
112.	Yamaguchi Kazunori, Takeyoshi Abe, Toshiki Takeuchi, Masahiro Watanabe, Koichiro Tsuchiya, 猪川和朗, 福岡憲泰, 加地雅人, 田中裕章, 朝倉正登, 小坂信二 and Hitoshi Houchi : アルベカシンのCpeak 到達時間の予測 ∼モンテカルロシミュレーションによる検討∼, 第27回日本医療薬学会年会・講演要旨集, 1288, Nov. 2017. (Keyword) TDM
113.	Takahiro Niimura, Yoshito Zamami, 小山敏広, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニングを切り口とした心肺蘇生後症候群治療薬の探索研究, 第27回日本医療薬学会年会, Nov. 2017.
114.	Yoshito Zamami, 小山敏広, Yuki Izawa-Ishizawa, Takahiro Niimura, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, 桐野靖, 中村敏己, 寺岡和彦, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用して心肺停止患者の生存率向上を志向したドラッグリポジショニング研究, 第27回日本医療薬学会年会, Nov. 2017.
115.	Marin Mitsui, Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを基にしたベバシズマブと相互作用を起こす薬剤の探索研究, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
116.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 心肺停止患者の予後に与えるニコランジルの影響-大規模レセプト情報を用いた検討, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
117.	Shiori Urushizaki, Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用して新規心肺蘇生後症候群治療薬の開発を志向したドラッグリポジショニング研究, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
118.	細井麻由, Licht Miyamoto, 川崎彩, 芳野真奈 and Koichiro Tsuchiya : 交感神経系刺激による肝臓の糖脂質代謝制御におけるAMPKの意義, 第56回中国四国支部学術大会, Oct. 2017.
119.	Mana Yoshino, Licht Miyamoto, Tomomi Yamaoka, Mayu Hosoi, Takuya Morisaki, Keitaroh Anyohji, Akira Shigenaga, Akira Otaka and Koichiro Tsuchiya : 骨格筋培養細胞でのレプチン作用におけるSIRT1の役割, 第56回中国四国支部学術大会, Oct. 2017.
120.	Yu Kagimoto, Yuki Izawa-Ishizawa, Mayuko Hosohka, Naoko Saito, Kotoko Suzuki, Masaki Imanishi, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 急性大動脈解離易発症マウスにおけるquercetinの効果, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
121.	Kyohei Tanaka, Masaki Imanishi, Masateru Kondoh, Raiki Ikutoh, Yoichi Murai, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : フェブキソスタットの尿酸合成抑制剤作用とは独立した血管線維化抑制作用の検討, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
122.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 肥満・糖尿病におけるマクロファージ鉄の役割の検討, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2017.
123.	Licht Miyamoto, 梅本果奈, 上島沙弥香, 友成奈央実, 土橋有希, 井上貴久, 許文婷, 津田勝範 and Koichiro Tsuchiya : 食と運動による代謝制御のクロスロードとしての新たなAMPK活性制御機構, 第38回日本肥満学会, Oct. 2017.
124.	Chiemi Sato, Shinji Abe, Koichiro Tsuchiya and Tetsuya Kume : 改訂コアカリキュラムに提示された「代表的な疾患」に関する実習状況と今後の課題, 第56回日本薬学会・日本薬剤師会・日本病院薬剤師会学術大会中国四国支部大会, Oct. 2017.
125.	近藤友宏, Licht Miyamoto and Koichiro Tsuchiya : The essential oil from Sudachi peal improves glucose and lipid metabolism, 2017 Tokushima Bioscience Retreat, Sep. 2017.
126.	芳野真奈, Licht Miyamoto and Koichiro Tsuchiya : The role of SIRT1 in regulation of C2C12 myotube metabolism by leptin,, 2017 Tokushima Bioscience Retreat, Sep. 2017.
127.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎臓病における尿毒素蓄積によるヘプシジン制御と鉄代謝破綻のメカニズムの解明, 第41回日本鉄バイオサイエンス学会学術集会, Sep. 2017.
128.	Yasumasa Ikeda, Yuya Horinouchi, Hirofumi Hamano, 平山祐, Seiji Kishi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Ken-ichi Aihara, Hideko Nagasawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄摂取制限による尿細管間質障害の抑制効果の検討, 第41回日本鉄バイオサイエンス学会学術集会, Sep. 2017.
129.	Licht Miyamoto, Kana Umemoto, Sayaka Ueshima, Naomi Tomonari, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食後のエネルギー代謝調節を担うAMPK活性制御機構, 次世代を担う創薬医療薬理シンポジウム2017, Aug. 2017.
130.	Licht Miyamoto, Kana Umemoto, Sayaka Ueshima, Naomi Tomonari, 土橋有希, 井上貴久, 許文婷, 津田勝範 and Koichiro Tsuchiya : 食後のエネルギー代謝調節を担うAMPK活性制御機構, 生体機能と創薬シンポジウム, Aug. 2017.
131.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素蓄積はヘプシジンを介した鉄代謝恒常性破綻に関与する, 大阪市大フォーラム, Aug. 2017.
132.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 心肺蘇生後症候群治療薬の開発を目的としたドラッグリポジショニング研究-大規模医療情報を活用した検討-, 第255回徳島医学会学術集会, Aug. 2017.
133.	細井麻由, Licht Miyamoto and Koichiro Tsuchiya : AMPKを介した交感神経系刺激による肝臓の糖代謝制御の検討, 第3回徳島大学薬理カンファレンス, Jul. 2017.
134.	服部真奈, Licht Miyamoto and Koichiro Tsuchiya : 亜硝酸塩がグルカゴン分泌に与える影響の検討, 第3回徳島大学薬理カンファレンス, Jul. 2017.
135.	Yoshito Zamami, Yuki Izawa-Ishizawa, 桐野靖, Marin Mitsui, Shiori Urushizaki, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを切り口としたベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 医療薬学フォーラム2017 第25回クリニカルファーマシーシンポジウム, Jul. 2017.
136.	Yuya Horinouchi, Yasumasa Ikeda, Masaki Imanishi, Yoshito Zamami, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 経口FXa阻害剤の腎線維化抑制効果, 医療薬学フォーラム2017 第25回クリニカルファーマシーシンポジウム, Jul. 2017.
137.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 第Xa因子阻害剤は腎間質線維化を抑制する, 第131回日本薬理学会近畿部会, Jun. 2017.
138.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インドキシル硫酸蓄積はヘプシジン制御を介して鉄代謝恒常性破綻に関与する, 第131回日本薬理学会近畿部会, Jun. 2017.
139.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インドキシル硫酸はヘプシジンを介した鉄代謝異常に関与する, 第60回日本腎臓学会学術総会, May 2017.
140.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FXa阻害剤は腎間質線維化を抑制する, 第60回日本腎臓学会学術総会, May 2017.
141.	Licht Miyamoto, Aihara Haruna, Xu Wenting, Jin Meina, Tomida Yosuke, Yamaoka Tomomi, Tanaka Naonobu, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : A limonene-derivative purified from Sudachi peel upregulates sirt1 and improves lipid /glucose metabolism in HFD-fed mice., 第60回日本糖尿病学会, May 2017.
142.	Marin Mitsui, Yoshito Zamami, Yuki Izawa-Ishizawa, Shiori Urushizaki, 桐野靖, Kazuhito Saike, Hiroshi Moriguchi, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを基にしたベバシズマブの抗腫瘍効果を減弱させる薬剤の探索研究, 日本薬学会第137年会, Mar. 2017.
143.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : FXa 阻害剤の片側尿管結紮モデルマウスにおける腎間質線維化抑制作用, 日本薬学会第137年会, Mar. 2017.
144.	Raiki Ikutoh, Masaki Imanishi, Kyohei Tanaka, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : アンジオテンシンII 誘発性血管リモデリングに対するキサンチンオキシダーゼ阻害剤の影響, 日本薬学会第137年会, Mar. 2017.
145.	Yuya Horinouchi, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Factor Xa inhibitor attenuates renal fibrosis in mice with unilateral ureteral obstruction, 第90回日本薬理学会年会, Mar. 2017.
146.	Masaki Imanishi, Kyohei Tanaka, Raiki Ikuto, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Febuxostat suppresses angiotensin II-induced aortic fibrosis, 第90回日本薬理学会年会, Mar. 2017.
147.	Masaki Imanishi, 田中恭平, 生藤来希, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : フェブキソスタットはアンジオテンシンII誘発性大動脈繊維化を抑制する, 第90回日本薬理学会年会(長崎), Mar. 2017.
148.	Yuki Izawa-Ishizawa, Mayuko Hosooka, Naoko Saito, Masaki Imanishi, Yuya Horinouchi, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : The effect of quercetin on the aortic dissection onset via its endothelial protective effect in mice, 第90回日本薬理学会年会, Mar. 2017.
149.	Licht Miyamoto, Goki Tomokawa, Yuki Matsuda, Moe Yamane, Mana Hattori, Reina Oonishi, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Significance of central regulation in physical exercise-induced metabolic alterations in skeletal muscles, The 90th Annual Meeting of The Japanese Pharmacology Society, Mar. 2017.
150.	Licht Miyamoto and Koichiro Tsuchiya : SGLT as a therapeutic target for diabetes - from a view of drug discovery and pharmacotherapy, 日本薬学会第137年会シンポジウムS44, Mar. 2017.
151.	Koichiro Tsuchiya, Yasumasa Ikeda, Yuki Izawa-Ishizawa, Yuya Horinouchi, Licht Miyamoto and Toshiaki Tamaki : 鉄ストレスと代謝性疾患-鉄ストレスによる疾患と，鉄ストレスによる治療, 日本薬学会第137年会, Mar. 2017.
152.	Chiemi Sato, Shinji Abe, Naoto Okada, Koichiro Tsuchiya and Kazuyoshi Kawazoe : 薬物療法における実践的能力育成に向けたルーブリック評価の活用, 日本薬学会第137年会(仙台), Mar. 2017.
153.	Yoshito Zamami, Yuki Izawa-Ishizawa, 桐野靖, 三井茉綸, 漆崎汐里, 斉家和仁, 森口浩史, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 有害事象自発報告データベースを切り口としたベバシズマブと相互作用を起こす薬剤の探索研究, 第46回日本心脈管作動物質学会年会, Feb. 2017.
154.	Masaki Imanishi, 田中恭平, 生藤来希, Yoshito Zamami, Kenshi Takechi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Angiotensin II誘発性血管リモデリングに対するfebuxostatの効果, 第46回日本心脈管作動物質学会, Feb. 2017.
155.	Licht Miyamoto, 友川剛己, 松田裕樹, 山根萌, 服部真奈, 大西伶奈, Yasumasa Ikeda, Toshiaki Tamaki, Koichiro Tsuchiya and Koichiro Tsuchiya : 身体運動時に生じる骨格筋代謝状態の変化における，中枢を介した調節機構の意義, 第46回日本心脈管作動物質学会, Feb. 2017.
156.	Hirofumi Hamano, Yasumasa Ikeda, Hiroaki Watanabe, Yuya Horinouchi, Akiho Satoh, Keisuke Oshima, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素蓄積が生体内鉄代謝に与える影響の検討, 第46回日本心脈管作動物質学会, Feb. 2017.
157.	Yuki Izawa-Ishizawa, 細岡真由子, 斎藤尚子, 鍵本優有, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ケルセチンによるマウス大動脈解離発症予防効果の検討, 第46回日本心脈管作動物質学会年会, Feb. 2017.
158.	友川剛己, Licht Miyamoto, 松田裕樹, 山根萌, 服部真奈, 大西怜奈, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 水泳運動負荷時に生じる骨格筋AMPK活性化の新たなメカニズム，第46回日本心脈管作動物質学会年会, Feb. 2017.
159.	Licht Miyamoto and Koichiro Tsuchiya : 香酸柑橘類研究ネットワークの事業化可能性調査, 中国四国農林水産食品先進技術研究会(岡山), Jan. 2017.
160.	芳野真奈, Licht Miyamoto and Koichiro Tsuchiya : Leptinによる骨格筋培養細胞での代謝制御作用におけるSIRT1の役割, 夏の生物系勉強会, 2017.
161.	土橋有希, Licht Miyamoto and Koichiro Tsuchiya : 3T3-L1細胞の脂肪分化誘導に対する加圧刺激の影響, 夏の生物系勉強会, 2017.
162.	土橋有希, Licht Miyamoto and Koichiro Tsuchiya : 3T3-L1脂肪前駆細胞の分化誘導に対する加圧刺激の影響, 第24回市大フォーラム, 2017.
163.	Yumi Kangawa, Chiharu Fukue, Katsunori Tsuda, Licht Miyamoto, Koichiro Tsuchiya, Yasumasa Ikeda, Toshiaki Tamaki and Shuichi Hamano : Artesunateによる細胞傷害発現機序の解明1, 第40回徳島県医学検査学会, Dec. 2016.
164.	Chiharu Fukue, Yumi Kangawa, Katsunori Tsuda, Licht Miyamoto, Koichiro Tsuchiya, Yasumasa Ikeda, Toshiaki Tamaki and Shuichi Hamano : Artesunateによる細胞傷害発現機序の解明2, 第40回徳島県医学検査学会, Dec. 2016.
165.	Yuki Izawa-Ishizawa, Yutaka Fukunaga, 西良恵理子, Masaki Imanishi, Yuya Horinouchi, Yasumasa Ikeda, Yoshito Zamami, Kenshi Takechi, Keisuke Ishizawa, Koichiro Tsuchiya, Ichiro Hashimoto and Toshiaki Tamaki : ニトロソニフェジピンは虚血性皮弁モデルにおいて皮弁壊死を抑制する, 第26回日本循環薬理学会, Dec. 2016.
166.	高橋梨恵, Licht Miyamoto, 友川剛己, 宮武由実子, Hiroshi Sakaue, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 脳内グリコーゲンによる代謝調節効果の検討, 第130回日本薬理学会近畿部会, Nov. 2016.
167.	福田恵介, Licht Miyamoto, 高橋梨恵, Toshiaki Tamaki, Yasumasa Ikeda and Koichiro Tsuchiya : スダチ果皮芳香成分が糖脂質代謝に与える影響, 第130回日本薬理学会近畿部会, Nov. 2016.
168.	細岡真由子, Yuki Izawa-Ishizawa, 斎藤尚子, Masaki Imanishi, Yoshito Zamami, Licht Miyamoto, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : Quercetin による血管内皮細胞保護効果の検討, 第130回日本薬理学会近畿部会, Nov. 2016.
169.	Akiho Satoh, Yasumasa Ikeda, Hirofumi Hamano, Yuya Horinouchi, Mizuki Imao, Hiroaki Watanabe, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄欠乏が骨格筋に与える作用の検討, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
170.	梅本果奈, Licht Miyamoto, 上島沙弥香, 友川剛己, 細井麻由 and Koichiro Tsuchiya : 肝臓における食後AMPK活性抑制経路の解明，, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
171.	奥野貴子, Licht Miyamoto, 高橋梨恵 and Koichiro Tsuchiya : 大豆熱水抽出物の糖代謝に及ぼす影響の検討，第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
172.	Chiemi Sato, Shinji Abe, Naoto Okada, Tatsuhiro Ishida, Koichiro Tsuchiya, Akira Otaka and Kazuyoshi Kawazoe : 地域薬局における災害対策の現状と課題, 第55回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2016.
173.	Licht Miyamoto, 友川剛己, 松田裕樹, 山根萌, 服部真奈, 大西伶奈 and Koichiro Tsuchiya : 身体運動時に生じる骨格筋AMPK活性化における中枢性代謝調節シグナルの関与, 日本肥満学会, Oct. 2016.
174.	友川剛己, Licht Miyamoto and Koichiro Tsuchiya : 水泳運動時におけるAMPK活性機構の検討, 大学間連携事業評価委員会C, Sep. 2016.
175.	Yutaka Fukunaga, Yuki Izawa-Ishizawa, Yuya Horinouchi, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Ichiro Hashimoto : 虚血性皮弁壊死モデルにおける抗酸化薬ニトロソニフェジピンの壊死抑制効果, 第25回日本形成外科学会基礎学術集会, Sep. 2016.
176.	Shinji Abe, デニスウィリアムズ, Chiemi Sato, Naoto Okada, Koichiro Tsuchiya and Kazuyoshi Kawazoe : ビデオ会議システムを用いた米国薬学部学生との症例検討会実施の試み, 第1回日本薬学教育学会, Aug. 2016.
177.	三井茉綸, Yoshito Zamami, 漆崎汐里, 斉家和仁, 森口浩史, Kenshi Takechi, Masaki Imanishi, Yuya Horinouchi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニングを切り口としたベバシズマブ誘発高血圧に対する予防薬の探索研究, 第27回霧島神経薬理フォーラム(福岡), Aug. 2016.
178.	奥野貴子, Licht Miyamoto and Koichiro Tsuchiya : 大豆熱水抽出物の薬理学的作用の検討，第253回徳島医学会, Jul. 2016.
179.	Licht Miyamoto, 秦野彩, 竹之熊和也, 土橋有希, 矢野友章, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 速効型インスリン分泌促進薬とSGLT2阻害薬の併用による薬効の検討, 第129回日本薬理学会近畿部会, Jun. 2016.
180.	Yuki Izawa-Ishizawa, 細岡真由子, 斎藤尚子, Yuya Horinouchi, Masaki Imanishi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチン代謝産物Q3GAの血管内皮膚細胞に対する短期及び長期効果の検討, 第129回日薬理学会学会近畿部会( 広島), Jun. 2016.
181.	Yasumasa Ikeda, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 骨格筋分化における鉄の役割, 第129回日薬理学会学会近畿部会 (広島), Jun. 2016.
182.	Yasumasa Ikeda, Keisuke Oshima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄は低酸素誘導因子を抑制してエリスロポエチン発現を低下させる, 第59回日本腎臓学会学術総会, Jun. 2016.
183.	Licht Miyamoto, 粟飯原遥菜, 許文婷, 靳美娜, 冨田洋輔, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : スダチ果皮における抗メタボリックシンドローム作用を有する物質の同定, 日本薬学会第136年会(横浜), Mar. 2016.
184.	細岡真由子, Yuki Izawa-Ishizawa, 斎藤尚子, Licht Miyamoto, Masaki Imanishi, Yoshito Zamami, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ケルセチン生体内代謝産物 quercetin -3-O-β-Dglucuronideによる血管内皮細胞保護効果, 日本薬学会第136年会(横浜), Mar. 2016.
185.	鍵本優有, Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshito Zamami, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 無機リン刺激による血管平滑筋細胞石灰化におけるrho-kinase 及び cyclophilinA の関与, 日本薬学会第136年会(横浜), Mar. 2016.
186.	Hiroaki Watanabe, Yasumasa Ikeda, Hirofumi Hamano, Akiho Satoh, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : 慢性腎臓病におけるヘプシジン制御メカニズムの検討, 日本薬学会第136年会(横浜), Mar. 2016.
187.	佐藤明穂, Yasumasa Ikeda, Yuya Horinouchi, 濱野裕章, 今尾瑞季, 渡邉大晃, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Toshiaki Tamaki, Licht Miyamoto and Koichiro Tsuchiya : 鉄過剰による骨格筋分化抑制作用の解明, 日本薬学会第136年会(横浜), Mar. 2016.
188.	Yasumasa Ikeda, Keisuke Oshima, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Iron Supplementation Suppressed Erythropoietin Expression through HIF-dependent Pathway, The 80th Annual Scientific Meeting of the Japanese Circulation Society, Mar. 2016.
189.	太田和馬, Yoshitaka Kihira, 岸渕麗奈, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 電位依存性カリウムチャネルKv2.2は腎虚血再灌流障害の軽減に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
190.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : HIF-1aはアポトーシス制御因子Bcl-2及びCHAC1の発現制御を介して腎虚血再灌流障害からの回復に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
191.	斎藤尚子, Yuki Izawa-Ishizawa, 細岡真由子, Yoshitaka Kihira, Masaki Imanishi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチン代謝物Q3GAによる血管内皮細胞保護効果の検討, 第89回日本薬理学会年会(神奈川), Mar. 2016.
192.	青木友里, Yuki Izawa-Ishizawa, 高田真衣, 田渕正樹, Masaki Imanishi, Yoshito Zamami, 福永豊, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Keisuke Ishizawa and Toshiaki Tamaki : 神経突起伸長および脳卒中後神経症状に対するニトロソニフェジピンの効果, 第89回日本薬理学会年会(神奈川), Mar. 2016.
193.	大島啓亮, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄のエリスロポエチン発現への影響の検討, 第89回日本薬理学会年会(神奈川), Mar. 2016.
194.	佐藤明穂, Yasumasa Ikeda, Yuya Horinouchi, 濱野裕章, 今尾瑞季, 渡邉大晃, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄欠乏に伴う骨格筋萎縮メカニズム, 第89回日本薬理学会年会(神奈川), Mar. 2016.
195.	Licht Miyamoto, Haruna Aihara, Wenting Xu, Meina Jin, Yosuke Tomida, Tomomi Yamaoka, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : Identification of an active compound on lipid metabolism from Sudachi peel, 薬理学会(パシフィコ), Mar. 2016.
196.	Licht Miyamoto, 粟飯原遥菜, Xu Wenting, Jin Meina, 冨田洋輔, 山岡朋美, Naonobu Tanaka, Yasumasa Ikeda, Toshiaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : 脂質低下作用を有するスダチ果皮由来化合物の薬理作用, 第89回日本薬理学会年会(神奈川), Mar. 2016.
197.	濱野裕章, Yasumasa Ikeda, 渡邉大晃, 佐藤明穂, 大島啓亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 尿毒素は慢性腎不全におけるヘプシジン発現に関与する, 第89回日本薬理学会年会(神奈川), Mar. 2016.
198.	Yuki Izawa-Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Licht Miyamoto, Yoshito Zamami, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Keisuke Ishizawa : Development of endothelial dysfunction-induced aortic dissection model and search for a preventive strategy, 第89回日本薬理学会年会(神奈川), Mar. 2016.
199.	Chiemi Sato, Shinji Abe, Naoto Okada, Kaori Yamamoto, Mami Azuma, Koichiro Tsuchiya and Kazuyoshi Kawazoe : 薬局実務実習における能動的な学びの促進と課題解決能力の醸成に向けた連携指導の検討, 日本薬学会第136年会(横浜), Mar. 2016.
200.	Masaki Imanishi, Keisuke Ishizawa, 小原佑介, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニフェジピン光分解産物による血管リモデリング抑制効果, 第252回徳島医学会学術集会(平成27年度冬期), Feb. 2016.
201.	Keisuke Oshima, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄のエリスロポエチン発現への影響の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
202.	Licht Miyamoto, 江川達郎, 大島里詠子, 黒木英梨子, Koichiro Tsuchiya and 林達也 : メタボローム解析による，運動療法の代謝改善効果におけるAMPK活性化の意義の解明, 心脈管作動物質学会, Feb. 2016.
203.	Masaki Imanishi, Keisuke Ishizawa, 小原佑介, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンによる抗大動脈瘤機序の検討, 第45回日本心脈管作動物質学会, Feb. 2016.
204.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 鍵本優有, 斎藤尚子, 高田真衣, Yoshitaka Kihira, Masaki Imanishi, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 高リン刺激は血管平滑筋細胞においてrho-kinase-cyclophilin A経路を活性化させる, 第45回日本心脈管作動物質学会, Feb. 2016.
205.	Asuka Shigetomi, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Shuichi Hamano : LED灯によるビリルビン光分解の検討, 徳島検査医学会, Dec. 2015.
206.	Yasumasa Ikeda, 濱野裕章, 渡邉大晃, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎臓病におけるヘプシジン制御メカニズムの検討, 第25回日本循環薬理学会, Dec. 2015.
207.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 高田真衣, 田渕正樹, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは悪性脳卒中易発性高血圧自然発症ラットの生命予後を改善する, 第25回日本循環薬理学会, Dec. 2015.
208.	斎藤尚子, Yuki Izawa-Ishizawa, Keisuke Ishizawa, 戸谷紘基, Masaki Imanishi, 鍵本優有, 細岡真由子, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離発症における内皮障害の関与, 第25回日本循環薬理学会, Dec. 2015.
209.	Yamaguchi Kazunori, Takeyoshi Abe, Masahiro Watanabe, Toshiki Takeuchi, Koichiro Tsuchiya, 高橋功一, 元木貴大, 田中裕章, 朝倉正登, 小坂信二 and Hitoshi Houchi : Easy TDMを用いた2-コンパートメントモデルによるアミノグリコシド系抗菌薬のCpeak到達時間の探索, 第25回日本医療薬学会年会・講演要旨集, 327, Nov. 2015. (Keyword) TDM
210.	Licht Miyamoto, 江川達郎, 大島里詠子, 黒木英梨子, Koichiro Tsuchiya and 林達也 : AMPK活性化剤は運動療法による代謝改善効果をどこまで模倣できるか?―メタボローム分析によるAMPK仮説の検証―, 薬理学会近畿部会, Nov. 2015.
211.	Hirofumi Hamano, Yasumasa Ikeda, Yuya Horinouchi, Akiho Satoh, Hiroaki Watanabe, Keisuke Oshima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 慢性腎不全における尿毒素によるヘプシジン制御機構, 第128回日本薬理学会近畿部会, Nov. 2015.
212.	今尾瑞季, Yasumasa Ikeda, 佐藤明穂, 濱野裕章, Yuya Horinouchi, Licht Miyamoto, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄蓄積によって引き起こされる骨格筋萎縮のメカニズム, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
213.	高田真衣, Keisuke Ishizawa, 田渕正樹, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 悪性脳卒中易発性高血圧自然発症ラットの神経症状に対するニトロソニフェジピンの効果, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
214.	戸谷紘基, Keisuke Ishizawa, Yuki Izawa-Ishizawa, 細岡真由子, 鍵本優有, 斎藤尚子, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 大動脈解離発症における内皮障害の関与の検討, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
215.	Chiemi Sato, Kaori Yamamoto, Shinji Abe, Naoto Okada, Koichiro Tsuchiya, Mami Azuma and Akira Otaka : 病院・薬局実務実習における実習生の主体性育成に向けての取組み:課題発見型レポートの効果の検証, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2015.
216.	秦野彩, Licht Miyamoto, 竹之熊和也, 友川剛己, 松田裕樹, 服部真奈 and Koichiro Tsuchiya : グリニド薬とSGLT2 阻害薬の併用療法による有効性, 日本薬学会中国四国地方会, Oct. 2015.
217.	竹之熊和也, 山根萌, 友川剛己, Licht Miyamoto and Koichiro Tsuchiya : カフェインによるAMPK活性化メカニズムの解析, 日本薬学会中国四国地方会, Oct. 2015.
218.	上島沙弥香, Licht Miyamoto, 梅本果奈 and Koichiro Tsuchiya : インスリン刺激による新たなAMPK翻訳後修飾の分子機構, 日本薬学会中国四国地方会, Oct. 2015.
219.	土橋有希, Shinji Abe, Licht Miyamoto, 松下剛史, 片桐彩人, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロールを用いたPaclitaxelの物性及び薬効の改善, 第54回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会 (高知), Oct. 2015.
220.	Yasumasa Ikeda, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄欠乏は骨格筋量減少の原因となる, 第39回日本鉄バイオサイエンス学会学術集会, Aug. 2015.
221.	Ariunzaya Burentogtokh, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : YC1 increased adiponectin expression in 3T3-L1 adipocytes, 次世代を担う創薬・医療薬理シンポジウム2015, Aug. 2015.
222.	秦野彩, Licht Miyamoto, 竹之熊和也, 土橋有希, 矢野友章 and Koichiro Tsuchiya : 速効型インスリン分泌促進剤，ナテグリニドとSGLT2 阻害剤，カナグリフロジンの併用による効果の検討, 日本糖尿病学会, May 2015.
223.	Licht Miyamoto, 江川達郎, 大島里詠子, 黒木英梨子, Koichiro Tsuchiya and 林達也 : 骨格筋収縮時のメタボローム変化におけるAMPKの意義, 日本糖尿病学会, May 2015.
224.	Yasumasa Ikeda, Kanai Yusuke, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bilirubin Promotes Ischemic-Induced Revascularization through Akt-eNOS Pathway, 第79回日本循環器学会学術集会, Apr. 2015.
225.	Yoshitaka Kihira, 岸渕麗奈, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 腎虚血再灌流障害において低酸素誘導因子が制御する因子の探索, 日本薬学会第135年会(神戸), Mar. 2015.
226.	Shinji Abe, 土橋有希, Chiemi Sato, Kaori Yamamoto, Licht Miyamoto, Koichiro Tsuchiya, Mami Azuma and Yasuhiko Nishioka : 悪性胸膜中皮腫胸腔内移植マウスに対するヒト・キメラ型抗ポドプラニン抗体NZ-8の効果, 日本薬学会第135年会, Mar. 2015.
227.	Mai Takata, Keisuke Ishizawa, 田渕正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 悪性脳卒中易発性高血圧自然発症ラットに対するニトロソニフェジピンの効果, 日本薬学会第135年会(神戸), Mar. 2015.
228.	Takeyoshi Abe, Masahiro Watanabe, Nariyasu Yoshino, Noriyasu Fukuoka, Toshiki Takeuchi and Koichiro Tsuchiya : Cpeak blood sampling time of arbekacin using the 2-compartment model to evaluate the bacteriological effect, 日本薬学会第135年会要旨集, Vol.4, 195, Mar. 2015. (Keyword) Cpeak / TDM / compartment model
229.	Keiji Ogura, Hiroko Hirakawa, Takuya Morisaki, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya, Akira Shigenaga and Akira Otaka : 低酸素環境応答型アミノ酸の開発研究, 日本薬学会第135年会, Mar. 2015.
230.	Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンは虚血後血管新生を促進する, 第88回日本薬理学会年会(愛知), Mar. 2015.
231.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 田渕正樹, Mai Takata, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは悪性脳卒中易発性高血圧自然発症ラットの生存期間を延長させる, 第88回日本薬理学会年会(愛知), Mar. 2015.
232.	Hiroki Toya, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Yusuke Kohara, Tomoko Nagao, 今西正樹, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離発症における血管内皮機能障害の関与, 第88回日本薬理学会年会(愛知), Mar. 2015.
233.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible factor-1 participates in induction of apoptosis in renal reperfusion injury, 第88回日本薬理学会年会(愛知), Mar. 2015.
234.	Mizuho Ogoshi, Yuki Izawa-Ishizawa, Sakiko Doi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管平滑筋細胞において無機リンによる石灰化シグナルにはRho-kinaseおよびcyclophilin Aが関与する, 第88回日本薬理学会年会(愛知), Mar. 2015.
235.	Burentogtokh Ariunzaya, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia decreases glucagon-like peptide-1 secretion from glutag cell lines, 第88回日本薬理学会年会(愛知), Mar. 2015.
236.	Yasumasa Ikeda, 金井佑亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンの血管新生促進作用の検討, 第44回日本心脈管作動物質学会, Feb. 2015.
237.	Yuri Morimoto, Licht Miyamoto, Koichiro Tsuchiya, Toshiaki Tamaki and Shuichi Hamano : セスキテルペンラクトン誘導体の鉄依存細胞障害機構の解明, 第38回徳島県医学検査学会, Dec. 2014.
238.	Yasumasa Ikeda, 金井佑亮, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : ビリルビンは血管内皮細胞を活性化させて，虚血後血管新生を促進する, 第24回循環薬理学会, Dec. 2014.
239.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, 長尾朋子, 戸谷紘基, 小原佑介, 細岡真由子, 高田真衣, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 新規薬剤誘発性大動脈解離モデルを用いたスタチンの効果の検討, 第24回循環薬理学会, Dec. 2014.
240.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 低酸素誘導因子の機能不全は腎虚血再灌流障害からの回復を阻害する, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
241.	Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 高脂肪食誘発肥満に対する脂肪特異的低酸素誘導因子欠損の影響, 第36回生体膜と薬物の相互作用シンポジウム, Nov. 2014.
242.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : HMG-CoA 還元酵素阻害薬の大動脈解離に対する効果, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
243.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, 川崎彩, 山岡朋美, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞における亜硝酸塩によるAMPK-eNOS活性化経路の検討, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
244.	川崎彩, Licht Miyamoto, 山岡朋美, 山根萌, Keisuke Ishizawa and Koichiro Tsuchiya : 交感神経系刺激による肝臓の糖代謝および脂質代謝の制御におけるAMPKの意義, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
245.	山岡朋美, Licht Miyamoto, 川崎彩, 山根萌, 高橋梨恵, Keisuke Ishizawa, Rin Miyajima, Akira Shigenaga, Akira Otaka and Koichiro Tsuchiya : Leptinによる骨格筋培養細胞での代謝制御作用におけるSIRT1の役割, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
246.	Wenting Xu, Licht Miyamoto, Haruna Aihara, Tomomi Yamaoka, Keisuke Ishizawa, Toshaki Tamaki, Yoshiki Kashiwada and Koichiro Tsuchiya : The Mechanism of Citrus Sudachi Peel Extraction Exerts Lipid Reducing Effect in Cells., 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
247.	Shinji Abe, デニスウィリアムズ, Chiemi Sato, Kaori Yamamoto, Mami Azuma and Koichiro Tsuchiya : 屋根瓦方式を用いた症例検討ビデオカンファレンスの有用性, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
248.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : HMG-CoA 還元酵素阻害薬の大動脈解離に対する効果, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
249.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈瘤形成に対する新規抗酸化薬の効果, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
250.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, 川崎彩, 山岡朋美, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による AMPK-eNOS 経路活性化, 第53回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2014.
251.	岸渕麗奈, Yoshitaka Kihira, Kunihisa Yamaguchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 低酸素誘導因子の腎虚血再灌流障害に対する役割, 第126回日本薬理学会近畿部会, Oct. 2014.
252.	長尾朋子, Keisuke Ishizawa, 戸谷紘基, 小原佑介, 今西正樹, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 大動脈解離に対するピタバスタチンの効果, 第126回日本薬理学会近畿部会, Oct. 2014.
253.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : ヒト腎糸球体内皮細胞におけるAMPK-eNOS経路の活性化, 第126回日本薬理学会近畿部会, Oct. 2014.
254.	Yasumasa Ikeda, 今尾瑞季, 佐藤明穂, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄による骨格筋萎縮メカニズムの検討, 日本鉄バイオサイエンス学会第38回学術集会, Sep. 2014.
255.	Licht Miyamoto, 渡辺勝志, 土橋有希, 山根萌, 田岡千明, 松下剛史, 笠原真一郎, 神谷昌樹, Keisuke Ishizawa, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロールを用いた難水溶性化合物の物性，薬物動態，薬効の改善, 次世代を担う創薬・医療薬理シンポジウム2014, Aug. 2014.
256.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, 細岡真由子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは大動脈瘤の形成を抑制する, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
257.	戸谷紘基, Keisuke Ishizawa, 小原佑介, 長尾朋子, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管内皮障害を介する新規大動脈解離モデルの作製, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
258.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による AMPK-eNOS 経路活性化, 次世代を担う創薬・医療薬理シンポジウム 2014, Aug. 2014.
259.	山根萌, Licht Miyamoto, 冨田洋輔, 竹之熊和也, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩によるAMPK-eNOS経路活性化, 生体機能と創薬シンポジウム 2014, Aug. 2014.
260.	矢野友章, Licht Miyamoto, 竹之熊和也, 福田恵介, 津田勝範, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 食事による血中NOレベル変動の検討, 第249回徳島医学会, Jul. 2014.
261.	小原佑介, Keisuke Ishizawa, 櫻田巧, 戸谷紘基, 長尾朋子, 壱岐豊, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 薬剤誘導性大動脈瘤モデルに対するニトロソニフェジピンの効果, 第125回日本薬理学会近畿部会, Jun. 2014.
262.	Yasumasa Ikeda, 田島壮一郎, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : アンジオテンシンIIは鉄吸収制御と生体内鉄分布変化に関与する, 第125回日本薬理学会近畿部会, Jun. 2014.
263.	Miku Kita, Jun Yamamoto, Koji Ebisuno, Chiaki Komiya, Licht Miyamoto, Koichiro Tsuchiya, Akira Shigenaga and Akira Otaka : 過酸化水素応答型ペプチド結合切断デバイスの開発研究, 日本ケミカルバイオロジー学会第9回年会, Jun. 2014.
264.	鞍野佳孝, 斉藤辰也, Koichiro Tsuchiya, Miyuki Oshimura, Tomohiro Hirano and Koichi Ute : Li塩存在下でのアクリレート系モノマーのラジカル重合の機構, 第63回高分子学会年次大会, May 2014.
265.	Licht Miyamoto, 渡邊勝志, 田岡千秋, 土橋有希, 松下剛史, Keisuke Ishizawa, Shinji Abe, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロール修飾による疎水性化合物の物性，薬物動態および薬効の改善, 日本薬学会第134年会, Mar. 2014.
266.	土橋有希, Shinji Abe, Licht Miyamoto, 松下剛史, 片桐彩人, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : 新規水溶性Paclitaxelの肺癌に対する抗腫瘍効果の検討, 日本薬学会第134年会, Mar. 2014.
267.	智子中西, Keisuke Ishizawa, Shinji Abe, Mari Nakase, Hirofumi Shibata, Chiemi Sato, Naokatu Arakaki, Youichi Sato, Naoshi Yamazaki, Jiro Kasahara, Mami Azuma, Tetsuo Yamazaki, Aiko Yamauchi, Yoshiharu Takiguchi and Koichiro Tsuchiya : Study of the method for development of case-problem solving abilities through advanced practice and the results that have been achieved, 日本薬学会第134年会, Mar. 2014.
268.	今西正樹, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya and Toshiaki Tamaki : 血管リモデリングにおける低酸素誘導因子HIF-1αの役割, 日本薬学会第134年会, Mar. 2014.
269.	Yoshitaka Kihira, Ariunzaya BURENTOGTOKH, Mari Itoh, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 腸管L細胞のグルカゴン様ペプチド-1分泌に対する低酸素の影響, 日本薬学会第134年会, Mar. 2014.
270.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Noriko Yamano, 布あさ美, 今西正樹, 櫻田巧, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates the progression of renal disease associated with endothelial dysfunction independently of eNOS, 第87回日本薬理学会年会, Mar. 2014.
271.	Licht Miyamoto, Megumi Yamane, Yohsuke Tomida, Kazuya Takenokuma, Keisuke Ishizawa, Toshiaki Tamaki and Koichiro Tsuchiya : 亜硝酸塩による腎保護作用および糖脂質代謝改善作用におけるAMPKの意義, 第87回日本薬理学会年会, Mar. 2014.
272.	Mizuki Imao, Yasumasa Ikeda, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The mechanism of sj=keletal muscle atroph induced by iron, 第87回日本薬理学会年会, Mar. 2014.
273.	Yuya Horinouchi, Summers A. Fiona, Ehrenshaft Marilyn, Koichiro Tsuchiya, Toshiaki Tamaki and Mason P. Ronald : Investigating free radical generation in HepG2 cells induced by aromatic amine compounds using immuno-spin trapping, 第87回日本薬理学会年会, Mar. 2014.
274.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : アンジオテンシンIIは十二指腸鉄輸送体発現とマクロファージ鉄量を増加させる, 第43回日本心脈管作動物質学会, Feb. 2014.
275.	山脇早穂, 佐藤佑太, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuichi Hamano : リチウム定量にあたえる共存物質の影響, 第37回徳島県医学検査学会, Dec. 2013.
276.	佐藤佑太, 山脇早穂, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuichi Hamano : セスキテルペンラクトン誘導体の鉄依存ラジカル生成過程の解明, 第37回徳島県医学検査学会, Dec. 2013.
277.	Masaki Imanishi, Shuhei Tomita, Hirotsugu Kurobe, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 薬剤誘導性大動脈瘤モデルにおける平滑筋由来hypoxia-inducible factor-1αの役割, 第23回日本循環薬理学会, Dec. 2013.
278.	Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 肥満に伴う脂肪組織炎症に対する低酸素誘導因子の役割, 第124回日本薬理学会近畿部会, Nov. 2013.
279.	Shinji Abe, デニスウィリアムズ, Mari Nakase, Chiemi Sato, Hirofumi Shibata, Mami Azuma and Koichiro Tsuchiya : 症例検討能力向上に向けての徳島大学薬学部の取り組み∼米国UNC薬学部とのビデオカンファレンス実施の効果∼, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
280.	布あさ美, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, 櫻田巧, Masaki Imanishi, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : ニトロソニフェジピンは血管内皮機能を改善することで糖尿病性腎症の進展を抑制する, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
281.	Yuta Suzuki, Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 平滑筋由来HIF-1 αがアンジオテンシンII 誘発血管リモデリングに関与するメカニズム, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
282.	Masaki Murakami, Yusaku Maeda, Shuhei Tomita, Masaki Imanishi, Yoshitaka Kihira, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリングにおける骨髄由来細胞のHIF1 αの役割, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
283.	Mariko Miyake, Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 脂肪細胞の低酸素誘導因子欠損による耐糖能改善メカニズムの解析, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
284.	智子中西, Keisuke Ishizawa, Shinji Abe, Mari Nakase, Hirofumi Shibata, Chiemi Sato, Naokatu Arakaki, Youichi Sato, Naoshi Yamazaki, Jiro Kasahara, Mami Azuma, Tetsuo Yamazaki, Aiko Yamauchi, Yoshiharu Takiguchi and Koichiro Tsuchiya : Study of the method for development of case-problem solving abilities through advanced practice and the results that have been achieved, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
285.	Chiemi Sato, Mari Nakase, Shinji Abe, Hirofumi Shibata, Koichiro Tsuchiya, Hideji TANAKA and Mami Azuma : 生涯学習の必要性に目覚めさせる徳島大学の取組∼能動学習制度∼, 第52回日本薬学会·日本薬剤師会·日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
286.	中野扶佐子, 栗本慎一郎, Kazuyoshi Kawazoe, Kotarou Murakami, 孫漢董, 李順林, Yoshihisa Takaishi, Licht Miyamoto, Koichiro Tsuchiya and Yoshiki Kashiwada : キク科植物Saussurea lanicepsの成分研究, 第55回天然有機化合物討論会, Sep. 2013.
287.	Yasumasa Ikeda, 田島壮一郎, Mizuki Imao, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : フェリチンの炎症惹起作用, 第37回日本鉄バイオサイエンス学会, Sep. 2013.
288.	Masaki Murakami, Shuhei Tomita, Yusaku Maeda, Masaki Imanishi, Noriko Yamano, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリング形成過程には，傷害部位に動員される骨髄由来細胞のHIFが関与する, 次世代を担う創薬・医療薬理シンポジウム2013, Aug. 2013.
289.	Noriko Yamano, Keisuke Ishizawa, 小堀浩幸, Maki Urushihara, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病性腎症における腎内局所アンジオテンシノーゲンに対するニトロソニフェジピンの効果, 第123回日本薬理学会近畿部会, Jul. 2013.
290.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αがangiotensinⅡ誘発血管リモデリング形成に関与するメカニズムの解析, 第34回日本炎症・再生医学会, Jul. 2013.
291.	Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, 櫻田巧, Masaki Imanishi, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは血管内皮保護作用を示して糖尿病性腎症進展を抑制する, 第56回日本腎臓学会学術総会, May 2013.
292.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, Yuki Izawa-Ishizawa, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 酸化ストレスに起因する心腎血管障害の克服を目指す新規治療薬開発, 日本薬学会第133年会, Mar. 2013.
293.	Koichiro Tsuchiya, Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Licht Miyamoto, Noriko Yamano and Toshiaki Tamaki : 糖尿病に対する鉄の関与とキレート療法, 日本薬学会第133年会, Mar. 2013.
294.	Licht Miyamoto, Masashi Watanabe, 河野舞, Yohsuke Tomida, Tsuyoshi Matsushita, 服部初彦, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖オリゴグリセロール修飾によるフェノフィブラートの物性および薬物動態，薬効の改善, 日本若学会第133年会, Mar. 2013.
295.	Tsuyoshi Matsushita, Masashi Watanabe, Licht Miyamoto, Koichiro Tsuchiya and Hisao Nemoto : 脂質異常症治療薬であるフェノフィブラートのBGL化と活性評価, 日本若学会第133年会, Mar. 2013.
296.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Hypoxia-inducible factor-1a; in vascular smooth muscle cells contributes to AT1 receptor expression in angiotensin II-induced vascular remodeling in mice, 第86回日本薬理学会年会, Mar. 2013.
297.	Mari Itoh, Yoshitaka Kihira, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : Secretion of glucagon-like peptide-1 from Intestinal L cell in hypoxia, 第86回日本薬理学会年会, Mar. 2013.
298.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : The influence of angiotensin II on duodenal iron absorption, 第86回日本薬理学会年会, Mar. 2013.
299.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine lactoferrin stimulated angiogenesis in response to ischemic hindlimb, 第86回日本薬理学会年会, Mar. 2013.
300.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Sakiko Doi, Masaki Imanishi, Takumi Sakurada, Noriko Yamano, Yusuke Kohara, Tomoko Nagao, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Y-27632, a rho-kinase inhibitor, inhibits inorganic phosphate-induced ERK1/2 phosphorylation and ALP activity in vascular smooth muscle cells, 第86回日本薬理学会年会, Mar. 2013.
301.	Iori Ohzono, Yasumasa Ikeda, Souichirou Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : The Effects of Iron chelatoion against Renal Fibrosis in Unilateral Ureteral Obstruction Mice Model, 第86回日本薬理学会年会, Mar. 2013.
302.	Yoji Hoshina, Yoshitaka Kihira, Shuhei Tomita, Mariko Miyake, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Adipocyte-specific hypoxia-inducible factor-1alpha knockout stimulated GLP-1 and insulin secretions in mice, 第86回日本薬理学会年会, Mar. 2013.
303.	Noriko Yamano, Keisuke Ishizawa, Shoko Fujii, Asami Nuno, Masaki Imanishi, Takumi Sakurada, Yuta Suzuki, Furi Endo, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Effects of nitrosonifedipine on the diabetic nephropathy with the endothelial dysfunction, 第86回日本薬理学会年会, Mar. 2013.
304.	Yasumasa Ikeda, Hideaki Enomoto, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Low Iron Diet Limits Development of Diabetic Nephropathy In db/db Mice, 第77回日本循環器学会学術集会, Mar. 2013.
305.	Yuki Izawa-Ishizawa, Keisuke Ishizawa, Noriko Yamano, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Asami Nuno, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : ニトロソニフェジピンは血管内皮細胞障害を伴う糖尿病性腎症の進展を抑制する, 第42回日本心脈管作動物質学会, Feb. 2013.
306.	田島壮一郎, Yasumasa Ikeda, Hideaki Enomoto, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : 鉄制限食によってdb/dbマウスの糖尿病性腎症進展は抑制される, 第42回日本心脈管作動物質学会, Feb. 2013.
307.	Sakiko Doi, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Yusuke Kohara, Tomoko Nagao, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 無機リン刺激による血管平滑筋細胞石灰化におけるRho-kinaseの関与, 第42回日本心脈管作動物質学会, Feb. 2013.
308.	Yoshitaka Kihira, Shuhei Tomita, Mariko Miyake, Yoji Hoshina, Noriko Yamano, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 脂肪細胞特異的低酸素誘導因子欠損マウスに観察される耐糖能の改善にはglucagon-like peptide-1が関与する, 第42回日本心脈管作動物質学会, Feb. 2013.
309.	Keisuke Ishizawa, Masaki Imanishi, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Angiotensin II慢性投与はhypoxia-inducible factor-1αを介して血管リモデリングを惹起する, 第33回日本臨床薬理学会学術総会, Dec. 2012.
310.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 血管平滑筋細胞のhypoxia-inducible factor-1αがangiotensinⅡ誘発血管リモデリング形成に寄与するメカニズムの解析, 第22回日本循環薬理学会, Nov. 2012.
311.	Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄吸収機構におけるAngiotensinⅡの効果の検討, 第122回日本薬理学会近畿部会, Nov. 2012.
312.	中西智子, Youichi Sato, Aiko Yamauchi and Koichiro Tsuchiya : 薬学部での臨床思考プロセスを取り入れた医薬品情報提供実習, 51回日本薬学会・日本薬剤師会，日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
313.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : Nifedipine 光分解産物であるnitrosonifedipine は糖尿病性腎症進展を抑制する, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
314.	Akira Shigenaga, Keiji Ogura, Hiroko Hirakawa, Jun Yamamoto, Koji Ebisuno, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Akira Otaka : Design and synthesis of hypoxia-responsive amino acid which causes peptide bond cleavage in hypoxic cells, 第49回ペプチド討論会, Nov. 2012.
315.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 血管平滑筋細胞におけるHIF-1αのangiotensinⅡ誘発血管リモデリング形成およびAT1受容体発現への関与;平滑筋特異的HIF-1α遺伝子欠損マウスを用いた検討 The Role of HIF-1α in angiotensin Ⅱ-induced Vascular Remodeling and AT1 Receptor Expression in Vascular Smooth Muscle Cells, 第35回日本高血圧学会総会, Sep. 2012.
316.	Asami Nuno, Keisuke Ishizawa, Shoko Fujii, 櫻田巧, Noriko Yamano, Yuki Izawa-Ishizawa, Masaki Imanishi, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病性腎症進展に対するニトロソニフェジピンの抑制作用, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
317.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおける血管平滑筋細胞内HIFシグナルの解析, 次世代を担う創薬・医療薬理シンポジウム2012, Sep. 2012.
318.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 十二指腸からの鉄吸収に対するAngiotensinⅡの影響, 第36回日本鉄バイオサイエンス学会学術集会, Sep. 2012.
319.	渡邊勝志, Licht Miyamoto, 冨田洋輔, 河野舞, 田岡千明, 松下剛史, 神谷昌樹, 服部初彦, Keisuke Ishizawa, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖グリセロールオリゴマーによるフェノフィブラートの物性および薬物動態の改善, 生体機能と創薬シンポジウム2012, Aug. 2012.
320.	Yusaku Maeda, Shuhei Tomita, Masaki Murakami, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 血管傷害モデルに伴う血管リモデリング形成過程には，傷害部位に動員される骨髄由来細胞のHIFが関与する, 第121回日本薬理学会近畿部会, Jun. 2012.
321.	Masaki Imanishi, Shuhei Tomita, Keisuke Ishizawa, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 平滑筋特異的hypoxia-inducible factor-1α欠損がangiotensin II誘発血管リモデリング形成に及ぼす影響, 第121回日本薬理学会近畿部会, Jun. 2012.
322.	Yasumasa Ikeda, 田島壮一郎, Koichiro Tsuchiya and Toshiaki Tamaki : 肥満進展における鉄と酸化ストレス, 第65回日本酸化ストレス学会学術集会シンポジウム「金属と酸化ストレスの関係を探る:基礎から臨床研究へ」, Jun. 2012.
323.	Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Shoko Fujii, Yuki Izawa-Ishizawa, Licht Miyamoto, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine はangiotensin II 誘発のマウス血管リモデリングを改善する, 第65回日本酸化ストレス学会学術集会, Jun. 2012.
324.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病モデルマウスにおいてニトロソニフェジピンは腎症の進展を抑制する, 第55回日本腎臓学会学術総会, Jun. 2012.
325.	Licht Miyamoto, 河野舞, 中川剛夫, 服部初彦, 吉富康亮, Keisuke Ishizawa, Yoshiyuki Yoshimura, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖グリセロール修飾による新規水溶性プロブコール誘導体の開発と耐糖能改善作用のメカニズム, 第55回日本糖尿病学会年次学術集会, May 2012.
326.	Yoshiki Kashiwada, JIN Meina, 柴山恵美子, 和田悠, Keisuke Ishizawa, Licht Miyamoto, Koichiro Tsuchiya and 井端和郎 : スダチ(Citrus sudachi)果皮の有効利用に関する研究 (5) ―3-O-Feruloyl aldaric acid 1,4-lactone methyl esterの立体構造について―, 日本薬学会第132年会, No.2, 189, Mar. 2012.
327.	Mariko Miyake, Yoshitaka Kihira, Manami Hirata, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 脂肪細胞における低酸素誘導因子1a欠損は高脂肪食負荷による耐糖能異常の発現を抑制する, 日本薬学会第132年会, Mar. 2012.
328.	Shuichi Hamano, Yoko Kagawa, Licht Miyamoto, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : セスキテルペンラクトン誘導体の鉄依存ラジカル生成機構の検討, 日本薬学会大132年会, Mar. 2012.
329.	Asami Nuno, Keisuke Ishizawa, 藤井聖子, Yuki Izawa-Ishizawa, Masaki Imanishi, Takumi Sakurada, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 2型糖尿病性腎症に対するニトロソニフェジピンの効果, 日本薬学会第132年会, Mar. 2012.
330.	Licht Miyamoto, 河野舞, 中川剛夫, 服部初彦, 吉富康亮, Keisuke Ishizawa, Yoshiyuki Yoshimura, Hisao Nemoto and Koichiro Tsuchiya : 分岐鎖グリセロール修飾による新規水溶性プロブコール誘導体の開発と耐糖能改善作用のメカニズム, 日本薬学会年会, Mar. 2012.
331.	Yasumasa Ikeda, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Bovine Lactoferin Promotes Angiogenesis Via Akt-eNOS Dependent Pathway in Vascular Endothelial Cells, 第76回日本循環器学会学術集会, Mar. 2012.
332.	Hideaki Enomoto, Yasumasa Ikeda, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Protective effect of dietary iron restriction on diabetic nephropathy, 第85回日本薬理学会年会, Mar. 2012.
333.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Accumulated iron storage in high fat diet-induced obese and diabetic mice, 第85回日本薬理学会年会, Mar. 2012.
334.	Shoko Fujii, Keisuke Ishizawa, Takumi Sakurada, Yuki Izawa-Ishizawa, Masaki Imanishi, Asami Nuno, Yuta Suzuki, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine prevents the progression of diabetic nephropathy in type 2 diabetic mice, 第85回日本薬理学会年会, Mar. 2012.
335.	Shuhei Tomita, Mitsuru Takaku, Noriko Yamano, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Preoperative stabilization of HIF-1 by systemic introduction of dimethyloxalylglycine (DMOG), improves skin flap survival, 第85回日本薬理学会年会, Mar. 2012.
336.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : The inhibitory effects of smooth muscle cell-specific hypoxia-inducible factor-1a deficiency on angiotensin 2-induced vascular remodeling in mice, 第85回日本薬理学会年会, Mar. 2012.
337.	Manami Hirata, Yoshitaka Kihira, Mariko Miyake, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : High fat diet-induced inflammation in adipose tissues is reduced in adipocyte-specific hypoxia-inducible factor-1a knockout mice, 第85回日本薬理学会年会, Mar. 2012.
338.	Licht Miyamoto, 河野舞, 中川剛夫, 服部初彦, 吉富康亮, Keisuke Ishizawa, Yoshiyuki Yoshimura, Hisao Nemoto and Koichiro Tsuchiya : 水溶性プロブコール誘導体による新たなメカニズムを介した耐糖能およびインスリン感受性の改善, 第244回徳島医学会学集会, Feb. 2012.
339.	Keisuke Ishizawa, Shoko Fujii, Asami Nuno, Yuki Izawa-Ishizawa, Masaki Imanishi, Takumi Sakurada, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineは2型糖尿病モデルマウスにおける腎症進展を抑制する, 第41回心脈管作動物質学会, Feb. 2012.
340.	Yoshitaka Kihira, Mariko Miyake, Manami Hirata, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : 肥満に伴う耐糖能異常の発現に対する脂肪細胞の低酸素誘導因子の役割, 第41回心脈管作動物質学会, Feb. 2012.
341.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Soichiro Tajima, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The alternation of iron metabolism in high fat diet-induced obese and diabetic mice, 第34回日本分子生物学会年会, Dec. 2011.
342.	Yasumasa Ikeda, Hideaki Enomoto, 田島壮一郎, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 糖尿病腎症進展における鉄除去の効果, 腎と高血圧update, Dec. 2011.
343.	智子中西, Youichi Sato, Aiko Yamauchi and Koichiro Tsuchiya : 問題解決能力の向上を目指した病院実務実習を考える, 第33 回徳島大学薬学部卒後教育公開講座, Dec. 2011.
344.	Mitsuru Takaku, Shuhei Tomita, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Hideki Nakanishi and Toshiaki Tamaki : PHD阻害剤の虚血皮弁生存拡大に対する効果, 第21回日本循環薬理学会, Dec. 2011.
345.	八木祐子, Koichiro Tsuchiya, Masayuki Shono, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト結腸癌由来Caco-2細胞における抗癌剤耐性に及ぼす酸素分圧の影響, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
346.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αはangiotensinⅡ誘発血管リモデリングの形成に関与する, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
347.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Jumpei Taniguchi, Shoko Fujii, Asami Nuno, Yuta Suzuki, Licht Miyamoto, Yoshitaka Kihira, Koichiro Tsuchiya, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : マウス血管リモデリングに対するnitrosonifedipineの抑制効果, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
348.	Licht Miyamoto, 海老原健, Hisao Nemoto, 中尾一和 and Koichiro Tsuchiya : 自律神経系による肝AMPK活性制御のメカニズムと糖脂質代謝制御における意義, 第244回徳島医学会学集会, Nov. 2011.
349.	玉川晋也, 八塚研治, Shinji Abe, Hitoshi Kubo, Koichiro Tsuchiya, Masafumi Harada and Hisao Nemoto : The new development of MRI contrast medium, 第37回反応と合成の進歩シンポジウム, Nov. 2011.
350.	智子中西, Youichi Sato, Aiko Yamauchi and Koichiro Tsuchiya : 問題解決能力の向上を目指した病院実務実習を考える, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国支部学術大会, Nov. 2011.
351.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : AngiotensinⅡ誘発性血管リモデリングは平滑筋特異的HIF-1α遺伝子欠損により抑制される, 第34回日本高血圧学会総会, Oct. 2011.
352.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : AngiotensinⅡ誘発性血管リモデリングは平滑筋特異的HIF-1α遺伝子欠損により抑制される, 第34回日本高血圧学会総会, Oct. 2011.
353.	Koichiro Tsuchiya : 亜硝酸による腎保護作用, 23, Oct. 2011.
354.	Shinji Abe, Dennis Williams, Mami Azuma, Koichiro Tsuchiya, 美妃山下, 麻衣子町田 and Hiroshi Kiwada : 日米の薬学部学生間におけるビデオ会議システムを用いた症例検討カンファレンス実施の試み, 日本医療薬学会第21回年会, Oct. 2011.
355.	Licht Miyamoto, 海老原健, Hisao Nemoto, 中尾一和 and Koichiro Tsuchiya : 自律神経系による肝AMPK活性制御のメカニズムと糖脂質代謝制御における意義, 第32回日本肥満学会, Sep. 2011.
356.	Kazuma Okano, Daisuke Tsuji, Takahiro Nakamura, Koichiro Tsuchiya and Kouji Itou : ヒト多発性骨髄腫細胞株におけるSide Population細胞の性質解析, 第84回日本生化学会大会, Sep. 2011.
357.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 肥満の脂肪組織における鉄の役割, 第35回日本鉄バイオサイエンス学会学術集会, Sep. 2011.
358.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Jumpei Taniguchi, Shoko Fujii, Asami Nuno, Yuta Suzuki, Yuki Izawa-Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineによるマウス血管リモデリング抑制機構の解明, 次世代を担う創薬・医療薬理シンポジウム2011, Aug. 2011.
359.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1a in vascular smooth muscle cells contributes to the development of angiotensin -induced vascular remodeling, 第43回日本動脈硬化学会総会・学術集会, Jul. 2011.
360.	Masashi Akaike, Koichiro Tsuchiya, Yoshiki Kashiwada, Yoshihisa Takaishi, Toshiaki Tamaki, Takashi Iwase, Masataka Sata, Ken-ichi Aihara, Sumiko Yoshida, Toshio Matsumoto, 佐藤千穂, 西条伴香 and Hiroaki Yanagawa : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果 ∼探索的臨床試験による検討∼, 第243回徳島医学会学術集会公開シンポジウム, Jul. 2011.
361.	Masashi Akaike, Koichiro Tsuchiya, Yoshiki Kashiwada, Yoshihisa Takaishi, Toshiaki Tamaki, Takashi Iwase, Masataka Sata, Ken-ichi Aihara, 吉田守実子, Toshio Matsumoto, 佐藤千穂, 西条伴香 and Hiroaki Yanagawa : 生活習慣病関連リスクファクターに及ぼすスダチ果皮加工品の効果-探索的臨床試験による検討-, 第243回徳島医学会学術集会, Jul. 2011.
362.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, 久次米敏秀, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 動脈硬化におけるhypoxia-inducible factor-1αの新規治療標的分子としての可能性, 医療薬学フォーラム2011/第19回クリニカルファーマシーシンポジウム, Jul. 2011.
363.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Noriko Yamano, Yuki Izawa-Ishizawa, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensisⅡ誘発血管リモデリングは血管平滑筋細胞のhypoxia-inducible factor-1αを介して形成される, 第119回日本薬理学会近畿部会, Jul. 2011.
364.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : ヒト腎糸球体血管内皮細胞において細胞内遊離鉄はangiotensin ⅡによるICAM-1の発現を増強する, 第54回日本腎臓学会学術集会, Jun. 2011.
365.	Yasumasa Ikeda, 田島壮一郎, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄除去薬による糖尿病の病態改善効果の検討, 第84回日本内分泌学会学術集会, Apr. 2011.
366.	Yasumasa Ikeda, Soichiro Tajima, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Iron elimination ameliorated glucose tolerance through suppression of oxidative stress and inflammation on fat in diabetic mice, 第75回日本循環器学会総会・学術集会, Mar. 2011.
367.	Noriko Yamano, Yasumasa Ikeda, Minoru Sakama, Soichiro Tajima, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : The alternation of iron transport-related genes in high fat diet-induced obese and diabetic mice, 第84回日本薬理学会年会, Mar. 2011.
368.	Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : bFGF and insulin differentially regulate hypoxia-inducible factor-1 alpha in adipocytes, 第84回日本薬理学会年会, Mar. 2011.
369.	Yayoi Fukuhara, Shuhei Tomita, Masahisa Urata, Yoshitaka Kihira, Mitsuru Takaku, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya and Toshiaki Tamaki : Role of HIF-1b in endothelial cells in monocrotaline-induced pulmonary hypertension, 第84回日本薬理学会年会, Mar. 2011.
370.	Yasumasa Ikeda, Soichiro Tajima, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, promotes revascularization via endothelial cells activation, 第84回日本薬理学会年会, Mar. 2011.
371.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Erika Tominaga, Junpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine, a photodegrative metabolite of nifedipine, improves angiotensin -induced vascular remodeling, 第84回日本薬理学会年会, Mar. 2011.
372.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : Angiotensin -induced vascular remodeling is surpressed in smooth muscle cell-specific hypoxia-inducible factor-1a deficient mice, 第84回日本薬理学会年会, Mar. 2011.
373.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, 富永えりか, Yuya Horinouchi, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineによる血管リモデリング抑制効果の検討, 日本薬学会第131回年会, Mar. 2011.
374.	Yuya Horinouchi, Koichiro Tsuchiya, 田島壮一郎, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Nitrosonifedipine の細胞保護効果に関する検討, 日本薬学会第131年会, Mar. 2011.
375.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおけるhypoxia-inducible factor-1αの役割, 第40回日本心脈管作動物質学会, Feb. 2011.
376.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
377.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, 富永えりか, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : AngiotensinⅡ誘発血管リモデリングに対するニトロソニフェジピンの抑制作用, 第40回日本心脈管作動物質学会, Feb. 2011.
378.	Yasumasa Ikeda, 田島壮一郎, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : マウス下肢虚血モデルにおいて鉄キレート剤Deferoxamineは酸化ストレスとアポトーシスを抑制する, 第40回日本心脈管作動物質学会, Feb. 2011.
379.	Noriko Yamano, Yasumasa Ikeda, 田島壮一郎, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : 高脂肪食負荷肥満マウスにおける鉄吸収動態の検討, 第40回日本心脈管作動物質学会, Feb. 2011.
380.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
381.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuya Horinouchi, 富永えりか, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : AngiotensinⅡ誘発血管リモデリングに対するニトロソニフェジピンの抑制作用, 第40回日本心脈管作動物質学会, Feb. 2011.
382.	Masaki Imanishi, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Koichiro Tsuchiya, Toshiaki Tamaki and Shuhei Tomita : AngiotensinⅡ誘発血管リモデリングにおけるhypoxia-inducible factor-1αの役割, 第40回日本心脈管作動物質学会, Feb. 2011.
383.	Yasumasa Ikeda, 田島壮一郎, Sumiko Yoshida, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Ken-ichi Aihara, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Deferoxamine, an iron chelator, enhances angiogenesis through Akt-eNOS-dependent pathway in endothelial cells, 第18回日本血管生物医学会学術集会, Dec. 2010.
384.	Yuuko Imamura, Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : HIF-2/ARNT control hair differentiation by up-regulating p21Waf1/Cip1, 第33回日本分子生物学会年会, Dec. 2010.
385.	Yoshitaka Kihira, Keisuke Ishizawa, Yasumasa Ikeda, Koichiro Tsuchiya, Shuhei Tomita and Toshiaki Tamaki : 脂肪細胞における塩基性繊維芽細胞増殖因子による低酸素誘導因子誘導とそれを介した糖輸送担体発現誘導, 第118回日本薬理学会近畿部会, Nov. 2010. (Keyword) 第118回日本薬理学会近畿部会
386.	Keisuke Ishizawa, 中西智子, Hirofumi Shibata, Shinji Abe, Mayumi Sugimura, Chieko Okumura, Yoshiyuki Yoshimura, Youichi Sato, Naokatu Arakaki, Kazuyoshi Kawazoe, Mami Azuma, Koichiro Tsuchiya, Aiko Yamauchi, Tetsuo Yamazaki and Kazuo Minakuchi : 徳島大学における薬学部・薬剤部連携による病院実務実習の実践, 第20回日本医療薬学会年会, Nov. 2010.
387.	富永えりか, Keisuke Ishizawa, Masaki Imanishi, 櫻田巧, 谷口順平, 藤井聖子, Yuya Horinouchi, Yoshitaka Kihira, Shinji Abe, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : アンジオテンシンII による血管リモデリングに対するニトロソニフェジピンの影響, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
388.	田島壮一郎, Yasumasa Ikeda, Yuya Horinouchi, Yoshitaka Kihira, Shuhei Tomita, Noriko Yamano, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 鉄キレート剤 deferoxamine は内皮細胞活性化により血管新生を促進する, 第20回日本循環薬理学会, Nov. 2010.
389.	Koichiro Tsuchiya, Keisuke Ishizawa, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita and Toshiaki Tamaki : 亜硝酸塩由来血中NO動態に与える経口鉄の影響, 第22回腎とフリーラジカル研究会, Oct. 2010.
390.	Masaki Imanishi, Keisuke Ishizawa, 富永えりか, 櫻田巧, Yuya Horinouchi, 谷口順平, 藤井聖子, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II による血管平滑筋細胞の遊走および増殖に対するnifedipine代謝物の抑制作用とそのメカニズム, 第33回日本高血圧学会, Oct. 2010.
391.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 2型糖尿病モデルマウスに対する鉄キレート剤による糖尿病改善効果の検討, 第34回日本鉄バイオサイエンス学会学術集会, Sep. 2010.
392.	藤井聖子, Keisuke Ishizawa, Masaki Imanishi, 富永えりか, 桜田巧, 谷口順平, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : AngiotensinⅡ誘発血管リモデリングに対するnitrosonifedipineの抑制効果, 次世代を担う創薬・医療薬理シンポジウム2010, Sep. 2010.
393.	Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : 動脈硬化に伴う血管リモデリングに対してT細胞のHIF-1 は抑制的に機能する．, 第31回日本炎症再生医学会, Aug. 2010.
394.	Masaki Imanishi, Keisuke Ishizawa, 富永えりか, Yuya Horinouchi, 谷口順平, 藤井聖子, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Nifedipine代謝物によるangiotensin II 誘発血管平滑筋細胞遊走及び増殖に対する抑制作用, 第117回日本薬理学会近畿部会, Jul. 2010.
395.	Keisuke Ishizawa, Masaki Imanishi, Erika Tminaga, Yuya Horinouchi, Takumi Sakurada, Zyunpei Taniguchi, Seiko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Toshiaki Tamaki and Koichiro Tsuchiya : Nifedipine代謝物はangiotensinⅡによる血管平滑筋細胞遊走および増殖を抑制する, 第63回日本酸化ストレス学会, Jun. 2010.
396.	Yasumasa Ikeda, Koichiro Tsuchiya, 田島壮一郎, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Shuhei Tomita, Yoshihisa Takaishi and Toshiaki Tamaki : The effect of SUDACHI peel, a specialty of Tokushima, as anti-metabolic syndrome, 第83回日本薬理学会年会シンポジウム「肥満の栄養ゲノミクスと薬理ゲノミクス」, Mar. 2010.
397.	Keisuke Ishizawa, Masanori Yoshizumi, Dortsuren Naruantungalag, 今村優子, Yasumasa Ikeda, Junji Terao, Koichiro Tsuchiya and Toshiaki Tamaki : ケルセチンの生体内代謝と動脈硬化予防効果, 第83回日本薬理学会年会シンポジウム「健康食品の薬理学」, Mar. 2010.
398.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : KK-Ay マウスにおける鉄キレート剤Deferoxamineによる糖尿病病態改善効果の検討, 第83回日本薬理学会, Mar. 2010.
399.	Yayoi Fukuhara, Shuhei Tomita, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Koichiro Tsuchiya, Masanori Yoshizumi and Toshiaki Tamaki : T細胞のHIF-1aは，動脈硬化に伴う血管リモデリングを抑制的に制御する, 第39回日本心脈管作動物質学会, Feb. 2010.
400.	Keisuke Ishizawa, Kazuyoshi Kawazoe, Mami Azuma, Koichiro Tsuchiya, Aiko Yamauchi, Tetsuo Yamazaki, Kazuo Minakuchi, 智子中西, Hirofumi Shibata, Shinji Abe, Mayumi Sugimura, Chieko Okumura, Yoshiyuki Yoshimura, Youichi Sato and Naokatu Arakaki : P1-571 徳島大学における薬学部・薬剤部連携による病院実務実習の実践(一般演題ポスター発表,薬学教育(実務実習),臨床から学び臨床へと還元する医療薬学), The Annual Meeting of Japanese Society of Pharmaceutical Health Care and Sciences, Vol.20, No.0, 382, 2010. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390845713041900800 (CiNii: 1390845713041900800)
401.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, Kazuyoshi Kawazoe, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Angiotensin IIによる血管平滑筋細胞遊走に対するnifedipine代謝物の影響, 第30回日本臨床薬理学会年会, Dec. 2009.
402.	Yoshihisa Takaishi, Yoshiki Kashiwada, 橋田和佳, 北岡信, 三口弘介, 中川剛夫, Koichiro Tsuchiya and 井端和郎 : スダチ(Citrus sudachi)果皮のSIRT1活性化成分について, 第3回食品薬学シンポジウム, 114-116, Nov. 2009.
403.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, 山﨑有希子, Yoshitaka Kihira, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : ニフェジピン代謝物はアンジオテンシンⅡ誘発血管平滑筋細胞遊走を抑制する, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
404.	山﨑有希子, Keisuke Ishizawa, 富永えりか, 谷口順平, 櫻田巧, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : アンジオテンシンⅡによる血管平滑筋細胞遊走・増殖における細胞内鉄の関与, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
405.	福原弥生, Shuhei Tomita, 浦田将久, Yoshitaka Kihira, 池田康将, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : モノクロタリン誘導肺高血圧症モデルマウスにおける血管内皮細胞の低酸素応答因子(HIF-1b)の役割, 第116回日本薬理学会近畿部会, Jun. 2009.
406.	三木あかね, 菊石美也子, Harumi Hinode, Mami Azuma, Tomihiko Higuti, Koichiro Tsuchiya, Masaru Kihara and Yoshihisa Takaishi : 徳島大学薬学部における自学能力育成への取組, 日本薬学会129年会, 0, Mar. 2009.
407.	田島壮一郎, Koichiro Tsuchiya, 濱本磨以, Yuya Horinouchi, Shuhei Tomita, Keisuke Ishizawa, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Angiotensin IIによるヒト腎糸球体血管内皮細胞(HGEC)内における鉄動態の検討, 日本薬学会129年会, Mar. 2009.
408.	Mami Azuma, Harumi Hinode, Yoshiki Kashiwada, Masahiro Yoshida, Naoshi Yamazaki, Koichiro Tsuchiya, Aiko Yamauchi, Hirofumi Shibata, Naokatu Arakaki, Yoshiharu Takiguchi, Tsutomu Araki, Yoshiyuki Yoshimura, Toshiki Himeda, Tatsuhiro Ishida, Daisuke Tsuji and Masaru Kihara : 徳島大学薬学部OSCEトライアル実施体制の確立と検証, 第17回日本医療薬学会年会, Sep. 2007.
409.	田岡千明, Koichiro Tsuchiya, 神谷昌樹, Hisao Nemoto, Keisuke Ishizawa, Kunihisa Yamaguchi, Yoshiharu Takiguchi and Toshiaki Tamaki : 水溶性Fenofibrate製剤の作成と中性脂肪低下作用の検討, 第111回日本薬理学会近畿部会, 81, Jun. 2007.
410.	佐野真純, Akira Tokumura, Koichiro Tsuchiya, Akira Shibata and Kenji Fukuzawa : 過酸化脂質の簡易比色定量法:発色成分 [キシレノールオレンジFe3+錯体ー膜ホスファチジルコリン] 複合体の性質, 日本過酸化脂質フリーラジカル学会第31回大会, Jun. 2007.
411.	神谷昌樹, 中本亜樹, 河村知志, Hisao Nemoto, Koichiro Tsuchiya and Yoshiharu Takiguchi : 高脂血症治療薬・フェノフィブラートのBGL Modificationによる中性脂肪低下効果の検討, 日本薬学会第127年会, Vol.31-0567, Mar. 2007.
412.	松村敏彦, 宮本由加里, 黒川ふみ, Shinji Abe, 榊原啓之, Keisuke Ishizawa, Koichiro Tsuchiya, 清水寛, Junji Terao, Toshiaki Tamaki, Kazuyoshi Kawazoe and Kazuo Minakuchi : ラット強制水泳試験における漢方薬の抗うつ作用の検討, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 125, Oct. 2006.
413.	Naonobu Tanaka, 中川博之, Waka Hashida, Masatoshi Satou, Yui Okuse, Chiaki Taoka, Satoshi Iwanaga, Koichiro Tsuchiya and Yoshihisa Takaishi : スダチCitrus sudachi)の含有成分並びに血糖値上昇抑制作用について, 第一回食品薬学シンポジウム, Oct. 2006.
414.	Kazuyoshi Kawazoe, 松村敏彦, 黒川ふみ, 榊原啓之, Keisuke Ishizawa, Koichiro Tsuchiya, 清水寛, Junji Terao, Toshiaki Tamaki and Kazuo Minakuchi : ラット強制水泳試験による漢方薬の抗うつ作用評価, 第109回日本薬理学会近畿部会, 30, Jun. 2006.
415.	堀長志帆, 吉村祥穂, 村田有希, Koichiro Tsuchiya, 峰松敏彦, Kazuyoshi Kawazoe, Yoshihisa Takaishi and Hiroyuki Fukui : 苦参，小青竜湯のアレルギー疾患関連遺伝子発現機構への影響, 第43回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2004.
416.	石上まみ, 池平しのぶ, 三好真紀, Koichiro Tsuchiya, Yoshiharu Takiguchi and Yoshihisa Takaishi : 竹粉末のロペラミン誘発便秘改善作用, 第43回日本薬学会・日本病院薬剤師会中国四国支部学術大会, Nov. 2004.
417.	生田雅子, 石澤啓介, Kazuo Minakuchi, Koichiro Tsuchiya, Aiko Yamauchi and Masaru Kihara : 徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良, 日本薬学会第124年会, Mar. 2004.
418.	合田真規, Aiko Yamauchi, Masaru Kihara, Koichiro Tsuchiya and Kazuo Minakuchi : 徳島大·医·病院におけるIVH処方設計支援ソフトを使用してみて, 第36回日本薬学会·日本病院薬剤師会学術大会中国四国支部大会, Nov. 1997.

Et cetera, Workshop:

1.	Koichiro Tsuchiya : Nitrate exerts its physiological effects through NO-dependent and -independent manner, Apr. 2022.
2.	Rina Murata, Keiji Murakami, Yuka Hiroshima, Koichiro Tsuchiya, Keiko Kataoka and Hideki Fujii : 緑膿菌における抗菌薬添加によるスーパーオキシドの発生について, 徳島大学研究クラスター Joint Meeting on Microbiology 2020, Nov. 2020.
3.	Toshitaka Ikehara, Mutsumi Nakahashi, Koichiro Tsuchiya, Takahiro Emoto, Masatake Akutagawa, Akira Takahashi and Yohsuke Kinouchi : Effects of reactive oxygen species induced by 405 nm LED light irradiation on cultured HeLa S3 cells, LED総合フォーラム2020 in 徳島, 145-148, Feb. 2020.
4.	Licht Miyamoto, 中山卓, 服部真奈, 井上陽加 and Koichiro Tsuchiya : α-TC SGLT2, 循環器ミニリトリート, Feb. 2019.
5.	Yasuoka Takashi, Licht Miyamoto, Tsuchihashi Yuki, Sone Tsubasa, Masuda Shiori and Koichiro Tsuchiya : Circadian disruption during the late gestation period does not affect offspring birth weight, 小豆島リトリート, Sep. 2018.
6.	桂明里, Licht Miyamoto and Koichiro Tsuchiya : 藍含有成分がAhRに与える影響の検討, 夏の生物系勉強会, Aug. 2018.
7.	大西伶奈, Licht Miyamoto and Koichiro Tsuchiya : CaffeineによるAMPK活性調節メカニズムの検討, 第4回徳島大学薬理カンファレンス, Jul. 2018.
8.	竹之熊和也, Licht Miyamoto and Koichiro Tsuchiya : カフェインによるAMPK活性化メカニズムの解析, 心血管ミニリトリート, Jan. 2016.
9.	友川剛己, Licht Miyamoto and Koichiro Tsuchiya : 運動によるAMPK の活性化に関与する機構の検討, 心血管ミニリトリート, Jan. 2016.
10.	秦野彩, Licht Miyamoto and Koichiro Tsuchiya : グリニド薬とSGLT2阻害薬の併用療法, 大学間連携事業評価委員会C, Sep. 2015.
11.	上島沙弥香, Licht Miyamoto and Koichiro Tsuchiya : 肝AMPK活性の新たな調節機構の検討, 大学間連携事業評価委員会C, Sep. 2015.
12.	Yuki Tsuchihashi, Licht Miyamoto, Hisao Nemoto and Koichiro Tsuchiya : Effect of novel branched oligoglycerols-conjugated (BGL) paclitaxels against lung cancer, Tokushima Bioscience Retreat, Sep. 2015.
13.	Goki Tomokawa, Licht Miyamoto and Koichiro Tsuchiya : Mechanism involved in AMPK activation by exercise, Tokushima Bioscience Retreat, Sep. 2015.
14.	Licht Miyamoto, 江川達郎, 大島里詠子, 黒木英梨子, Koichiro Tsuchiya and 林達也 : AMPK活性化剤はどこまで運動療法の代謝改善効果を模倣できるか?―メタボローム分析による検証―, 次世代を担う創薬・医療薬理シンポジウム, Aug. 2015.
15.	津田勝範, Licht Miyamoto and Koichiro Tsuchiya : 鉄による脂質過酸化生成に対するニトロソニフェジピン(NO-NIF)の抑制機構の検討, 夏の生物系勉強会, Aug. 2015.
16.	秦野彩, Licht Miyamoto and Koichiro Tsuchiya : グリニド薬とSGLT2 阻害薬の併用による有用性, 夏の生物系勉強会, Aug. 2015.
17.	許文婷, Licht Miyamoto and Koichiro Tsuchiya : The Mechanism of Citrus Sudachi Peel Extract Exerts Lipid Reducing Effect in Cells, 夏の生物系勉強会, Aug. 2015.
18.	秦野彩, Licht Miyamoto and Koichiro Tsuchiya : Combination therapy of the glinide and SGLT2 inhibitor effectively lowers blood glucose level., アディポサイエンス研究会, Aug. 2015.
19.	秦野彩, Licht Miyamoto, 竹之熊和也, 友川剛己, 松田裕樹, 服部真奈 and Koichiro Tsuchiya : 速効型インスリン分泌促進剤，ナテグリニドとSGLT2 阻害剤，カナグリフロジンの併用による効果の検討, 徳島医学会, Aug. 2015.
20.	津田勝範, Licht Miyamoto, 森本悠里, Shuichi Hamano, Keisuke Ishizawa, 木平考高, Yasumasa Ikeda, Toshiaki Tamaki and Koichiro Tsuchiya : 鉄過剰ストレスに対するニトロソニフェジピン(NO-NIF)の抗酸化メカニズム検討, 徳島医学会, Aug. 2015.

Report:

1.	Masanori Yoshizumi, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : インスリン抵抗性に対するロサルタンおよびロサルタンと運動の併用による効果-モデルラットを用いたin vivoでの検討-, 第17回健康医科学研究助成論文集, No.17, 124-134, Tokyo, Mar. 2002.

Patent:

1.	Yoshihisa Takaishi and Koichiro Tsuchiya : 新規ポリフェノール化合物, P2005-237783, P2007-51099A, .
2.	Yoshihisa Takaishi and Koichiro Tsuchiya : 天然素材を有効に利用した組成物，並びに当該組成物を含有する医薬組成物，健康食品及びサプリメントを提供すること, 2006-2211171, 2007-77139, .
3.	Koichiro Tsuchiya and 木下良治 : 前処理装置, (Oct. 2016), (Apr. 2017), 2017-78716(P2017-78716A) (Apr. 2017).
4.	Koichiro Tsuchiya : 光応答性消臭抗菌剤, (Feb. 2016), (Sep. 2017), 2017-154985(P2017-154985A) (Sep. 2017).
5.	Toshiki Takeuchi, Koichiro Tsuchiya, 阿部武由 and 福岡憲泰 : 薬物動態パラメータの推定方法及び薬物動態パラメータの推定プログラム, 2014-63011 (Jun. 2014), 2015-181853 (Oct. 2015), .
6.	Toshiaki Tamaki, Yasumasa Ikeda and Koichiro Tsuchiya : マクロファージの浸潤抑制によるインスリン抵抗性改善剤, (2011), 2011-174001 (2011).
7.	Hisao Nemoto, Koichiro Tsuchiya and 片桐彩人 : パクリタキセル誘導体, 2010-270797 (Oct. 2010), 2012-999999 (Apr. 2012), 9999999999 (2010).
8.	Yoshihisa Takaishi and Koichiro Tsuchiya : 新規NAD依存性脱アセチル化酵素活性化剤, 2007-301398 (Nov. 2007), 2009-126799 (Jun. 2009), .
9.	Hisao Nemoto, Masaki Kamiya and Koichiro Tsuchiya : ポリアルコール化合物, 2007-020062 (Jan. 2007), .

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

将来の抗がん剤誘導性血行性がん転移制御も考慮した効率的がん治療戦略の開発 (Project/Area Number: 24K09845 )
Antioxidant activity of nitrite and its physiological significance. (Project/Area Number: 22K06645 )
The effects of mild pressure stress on adipocyte differentiation and function. (Project/Area Number: 20K11389 )
Elucidation of the conversion mechanism from white adipocytes to beige cells by nitrite anion (Project/Area Number: 19K07100 )
Effect of glucagon on antidiabetic effect induced by nitrite (Project/Area Number: 16K08550 )
Physiological role of dietary nitrite (Project/Area Number: 15H02898 )
Activation mechanisms of AMPK by nitrite (Project/Area Number: 25460332 )
The renal protective effects of nitrite salts in diabetic nephropathy model rats. (Project/Area Number: 22590241 )
Elucidation of the formation pathways of nitric oxide involved in the reduction of orally-ingested nitrite in vivo (Project/Area Number: 18590235 )
Physiological and pathophysiological role of nitrite-derived nitric oxide formation (Project/Area Number: 17390066 )
Nitrite-derived nitric oxide formation and its pathophysiological effects following ischemia-reperfusion injury in kidney (Project/Area Number: 16590196 )
Investigation of the pathophysiological significance of big mitogen-activated protein kinase 1 in diabetic microangiopathy for the development of molecular-targeted drugs (Project/Area Number: 16590195 )
生体内でのフラボノイド代謝物の抗酸化機序の解明 (Project/Area Number: 14770034 )
Investigation of the pathophysiological significance of big mitogen-acivated protein kinase 1 in diabetic nephropathy for the development of molecular-targeted drugs (Project/Area Number: 14570078 )
Mechanism of the production of reactive nitrogen species during renal ischemic-reperfusion insult (Project/Area Number: 13670087 )
Pathophysiological role of ET-1(1-31) on the inflammatory diseases. (Project/Area Number: 12557008 )
電子スピン共鳴（ESR）法を用いた生体内一酸化窒素（NO）の直接測定 (Project/Area Number: 10770041 )
Search by Researcher Number (70301314)

Professor : Tsuchiya, Koichiro

Research

Personal Web Page

Field of Study

Subject of Study

Book / Paper

Book:

Academic Paper (Judged Full Paper):

Academic Paper (Unrefereed Paper):

Review, Commentary:

Proceeding of International Conference:

Proceeding of Domestic Conference:

Et cetera, Workshop:

Report:

Patent:

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)