Tokushima University / Educator and Researcher Directory --- Fukushima, Keijo

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Academic Paper (Judged Full Paper):

1.	Haruka Okabayashi, Miki Yasuda, Chinatsu Nii, Ryo Sugishita, Keijo Fukushima, Kouki Yuasa, Satoshi Kotoura and Hiromichi Fujino : Phosphatidylcholine-Plasmalogen-Oleic Acid Reduces BACE1 Expression in Human SH-SY5Y Cells., Biological & Pharmaceutical Bulletin, Vol.47, No.1, 192-195, 2024. (Summary) Plasmalogens are a family of glycerophospholipids containing one vinyl-ether bond at the sn-1 position in the glycerol backbone, and play important roles in cellular homeostasis including neural transmission. Therefore, reductions of plasmalogens have been associated with neurodegenerative disorders, such as Alzheimer's disease (AD). To evaluate the potential protective effects of plasmalogens against the pathology of AD, protein expression levels of key factors in amyloid precursor protein (APP) metabolic processes were examined using human neuroblastoma SH-SY5Y cells. Here, phosphatidylcholine-plasmalogen-oleic acid (PC-PLS-18) was shown to reduce protein expression levels of β-site APP cleaving enzyme 1 (BACE1), clusterin, and Tau, factors involved in the amyloid β-associated pathogenesis of AD. Thus, PC-PLS-18 may have preventive effects against AD by delaying the onset risk for a certain period. (Keyword) Humans / Amyloid beta-Peptides / Amyloid Precursor Protein Secretases / Plasmalogens / Aspartic Acid Endopeptidases / Oleic Acid / Phosphatidylcholines / Neuroblastoma / Alzheimer Disease / Amyloid beta-Protein Precursor (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b23-00787 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38233149 ● Search Scopus @ Elsevier (PMID): 38233149 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b23-00787 (DOI: 10.1248/bpb.b23-00787, PubMed: 38233149)
2.	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): 1050018428980929664 ● 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: 1050018428980929664)
3.	Ayaka Hamaguchi, Hayato Fukuda, Koichi Fujiwara, Tomofumi Harada, Keijo Fukushima, Satoshi Shuto and Hiromichi Fujino : Individual resolvin E family members work distinctly and in a coordinated manner in the resolution of inflammation., Prostaglandins & Other Lipid Mediators, Vol.168, 106759, 2023. (Summary) Three main E-type resolvins (RvEs): RvE1, RvE2, and RvE3, have roles in the resolution of inflammation as anti-inflammatory activities. To investigate the roles of each RvE in the resolution of inflammation, timing of interleukin (IL)- 10 release and IL-10 receptor expressions, and phagocytosis evoked by each RvE in differentiated human monocytes, macrophage-like U937 cells were examined. Here, we show that RvEs enhance the expression of IL-10, and IL-10 receptor-mediated signaling pathways and IL-10-mediated-signaling-independent resolution of inflammatory effects by activating the phagocytotic function. Thus, RvE2 mainly evoked an IL-10-mediated anti-inflammatory function, whereas RvE3 principally activated phagocytotic activity of macrophages, which may be involved in tissue repair. On the other hand, RvE1 showed both functions, although not prominent but rather acting as a relief mediator that takes over the RvE2 function and passes over to the RvE3 function. Therefore, each RvE may act as an important role/stage-specific mediator in a coordinated manner with other RvEs in the processes of the resolution of inflammation. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.prostaglandins.2023.106759 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37327943 ● Summary page in Scopus @ Elsevier: 2-s2.0-85163220563 (DOI: 10.1016/j.prostaglandins.2023.106759, PubMed: 37327943, Elsevier: Scopus)
4.	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)
5.	Takahiro Niimura, Yoshito Zamami, Koji Miyata, Takahisa Mikami, Mizuho Asada, Keijo Fukushima, Masaki Yoshino, Satoru Mitsuboshi, Naoto Okada, Hirofumi Hamano, Takumi Sakurada, Rie Matsuoka-Ando, Fuka Aizawa, Kenta Yagi, Mitsuhiro Goda, Masayuki Chuma, Toshihiro Koyama, Yuki Izawa-Ishizawa, Hiroaki Yanagawa, Hiromichi Fujino, Yoshihiro Yamanishi and Keisuke Ishizawa : Characterization of Immune Checkpoint Inhibitor-Induced Myasthenia Gravis Using the US Food and Drug Administration Adverse Event Reporting System., Journal of Clinical Pharmacology, Vol.63, No.4, 473-479, 2022. (Summary) Myasthenia gravis (MG) is a rare but fatal adverse event of immune checkpoint inhibitors (ICIs). We assessed whether patient characteristics differed between those with ICI-related myasthenia gravis and those with idiopathic myasthenia gravis. Reports from the US Food and Drug Administration Adverse Event Reporting System were analyzed. Multivariate analyses were conducted to evaluate the associations between age, sex, and ICI treatment and the reporting rate of myasthenia gravis. Among 5 464 099 cases between 2011 and 2019, 53 447 were treated with ICIs. Myasthenia gravis was reported more often in ICI users. Multiple logistic regression analyses showed that the reporting rate of ICI-related myasthenia gravis did not differ significantly between men and women; however, it was higher in older people than in younger people (adjusted odds ratio, 2.4 [95%CI, 1.84-3.13]). We also investigated useful signs for the early detection of myositis and myocarditis, which are fatal when overlapping with ICI-related myasthenia gravis. Patients with elevated serum creatine kinase or troponin levels were more likely to have concurrent myositis and myocarditis. Unlike idiopathic myasthenia gravis, there was no sex difference in the development of ICI-related myasthenia gravis, which may be more common in older people. Considering the physiological muscle weakness that occurs in the elderly, it may be necessary to monitor ICI-related myasthenia gravis more closely in older people. (Keyword) Male / United States / Humans / Female / Aged / Immune Checkpoint Inhibitors / United States Food and Drug Administration / Myocarditis / Myasthenia Gravis / Myositis (Link to Publication Site) ● Publication site (DOI): 10.1002/jcph.2187 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36453166 ● Search Scopus @ Elsevier (PMID): 36453166 ● Search Scopus @ Elsevier (DOI): 10.1002/jcph.2187 (DOI: 10.1002/jcph.2187, PubMed: 36453166)
6.	Natsuki Yamagiwa, Haruka Kobayashi, Haruka Okabayashi, Miki Yasuda, Keijo Fukushima, Jun Kawamura, Satoshi Kotoura and Hiromichi Fujino : Phosphatidylcholine-Plasmalogen-Oleic Acid Has Protective Effects against Arachidonic Acid-Induced Cytotoxicity., Biological & Pharmaceutical Bulletin, Vol.45, No.5, 643-648, 2022. (Summary) Plasmalogens are a group of glycerophospholipids containing a vinyl-ether bond at the sn-1 position in the glycerol backbone. Cellular membrane plasmalogens are considered to have important roles in homeostasis as endogenous antioxidants, differentiation, and intracellular signal transduction pathways including neural transmission. Therefore, reduced levels of plasmalogens have been suggested to be associated with neurodegenerative diseases such as Alzheimer's disease. Interestingly, although arachidonic acid is considered to be involved in learning and memory, it could be liberated and excessively activate neuronal activity to the excitotoxic levels seen in Alzheimer's disease patients. Here, we examined the protective effects of several kinds of plasmalogens against cellular toxicity caused by arachidonic acid in human neuroblastoma SH-SY5Y cells. As a result, only phosphatidylcholine-plasmalogen-oleic acid (PC-PLS-18) showed protective effects against arachidonic acid-induced cytotoxicity based on the results of lactate dehydrogenase release and ATP depletion assays, as well as cellular morphological changes in SH-SY5Y cells. These results indicate that PC-PLS-18 protects against arachidonic acid-induced cytotoxicity, possibly via improving the stability of the cellular membrane in SH-SY5Y cells. (Keyword) Alzheimer Disease / Arachidonic Acid / Humans / Lecithins / Oleic Acid / Plasmalogens (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b22-00035 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35236811 ● Search Scopus @ Elsevier (PMID): 35236811 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.b22-00035 (DOI: 10.1248/bpb.b22-00035, PubMed: 35236811)
7.	Yoshito Zamami, Takahiro Niimura, Takehiro Kawashiri, Mitsuhiro Goda, Yutaro Naito, Keijo Fukushima, Soichiro Ushio, Fuka Aizawa, Hirofumi Hamano, Naoto Okada, Kenta Yagi, Koji Miyata, Kenshi Takechi, Masayuki Chuma, Toshihiro Koyama, Daisuke Kobayashi, Takao Shimazoe, Hiromichi Fujino, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Identification of prophylactic drugs for oxaliplatin-induced peripheral neuropathy using big data., Biomedicine & Pharmacotherapy, Vol.148, 2022. (Summary) Thus, drug repositioning using data from large-scale basic and clinical databases enables the discovery of new indications for approved drugs with a high probability of success. (Keyword) Animals / Anticholesteremic Agents / Antineoplastic Agents / Big Data / Databases, Factual / Drug Repositioning / Humans / Hyperalgesia / Japan / Male / Mice / Mice, Inbred BALB C / Oxaliplatin / Peripheral Nervous System Diseases / Pre-Exposure Prophylaxis / Rats / Rats, Sprague-Dawley / Retrospective Studies / Simvastatin (Tokushima University Institutional Repository) ● Metadata: 117414 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.biopha.2022.112744 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35240525 ● Search Scopus @ Elsevier (PMID): 35240525 ● Search Scopus @ Elsevier (DOI): 10.1016/j.biopha.2022.112744 (Tokushima University Institutional Repository: 117414, DOI: 10.1016/j.biopha.2022.112744, PubMed: 35240525)
8.	Kana Kitagawa, Ayaka Hamaguchi, Keijo Fukushima, Yuki Nakano, W John Regan, Masato Mashimo and Hiromichi Fujino : Interleukin-4 may suppress expression of E-type prostanoid receptor4 in human colorectal cancer HCA-7 cells, European Journal of Pharmacology, Vol.920, 2022. (Summary) ) and cyclooxygenase-2 (COX-2), the hallmarks of colorectal carcinogenesis. In the present study, using an in silico analysis and pharmacological experiments, we demonstrated that interleukin (IL)-4, a signature cytokine of Th2 cells, down-regulated the expression of COX-2 and PGE (Keyword) Colonic Neoplasms / Cyclooxygenase 2 / Dinoprostone / Down-Regulation / Humans / Interleukin-4 / Prostaglandins E / Receptors, Prostaglandin E, EP2 Subtype / Receptors, Prostaglandin E, EP4 Subtype (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2022.174863 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35240193 ● Search Scopus @ Elsevier (PMID): 35240193 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2022.174863 (DOI: 10.1016/j.ejphar.2022.174863, PubMed: 35240193)
9.	Keijo Fukushima, Kanaho Senoo, Naoki Kurata, W John Regan and Hiromichi Fujino : The Gαs-protein-mediated pathway may be steadily stimulated by prostanoid EP2 receptors, but not by EP4 receptors., FEBS Open Bio, Vol.12, No.4, 775-783, 2022. (Summary) causes accumulation of cAMP in EP2 receptors, whereas markedly low levels of cAMP accumulated in EP4 receptors. By applying the Black/Leff operational model calculation, we found that EP2 receptors have a biased ability to intrinsically activate the Gαs-protein-mediated pathway, whereas EP4 receptors have strong biased activity for the Gαi-protein-mediated pathway. Thus, EP2 and EP4 receptors may not be similar Gαs-coupled receptors but instead substantially different receptors with distinct roles. (Keyword) Prostaglandins / Receptors, Prostaglandin E, EP2 Subtype / Receptors, Prostaglandin E, EP4 Subtype / Signal Transduction (Tokushima University Institutional Repository) ● Metadata: 117444 (Link to Publication Site) ● Publication site (DOI): 10.1002/2211-5463.13378 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35124898 ● Search Scopus @ Elsevier (PMID): 35124898 ● Search Scopus @ Elsevier (DOI): 10.1002/2211-5463.13378 (Tokushima University Institutional Repository: 117444, DOI: 10.1002/2211-5463.13378, PubMed: 35124898)
10.	Keijo Fukushima and Hiromichi Fujino : Identification and Characterization of Human Colorectal Cancer Cluster Predominantly Expressing EP3 Prostanoid Receptor Subtype., Biological & Pharmaceutical Bulletin, Vol.45, No.6, 698-702, 2022. (Summary) ) is a well-known mediator of colorectal cancer through stimulation of four E-type prostanoid (EP) receptor subtypes: EP1, EP2, EP3, and EP4 receptors. All subtypes of EP receptors are involved in CRC promotion or malignancy. However, the characteristics of CRC that highly expresses EP receptor subtypes have not been clarified. In the present study, we classified CRC from a cancer genomic database and identified CRC clusters which highly express EP receptor subtypes. Most of these clusters predominantly expressed one subtype of EP receptor and showed different gene expression patterns. Among them, we focused on the cluster highly expressing the EP3 receptor (CL-EP3). As the result of characterization of gene expression, CL-EP3 was characterized as: epithelial mesenchymal transition (EMT)-induced progressed cancer with activation of transforming growth factor-β pathway, activation of hypoxia-inducible factor-1α, and suppression of runt-related transcription factor 3. Since we previously reported that EP3 receptor is involved in and induce colon cancer cell migration, EP3 receptor-expressing CRC may induce metastasis through these signaling pathways. Thus, the findings suggest the effectiveness of cancer clustering by gene expression of the EP receptor subtype to elucidate the mechanism of human CRC. (Keyword) Colorectal Neoplasms / Dinoprostone / Humans / Receptors, Prostaglandin E / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b22-00104 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35650098 ● CiNii @ National Institute of Informatics (CRID): 1390292251338536320 ● Summary page in Scopus @ Elsevier: 2-s2.0-85131270255 (DOI: 10.1248/bpb.b22-00104, PubMed: 35650098, CiNii: 1390292251338536320, Elsevier: Scopus)
11.	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)
12.	Iori Okura, Nanae Hasuoka, Kanaho Senoo, Akiko Suganami, Keijo Fukushima, W John Regan, Masato Mashimo, Toshihiko Murayama, Yutaka Tamura and Hiromichi Fujino : The differential functional coupling of phosphodiesterase 4 to human DP and EP2 prostanoid receptors stimulated with PGD 2 or PGE 2, Pharmacological Reports : PR, Vol.73, No.3, 946-953, 2021. (Keyword) Adenylyl Cyclases / Cell Line / Cyclic AMP / Cyclic Nucleotide Phosphodiesterases, Type 4 / Dinoprostone / HEK293 Cells / Humans / Ligands / Prostaglandin D2 / Receptors, Immunologic / Receptors, Prostaglandin / Receptors, Prostaglandin E, EP2 Subtype / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1007/s43440-021-00247-x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33786738 ● Search Scopus @ Elsevier (PMID): 33786738 ● Search Scopus @ Elsevier (DOI): 10.1007/s43440-021-00247-x (DOI: 10.1007/s43440-021-00247-x, PubMed: 33786738)
13.	Motofumi Suzuki, Atsumi Urabe, Sayaka Sasaki, Ryo Tsugawa, Satoshi Nishio, Haruka Mukaiyama, Yoshiko Murata, Hiroshi Masuda, M. Sann Aung, Akane Mera, Masaki Takeuchi, Keijo Fukushima, Michika Kanaki, Kaori Kobayashi, Yudai Chiba, Binod Babu Shrestha, Hiromi Nakanishi, T. Watanabe, Atsushi Nakayama, Hiromichi Fujino, Takanori Kobayashi, Keiji Tanino, Naoko Nishizawa and Kosuke Namba : Development of a mugineic acid family phytosiderophore analog as an iron fertilizer, Nature Communications, Vol.12, No.1, 1558, 2021. (Summary) Iron (Fe) is an essential nutrient, but is poorly bioavailable because of its low solubility in alkaline soils; this leads to reduced agricultural productivity. To overcome this problem, we first showed that the soil application of synthetic 2'-deoxymugineic acid, a natural phytosiderophore from the Poaceae, can recover Fe deficiency in rice grown in calcareous soil. However, the high cost and poor stability of synthetic 2'-deoxymugineic acid preclude its agricultural use. In this work, we develop a more stable and less expensive analog, proline-2'-deoxymugineic acid, and demonstrate its practical synthesis and transport of its Fe-chelated form across the plasma membrane by Fe(III)·2'-deoxymugineic acid transporters. Possibility of its use as an iron fertilizer on alkaline soils is supported by promotion of rice growth in a calcareous soil by soil application of metal free proline-2'-deoxymugineic acid. (Keyword) Azetidinecarboxylic Acid / Fertilizers / Iron / Siderophores / Soil (Tokushima University Institutional Repository) ● Metadata: 116178 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41467-021-21837-6 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33692352 ● Search Scopus @ Elsevier (PMID): 33692352 ● Search Scopus @ Elsevier (DOI): 10.1038/s41467-021-21837-6 (Tokushima University Institutional Repository: 116178, DOI: 10.1038/s41467-021-21837-6, PubMed: 33692352)
14.	Suzu Endo, Akiko Suganami, Keijo Fukushima, Kanaho Senoo, Yumi Araki, W John Regan, Masato Mashimo, Yutaka Tamura and Hiromichi Fujino : 15-Keto-PGE 2 acts as a biased/partial agonist to terminate PGE 2-evoked signaling, The Journal of Biological Chemistry, Vol.295, No.38, 13338-13352, 2020. (Summary) -evoked inflammation and/or maintaining homeostasis of colorectal tissues/cells functions. (Keyword) Computer Simulation / Dinoprostone / HEK293 Cells / Humans / Inflammation / Models, Biological / Receptors, Prostaglandin E, EP2 Subtype / Receptors, Prostaglandin E, EP4 Subtype / Signal Transduction (Tokushima University Institutional Repository) ● Metadata: 116544 (Link to Publication Site) ● Publication site (DOI): 10.1074/jbc.RA120.013988 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32727851 ● Search Scopus @ Elsevier (PMID): 32727851 ● Search Scopus @ Elsevier (DOI): 10.1074/jbc.RA120.013988 (Tokushima University Institutional Repository: 116544, DOI: 10.1074/jbc.RA120.013988, PubMed: 32727851)
15.	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)
16.	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)
17.	Yoshito Zamami, Takahiro Niimura, Naoto Okada, Toshihiro Koyama, Keijo Fukushima, Yuki Izawa-Ishizawa and Keisuke Ishizawa : Factors Associated With Immune Checkpoint Inhibitor-Related Myocarditis., JAMA Oncology, 2019. (Link to Publication Site) ● Publication site (DOI): 10.1001/jamaoncol.2019.3113 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31436802 ● Search Scopus @ Elsevier (PMID): 31436802 ● Search Scopus @ Elsevier (DOI): 10.1001/jamaoncol.2019.3113 (DOI: 10.1001/jamaoncol.2019.3113, PubMed: 31436802)
18.	Naoki Kurata, Natsumi Tokashiki, Keijo Fukushima, Takaya Misao, Nanae Hasuoka, Kana Kitagawa, Masato Mashimo, W John Regan, Toshihiko Murayama and Hiromichi Fujino : Short chain fatty acid butyrate uptake reduces expressions of prostanoid EP4 receptors and their mediation of cyclooxygenase-2 induction in HCA-7 human colon cancer cells., European Journal of Pharmacology, Vol.853, 308-315, 2019. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2019.04.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30980797 ● Search Scopus @ Elsevier (PMID): 30980797 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2019.04.014 (DOI: 10.1016/j.ejphar.2019.04.014, PubMed: 30980797)
19.	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)
20.	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)
21.	Naofumi Seira, Kazuyuki Yamagata, Keijo Fukushima, Yumi Araki, Naoki Kurata, Naoki Yanagisawa, Masato Mashimo, Hiroyuki Nakamura, W John Regan, Toshihiko Murayama and Hiromichi Fujino : Cellular density-dependent increases in HIF-1α compete with c-Myc to down-regulate human EP4 receptor promoter activity through Sp-1-binding region., Pharmacology Research & Perspectives, Vol.6, No.6, 2018. (Summary) The up-regulated expression of E-type prostanoid (EP) 4 receptors has been implicated in carcinogenesis; however, the expression of EP4 receptors has also been reported to be weaker in tumor tissues than in normal tissues. Indeed, EP4 receptors have been suggested to play a role in the maintenance of colorectal homeostasis. This study aimed to examine the underlying mechanisms/reasons for why inconsistent findings have been reported regarding EP4 receptor expression levels in homeostasis and carcinogenesis by focusing on cellular densities. Thus, the human colon cancer HCA-7 cells, which retain some functional features of normal epithelia, and luciferase reporter genes containing wild-type or mutated EP4 receptor promoters were used for elucidating the cellular density-dependent mechanisms about the regulation of EP4 receptor expression. In silico analysis was also utilized for confirming the relevance of the findings with respect to colon cancer development. We here demonstrated that the expression of EP4 receptors was up-regulated by c-Myc by binding to Sp-1 under low cellular density conditions, but was down-regulated under high cellular density conditions via the increase in the expression levels of HIF-1α protein, which may pull out c-Myc and Sp-1 from DNA-binding. The tightly regulated EP4 receptor expression mechanism may be a critical system for maintaining homeostasis in normal colorectal epithelial cells. Therefore, once the system is altered, possibly due to the transient overexpression of EP4 receptors, it may result in aberrant cellular proliferation and transformation to cancerous phenotypes. However, at the point, EP4 receptors themselves and their mediated homeostasis would be no longer required. (Keyword) Carcinogenesis / Cell Count / Cell Line, Tumor / Colonic Neoplasms / Computational Biology / Down-Regulation / Gene Expression Regulation, Neoplastic / Humans / Hypoxia-Inducible Factor 1, alpha Subunit / Promoter Regions, Genetic / Proto-Oncogene Proteins c-myc / Receptors, Prostaglandin E, EP4 Subtype / Sp1 Transcription Factor / Up-Regulation (Tokushima University Institutional Repository) ● Metadata: 115684 (Link to Publication Site) ● Publication site (DOI): 10.1002/prp2.441 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30455960 ● Search Scopus @ Elsevier (PMID): 30455960 ● Search Scopus @ Elsevier (DOI): 10.1002/prp2.441 (Tokushima University Institutional Repository: 115684, DOI: 10.1002/prp2.441, PubMed: 30455960)
22.	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)
23.	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)
24.	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)
25.	Araki Yumi, Suganami Akiko, Endo Suzu, Masuda Yuta, Keijo Fukushima, Regan W. John, Murayama Toshihiko, Tamura Yutaka and Hiromichi Fujino : PGE1 and E3 show lower efficacies than E2 to -catenin-mediated activity as biased ligands of EP4 prostanoid receptors., FEBS Letters, Vol.591, No.22, 3771-3780, 2017. (Summary) The 2-series of prostaglandin E (PGE ) is regarded as a pro-cancer prostanoid, whereas the 1-series (PGE ) and the 3-series (PGE ) are considered to act as anti-cancer prostanoids. In the present study, we provide possible reasons why PGE and PGE , but not PGE , exert anti-cancer effects by focusing on each diverged E-type prostanoid (EP)4 receptor-mediated signaling pathway. PGE , PGE and PGE function as full agonists in terms of G - and G -protein-mediated signaling. However, PGE and PGE function as partial agonists of T-cell factor (TCF)/β-catenin (β-cat)-mediated activity, the well-known cancer-related signaling pathway. Furthermore, pretreatment with PGE or PGE almost completely reduces PGE -induced TCF/β-cat activity. These results provide a plausible reason why PGE and PGE function as anti-cancer prostanoids as a result of novel biased activity for EP4 receptors. (Keyword) Alprostadil / Binding Sites / Crystallography, X-Ray / Dinoprostone / Gene Expression Regulation / HEK293 Cells / Humans / Hydrogen Bonding / Ligands / Models, Molecular / Protein Binding / Receptors, Prostaglandin E, EP4 Subtype / Signal Transduction / beta Catenin (Link to Publication Site) ● Publication site (DOI): 10.1002/1873-3468.12878 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28986997 ● Search Scopus @ Elsevier (PMID): 28986997 ● Search Scopus @ Elsevier (DOI): 10.1002/1873-3468.12878 (DOI: 10.1002/1873-3468.12878, PubMed: 28986997)

Academic Paper (Unrefereed Paper):

1.	Keijo Fukushima, Tadanobu Takahashi and Takashi Suzuki : Characterization of Human Parainfluenza Virus Receptor Using Terminal Sialic Acid Linkage-Modified Cells., Methods in Molecular Biology, Vol.2556, 169-178, 2022. (Summary) Human parainfluenza virus type 1 (hPIV1) and type 3 (hPIV3) are respiratory pathogen viruses that bind to terminal sialic acids of glycoconjugates on the cell surface hemagglutinin-neuraminidase glycoprotein. Sialic acid residues are linked to the galactose residue primarily by α2,3 or α2,6 linkages on the terminal of glycoprotein or glycolipids. One of the major determinants of pathogenicity or tissue tropism is virus binding or infection specificity for each sialyl linkage. Sialic linkage-modified human blood cells or mammalian cells that mainly have α2,3- or α2,6-linked sialic acid residues on the surface can be prepared by treatment with linkage-specific sialidases or sialyltransferases. These linkage-modified cells can be used in hemagglutination assays to estimate virus particles' binding specificity, hemadsorption assays to estimate virus glycoproteins' binding specificity, and virus infectivity assays. These methods contribute to identifying the specificity of sialic acid lineage recognition of the hPIV or other sialic acid-binding viruses. (Keyword) Animals / Galactose / Glycolipids / HN Protein / Humans / Mammals / Membrane Glycoproteins / N-Acetylneuraminic Acid / Parainfluenza Virus 1, Human / Paramyxoviridae Infections / Receptors, Virus / Sialyltransferases (Link to Publication Site) ● Publication site (DOI): 10.1007/978-1-0716-2635-1_13 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36175634 ● Search Scopus @ Elsevier (PMID): 36175634 ● Search Scopus @ Elsevier (DOI): 10.1007/978-1-0716-2635-1_13 (DOI: 10.1007/978-1-0716-2635-1_13, PubMed: 36175634)

Academic Letter:

1.	Masato Mashimo, Asuka Shimizu, Aimi Mori, Ayaka Hamaguchi, Keijo Fukushima, Naofumi Seira, Takeshi Fujii and Hiromichi Fujino : PARP14 regulates EP4 receptor expression in human colon cancer HCA-7 cells., Biochemical and Biophysical Research Communications, Vol.623, 133-139, 2022. (Summary) E type prostanoid 4 (EP4) receptors and their signaling pathways have been implicated in the development and malignant transformation of colorectal cancer. We herein demonstrated that the mono(ADP-ribosyl)ation of histone deacetylase (HDAC)1 and HDAC2 by poly(ADP-ribose) polymerase 14 (PARP14) may be required to induce the expression of EP4 receptors. The suppression of PARP14 activity by siRNA and/or its inhibitors reduced the mRNA expression of EP4 receptors. Thus, the expression of their proteins to approximately 50-80% in human colon cancer HCA-7 cells, however, which retained the activities of EP4 receptors to some extent. Since the expression levels of EP4 receptors are important factors for the maintenance of homeostasis, the adequate inhibition of PARP14 activity will be a good target for the prevention of colon cancer and/or as an alternative therapy for this disease. Since non-steroidal anti-inflammatory drugs (NSAIDs) are associated with a risk of heart attacks and stroke, novel PARP14 inhibitors will supersede NSAIDs without causing heart attacks and stroke, while maintaining appropriate EP4 receptor-mediated intestinal homeostasis. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2022.07.055 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35914351 ● CiNii @ National Institute of Informatics (CRID): 1360861707370271744 ● Summary page in Scopus @ Elsevier: 2-s2.0-85135092033 (DOI: 10.1016/j.bbrc.2022.07.055, PubMed: 35914351, CiNii: 1360861707370271744, Elsevier: Scopus)
2.	Keijo Fukushima, Tadanobu Takahashi, Masahiro Takaguchi, Seigo Ito, Chihiro Suzuki, Takashi Agarikuchi, Yuuki Kurebayashi, Akira Minami and Takashi Suzuki : A I131V Substitution in the Fusion Glycoprotein of Human Parainfluenza Virus Type 1 Enhances Syncytium Formation and Virus Growth., Biological & Pharmaceutical Bulletin, Vol.42, No.5, 827-832, 2019. (Summary) Human parainfluenza virus type 1 (hPIV1) has two spike glycoproteins, the hemagglutinin-neuraminidase (HN) glycoprotein as a receptor-binding protein and the fusion (F) glycoprotein as a membrane-fusion protein. The F glycoprotein mediates both membrane fusion between the virus and cell and membrane fusion between cells, called syncytium formation. Wild-type C35 strain (WT) of hPIV1 shows little syncytium formation of infected cells during virus growth. In the present study, we isolated a variant virus (Vr) from the WT that showed enhanced syncytium formation of infected cells by using our previously established hPIV1 plaque formation assay. Vr formed a larger focus and showed increased virus growth compared with WT. Sequence analysis of the spike glycoprotein genes showed that the Vr had a single amino acid substitution of Ile to Val at position 131 in the fusion peptide region of the F glycoprotein without any substitutions of the HN glycoprotein. The Vr F glycoprotein showed enhanced syncytium formation in F and HN glycoprotein-expressing cells. Additionally, expression of the Vr F glycoprotein increased the focus area of the WT-infected cells. The single amino acid substitution at position 131 in the F glycoprotein of hPIV1 gives hPIV1 abilities to enhance syncytium formation and increase cell-to-cell spread. The present study supports the possibility that hPIV1 acquires increased virus growth in vitro from promotion of direct cell-to-cell transmission by syncytium formation. (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b18-00714 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31061326 ● Summary page in Scopus @ Elsevier: 2-s2.0-85065672034 (DOI: 10.1248/bpb.b18-00714, PubMed: 31061326, Elsevier: Scopus)
3.	Seira Naofumi, Yanagisawa Naoki, Suganami Akiko, Takuya Honda, Wasai Makiko, Regan W John, Keijo Fukushima, Yamaguchi Naoto, Tamura Yutaka, Arai Takayoshi, Murayama Toshihiko and Hiromichi Fujino : Anti-cancer effects of MW-03, a novel indole compound, by inducing 15-hydroxyprostaglandin dehydrogenase and cellular growth inhibition in the LS174T human colon cancer cell line, Biological & Pharmaceutical Bulletin, Vol.40, No.10, 1806-1812, 2017. (Summary) Increases in the expression of prostaglandin E (PGE) are widely known to be involved in aberrant growth in the early stage of colon cancer development. We herein demonstrated that the novel indole compound MW-03 reduced PGE-induced cAMP formation by catalization to an inactive metabolite by inducing 15-hydroxyprostaglandin dehydrogenase through the activation of peroxisome proliferator-activated receptor-γ. MW-03 also inhibited colon cancer cell growth by arresting the cell cycle at the S phase. Although the target of MW-03 for cell cycle inhibition has not yet been identified, these dual anti-cancer effects of MW-03 itself and/or its leading compound(s) on colon cancer cells may reduce colon cancer development and, thus, have potential as a novel treatment for the early stage of this disease. (Keyword) Antineoplastic Agents / Cell Line, Tumor / Cell Proliferation / Colonic Neoplasms / Cyclic AMP / Dinoprostone / Humans / Hydroxyprostaglandin Dehydrogenases / Indoles / PPAR gamma (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b17-00458 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28966256 ● Summary page in Scopus @ Elsevier: 2-s2.0-85030767955 (DOI: 10.1248/bpb.b17-00458, PubMed: 28966256, Elsevier: Scopus)

Proceeding of International Conference:

1.	Yoshito Zamami, Yuki Izawa-Ishizawa, Takahiro Niimura, Mitsuhiro Goda, Naoto Okada, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yasumasa Ikeda, Koichiro Tsuchiya and Keisuke Ishizawa : Development of therapeutic agents using drug discovery tools and large-scale medical information, FIP2019, Abu Dhabi, Sep. 2019.
2.	Niimura Takahiro, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : Nicorandil improve prognosis of cardiac arrest patient: A large-scale medical information analysis, FIP2019, Abu Dhabi, Sep. 2019.
3.	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.
4.	Seira Naofumi, Yamagata Kazuyuki, Keijo Fukushima, Araki Yumi, Kurata Naoki, Yanagisawa Naoki, Mashimo Masato, Nakamura Hiroyuki, Regan W. John, Murayama Toshihiko and Hiromichi Fujino : Hypoxia inducible factor-1alpha regulates human EP4 receptor expression by binding to specificity protein-1, The 3rd Chiba University-Mahidol University Joint Symposium on Pharmaceutical Sciences, Aug. 2018.
5.	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.
6.	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.
7.	Hiromichi Fujino, Araki Yumi, Suganami Akiko, Endo Suzu, Takano Harumi, Masuda Yuta, Keijo Fukushima, Regan W. John, Murayama Toshihiko and Tamura Yutaka : PGE1 and E3 show lower efficacies than E2 to beta-catenin-mediated activity as biased ligands of EP4 prostanoid receptors, 18th World Congress of Basic and Clinical Pharmacology, Jul. 2018.

Proceeding of Domestic Conference:

1.	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.
2.	ISAMU Konishi, Keijo Fukushima, W. John Regan and Hiromichi Fujino : EP4プロスタノイド受容体下流の大腸がん原因因子の同定と誘導メカニズムの解明, 第144回日本薬理学会近畿部会，高槻, 2024.
3.	Shunya Yanagawa, Akiko Higashiyama, Keijo Fukushima, W. John Regan and Hiromichi Fujino : ProteinkinaseAが制御するEP4受容体シグナル伝達メカニズムの解明, 第144回日本薬理学会近畿部会，高槻, 2024.
4.	Kaori Ueki, Junichiroh Kawasaki, YOSHIMATSU Keisei, Rei Matsumoto, Keijo Fukushima and Hiromichi Fujino : histamineH1受容体の発現量とloratadineへの感受性について, 日本薬学会第144年会，横浜，2024年3月29日, 2024.
5.	Akiko Higashiyama, Akito Ohnishi, Shunya Yanagawa, 清良尚史, W John Regan, OHKAWACHI Kento, Masaya Denda, Keijo Fukushima, 西野耕平, Akira Otaka, Hidetaka Kosako and Hiromichi Fujino : EP4受容体の細胞内第3ループ領域に相互作用する因子の探索, 日本薬学会第144年会,横浜,2024年3月29日, 2024.
6.	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.
7.	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.
8.	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.
9.	Mayu Yamashita, Hitomi Yamamoto, SHINOHARA Mayu, Keijo Fukushima, 菅波晃子, 田村裕 and Hiromichi Fujino : PGJ2のヒトEP2プロスタノイド受容体を介したcAMP産生に対する影響, 日本薬学会第143年会, Mar. 2023.
10.	Yuki Nakano, Kiyoka Matsumoto, Ayaka Ohgimoto, SOMEYA Saki, Keijo Fukushima and Hiromichi Fujino : EP4プロスタノイド受容体シグナルの代謝機構への影響, 日本薬学会第143年会, Mar. 2023.
11.	Haruka Okabayashi, Miki Yasuda, NII Chinatsu, Keijo Fukushima, 湯浅浩気, 琴浦聡 and Hiromichi Fujino : プラズマローゲンによるアルツハイマー病発症予防メカニズムの解明, 日本薬学会第143年会, Mar. 2023.
12.	Miho Agata, Nanae Hasuoka, 間下雅士, Keijo Fukushima and Hiromichi Fujino : プロスタグランジンD2代謝物のCRTH2受容体を介した機能的差異の解明, 日本薬学会第143年会, Mar. 2023.
13.	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.
14.	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.
15.	Shunya Yanagawa, Akito Ohnishi, Akiko Higashiyama, W John Regan, Keijo Fukushima and Hiromichi Fujino : EP4プロスタノイド受容体の1アミノ酸変異によるシグナル伝達変化, 生体機能と創薬シンポジウム2023，徳島, 2023.
16.	Takaya Misao, Keijo Fukushima and Hiromichi Fujino : Arachidonicacidおよび2-arachidonoylglycerolによるcyclooxygenase-2分解促進作用, 生体機能と創薬シンポジウム2023，徳島, 2023.
17.	SHINOHARA Mayu, Nanae Hasuoka, Miho Agata, Keijo Fukushima and Hiromichi Fujino : プロスタグランジンD2代謝物のCRTH2受容体を介した機能的差異の解明, 生体機能と創薬シンポジウム2023，徳島, 2023.
18.	SHINOHARA Mayu, Nanae Hasuoka, Miho Agata, Keijo Fukushima and Hiromichi Fujino : プロスタグランジンD₂代謝物のCRTH2受容体を介したバイアス活性の解明, 第97回日本薬理学会年会，神戸, 2023.
19.	Takaya Misao, Keijo Fukushima and Hiromichi Fujino : 内因性カンナビノイド2-アラキドノイルグリセロール(2-AG)の抗結腸がんメカニズムの解明, 第97回日本薬理学会年会，神戸, 2023.
20.	Keijo Fukushima, Suzu Endoh, Kanaho Senoh, W John Regan and Hiromichi Fujino : 15-Keto-PGE2はPGE2によるシグナルを抑制するバイアスアゴニストとして作用する, 第97回日本薬理学会年会，神戸, 2023.
21.	Ayaka Hamaguchi, 福田隼, 藤原広一, Tomofumi Harada, Keijo Fukushima, 高栁和伸, 周東智 and Hiromichi Fujino : Eタイプresolvinファミリーの異なる作用は，協奏的に炎症を終息させる, 第97回日本薬理学会年会，神戸, 2023.
22.	Keijo Fukushima and Hiromichi Fujino : EP3プロスタノイド受容体サブタイプを高発現するヒト大腸がんクラスターの同定と性質評価, 第96回日本薬理学会年会, Nov. 2022.
23.	Takaya Misao, 北島満里子, 村木拓斗, 林隼太郎, Kohki Takahashi, Keijo Fukushima, 北井淳一郎, 奥村明子, 吉田博也, 石川勇人 and Hiromichi Fujino : パラグアイ原産ハーブCyclollepis genistoides D. Don(パロアッスル)の抗糖尿病生物活性成分含有画分の活性評価, 第96回日本薬理学会年会, Nov. 2022.
24.	村嶋優香, Yuya Horinouchi, 山田佑人, 吉岡駿, Keijo Fukushima, 久禮匠, 佐々木尚史, Hiromichi Fujino, 四宮一昭 and Yasumasa Ikeda : フィブラート系薬剤の腎保護効果に関する検討, 第61回日本薬学会中四国支部学術大会, Nov. 2022.
25.	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.
26.	Keijo Fukushima and Hiromichi Fujino : プロスタノイドEP2受容体とEP4受容体, 生体機能と創薬シンポジウム2022, Aug. 2022.
27.	Takaya Misao, Keijo Fukushima and Hiromichi Fujino : 内因性カンナビノイドによる抗結腸がんメカニズムの解明, 第63回日本生化学会中国・四国支部例会, May 2022.
28.	Haruka Kobayashi, Haruka Okabayashi, Miki Yasuda, Keijo Fukushima, 川村純, 琴浦聡 and Hiromichi Fujino : アラキドン酸による神経毒生を緩和するプラズマローゲン作用の解明, 日本薬学会第142年会，名古屋, Mar. 2022.
29.	Ayaka Hamaguchi, Keijo Fukushima, 福田隼人, 藤原広一, 周東智 and Hiromichi Fujino : Resolvin E-seriesの炎症収束作用の検討, 日本薬学会第142年会，名古屋, Mar. 2022.
30.	Kanaho Senoh, Hitomi Yamamoto, Suzu Endoh, W John Regan, Keijo Fukushima and Hiromichi Fujino : プロスタグランジンD2の代謝物はDPプロスタノイド受容体に対してバイアスアゴニストとして働く, 第95回日本薬理学会年会，福岡, Mar. 2022.
31.	Akito Ohnishi, Akiko Higashiyama, Shunya Yanagawa, 清良尚史, W John Regan, Kento Ohkawachi, Masaya Denda, Keijo Fukushima, Akira Otaka and Hiromichi Fujino : プロスタノイドEP4受容体の1アミノ酸変異によるシグナル伝達プロファイル変化, 第95回日本薬理学会年会，福岡, Mar. 2022.
32.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Masayuki Chuma, Yoshito Zamami, Licht Miyamoto, 石澤啓介, Hiromichi Fujino, Ken-ichi Aihara, Koichiro Tsuchiya and Toshiaki Tamaki : Identification of a candidate drug for the prevention of cisplatin-induced nephrotoxicity by a database analysis -basic research-clinical study, 第94回日本薬理学会年会, Mar. 2021.
33.	Nanae Hasuoka, Miho Agata, 間下雅士, Keijo Fukushima and Hiromichi Fujino : PGD2およびその代謝物によるCRTH2受容体へのバイアス作用の解明, 日本薬学会第141年会, Mar. 2021.
34.	Kiyoka Matsumoto, Yuki Nakano, 高橋弘喜, 楠屋陽子, 村山俊彦, Keijo Fukushima and Hiromichi Fujino : PGE2による結腸がん細胞内代謝変化の解析, 日本薬学会第141年会, Mar. 2021.
35.	Harumi Takano, Kanaho Senoh, Mayu Yamashita, Yumi Araki, Regan John W, Keijo Fukushima and Hiromichi Fujino : EP4プロスタノイド受容体を介したプロスタグランジンD2のバイアス性による抗癌作用, 第94回日本薬理学会年会, Mar. 2021.
36.	Rei Matsumoto, Kaori Ueki, Yuta Masuda, 間下雅士, Keijo Fukushima and Hiromichi Fujino : 結腸癌転移に関与するヒスタミンH1受容体作用の解明, Mar. 2021.
37.	Takaya Misao, Keijo Fukushima and Hiromichi Fujino : 内因性カンナビノイドによる抗結腸がんメカニズムの解明, 日本薬学会第141年会, 2021.
38.	Yasumasa Ikeda, Hirofumi Hamano, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, 石澤啓介, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン起因性腎障害を予防する既存薬の同定, 第63回日本腎臓学会学術総会, Aug. 2020.
39.	Manabu Sugiyama, Akito Ohnishi, Takuya Morisaki, Akira Shigenaga, Keijo Fukushima, Akira Otaka and Hiromichi Fujino : inteinシステムを用いたプロスタノイドEP4受容体の局在解析を目指して, 日本薬学会第140年会, Mar. 2020.
40.	Natsuki Yamagiwa, Haruka Kobayashi, Keijo Fukushima, Haruka Okabayashi, 川村純, 琴浦聡 and Hiromichi Fujino : アラキドン酸による神経毒性作用を緩和する有効な生理活性脂質としてのプラズマローゲン種の同定, 日本薬学会第140年会, Mar. 2020.
41.	Kana Kitagawa, Ayaka Hamaguchi, 間下雅士, Regan John W., Keijo Fukushima and Hiromichi Fujino : ヒト結腸がんHCA-7細胞においてインターロイキン4はEP4プロスタノイド受容体発現を抑制する, 第93回日本薬理学会年会, Mar. 2020.
42.	Suzu Endoh, Kanaho Senoh, Harumi Takano, Yumi Araki, Regan John W., Keijo Fukushima and Hiromichi Fujino : PGE2代謝物 15-keto-PGE2はバイアスアゴニストとしてEP2およびEP4プロスタノイド受容体に作用する, 第93回日本薬理学会年会, Mar. 2020.
43.	Hirofumi Hamano, Yasumasa Ikeda, Mitsuhiro Goda, Keijo Fukushima, Seiji Kishi, Kenshi Takechi, Masayuki Chuma, Yoshito Zamami, Yuya Horinouchi, Licht Miyamoto, Hiromichi Fujino, Keisuke Ishizawa, Koichiro Tsuchiya and Toshiaki Tamaki : シスプラチン誘発性腎障害を予防する既存薬物の同定, 第260回徳島医学会学術集会(令和元年度冬期), Feb. 2020.
44.	Masayuki Chuma, Mitsuhiro Goda, Takahiro Niimura, Yoshito Zamami, Kenshi Takechi, Yuki Izawa-Ishizawa, 濱野裕章, 石田俊介, Takahiro Niimura, Masateru Kondoh, Takashi Bandoh, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : ドラッグリポジショニング手法を用いたバンコマイシン関連腎障害の予防薬探索とその有用性の検討, 第13回日本腎臓病薬物療法学会学術集会・総会, Nov. 2019.
45.	Yuta Masuda, Kiyoka Matsumoto, Rei Matsumoto, Keijo Fukushima and Hiromichi Fujino : 抗ヒスタミン薬による大腸がん誘発への有害事象の検討, 第26回日本免疫毒性学会学術年会, Jul. 2019.
46.	新村貴博, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 大規模医療情報を用いたニコランジルの心肺停止後予後改善効果の検討, 医療薬学フォーラム2019/第27回クリニカルファーマシーシンポジウム, Jul. 2019.
47.	Mitsuhiro Goda, 斉家和仁, Akiko Maegawa, Masaya Kanda, Ami Yoshida, Yoichi Murai, Takahiro Niimura, Yuki Izawa-Ishizawa, Yoshito Zamami, Masayuki Chuma, Kenshi Takechi, Hirofumi Hamano, Naoto Okada, Keijo Fukushima, Hiromichi Fujino, Koichiro Tsuchiya, Yuya Horinouchi, Yasumasa Ikeda, Hiroaki Yanagawa and Keisuke Ishizawa : 医療ビッグデータを活用したシスプラチン誘発腎障害に対する新規予防薬の探索とその有効性の検証, 第4回中四国臨床薬理学会, Jul. 2019.
48.	Takahiro Niimura, Yoshito Zamami, Yuki Izawa-Ishizawa, Mitsuhiro Goda, Kenshi Takechi, Masayuki Chuma, Keijo Fukushima, Yuya Horinouchi, Yasumasa Ikeda, Hiromichi Fujino, Koichiro Tsuchiya and Keisuke Ishizawa : 医療ビッグデータ解析と基礎研究を融合した薬剤性副作用の機序解明および治療薬の開発, 第29回日本医療薬学会年会シンポジウム13, Mar. 2019.
49.	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.
50.	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.
51.	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.
52.	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.
53.	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.
54.	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.
55.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Yuki Izawa-Ishizawa, Hiromichi Fujino and Toshiaki Tamaki : リアルワールドデータを活用した新規腎保護薬の探索, 第48回日本腎臓学会西部学術大会, Sep. 2018.
56.	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.
57.	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.
58.	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.
59.	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.
60.	Natsumi Tokashiki, Naoki Kurata, Takaya Misao, Yumi Araki, 清良尚史, Natsuki Yamagiwa, Manabu Sugiyama, Keijo Fukushima, W John REGAN, 村山俊彦 and Hiromichi Fujino : ヒト結腸がんHCA-7 細胞における酪酸によるEP4 受容体発現系への影響, 日本薬学会第138年会, Mar. 2018.
61.	Keijo Fukushima, 市川和哉, 上野崇宏, 稲垣孝行, 宮川泰宏, 千﨑康司, Hiromichi Fujino and 山田清文 : 関節リウマチ治療薬を対象とした有害事象自発報告データベースFAERSを用いた感染症リスクの比較, 第256回徳島医学会学術集会, Feb. 2018.
62.	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.
63.	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.
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因子阻害剤の腎保護効果, 第47回日本心脈管作動物質学会, Feb. 2018.
65.	Yuya Horinouchi, Yasumasa Ikeda, Keijo Fukushima, Yuki Izawa-Ishizawa, Hiromichi Fujino and Toshiaki Tamaki : 医療ビッグデータを活用した腎保護薬の探索, 2017年度肥満・糖尿病クラスター・ミニリトリート, Feb. 2018.
66.	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.
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.	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.
69.	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.
70.	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.
71.	荒木祐美, 菅波晃子, Suzu Endoh, Hiroyuki Mizuguchi, Keijo Fukushima, W John REGAN, 村山俊彦, 田村裕 and Hiromichi Fujino : PGE1とPGE3のバイアス性と癌抑制機構の解明, 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.
72.	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.

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

プロスタノイドEP4受容体高発現大腸がんの治療的探索を目指した機能解析 (Project/Area Number: 22K15293 )
Elucidation of prostanoid receptor subtype conversion and colorectal cancer development/malignancy mechanism (Project/Area Number: 19K16374 )
Search by Researcher Number (10805112)

Assistant Professor : Fukushima, Keijo

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