Tokushima University / Educator and Researcher Directory --- Imanishi, Masaki

Personal Web Page

https://orcid.org/0000-0003-1305-5943 (ORCID)

Field of Study

○	Pharmacology, Cardiovascular Pharmacology, Clinical Pharmacology, Molecular Pharmacology

Subject of Study

○

Book / Paper

Book:

1.	Masaki Imanishi : テキサス・メディカルセンター最前線「第197回抗がん剤の副作用ってこわいの?」, ヒューストン日本商工会, Houston, May 2021.
2.	Yoshito Zamami, Naoto Okada, Kenshi Takechi, Masaki Imanishi and Keisuke Ishizawa : あ，検査値が変わった」そのとき，薬のリスクは?(分担執筆), 株式会社じほう, Jun. 2017.

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.	H Minh T Nguyen, Masaki Imanishi, Shengyu Li, Khanh Chau, Priyanka Banerjee, Reddy Loka Velatooru, Ae Kyung Ko, K Venkata S Samanthapudi, J Young Gi, Ling-Ling Lee, J Rei Abe, Elena McBeath, Anita Deswal, H Steven Lin, L Nicolas Palaskas, Robert Dantzer, Keigi Fujiwara, K Mae Borchrdt, Berrios Estefani Turcios, A Elizabeth Olmsted-Davis, Sivareddy Kotla, P John Cooke, Guangyu Wang, Jun-Ichi Abe and Nhat-Tu Le : Endothelial activation and fibrotic changes are impeded by laminar flow-induced CHK1-SENP2 activity through mechanisms distinct from endothelial-to-mesenchymal cell transition., Frontiers in Cardiovascular Medicine, Vol.10, 2023. (Summary) In this study, we have revealed a novel mechanism underlying the suppressive effects of L-flow on EC inflammation, migration, proliferation, apoptosis, and fibrotic changes through promoting CHK1-induced SENP2 S344 phosphorylation. The phospho-site mutation SENP2 S344A responds to L-flow through a distinct mechanism, which involves the upregulation of both mesenchymal and EC marker genes. (Tokushima University Institutional Repository) ● Metadata: 119175 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2023.1187490 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37711550 ● Search Scopus @ Elsevier (PMID): 37711550 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2023.1187490 (Tokushima University Institutional Repository: 119175, DOI: 10.3389/fcvm.2023.1187490, PubMed: 37711550)
6.	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)
7.	Hannah Savage, Sumedha Pareek, Jonghae Lee, Riccardo Ballarò, Darlan Minussi Conterno, Karma Hayek, Mumina Sadullozoda, S Brooke Lochmann, L Jennifer McQuade, C Emily LaVoy, Enrica Marmonti, Hetal Patel, Guangyu Wang, Masaki Imanishi, Sivareddy Kotla, Jun-Ichi Abe and L Keri Schadler : Aerobic exercise alters the melanoma microenvironment and modulates ERK5 S496 phosphorylation., Cancer Immunology Research, Vol.11, No.9, 1168-1183, 2023. (Summary) Exercise changes the tumor microenvironment by remodeling blood vessels and increasing infiltration by cytotoxic immune cells. The mechanisms driving these changes remain unclear. Herein, we demonstrate that exercise normalizes tumor vasculature and upregulates endothelial expression of VCAM1 in YUMMER 1.7 and B16F10 murine models of melanoma but differentially regulates tumor growth, hypoxia, and the immune response. We found that exercise suppressed tumor growth and increased CD8+ T-cell infiltration in YUMMER but not in B16F10 tumors. Single-cell RNA sequencing and flow cytometry revealed exercise modulated the number and phenotype of tumor-infiltrating CD8+ T cells and myeloid cells. Specifically, exercise caused a phenotypic shift in the tumor-associated macrophage population and increased the expression of MHC class II transcripts. We further demonstrated that ERK5 S496A knock-in mice, which are phosphorylation deficient at the S496 residue, "mimicked" the exercise effect when unexercised, yet when exercised, these mice displayed a reversal in the effect of exercise on tumor growth and macrophage polarization compared with wild-type mice. Taken together, our results reveal tumor-specific differences in the immune response to exercise and show that ERK5 signaling via the S496 residue plays a crucial role in exercise-induced tumor microenvironment changes. See related Spotlight by Betof Warner, p. 1158. (Link to Publication Site) ● Publication site (DOI): 10.1158/2326-6066.CIR-22-0465 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37307577 ● Search Scopus @ Elsevier (PMID): 37307577 ● Search Scopus @ Elsevier (DOI): 10.1158/2326-6066.CIR-22-0465 (DOI: 10.1158/2326-6066.CIR-22-0465, PubMed: 37307577)
8.	Jun-Ichi Abe, Masaki Imanishi, Shengyu Li, Aijun Zhang, Ae Kyung Ko, K Venkata S Samanthapudi, Ling-Ling Lee, Paniagua Angelica Bojorges, Jin Young Gi, P Brian Hobbs, Anita Deswal, Joerg Herrmann, H Steven Lin, N Eduardo Chini, H Ying Shen, L Keri Schadler, Thi-Hong-Minh Nguyen, A Anisha Gupte, Cielito Reyes-Gibby, J Sai-Ching Yeung, J Rei Abe, A Elizabeth Olmsted-Davis, Sunil Krishnan, Robert Dantzer, L Nicolas Palaskas, P John Cooke, J Henry Pownall, Momoko Yoshimoto, Keigi Fujiwara, J Dale Hamilton, K Jared Burks, Guangyu Wang, Nhat-Tu Le and Sivareddy Kotla : An ERK5-NRF2 Axis Mediates Senescence-Associated Stemness and Atherosclerosis., Circulation Research, Vol.133, No.1, 25-44, 2023. (Summary) We discovered a novel mechanism by which the macrophage ERK5-NRF2 axis develops a unique senescence-associated secretory phenotype/stemness phenotype by upregulating AHR to engender atherogenesis. The finding of senescence-associated stemness phenotype provides a molecular explanation to resolve the paradox of senescence in proliferative plaque by permitting myeloid cells to escape the senescence-induced cell cycle arrest during atherosclerosis formation. (Keyword) Animals / knockout mice / atherosclerosis / inflammation / Mitogen-Activated Protein Kinase 7 / NF-E2-Related Factor 2 / Plaque, Atherosclerotic (Link to Publication Site) ● Publication site (DOI): 10.1161/CIRCRESAHA.122.322017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37264926 ● Search Scopus @ Elsevier (PMID): 37264926 ● Search Scopus @ Elsevier (DOI): 10.1161/CIRCRESAHA.122.322017 (DOI: 10.1161/CIRCRESAHA.122.322017, PubMed: 37264926)
9.	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)
10.	Masaki Imanishi, Haizi Cheng, Sivareddy Kotla, Anita Deswal, Nhat-Tu Le, Eduardo Chini, Ae Kyung Ko, K Venkata S Samanthapudi, Ling-Ling Lee, Joerg Herrmann, Xiaolei Xu, Cielito Reyes-Gibby, J Sai-Ching Yeung, L Keri Schadler, Wamique Syed Yusuf, Zhongxing Liao, Roza Nurieva, David El-Ad Amir, K Jared Burks, L Nicolas Palaskas, P John Cooke, H Steven Lin, Michihiro Kobayashi, Momoko Yoshimoto and Jun-Ichi Abe : Radiation therapy induces immunosenescence mediated by p90RSK., Frontiers in Cardiovascular Medicine, Vol.9, 2022. (Summary) memory and naïve B, and myeloid cells, (2) senescence-associated β-gal staining, and (3) mitochondrial reactive oxygen species (ROS) after ionizing radiation (IR). These data suggest the crucial role of p90RSK activation in immunosenescence. The critical role of p90RSK activation in immune cells and T-bet induction in upregulating atherosclerosis formation has been reported. Furthermore, T-bet directly binds to the CD38 promoter region and upregulates CD38 expression. Since both T-bet and CD38 play a significant role in the process of immunosenescence, our data provide a cellular and molecular mechanism that links RT-induced p90RSK activation and the immunosenescence with T-bet and CD38 induction observed in thoracic cancer patients treated by RT and suggests that targeting the p90RSK/T-bet/CD38 pathway could play a role in preventing the radiation-associated CVD and improving cancer prognosis by inhibiting immunosenescence. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2022.988713 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36426217 ● Search Scopus @ Elsevier (PMID): 36426217 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2022.988713 (DOI: 10.3389/fcvm.2022.988713, PubMed: 36426217)
11.	Yin Wang, Jun-Ichi Abe, M Khanh Chau, Yongxing Wang, Thi Hang Vu, Loka Velatooru Reddy, Fahad Gulraiz, Masaki Imanishi, K Venkata S Samanthapudi, H Minh T Nguyen, Ae Kyung Ko, Ling-Ling Lee, N Tamlyn Thomas, A Elizabeth Olmsted-Davis, Sivareddy Kotla, Keigi Fujiwara, P John Cooke, Di Zhao, E Scott Evans and Nhat-Tu Le : MAGI1 inhibits interferon signaling to promote influenza A infection., Frontiers in Cardiovascular Medicine, Vol.9, 2022. (Summary) mRNA and MX1 expression, again supporting the pro-viral response mediated by MAGI1. MAGI1 depletion induces the expression of MX1 and virus suppression. The data suggests that IAV suppression by MAGI1 depletion may, in part, be due to MX1 induction. Lastly, interferon regulatory factor 3 (IRF3) translocates to the nucleus in the absence of IRF3 phosphorylation, and IRF3 SUMOylation is abolished in MAGI1-depleted ECs. The data suggests that MAGI1 inhibits IRF3 activation by maintaining IRF3 SUMOylation. In summary, IAV infection occurs in ECs in a MAGI1 expression-dependent manner by inhibiting anti-viral responses including STATs and IRF3 activation and subsequent MX1 induction, and MAGI1 plays a role in EC activation, and in upregulating a pro-viral response. Therefore, the inhibition of MAGI1 is a potential therapeutic target for IAV-induced cardiovascular disease. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2022.791143 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36082118 ● Search Scopus @ Elsevier (PMID): 36082118 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2022.791143 (DOI: 10.3389/fcvm.2022.791143, PubMed: 36082118)
12.	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)
13.	Loka Reddy Velatooru, Rei J. Abe, Masaki Imanishi, Young Jin Gi, Kyung Ae Ko, Kyung-Sun Heo, Keigi Fujiwara, Nhat-Tu Le and Sivareddy Kotla : Disturbed flow-induced FAK K152 SUMOylation initiates the formation of pro-inflammation positive feedback loop by inducing reactive oxygen species production in endothelial cells., Free Radical Biology and Medicine, Vol.177, 404-418, 2021. (Summary) Focal adhesion kinase (FAK) activation plays a crucial role in vascular diseases. In endothelial cells, FAK activation is involved in the activation of pro-inflammatory signaling and the progression of atherosclerosis. Disturbed flow (D-flow) induces endothelial activation and senescence, but the exact role of FAK in D-flow-induced endothelial activation and senescence remains unclear. The objective of this study is to investigate the role of FAK SUMOylation in D-flow-induced endothelial activation and senescence. The results showed that D-flow induced reactive oxygen species (ROS) production via NADPH oxidase activation and activated a redox-sensitive kinase p90RSK, leading to FAK activation by upregulating FAK K152 SUMOylation and the subsequent Vav2 phosphorylation, which in turn formed a positive feedback loop by upregulating ROS production. This feedback loop played a crucial role in regulating endothelial activation and senescence. D-flow-induced endothelial activation and senescence were significantly inhibited by mutating a FAK SUMOylation site lysine152 to arginine. Collectively, we concluded that FAK K152 SUMOylation plays a key role in D-flow-induced endothelial activation and senescence by forming a positive feedback loop through ROS production. (Keyword) Endothelial Cells / Feedback / Focal Adhesion Protein-Tyrosine Kinases / Humans / Inflammation / Phosphorylation / Reactive Oxygen Species / Sumoylation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.freeradbiomed.2021.09.023 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34619327 ● Search Scopus @ Elsevier (PMID): 34619327 ● Search Scopus @ Elsevier (DOI): 10.1016/j.freeradbiomed.2021.09.023 (DOI: 10.1016/j.freeradbiomed.2021.09.023, PubMed: 34619327)
14.	Sivareddy Kotla, Aijun Zhang, Masaki Imanishi, Kyung Ae Ko, Steven H. Lin, Young Jin Gi, Margie Moczygemba, Sevinj Isgandarova, Keri L. Schadler, Caroline Chung, Sarah A. Milgrom, Jose Banchs, Syed Wamique Yusuf, Diana N. Amaya, Huifang Guo, Tamlyn N. Thomas, Ying H. Shen, Anita Deswal, Joerg Herrmann, Eugenie S. Kleinerman, Mark L. Entman, John P. Cooke, Giovanni Schifitto, Sanjay B. Maggirwar, Elena McBeath, Anisha A. Gupte, Sunil Krishnan, Zarana S. Patel, Yisang Yoon, Jared K. Burks, Keigi Fujiwara, Paul S. Brookes, Nhat-Tu Le, Dale J. Hamilton and Jun-Ichi Abe : Nucleus-mitochondria positive feedback loop formed by ERK5 S496 phosphorylation-mediated poly (ADP-ribose) polymerase activation provokes persistent pro-inflammatory senescent phenotype and accelerates coronary atherosclerosis after chemo-radiation., Redox Biology, Vol.47, 102132, 2021. (Summary) The incidence of cardiovascular disease (CVD) is higher in cancer survivors than in the general population. Several cancer treatments are recognized as risk factors for CVD, but specific therapies are unavailable. Many cancer treatments activate shared signaling events, which reprogram myeloid cells (MCs) towards persistent senescence-associated secretory phenotype (SASP) and consequently CVD, but the exact mechanisms remain unclear. This study aimed to provide mechanistic insights and potential treatments by investigating how chemo-radiation can induce persistent SASP. We generated ERK5 S496A knock-in mice and determined SASP in myeloid cells (MCs) by evaluating their efferocytotic ability, antioxidation-related molecule expression, telomere length, and inflammatory gene expression. Candidate SASP inducers were identified by high-throughput screening, using the ERK5 transcriptional activity reporter cell system. Various chemotherapy agents and ionizing radiation (IR) up-regulated p90RSK-mediated ERK5 S496 phosphorylation. Doxorubicin and IR caused metabolic changes with nicotinamide adenine dinucleotide depletion and ensuing mitochondrial stunning (reversible mitochondria dysfunction without showing any cell death under ATP depletion) via p90RSK-ERK5 modulation and poly (ADP-ribose) polymerase (PARP) activation, which formed a nucleus-mitochondria positive feedback loop. This feedback loop reprogramed MCs to induce a sustained SASP state, and ultimately primed MCs to be more sensitive to reactive oxygen species. This priming was also detected in circulating monocytes from cancer patients after IR. When PARP activity was transiently inhibited at the time of IR, mitochondrial stunning, priming, macrophage infiltration, and coronary atherosclerosis were all eradicated. The p90RSK-ERK5 module plays a crucial role in SASP-mediated mitochondrial stunning via regulating PARP activation. Our data show for the first time that the nucleus-mitochondria positive feedback loop formed by p90RSK-ERK5 S496 phosphorylation-mediated PARP activation plays a crucial role of persistent SASP state, and also provide preclinical evidence supporting that transient inhibition of PARP activation only at the time of radiation therapy can prevent future CVD in cancer survivors. (Keyword) Adenosine Diphosphate / Animals / Coronary Artery Disease / Feedback / Humans / Mice / Mitochondria / Mitogen-Activated Protein Kinase 7 / Phenotype / Phosphorylation / Poly (ADP-Ribose) Polymerase-1 / Poly(ADP-ribose) Polymerases / Ribose (Link to Publication Site) ● Publication site (DOI): 10.1016/j.redox.2021.102132 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34619528 ● Search Scopus @ Elsevier (PMID): 34619528 ● Search Scopus @ Elsevier (DOI): 10.1016/j.redox.2021.102132 (DOI: 10.1016/j.redox.2021.102132, PubMed: 34619528)
15.	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)
16.	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)
17.	J Rei Abe, Hannah Savage, Masaki Imanishi, Priyanka Banerjee, Sivareddy Kotla, Jesus Paez-Mayorga, Jack Taunton, Keigi Fujiwara, Hak Jong Won, Wamique Syed Yusuf, L Nicolas Palaskas, Jose Banchs, H Steven Lin, L Keri Schadler, Jun-Ichi Abe and Nhat-Tu Le : p90RSK-MAGI1 Module Controls Endothelial Permeability by Post-translational Modifications of MAGI1 and Hippo Pathway., Frontiers in Cardiovascular Medicine, Vol.7, 2020. (Summary) These results provide novel insights into crucial roles for p90RSK-mediated MAGI1 PTMs and the Hippo pathway in EC permeability, as well as p90RSK activation in tumor vessel leakiness. (Link to Publication Site) ● Publication site (DOI): 10.3389/fcvm.2020.542485 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33304925 ● Search Scopus @ Elsevier (PMID): 33304925 ● Search Scopus @ Elsevier (DOI): 10.3389/fcvm.2020.542485 (DOI: 10.3389/fcvm.2020.542485, PubMed: 33304925)
18.	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)
19.	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)
20.	Tatsuya Tsuda, Masaki Imanishi, Mizuho Oogoshi, Mitsuhiro Goda, Yoshitaka Kihira, Yuya Horinouchi, Yoshito Zamami, Keisuke Ishizawa, Yasumasa Ikeda, Ichiro Hashimoto, Toshiaki Tamaki and Yuki Izawa-Ishizawa : Rho-associated protein kinase and cyclophilin a are involved in inorganic phosphate-induced calcification signaling in vascular smooth muscle cells., Journal of Pharmacological Sciences, Vol.142, No.3, 109-115, 2020. (Summary) Arterial calcification, a risk factor of cardiovascular events, develops with differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Cyclophilin A (CypA) is a peptidyl-prolyl isomerase involved in cardiovascular diseases such as atherosclerosis and aortic aneurysms, and rho-associated protein kinase (ROCK) is involved in the pathogenesis of vascular calcification. CypA is secreted in a ROCK activity-dependent manner and works as a mitogen via autocrine or paracrine mechanisms in VSMCs. We examined the involvement of the ROCK-CypA axis in VSMC calcification induced by inorganic phosphate (Pi), a potent cell mineralization initiator. We found that Pi stimulated ROCK activity, CypA secretion, extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation, and runt-related transcription factor 2 expression, resulting in calcium accumulation in rat aortic smooth muscle cells (RASMCs). The ROCK inhibitor Y-27632 significantly suppressed Pi-induced CypA secretion, ERK1/2 phosphorylation, and calcium accumulation. Recombinant CypA was found to be associated with increased calcium accumulation in RASMCs. Based on these results, we suggest that autocrine CypA is mediated by ROCK activity and is involved in Pi-induced ERK1/2 phosphorylation following calcification signaling in RASMCs. (Tokushima University Institutional Repository) ● Metadata: 115530 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphs.2019.12.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31882204 ● Search Scopus @ Elsevier (PMID): 31882204 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphs.2019.12.005 (Tokushima University Institutional Repository: 115530, DOI: 10.1016/j.jphs.2019.12.005, PubMed: 31882204)
21.	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)
22.	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)
23.	Sivareddy Kotla, Thi Hang Vu, Ae Kyung Ko, Yin Wang, Masaki Imanishi, Kyung-Sun Heo, Yuka Fujii, N Tamlyn Thomas, Jin Young Gi, Hira Mazhar, Jesus Paez-Mayorga, Ji-Hyun Shin, Yunting Tao, J Carolyn Giancursio, Lm Jan Medina, Jack Taunton, J Aldos Lusis, P John Cooke, Keigi Fujiwara, Nhat-Tu Le and Jun-Ichi Abe : Endothelial senescence is induced by phosphorylation and nuclear export of telomeric repeat binding factor 2-interacting protein., JCI Insight, Vol.4, No.9, 2019. (Summary) The interplay among signaling events for endothelial cell (EC) senescence, apoptosis, and activation and how these pathological conditions promote atherosclerosis in the area exposed to disturbed flow (d-flow) in concert remain unclear. The aim of this study was to determine whether telomeric repeat-binding factor 2-interacting protein (TERF2IP), a member of the shelterin complex at the telomere, can regulate EC senescence, apoptosis, and activation simultaneously, and if so, by what molecular mechanisms. We found that d-flow induced p90RSK and TERF2IP interaction in a p90RSK kinase activity-dependent manner. An in vitro kinase assay revealed that p90RSK directly phosphorylated TERF2IP at the serine 205 (S205) residue, and d-flow increased TERF2IP S205 phosphorylation as well as EC senescence, apoptosis, and activation by activating p90RSK. TERF2IP phosphorylation was crucial for nuclear export of the TERF2IP-TRF2 complex, which led to EC activation by cytosolic TERF2IP-mediated NF-κB activation and also to senescence and apoptosis of ECs by depleting TRF2 from the nucleus. Lastly, using EC-specific TERF2IP-knockout (TERF2IP-KO) mice, we found that the depletion of TERF2IP inhibited d-flow-induced EC senescence, apoptosis, and activation, as well as atherosclerotic plaque formation. These findings demonstrate that TERF2IP is an important molecular switch that simultaneously accelerates EC senescence, apoptosis, and activation by S205 phosphorylation. (Keyword) Active Transport, Cell Nucleus / Animals / Apoptosis / Atherosclerosis / Cellular Senescence / DNA Damage / Disease Models, Animal / Endothelial Cells / Male / Mice / Mice, Inbred C57BL / Mice, Knockout / Phosphorylation / Plaque, Atherosclerotic / Shelterin Complex / Signal Transduction / Telomere / Telomere-Binding Proteins / Telomeric Repeat Binding Protein 2 / Transcriptome (Link to Publication Site) ● Publication site (DOI): 10.1172/jci.insight.124867 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31045573 ● Search Scopus @ Elsevier (PMID): 31045573 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.124867 (DOI: 10.1172/jci.insight.124867, PubMed: 31045573)
24.	Jun-Ichi Abe, Ae Kyung Ko, Sivareddy Kotla, Yin Wang, Jesus Paez-Mayorga, Jae Ik Shin, Masaki Imanishi, Thi Hang Vu, Yunting Tao, M Miguel Leiva-Juarez, N Tamlyn Thomas, L Jan Medina, Hak Jong Won, Yuka Fujii, J Carolyn Giancursio, Elena McBeath, Ji-Hyun Shin, Liliana Guzman, J Rei Abe, Jack Taunton, Naoki Mochizuki, William Faubion, P John Cooke, Keigi Fujiwara, E Scott Evans and Nhat-Tu Le : MAGI1 as a link between endothelial activation and ER stress drives atherosclerosis., JCI Insight, Vol.4, No.7, 2019. (Summary) The possible association between the membrane-associated guanylate kinase with inverted domain structure-1 (MAGI1) and inflammation has been suggested, but the molecular mechanisms underlying this link, especially during atherogenesis, remain unclear. In endothelial cells (ECs) exposed to disturbed flow (d-flow), p90 ribosomal S6 kinase (p90RSK) bound to MAGI1, causing MAGI1-S741 phosphorylation and sentrin/SUMO-specific protease 2 T368 phosphorylation-mediated MAGI1-K931 deSUMOylation. MAGI1-S741 phosphorylation upregulated EC activation via activating Rap1. MAGI1-K931 deSUMOylation induced both nuclear translocation of p90RSK-MAGI1 and ATF-6-MAGI1 complexes, which accelerated EC activation and apoptosis, respectively. Microarray screening revealed key roles for MAGI1 in the endoplasmic reticulum (ER) stress response. In this context, MAGI1 associated with activating transcription factor 6 (ATF-6). MAGI1 expression was upregulated in ECs and macrophages found in atherosclerotic-prone regions of mouse aortas as well as in the colonic epithelia and ECs of patients with inflammatory bowel disease. Further, reduced MAGI1 expression in Magi1-/+ mice inhibited d-flow-induced atherogenesis. In sum, EC activation and ER stress-mediated apoptosis are regulated in concert by two different types of MAGI1 posttranslational modifications, elucidating attractive drug targets for chronic inflammatory disease, particularly atherosclerosis. (Keyword) Activating Transcription Factor 6 / Adaptor Proteins, Signal Transducing / Adult / Animals / Aorta / Apoptosis / Atherosclerosis / Cell Adhesion Molecules / Cells, Cultured / Colon / Cysteine Endopeptidases / Disease Models, Animal / Endoplasmic Reticulum Stress / Endothelial Cells / Endothelium, Vascular / Female / Guanylate Kinases / Humans / Inflammatory Bowel Diseases / Intestinal Mucosa / Male / Mice / Middle Aged / Phosphorylation / Primary Cell Culture / Ribosomal Protein S6 Kinases, 90-kDa / Signal Transduction / Sumoylation (Link to Publication Site) ● Publication site (DOI): 10.1172/jci.insight.125570 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30944250 ● Search Scopus @ Elsevier (PMID): 30944250 ● Search Scopus @ Elsevier (DOI): 10.1172/jci.insight.125570 (DOI: 10.1172/jci.insight.125570, PubMed: 30944250)
25.	Hirofumi Hamano, Marin Mitsui, Yoshito Zamami, Kenshi Takechi, Takahiro Nimura, Naoto Okada, Keijo Fukushima, Masaki Imanishi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Yasumasa Ikeda, Hiromichi Fujino, Hiroaki Yanagawa, Toshiaki Tamaki and Keisuke Ishizawa : Irinotecan-induced neutropenia is reduced by oral alkalization drugs: analysis using retrospective chart reviews and the spontaneous reporting database., Supportive Care in Cancer, Vol.27, No.3, 849-856, 2019. (Summary) These data indicate that oral alkalization drugs may reduce the frequency of neutropenia caused by irinotecan administration, making it possible to increase the dose safely. (Link to Publication Site) ● Publication site (DOI): 10.1007/s00520-018-4367-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30062585 ● Search Scopus @ Elsevier (PMID): 30062585 ● Search Scopus @ Elsevier (DOI): 10.1007/s00520-018-4367-y (DOI: 10.1007/s00520-018-4367-y, PubMed: 30062585)
26.	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)
27.	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)
28.	Ken Konaka, Takumi Sakurada, Tatsuhiko Saito, Sachiko Mori, Masaki Imanishi, Soji Kakiuchi, Shuji Fushitani and Keisuke Ishizawa : Study on the Optimal Dose of Irinotecan for Patients with Heterozygous Uridine Diphosphate-Glucuronosyltransferase 1A1 (UGT1A1)., Biological & Pharmaceutical Bulletin, Vol.42, No.11, 1839-1845, 2019. (Summary) Uridine 5'-diphospho-glucuronosyltransferase (UGT), a metabolic enzyme of irinotecan active metabolite, has two genetic polymorphisms (UGT1A16 and UGT1A128). In UGT1A1 homozygous or heterozygous patients, metabolism is delayed and the risk of developing adverse effects is increased, and therefore, dose reduction of irinotecan is considered. However, the specific dose reduction rate of irinotecan for heterozygous patients is uncertain. We studied the necessity of irinotecan dose reduction and its optimal dose in UGT1A1 heterozygous patients with lung cancer. Patients with lung cancer treated with irinotecan in the Tokushima University Hospital or Tokushima Municipal Hospital were included in this study. The dose of irinotecan was evaluated based on the relative dose intensity (RDI). The time to treatment failure (TTF) was defined as the period until treatment change, death, or progressive disease based on response evaluation criteria of solid tumors. We targeted 31 patients treated with irinotecan: 12 wild types (WT), 14 heterozygotes, and 1 complex heterozygote and 4 homozygotes. There was no significant difference in the TTF, but the mean RDI during the entire treatment period was significantly different in the wild type (79%), heterozygous (62%), and complex heterozygous and homozygous groups (46%). In addition, the proportion of patients who completed treatment without dose reduction in the WT group tended to be higher than that in the other groups. For lung cancer patients with UGT1A1 heterozygote types who start irinotecan therapy, reducing the initial dose by approximately 20% might be a safer chemotherapy without decreasing the therapeutic effect. (Keyword) Aged / Dose-Response Relationship, Drug / Female / Genotype / Glucuronosyltransferase / Heterozygote / Homozygote / Humans / Irinotecan / Lung Neoplasms / Male / Middle Aged / Polymorphism, Genetic (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b19-00357 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31685767 ● Search Scopus @ Elsevier (PMID): 31685767 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b19-00357 (DOI: 10.1248/bpb.b19-00357, PubMed: 31685767)
29.	Naoto Okada, Takahiro Niimura, Yoshito Zamami, Hirofumi Hamano, Shunsuke Ishida, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Masaki Imanishi and Keisuke Ishizawa : Pharmacovigilance evaluation of the relationship between impaired glucose metabolism and BCR-ABL inhibitor use by using an adverse drug event reporting database., Cancer Medicine, 2018. (Summary) Breakpoint cluster region-Abelson murine leukemia (BCR-ABL) inhibitors markedly improve the prognosis of chronic myeloid leukemia. However, high treatment adherence is necessary for successful treatment with BCR-ABL inhibitors. Therefore, an adequate understanding of the adverse event profiles of BCR-ABL inhibitors is essential. Although many adverse events are observed in trials, an accurate identification of adverse events based only on clinical trial results is difficult because of strict entry criteria or limited follow-up durations. In particular, BCR-ABL inhibitor-induced impaired glucose metabolism remains controversial. Pharmacovigilance evaluations using spontaneous reporting systems are useful for analyzing drug-related adverse events in clinical settings. Therefore, we conducted signal detection analyses for BCR-ABL inhibitor-induced impaired glucose metabolism by using the FDA Adverse Event Reporting System (FAERS) and Japanese Adverse Drug Event Report (JADER) database. Signals for an increased reporting rate of impaired glucose metabolism were detected only for nilotinib use, whereas these signals were not detected for other BCR-ABL inhibitors. Subgroup analyses showed a clearly increased nilotinib-associated reporting rate of impaired glucose metabolism in male and younger patients. Although FAERS- and JADER-based signal detection analyses cannot determine causality perfectly, our study suggests the effects on glucose metabolism are different between BCR-ABL inhibitors and provides useful information for the selection of appropriate BCR-ABL inhibitors. (Tokushima University Institutional Repository) ● Metadata: 115037 (Link to Publication Site) ● Publication site (DOI): 10.1002/cam4.1920 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30561126 ● Search Scopus @ Elsevier (PMID): 30561126 ● Search Scopus @ Elsevier (DOI): 10.1002/cam4.1920 (Tokushima University Institutional Repository: 115037, DOI: 10.1002/cam4.1920, PubMed: 30561126)
30.	Naoto Okada, Hitoshi Kawazoe, Kenshi Takechi, Yoshihiro Matsudate, Ryo Utsunomiya, Yoshito Zamami, Mitsuhiro Goda, Masaki Imanishi, Masayuki Chuma, Noriaki Hidaka, Koji Sayama, Yoshiaki Kubo, Akihiro Tanaka and Keisuke Ishizawa : Association Between Immune-Related Adverse Events and Clinical Efficacy in Patients with Melanoma Treated With Nivolumab: A Multicenter Retrospective Study., Clinical Therapeutics, Vol.41, No.1, 59-67, 2018. (Summary) Our study indicated that clinical response with nivolumab treatment improves with irAE occurrence in patients with melanoma. Moreover, the early increase in peripheral lymphocyte count may act as a biomarker for predicting the occurrence of irAEs induced by nivolumab. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinthera.2018.11.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30528047 ● Summary page in Scopus @ Elsevier: 2-s2.0-85057595502 (DOI: 10.1016/j.clinthera.2018.11.004, PubMed: 30528047, Elsevier: Scopus)
31.	Yoshito Zamami, Y Kouno, T Niimura, Masayuki Chuma, T Imai, M Mitsui, T Koyama, M Kayano, Naoto Okada, H Hamano, Mitsuhiro Goda, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Y Kondo, Hiroaki Yanagawa, Y Kitamura, T Sendo, Y Ujike and Keisuke Ishizawa : Relationship between the administration of nicardipine hydrochloride and the development of delirium in patients on mechanical ventilation., Die Pharmazie, Vol.73, No.12, 740-743, 2018. (Summary) A history of hypertension is a known risk factor for delirium in patients in intensive care units, but the effect of antihypertensive agents on delirium development is unclear. Nicardipine, a calcium channel blocker, is widely used in ICU as a treatment agent for hypertensive emergency. This study investigated the relationship between the administration of nicardipine hydrochloride and delirium development in patients under mechanical ventilation. We conducted a medical chart review of 103 patients, who were divided into two groups according to the use of nicardipine hydrochloride. The prevalence of delirium was compared with respect to factors such as age, sex, laboratory data, and medical history, by multivariate analysis. 21 patients (20.4 %) were treated with nicardipine hydrochloride in 103 patients. The treatment and non-treatment groups differed significantly in age (72 vs. 65 years) and history of high blood pressure (57% vs. 11%). Multivariate analysis revealed that patients in the treatment group developed delirium significantly less often than those in the non-treatment group (19% vs. 48%). These results suggested that treatment of high blood pressure with nicardipine hydrochloride is a possible method for preventing the development of delirium. (Link to Publication Site) ● Publication site (DOI): 10.1691/ph.2018.8711 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30522561 ● Search Scopus @ Elsevier (PMID): 30522561 ● Search Scopus @ Elsevier (DOI): 10.1691/ph.2018.8711 (DOI: 10.1691/ph.2018.8711, PubMed: 30522561)
32.	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)
33.	Shunsuke Ishida, Kenshi Takechi, Hiroshi Bando, Masaki Imanishi, Yoshito Zamami, Masayuki Chuma, Hiroaki Yanagawa, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka and Keisuke Ishizawa : Development and pharmacist-mediated use of tools for monitoring atypical antipsychotic-induced side effects related to blood glucose levels., Pharmacoepidemiology and Drug Safety, 2018. (Summary) The results suggested that regardless of pharmacists' experience or skill, the introduction of this tool enables centralization of side effect monitoring and can contribute to proper drug use. (Tokushima University Institutional Repository) ● Metadata: 112203 (Link to Publication Site) ● Publication site (DOI): 10.1002/pds.4656 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30221424 ● Search Scopus @ Elsevier (PMID): 30221424 ● Search Scopus @ Elsevier (DOI): 10.1002/pds.4656 (Tokushima University Institutional Repository: 112203, DOI: 10.1002/pds.4656, PubMed: 30221424)
34.	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)
35.	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)
36.	Naoto Okada, Momoyo Azuma, Masaki Imanishi, Yoshito Zamami, Yasushi Kirino, Toshimi Nakamura, Kazuhiko Teraoka, Masahiro Abe and Keisuke Ishizawa : Potential Usefulness of Early Potassium Supplementation for Preventing Severe Hypokalemia Induced by Liposomal Amphotericin B in Hematologic Patients: A Retrospective Study., Clinical Therapeutics, Vol.40, No.2, 252-260, 2018. (Summary) This study showed that starting administration of a potassium formulation within 2 days from the start of L-AMB administration was a risk reduction factor for L-AMB-induced hypokalemia. This finding indicates that early potassium supplementation should be incorporated into the regimen of hypokalemia management when L-AMB is used. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.clinthera.2017.12.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29305017 ● Search Scopus @ Elsevier (PMID): 29305017 ● Search Scopus @ Elsevier (DOI): 10.1016/j.clinthera.2017.12.006 (DOI: 10.1016/j.clinthera.2017.12.006, PubMed: 29305017)
37.	Takahiro Niimura, Yoshito Zamami, Toru Imai, Tsuyoshi Ito, Hidenori Sagara, Hichiya Hiroyuki, Satoru Esumi, Kenshi Takechi, Masaki Imanishi, Toshihiro Koyama, Manabu Amano, Naomi Kurata, Yoshihisa Kitamura, Hironori Nakura, Toshiaki Sendo and Keisuke Ishizawa : Administration of Kampo medicine through a tube at an advanced critical care center., The Journal of Medical Investigation : JMI, Vol.65, No.1.2, 32-36, 2018. (Summary) n emergency and critical care medical centers, tube administration is employed for patients who have difficulty swallowing oral drugs owing to decreased consciousness or mechanical ventilation. However, tube clogging due to drug injection is a concern. We compared the crushing method with the simple suspension method for the passage of amlodipine, an antihypertensive drug, in combination with rikkunshito, which has been used to treat upper gastrointestinal disorders such as functional dyspepsia and gastroesophageal reflux in emergency and critical care medical centers, to ascertain the effect of Kampo products on the passage of other drugs during tube administration. When the crushing method was employed, poorly water-soluble solid products were formed, while a uniformly dispersed suspension was obtained using the simple suspension method. In addition, the passage rate of amlodipine through the tube was 64% and 93% in the crushing and simple suspension methods, respectively, thereby indicating that the simple suspension method provided more favorable than the crushing method. The results of this study suggested that the passage rate of amlodipine for patients who received Kampo products concurrently was higher when the simple suspension method was used, and an appropriate drug amount might well be able to administered to patients using this method. J. Med. Invest. 65:32-36, February, 2018. (Tokushima University Institutional Repository) ● Metadata: 111388 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.32 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29593190 ● Search Scopus @ Elsevier (PMID): 29593190 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.32 (Tokushima University Institutional Repository: 111388, DOI: 10.2152/jmi.65.32, PubMed: 29593190)
38.	Takahiro Niimura, Yoshito Zamami, Toru Imai, Kanako Nagao, Masafumi Kayano, Hidenori Sagara, Mitsuhiro Goda, Naoto Okada, Masayuki Chuma, Kenshi Takechi, Masaki Imanishi, Toshihiro Koyama, Tadashi Koga, Hironori Nakura, Toshiaki Sendo and Keisuke Ishizawa : Evaluation of the Benefits of De-Escalation for Patients with Sepsis in the Emergency Intensive Care Unit., Journal of Pharmacy & Pharmaceutical Sciences, Vol.21, No.1, 54-59, 2018. (Summary) The length of hospital stay after diagnosis was significantly shorter for the de-escalation group than for the non-de-escalation group. In the subgroup analysis, de-escalation for blood culture-positive patients was beneficial in terms of the length of hospital stay and length of antibiotic administration. (Link to Publication Site) ● Publication site (DOI): 10.18433/jpps29737 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29455711 ● Summary page in Scopus @ Elsevier: 2-s2.0-85044119660 (DOI: 10.18433/jpps29737, PubMed: 29455711, Elsevier: Scopus)
39.	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)
40.	Nishimura Yoshiro, Ueki Masaaki, Masaki Imanishi, Shuhei Tomita, Ueno Masaki, Morishita Jun and Nishiyama Takashi : Reoxygenation With 100% Oxygen Following Hypoxia in Mice Causes Apoptosis, Shock, Vol.48, No.5, 590-594, 2017. (Summary) After hypoxia, reoxygenation with air is the consensus treatment for full-term neonates; however, the effect of hyperoxic reoxygenation of adults is unknown. The present study was designed to investigate the effects of reoxygenation with 100% oxygen after hypoxia on inflammation and apoptosis in mice. Eight-week-old mice were either subjected to hypoxia in 8% oxygen for 30 min or air served as controls. Following hypoxia, mice underwent reoxygenation for 30 min with 21% or 100% oxygen. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), caspase-3 and brain derived neurotrophic factor (BDNF) mRNA study and histopathological study were performed. Reoxygenation with 100% oxygen significantly increased TNF-α (2.5 h after hypoxia), IL-1β (5 h after hypoxia), caspase-3 (8 h after hypoxia) mRNA levels in the whole brain compared with 21% oxygen, and significantly decreased erythropoietin mRNA expression compared with 21% oxygen 9 h after reoxygenation. However, reoxygenation with 100% oxygen and 21% oxygen significantly decreased BDNF mRNA levels compared with control air group. There were no clear abnormal findings showing neuronal death among the three groups. Reoxygenation with 100% oxygen after hypoxia induced inflammation and apoptosis in adult mice. Therefore, these results suggest that the reoxygenation with 100% oxygen after hypoxia has harmful effects on adult brain as well as on neonatal brain. (Keyword) Animals / apoptosis / Brain-Derived Neurotrophic Factor / Caspase 3 / Erythropoietin / Hypoxia / Interleukin-1 / Male / Mice / Mice, Inbred C57BL / Oxygen / RNA, Messenger / Tumor Necrosis Factor-alpha (Link to Publication Site) ● Publication site (DOI): 10.1097/SHK.0000000000000891 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28472013 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030762981 (DOI: 10.1097/SHK.0000000000000891, PubMed: 28472013, Elsevier: Scopus)
41.	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)
42.	Ken Konaka, Kota Moriyama, Takumi Sakurada, Naoto Okada, Masaki Imanishi, Yoshito Zamami, Kazuyoshi Kawazoe, Shuji Fushitani and Keisuke Ishizawa : Kamishoyosan and Shakuyakukanzoto promote recovery from paclitaxel-induced neurite retraction in PC12 cells, Journal of Pharmaceutical Health Care and Sciences, Vol.3, 20, 2017. (Summary) In chemotherapy, the full round of treatment must be completed as scheduled to achieve the strongest therapeutic effect. However, peripheral neuropathy, a severe side effect of the chemotherapeutic agent paclitaxel, can force the premature discontinuation of treatment. As some kampo practitioners have suggested that it may be possible to counteract such side effects, we analyzed the effects of Kamishoyosan, Shakuyakukanzoto, and Goshajinkigan in an in vitro model of paclitaxel-induced peripheral neuropathy. Paclitaxel-treated PC12 cells were assessed for neurite length and performed Western blot analysis for growth-associated protein-43 (GAP-43) and light neurofilament protein (NF-L) levels in the presence of nerve growth factor (NGF); they were re-assessed, with additional testing for acetylcholinesterase levels, after application of one of the kampo. We also compared phosphorylation of extracellular signal-regulated kinase (Erk)1/2 and Akt via Western blot analysis. About effect of kampo to anticancer efficacy, we confirmed cell cytotoxicity in A549 cells using MTT assay. Addition of Kamishoyosan or Shakuyakukanzoto, but not Goshajinkigan, significantly improved neurite length and GAP-43 and NF-L levels from paclitaxel-treated PC12 cells, relative to those of only NGF-treated PC12 cells. The promoting effect of Kamishoyosan and Shakuyakukanzoto in neurite outgrowth is confirmed when NGF promoted neurite outgrowth, and it was inhibited partially when Erk1/2 and Akt were blocked by Erk1/2 inhibitor or Akt inhibitor alone. Furthermore, neurite outgrowth induced by TJ24 and TJ68 was inhibited more strongly when Erk1/2 inhibitor and Akt inhibitor were treated at the same time. NGF with Kamishoyosan or Shakuyakukanzoto promoted the proportion of phosphorylated Erk1/2 and phosphorylated Akt compare with NGF only. On the other hand, Kamishoyosan or Shakuyakukanzoto didn't influence cytotoxicity of paclitaxel in A549 cells. Kamishoyosan or Shakuyakukanzoto promotes neurite outgrowth with NGF via increasing the proportion of phosphorylated Erk1/2 and phosphorylated Akt in PC12 cells. The effect applies to recovery from paclitaxel-induced axonal involvement and might promote recovery from paclitaxel-induced neuropathy without influence of anticancer effect of paclitaxel. (Tokushima University Institutional Repository) ● Metadata: 114522 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40780-017-0090-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28748102 ● Search Scopus @ Elsevier (PMID): 28748102 ● Search Scopus @ Elsevier (DOI): 10.1186/s40780-017-0090-y (Tokushima University Institutional Repository: 114522, DOI: 10.1186/s40780-017-0090-y, PubMed: 28748102)
43.	Koyama Satoshi, Matsunaga Shinji, Masaki Imanishi, Yoichi Maekawa, Kitano Hiroya, Takeuchi Hiromi and Shuhei Tomita : Tumour blood vessel normalisation by prolyl hydroxylase inhibitor repaired sensitivity to chemotherapy in a tumour mouse model, Scientific Reports, Vol.7, 45621, 2017. (Summary) Blood vessels are important tissue structures that deliver oxygen and nutrition. In tumour tissue, abnormal blood vessels, which are hyperpermeable and immature, are often formed; these tissues also have irregular vascularisation and intravasation. This situation leads to hypoperfusion in tumour tissue along with low oxygen and nutrition depletion; this is also called the tumour microenvironment and is characterised by hypoxia, depleted nutrition, low pH and high interstitial pressure. This environment induces resistance to anticancer drugs, which causes an increase in anticancer drug doses, leading to increased side effects. We hypothesised that normalised tumour blood vessels would improve tumour tissue perfusion, resupply nutrition and re-oxygenate the tumour tissue. Chemotherapy would then be more effective and cause a decrease in anticancer drug doses. Here we report a neovascularisation-inducing drug that improved tumour vascular abnormalities, such as low blood flow, blood leakage and abnormal vessel structure. These results could lead to not only an increased chemo-sensitivity and tissue-drug distribution but also an up-regulated efficiency for cancer chemotherapy. This suggests that tumour blood vessel normalisation therapy accompanied by angiogenesis may be a novel strategy for cancer therapy. (Tokushima University Institutional Repository) ● Metadata: 112382 (Link to Publication Site) ● Publication site (DOI): 10.1038/srep45621 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28361934 ● Summary page in Scopus @ Elsevier: 2-s2.0-85016642181 (Tokushima University Institutional Repository: 112382, DOI: 10.1038/srep45621, PubMed: 28361934, Elsevier: Scopus)
44.	Kenshi Takechi, Yurika Yoshioka, Hitoshi Kawazoe, Mamoru Tanaka, Shingo Takatori, Miwako Kobayashi, Ichiro Matsuoka, Hiroaki Yanagawa, Yoshito Zamami, Masaki Imanishi, Keisuke Ishizawa, Akihiro Tanaka and Hiroaki Araki : Psychiatric patients with antipsychotic drug-induced hyperprolactinemia and menstruation disorders, Biological & Pharmaceutical Bulletin, Vol.40, No.10, 1775-1778, 2017. (Summary) Treatment with antipsychotic drugs has been associated with hyperprolactinemia. The same antipsychotic drugs have also been associated with side effects such as menstruation disorders. The aim of this study was to evaluate the prevalence of hyperprolactinemia and menstruation disorders in women undergoing antipsychotic treatment. We performed a retrospective chart review study of psychiatric patients who underwent laboratory testing for serum prolactin (PRL) level between March 2011 and March 2015 in Ehime University Hospital. Patients presenting with and without menstruation disorders were evaluated to determine if they presented concomitant hyperprolactinemia. Patients with menstrual disorders had a significant increase in serum PRL level with a mean of approximately 90 ng/mL. Those with menstrual disorders presented increased PRL levels by 2-fold that of patients without menstrual disorder. However, there was no significant difference in the equivalent dose of chlorpromazine between these two groups. Additionally, about 70% of patients with menstrual disorders received risperidone treatment. The receiver operating characteristic curve showed that the optimal cutoff point of serum PRL level associated with the development of menstrual disorders was 60 ng/mL. Based on these results, we concluded that patients with menstrual disorders presented increased serum PRL, and that most of them underwent treatment with risperidone. (Keyword) Adolescent / Adult / Antipsychotic Agents / Female / Humans / Hyperprolactinemia / Menstruation Disturbances / Mental Disorders / Prolactin / Young Adult (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b17-00053 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28966250 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030761013 (DOI: 10.1248/bpb.b17-00053, PubMed: 28966250, Elsevier: Scopus)
45.	Yoshito Zamami, Toru Imai, Masaki Imanishi, Kenshi Takechi, Naoko Shiraishi, Toshihiro Koyama, Hidenori Sagara, Yasukazu Shiino, Toshiaki Sendo and Keisuke Ishizawa : Evaluation of pharmaceutical lifesaving skills training oriented pharmaceutical intervention., Journal of Pharmaceutical Health Care and Sciences, Vol.2, No.1, 21, 2016. (Summary) Our high-performance patient simulator-based lifesaving skills training program not only increased the participants' understanding of the training content but also increased their confidence in their ability to perform pharmaceutical interventions. Therefore, the pharmaceutical lifesaving skills training program we developed will contribute to the education of emergency care pharmacists who can perform pharmaceutical interventions for emergency patients. (Tokushima University Institutional Repository) ● Metadata: 114521 (Link to Publication Site) ● Publication site (DOI): 10.1186/s40780-016-0054-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27606071 ● Search Scopus @ Elsevier (PMID): 27606071 ● Search Scopus @ Elsevier (DOI): 10.1186/s40780-016-0054-7 (Tokushima University Institutional Repository: 114521, DOI: 10.1186/s40780-016-0054-7, PubMed: 27606071)
46.	Masaki Imanishi, Chiba Yoichi, Tomita Noriko, Matsunaga Shinji, Nakagawa Toshitaka, Ueno Masaki, Yamamoto Kazuhiro, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-Inducible Factor-1α in Smooth Muscle Cells Protects Against Aortic Aneurysms-Brief Report., Arteriosclerosis, Thrombosis, and Vascular Biology, Vol.36, No.11, 2158-2162, 2016. (Summary) The purpose of this study was to determine the role of smooth muscle cell-derived hypoxia-inducible factor-1α (Hif-1α) in the pathogenesis of aortic aneurysms. Control mice and smooth muscle cell-specific hypoxia-inducible factor-1α-deficient mice were infused with β-aminopropionitrile for 2 weeks and angiotensin II for 6 weeks to induce aortic aneurysm formation. Mutant mice experienced increased levels of aneurysm formation of the thoracic or abdominal aorta with more severe elastin disruption, compared with control mice. Smooth muscle cell-specific hypoxia-inducible factor-1α deficiency did not affect matrix metalloproteinase-2 activity; however, the activity of lysyl oxidase and the levels of tropoelastin mRNA in the angiotensin II- and β-aminopropionitrile-treated aortae, associated with elastin fiber formation, were suppressed. Furthermore, we observed reduced volumes of mature cross-linked elastin in the thoracoabdominal aorta after treatment with angiotensin II and β-aminopropionitrile. Deficiency of smooth muscle cell-derived hypoxia-inducible factor-1α augments aortic aneurysms, accompanied by disruption of elastin fiber formation, but not changes of elastin fiber degradation. (Keyword) Aminopropionitrile / Angiotensin II / Animals / Aorta, Abdominal / Aorta, Thoracic / Aortic Aneurysm, Abdominal / Aortic Aneurysm, Thoracic / Cells, Cultured / Dilatation, Pathologic / Disease Models, Animal / Elastic Tissue / Genetic Predisposition to Disease / Hypoxia-Inducible Factor 1, alpha Subunit / male / Mice, Knockout / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Phenotype / Protein-Lysine 6-Oxidase / Tropoelastin / Vascular Remodeling (Link to Publication Site) ● Publication site (DOI): 10.1161/ATVBAHA.116.307784 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27562915 ● Summary page in Scopus @ Elsevier: 2-s2.0-84983748456 (DOI: 10.1161/ATVBAHA.116.307784, PubMed: 27562915, Elsevier: Scopus)
47.	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)
48.	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)
49.	Atsushi Morimoto, Shuhei Tomita, Masaki Imanishi, Go Shioi, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Mitsuru Takaku, Ichiro Hashimoto, Yasumasa Ikeda, Hideki Nakanishi and Toshiaki Tamaki : Overexpressed HIF-2α in Endothelial Cells Promotes Vascularization and Improves Random Pattern Skin Flap Survival., Plastic and Reconstructive Surgery. Global Open, Vol.2, No.4, e132, 2014. (Summary) Specific overexpression of HIF-2 in ECs promoted vascularization and enhanced skin flap survival in vivo in a mouse model. (Tokushima University Institutional Repository) ● Metadata: 106138 (Link to Publication Site) ● Publication site (DOI): 10.1097/GOX.0000000000000083 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25289325 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897362750 (Tokushima University Institutional Repository: 106138, DOI: 10.1097/GOX.0000000000000083, PubMed: 25289325, Elsevier: Scopus)
50.	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)
51.	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)
52.	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)
53.	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)

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.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi and Keisuke Ishizawa : Pharmacological approach for drug repositioning against cardiorenal diseases., The Journal of Medical Investigation : JMI, Vol.64, No.3.4, 197-201, 2017. (Summary) New applications of approved clinically used drugs are being discovered. Drug repositioning is a proposed strategy for developing these drugs as therapeutic agents for different diseases. Currently, approximately 2000 drugs are used in Japan. However, the compound targets and pathways involved in the pharmacological actions of 70-80% of these drugs have not been adequately clarified. Pharmacological examination of approved drugs is an important task in drug repositioning and vital for improving drug development efficiency. This review reports that angiotensin II type 1 receptor blockers show receptor-independent effects against reactive oxygen species generation in renal cells. Additionally, nitrosonifedipine has an antioxidative effect and protects endothelial cells against oxidative stress, and pioglitazone has multiple effects that improve dysfunctions in vascular control regulated by adrenergic and calcitonin gene-related peptide-containing nerves in animal models of diabetes. These data suggest that some approved drugs could be useful for treating cardiorenal diseases. Since cardiorenal diseases are likely to have chronic pathological conditions and require chronic drug administration, highly safe drugs are needed. Compared to newly developed drugs, drug repositioning of approved drugs with safety information is considered a particularly useful technique for searching new treatments for cardiorenal diseases. J. Med. Invest. 64: 197-201, August, 2017. (Tokushima University Institutional Repository) ● Metadata: 111115 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.197 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954981 ● Search Scopus @ Elsevier (PMID): 28954981 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.197 (Tokushima University Institutional Repository: 111115, DOI: 10.2152/jmi.64.197, PubMed: 28954981)
3.	Masaki Imanishi and Shuhei Tomita : 血管リモデリング形成における低酸素誘導因子の機能解析, Japanese Journal of Circulation Research, Vol.39, No.4, 127-132, 2017.
4.	Yoshito Zamami, Takahiro Niimura, Kenshi Takechi, Masaki Imanishi, T Koyama and Keisuke Ishizawa : Drug repositioning research to improve the survival rate after cardiopulmonary arrest - utilizing large scale Medical Claims Database -, Journal of the Pharmaceutical Society of Japan, Vol.137, No.12, 1439-1442, 2017. (Summary) Approximately 100000 people suffer cardiopulmonary arrest in Japan every year, and the aging of society means that this number is expected to increase. Worldwide, approximately 100 million develop cardiac arrest annually, making it an international issue. Although survival has improved thanks to advances in cardiopulmonary resuscitation, there is a high rate of postresuscitation encephalopathy after the return of spontaneous circulation, and the proportion of patients who can return to normal life is extremely low. Treatment for postresuscitation encephalopathy is long term, and if sequelae persist then nursing care is required, causing immeasurable economic burdens as a result of ballooning medical costs. As at present there is no drug treatment to improve postresuscitation encephalopathy as a complication of cardiopulmonary arrest, the development of novel drug treatments is desirable. In recent years, new efficacy for existing drugs used in the clinical setting has been discovered, and drug repositioning has been proposed as a strategy for developing those drugs as therapeutic agents for different diseases. This review describes a large-scale database study carried out following a discovery strategy for drug repositioning with the objective of improving survival rates after cardiopulmonary arrest and discusses future repositioning prospects. (Keyword) Databases, Factual / Drug Repositioning / Heart Arrest / Humans / Hypoxia-Ischemia, Brain / Japan / Research Design / Survival Rate (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.17-00139-3 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29199254 ● Summary page in Scopus @ Elsevier: 2-s2.0-85037339843 (DOI: 10.1248/yakushi.17-00139-3, PubMed: 29199254, Elsevier: Scopus)
5.	Masaki Imanishi : 間葉内皮転換が心臓の血管新生に関与する, Farumashia, Vol.51, No.7, 2015.
6.	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)
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.	Shuhei Tomita, Masaki Imanishi, Takumi Sakurada, Noriko Yamano, Yoshitaka Kihira, Yasumasa Ikeda and Toshiaki Tamaki : Role of Hypoxia-Inducible Factor1a (HIF-1a) in T cells in development of vascular remodeling, Shikoku Acta Medica, Vol.67, No.1, 2, 3-6, Apr. 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 factor1(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) vascular remodeling / hypoxia / hypoxia-inducible factor (Tokushima University Institutional Repository) ● Metadata: 110344 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050865122807543808 (Tokushima University Institutional Repository: 110344, CiNii: 1050865122807543808)

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.	Nguyen TH Minh, Masaki Imanishi, Li Shengyu, Ko Ae Kyung, Banerjee Priyanka, Velatooru reddy Loka, McBeath Elena, Fujiwara Keigi, Kotla Sivareddy, Chau Khanh, Abe J. Rei, Borchrdt K. Mae, Yeh T.H. Edward, Cooke P. John, Wang Guangyu, Abe Jun-ichi and Le Nhat-Tu : Checkpoint Kinase 1-associated SENP2 S344 phosphorylation under laminar flow attenuates Endothelial-Mesenchymal Transition and atherogenesis, AHA Scientific Sessions 2022, Nov. 2022.
3.	Li Shengyu, Kotla Sivareddy, Masaki Imanishi, Ko Ae Kyung, Samanthapudi K Venkatasubrahman, Savage Hannah, Schadler L. Keri, Deswal Anita, Lin H. Steven, Reyes-Gibby Cielito, Yeung J. Sai-ching, Pownall J. Henry, Fujiwara Keigi, Le Nhat-Tu, Wang Guangyu and Abe Jun-ichi : Differentially expressed genes mediated by ERK5 S496 phosphorylation in hypercholesterolemia-induced macrophage reprogramming, VASCULAR DISCOVERY: From Genes to Medicine Scientific Sessions 2022, May 2022.
4.	Kotla Sivareddy, Masaki Imanishi, Zhang Aijun, Ko Ae Kyung, Samanthapudi K Venkatasubrahman, Savage Hannah, Schadler L. Keri, Abe J. Rei, Gupte A. Anisha, Deswal Anita, Lin H. Steven, Reyes-Gibby Cielito, Yeung J. Sai-ching, Pownall J. Henry, Fujiwara Keigi, Hamilton J. Dale, Li Shengyu, Wang Guangyu, Le Nhat-Tu and Abe Jun-ichi : ERK5 S496 phosphorylation, but not ERK5 kinase or transcriptional activity, is responsible for promoting macrophage inflammation and mitochondrial dysfunction via upregulating novel site of NRF2 K518 SUMOylation, VASCULAR DISCOVERY: From Genes to Medicine Scientific Sessions 2022, May 2022.
5.	Masaki Imanishi, Cheng Haizi, Kotla Sivareddy, Lin H. Steven, Deswal Anita, Ko Ae Kyung, Samanthapudi K Venkatasubrahman, Le Nhat-Tu, Fujiwara Keigi, Liao Zhongxing, Palaskas L. Nicolas, Yusuf Wamique Syed, Nurieva Roza, Reyes-Gibby Cielito, Yeung J. Sai-ching, Gomez-Cabrero Azucena, Amir David El-ad, Burks K. Jared, Kobayashi Michihiro, Yoshimoto Momoko and Abe Jun-ichi : Multiparameter mass cytometry reveals the unique response of naïve B cell CD27 subset with the increase of T-bet and CD38 expression after radiation therapy in thoracic cancer patients, VASCULAR DISCOVERY: From Genes to Medicine Scientific Sessions 2022, May 2022.
6.	Ko ae Kyung, Abe Jun-ichi, Kotla Sivareddy, GI JIN YOUNG, Masaki Imanishi and Fujiwara Keigi : Novel Model Of Ionizing Radiation-induced Mouse Coronary Arteriosclerosis, Which Was Attenuated By Precise Time Treatment Of Poly (adp-ribose) Polymerase (parp) Inhibitor, VASCULAR DISCOVERY: From Genes to Medicine Scientific Sessions 2021, Sep. 2021.
7.	Masaki Imanishi, Velatooru Loka, Ko ae Kyung, Heo Kyung-Sun, Thomas Tamlyn, GI JIN YOUNG, Fujiwara Keigi, Le T Nhat, Kotla Sivareddy and Abe Junichi : The Roles Of Telomeric Repeat Binding Factor 2-interacting Protein (TERF2IP) K240 Sumoylation In Endothelial Cells On Atherogenesis, VASCULAR DISCOVERY: From Genes to Medicine Scientific Sessions 2021, Sep. 2021.
8.	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.
9.	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.
10.	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.
11.	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.
12.	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.
13.	Yoshito Zamami, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Toshiaki Tamaki and Keisuke Ishizawa : Search for drugs that attenuate the anti tumor effect of bevacizumab using adverse event database, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.
14.	Ishida Shunsuke, Bando Hiroshi, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, Krino Yashishi, Nakamura Toshimi, Teraoka Kazuhiko and Keisuke Ishizawa : Development and clinical application of management tool to monitor side effects for atypical antipsychotics, ASHPMidyear2017Clinical Meeting&Exhibition, フロリダ, Dec. 2017.
15.	Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, Hiroaki Yanagawa and Keisuke Ishizawa : Psychiatric patients with antipsychotic drug-induced hyperprolactinemia and menstruation disorders, ASHPMidyear2017Clinical Meeting&Exhibition, フロリダ, Dec. 2017.
16.	Yoshito Zamami, Takahiro Niimura, Yuki Izawa-Ishizawa, Kenshi Takechi, Masaki Imanishi, Krino Yashishi, Nakamura Toshimi, Teraoka Kazuhiko and Keisuke Ishizawa : Drug repositioning research aimed at improving the survival rate of patients with cardiopulmonary arrest using large-scale medical claims database, ASHPMidyear2017Clinical Meeting&Exhibition, Dec. 2017.
17.	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)
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	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.
24.	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.
25.	Masaki Imanishi, 井口道代, 冨田紀子, Tsounapi Panagiota, 松永慎司, Toshiaki Tamaki and Shuhei Tomita : 平滑筋由来HIF-1αは薬剤誘導性大動脈瘤形成に対して保護的に作用する, 第1回国際心血管薬物療法学会日本部会, 2015.
26.	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.
27.	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.
28.	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.
29.	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.
30.	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.
31.	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.
32.	Masaki Imanishi : The effects of angiotensin II on free radical generation in vascular smooth muscle cells: Immuno-spin-trapping investigation, 20th JSPS Core-to-Core Seminar: International Redox Core Symposium, 2012.
33.	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.
34.	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.
35.	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.
36.	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.
37.	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.
38.	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.
39.	Yayoi Fukuhara, Shuhei Tomita, Yuko Imamura, Yuya Horinouchi, Masaki Imanishi, Takumi Sakurada, Tetsuya Kitagawa and Toshiaki Tamaki : Role of HIF-1b in endothelial cells in monocrotaline-induced pulmonary hypertension in mice, 16th World Congress on Basic and Clinical Pharmacology, Jul. 2010.
40.	Junko Sugatani, Makoto Osabe, Satoshi Sadamitsu, Masaki Imanishi, Yasuhiro Yamazaki, Akira Ikari and Masao Miwa : Comparison of enzymatically synthesized inulin, clofibrate and fluvastatin effects on biomarkers of metabolic disease and drug metabolism in rats fed standard and cafeteria diets, 1st International conference on health and longevity sciences, Yaku-shoku Dogen, Medicine and food, sharing a common origin, University of Shizuoka, Shizuoka, 2008.

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.	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.
4.	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.
5.	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.
6.	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.
7.	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.
8.	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.
9.	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.
10.	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.
11.	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.
12.	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.
13.	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.
14.	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.
15.	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.
16.	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.
17.	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.
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	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.
29.	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.
30.	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.
31.	Masaki Imanishi, Ko Ae Kyung, Le Nhat-Tu, Kotla Sivareddy, Fujiwara Keigi, Amir David El-ad, Burks K. Jared and Abe Jun-ichi : Multiparameter mass cytometry reveals radiation therapy-induced clonal hematopoiesis driver genes-related profiling subset changes in cancer patient peripheral blood lymphocytes, 第51回心脈管作動物質学会, Jul. 2022.
32.	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.
33.	Yuki Izawa-Ishizawa, Yoshito Zamami, Niimura Takahiro, Mitsuhiro Goda, Kenta Yagi, Masayuki Chuma, Masaki Imanishi and Keisuke Ishizawa : New strategy for Cardio-Oncology study; the combination of big data analysis and basic research, 第79回日本癌学会学術集会シンポジウム8, Oct. 2020.
34.	鈴木琴子, Yuki Izawa-Ishizawa, Mitsuhiro Goda, 近藤正輝, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : ケルセチンによる薬剤誘発性急性大動脈疾患発症抑制効果の検討, 第58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. 2019.
35.	Kotoko Suzuki, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Masateru Kondoh, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬剤誘発性急性大動脈疾患に対するケルセチンの効果, 第135回日本薬理学会近畿部会, Jun. 2019.
36.	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.
37.	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.
38.	鈴木琴子, Yuki Izawa-Ishizawa, Masateru Kondoh, Masaki Imanishi, Yoshito Zamami, Yuya Horinouchi, Kenshi Takechi, Mitsuhiro Goda, Masayuki Chuma, Yasumasa Ikeda and Keisuke Ishizawa : 薬物誘発性大動脈瘤または大動脈解離モデルマウスに対するケルセチンの効果, 第92回日本薬理学会年会, Mar. 2019.
39.	新村貴博, Yoshito Zamami, 川尻雄大, Mitsuhiro Goda, Naoto Okada, 萱野純史, 小山敏広, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, 小林大介, 島添隆雄 and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたオキサリプラチン誘発末梢神経障害の予防薬探索, 第92回日本薬理学会年会学生セッション, Mar. 2019.
40.	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.
41.	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.
42.	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.
43.	Yoshito Zamami, Yuki Izawa-Ishizawa, 新村貴博, Masaki Imanishi, Kenshi Takechi, Masayuki Chuma, Yuya Horinouchi, Yasumasa Ikeda, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 救急・集中治療領域において大規模医療情報データベースを活用したトランスレーショナルリサーチ, 第29回霧島神経薬理フォーラム, Nov. 2018.
44.	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.
45.	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.
46.	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.
47.	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.
48.	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.
49.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yusuke Iwata, Kotoko Suzuki, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : 第40回徳島医学会賞受賞講演動脈硬化性疾患発症に対するケルセチンの効果, 第257回徳島医学会学術集会(平成30年度夏季), Aug. 2018.
50.	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.
51.	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.
52.	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.
53.	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.
54.	櫻田巧, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 腎機能がペメトレキセド治療における安全性に影響を与えるか, 日本臨床腫瘍薬学会学術大会2018, Mar. 2018.
55.	Yoshito Zamami, Marin Mitsui, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, 桐野靖, 中村敏己, 寺岡和彦 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, 日本臨床腫瘍薬学会学術大会2018, Mar. 2018.
56.	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.
57.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yusuke Iwata, Yuya Horinouchi, Kenshi Takechi, Yoshito Zamami, Yasumasa Ikeda, Keisuke Ishizawa and Toshiaki Tamaki : マウス大動脈瘤形成に対するケルセチンの効果, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
58.	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.
59.	Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, Yuya Horinouchi, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki, Keisuke Ishizawa and Hiroaki Yanagawa : てんかん誘発性精神症状の行動学的解析および治療薬の探索と作用機序の解明, 第256回徳島医学会学術集会(平成29年度冬期), Feb. 2018.
60.	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.
61.	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.
62.	Yoshito Zamami, 近藤正輝, 阿部奈都美, Masayuki Chuma, 今井徹, Kenshi Takechi, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 集中治療における薬剤師教育, 第45回日本集中治療医学会学術集会委員会企画4(CP4)「集中治療における薬剤師のポジションを考える」, Feb. 2018.
63.	石田俊介, 坂東寛, Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 副作用モニタリング管理ツールの開発と業務効率化, 平成29年度大学病院情報マネジメント部門連絡会議, Feb. 2018.
64.	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.
65.	Sakiko Hino, Yoshito Zamami, Yuki Izawa-Ishizawa, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : 大規模医療情報を活用した薬剤性腎障害に対する予防薬の探索, 西日本医学生学術フォーラム2017, Dec. 2017.
66.	Yuki Izawa-Ishizawa, Yu Kagimoto, Masaki Imanishi, Yuya Horinouchi, Kotoko Suzuki, Yusuke Iwata, Yoshito Zamami, Kenshi Takechi, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : ケルセチンによる動脈硬化性疾患発症に対する予防効果の検討, 第27回日本循環薬理学会, Dec. 2017.
67.	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.
68.	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.
69.	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.
70.	石田俊介, 坂東寛, Kenshi Takechi, Yoshito Zamami, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : 抗精神病薬を対象とする副作用モニタリング管理ツールの開発と臨床評価, 第27回日本医療薬学会年会, Nov. 2017.
71.	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.
72.	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.
73.	濱野裕章, 三井茉綸, Yoshito Zamami, Takahiro Niimura, Kenshi Takechi, 岡田直人, Masaki Imanishi, 桐野靖, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : アルカリ化剤はイリノテカン誘発性好中球減少症を予防する, 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.
74.	岡田直人, 東桃代, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦, 安倍正博 and Keisuke Ishizawa : リポソーム化アムホテリシンB製剤による低カリウム血症の発現関連因子の同定, 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.
75.	柴田高洋, Masaki Imanishi, Yoshito Zamami, 中村敏己, 寺岡和彦 and Keisuke Ishizawa : PCR法によるSCCmec タイピングを利用した動向調査から探る来院者とMRSAの院内伝播の関連性, 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.
76.	合田光寛, 高橋沙矢佳, 長田武, Masaki Imanishi, Kenshi Takechi, Yoshito Zamami, 桐野靖, 中村敏己, 寺岡和彦, 大塚正人 and Keisuke Ishizawa : シスプラチン誘発腎障害に対するSGLT2阻害薬の影響, 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.
77.	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.
78.	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.
79.	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.
80.	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.
81.	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.
82.	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.
83.	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.
84.	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.
85.	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.
86.	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.
87.	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.
88.	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.
89.	坂東寛, 石田俊介, Kenshi Takechi, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 薬剤師がマネジメントする非定型抗精神病薬における副作用モニタリングの効果, 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.
90.	石田俊介, Masaki Imanishi, Yoshito Zamami, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 医薬品管理モニタリングツールを活用した周術期における医薬品管理業務の効率化, 第20回日本医薬品情報学会総会・学術大会, Jul. 2017.
91.	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.
92.	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.
93.	中本亜樹, 岡田直人, 濱野裕章, Sonoko Yasui, 西麻希, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka, Yasuhiro Hamada and Keisuke Ishizawa : 頭頸部癌に対する化学放射線療法における CDDP 単独療法及び 52FU+CDDP 療法による副作用発現の比較, 第11回日本緩和医療薬学会年会, Jun. 2017.
94.	坂東左奈子, 櫻田巧, Naoto Okada, Masaki Imanishi, Yoshito Zamami, Kazuhiko Teraoka, 中村敏己 and Keisuke Ishizawa : エピルビシン，シクロフォスファミド投与による持続型G-CSF製剤の有効性の検討, 第42回日本外科系連合学会学術集会, Jun. 2017.
95.	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.
96.	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.
97.	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.
98.	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.
99.	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.
100.	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.
101.	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.
102.	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.
103.	Yoshito Zamami, 近藤正輝, 阿部奈都美, Masaki Imanishi, Kenshi Takechi, 桐野靖, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 薬剤師と考える感染症治療抗MRSA薬による抗菌薬治療, Journal of the Japanese Society of Intensive Care Medicine, Vol.24, No.Suppl., SS4-1, Feb. 2017.
104.	Masaki Imanishi, 松永慎司, Keisuke Ishizawa, Toshiaki Tamaki and Shuhei Tomita : 大動脈瘤形成における平滑筋由来HIF-1αの役割, 第26回日本循環薬理学会, Dec. 2016.
105.	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.
106.	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.
107.	中本亜樹, 野裕章, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : DPP-4阻害薬ーDPP-4阻害薬間の切り替えによるLDL-Cの変動, 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.
108.	木宿昌俊, Masaki Imanishi, 中村敏己, Kazuhiko Teraoka, Keisuke Ishizawa and 中村敏己 : 消化器外科病棟における専任薬剤師のチーム医療参画に対する評価, 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.
109.	井上貴久, 柴田高洋, 櫻田巧, Naoto Okada, Yoshito Zamami, Masaki Imanishi, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 抗EGFR抗体薬の使用における低Mg血症の発現率の比較検討, 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.
110.	坂東左奈子, Naoto Okada, 櫻田巧, Masaki Imanishi, Yoshito Zamami, Kazuhiko Teraoka, 中村敏己 and Keisuke Ishizawa : 乳がん患者におけるエピルビシン，シクロフォスファミド投薬による持続型G-CSF製剤の有効性の検討, 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.
111.	桑原絵美, Naoto Okada, 高瀬友佳子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 徳島大学病院におけるニボルマブの適正使用に向けた取り組み, 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.
112.	石田俊介, 坂東寛, 坂本久美子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 抗精神病薬を対象にした臨床検査値を指標とする副作用モニタリング管理ツール導入による効果, 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.
113.	櫻田巧, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ペメトレキセドによる骨髄抑制のリスク因子解析, 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.
114.	三井茉綸, Yoshito Zamami, Masaki Imanishi, Kenshi Takechi and Keisuke Ishizawa : オーストラリアのがん病棟における薬剤師業務に対する患者満足度調査, 第26回日本医療薬学会年会, Sep. 2016.
115.	小中健, 櫻田巧, Masaki Imanishi, Yoshito Zamami, Keisuke Ishizawa and 伏谷秀治 : 肺がん患者におけるUGT1A1 遺伝子多型とイリノテカンの投与量に関する検討, 第26回日本医療薬学会年会, Sep. 2016.
116.	濱野裕章, 中本亜樹, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : GEM + nabPTX 療法における高ビリルビン血症が副作用発現に与える影響, 第26回日本医療薬学会年会, Sep. 2016.
117.	中本亜樹, 濱野裕章, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : DPP-4 阻害薬服用患者における他のDPP-4 阻害薬への切り替えによるLDL-C 低下作用の検討, 第26回日本医療薬学会年会, Sep. 2016.
118.	桑原絵美, Naoto Okada, 高瀬友佳子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 徳島大学病院におけるニボルマブの使用状況と今後の有害事象対策, 第26回日本医療薬学会年会, Sep. 2016.
119.	櫻田巧, Naoto Okada, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : ペメトレキセド投与後の皮疹出現は好中球減少症のリスク因子となる, 第26回日本医療薬学会年会, Sep. 2016.
120.	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.
121.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, 小山敏広, 大島礼子, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : 症例データベースを活用して新規心肺蘇生薬の開発を目指したドラッグリポジショニング研究, 第2回日本医薬品安全性学会学術大会( 岐阜), Jul. 2016.
122.	Masaki Imanishi, Yuki Izawa-Ishizawa, Yoshito Zamami, 田淵正樹, Toshiaki Tamaki and Keisuke Ishizawa : 脳卒中後の神経症状増悪に対するニトロソニフェジピンの効果, 第46回日本神経精神薬理学会年会( ソウル), Jul. 2016.
123.	柴田高洋, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 外来診療棟を主としたMRSAの実態調査, 医療薬学フォーラム2016/第24回クリニカルファーマシーシンポジウム (大津), Jun. 2016.
124.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, 小山敏広, 大島礼子, 今井徹, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : ドラッグリポジショニングを切り口とした新規心肺蘇生薬の探索研究-大規模医療情報を活用した検討-, 医療薬学フォーラム2016/第24回クリニカルファーマシーシンポジウム (大津 ), Jun. 2016.
125.	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.
126.	石田俊介, 坂本久美子, Masaki Imanishi, Yoshito Zamami, 中村敏己, Kazuhiko Teraoka and Keisuke Ishizawa : 持参薬管理業務における周術期中止医薬品の管理ツール導入による効果, 第19回日本医薬品情報学会総会・学術大会 (町田市), Jun. 2016.
127.	Yoshito Zamami, Masaki Imanishi, 小山敏広, 大島礼子, 樋之津史郎, 狩野光伸 and Keisuke Ishizawa : 心肺停止患者における社会復帰率の向上を志向したドラッグリポジショニング研究, 日本薬学会第136年会シンポジスト( 横浜 ), Mar. 2016.
128.	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.
129.	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.
130.	小中健, 花房剛志, 田中恭平, Naoto Okada, Masaki Imanishi, Yoshito Zamami, Kazuyoshi Kawazoe and Keisuke Ishizawa : パクリタキセル誘発性神経障害に対する漢方製剤抽出物の影響, 日本薬学会第136 年会( 横浜), Mar. 2016.
131.	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.
132.	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.
133.	Masaki Imanishi, 井口道代, 冨田紀子, 松永慎司, Toshiaki Tamaki and Shuhei Tomita : Hypoxia-inducible factor-1 in smooth muscle cells protects against aortic aneurysm formation via elastin-fiber formation, 第89回日本薬理学会年会(神奈川), Mar. 2016.
134.	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.
135.	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.
136.	Masaki Imanishi, 井口道代, 冨田紀子, 松永慎司, Toshiaki Tamaki and Shuhei Tomita : 平滑筋由来HIF-1 αによる弾性繊維構築を介した大動脈瘤形成抑制メカニズムの検討, 第45回日本心脈管作動物質学会, Feb. 2016.
137.	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.
138.	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.
139.	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.
140.	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.
141.	Masaki Imanishi, 井口道代, 冨田紀子, Tsounapi Panagiota, 松永慎司, Toshiaki Tamaki and Shuhei Tomita : 血管リモデリングにおける平滑筋由来HIF-1αの作用, 第12回がんとハイポキシア研究会, Nov. 2014.
142.	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.
143.	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.
144.	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.
145.	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.
146.	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.
147.	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.
148.	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.
149.	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.
150.	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.
151.	Shuhei Tomita, Yoshitaka Kihira, Yayoi Fukuhara, 桜田巧, Masaki Imanishi and Toshiaki Tamaki : 病態に観られる低酸素応答の意義-血管リモデリングにおけるT細胞のHIF-1の役割-, 第83回日本薬理学会年会シンポジウム「病態における低酸素応答機構の解明と治療への応用」, Mar. 2010.

Et cetera, Workshop:

1.	Yoshito Zamami, Masaki Imanishi, Kenshi Takechi, Yuya Horinouchi, Licht Miyamoto, Yuki Izawa-Ishizawa, Yasumasa Ikeda, Toshiaki Tamaki and Keisuke Ishizawa : ドラッグリポジショニング手法を用いた新規循環器治療薬の探索研究, 第23回大阪市大フォーラム, Aug. 2016.

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 )
PARP阻害薬の血行性がん転移予防への適応拡大を志向した基盤研究 (Project/Area Number: 22K20711 )
Antioxidant activity of nitrite and its physiological significance. (Project/Area Number: 22K06645 )
大動脈周囲線維芽細胞を標的とした弾性線維構築促進による大動脈瘤薬物治療戦略の開発 (Project/Area Number: 18K14920 )
Development of a treatment for post-cardiopulmonary resuscitation encephalopathy utilizing existing approved drugs using large-scale medical claims database (Project/Area Number: 18K06785 )
Elucidation of pathophysiology of aortic dissection and development of the preventive strategies by medical big data and novel model mice (Project/Area Number: 18K06686 )
Investigation of the mechanisms of kidney ischemia-reperfusion injury via reactive oxygen species production (Project/Area Number: 16K18884 )
Clarification of ERK5-mediated endothelial mesenchymal transition suppression mechanism and its application to the prevention of arteriosclerosis (Project/Area Number: 16K08549 )
Search by Researcher Number (00734344)

Assistant Professor : Imanishi, Masaki

Research

Personal Web Page

Field of Study

Subject of Study

Book / Paper

Book:

Academic Paper (Judged Full Paper):

Review, Commentary:

Proceeding of International Conference:

Proceeding of Domestic Conference:

Et cetera, Workshop:

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