Tokushima University / Educator and Researcher Directory --- Mawatari, Kazuaki

Personal Web Page

https://researchmap.jp/read0119880 (researchmap)

https://orcid.org/0000-0003-2880-3801 (ORCID)

Field of Study

○	Nutrition

Subject of Study

○	Research of signal transduction by phytochemical (phytochemical, signal transduction)

Book / Paper

Book:

1.	Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Glycolate as a Biological Marker of B Vitamins, Springer, 2022. (Keyword) Glycolate / B-vitamins / Glyoxylate / Glycolate oxidase
2.	福田朔, Kazuaki Mawatari and Akira Takahashi : UV-LED照射によるウイルス不活化機構, Technical Information Institute Co., Ltd., Mar. 2021.
3.	柴田克己, 合田敏尚, Kazuaki Mawatari, 奥恒之, 田辺賢一, 加藤秀夫, 前田朝美, 佐藤匡央, 下村吉治, 樋口満, 渡邉敏明, 根來宗孝, 上原万里子 and 山本孝史 : 健康・栄養科学シリーズ基礎栄養学改訂第6版, Nankodo, Mar. 2020.
4.	土江節子, Kazuaki Mawatari, 橋本弘子, 井上久美子, 小川万紀子, 清水扶美, 小林実夏, 秋吉美穂子, 小倉有子, 高橋律子, 大瀬良知子 and 安田敬子 : 栄養教育論-第6版 (食物と栄養学基礎シリーズ), 学文社, Feb. 2020.
5.	岡﨑光子, 饗場直美, Akira Takahashi, Kazuaki Mawatari, 風見公子, 神田あづさ, 古賀みのり, 辻雅子, 土屋ひろ子, 角田伸代, 坪田(宇津木) 恵, 寺澤洋子, 長幡友実, 三好恵子, 山内惠子 and 渡邉純子 : 栄養教育論演習(第2版), KENPAKUSHA, Mar. 2015.
6.	土江節子, Kazuaki Mawatari, 橋本弘子, 井上久美子, 小川万紀子, 山下(清水) 扶美, 小林実夏, 秋吉美穂子, 藤井紘子, 小倉有子, 高橋律子, 佐川まさの, 大瀬良知子 and 安田敬子 : 栄養教育論(第2版), 学文社, Mar. 2015.
7.	Kazuaki Mawatari, 岡﨑光子, 饗場直美, 風見公子, 神田あづさ and 他共著者11名 : 栄養教育論演習第2版, KENPAKUSHA, Tokyo, 2015.
8.	Kazuaki Mawatari, 土江節子, 橋本弘子, 井上久美子, 小川万紀子 and (他共著者9名) : 栄養教育論第2版, 学文社, 2015.
9.	土江節子, Kazuaki Mawatari, 橋本弘子, 井上久美子, 小川万紀子, 山下(清水) 扶美, 小林実夏, 秋吉美穂子, 藤井紘子, 小倉有子, 高橋律子, 佐川まさの, 大瀬良知子 and 安田敬子 : 栄養教育論, 学文社, Mar. 2013.
10.	岡﨑光子, 岡﨑光子, Akira Takahashi, Kazuaki Mawatari, 風見公子, 神田あづさ, 古賀みのり, 辻雅子, 土屋ひろ子, 角田伸代, 坪田(宇津木) 恵, 寺澤洋子, 長幡友実, 三好恵子, 山内惠子 and 渡邉純子 : 栄養教育論演習, KENPAKUSHA, Apr. 2012.
11.	Mostafa Gadelmoula, Kazuaki Mawatari, Masayuki Yamato, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Microbiology book series2(2), --- UVA-LED Air Disinfection ---, Formatex research center, 2010.
12.	Yutaka Nakaya, Toshio Hosaka, Nagakatsu Harada and Kazuaki Mawatari : よくわかる臨床栄養管理実践マニュアル,Ⅱ.栄養管理の実際栄養不良と栄養管理の手順, 全日本病院出版社, Mar. 2009.
13.	Yutaka Nakaya, Toshio Hosaka, Nagakatsu Harada and Kazuaki Mawatari : Ⅱ.栄養管理の実際栄養不良と栄養管理の手順, 全日本病院出版社, Mar. 2009.
14.	Yutaka Nakaya and Kazuaki Mawatari : ニュートリションケア, 特集・合併症・病態の変化に合わせた栄養管理保存期腎不全+心不全, Medicus SHUPPAN, Feb. 2009.
15.	Yutaka Nakaya, 鈴木和枝, Kazuaki Mawatari, Masashi Kuwahata, Yutaka Taketani, Nagakatsu Harada and Hironori Yamamoto : 臨床栄養学(第4版), 医学出版社, Tokyo, Mar. 2004.
16.	上西一弘, 海老沢秀道, 遠藤章二, 岡部晋彦, 沖田卓雄, 小野章史, 小野尚美, 加藤秀夫, 金子佳代子, 川内美樹, 木戸康博, 木本眞順美, 久保田恵, 小柏道子, 小垂眞, 小松啓子, 志塚ふじ子, 陶山敦子, 高橋史江, 東條仁美, 中坊幸弘, 中村亜紀, 眞鍋祐之, Kazuaki Mawatari, 村上淳, 村松陽治 and 矢埜みどり : 健康科学シリーズNEXT 応用栄養学, 講談社サイエンティフィック, Dec. 2003.

Academic Paper (Judged Full Paper):

1.	Kai Ishida, Yushi Onoda, Yasuko Kadomura-Ishikawa, Miharu Nagahashi, Michiyo Yamashita, Shiho Fukushima, Toshihiko Aizawa, Shigeharu Yamauchi, Yasuo Fujikawa, Tomotake Tanaka, Takashi Uebanso, Masatake Akutagawa, Kazuaki Mawatari and Akira Takahashi : Development of a standard evaluation method for microbial UV sensitivity using light-emitting diodes, Heliyon, Vol.10, No.6, e27456, 2024. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.heliyon.2024.e27456 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.1016/j.heliyon.2024.e27456 (DOI: 10.1016/j.heliyon.2024.e27456)
2.	Ryo Higashiyama, Yuna Kanda, Takaaki Shimohata, Kai Ishida, Shiho Fukushima, Kohei Yamazaki, Takashi Uebanso, Kazuaki Mawatari, Takashige Kashimoto and Akira Takahashi : Characterization of Outer Membrane Vesicles Produced by Vibrio vulnificus, The Journal of Medical Investigation : JMI, Vol.71, No.1,2, 102-120, 2024. (Tokushima University Institutional Repository) ● Metadata: 119259 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.71.102 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.71.102 (Tokushima University Institutional Repository: 119259, DOI: 10.2152/jmi.71.102)
3.	Takashi Uebanso, Moeka Fukui, Chisato Naito, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : SLC16a6, mTORC1, and autophagy involves ketone body excretion in the intestinal cells, Biology, Vol.12, No.12, 1467, 2023. (Summary) Ketone bodies serve several functions in the intestinal epithelium, such as stem cell maintenance, cell proliferation and differentiation, and cancer growth. Nevertheless, there is limited understanding of the mechanisms governing the regulation of intestinal ketone body concentration. In this study, we elucidated the factors responsible for ketone body production and excretion using shRNA-mediated or pharmacological inhibition of specific genes or functions in the intestinal cells. We revealed that a fasting-mimicked culture medium, which excluded glucose, pyruvate, and glutamine, augmented ketone body production and excretion in the Caco2 and HT29 colorectal cells. This effect was attenuated by glucose or glutamine supplementation. On the other hand, the inhibition of the mammalian target of rapamycin complex1 (mTORC1) recovered a fraction of the excreted ketone bodies. In addition, the pharmacological or shbeclin1-mediated inhibition of autophagy suppressed ketone body excretion. The knockdown of basigin, a transmembrane protein responsible for targeting monocarboxylate transporters (MCTs), such as MCT1 and MCT4, suppressed lactic acid and pyruvic acid excretion but increased ketone body excretion. Finally, we found that MCT7 (SLC16a6) knockdown suppressed ketone body excretion. Our findings indicate that the mTORC1-autophagy axis and MCT7 are potential targets to regulate ketone body excretion from the intestinal epithelium. (Link to Publication Site) ● Publication site (DOI): 10.3390/biology12121467 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38132294 ● Search Scopus @ Elsevier (PMID): 38132294 ● Search Scopus @ Elsevier (DOI): 10.3390/biology12121467 (DOI: 10.3390/biology12121467, PubMed: 38132294)
4.	K. Shinoda, Kazuaki Mawatari, Ngan Thi Kim Bui, H. Hirakawa, K. Awamoto, M. Wakitani, M. Wakitani, T. Shinoda and Akira Takahashi : Development of novel far-UVC light source for high germicidal effects and low human health risk, 2023 IEEE Photonics Conference, IPC 2023 - Proceedings, 2023. (Link to Publication Site) ● Publication site (DOI): 10.1109/IPC57732.2023.10360681 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-85182552166 (DOI: 10.1109/IPC57732.2023.10360681, Elsevier: Scopus)
5.	Eunju Kim, Kazuaki Mawatari, Seung-Hee Yoo and Zheng Chen : The Circadian Nobiletin-ROR Axis Suppresses Adipogenic Differentiation and IκBα/NF-κB Signaling in Adipocytes., Nutrients, Vol.15, No.18, 2023. (Summary) Importantly, RORα/RORγ double knockdown in 3T3-L1 cells (Ror DKD) significantly attenuated the effects of NOB on circadian gene expression and lipid accumulation. Furthermore, whereas NOB upregulated the expression of IκBα, a target of RORs, to inhibit NF-κB activation and proinflammatory cytokine expression, Ror DKD cells exhibited a heightened activation of the NF-κB pathway, further indicating a requisite role of RORs for NOB efficacy in adipocytes. Together, these results highlight a significant regulatory function of the NOB-ROR axis in the circadian expression of clock and clock-controlled genes in adipocytes, thereby governing adipogenic differentiation, lipogenesis, and inflammation. (Keyword) Animals / knockout mice / NF-kappa B / NF-KappaB Inhibitor alpha / Adipocytes / inflammation / Lipids / 3T3-L1 Cells / Flavones (Tokushima University Institutional Repository) ● Metadata: 119579 (Link to Publication Site) ● Publication site (DOI): 10.3390/nu15183919 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37764703 ● Search Scopus @ Elsevier (PMID): 37764703 ● Search Scopus @ Elsevier (DOI): 10.3390/nu15183919 (Tokushima University Institutional Repository: 119579, DOI: 10.3390/nu15183919, PubMed: 37764703)
6.	Shinta Aizawa, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effects of the loss of maternal gut microbiota before pregnancy on gut microbiota, food allergy susceptibility, and epigenetic modification on subsequent generations, Bioscience of Microbiota, Food and Health, Vol.42, No.3, 203-212, 2023. (Summary) Maternal environments affect the health of offspring in later life. Changes in epigenetic modifications may partially explain this phenomenon. The gut microbiota is a critical environmental factor that influences epigenetic modifications of host immune cells and the development of food allergies. However, whether changes in the maternal gut microbiota affect the development of food allergies and related epigenetic modifications in subsequent generations remains unclear. Here, we investigated the effects of antibiotic treatment before pregnancy on the development of the gut microbiota, food allergies, and epigenetic modifications in F1 and F2 mice. We found that pre-conception antibiotic treatment affected the gut microbiota composition in F1 but not F2 offspring. F1 mice born to antibiotic-treated mothers had a lower proportion of butyric acid-producing bacteria and, consequently, a lower butyric acid concentration in their cecal contents. The methylation level in the DNA of intestinal lamina propria lymphocytes, food allergy susceptibility, and production of antigen-specific IgE in the F1 and F2 mice were not different between those born to control and antibiotic-treated mothers. In addition, F1 mice born to antibiotic-treated mothers showed increased fecal excretion related to the stress response in a novel environment. These results suggest that the maternal gut microbiota is effectively passed onto F1 offspring but has little effect on food allergy susceptibility or DNA methylation levels in offspring. (Link to Publication Site) ● Publication site (DOI): 10.12938/bmfh.2022-093 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37404565 ● Search Scopus @ Elsevier (PMID): 37404565 ● Search Scopus @ Elsevier (DOI): 10.12938/bmfh.2022-093 (DOI: 10.12938/bmfh.2022-093, PubMed: 37404565)
7.	Kai Ishida, Takaaki Shimohata, Yuna Kanda, Quoc Anh Nguyen, Rumiko Masuda, Kohei Yamazaki, Takashi Uebanso, Kazuaki Mawatari, Takashige Kashimoto and Akira Takahashi : Characteristic Metabolic Changes in Skeletal Muscle Due to Vibrio vulnificus Infection in a Wound Infection Model., mSystems, Vol.8, No.2, 2023. (Summary) V. vulnificus causes necrotizing skin and soft tissue infections (NSSTIs) in severe cases, with high mortality and sign of rapid deterioration. Despite the severity of the infection, the dysfunction of the host metabolism in skeletal muscle triggered by V. vulnificus is poorly understood. In this study, by using a mouse wound infection model, we revealed characteristic changes in muscle catabolism and energy metabolism in skeletal muscle associated with bacterial proliferation in the infected tissues. Understanding such metabolic changes in V. vulnificus-infected tissue may provide crucial information to identify the mechanism via which V. vulnificus induces severe infections. Moreover, our metabolite data may be useful for the recognition, identification, or detection of V. vulnificus infections in clinical studies. (Keyword) Humans / Bacterial Toxins / Vibrio Infections / Virulence Factors / Muscle, Skeletal (Tokushima University Institutional Repository) ● Metadata: 118290 (Link to Publication Site) ● Publication site (DOI): 10.1128/msystems.00682-22 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36939368 ● Search Scopus @ Elsevier (PMID): 36939368 ● Search Scopus @ Elsevier (DOI): 10.1128/msystems.00682-22 (Tokushima University Institutional Repository: 118290, DOI: 10.1128/msystems.00682-22, PubMed: 36939368)
8.	Kazuaki Mawatari, Nobuya Koike, Kazunari Nohara, Marvin Wirianto, Takashi Uebanso, Takaaki Shimohata, Yasuhiro Shikishima, Hiroyuki Miura, Yoshitaka Nii, J Mark Burish, Kazuhiro Yagita, Akira Takahashi, Seung-Hee Yoo and Zheng Chen : The Polymethoxyflavone Sudachitin Modulates the Circadian Clock and Improves Liver Physiology., Molecular Nutrition & Food Research, Vol.67, No.9, 2023. (Summary) This study elucidates Sudachitin as a new clock-modulating PMF with beneficial effects to improve diurnal metabolic homeostasis and liver physiology, suggesting the circadian clock as a fundamental mechanism to safeguard physiological well-being. (Keyword) Mice / Animals / Circadian Clocks / ARNTL Transcription Factors / Flavonoids / Liver / Circadian Rhythm / CLOCK Proteins (Tokushima University Institutional Repository) ● Metadata: 118294 (Link to Publication Site) ● Publication site (DOI): 10.1002/mnfr.202200270 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36829302 ● CiNii @ National Institute of Informatics (CRID): 1050299595815331328 ● Summary page in Scopus @ Elsevier: 2-s2.0-85150827501 (Tokushima University Institutional Repository: 118294, DOI: 10.1002/mnfr.202200270, PubMed: 36829302, CiNii: 1050299595815331328, Elsevier: Scopus)
9.	ANAYT ULLA, Kanae Osaki, Mizanur Md Rahman, Reiko Nakao, Takayuki Uchida, Isafumi Maru, Kazuaki Mawatari, Tomoya Fukawa, Hiro-omi Kanayama, Iori Sakakibara, Katsuya Hirasaka and Takeshi Nikawa : Morin improves dexamethasone-induced muscle atrophy by modulating atrophy-related genes and oxidative stress in female mice., Bioscience, Biotechnology, and Biochemistry, Vol.86, No.10, 1448-1458, 2022. (Summary) This study investigated the effect of morin, a flavonoid, on dexamethasone-induced muscle atrophy in C57BL/6J female mice. Dexamethasone (10 mg/kg body weight) for 10 days significantly reduced body weight, gastrocnemius and tibialis anterior muscle mass, and muscle protein in mice. Dexamethasone significantly upregulated muscle atrophy-associated ubiquitin ligases, including atrogin-1 and MuRF-1, and the upstream transcription factors FoxO3a and Klf15. Additionally, dexamethasone significantly induced the expression of oxidative stress-sensitive ubiquitin ligase Cbl-b and the accumulation of the oxidative stress markers malondialdehyde and advanced protein oxidation products in both the plasma and skeletal muscle samples. Intriguingly, morin treatment (20 mg/kg body weight) for 17 days effectively attenuated the loss of muscle mass and muscle protein and suppressed the expression of ubiquitin ligases while reducing the expression of upstream transcriptional factors. Therefore, morin might act as a potential therapeutic agent to attenuate muscle atrophy by modulating atrophy-inducing genes and preventing oxidative stress. (Keyword) Animals / Body Weight / Dexamethasone / Female / Flavones / Malondialdehyde / Mice / Mice, Inbred C57BL / Muscle Proteins / Muscle, Skeletal / Muscular Atrophy / Oxidative Stress / Tripartite Motif Proteins / Ubiquitin-Protein Ligases (Link to Publication Site) ● Publication site (DOI): 10.1093/bbb/zbac140 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35977398 ● Search Scopus @ Elsevier (PMID): 35977398 ● Search Scopus @ Elsevier (DOI): 10.1093/bbb/zbac140 (DOI: 10.1093/bbb/zbac140, PubMed: 35977398)
10.	Tomoki Ozaki, Yuta Yoshino, Ayumi Tachibana, Hideaki Shimizu, Takaaki Mori, Tomohiko Nakayama, Kazuaki Mawatari, Shusuke Numata, Junichi Iga, Akira Takahashi, Tetsuro Ohmori and Shu-ichi Ueno : Metabolomic alterations in the blood plasma of older adults with mild cognitive impairment and Alzheimer's disease (from the Nakayama Study)., Scientific Reports, Vol.12, No.1, 15205, 2022. (Summary) Alzheimer's disease (AD) is a progressive disease, and the number of AD patients is increasing every year as the population ages. One of the pathophysiological mechanisms of AD is thought to be the effect of metabolomic abnormalities. There have been several studies of metabolomic abnormalities of AD, and new biomarkers are being investigated. Metabolomic studies have been attracting attention, and the aim of this study was to identify metabolomic biomarkers associated with AD and mild cognitive impairment (MCI). Of the 927 participants in the Nakayama Study conducted in Iyo City, Ehime Prefecture, 106 were selected for this study as Control (n = 40), MCI (n = 26), and AD (n = 40) groups, matched by age and sex. Metabolomic comparisons were made across the three groups. Then, correlations between metabolites and clinical symptoms were examined. The blood mRNA levels of the ornithine metabolic enzymes were also measured. Of the plasma metabolites, significant differences were found in ornithine, uracil, and lysine. Ornithine was significantly decreased in the AD group compared to the Control and MCI groups (Control vs. AD: 97.2 vs. 77.4; P = 0.01, MCI vs. AD: 92.5 vs. 77.4; P = 0.02). Uracil and lysine were also significantly decreased in the AD group compared to the Control group (uracil, Control vs. AD: 272 vs. 235; P = 0.04, lysine, Control vs. AD: 208 vs. 176; P = 0.03). In the total sample, the MMSE score was significantly correlated with lysine, ornithine, thymine, and uracil. The Barthel index score was significantly correlated with lysine. The instrumental activities of daily living (IADL) score were significantly correlated with lysine, betaine, creatine, and thymine. In the ornithine metabolism pathway, the spermine synthase mRNA level was significantly decreased in AD. Ornithine was decreased, and mRNA expressions related to its metabolism were changed in the AD group compared to the Control and MCI groups, suggesting an association between abnormal ornithine metabolism and AD. Increased betaine and decreased methionine may also have the potential to serve as markers of higher IADL in elderly persons. Plasma metabolites may be useful for predicting the progression of AD. (Keyword) Activities of Daily Living / Aged / Alzheimer Disease / Betaine / Biomarkers / Cognitive Dysfunction / Humans / Lysine / Ornithine / plasma / RNA, Messenger / Thymine (Link to Publication Site) ● Publication site (DOI): 10.1038/s41598-022-19670-y (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36075959 ● Search Scopus @ Elsevier (PMID): 36075959 ● Search Scopus @ Elsevier (DOI): 10.1038/s41598-022-19670-y (DOI: 10.1038/s41598-022-19670-y, PubMed: 36075959)
11.	Toshiharu Kamishikiryo, Go Okada, Eri Itai, Yoshikazu Masuda, Satoshi Yokoyama, Masahiro Takamura, Manabu Fuchikami, Atsuo Yoshino, Kazuaki Mawatari, Shusuke Numata, Akira Takahashi, Tetsuro Ohmori and Yasumasa Okamoto : Left DLPFC activity is associated with plasma kynurenine levels and can predict treatment response to escitalopram in major depressive disorder., Psychiatry and Clinical Neurosciences, Vol.76, No.8, 367-376, 2022. (Summary) Decreased resting-state regional activity of the left DLPFC and decreased plasma kynurenine levels may predict treatment response to escitalopram, suggesting that it may be involved in the pathophysiology of major depressive disorder in response to escitalopram treatment. (Keyword) Depressive Disorder, Major / Escitalopram / Humans / Kynurenine / magnetic resonance imaging / Prefrontal Cortex / Transcranial Magnetic Stimulation (Tokushima University Institutional Repository) ● Metadata: 117849 (Link to Publication Site) ● Publication site (DOI): 10.1111/pcn.13373 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35543406 ● Search Scopus @ Elsevier (PMID): 35543406 ● Search Scopus @ Elsevier (DOI): 10.1111/pcn.13373 (Tokushima University Institutional Repository: 117849, DOI: 10.1111/pcn.13373, PubMed: 35543406)
12.	Shiho Fukushima, Takaaki Shimohata, Yuri Inoue, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Recruitment of LC3 by Campylobacter jejuni to Bacterial Invasion Site on Host Cells via the Rac1-Mediated Signaling Pathway, Frontiers in Cellular and Infection Microbiology, Vol.12, 829682, 2022. (Summary) Campylobacter jejuni is a leading cause of food-borne disease worldwide. The pathogenicity of C. jejuni is closely associated with the internalization process in host epithelial cells, which is related to a host immune response. Autophagy indicates a key role in the innate immune system of the host to exclude invasive pathogens. Most bacteria are captured by autophagosomes and degraded by autophagosome-lysosome fusion in host cells. However, several pathogens, such as Salmonella and Shigella, avoid and/or escape autophagic degradation to establish infection. But autophagy involvement as a host immune response to C. jejuni infection has not been clarified. This study revealed autophagy association in C. jejuni infection. During infection, C. jejuni activated the Rho family small GTPase Rac1 signaling pathway, which modulates actin remodeling and promotes the internalization of this pathogen. In this study, we found the LC3 contribution to C. jejuni invasion signaling via the Rac1 signaling pathway. Interestingly, during C. jejuni invasion, LC3 was recruited to bacterial entry site depending on Rac1 GTPase activation just at the early step of the infection. C. jejuni infection induced LC3-II conversion, and autophagy induction facilitated C. jejuni internalization. Also, autophagy inhibition attenuated C. jejuni invasion step. Moreover, Rac1 recruited LC3 to the cellular membrane, activating the invasion of C. jejuni. Altogether, our findings provide insights into the new function of LC3 in bacterial invasion. We found the interaction between the Rho family small GTPase, Rac1, and autophagy-associated protein, LC3. (Keyword) bacteria / Campylobacter Infections / Campylobacter jejuni / Epithelial Cells / Humans / Microtubule-Associated Proteins / signal transduction / Virulence / rac1 GTP-Binding Protein (Tokushima University Institutional Repository) ● Metadata: 117002 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcimb.2022.829682 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35310852 ● Search Scopus @ Elsevier (PMID): 35310852 ● Search Scopus @ Elsevier (DOI): 10.3389/fcimb.2022.829682 (Tokushima University Institutional Repository: 117002, DOI: 10.3389/fcimb.2022.829682, PubMed: 35310852)
13.	Ngan Thi Kim Bui, Kazuaki Mawatari, Takahiro Emoto, Shiho Fukushima, Takaaki Shimohata, Takashi Uebanso, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : UV-LED irradiation reduces the infectivity of herpes simplex virus type 1 by targeting different viral components depending on the peak wavelength., Journal of Photochemistry and Photobiology B: Biology, Vol.228, 112410, 2022. (Summary) Herpes simplex virus type 1 (HSV-1) is an enveloped virus that mainly infects humans. Given its high global prevalence, disinfection is critical for reducing the risk of infection. Ultraviolet-light-emitting diodes (UV-LEDs) are eco-friendly irradiating modules with different peak wavelengths, but the molecules degraded by UV-LED irradiation have not been clarified. To identify the target viral molecules of UV-LEDs, we exposed HSV-1 suspensions to UV-LED irradiation at wavelengths of 260-, 280-, 310-, and 365-nm and measured viral DNA, protein, and lipid damage and infectivity in host cells. All UV-LEDs substantially reduced by inhibiting host cell transcription, but 260- and 280-nm UV-LEDs had significantly stronger virucidal efficiency than 310- and 365-nm UV-LEDs. Meanwhile, 260- and 280-nm UV-LEDs induced the formation of viral DNA photoproducts and the degradation of viral proteins and some phosphoglycerolipid species. Unlike 260- and 280-nm UV-LEDs, 310- and 365-nm UV-LEDs decreased the viral protein levels, but they did not drastically change the levels of viral DNA photoproducts and lipophilic metabolites. These results suggest that UV-LEDs reduce the infectivity of HSV-1 by targeting different viral molecules based on the peak wavelength. These findings could facilitate the optimization of UV-LED irradiation for viral inactivation. (Keyword) Disinfection / Herpesvirus 1, Human / Humans / Ultraviolet Rays / Viral Structures / Virus Inactivation / Water Purification (Tokushima University Institutional Repository) ● Metadata: 117004 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jphotobiol.2022.112410 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35193038 ● Search Scopus @ Elsevier (PMID): 35193038 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jphotobiol.2022.112410 (Tokushima University Institutional Repository: 117004, DOI: 10.1016/j.jphotobiol.2022.112410, PubMed: 35193038)
14.	Tsubasa Kondo, Takashi Uebanso, Natsuki Arao, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effect of T1R3 Taste Receptor Gene Deletion on Dextran Sulfate Sodium-Induced Colitis in Mice., Journal of Nutritional Science and Vitaminology, Vol.68, No.3, 204-212, 2022. (Summary) Taste receptor type 1 member 3 (T1R3) recognize umami or sweet tastes and also contributes type 2 immunity and autophagy in small intestine and muscle cells, respectively. Since imbalance of type 1 and type 2 immunity and autophagy affect intestinal bowel disease (IBD), we hypothesized that T1R3 have a potential role in the incidence and progression of colitis. In the present study, we investigated whether genetic deletion of T1R3 impacted aggravation of DSS-induced colitis in mice. We found that T1R3-KO mice showed reduction in colon damage, including reduced inflammation and colon shrinking relative to those of WT mice following DSS treatment. mRNA expression of tight junction components, particularly claudin1 was significantly lower in T1R3-KO mice with trend to lower inflammation related gene mRNA expression in colon. Other parameters, such as response to microbial stimuli in splenic lymphocytes and peritoneal macrophages, gut microbiota composition, and expression of autophagy-related proteins, were similar between WT and KO mice. Together, these results indicated that deletion of T1R3 has a minor role in intestinal inflammation induced by DSS-induced acute colitis in mice. (Keyword) Animals / Colitis / Colon / Dextran Sulfate / Disease Models, Animal / Gene Deletion / inflammation / Mice / Mice, Inbred C57BL / knockout mice / RNA, Messenger / Taste (Link to Publication Site) ● Publication site (DOI): 10.3177/jnsv.68.204 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35768251 ● CiNii @ National Institute of Informatics (CRID): 1390011097096971008 ● Summary page in Scopus @ Elsevier: 2-s2.0-85133147656 (DOI: 10.3177/jnsv.68.204, PubMed: 35768251, CiNii: 1390011097096971008, Elsevier: Scopus)
15.	Takashi Uebanso, Mai Suyama, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effect of Vitamin B2-Deficient Diet on Hydroxyproline- or Obesity-Induced Hyperoxaluria in Mice., Molecular Nutrition & Food Research, Vol.65, No.15, e2100226, 2021. (Summary) Together these results suggest that VB2 restriction could be a new dietary approach to improve hyperoxaluria when endogenous production of oxalate is increased. (Keyword) Alcohol Oxidoreductases / Animals / Creatinine / Diet / Hydroxyproline / Hyperoxaluria / Kidney / male / Mice, Inbred C57BL / Mice, Obese / obesity / Oxalates / Riboflavin / Riboflavin Deficiency (Link to Publication Site) ● Publication site (DOI): 10.1002/mnfr.202100226 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34110671 ● Search Scopus @ Elsevier (PMID): 34110671 ● Search Scopus @ Elsevier (DOI): 10.1002/mnfr.202100226 (DOI: 10.1002/mnfr.202100226, PubMed: 34110671)
16.	J Mark Burish, Chorong Han, Kazuaki Mawatari, Marvin Wirianto, Eunju Kim, Kaori Ono, Randika Parakramaweera, Zheng Chen and Seung-Hee Yoo : The first-line cluster headache medication verapamil alters the circadian period and elicits sex-specific sleep changes in mice., Chronobiology International, Vol.38, No.6, 839-850, 2021. (Summary) reporter mice, perhaps due to the exceptionally tight coupling in the SCN. Thus, verapamil affects both peripheral (trigeminal ganglion) and central (hypothalamus and cerebellum) nervous system structures involved in cluster headache pathophysiology, possibly with network effects instead of isolated SCN effects. These studies suggest that verapamil is a circadian modulator in laboratory models at both molecular and behavioral levels, and sex is an important biological variable for cluster headache medications. These observations highlight the circadian system as a potential convergent target for cluster headache medications with different primary mechanisms of action. (Keyword) Animals / Circadian Clocks / Circadian Rhythm / Cluster Headache / female / male / Mice / Mice, Inbred C57BL / Period Circadian Proteins / sleep / Suprachiasmatic Nucleus / Verapamil (Tokushima University Institutional Repository) ● Metadata: 117436 (Link to Publication Site) ● Publication site (DOI): 10.1080/07420528.2021.1892127 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33829951 ● Search Scopus @ Elsevier (PMID): 33829951 ● Search Scopus @ Elsevier (DOI): 10.1080/07420528.2021.1892127 (Tokushima University Institutional Repository: 117436, DOI: 10.1080/07420528.2021.1892127, PubMed: 33829951)
17.	Hitomi Iba, Takaaki Shimohata, Junko Kido, Sho Hatayama, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Vibrio parahaemolyticus induces inflammation-associated fluid accumulation via activation of the cystic fibrosis transmembrane conductance regulator., The Journal of Medical Investigation : JMI, Vol.68, No.1.2, 59-70, 2021. (Summary) Vibrio parahaemolyticus is a foodborne bacterium that causes acute gastroenteritis through the consumption of contaminated, raw, or undercooked seafood. Cystic fibrosis transmembrane conductance regulator (CFTR) is a well-characterized chloride channel that regulates several other ion channels and transporters to maintain water homeostasis in the gut lumen. Also, CFTR is a main target of bacterial infection-associated diarrhea. Hence, the aim of this study was to clarify the contribution of CFTR in V. parahaemolyticus-induced diarrhea in a mouse model of intestinal loop fluid accumulation, with CFTR inhibitors and a CFTR knockout model. The results indicated that CFTR plays a critical role in fluid accumulation in response to V. parahaemolyticus infection. We also investigated the inflammatory association in CFTR-mediated V. parahaemolyticus-induced fluid secretion with cyclooxygenase inhibitors and found that fluid accumulation was decreased by inhibition of cyclooxygenase 2 produced by neutrophils. These findings suggest that V. parahaemolyticus-inducing infiltration and activation of neutrophils also participated in CFTR mediated fluid secretion. This study reveals an important relationship between V. parahaemolyticus-induced diarrhea and inflammation in a mouse model. J. Med. Invest. 68 : 59-70, February, 2021. (Keyword) Animals / Cystic Fibrosis Transmembrane Conductance Regulator / Diarrhea / Gastroenteritis / inflammation / Mice / Vibrio parahaemolyticus (Tokushima University Institutional Repository) ● Metadata: 115628 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.68.59 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33994481 ● Search Scopus @ Elsevier (PMID): 33994481 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.68.59 (Tokushima University Institutional Repository: 115628, DOI: 10.2152/jmi.68.59, PubMed: 33994481)
18.	Miki Yasui-Maetani, Kazuaki Mawatari, Airi Honjo, Bui Kim Thi Ngan, Takaaki Shimohata, Takashi Uebanso, Mutsumi Aihara, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Identification of Genes Associated with Sensitivity to Ultraviolet A (UVA) Irradiation by Transposon Mutagenesis of Vibrio parahaemolyticu, Applied Sciences, Vol.10, No.16, 2020. (Tokushima University Institutional Repository) ● Metadata: 115319 (Link to Publication Site) ● Publication site (DOI): 10.3390/app10165549 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3390/app10165549 (Tokushima University Institutional Repository: 115319, DOI: 10.3390/app10165549)
19.	Quoc Anh Nguyen, Takaaki Shimohata, Sho Hatayama, Aya Tentaku, Junko Kido, Huong Thi Mai Bui, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Type III Secretion Effector VopQ of Vibrio parahaemolyticus Modulates Central Carbon Metabolism in Epithelial Cells., mSphere, Vol.5, No.2, e00960--19, 2020. (Summary) infection. (Tokushima University Institutional Repository) ● Metadata: 114634 (Link to Publication Site) ● Publication site (DOI): 10.1128/mSphere.00960-19 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32188755 ● Search Scopus @ Elsevier (PMID): 32188755 ● Search Scopus @ Elsevier (DOI): 10.1128/mSphere.00960-19 (Tokushima University Institutional Repository: 114634, DOI: 10.1128/mSphere.00960-19, PubMed: 32188755)
20.	Takashi Uebanso, Ayumi Yoshimoto, Shinta Aizawa, Maya Nakamura, Rumiko Masuda, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Glycolate is a Novel Marker of Vitamin B2 Deficiency Involved in Gut Microbe Metabolism in Mice., Nutrients, Vol.12, No.3, E736, 2020. (Summary) (VB2) deficiency, and show that gut microbiota sense dietary VB2 deficiency and accumulate GA in response. The plasma GA concentration responded to reduced VB2 supply from both the gut microbiota and the diet. These results suggest that GA is a novel marker that can be used to assess whether or not the net supply of VB2 from dietary sources and gut microbiota is sufficient. We also found that gut microbiota can provide short-term compensation for host VB2 deficiency when dietary VB2 is withheld. (Tokushima University Institutional Repository) ● Metadata: 115656 (Link to Publication Site) ● Publication site (DOI): 10.3390/nu12030736 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32168816 ● Search Scopus @ Elsevier (PMID): 32168816 ● Search Scopus @ Elsevier (DOI): 10.3390/nu12030736 (Tokushima University Institutional Repository: 115656, DOI: 10.3390/nu12030736, PubMed: 32168816)
21.	Maria Ulfa, Momoyo Azuma, Masami Satou, Takaaki Shimohata, Shiho Fukushima, Junko Kido, Mariko Nakamoto, Takashi Uebanso, Kazuaki Mawatari, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Inactivation of Extended-spectrum β-Lactamase (ESBL)-producing Escherichia Coli by UVA-LED Irradiation System., The Journal of Medical Investigation : JMI, Vol.67, No.1-2, 163-169, 2020. (Summary) The prevalence of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli is increasing rapidly and spreading worldwide, particularly in Asia, compared to other regions. In the last ten years, in our hospital, in particular, there has been a < 30% increase. To prevent the spread of ESBL in hospitals and the community, the ultraviolet (UV) A-light-emitting diode (LED) irradiation device was used to inactivate ESBL-E. coli in human livestock and the environment. ESBL-E. coli and E. coli bacterial samples were collected from patients at Tokushima University Hospital (Tokushima City, Japan). The UVA-LED irradiation system had 365 nm single wavelength, and the current of the circuit was set to 0.23 or 0.50 A consistently. Results demonstrated that UVA-LED was useful for the inactivation of ESBL-E. coli and E. coli. The minimum energy dosage required to inactivate ESBL-E. coli and E. coli was 40.76 J/cm2 (45 min) in the first type of UVA-LED and 38.85 J/cm2 (5 min) in the second type. There were no significant differences between ESBL-E. coli and E. coli. The inactivation of ESBL-E. coli was dependent on energy. These findings suggest that UVA-LED with 365 nm single wavelength could be useful for surface decontamination in healthcare facilities. J. Med. Invest. 67 : 163-169, February, 2020. (Tokushima University Institutional Repository) ● Metadata: 114642 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.67.163 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378601 ● Summary page in Scopus @ Elsevier: 2-s2.0-85084329310 (Tokushima University Institutional Repository: 114642, DOI: 10.2152/jmi.67.163, PubMed: 32378601, Elsevier: Scopus)
22.	Takaaki Shimohata, Kazuaki Mawatari, Takashi Uebanso, Airi Honjo, Akari Tsunedomi, Sho Hatayama, Yuri Sato, Junko Kido, Risa Nishisaka, Ayumi Yoshimoto, Tomoko Yamashita, Sachie Amano, Miki Maetani-Yasui, Hitomi Iba, Yumi Harada, Mutsumi Nakahashi, Sonoko Yasui-Yamada, Yasuhiro Hamada, Tadahiko Nakagawa, Masahiro Sogabe, Takahiro Emoto, Masatake Akutagawa, Toshiya Okahisa, Yohsuke Kinouchi and Akira Takahashi : Bacterial Contamination of Hemodialysis Devices in Hospital Dialysis Wards., The Journal of Medical Investigation : JMI, Vol.66, No.1.2, 148-152, 2019. (Summary) Chronic care patients undergoing hemodialysis for treatment of end-stage renal failure experience higher rates of bloodstream-associated infection due to the patients' compromised immune system and management of the bloodstream through catheters. Staphylococcus species are acommon cause of hemodialysis catheterrelated bloodstream infections. We investigated environmental bacterial contamination of dialysis wards and contamination of hemodialysis devices to determine the source of bacteria for these infections. All bacterial samples were collected by the swab method and the agarose stamp method. And which bacterium were identified by BBL CRYSTAL Kit or 16s rRNA sequences. In our data, bacterial cell number of hemodialysis device was lower than environment of patient surrounds. But Staphylococcus spp. were found predominantly on the hemodialysis device (46.8%), especially on areas frequently touched by healthcare-workers (such as Touch screen). Among Staphylococcus spp., Staphylococcus epidermidis was most frequently observed (42.1% of Staphylococcus spp.), and more surprising, 48.2% of the Staphylococcus spp. indicated high resistance for methicillin. Our finding suggests that hemodialysis device highly contaminated with bloodstream infection associated bacteria. This study can be used as a source to assess the risk of contamination-related infection and to develop the cleaning system for the better prevention for bloodstream infections in patients with hemodialysis. J. Med. Invest. 66 : 148-152, February, 2019. (Tokushima University Institutional Repository) ● Metadata: 113411 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.66.148 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31064928 ● Search Scopus @ Elsevier (PMID): 31064928 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.66.148 (Tokushima University Institutional Repository: 113411, DOI: 10.2152/jmi.66.148, PubMed: 31064928)
23.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Junko Kido, Quoc Anh Nguyen, Yuna Kanda, Shiho Fukushima, Takashi Uebanso, Taketoshi Iwata, Kazuaki Mawatari, Nagakatsu Harada and Akira Takahashi : Host cellular unfolded protein response signaling regulates Campylobacter jejuni invasion., PLoS ONE, Vol.13, No.10, 2018. (Summary) Campylobacter jejuni is a major cause of bacterial foodborne illness in humans worldwide. Bacterial entry into a host eukaryotic cell involves the initial steps of adherence and invasion, which generally activate several cell-signaling pathways that induce the activation of innate defense systems, which leads to the release of proinflammatory cytokines and induction of apoptosis. Recent studies have reported that the unfolded protein response (UPR), a system to clear unfolded proteins from the endoplasmic reticulum (ER), also participates in the activation of cellular defense mechanisms in response to bacterial infection. However, no study has yet investigated the role of UPR in C. jejuni infection. Hence, the aim of this study was to deduce the role of UPR signaling via induction of ER stress in the process of C. jejuni infection. The results suggest that C. jejuni infection suppresses global protein translation. Also, 12 h of C. jejuni infection induced activation of the eIF2α pathway and expression of the transcription factor CHOP. Interestingly, bacterial invasion was facilitated by knockdown of UPR-associated signaling factors and treatment with the ER stress inducers, thapsigargin and tunicamycin, decreased the invasive ability of C. jejuni. An investigation into the mechanism of UPR-mediated inhibition of C. jejuni invasion showed that UPR signaling did not affect bacterial adhesion to or survival in the host cells. Further, Salmonella Enteritidis or FITC-dextran intake were not regulated by UPR signaling. These results indicated that the effect of UPR on intracellular intake was specifically found in C. jejuni infection. These findings are the first to describe the role of UPR in C. jejuni infection and revealed the participation of a new signaling pathway in C. jejuni invasion. UPR signaling is involved in defense against the early step of C. jejuni invasion and thus presents a potential therapeutic target for the treatment of C. jejuni infection. (Keyword) Caco-2 Cells / Campylobacter jejuni / Endoplasmic Reticulum Stress / Thapsigargin / Transcription Factor CHOP / Tunicamycin / Unfolded Protein Response (Tokushima University Institutional Repository) ● Metadata: 114338 (Link to Publication Site) ● Publication site (DOI): 10.1371/journal.pone.0205865 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30321237 ● Search Scopus @ Elsevier (PMID): 30321237 ● Search Scopus @ Elsevier (DOI): 10.1371/journal.pone.0205865 (Tokushima University Institutional Repository: 114338, DOI: 10.1371/journal.pone.0205865, PubMed: 30321237)
24.	Sho Hatayama, Takaaki Shimohata, Sachie Amano, Junko Kido, Q Anh Nguyen, Yuri Sato, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Invasion and Inflammatory Barrier Disruption Promoting Bacterial Invasion from Lateral Membrane in Polarized Intestinal Epithelial Cells., Frontiers in Cellular and Infection Microbiology, Vol.8, No.30, 2018. (Summary) Campylobacter jejuni invasion is closely related to C. jejuni pathogenicity. The intestinal epithelium contains polarized epithelial cells that form tight junctions (TJs) to provide a physical barrier against bacterial invasion. Previous studies indicated that C. jejuni invasion of non-polarized cells involves several cellular features, including lipid rafts. However, the dynamics of C. jejuni invasion of polarized epithelial cells are not fully understood. Here we investigated the interaction between C. jejuni invasion and TJ formation to characterize the mechanism of C. jejuni invasion in polarized epithelial cells. In contrast to non-polarized epithelial cells, C. jejuni invasion was not affected by depletion of lipid rafts in polarized epithelial cells. However, depletion of lipid rafts significantly decreased C. jejuni invasion in TJ disrupted cells or basolateral infection and repair of cellular TJs suppressed lipid raft-mediated C. jejuni invasion in polarized epithelial cells. In addition, pro-inflammatory cytokine, TNF- treatment that induce TJ disruption promote C. jejuni invasion and lipid rafts depletion significantly reduced C. jejuni invasion in TNF- treated cells. These data demonstrated that TJs prevent C. jejuni invasion from the lateral side of epithelial cells, where they play a main part in bacterial invasion and suggest that C. jejuni invasion could be increased in inflammatory condition. Therefore, maintenance of TJs integrity should be considered important in the development of novel therapies for C. jejuni infection. (Tokushima University Institutional Repository) ● Metadata: 111607 (Link to Publication Site) ● Publication site (DOI): 10.3389/fcimb.2018.00015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29441328 ● Search Scopus @ Elsevier (PMID): 29441328 ● Search Scopus @ Elsevier (DOI): 10.3389/fcimb.2018.00015 (Tokushima University Institutional Repository: 111607, DOI: 10.3389/fcimb.2018.00015, PubMed: 29441328)
25.	Ayumi Yoshimoto, Takashi Uebanso, Mutsumi Nakahashi, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effect of prenatal administration of low dose antibiotics on gut microbiota and body fat composition of newborn mice., Journal of Clinical Biochemistry and Nutrition, Vol.62, No.2, 155-160, 2017. (Summary) Several environmental factors during the prenatal period transgenerationally affect the health of newborns in later life. Because low-dose antibiotics have been used for promoting the growth of crops and livestock in agriculture, humans may have ingested residual antibiotics for several decades. However, the effect of prenatal administration of low-dose antibiotics on newborns' health in later life is unclear. In the present study, we found that prenatal treatment of murine mothers with low-dose antibiotics increased the abundance of bacteria of the phylum Firmicutes and the genera Clostridium IV and XIVa in feces from pups. In addition, the body fat percentage of mice in the antibiotic-treated group was higher than those in the control group at 12 weeks of age even though all pups were fed a standard diet. The body fat percentage of all mice was correlated with the abundance of fecal bacteria of Clostridium IV and XIVa. These results predict that low-dose antibiotic administration during the prenatal period affects the gut microbiota of newborns and possibly their health in later life. (Tokushima University Institutional Repository) ● Metadata: 114647 (Link to Publication Site) ● Publication site (DOI): 10.3164/jcbn.17-53 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29610555 ● Search Scopus @ Elsevier (PMID): 29610555 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.17-53 (Tokushima University Institutional Repository: 114647, DOI: 10.3164/jcbn.17-53, PubMed: 29610555)
26.	Junko Kido, Takaaki Shimohata, Sachie Amano, Syo Hatayama, Quoc Anh Nguyen, Yuri Sato, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR reduces microtubule-dependent Campylobacter jejuni invasion., Infection and Immunity, 2017. (Summary) Campylobacter jejuni (C. jejuni) is gastroenteritis inducible food-born pathogen. Invasion and adhesion process are essential for leading gastroenteritis in C. jejuni infection process. As against bacterial strategy for efficacy invasion and adhesion, mucosal layer play a key role in defense systems, which modulated by several ion channels and transporters mediated water flux on the intestine. Cystic fibrosis transmembrane conductance regulator (CFTR) play the main role in waterfulux in intestine, and it closely related with bacterial clearance. We previously reported that C. jejuni infection suppresses CFTR channel activity in intestinal epithelial cells, however the mechanism and importance of this suppression is unclear. This study seeks to elucidate the role of CFTR in C. jejuni-infection. Using HEK293 cells that stably express wild type and mutated CFTR, we found that CFTR attenuated C. jejuni invasion, it was not involved bacterial adhesion or intracellular survival but associated with microtubule-dependent cellular transport. Moreover we revealed that CFTR attenuated function of microtubule motor protein but not microtubule stability, which causes inhibition of C. jejuni-invasion. Meanwhile, the CFTR mutant G551D-CFTR, which has defects in channel activity, suppressed C. jejuni-invasion, whereasF508-CFTR, which has defects in maturation, did not suppress, suggesting that CFTR suppression of C. jejuni-invasion is related to CFTR maturation but not channel activity.Taken together, mature CFTR inhibited C. jejuni invasion by regulating microtubule-mediated pathways. We suggest that CFTR plays a critical role in cellular defenses against C. jejuni-invasion, and CFTR suppression may be an initial step in promoting cellular invasion during C. jejuni-infection. (Tokushima University Institutional Repository) ● Metadata: 114676 (Link to Publication Site) ● Publication site (DOI): 10.1128/IAI.00311-17 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28784926 ● Search Scopus @ Elsevier (PMID): 28784926 ● Search Scopus @ Elsevier (DOI): 10.1128/IAI.00311-17 (Tokushima University Institutional Repository: 114676, DOI: 10.1128/IAI.00311-17, PubMed: 28784926)
27.	Takashi Uebanso, Saki Kano, Ayumi Yoshimoto, Chisato Naito, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effects of Consuming Xylitol on Gut Microbiota and Lipid Metabolism in Mice., Nutrients, Vol.9, No.7, 756, 2017. (Summary) The sugar alcohol xylitol inhibits the growth of some bacterial species including Streptococcus mutans. It is used as a food additive to prevent caries. We previously showed that 1.5-4.0 g/kg body weight/day xylitol as part of a high-fat diet (HFD) improved lipid metabolism in rats. However, the effects of lower daily doses of dietary xylitol on gut microbiota and lipid metabolism are unclear. We examined the effect of 40 and 200 mg/kg body weight/day xylitol intake on gut microbiota and lipid metabolism in mice. Bacterial compositions were characterized by denaturing gradient gel electrophoresis and targeted real-time PCR. Luminal metabolites were determined by capillary electrophoresis electrospray ionization time-of-flight mass spectrometry. Plasma lipid parameters and glucose tolerance were examined. Dietary supplementation with low- or medium-dose xylitol (40 or 194 mg/kg body weight/day, respectively) significantly altered the fecal microbiota composition in mice. Relative to mice not fed xylitol, the addition of medium-dose xylitol to a regular and HFD in experimental mice reduced the abundance of fecal Bacteroidetes phylum and the genus Barnesiella, whereas the abundance of Firmicutes phylum and the genus Prevotella was increased in mice fed an HFD with medium-dose dietary xylitol. Body composition, hepatic and serum lipid parameters, oral glucose tolerance, and luminal metabolites were unaffected by xylitol consumption. In mice, 40 and 194 mg/kg body weight/day xylitol in the diet induced gradual changes in gut microbiota but not in lipid metabolism. (Tokushima University Institutional Repository) ● Metadata: 115660 (Link to Publication Site) ● Publication site (DOI): 10.3390/nu9070756 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28708089 ● Summary page in Scopus @ Elsevier: 2-s2.0-85025080133 (Tokushima University Institutional Repository: 115660, DOI: 10.3390/nu9070756, PubMed: 28708089, Elsevier: Scopus)
28.	Takashi Uebanso, Ai Ohnishi, Reiko Kitayama, Ayumi Yoshimoto, Mutsumi Nakahashi, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effects of Low-Dose Non-Caloric Sweetener Consumption on Gut Microbiota in Mice., Nutrients, Vol.9, No.6, 2017. (Summary) Abstract: Non-caloric artificial sweeteners (NASs) provide sweet tastes to food without adding calories or glucose. NASs can be used as alternative sweeteners for controlling blood glucose levels and weight gain. Although the consumption of NASs has increased over the past decade in Japan and other countries, whether these sweeteners affect the composition of the gut microbiome is unclear. In the present study, we examined the effects of sucralose or acesulfame-K ingestion (at most the maximum acceptable daily intake (ADI) levels, 15 mg/kg body weight) on the gut microbiome in mice. Consumption of sucralose, but not acesulfame-K, for 8 weeks reduced the relative amount of Clostridiumcluster XIVa in feces. Meanwhile, sucralose and acesulfame-K did not increase food intake, body weight gain or liver weight, or fat in the epididymis or cecum. Only sucralose intake increased the concentration of hepatic cholesterol and cholic acid. Moreover, the relative concentration of butyrate and the ratio of secondary/primary bile acids in luminal metabolites increased with sucralose consumption in a dose-dependent manner. These results suggest that daily intake of maximum ADI levels of sucralose, but not acesulfame-K, affected the relative amount of the Clostridium cluster XIVa in fecal microbiome and cholesterol bile acid metabolism in mice. (Tokushima University Institutional Repository) ● Metadata: 115661 (Link to Publication Site) ● Publication site (DOI): 10.3390/nu9060560 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28587159 ● Search Scopus @ Elsevier (PMID): 28587159 ● Search Scopus @ Elsevier (DOI): 10.3390/nu9060560 (Tokushima University Institutional Repository: 115661, DOI: 10.3390/nu9060560, PubMed: 28587159)
29.	Yumiko Miyatake, Tetsuya Shiuchi, Kazuaki Mawatari, Satomi Toda, Yasuko Taniguchi, Akari Futami, Fukiko Sato, Masashi Kuroda, Mayu Sebe, Rie Tsutsumi, Nagakatsu Harada, Yasuhiko Minokoshi, Tadahiro Kitamura, Koro Gotoh, Masaki Ueno, Yutaka Nakaya and Hiroshi Sakaue : Intracerebroventricular injection of ghrelin decreases wheel running activity in rats., Peptides, Vol.87, 12-19, 2017. (Summary) There is an increasing interest in elucidating the molecular mechanisms by which voluntary exercise is regulated. In this study, we examined how the central nervous system regulates exercise. We used SPORTS rats, which were established in our laboratory as a highly voluntary murine exercise model. SPORTS rats showed lower levels of serum ghrelin compared with those of the parental line of Wistar rats. Intracerebroventricular and intraperitoneal injection of ghrelin decreased wheel-running activity in SPORTS rats. In addition, daily injection of the ghrelin inhibitor JMV3002 into the lateral ventricles of Wistar rats increased wheel-running activity. Co-administration of obestatin inhibited ghrelin-induced increases in food intake but did not inhibit ghrelin-induced suppression of voluntary exercise in rats. Growth hormone secretagogue receptor (GHSR) in the hypothalamus and hippocampus of SPORTS rats was not difference that in control rats. We created an arcuate nucleus destruction model by administering monosodium glutamate (MSG) to neonatal SPORTS rats. Injection of ghrelin into MSG-treated rats decreased voluntary exercise but did not increase food intake, suggesting that wheel-running activity is not controlled by the arcuate nucleus neurons that regulate feeding. These results provide new insights into the mechanism by which ghrelin regulates voluntary activity independent of arcuate nucleus neurons. (Tokushima University Institutional Repository) ● Metadata: 113364 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.peptides.2016.11.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27825986 ● Summary page in Scopus @ Elsevier: 2-s2.0-84995961350 (Tokushima University Institutional Repository: 113364, DOI: 10.1016/j.peptides.2016.11.005, PubMed: 27825986, Elsevier: Scopus)
30.	Yanfei Hou, Mutsumi Nakahashi, Kazuaki Mawatari, Takaaki Shimohata, Takashi Uebanso, Yumi Harada, Akari Tsunedomi, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Combined treatment of UVA irradiation and antibiotics induces greater bactericidal effects on Vibrio parahaemolyticus., The Journal of Medical Investigation : JMI, Vol.63, No.1-2, 63-67, 2016. (Summary) The presence of antibiotics in the environment and their subsequent impact on the development of multi-antibiotic resistant bacteria has raised concerns globally. Consequently, much research is focused on a method to produce a better disinfectant. We have established a disinfectant system using UVA-LED that inactivates pathogenic bacteria. We assessed the bactericidal efficiency of a combination of UVA-LED and antibiotics against Vibrio parahaemolyticus. Combined use of antibiotic drugs and UVA irradiation was more bactericidal than UVA irradiation or antibacterial drugs alone. The bactericidal synergy was observed at low concentrations of each drug that are normally unable to kill the bacteria. This combination has the potential to become a sterilization technology. J. Med. Invest. 63: 63-67, February, 2016. (Tokushima University Institutional Repository) ● Metadata: 111155 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.63.63 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27040055 ● Search Scopus @ Elsevier (PMID): 27040055 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.63.63 (Tokushima University Institutional Repository: 111155, DOI: 10.2152/jmi.63.63, PubMed: 27040055)
31.	Quang Ngoc Phan, Takashi Uebanso, Takaaki Shimohata, Mutsumi Nakahashi, Kazuaki Mawatari and Akira Takahashi : DNA-binding protein HU coordinates pathogenicity in Vibrio parahaemolyticus., Journal of Bacteriology, 2015. (Summary) Nucleoid binding protein HU regulate cellular behaviors, including nucleoid structuring, general recombination, transposition, growth, replication, motility, metabolism, and virulence. It is concerned that both number of bacteria and number of virulence factors may affect pathogenecity of bacteria. In the present study, we investigated that which factor have dominant role during infection in one of the most rapidly growing bacteria Vibrio parahaemolyticus. We found that V. parahaemolyticus cytotoxicity is regulated, in a growth rate-independent manner, by the HU proteins through regulation of number of virulence factors including T3SS1 gene expression. (Tokushima University Institutional Repository) ● Metadata: 109503 (Link to Publication Site) ● Publication site (DOI): 10.1128/JB.00306-15 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26148713 ● Search Scopus @ Elsevier (PMID): 26148713 ● Search Scopus @ Elsevier (DOI): 10.1128/JB.00306-15 (Tokushima University Institutional Repository: 109503, DOI: 10.1128/JB.00306-15, PubMed: 26148713)
32.	Sachie Negoro, Takaaki Shimohata, Syo Hatayama, Yuri Sato, Mari Matsumoto, Hitomi Iba, Mutsumi Aihara, Takashi Uebanso, Yasuhiro Hamada, Yoshikazu Nishikawa, Shinji Yamasaki, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni infection suppressed Cl(-) secretion induced by CFTR activation in T-84 cells., Journal of Infection and Chemotherapy, Vol.20, No.11, 682-688, 2014. (Summary) Campylobacter jejuni causes foodborne disease associated with abdominal pain, gastroenteritis, and diarrhea. These symptoms are induced by bacterial adherence and invasion of host epithelial cells. C. jejuni infection can occur with a low infective dose, suggesting that C. jejuni may have evolved strategies to cope with the bacterial clearance system in the gastrointestinal tract. The mucosa layer is the first line of defense against bacteria. Mucus conditions are maintained by water and anion (especially Cl(-)) movement. Cystic fibrosis transmembrane conductance regulator (CFTR) is the main Cl(-) channel transporting Cl(-) to the lumen. Mutations in CFTR result in dehydrated secreted mucus and bacterial accumulation in the lungs, and recent studies suggest that closely related pathogenic bacteria also may survive in the intestine. However, the relationship between C. jejuni infection and CFTR has been little studied. Here, we used an (125)I(-) efflux assay and measurement of short-circuit current to measure Cl(-) secretion in C. jejuni-infected T-84 human intestinal epithelial cells. The basic state of Cl(-) secretion was unchanged by C. jejuni infection, but CFTR activator was observed to induce Cl(-) secretion suppressed in C. jejuni-infected T-84 cells. The suppression of activated Cl(-) secretion was bacterial dose-dependent and duration-dependent. A similar result was observed during infection with other C. jejuni strains. The mechanism of suppression may occur by affecting water movement or mucus condition in the intestinal tract. A failure of mucus barrier function may promote bacterial adhesion or invasion of host intestinal epithelial cells, thereby causing bacterial preservation in the host intestinal tract. (Tokushima University Institutional Repository) ● Metadata: 110108 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jiac.2014.07.007 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25107576 ● Summary page in Scopus @ Elsevier: 2-s2.0-84908232552 (Tokushima University Institutional Repository: 110108, DOI: 10.1016/j.jiac.2014.07.007, PubMed: 25107576, Elsevier: Scopus)
33.	Mutsumi Nakahashi, Kazuaki Mawatari, Akiko Hirata, Miki Maetani, Takaaki Shimohata, Takashi Uebanso, Yasuhiro Hamada, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Simultaneous irradiation with different wavelengths of ultraviolet light has synergistic bactericidal effect on Vibrio parahaemolyticus., Photochemistry and Photobiology, Vol.90, No.6, 1397-1403, 2014. (Summary) Ultraviolet (UV) irradiation is an increasingly used method of water disinfection. UV rays can be classified by wavelength into UVA (320-400 nm), UVB (280-320 nm), and UVC (< 280 nm). We previously developed UVA sterilization equipment with a UVA-light emitting diode (LED). The aim of this study was to establish a new water disinfection procedure using the combined irradiation of the UVA-LED and another UV wavelength. An oxidative DNA product, 8-hydroxy-2'-deoxyguanosine (8-OHdG), increased after irradiation by UVA-LED alone, and the level of cyclobutane pyrimidine dimers (CPDs) was increased by UVC alone in Vibrio parahaemolyticus. Although sequential irradiation of UVA-LED and UVC induced additional bactericidal effects, simultaneous irradiation with UVA-LED and UVC induced bactericidal synergistic effects. 8-OHdG and CPDs production showed no differences between sequential and simultaneous irradiation. Interestingly, the recovery of CPDs was delayed by simultaneous irradiation. The synergistic effect was absent in SOS response-deficient mutants, such as the recA and lexA strains. Because recA- and lexA-mediated SOS responses have crucial roles in a DNA repair pathway, the synergistic bactericidal effect produced by the simultaneous irradiation could depend on suppression of the CPDs repair. The simultaneous irradiation of UVA-LED and UVC is a candidate new procedure for effective water disinfection. This article is protected by copyright. All rights reserved. (Link to Publication Site) ● Publication site (DOI): 10.1111/php.12309 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25041035 ● Summary page in Scopus @ Elsevier: 2-s2.0-84915794877 (DOI: 10.1111/php.12309, PubMed: 25041035, Elsevier: Scopus)
34.	Kazuaki Mawatari, Emiko Yoshioka, Satomi Toda, Sonoko Yasui, Hiroko Furukawa, Takaaki Shimohata, Takamasa Ohnishi, Masaki Morishima, Nagakatsu Harada, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : Enhancement of endothelial function inhibits left atrial thrombi development in an animal model of spontaneous left atrial thrombosis., Circulation Journal, Vol.78, No.8, 1980-1988, 2014. (Summary) Left atrial (LA) thrombosis is an important cause of systemic embolization. The SPORTS rat model of LA thrombi (Spontaneously-Running Tokushima-Shikoku), which have a unique characteristic of high voluntary wheel running, was previously established. The aim of the present study was to investigate how SPORTS rats develop LA thrombi.Methods and Results:Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in the local regulation of blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in SPORTS rats regardless of age was found; however, SPORTS rats demonstrated endothelial dysfunction and a decrease of NO production from a young age. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of SPORTS rats. While voluntary wheel running was able to intermittently increase NO levels, running did not statistically decrease the incidence of LA thrombi at autopsy. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in SPORTS rats. They present study results indicate that NO has an important role in the development of LA thrombus, and endothelia pathways could provide new targets of therapy to prevent LA thrombosis. (Circ J 2014; 78: 1980-1988). (Link to Publication Site) ● Publication site (DOI): 10.1253/circj.CJ-13-1398 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24859498 ● Summary page in Scopus @ Elsevier: 2-s2.0-84905043629 (DOI: 10.1253/circj.CJ-13-1398, PubMed: 24859498, Elsevier: Scopus)
35.	Mutsumi Aihara, Xin Lian, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Yumi Harada, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Vegetable surface sterilization system using UVA light-emitting diodes., The Journal of Medical Investigation : JMI, Vol.61, No.3-4, 285-290, 2014. (Summary) Surface sterilization of fresh produce has been needed in the food manufacturing/processing industry. Here we report a UVA-LED (Ultra Violet A-Light Emitting Diode) system for surface sterilization that is safe, efficacious, low cost, and apparently harmless to fresh produce. To test the system, Escherichia coli strain DH5 was spot-inoculated onto vegetable tissues, and treated under UVA-LED. Tissues were homogenized and bacteria quantified by colony-forming assay. Possible effects of UVA-LED on vegetable quality were evaluated by HPLC. Tissue weight changes were checked after treatment at 4, 15, and 30. Bacterial inactivation by UVA-LED radiation was observed after a 10 min treatment and increased with increasing time of irradiation. The log survival ratio reached -3.23 after a 90 min treatment. Bacterial cells surviving treatment grew slowly compared to non-irradiated control cells. Cabbage tissue lost weight over time after treatment, and weight loss increased with increasing incubation temperature, but there was no difference between losses by UVA-LED treated and control tissues at any temperature tested. In addition, no differences of Vitamin C content in cabbage tissue were detected by HPLC after UVA-LED treatment. These results suggest that UVA-LED treatment has great potential for vegetable surface sterilization in the food manufacturing/processing industry. (Tokushima University Institutional Repository) ● Metadata: 109573 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.285 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25264046 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907509465 (Tokushima University Institutional Repository: 109573, DOI: 10.2152/jmi.61.285, PubMed: 25264046, Elsevier: Scopus)
36.	Hirokazu Takechi, Kazuaki Mawatari, Nagakatsu Harada, Yutaka Nakaya, Megumi Asakura, Mutsumi Aihara, Hiromitsu Takizawa, Masakazu Goto, Takeshi Nishino, Takuya Minato, Yoshihito Furukita, Yota Yamamoto, Yasuhiro Yuasa, Hiromichi Yamai, Takahiro Yoshida, Jun-ichi Seike and Akira Tangoku : Glutamine protects the small intestinal mucosa in anticancer drug-induced rat enteritis model., The Journal of Medical Investigation : JMI, Vol.61, No.1-2, 59-64, 2014. (Summary) Supportive therapy during chemotherapy has become essential, but effective preventive therapies to gastrointestinal mucosal injury are few. We investigated the efficacy of glutamine in rat anticancer drug-induced enteritis model. In this study, we used twenty male SD rats. They were divided into control, 5-fluorouracil (5-FU) (orally administered at 20 mg/kg day), 5-FU+glutamine (1000 mg/kg/day) and 5-FU+glutamine+fiber and oligosaccharide (GFO(®)) (1000 mg/kg/day) groups. All groups were sacrificed on day 6 and upper jejunums were excised. The jejunal villous height was measured in specimens. IgA level in jejunal washing solution, and serum diamine oxidase activity were also measured. The jejunal villous height was recognized as shorter in the specimen from 5-FU treated rats compared with 5-FU+glutamine treated rats (p<0.001). Serum diamine oxidase activity in 5-FU+glutamine group were significantly superior to that in 5-FU group (p=0.028). IgA level in jejunal washing solution tended to be higher in 5-FU+glutamine group than that in 5-FU group (p=0.076). On the other hand, serum diamine oxidase activity and IgA level in jejunal washing solution showed no significant difference between 5-FU+GFO and 5-FU treatment group. Our results suggest that glutamine showed protective effects on mucosal injury of small intestine in rat anticancer drug-induced enteritis model. (Keyword) glutamine / gastrointestinal toxity / anticancer drug / diamine oxidase / IgA (Tokushima University Institutional Repository) ● Metadata: 109521 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.61.59 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24705750 ● CiNii @ National Institute of Informatics (CRID): 1390001204244693120 ● Summary page in Scopus @ Elsevier: 2-s2.0-84897937797 (Tokushima University Institutional Repository: 109521, DOI: 10.2152/jmi.61.59, PubMed: 24705750, CiNii: 1390001204244693120, Elsevier: Scopus)
37.	A Rodriguez-Mateos, Akari Ishisaka, Kazuaki Mawatari, Alberto Vidal-Diez, Jeremy Spencer and Junji Terao : Blueberry intervention improves vascular reactivity and lowers blood pressure in high fat, high cholesterol fed rats, British Journal of Nutrition, Vol.109, No.10, 1746-1754, 2013. (Summary) Growing evidence suggests that intake of flavonoid-containing foods may exert cardiovascular benefits in human subjects. We have investigated the effects of a 10-week blueberry (BB) supplementation on blood pressure (BP) and vascular reactivity in rats fed a high-fat/high-cholesterol diet, known to induce endothelial dysfunction. Rats were randomly assigned to follow a control chow diet, a chow diet supplemented with 2 % (w/w) BB, a high-fat diet (10 % lard; 0·5 % cholesterol) or the high fat plus BB for 10 weeks. Rats supplemented with BB showed significant reductions in systolic BP (SBP) of 11 and 14 %, at weeks 8 and 10, respectively, relative to rats fed the control chow diet (week 8 SBP: 107·5 (SEM 4·7) v. 122·2 (SEM 2·1) mmHg, P= 0·018; week 10 SBP: 115·0 (SEM 3·1) v. 132·7 (SEM 1·5) mmHg, P< 0·0001). Furthermore, SBP was reduced by 14 % in rats fed with the high fat plus 2 % BB diet at week 10, compared to those on the high-fat diet only (SBP: 118·2 (SEM 3·6) v. 139·5 (SEM 4·5) mmHg, P< 0·0001). Aortas harvested from BB-fed animals exhibited significantly reduced contractile responses (to L-phenylephrine) compared to those fed the control chow or high-fat diets. Furthermore, in rats fed with high fat supplemented with BB, aorta relaxation was significantly greater in response to acetylcholine compared to animals fed with the fat diet. These data suggest that BB consumption can lower BP and improve endothelial dysfunction induced by a high fat, high cholesterol containing diet. (Keyword) Acetylcholine / Animals / Aorta / Blood Pressure / Cholesterol, Dietary / Diet, High-Fat / Dietary Fats / Dietary Supplements / Endothelium, Vascular / Flavonoids / Fruit / Male / Muscle, Smooth, Vascular / Phenylephrine / Phytotherapy / Plant Preparations / Rats / Rats, Wistar / Vaccinium / Vascular Diseases / Vasoconstriction / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1017/S0007114512003911 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23046999 ● Search Scopus @ Elsevier (PMID): 23046999 ● Search Scopus @ Elsevier (DOI): 10.1017/S0007114512003911 (DOI: 10.1017/S0007114512003911, PubMed: 23046999)
38.	Atsushi Hashimoto, Kazuaki Mawatari, Yohsuke Kinouchi, Masatake Akutagawa, Naotomo Ota, Kazuyuki Nishimura, Tsuyoshi Hirata and Akira Takahashi : Inactivation of MS2 Phage and Cryptosporidium parvum Oocysts Using UV-A from High-Intensity Light-Emitting Diode for Water Disinfection, Journal of Water and Environment Technology, Vol.11, No.4, 299-307, 2013. (Summary) In this study, high-intensity, UV-A (ranging from 360 to 370 nm, peak wavelength at 365 nm) produced by a light-emitting diode was used for the inactivation of MS2 phage and <I>Cryptosporidium parvum</I> oocyst. In the irradiation experiment with MS2 phage, approximately 44 and 65 J/cm<SUP>2</SUP> of UV-A were required to obtain -2 and -3 log inactivations, respectively. The -2 and -3 log inactivations of <I>Cryptosporidium</I> oocysts required 338 and 508 J/cm<SUP>2</SUP> UV-A, respectively, which were 7.7 - 7.8 times greater than those required for MS2 phage. The possibility that high-intensity UV-A irradiation can inactivate both protozoa and viruses (phage) was demonstrated in this study. (Keyword) <I>Cryptosporidium</I> / inactivation / LED, MS2 phage / UV-A (Link to Publication Site) ● Publication site (DOI): 10.2965/jwet.2013.299 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680154853888 ● Search Scopus @ Elsevier (DOI): 10.2965/jwet.2013.299 (DOI: 10.2965/jwet.2013.299, CiNii: 1390282680154853888)
39.	Takaaki Shimohata, Kazuaki Mawatari, Hitomi Iba, Masakazu Hamano, Sachie Negoro, Shoko Asada, Mutsumi Aihara, Akiko Hirata, Zehong Su and Akira Takahashi : VopB1 and VopD1 are essential for translocation of type III secretion system 1 effectors of Vibrio parahaemolyticus., Canadian Journal of Microbiology, Vol.58, No.8, 1002-1007, 2012. (Summary) Vibrio parahaemolyticus is a pathogenic Vibrio species that causes food-borne acute gastroenteritis, often related to the consumption of raw or undercooked seafood. Vibrio parahaemolyticus has 2 type III secretion systems (T3SS1 and T3SS2). Here, we demonstrate that VP1657 (VopB1) and VP1656 (VopD1), which share sequence similarity with Pseudomonas genes popB (38%) and popD (36%), respectively, are essential for translocation of T3SS1 effectors into host cells. A VP1680CyaA fusion reporter system was constructed to observe effector translocation. Using this reporter assay we showed that the VopB1 and VopD1 deletion strains were unable to translocate VP1680 to host cell but that the secretion of VP1680 into the culture medium was not affected. VopB1 or VopD1 deletion strains did not enhance cytotoxicity and failed to activate mitogen-activated protein kinases and secretion of interleukin-8, which depend on VP1680. Thus, we conclude that VopB1 and VopD1 are essential components of the translocon. To target VopB1 and VopD1 may have therapeutic potential for the treatment or prevention in V. parahaemolyticus infection. (Link to Publication Site) ● Publication site (DOI): 10.1139/w2012-081 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22827847 ● Summary page in Scopus @ Elsevier: 2-s2.0-84864769777 (DOI: 10.1139/w2012-081, PubMed: 22827847, Elsevier: Scopus)
40.	Thanh Tam Thi Le, Kazuaki Mawatari, Miki Maetani, Tomomi Yamamoto, Sayaka Hayashida, Hitomi Iba, Mutsumi Aihara, Akiko Hirata, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : VP2118 has major roles in Vibrio parahaemolyticus response to oxidative stress., Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1820, No.10, 1686-1692, 2012. (Summary) The V. parahaemolyticus FeSOD VP2118 may enhance ROS resistance and could promote its survival in the intestinal tract to facilitate host tissue infection. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2012.06.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22771831 ● Summary page in Scopus @ Elsevier: 2-s2.0-84863814713 (DOI: 10.1016/j.bbagen.2012.06.019, PubMed: 22771831, Elsevier: Scopus)
41.	Tuyet Le Thi Nhung, Hirofumi Nagata, Akira Takahashi, Mutsumi Aihara, Toshihiro Okamoto, Takaaki Shimohata, Kazuaki Mawatari, Masatake Akutagawa, Yohsuke Kinouchi and Masanobu Haraguchi : Sterilization effect of UV light on Bacillus spores using TiO(2) films depends on wavelength., The Journal of Medical Investigation : JMI, Vol.59, No.1-2, 53-58, 2012. (Summary) UV light and photocatalysts such as titanium dioxide (TiO(2)) and silver (Ag) are useful for disinfection of water and surfaces. However, the effect of UV wavelength on photocatalytic disinfection of spores is not well understood. Inactivation of Bacillus spores has been examined using different UV wavelengths and TiO(2) or TiO(2)/Ag composite materials. The level of UVA disinfection of Bacillus anthracis and Bacillus brevis vegetative cells increased with the presence of the TiO(2) and Ag photocatalysts, but had little effect on their spores. B. brevis spores were slightly more sensitive to UVB and UVC than the spores of B. atrophaeus. Photocatalytic sterilization against spores was strongest in UVC and UVB and weakest in UVA. The rate of inactivation of Bacillus spores was significantly increased by the presence of TiO(2), but was not markedly different from that induced by the presence of Ag. Therefore, TiO(2)/Ag plus UVA can be used for the sterilization of vegetative cells, while TiO(2) and UVC are effective against spores. (Keyword) Bacillus anthracis / Silver / Spores, Bacterial / sterilization / titanium / Ultraviolet Rays (Tokushima University Institutional Repository) ● Metadata: 106002 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.59.53 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22449993 ● Search Scopus @ Elsevier (PMID): 22449993 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.53 (Tokushima University Institutional Repository: 106002, DOI: 10.2152/jmi.59.53, PubMed: 22449993)
42.	Nakagawa Tadahiko, Nagakatsu Harada, Miyamoto Aiko, Kawanishi Yukiko, Yoshida Masaki, Masayuki Shono, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : Membrane topology of murine glycerol-3-phosphate acyltransferase 2., Biochemical and Biophysical Research Communications, Vol.418, No.3, 506-511, 2012. (Summary) Glycerol-3-phosphate acyltransferase (GPAT) is a rate-limiting enzyme in mammalian triacylglycerol biosynthesis. GPAT is a target for the treatment of metabolic disorders associated with high lipid accumulation. Although the molecular basis for GPAT1 activation has been investigated extensively, the activation of other isoforms, such as GPAT2, is less well understood. Here the membrane topology of the GPAT2 protein was examined using an epitope-tag-based method. Exogenously expressed GPAT2 protein was present in the membrane fraction of transformed HEK293 cells even in the presence of Na(2)CO(3) (100 mM), indicating that GPAT2 is a membrane-bound protein. Trypsin treatment of the membrane fraction degraded the N-terminal (FLAG) and C-terminal (myc-epitope) protein tags of the GPAT2 protein. Bioinformatic analysis of the GPAT2 protein sequence indicated four hydrophobic sequences as potential membrane-spanning regions (TM1-TM4). Immunoblotting of the myc-epitope tag, which was inserted between each TM region of the GPAT2 protein, showed that the amino acid sequence between TM3 and TM4 was protected from trypsin digestion. These results suggest that the GPAT2 protein has two transmembrane segments and that the N-terminal and C-terminal regions of this protein face the cytoplasm. These results also suggest that the enzymatically active motifs I-III of the GPAT2 protein face the cytosol, while motif IV is within the membrane. It is expected that the use of this topological model of GPAT2 will be essential in efforts to elucidate the molecular mechanisms of GPAT2 activity in mammalian cells. (Keyword) Amino Acid Motifs / Animals / Cell Membrane / Cytoplasm / Glycerol-3-Phosphate O-Acyltransferase / HEK293 Cells / Humans / Mice / Molecular Sequence Data / Protein Structure, Tertiary (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2012.01.055 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22285183 ● Search Scopus @ Elsevier (PMID): 22285183 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2012.01.055 (DOI: 10.1016/j.bbrc.2012.01.055, PubMed: 22285183)
43.	Sonoko Yasui, Kazuaki Mawatari, Ran Morizumi, Hiroko Furukawa, Takaaki Shimohata, Nagakatsu Harada, Akira Takahashi and Yutaka Nakaya : Hydrogen peroxide inhibits insulin-induced ATP-sensitive potassium channel activation independent of insulin signaling pathway in cultured vascular smooth muscle cells., The Journal of Medical Investigation : JMI, Vol.59, No.1-2, 36-44, 2012. (Summary) Both reactive oxygen species (ROS) and insulin resistance have been reported to play essential pathophysiological roles in cardiovascular diseases, such as hypertension and atherosclerosis. However, the mechanistic link between ROS and insulin resistance in the vasculature remains unclear. Recently we have shown that insulin causes membrane hyperpolarization via ATP-sensitive potassium (K(ATP)) channel activation, which is mediated by phosphatidylinositol 3-kinase (PI3-K) in cultured vascular smooth muscle cells (VSMCs). K(ATP) channel in the vasculature is critical in the regulation of vascular tonus. Here we examined the effects of ROS induced by hydrogen peroxide (H(2)O(2)) on insulin-induced K(ATP) channel activities in cultured VSMCs, A10 cells. H(2)O(2) (10 µM) increased significantly intercellular ROS in A10 cells. By using a cell-attached patch clamp experiment, 10 µM H(2)O(2) suppressed significantly insulin-induced K(ATP) channel activation without inhibition of insulin receptor signal transduction component including IRS and Akt in A10 cells. Furthermore 10 µM H(2)O(2) suppressed significantly pinacidil-induced K(ATP) channel activation in A10 cells. These data suggest that H(2)O(2) might inhibit directly K(ATP) channel independent of insulin signaling pathway. This study may contribute to our understanding of mechanisms of insulin resistance-associated cardiovascular disease. (Keyword) Animals / Aorta, Thoracic / Cell Line / hydrogen peroxide / Hypoglycemic Agents / insulin / KATP Channels / Muscle, Smooth, Vascular / Oxidants / Patch-Clamp Techniques / Rats / signal transduction (Tokushima University Institutional Repository) ● Metadata: 99853 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.59.36 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22449991 ● Search Scopus @ Elsevier (PMID): 22449991 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.36 (Tokushima University Institutional Repository: 99853, DOI: 10.2152/jmi.59.36, PubMed: 22449991)
44.	Tuyet Nhung Thi Le, Hirofumi Nagata, Mutsumi Aihara, Akira Takahashi, Toshihiro Okamoto, Takaaki Shimohata, Kazuaki Mawatari, Yhosuke Kinouchi, Masatake Akutagawa and Masanobu Haraguchi : Additional effects of silver nanoparticles on bactericidal efficiency depend on calcination temperature and dip-coating speed., Applied and Environmental Microbiology, Vol.77, No.16, 5629-5634, 2011. (Summary) There is an increasing interest in the application of photocatalytic properties for disinfection of surfaces, air, and water. Titanium dioxide is widely used as a photocatalyst, and the addition of silver reportedly enhances its bactericidal action. However, the synergy of silver nanoparticles and TiO(2) is not well understood. The photocatalytic elimination of Bacillus atrophaeus was examined under different calcination temperatures, dip-coating speeds, and ratios of TiO(2), SiO(2), and Ag to identify optimal production conditions for the production of TiO(2)- and/or TiO(2)/Ag-coated glass for surface disinfection. Photocatalytic disinfection of pure TiO(2) or TiO(2) plus Ag nanoparticles was dependent primarily on the calcination temperature. The antibacterial activity of TiO(2) films was optimal with a high dip-coating speed and high calcination temperature (600°C). Maximal bacterial inactivation using TiO(2)/Ag-coated glass was also observed following high-speed dip coating but with a low calcination temperature (250°C). Scanning electron microscopy (SEM) showed that the Ag nanoparticles combined together at a high calcination temperature, leading to decreased antibacterial activity of TiO(2)/Ag films due to a smaller surface area of Ag nanoparticles. The presence of Ag enhanced the photocatalytic inactivation rate of TiO(2), producing a more pronounced effect with increasing levels of catalyst loading. (Keyword) Anti-Bacterial Agents / Bacillus / Catalysis / Disinfectants / Glass / Hot Temperature / Metal Nanoparticles / Microbial Sensitivity Tests / Microscopy, Electron, Scanning / photochemistry / Silicon Dioxide / Silver / Time Factors / titanium / Ultraviolet Rays (Link to Publication Site) ● Publication site (DOI): 10.1128/AEM.00049-11 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21724887 ● Summary page in Scopus @ Elsevier: 2-s2.0-80052609659 (DOI: 10.1128/AEM.00049-11, PubMed: 21724887, Elsevier: Scopus)
45.	Hiroko Furukawa, Kazuaki Mawatari, Kei Koyama, Sonoko Yasui, Ran Morizumi, Takaaki Shimohata, Nagakatsu Harada, Akira Takahashi and Yutaka Nakaya : Telmisartan increases localization of glucose transporter 4 to the plasma membrane and increases glucose uptake via peroxisome proliferator-activated receptor γ in 3T3-L1 adipocytes., European Journal of Pharmacology, Vol.660, No.2-3, 485-491, 2011. (Summary) Angiotensin II is a peptide hormone with strong vasoconstrictive action, and recent reports have shown that Angiotensin II receptor type 1 antagonists (angiotensin II receptor blockers) also improve glucose metabolism. The angiotensin II receptor blocker telmisartan acts as an agonistic ligand of the peroxisome proliferator-activated receptor gamma (PPARγ). In this study, we investigated the effects of telmisartan on glucose uptake and insulin sensitivity in 3T3-L1 adipocytes and compared it with the action of other angiotensin II receptor blockers. Telmisartan treatment dose-dependently increased (from 1 μM) protein expression of PPARγ-regulated molecules such as fatty acid binding protein 4 (FABP4), insulin receptor, and glucose transporter 4 (GLUT4). Telmisartan increased glucose uptake both with and without insulin stimulation in 3T3-L1 adipocytes. Telmisartan increased the up-regulation of phosphorylated insulin receptor, insulin receptor substrate-1 (IRS-1) and Akt by insulin, suggesting that telmisartan increases insulin sensitivity. Furthermore, in the absence of insulin, telmisartan, but not candesartan, increased GLUT4 levels at the plasma membrane. These effects by 10 μM telmisartan were similar potency to those of 1 μM troglitazone, an activator of PPARγ. In addition, up-regulation of glucose uptake by telmisartan was inhibited by a PPARγ antagonist, T0070907 (2-chloro-5-nitro-N-4-pyridinyl-benzamide). These results indicate that telmisartan acts via PPARγ activation in adipose tissue and may be an effective therapy for the metabolic syndrome. (Keyword) 3T3-L1 Cells / Adipocytes / Angiotensin II Type 1 Receptor Blockers / Animals / Benzimidazoles / Benzoates / Cell Membrane / Fatty Acid-Binding Proteins / Glucose / Glucose Transporter Type 4 / Insulin / Mice / PPAR gamma / Protein Transport / Receptor, Insulin / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2011.04.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21514293 ● Search Scopus @ Elsevier (PMID): 21514293 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2011.04.008 (DOI: 10.1016/j.ejphar.2011.04.008, PubMed: 21514293)
46.	Yasuo M. Tsutsumi, Rie Tsutsumi, Kazuaki Mawatari, Yutaka Nakaya, Michiko Kinoshita, Katsuya Tanaka and Shuzo Oshita : Compound K, a metabolite of ginsenosides, induces cardiac protection mediated nitric oxide via Akt/PI3K pathway., Life Sciences, Vol.88, No.15-16, 725-729, 2011. (Summary) Compound K (C-K; 20-O-D-glucopyranosyl-20(S)-protopanaxadiol) is a novel ginsenoside metabolite formed by intestinal bacteria and does not occur naturally in ginseng. In this study, we investigated whether administration of C-K has protective effects on myocardial ischemia-reperfusion injury and its potential mechanisms. (Keyword) Androstadienes / Animals / calcium / Ginsenosides / Immunoblotting / male / Mice / Mice, Inbred C57BL / Mitochondria, Heart / Myocardial Infarction / Myocardial Reperfusion Injury / nitric oxide / Nitric Oxide Synthase Type III / Phosphatidylinositol 3-Kinases / Proto-Oncogene Proteins c-akt (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2011.02.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21338613 ● Summary page in Scopus @ Elsevier: 2-s2.0-79953283184 (DOI: 10.1016/j.lfs.2011.02.011, PubMed: 21338613, Elsevier: Scopus)
47.	Takaaki Shimohata, Masayuki Nakano, Xin Lian, Tomomi Shigeyama, Hitomi Iba, Akiko Hamamoto, Masaki Yoshida, Nagakatsu Harada, Hironori Yamamoto, Masayuki Yamato, Kazuaki Mawatari, Toshiaki Tamaki, Yutaka Nakaya and Akira Takahashi : Vibrio parahaemolyticus infection induces modulation of IL-8 secretion through dual pathway via VP1680 in Caco-2 cells., The Journal of Infectious Diseases, Vol.203, No.4, 537-544, 2011. (Summary) Vibrio parahaemolyticus causes acute gastroenteritis and inflammations in humans. A variety of pathogenic bacteria can stimulate mitogen-activated protein kinases (MAPKs) in host cells. Phosphorylation of MAPKs leads to production of interleukin (IL)- 8 and subsequently causes inflammations. Thus, MAPK cascades were strong candidates for the main signaling pathway of V. parahaemolyticus-induced acute inflammation. (Keyword) Caco-2 Cells / Humans / Interleukin-8 / Mitogen-Activated Protein Kinases / Phosphorylation / Signal Transduction / Vibrio parahaemolyticus / Viral Proteins / Virulence Factors (Link to Publication Site) ● Publication site (DOI): 10.1093/infdis/jiq070 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21177635 ● Search Scopus @ Elsevier (PMID): 21177635 ● Search Scopus @ Elsevier (DOI): 10.1093/infdis/jiq070 (DOI: 10.1093/infdis/jiq070, PubMed: 21177635)
48.	Yasunobu Hayabuchi, Yutaka Nakaya, Kazuaki Mawatari, Miki Inoue, Miho Sakata and Shoji Kagami : Cell membrane stretch activates intermediate-conductance Ca2+-activated K+ channels in arterial smooth muscle cells, Heart and Vessels, Vol.26, No.1, 91-100, 2011. (Summary) The aim of this study is to determine the signal transduction of membrane stretch on intermediate-conductance Ca(2+)-activated K(+) (IKca) channels in rat aorta smooth muscle cells using the patch-clamp technique. To stretch the cell membrane, both suction to the rear end of patch pipette and hypotonic shock were used. In cell-attached and inside-out patch configurations, the open probability of IKca channels increased when 20- to 45-mmHg suction was applied. Hyposmotic swelling efficiently increased IKca channel current. When the Ca(2+)-free solution was superfused, the activation of IKca current by the hyposmotic swelling was reduced. Furthermore, gadolinium (Gd(3+)) attenuated the activation of IKca channels induced by hyposmotic swelling, whereas nicardipine did not. In the experiments with Ca(2+)-free bath solution, pretreatment with GF109203X, a protein kinase C (PKC) inhibitor, completely abolished the stretch-induced activation of IKca currents. The stretch-induced activation of IKca channels was strongly inhibited by cytochalasin D, indicating a role for the F-actin in modulation of IKca channels by changes in cell stretching. These data suggest that cell membrane stretch activates IKca channels. In addition, the activation is associated with extracellular Ca(2+) influx through stretch-activated nonselective cation channels, and is also modulated by the F-actin cytoskeleton and the activation of PKC. (Keyword) Actins / Animals / Aorta / Cell Line / Cell Size / Enzyme Activation / Hypotonic Solutions / Intermediate-Conductance Calcium-Activated Potassium Channels / Ion Channel Gating / Mechanotransduction, Cellular / Membrane Potentials / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Osmotic Pressure / Patch-Clamp Techniques / Potassium Channel Blockers / Protein Kinase C / Protein Kinase Inhibitors / Rats / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1007/s00380-010-0025-0 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21063882 ● Search Scopus @ Elsevier (PMID): 21063882 ● Search Scopus @ Elsevier (DOI): 10.1007/s00380-010-0025-0 (DOI: 10.1007/s00380-010-0025-0, PubMed: 21063882)
49.	A Hamamoto, M Bandou, K Nakano, Kazuaki Mawatari, Nagakatsu Harada, Masatake Akutagawa, Yohsuke Kinouchi, Yutaka Nakaya and Akira Takahashi : Differences in stress response after UVC or UVA irradiation in Vibrio parahaemolyticus., Environmental Microbiology Reports, Vol.2, No.5, 660-666, 2010. (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1758-2229.2010.00154.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23766253 ● Search Scopus @ Elsevier (PMID): 23766253 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1758-2229.2010.00154.x (DOI: 10.1111/j.1758-2229.2010.00154.x, PubMed: 23766253)
50.	Zehong Su, Masayuki Nakano, Tetsuro Koga, Xin Lian, Akiko Hamamoto, Takaaki Shimohata, Yumi Harada, Kazuaki Mawatari, Nagakatsu Harada, Masatake Akutagawa, Yutaka Nakaya and Akira Takahashi : Hfq regulates anti-oxidative ability in Vibrio parahaemolyticus., The Journal of General and Applied Microbiology, Vol.56, No.3, 181-186, 2010. (Summary) Hfq plays a fundamental role in bacterial cell physiology. It can stimulate or repress the expression of certain target genes, and there is a possibility that Hfq regulates the oxidative stress response. However, how Hfq functions that in Vibrio parahaemolyticus remains speculative. In this paper, we explain the functions Hfq plays in V. parahaemolyticus in the gene expression of superoxide dismutase gene and catalase gene, comparing the hfq deletion mutant strain to the parental strain. The results show that the hfq deletion mutant V. parahaemolyticus has a stronger ability to resist H(2)O(2). Superoxide dismutase (SOD) and catalase (CAT) activities in the hfq deletion mutant were remarkably higher than in the parental strain. Genetic experiments indicated that the gene expression of sod and kat was up-regulated in the mutant strain. These results indicate that Hfq down-regulates CAT and SOD activity, and Hfq is associated with the oxidative stress response. (Keyword) Catalase / Host Factor 1 Protein / Oxidative Stress / Superoxide Dismutase / Vibrio parahaemolyticus (Link to Publication Site) ● Publication site (DOI): 10.2323/jgam.56.181 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20647674 ● Summary page in Scopus @ Elsevier: 2-s2.0-77954735342 (DOI: 10.2323/jgam.56.181, PubMed: 20647674, Elsevier: Scopus)
51.	Xin Lian, Kayo Tetsutani, Akiko Hamamoto, Masayuki Nakano, Kazuaki Mawatari, Nagakatsu Harada, Masayuki Yamato, Masatake Akutagawa, Yohsuke Kinouchi, Yutaka Nakaya and Akira Takahashi : A new colored beverage disinfection system using UV-A light-emitting diodes, Biocontrol Science, Vol.15, No.1, 33-37, 2010. (Summary) In this study we evaluated the ability of the UV-A-LED to eliminate bacteria in a colored beverage. Ten edible pigments were used to make a colored solution at concentrations of 1.0%, 0.1%, 0.01% and 0.001%. We used a colony-forming assay to monitor the bactericidal action against the bacteria. The bactericidal effect of UV-A-LED against Escherichia coli DH5 a decreased with the increasing concentration of almost all of the edible pigments. Although less effective in colored solutions and commercially available orange juice than in the positive control PBS, it holds potential for further development and use to ensure food and water safety. (Keyword) Beverages / Colony Count, Microbial / Escherichia coli / Food Irradiation / Ultraviolet Rays (Link to Publication Site) ● Publication site (DOI): 10.4265/bio.15.33 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20361521 ● CiNii @ National Institute of Informatics (CRID): 1390001204463296896 ● Search Scopus @ Elsevier (PMID): 20361521 ● Search Scopus @ Elsevier (DOI): 10.4265/bio.15.33 (DOI: 10.4265/bio.15.33, PubMed: 20361521, CiNii: 1390001204463296896)
52.	Masaki Yoshida, Nagakatsu Harada, Keiko Yoshida, Tadahiko Nakagawa, Takaaki Shimohata, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : High density lipoprotein inhibits the activation of sterol regulatory element-binding protein-1 in cultured cells., FEBS Letters, Vol.584, No.6, 1217-1222, 2010. (Summary) A link between cellular uptake of high density lipoprotein (HDL) and regulation of sterol regulatory element-binding protein-1 (SREBP-1) was investigated in vitro. HDL decreased nuclear SREBP-1 levels as well as SREBP-1 target gene expression in HepG2 and HEK293 cells. However, HDL did not repress an exogenously expressed, constitutively active form of SREBP-1. HDL increased cellular cholesterol levels, and cellular cholesterol depletion by methyl-beta-cyclodextrin abolished the effects of HDL. These results suggest that HDL inhibits the activation of SREBP-1 through a cholesterol-dependent mechanism, which may play an important role in regulating lipid synthetic pathways mediated by SREBP-1. (Keyword) Acetyl-CoA Carboxylase / Animals / Cells, Cultured / Fatty Acid Synthetase Complex / Gene Expression Regulation, Enzymologic / Hep G2 Cells / Humans / Lipid Metabolism / Lipoproteins, HDL / Male / Promoter Regions, Genetic / Rats / Rats, Sprague-Dawley / Stearoyl-CoA Desaturase / Sterol Regulatory Element Binding Protein 1 / Transcriptional Activation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.febslet.2010.02.034 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20171215 ● Summary page in Scopus @ Elsevier: 2-s2.0-77950369388 (DOI: 10.1016/j.febslet.2010.02.034, PubMed: 20171215, Elsevier: Scopus)
53.	Hattori Atsushi, Kazuaki Mawatari, Tuzuki Satomi, Yoshioka Emiko, Toda Satomi, Yoshida Masaki, Yasui Sonoko, Furukawa Hiroko, Morishima Masaki, Ono Katsushige, Takamasa Ohnishi, Nakano Masayuki, Nagakatsu Harada, Akira Takahashi and Yutaka Nakaya : β-Adrenergic-AMPK Pathway Phosphorylates Acetyl-CoA Carboxylase in a High-epinephrine Rat Model, SPORTS, Obesity, Vol.18, No.1, 48-54, 2010. (Summary) We established a new animal model called SPORTS (Spontaneously-Running Tokushima-Shikoku) rats, which show high-epinephrine (Epi) levels. Recent reports show that Epi activates adenosine monophosphate (AMP)-activated protein kinase (AMPK) in adipocytes. Acetyl-CoA carboxylase (ACC) is the rate-limiting enzyme in fatty acid synthesis, and the enzymatic activity is suppressed when its Ser-79 is phosphorylated by AMPK. The aim of this study was to investigate the in vivo effect of Epi on ACC and abdominal visceral fat accumulation. We divided both 6-week male control and SPORTS rats into two groups, which were fed either normal diet or high fat and sucrose (HFS) diet for 16 weeks. At the end of diet treatment, retroperitoneal fat was collected for western blotting and histological analysis. Food intake was not different among the groups, but SPORTS rats showed significantly lower weight gain than control rats in both diet groups. After 10 weeks of diet treatment, glucose tolerance tests (GTTs) revealed that SPORTS rats had increased insulin sensitivity. Furthermore, SPORTS rats had lower quantities of both abdominal fat and plasma triglyceride (TG). In abdominal fat, elevated ACC Ser-79 phosphorylation was observed in SPORTS rats and suppressed by an antagonist of beta-adrenergic receptor (AR), propranolol, or an inhibitor of AMPK, Compound C. From these results, high level of Epi induced ACC phosphorylation mediated through beta-AR and AMPK signaling pathways in abdominal visceral fat of SPORTS rats, which may contribute to reduce abdominal visceral fat accumulation and increase insulin sensitivity. Our results suggest that beta-AR-regulated ACC activity would be a target for treating lifestyle-related diseases, such as obesity. (Keyword) AMP-Activated Protein Kinases / Acetyl-CoA Carboxylase / Adrenergic beta-Antagonists / analysis of variance / Animals / Blood Glucose / Blotting, Western / Body Weight / Eating / Enzyme-Linked Immunosorbent Assay / Epinephrine / Glucose Tolerance Test / insulin / Intra-Abdominal Fat / Male / obesity / phosphorylation / Propranolol / Pyrazoles / Pyrimidines / Rats / Receptors, Adrenergic, beta / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1038/oby.2009.145 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19444233 ● Search Scopus @ Elsevier (PMID): 19444233 ● Search Scopus @ Elsevier (DOI): 10.1038/oby.2009.145 (DOI: 10.1038/oby.2009.145, PubMed: 19444233)
54.	Gadelmoula Mostafa, Lian Xin, Maeda Miku, Aihara Mutsumi, Kazuaki Mawatari, Hamamoto Akiko, Harada Yumi, Masayuki Yamato, Masatake Akutagawa, Yutaka Nakaya, Yohsuke Kinouchi and Akira Takahashi : Suitability of ultraviolet(A)-light emitting diode for air stream disinfection, The Journal of Medical Investigation : JMI, Vol.56, No.3-4, 150-156, 2009. (Summary) We previously developed a high powered light-emitting diode device capable of discharging germicidal ultraviolet irradiation (UVA-LED) at an approximate wavelength of 365 nm. This study examined the bactericidal activity of UVA-LED in moving air streams. Aerosols of Escherichia coli DH5alpha were exposed to UVA-LED irradiation using a stable current (0.5 A and 1.2 mW/cm(2)) or pulse current (1.0 A and 0.2 mW/cm(2)). Settle plate analysis was used for bioaerosol sampling, where results were expressed as Colony Forming Units. A -3 Log inactivation of the E. coli population occurred after 75 minutes of constant exposure to stable current. The pulse current produced inactivation within a similar timeframe. Our results might be significant as a basic study for further investigations about the effect of UVA-LED on airborne bacteria and its suitability for air disinfection applications. (Keyword) Aerosols / Air Microbiology / Air Pollution, Indoor / Disinfection / Escherichia coli / Humans / Sick Building Syndrome / Ultraviolet Rays (Tokushima University Institutional Repository) ● Metadata: 111322 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.56.150 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19763028 ● Search Scopus @ Elsevier (PMID): 19763028 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.56.150 (Tokushima University Institutional Repository: 111322, DOI: 10.2152/jmi.56.150, PubMed: 19763028)
55.	hua Yin, Nagakatsu Harada, Kazuaki Mawatari, Yasui Sonoko, Hiroko Segawa, Akira Takahashi, Shuzo Oshita and Yutaka Nakaya : L-DOPA inhibits nitric oxide-dependent vasorelaxation via production of reactive ozygen species in rat aorta, The Journal of Medical Investigation : JMI, Vol.56, No.3,4, 120-129, 2009. (Summary) To clarify the underlying mechanisms of L-DOPA induced vasoconstriction in rat aorta. Methods: The effect of L-DOPA on phenylephrine-induced contractile force of blood vessels was examined in vitro using rat aortic ring preparations by isometric tension experiment. Involvement of nitric oxide (NO) in the effect of L-DOPA on vascular smooth muscle was studied by using N(omega)-Nitro-L-arginine (L-NNA), Sodium nitroprusside (SNP) in endothelium-intact and endothelium-denuded aortic rings. L-DOPA potentiated alpha-adrenergic receptor- and depolarization-induced vascular contraction and inhibited acetylcholine-induced vasorelaxation. This effect was diminished by pretreatment of the aortic rings with L-NNA, an inhibitor of NO synthesis, or by removing the endothelium from the ring preparations. In endothelium-denuded rings, L-DOPA inhibited exogenous NO-dependent but not cGMP-mediated vasorelaxation. Increases in cGMP levels in response to an NO donor were attenuated by L-DOPA in cultured rat aortic smooth muscle cells. L-DOPA could not contract rings (without endothelium) pretreated with 3-(5'-hydroxymethyl- 2'-furyl)-1-benzyl indazole (YC-1), an activator of guanylyl cyclase, but SOD (150 U/ml) pretreatment of rings with endothelium inhibited contraction by L-DOPA. These results suggest that L-DOPA inhibits nitric-dependent vasorelaxation on vascular smooth muscle cells via production of reactive oxygen species. (Keyword) Animals / Aorta, Thoracic / Cells, Cultured / Cyclic GMP / Drug Synergism / Endothelium, Vascular / Guanylate Cyclase / Levodopa / Male / Myocytes, Smooth Muscle / Nitric Oxide / Phenylephrine / Rats / Rats, Wistar / Reactive Oxygen Species / Receptors, Cytoplasmic and Nuclear / Vasodilation (Tokushima University Institutional Repository) ● Metadata: 111318 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.56.120 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19763024 ● Search Scopus @ Elsevier (PMID): 19763024 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.56.120 (Tokushima University Institutional Repository: 111318, DOI: 10.2152/jmi.56.120, PubMed: 19763024)
56.	Masaki Yoshida, Nagakatsu Harada, Hironori Yamamoto, Yutaka Taketani, Nagakatsu Harada, Yunjie Yin, Atsushi Hattori, Tomoe Zenitani, Sayuri Hara, Haruka Yonemoto, Aki Nakamura, Masayuki Nakano, Kazuaki Mawatari, Kiyoshi Teshigawara, Hidekazu Arai, Toshio Hosaka, Akira Takahashi, Katsuhiko Yoshimoto and Yutaka Nakaya : Identification of cis-acting promoter sequences required for expression of the glycerol-3-phosphate acyltransferase 1 gene in mice., Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Vol.1791, No.1, 39-52, 2009. (Summary) Glycerol-3-phosphate acyltransferase 1 (GPAT1) is a rate limiting enzyme in de novo glycerophospholipid synthesis. The murine GPAT1 promoter sequence (the "classical" sequence) was reported previously. However, the organization of this DNA sequence does not fully match the mouse genome sequences on NCBI/GenBank. Here we have identified net cis-acting promoter sequences for the mouse GPAT1 gene: promoter 1a which includes part of the classical sequence and the downstream promoter 1b. Promoter 1a facilitates transcription of two alternative GPAT1 transcript variants, GPAT1-V1 and V2, while promoter 1b produces a third transcript variant, GPAT1-V3. Upstream stimulating factor-1 (USF-1) controlled both promoters whereas sterol regulatory element-binding protein-1 (SREBP-1) exclusively regulated promoter 1a activity in vitro. Feeding increased GPAT1-V1 and V2, but not V3 mRNA levels in mouse liver. The obese condition of db/db mice did not alter the hepatic expression levels of any of the three GPAT1 variants. Feeding enhanced hepatic mRNA levels, intranuclear protein levels and promoter 1a-binding levels of SREBP-1, but not of USF-1. Thus, promoter 1a was exclusively activated by routine feeding in vivo. Our results indicate differential roles of the two promoters in the regulation of hepatic GPAT1 gene expression in mice. (Keyword) Animals / Base Sequence / Cell Line, Tumor / Gene Expression Regulation, Enzymologic / Glycerol-3-Phosphate O-Acyltransferase / Hepatocytes / Humans / Male / Mice / Mice, Obese / Promoter Regions, Genetic / RNA Interference / Sterol Regulatory Element Binding Protein 1 / Upstream Stimulatory Factors (Tokushima University Institutional Repository) ● Metadata: 113301 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbalip.2008.09.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18983939 ● Search Scopus @ Elsevier (PMID): 18983939 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbalip.2008.09.005 (Tokushima University Institutional Repository: 113301, DOI: 10.1016/j.bbalip.2008.09.005, PubMed: 18983939)
57.	M Nakano, Akira Takahashi, Z Su, Nagakatsu Harada, Kazuaki Mawatari and Yutaka Nakaya : Hfq regulates the expression of the thermostable direct hemolysin gene in Vibrio parahaemolyticus, BMC Microbiology, Vol.8, 155, 2008. (Summary) The hfq gene is conserved in a wide variety of bacteria and Hfq is involved in many cellular functions such as stress responses and the regulation of gene expression. It has also been reported that Hfq is involved in bacterial pathogenicity. However, it is not clear whether Hfq regulates virulence in Vibrio parahaemolyticus. To evaluate this, we investigated the effect of Hfq on the expression of virulence-associated genes including thermostable direct hemolysin (TDH), which is considered to be an important virulence factor in V. parahaemolyticus, using an hfq deletion mutant. The production of TDH in the hfq deletion mutant was much higher than in the parental strain. Quantification of tdh promoter activity and mRNA demonstrated that transcription of the tdh gene was up-regulated in the mutant strain. The hfq-complemented strain had a normal (parental) amount of tdh expression. The transcriptional activity of tdhA was particularly increased in the mutant strain. These results indicate that Hfq is closely associated with the expression level of the tdh gene. Interestingly, other genes involved in the pathogenicity of V. parahaemolyticus, such as VP1680, vopC, and vopT, were also up-regulated in the mutant strain. Hfq regulates the expression of virulence-associated factors such as TDH and may be involved in the pathogenicity of V. parahaemolyticus. (Keyword) Amino Acid Sequence / Bacterial Proteins / Bacterial Toxins / Gene Expression Regulation, Bacterial / Hemolysin Proteins / Host Factor 1 Protein / Humans / Molecular Sequence Data / Promoter Regions, Genetic / Sequence Alignment / Transcription, Genetic / Vibrio Infections / Vibrio parahaemolyticus / Virulence Factors (Link to Publication Site) ● Publication site (DOI): 10.1186/1471-2180-8-155 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18803872 ● Search Scopus @ Elsevier (PMID): 18803872 ● Search Scopus @ Elsevier (DOI): 10.1186/1471-2180-8-155 (DOI: 10.1186/1471-2180-8-155, PubMed: 18803872)
58.	Takashi Kawano, Katsuya Tanaka, Kazuaki Mawatari, Shuzo Oshita, Akira Takahashi and Yutaka Nakaya : Hyperglycemia impairs isoflurane-induced adenosine triphosphate-sensitive potassium channel activation in vascular smooth muscle cells, Anesthesia & Analgesia, Vol.106, No.3, 858-864, 2008. (Summary) Isoflurane activates vascular adenosine triphosphate sensitive potassium (K(ATP)) channels, and may induce vasodilation. In the present study, we investigated whether hyperglycemia modifies isoflurane activation of vascular K(ATP) channel. We used a cell-attached patch-clamp configuration to test the effects of isoflurane on K(ATP) channel activity in vascular smooth muscle cells (VSMCs) after incubation for 24 h in medium containing normal glucose (NG, 5.5 mM D-glucose), L-glucose (LG, 5.5 mM D-glucose plus 17.5 mM L-glucose), or high glucose (HG, 23 mM D-glucose). Superoxide levels in aortas were measured by the lucigenin-enhanced chemiluminescence technique. Isoflurane-induced open probabilities were significantly reduced in VSMCs from arteries incubated in HG (0.06 +/- 0.01) compared with NG (0.17 +/- 0.02; P < 0.05) and LG (0.15 +/- 0.02; P < 0.05). Pretreatment of VSMCs with protein kinase C (PKC) inhibitors, calphostin C and PKC inhibitor 20-28, greatly reduced HG inhibition of isoflurane-induced K(ATP) channel activity. In addition, a PKC activator, PMA, mimicked the effects of HG. Superoxide release was significantly increased in arteries incubated in HG (18.3 +/- 11.5 relative light units (RLU) x s(-1) x mg(-1); P < 0.05 versus NG). Coincubated with polyethylene glycol-superoxide dismutase (250 U/mL), a cell-permeable superoxide scavenger, greatly reduced the HG-induced increase of superoxide, but failed to reduce HG inhibition of isoflurane-induced K(ATP) channel activity. Our results suggest that the metabolic stress of hyperglycemia can impair isoflurane-induced vascular K(ATP) channel activity mediated by excessive activation of PKC. This could impede the coronary vasodilation response to isoflurane, causing ischemia or hypoxia in patients with perioperative hyperglycemia. (Keyword) Anesthetics, Inhalation / Animals / Cells, Cultured / Enzyme Activators / Free Radical Scavengers / Glucose / Hyperglycemia / Isoflurane / KATP Channels / Male / Membrane Potentials / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Naphthalenes / Polyethylene Glycols / Protein Kinase C / Protein Kinase Inhibitors / Rats / Rats, Wistar / Signal Transduction / Superoxide Dismutase / Superoxides / Tetradecanoylphorbol Acetate / Time Factors / Vasodilation (Link to Publication Site) ● Publication site (DOI): 10.1213/ane.0b013e318163fd5b (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18292430 ● Search Scopus @ Elsevier (PMID): 18292430 ● Search Scopus @ Elsevier (DOI): 10.1213/ane.0b013e318163fd5b (DOI: 10.1213/ane.0b013e318163fd5b, PubMed: 18292430)
59.	Nagakatsu Harada, Haruka Yonemoto, Masaki Yoshida, Hironori Yamamoto, Yunjie Yin, Aiko Miyamoto, Atsushi Hattori, Qishisan Wu, Tadahiko Nakagawa, Masayuki Nakano, Kiyoshi Teshigawara, Kazuaki Mawatari, Toshio Hosaka, Akira Takahashi and Yutaka Nakaya : Alternative splicing produces a constitutively active form of human SREBP-1., Biochemical and Biophysical Research Communications, Vol.368, No.3, 820-826, 2008. (Summary) We identified a novel alternative splicing event that constitutively produces a truncated active form of human sterol regulatory element-binding protein 1 (SREBP-1). A cDNA of this splicing variant (named SREBP-1Delta) contains a translational stop codon-encoding exon sequence between exons 7 and 8. It produces SREBP-1aDelta (470 a.a.) and SREBP-1cDelta (446 a.a.) proteins that lack transmembrane and C-terminal regulatory sequences necessary for localization of SREBP-1 to the endoplasmic reticulum. A luciferase reporter assay showed that SREBP-1aDelta and SREBP-1cDelta transactivated lipogenic gene promoters to the same extent as that induced by N-terminal active fragments of SREBP-1a and SREBP-1c, respectively. SREBP-1Delta mRNA is expressed in human cell lines as well as adipose and liver tissues. Expression levels ranged from 5% to 16% of total SREBP-1 expression. The ratio of SREBP-1Delta expression to total SREBP-1 expression in HepG2 cells was not affected by either insulin or high glucose treatment. (Keyword) Adipose Tissue / Alternative Splicing / Cell Line / Humans / Liver / Organ Specificity / Protein Isoforms / RNA Splice Sites / Sterol Regulatory Element Binding Protein 1 / Tissue Distribution (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2008.02.004 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18267114 ● Search Scopus @ Elsevier (PMID): 18267114 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2008.02.004 (DOI: 10.1016/j.bbrc.2008.02.004, PubMed: 18267114)
60.	Qishisan Wu, Nagakatsu Harada, Aki Nakamura, Masaki Yoshida, Kazuaki Mawatari, Atsushi Hattori, Qinkai Li, Takaaki Shimohata, (名) Yinhua, Xin Lian, Masayuki Nakano, Toshio Hosaka, Akira Takahashi and Yutaka Nakaya : NO-1886, a lipoprotein lipase activator, attenuates contraction of rat intestinal ring preparations, The Journal of Medical Investigation : JMI, Vol.55, No.1,2, 61-70, 2008. (Summary) Various intestinal symptoms or diseases are closely associated with intestinal motility, which may be altered by metabolic disturbances associated with diabetes and obesity. It is therefore important that drugs used in the treatment of metabolic disorders should not have any adverse effects on the intestine. In the present study, we examined whether [4-(4-bromo-2-cyano-phenylcarbamoyl)-benzyl]-phosphonic acid diethyl ester (NO-1886), a lipoprotein lipase activator with anti-diabetic and/or anti-obese activity, affects stimulant-induced intestinal contractility. Administration of NO-1886 to intestinal ring preparations of ileum, rectum and colon isolated from Wistar rats attenuated or relaxed contraction induced by a high K+ environment or acetylcholine (ACh). This effect of NO-1886 was dependent on extracellular Ca(2+) and intracellular myosin light chain kinase activity. Our results also showed that ACh-induced colonic contraction was significantly higher in the obese Otsuka Long-Evans Tokushima Fatty (OLETF) than in the non-obese Long-Evans Tokushima Otsuka (LETO) rats. The hypercontractility observed in the colons of OLETF rats occurred concomitantly with an elevation in muscarinic M3 ACh receptor protein levels. Administration of NO-1886 attenuated the obesity-induced hypercontractility of the colonic rings of OLETF rats. Thus, intestinal contractile system would be a novel pharmacological target of the lipoprotein lipase activator NO-1886. (Keyword) Animals / Benzamides / Calcium / Diabetes Mellitus, Type 2 / Gastrointestinal Motility / Hypolipidemic Agents / Intestinal Diseases / Intestines / Lipoprotein Lipase Activators / Male / Muscle Contraction / Muscle, Smooth / Myosin-Light-Chain Kinase / Obesity / Organophosphorus Compounds / Peptides / Rats / Rats, Inbred OLETF / Rats, Wistar (Tokushima University Institutional Repository) ● Metadata: 110840 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.55.61 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18319547 ● Search Scopus @ Elsevier (PMID): 18319547 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.55.61 (Tokushima University Institutional Repository: 110840, DOI: 10.2152/jmi.55.61, PubMed: 18319547)
61.	Satoru Eguchi, Takashi Kawano, hua Yin, Katsuya Tanaka, Sonoko Yasui, Kazuaki Mawatari, Akira Takahashi, Yutaka Nakaya, Shuzo Oshita and Nobuyoshi Nakajo : Effects of prostaglandin E1 on vascular ATP-sensitive potassium channels., Journal of Cardiovascular Pharmacology, Vol.50, No.6, 686-691, 2007. (Summary) BACKGROUND: Prostaglandin E1 (PGE1) has been reported to activate ATP-sensitive potassium (KATP) channels, which induces vasorelaxation. However, direct evidence of PGE1 interactions with vascular KATP channels is limited. METHODS: The present study investigated the effects and mechanisms of PGE1 on vascular KATP channels in both isometric tension and patch clamp experiments.Isometric tension experiments were performed in rat thoracic aortic rings without an endothelium. Electrophysiologic experiments were performed using patch-clamp techniques to monitor KATP channels in rat vascular smooth muscle cells. RESULTS: PGE1 significantly decreased the isometric tension in a concentration-dependent manner, which was partially inhibited by pretreating with a KATP channel inhibitor, glibenclamide (1 microM), or an inhibitor of protein kinase A (PKA), Rp-cAMPS (100 microM). Application of PGE1 to the bath solution during cell-attached recordings induced a significant increase in KATP channel activity, whereas PGE1 failed to activate KATP channels in the inside-out patches. The PGE1-induced KATP channel currents in cell-attached patches were abolished by pretreating with Rp-cAMPS (100 microM). CONCLUSIONS: The results indicate that the activation of vascular KATP channels played an important role in the PKA-dependent PGE1-induced vasorelaxation. Furthermore, an electrophysiological experiment demonstrated that PGE1 activated vascular KATP channels via PKA activation. (Keyword) Algorithms / Alprostadil / Analysis of Variance / Animals / Aorta, Thoracic / Cyclic AMP / Cyclic AMP-Dependent Protein Kinases / Dose-Response Relationship, Drug / Forskolin / Glyburide / KATP Channels / Male / Patch-Clamp Techniques / Phenylephrine / Pinacidil / Protein Kinase Inhibitors / Rats / Rats, Wistar / Thionucleotides / Vasoconstriction / Vasodilation / Vasodilator Agents (Link to Publication Site) ● Publication site (DOI): 10.1097/FJC.0b013e3181583d9b (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18091586 ● Search Scopus @ Elsevier (PMID): 18091586 ● Search Scopus @ Elsevier (DOI): 10.1097/FJC.0b013e3181583d9b (DOI: 10.1097/FJC.0b013e3181583d9b, PubMed: 18091586)
62.	Hirohide Yamada, Takashi Kawano, Katsuya Tanaka, Sonoko Yasui, Kazuaki Mawatari, Akira Takahashi, Yutaka Nakaya and Shuzo Oshita : Effects of intracellular MgADP and acidification on the inhibition of cardiac sarcolemmal ATP-sensitive potassium channels by propofol, Journal of Anesthesia, Vol.21, No.4, 472-479, 2007. (Summary) Propofol inhibits adenosine triphosphate-sensitive potassium (K(ATP)) channels, which may result in the blocking of ischemic preconditioning in the heart. During cardiac ischemia, sarcolemmal K(ATP) channel activity is regulated by the increased levels of cytosolic metabolites, such as adenosine diphosphate (ADP) and protons. However, it remains unclear whether these cytosolic metabolites modulate the inhibitory action of propofol. The aim of this study was to investigate the effects of intracellular MgADP and acidification on K(ATP) channel inhibition by propofol. We used inside-out patch-clamp configurations to investigate the effects of propofol on the activities of recombinant cardiac sarcolemmal K(ATP) channels, which are reassociated by expressed subunits, sulfonylurea receptor (SUR) 2A, and inwardly rectifying potassium channels (Kir6.2). In the absence of MgADP, propofol inhibited the SUR2A/Kir6.2 channel currents in a concentration-dependent manner, and an IC(50) of 78 microM. Increasing the intracellular MgADP concentrations to 0.1 and 0.3 mM markedly attenuated the inhibitory potency of propofol, and shifted the IC(50) to 183 and 265 microM, respectively. Moreover, decreasing the intracellular pH from 7.4 to 6.5 attenuated the inhibitory potency of propofol, and shifted the IC(50) to 277 microM. In addition, propofol-induced inhibition of truncated Kir6.2DeltaC36 currents, which form a functional channel without SUR2A, was not affected by an increase in intracellular MgADP. However, intracellular acidification (pH 6.5) significantly reduced the propofol sensitivity of Kir6.2DeltaC36 channels. Our results demonstrated that the existence of intracellular MgADP and protons attenuated the direct inhibitory potency of propofol on recombinant cardiac sarcolemmal K(ATP) channels, via SUR2A and Kir6.2 subunits, respectively. (Keyword) ATP-Binding Cassette Transporters / Adenosine Diphosphate / Anesthetics, Intravenous / Animals / COS Cells / Cercopithecus aethiops / heart / Hydrogen-Ion Concentration / KATP Channels / Potassium Channel Blockers / Potassium Channels / Potassium Channels, Inwardly Rectifying / Propofol / Receptors, Drug / Recombinant Proteins / Sarcolemma (Link to Publication Site) ● Publication site (DOI): 10.1007/s00540-007-0551-9 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18008114 ● CiNii @ National Institute of Informatics (CRID): 1570572700582815104 ● Search Scopus @ Elsevier (PMID): 18008114 ● Search Scopus @ Elsevier (DOI): 10.1007/s00540-007-0551-9 (DOI: 10.1007/s00540-007-0551-9, PubMed: 18008114, CiNii: 1570572700582815104)
63.	Katsuya Hirasaka, S Kohno, J Goto, H Furochi, Kazuaki Mawatari, Nagakatsu Harada, Toshio Hosaka, Yutaka Nakaya, K Ishidoh, Toshiyuki Obata, Yousuke Ebina, H Gu, S Takeda, Kyoichi Kishi and Takeshi Nikawa : Deficiency of Cbl-b gene enhances infiltration and activation of macrophages in adipose tissue and causes peripheral insulin resistance in mice., Diabetes, Vol.56, No.10, 2511-2522, 2007. (Summary) c-Cbl plays an important role in whole-body fuel homeostasis by regulating insulin action. In the present study, we examined the role of Cbl-b, another member of the Cbl family, in insulin action. C57BL/6 (Cbl-b(+/+)) or Cbl-b-deficient (Cbl-b(-/-)) mice were subjected to insulin and glucose tolerance tests and a hyperinsulinemic-euglycemic clamp test. Infiltration of macrophages into white adipose tissue (WAT) was assessed by immunohistochemistry and flow cytometry. We examined macrophage activation using co-cultures of 3T3-L1 adipocytes and peritoneal macrophages. Elderly Cbl-b(-/-) mice developed glucose intolerance and peripheral insulin resistance; serum insulin concentrations after a glucose challenge were always higher in elderly Cbl-b(-/-) mice than age-matched Cbl-b(+/+) mice. Deficiency of the Cbl-b gene significantly decreased the uptake of 2-deoxyglucose into WAT and glucose infusion rate, whereas fatty liver was apparent in elderly Cbl-b(-/-) mice. Cbl-b deficiency was associated with infiltration of macrophages into the WAT and expression of cytokines, such as tumor necrosis factor-alpha, interleukin-6, and monocyte chemoattractant protein (MCP)-1. Co-culture of Cbl-b(-/-) macrophages with 3T3-L1 adipocytes induced leptin expression and dephosphorylation of insulin receptor substrate 1, leading to impaired glucose uptake in adipocytes. Furthermore, Vav1, a key factor in macrophage activation, was highly phosphorylated in peritoneal Cbl-b(-/-) macrophages compared with Cbl-b(+/+) macrophages. Treatment with a neutralizing anti-MCP-1 antibody improved peripheral insulin resistance and macrophage infiltration into WAT in elderly Cbl-b(-/-) mice. Cbl-b is a negative regulator of macrophage infiltration and activation, and macrophage activation by Cbl-b deficiency contributes to the peripheral insulin resistance and glucose intolerance via cytokines secreted from macrophages. (Keyword) 3T3 Cells / Adaptor Proteins, Signal Transducing / Adipocytes / Adipose Tissue / Animals / Biological Transport / Blood Glucose / Coculture Techniques / Crosses, Genetic / Energy Metabolism / Flow Cytometry / Glucose / Glucose Intolerance / Glucose Tolerance Test / Homeostasis / Insulin / Insulin Resistance / Macrophage Activation / Mice / Mice, Inbred C57BL / Mice, Knockout / Proto-Oncogene Proteins c-cbl (Link to Publication Site) ● Publication site (DOI): 10.2337/db06-1768 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17601987 ● Search Scopus @ Elsevier (PMID): 17601987 ● Search Scopus @ Elsevier (DOI): 10.2337/db06-1768 (DOI: 10.2337/db06-1768, PubMed: 17601987)
64.	Lian Xin, Akira Takahashi, Nakano Masayuki, Hori Emiko, Kazuaki Mawatari, Nagakatsu Harada, Toshio Hosaka and Yutaka Nakaya : Vibrio parahaemolytics elevates interferon aloha production in intestinal-like epithelial Caco-2 cells, Canadian Journal of Microbiology, Vol.53, No.9, 1084-1090, 2007. (Summary) Vibrio parahaemolyticus is the leading cause of gastroenteritis from seafood consumption. We tried to determine how the gene expression levels of intestinal-like epithelial cells (Caco-2 cells) and mouse intestinal loop mucosal cells change upon infection with this bacterium. Since we found the robust production of interferon alpha (IFN-alpha) by the V. parahaemolyticus infection, we also assessed the upregulation of a number of IFN-stimulated genes (ISGs). The expressions of IFN protein were determined by Western blotting, and the gene expressions of Caco-2 cells after V. parahaemolyticus infection were determined by quantitative real-time reverse-transcription polymerase chain reaction. Three ISGs (i.e., IFN-alpha-inducible protein 15, IFN-alpha-inducible protein 6-16, and IFN-induced protein with tetratricopeptide repeats 1) were upregulated by V. parahaemolyticus infection. Infection induced the production of IFN-alpha, but not IFN-beta or IFN-gamma. The upregulation of the 3 ISGs was suppressed by treatment with a neutralizing IFN-alpha antibody. Moreover, the production of infection-induced IFN-alpha was found in the mouse intestinal loop mucosal cells. V. parahaemolyticus infection of Caco-2 cells results in IFN-alpha production and the expression of IFN-regulated genes. (Keyword) Animals / Caco-2 Cells / Disease Models, Animal / Epithelial Cells / Humans / Interferon-alpha / Intestines / Mice / Proteins / Up-Regulation / Vibrio Infections / Vibrio parahaemolyticus (Link to Publication Site) ● Publication site (DOI): 10.1139/w07-075 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18026229 ● Search Scopus @ Elsevier (PMID): 18026229 ● Search Scopus @ Elsevier (DOI): 10.1139/w07-075 (DOI: 10.1139/w07-075, PubMed: 18026229)
65.	Masori Maria, Hamamoto Akiko, Kazuaki Mawatari, Nagakatsu Harada, Akira Takahashi and Yutaka Nakaya : Angiotensin Decreases Glucose Uptake by Downregulation of GLUT1 in the Cell Membrene of the Vascular Smooth Muscule Cell Line A10, Journal of Cardiovascular Pharmacology, Vol.50, No.3, 267-273, 2007. (Summary) Recent evidence suggests a crosstalk between angiotensin II (Ang II) and insulin. However, whether this crosstalk affects glucose uptake, particularly in terms of actin filament involvement, has not yet been studied in vascular smooth muscle cells. Pretreatment of cells with either Ang II or cytochalasin D disarranged actin filaments in a time-dependent manner and inhibited glucose uptake. However, insulin increased actin reorganization and glucose uptake. Membrane fractionation studies showed that Ang II decreased GLUT-1 at the cell membrane, whereas it increased GLUT-1 in the cytoplasm, indicating that Ang II may cause internalization of GLUT-1 via actin disorganization, consequently decreasing glucose uptake. The effects of Ang II on glucose uptake and actin reorganization were blocked by AT1 receptor antagonist, but not by AT2 antagonist. Either P38 or ERK1/2 inhibitors partially reversed the Ang II-inhibited actin reorganization and glucose uptake, suggesting that MAPK signaling pathways could be involved as downstream events in Ang II signaling, and this signaling may interfere with insulin-induced actin reorganization and glucose uptake. These data imply that Ang II induces insulin resistance by decreasing glucose uptake via disarrangement of actin filaments, which provides a novel insight into understanding of insulin resistance by Ang II at the molecular level. (Keyword) Actins / Angiotensin II / Animals / Cell Fractionation / Cell Line / Cell Membrane / Cytochalasin D / Down-Regulation / Glucose / Glucose Transporter Type 1 / Insulin / Insulin Resistance / MAP Kinase Signaling System / Muscle, Smooth, Vascular / Rats / Time Factors (Link to Publication Site) ● Publication site (DOI): 10.1097/FJC.0b013e318093ec74 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17878754 ● Search Scopus @ Elsevier (PMID): 17878754 ● Search Scopus @ Elsevier (DOI): 10.1097/FJC.0b013e318093ec74 (DOI: 10.1097/FJC.0b013e318093ec74, PubMed: 17878754)
66.	Ono Kaori, Kazuaki Mawatari, Nagakatsu Harada, Akira Takahashi, Tohru Sakai, Ogoshi Shohei and Yutaka Nakaya : Nucleoside and nucleotide mixture OG-VI rescues cytotoxicity induced by chemotherapeutic agents in intestinal-like epithelial cell., The Journal of Medical Investigation : JMI, Vol.54, No.3,4, 235-242, 2007. (Summary) Immune cells and cells undergoing rapid turn-over can obtain exogenous nucleotides via salvage synthesis. We evaluated whether or not the balanced nucleoside and nucleotide mixture OG-VI, could rescue intestinal epithelial-like Caco-2 cells from the cytotoxic effects of several chemotherapeutic agents, in the presence and absence of glutamine (Gln). Cells were exposed to 5-fluorouracil (5FU), methotrexate (MTX) or 6-mercaptopurine (6MP), after which proliferation and cell cycle analyses were performed. Following exposure to the chemotherapeutic agents, we observed that cells treated with OG-VI proliferated well, whereas those without the supplement did not proliferate. Furthermore, following treatment with either 5FU or MTX, we observed that the number of cells in the G0/G1 phase decreased and those in the S phases increased. However, these cell cycle alterations were prevented by the addition of OG-VI. With the exception of 6MP-treated cells, we did not observe any effects on proliferation or cell cycle regulation that could be ascribed to the presence of Gln. Thus, we have demonstrated that OG-VI rescues cells from the cytotoxic effects of several chemotherapeutic agents. (Keyword) 6-Mercaptopurine / Antineoplastic Agents / Caco-2 Cells / Cell Cycle / Cell Proliferation / Cell Survival / Epithelial Cells / Fluorouracil / Humans / Intestines / Methotrexate / Nucleosides / Nucleotides (Tokushima University Institutional Repository) ● Metadata: 111518 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.54.235 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17878671 ● Search Scopus @ Elsevier (PMID): 17878671 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.54.235 (Tokushima University Institutional Repository: 111518, DOI: 10.2152/jmi.54.235, PubMed: 17878671)
67.	Masayuki Nakano, Akira Takahashi, Y Sakai, M Kawano, Nagakatsu Harada, Kazuaki Mawatari and Yutaka Nakaya : Catecholamine-induced stimulation of growth in Vibrio species., Letters in Applied Microbiology, Vol.44, No.6, 649-653, 2007. (Summary) To evaluate the effect of norepinephrine (NE) and related compounds on the growth of bacteria, we have examined the effect of the neuroendocrine hormone NE and related compounds on the growth of Vibrio parahaemolyticus and other human-pathogenic Vibrio species (Vibrio cholerae, Vibrio vulnificus, and Vibrio mimicus). The effects on bacterial growth were examined using the serum-based medium and viable cells were counted using agar plates. We have shown that NE and its related compounds stimulate growth of V. parahaemolyticus in serum-based medium. This NE-induced growth stimulation was dependent upon the presence of transferrin. NE also stimulated growth of V. mimicus, but not V. cholerae and V. vulnificus. These results suggest that the Vibrio species differ in their ability to respond to NE. It is possible that NE and related compounds modulate the pathogenicity of V. parahaemolyticus and V. mimicus. (Keyword) Adrenergic alpha-Agonists / Catecholamines / Culture Media / Norepinephrine / Transferrin / Vibrio / Virulence (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1472-765X.2007.02136.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17576228 ● Search Scopus @ Elsevier (PMID): 17576228 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1472-765X.2007.02136.x (DOI: 10.1111/j.1472-765X.2007.02136.x, PubMed: 17576228)
68.	Hossein Nazari, Akira Takahashi, Nagakatsu Harada, Kazuaki Mawatari, Masayuki Nakano, Kazuhiro Kishi, Yousuke Ebina and Yutaka Nakaya : Angiotensin II inhibits insulin-induced actin stress fiber formation and glucose uptake via ERK1/2., The Journal of Medical Investigation : JMI, Vol.54, No.1,2, 19-27, 2007. (Summary) There is crosstalk in intracellular signaling between Angiotensin II (Ang II) and insulin. We hypothesized that the underlying mechanism might be related to changes in cytoskeleton. In the presence of 100 nM of Ang II, insulin-induced glucose uptake was decreased and insulin-induced actin filament organization was inhibited. PKC inhibitors, including GF109203x and p38MAPK inhibitor (SB203580) neither improved insulin-induced actin reorganization nor glucose uptake. In contrast, the Ang II-induced inhibition of glucose uptake and actin filament disorganization was reversed by 10 micromol ERK 1/2 MAPK inhibitor (PD98059). Pretreatment of Ang II increased ERK1/2 phosphorylation and inhibited insulin-induced Akt phosphorylation. The effect of Ang II on ERK1/2 phosphorylation was blocked by Ang II type 1 receptor antagonists, RNH6270 and PD98059 but not by SB203580 or Guanosine-5'-O-(2-ThioDiphosphate), a G-protein inhibitor. We next tested the effect of broad-spectrum matrix metalloproteinase (MMP) inhibitor (GM6001) on Ang II-inhibition of insulin signaling pathway. GM6001 did not improve Ang II-induced actin filament disorganization and did not inhibit ERK1/2 phosphorylation. From these data in L6 myotube, we conclude that Ang II negatively regulates the insulin signal not through MMP signaling pathway but specifically through MMP-independent ERK1/2 activation pathway, providing an alternative molecular mechanism for angiotensin-induced insulin resistance. (Keyword) Angiotensin II / Cell Line / glucose / Humans / insulin / MAP Kinase Signaling System / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / phosphorylation / Proto-Oncogene Proteins c-akt / Receptor, Angiotensin, Type 1 / Stress Fibers (Tokushima University Institutional Repository) ● Metadata: 111490 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.54.19 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17380010 ● Search Scopus @ Elsevier (PMID): 17380010 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.54.19 (Tokushima University Institutional Repository: 111490, DOI: 10.2152/jmi.54.19, PubMed: 17380010)
69.	Kazuhiro Kishi, Kazuaki Mawatari, K Sakai-Wakamatsu, Tomoyuki Yuasa, M Wang, M Ogura-Sawa, Yutaka Nakaya, S Hatakeyama and Yousuke Ebina : APS-mediated Ubiquitination of the Insulin Receptor Enhances its Internalization but does not Induce its Degradation., Endocrine Journal, Vol.54, No.1, 77-88, 2007. (Summary) APS, a tyrosine kinase adaptor protein with pleckstrin homology and Src homology 2 domains, is rapidly and strongly tyrosine-phosphorylated by insulin receptor kinase upon insulin stimulation. We have previously shown that APS knockout mice have increased insulin sensitivity, and that this enhancement is possibly due to increased insulin-response on adipose tissues. However, the function of APS in insulin signaling has so far been controversial. Here, we report that APS enhanced ligand-dependent multi-ubiquitination of the insulin receptor (IR) in CHO cells overexpressing the IR. APS-mediated ubiquitination of the IR induced enhancement of the IR internalization, but did not affect the IR degradation. This finding shows one of the pleiotropic functions of APS in insulin signaling. (Keyword) Adaptor Proteins, Signal Transducing / Animals / CHO Cells / Cricetinae / Cricetulus / Humans / Insulin / Mice / Protein Processing, Post-Translational / Protein Transport / Receptor, Insulin / Signal Transduction / Transfection / Ubiquitin (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.K06-056 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17102568 ● Search Scopus @ Elsevier (PMID): 17102568 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.K06-056 (DOI: 10.1507/endocrj.K06-056, PubMed: 17102568)
70.	Nagakatsu Harada, S Hara, M Yoshida, T Zenitani, Kazuaki Mawatari, M Nakano, Akira Takahashi, Toshio Hosaka, Katsuhiko Yoshimoto and Yutaka Nakaya : Molecular cloning of a murine glycerol-3-phosphate acyltransferase-like protein 1 (xGPAT1)., Molecular and Cellular Biochemistry, Vol.297, No.1-2, 41-51, 2007. (Summary) A novel murine glycerol-3-phosphate acyltransferase-like protein 1 (named xGPAT1) has been cloned. The mouse xGPAT1 gene is located on mouse Chromosome 2, spans >19 kb, and consists of at least 23 exons. The protein is 32% identical and 72% similar to mouse mitochondrial GPAT (mtGPAT) on the amino acid level. Sequencing analysis confirmed that xGPAT1 has a 2403-bp open reading frame (ORF) that encodes an 801-amino acid protein with an estimated molecular mass of 89.1 kDa. A hydropathy plot of the deduced xGPAT1 protein showed a high degree of similarity with that of the mtGPAT protein. Using 5'-rapid amplification of cDNA ends, two alternate, untranslated exon 1 (1a and b) isoforms were obtained, generating variants xGPAT1-v1 and xGPAT1-v2. xGPAT1-v1 is expressed in mouse heart, liver, spleen, kidney and murine inner medullary collecting duct 3 (mIMCD3) cells, while xGPAT1-v2 is expressed in mouse liver, spleen, kidney, white and brown adipose tissues and 3T3-L1 pre- and post-adipocytes. xGPAT1 was distributed in the membrane fraction and showed GPAT activity when epitope-tagged xGPAT1 was expressed in Chinese hamster ovary (CHO)-K1 cells. (Keyword) Amino Acid Sequence / Animals / Base Sequence / CHO Cells / Cell Line / Chromosomes, Mammalian / Cloning, Molecular / Cricetinae / Cricetulus / Epitopes / Exons / Gene Expression Profiling / Gene Expression Regulation, Enzymologic / Glycerol-3-Phosphate O-Acyltransferase / Introns / Mice / Mice, Inbred C57BL / Mitochondria / Molecular Sequence Data / RNA, Messenger / Sequence Homology, Amino Acid (Link to Publication Site) ● Publication site (DOI): 10.1007/s11010-006-9321-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17013544 ● Search Scopus @ Elsevier (PMID): 17013544 ● Search Scopus @ Elsevier (DOI): 10.1007/s11010-006-9321-5 (DOI: 10.1007/s11010-006-9321-5, PubMed: 17013544)
71.	A Nakamura, Nagakatsu Harada, Akira Takahashi, Kazuaki Mawatari, M Nakano, K Tsutsumi and Yutaka Nakaya : NO-1886, a lipoprotein lipase activator, attenuates vascular smooth muscle contraction in rat aorta, European Journal of Pharmacology, Vol.554, No.2-3, 183-190, 2007. (Summary) The chemical compound [4-(4-bromo-2-cyano-phenylcarbamoyl)-benzyl]-phosphonic acid diethyl ester (NO-1886) is a lipoprotein lipase activator having beneficial effects on both diabetes control and the cardiovascular system. Preventing accumulation of lipids in the cell wall, in addition to improving insulin actions on vasculature, may indirectly contribute to the reducing effect of NO-1886 on vascular resistance. However, the direct effect of NO-1886 on vascular resistance, i.e., whether NO-1886 directly modulates the function of vascular endothelium and/or smooth muscle cells has not been investigated. In this study we therefore investigated the direct effect of NO-1886 on vascular contractility using rat aortic rings and cultured smooth muscle cell-line A10. The results show that administration of NO-1886 attenuated aortic contraction induced by phenylephrine and/or a high K(+) environment, in both the presence and absence of aortic endothelium. 1-(5-Chloronaphthalene-1-sulfonyl)homopiperazine hydrochloride (ML-9), a myosin light chain kinase (MLCK) inhibitor, blocked this inhibitory effect of NO-1886, whereas inhibitors of other signaling molecules such as calmodulin, protein kinase C and Rho-kinase had no effect. The vasorelaxant effect of NO-1886 was blocked in the absence of extracellular Ca(2+), or in the presence of the Ca(2+) channel inhibitor, verapamil. NO-1886 attenuated smooth muscle contraction induced by the cumulative addition of CaCl(2). In A10 cells, NO-1886 inhibited the membrane depolarization-induced initial peak of [Ca(2+)](i) in the presence of extracellular Ca(2+). This inhibition did not occur in the absence of extracellular Ca(2+). Taken together these results demonstrate that NO-1886 attenuates smooth muscle contraction and causes vasorelaxation by an extracellular Ca(2+)- and MLCK-dependent mechanism. (Keyword) Adrenergic alpha-Agonists / Animals / Aorta, Thoracic / Benzamides / Calcium / Calcium Channel Blockers / Calcium Channels, N-Type / Calcium-Calmodulin-Dependent Protein Kinases / Dose-Response Relationship, Drug / Enzyme Activators / Flavonoids / Hypolipidemic Agents / Lipoprotein Lipase / Male / Muscle Contraction / Muscle, Smooth, Vascular / Organophosphorus Compounds / Phenylephrine / Potassium Chloride / Protein Kinase C / Rats / Rats, Wistar / Signal Transduction / Staurosporine / Vasoconstriction / Vasodilation / Verapamil (Link to Publication Site) ● Publication site (DOI): 10.1016/j.ejphar.2006.09.059 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17109854 ● Search Scopus @ Elsevier (PMID): 17109854 ● Search Scopus @ Elsevier (DOI): 10.1016/j.ejphar.2006.09.059 (DOI: 10.1016/j.ejphar.2006.09.059, PubMed: 17109854)
72.	Akira Takahashi, SI Miyoshi, N Takata, M Nakano, A Hamamoto, Kazuaki Mawatari, Nagakatsu Harada, S Shinoda and Yutaka Nakaya : Haemolysin produced by Vibrio mimicus activates two Cl secretory pathways in cultured intestinal-like Caco-2 cells., Cellular Microbiology, Vol.9, No.3, 583-595, 2007. (Summary) Haemolysin (VMH) is a virulent factor produced by Vibrio mimicus, a human pathogen that causes diarrhoea. As intestinal epithelial cells are the primary targets of haemolysin, we investigated its effects on ion transport in human colonic epithelial Caco-2 cells. VMH increased the cellular short circuit current (Isc), used to estimated ion fluxes, and 125I efflux of the cells. The VMH-induced increases in Isc and 125I efflux were suppressed by depleting Ca2+ from the medium or by pretreating the cells with BAPTA-AM or by Rp-adenosin 3',5'-cyclic monophosphorothioate triethylammonium salt (Rp-cAMPS). The Cl- channel inhibitors 4,4'-disothiocyanatostibene-2,2'-disulfonic acid (DIDS), glybenclamide, and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) suppressed the VMH-induced increases in Isc and 125I efflux. Moreover, VMH increased the intracellular concentrations of Ca2+ and cAMP. Thus, VMH stimulates Caco-2 cells to secrete Cl- by activating both Ca2+ -dependent and cAMP-dependent Cl- secretion mechanisms. VMH forms ion-permeable pores in the lipid bilayer that are non-selectively permeable to small ions. However, the ion permeability of these pores was not inhibited by glybenclamide and DIDS, and VMH did not change the cell membrane potential. These observations indicate that the pores formed on the cell membrane by VMH are unlikely to be involved in VMH-induced Cl- secretion. Notably, VMH stimulated fluid accumulation in the iliac loop test that was fully suppressed by a combination of DIDS and glybenclamide. Thus, Ca2+-dependent and cAMP-dependent Cl- secretion may be important therapeutic targets with regard to the diarrhoea that is induced by Vibrio mimicus. (Keyword) 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Animals / Bacterial Proteins / Biological Transport / Caco-2 Cells / Calcium / Chlorides / Cyclic AMP / Egtazic Acid / Glyburide / Hemolysin Proteins / Humans / Intestines / Iodine Radioisotopes / Membrane Potentials / Mice / Vibrio mimicus (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1462-5822.2006.00809.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17026482 ● Search Scopus @ Elsevier (PMID): 17026482 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1462-5822.2006.00809.x (DOI: 10.1111/j.1462-5822.2006.00809.x, PubMed: 17026482)
73.	Yasunobu Hayabuchi, Yutaka Nakaya, Yasui Sonoko, Kazuaki Mawatari, Kazuhiro Mori, Suzuki Mitsujiro and Shoji Kagami : Angiotensin II activates intermediate-conductance Ca²⁺-activated K⁺ channels in arterial smooth muscle cells., Journal of Molecular and Cellular Cardiology, Vol.41, No.6, 972-929, 2006. (Summary) Angiostensin II (Ang II) regulates the migration and proliferation of vascular smooth muscle cells. Recent studies indicate that intermediate-conductance Ca2+ -activated K+ (IKca) channels have an important role in cell migration and proliferation. It is not known, however, whether the action of Ang II is linked to IKca channel regulation. Here, we investigated the modulation of IKca channels by Ang II in artery smooth muscle cells. Functional IKca channel expression in cultured embryonic rat aorta smooth muscle (A10) cells was studied using the patch-clamp technique. These cells predominantly express IKca channels. In contrast, large-conductance Ca2+ -activated K+ (BKca) currents were rarely observed in excised patches. Ang II increased the IKca current in a contration-dependent manner. Losartan (1.0 microM), an AT1 selective antagonist, abolished the activation of IKca channels by Ang II. Pretreatment with 100 microM myristoylated protein kinase C inhibitor peptide 20-28 or 10 microM GF109203X completely abolished the AngII-induced activation of IKca currents, whereas the action of Ang II was not prevented in the presence of 100 microM Rp-cyclic 3', 5'-hydrogen phosphotiate adenosine triethylammonium, a protein kinase A inhibitor, or 1.0 microM KT-5823, a protein kinase G inhibitor. A membrane permeant analogue of diacylglycerol 1, 2-dioctanoyl-sn-glycerol (10 microM) induced the activation of IKca currents. These data suggest that Ang II activates IKca channels through the activation of protein kinase C, and the AT1 receptor is involved in the regulation of these channels. (Keyword) Angiotensin II / Angiotensin II Type 1 Receptor Blockers / Animals / Cells, Cultured / Diglycerides / Enzyme Inhibitors / Intermediate-Conductance Calcium-Activated Potassium Channels / Losartan / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Patch-Clamp Techniques / Protein Kinase C / Rats / Receptor, Angiotensin, Type 1 / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yjmcc.2006.07.010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16919291 ● Search Scopus @ Elsevier (PMID): 16919291 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yjmcc.2006.07.010 (DOI: 10.1016/j.yjmcc.2006.07.010, PubMed: 16919291)
74.	Akira Takahashi, Nakano Masayuki, Keinosuke Okamoto, Fujii Yoshio, Kazuaki Mawatari, Nagakatsu Harada and Yutaka Nakaya : Aeromonas sobria hemolysin causes diarrhea by increasing secretion of HCO₃^-, FEMS Microbiology Letters, Vol.258, No.1, 92-95, 2006. (Summary) Aeromonas sobria hemolysin (ASH) is one of the major virulence factors produced by A. sobria, a causative agent of diarrhea in humans. We investigated the effects of ASH on anion transport in human colonic epithelial cells. ASH increased short circuit currents across the intestinal epithelia, which were suppressed by anion channel antagonists, such as carbonic anhydrase inhibitors, and by the removal of external HCO3-. Iliac fluid accumulation was also inhibited by carbonic anhydrase inhibitors. The results suggest that ASH activates HCO3- secretion, whose level correlates with the severity of diarrhea. (Keyword) Aeromonas / Animals / Bicarbonates / Caco-2 Cells / Chlorides / Cystic Fibrosis Transmembrane Conductance Regulator / Diarrhea / Hemolysin Proteins / Humans / Intestinal Mucosa / Mice (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1574-6968.2006.00204.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16630261 ● Search Scopus @ Elsevier (PMID): 16630261 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1574-6968.2006.00204.x (DOI: 10.1111/j.1574-6968.2006.00204.x, PubMed: 16630261)
75.	Kazuaki Mawatari, Kakui Sae, Nagakatsu Harada, Takamasa Ohnishi, Yasuharu Niwa, Kazuko Okada, Akira Takahashi, Keisuke Izumi and Yutaka Nakaya : Endothelin-1(1 31) levels are increased in atherosclerotic lesions of the thoracic aorta of hypercholesterolemic hamsters, Atherosclerosis, Vol.175, No.2, 203-212, 2004. (Summary) The novel vaso-constricting 31-amino acid-length endothelin-1 [ET-1(1-31)] is selectively produced by human mast cell chymase via its action on big ET-1. However, the pathological role of ET-1(1-31) in atherosclerosis remains unclear. The aim of this study was to clarify vasoconstrictive response and expression of ET-1(1-31) in atherosclerotic aorta. Syrian golden hamster, was used for preparing the atherosclerotic models by the administration of a high cholesterol diet (HC), treatment with the nitric oxide synthase inhibitor (Nomega-nitro-L-arginine methylester, L-NAME) alone, or both (HC and L-NAME) for 40 weeks. Early atherosclerosis was observed in the case of HC or L-NAME alone treatments respectively and severe atherosclerosis was observed in the case of combined HC and L-NAME treatment. Vasoconstriction induced by ET-1(1-31) was not altered by the atherosclerotic changes, but the expression pattern of ET-1(1-31) was different at each stage of the atherosclerotic aorta. ET-1(1-31) was observed rarely in normal aortas or in early atherosclerotic lesions, but ET-1(1-31) expression was dramatically increased in aortic neointima and adventitia in a state of atherosclerosis with severe inflammation. ET-1(1-31) might play in a role of promoting atherosclerosis, and especially be involved in inflammatory mediation during the progression of atherosclerosis. (Keyword) Animals / Aorta, Thoracic / Arteriosclerosis / blood pressure / cholesterol / Cricetinae / Disease Models, Animal / Endothelin-1 / Heart Rate / Hypercholesterolemia / Male / Peptide Fragments / Triglycerides / Vasoconstriction (Link to Publication Site) ● Publication site (DOI): 10.1016/j.atherosclerosis.2003.10.015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15262175 ● Search Scopus @ Elsevier (PMID): 15262175 ● Search Scopus @ Elsevier (DOI): 10.1016/j.atherosclerosis.2003.10.015 (DOI: 10.1016/j.atherosclerosis.2003.10.015, PubMed: 15262175)
76.	Nagakatsu Harada, Chika Ninomiya, Yoshie Osako, Masaki Morishima, Kazuaki Mawatari, Akira Takahashi and Yutaka Nakaya : Taurine alters respiratory gas exchange and nutrient metabolism in type 2, Obesity Research, Vol.12, No.7, 1077-1084, 2004. (Summary) To assess the effect of taurine supplementation on respiratory gas exchange, which might reflect the improved metabolism of glucose and/or lipid in the type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Male OLETF rats (16 weeks of age) were randomly divided into two groups: unsupplemented group and taurine-supplemented (3% in drinking water) group. After 9 weeks of treatment, indirect calorimetry and insulin tolerance tests were conducted. The amounts of visceral fat pads, tissue glycogen, the blood concentrations of glucose, triacylglycerol, taurine, and electrolytes, and the level of hematocrit were compared between groups. A nondiabetic rat strain (Long-Evans Tokushima Otsuka) was used as the age-matched normal control. The indirect calorimetry showed that the treatment of OLETF rats with taurine could reduce a part of postprandial glucose oxidation possibly responsible for the increase of triacylglycerol synthesis in the body. Taurine supplementation also improved hyperglycemia and insulin resistance and increased muscle glycogen content in the OLETF rats. Supplementation with taurine increased the blood concentration of taurine and electrolyte and fluid volume, all of which were considered to be related to the improvement of metabolic disturbance in OLETF rats. Taurine supplementation may be an effective treatment for glucose intolerance and fat/lipid accumulation observed in type 2 diabetes associated with obesity. These metabolic changes might be ascribed, in part, to the alteration of circulating blood profiles, where the improved hyperglycemia and/or the blood accumulation of taurine itself would play roles. (Keyword) Animal Nutritional Physiological Phenomena / Animals / Blood / Blood Glucose / Blood Pressure / Body Weight / Calorimetry, Indirect / Diabetes Mellitus, Type 2 / Dietary Supplements / Drinking / Eating / Electrolytes / Food / Glycogen / Hematocrit / Insulin / Insulin Resistance / Male / Osmolar Concentration / Pulmonary Gas Exchange / Rats / Rats, Inbred OLETF / Taurine (Link to Publication Site) ● Publication site (DOI): 10.1038/oby.2004.135 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15292471 ● Summary page in Scopus @ Elsevier: 2-s2.0-6344221730 (DOI: 10.1038/oby.2004.135, PubMed: 15292471, Elsevier: Scopus)
77.	Sae Kakui, Kazuaki Mawatari, Takamasa Ohnishi, Yasuharu Niwa, Naomi Tanoue, Nagakatsu Harada, Akira Takahashi, Keisuke Izumi and Yutaka Nakaya : Localization of the 31-amino-acid endothelin-1 in hamster tissue, Life Sciences, Vol.74, No.11, 1435-1443, 2004. (Summary) Endothelin (ET)-1(1-31) is a novel vasoconstrictor peptide produced by human mast cell chymase, which selectively cleaves big ET-1 at the Try(31)-Gly(32) bond. We investigated the localization of ET-1(1-31) in various hamster tissues by immunohistochemistry and compared it to the distribution of ET-1(1-21). We found that the localization and amount of ET-1(1-31) were different from those of ET-1(1-21) in each tissue. ET-1(1-31)-like immunoreactivities (IR) in the heart, lung, and adrenal gland were observed in the same areas as ET-1(1-21) but were significantly weaker, suggesting that ET-1(1-31) might play a role only in mast cell/chymase-related pathological conditions in these tissues. In the liver, ET-1(1-31)-like IR was strongly detected in Kupffer cells where ET-1(1-21)-like IR was seen more weakly. In the kidney, ET-1(1-31)-like IR was slightly higher than ET-1(1-21). These results suggest that ET-1(1-31) might have physiological roles distinct from those of ET-1(1-21) in some hamster tissues. (Keyword) Animals / Chromatography, Affinity / Chromatography, High Pressure Liquid / Chymases / Cricetinae / Endothelin-1 / Immunochemistry / Immunohistochemistry / Male / Mesocricetus / Peptide Fragments / Peptides / Serine Endopeptidases / Tissue Distribution (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2003.08.021 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14706574 ● Search Scopus @ Elsevier (PMID): 14706574 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lfs.2003.08.021 (DOI: 10.1016/j.lfs.2003.08.021, PubMed: 14706574)
78.	Asako Minami, Noriko Ishimura, Sadaichi Sakamoto, Eiko Takishita, Kazuaki Mawatari, Kazuko Okada and Yutaka Nakaya : Effect of eicosapentaenoic acid ethyl ester v. oleic acid-rich safflower oil on insulin resistance in type 2 diabetic model rats with hypertriacylglycerolaemia, British Journal of Nutrition, Vol.87, No.2, 157-162, 2002. (Summary) The purpose of the present study was to test whether hyperlipidaemia and insulin resistance in type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats can be improved by dietary supplementation with purified eicosapentaenoic acid (EPA) or oleic acid (OA). Male OLETF rats were fed powdered chow (510 g fat/kg) alone (n 8) or chow supplemented with 10 g EPA- (n 8) or OA- (n 8) rich oil/kg per d from 5 weeks until 30 weeks of age. An oral glucose tolerance test and hyperinsulinaemic euglycaemic clamp was performed at 25 and 30 weeks of age. EPA supplementation resulted in significantly (P<0.05) reduced plasma lipids, hepatic triacylglycerols, and abdominal fat deposits, and more efficient in vivo glucose disposal compared with OA supplementation and no supplementation. OA supplementation was associated with significantly increased insulin response to oral glucose compared with EPA supplementation and no supplementation. Inverse correlation was noted between glucose uptake and plasma triacylglycerol levels (r -086, P<0.001) and abdominal fat volume (r -0.80, P<0.001). The result of oral glucose tolerance test study showed that the rats fed EPA tended to improve glucose intolerance, although this was not statistically significant. Levels of plasma insulin at 60 min after glucose was significantly increased in rats fed OA compared with the other two groups. The results indicate that long-term feeding of EPA might be effective in preventing insulin resistance in diabetes-prone rats, at least in part, due to improving hypertriacylglycerolaemia. (Keyword) Abdomen / Adipose Tissue / Animals / Blood Glucose / Body Weight / Diabetes Mellitus, Type 2 / Dietary Supplements / Disease Models, Animal / Eating / Eicosapentaenoic Acid / Glucose Clamp Technique / Glucose Tolerance Test / Hypertriglyceridemia / Insulin Resistance / Lipid Metabolism / Liver / Male / Oleic Acid / Rats / Rats, Inbred OLETF / Safflower Oil / Triglycerides (Link to Publication Site) ● Publication site (DOI): 10.1079/BJN2001496 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11895168 ● Search Scopus @ Elsevier (PMID): 11895168 ● Search Scopus @ Elsevier (DOI): 10.1079/BJN2001496 (DOI: 10.1079/BJN2001496, PubMed: 11895168)
79.	Akira Takahashi, Wada Akihiro, Ogushi Ken-ichi, Maeda Kyoko, Kawahara Tsukasa, Kazuaki Mawatari, Hisao Kurazono, Moss Joel, Hirayama Toshiya and Yutaka Nakaya : Production of L-defensin-2 by human colonic epithelial cells induced by Salmonella enteritidis flagella filament structural protein, FEBS Letters, Vol.508, No.3, 484-488, 2001. (Summary) We recently showed that FliC of Salmonella enteritidis increased human beta-defensin-2 (hBD-2) expression, and now describe the signaling responsible pathway. FliC increased the intracellular Ca(2+) concentration ([Ca(2+)](in)) in Caco-2 cells. The [Ca(2+)](in) increase induced by FliC was prevented by U73122 and heparin, but not by chelating extracellular Ca(2+) or pertussis toxin. The FliC-induced increase in hBD-2 promoter activity via nuclear factor kappaB (NF-kappaB) was also inhibited by chelation of intracellular Ca(2+) or by U73122. We conclude that FliC increased [Ca(2+)](in) via inositol 1,4,5-trisphosphate, which was followed by up-regulating hBD-2 mRNA expression via an NF-kappaB-dependent pathway. (Keyword) Caco-2 Cells / Calcium / Cell Nucleus / Chelating Agents / Colon / Culture Media / Egtazic Acid / Estrenes / Flagellin / Heparin / Humans / Inositol 1,4,5-Trisphosphate / Intestinal Mucosa / NF-kappa B / Pertussis Toxin / Promoter Regions, Genetic / Pyrrolidinones / RNA, Messenger / Salmonella enteritidis / Signal Transduction / Up-Regulation / Virulence Factors, Bordetella / beta-Defensins (Link to Publication Site) ● Publication site (DOI): 10.1016/S0014-5793(01)03088-5 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11728477 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035941137 (DOI: 10.1016/S0014-5793(01)03088-5, PubMed: 11728477, Elsevier: Scopus)

Academic Paper (Unrefereed Paper):

1.	Hiroki Mori, Yuji Morine, Kazuaki Mawatari, Ayumi Chiba, Shin-ichiro Yamada, Yu Saitou, Hiroki Ishibashi, Akira Takahashi and Mitsuo Shimada : Bile Metabolites and Risk of Carcinogenesis in Patients With Pancreaticobiliary Maljunction: A Pilot Study., Anticancer Research, Vol.41, No.1, 327-334, 2021. (Summary) Pancreaticobiliary maljunction (PBM), a disease with reflux of pancreatic and bile juice in the pancreaticobiliary tract, is a high-risk factor for biliary tract cancer. The aim of this study was to investigate the mechanism of carcinogenesis in PBM using a metabolomics analysis of bile sampled during surgery. Three patients with PBM without biliary tract cancer, four patients with extrahepatic bile duct cancer (EHBC), and three controls with benign disease were enrolled. Metabolomics analysis of bile samples was performed using capillary electrophoresis-mass spectrometry and liquid chromatography-mass spectrometry to discriminate the amino acid and lipidomic profiles. The principal component analysis in the capillary electrophoresis-mass spectrometry and liquid chromatography-mass spectrometry revealed similar metabolites in patients with PBM and those with EHBC; furthermore, there was a clear difference between patients with PBM or EHBC compared to controls. The amino acid profiles revealed the following 20 potential carcinogenic candidates for PBM: isoleucine, phenylalanine, tyrosine, leucine, tryptophan, arginine, lysine, valine, asparagine, methionine, aspartic acid, serine, threonine, histidine, glutamine, alanine, proline, glutamic acid, and pyruvic acid. The lipidomic profiles revealed the following 11 carcinogenic candidates: lysophosphatidylcholine, lysophosphatidylethanolamine, phosphatidyl glycerol, lysophosphatidyl glycerol, triacylglycerol, diacylglycerol, ceramide, sphyngomyeline, fatty acid, hyperforin, and vitamin D. Among these characteristic metabolites, the branched-chain amino acids, methionine and lysophosphatidylcholine are known to be related to carcinogenesis. The bile metabolites were extremely similar in patients with PBM and those with EHBC. Furthermore, amino acid and lipid metabolism was markedly different in patients with PBM or EHBC compared to healthy controls. (Keyword) Bile / Bile Duct Neoplasms / Cell Transformation, Neoplastic / Chromatography, Liquid / Disease Susceptibility / Electrophoresis, Capillary / Female / Humans / Male / Mass Spectrometry / Metabolomics / Pancreaticobiliary Maljunction / Pilot Projects / Risk Assessment / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.21873/anticanres.14779 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33419827 ● Search Scopus @ Elsevier (PMID): 33419827 ● Search Scopus @ Elsevier (DOI): 10.21873/anticanres.14779 (DOI: 10.21873/anticanres.14779, PubMed: 33419827)

Review, Commentary:

1.	SHINODA Koichi, Kazuaki Mawatari and Akira Takahashi : 家庭の安全・安心科学 ―家庭における微生物汚染とその対策―, Journal of Antibacterial and Antifungal Agents, Vol.52, No.2, 51-56, 2024.
2.	Akira Takahashi, Mutsumi Aihara, Kazuaki Mawatari and Masatake Akutagawa : 近紫外線発光ダイオードを用いた殺菌システム, 食品分野における非加熱殺菌技術, 150-166, Nov. 2013.
3.	Yutaka Nakaya, Nagakatsu Harada and Kazuaki Mawatari : 臨床スポーツ医学, 運動習慣形成と脳内神経伝達物質, 臨床スポーツ医学, Vol.25, No.10, 1181-1186, 2008.
4.	Yutaka Nakaya, Kazuaki Mawatari, Nagakatsu Harada and Akira Takahashi : 侵襲時の栄養評価法, 機能性食品と薬理栄養, Vol.4, No.4, 215-218, Sep. 2007.
5.	Yutaka Nakaya, Nagakatsu Harada, Kazuaki Mawatari, Akira Takahashi and Toshio Hosaka : Control of hypertension in metabolic syndrome, Shikoku Acta Medica, Vol.63, No.3,4, 97-100, Aug. 2007. (Summary) Metabolic syndrome includes abdominal obesity, hyperlipidemia, diabetes, and hypertension. All, but hypertension, are obviously related to metabolism. However, hypertension might result from, at least in part, abdominal obesity, because adipose tissue produces bioactive mediators (adipocytokines)which increase blood pressure. In treatment of hypertension, we should concern insulin resistance, which is a major risk factor of cardiovascular events. Angiotensin converting enzyme inhibitor is known to improve insulin resistance, but results of angiotensin receptor blocker in animal studies are controversial. In clinical trial, there are many established data that ARBs prevent new onset of diabetes mellitus, suggesting that this agent also has a beneficial effect on glucose metabolism. Short acting Ca-antagonists, such as nifedipine, decrease insulin sensitivity, but long-acting Ca-antagonists increase it. βblockers decrease insulin sensitivity but those with α-blocking action improve insulin resistance. Recent study, ARB is more potent to reduce cardiovascular risk in those with obesity than in those with normal body weight, suggesting some drugs are more effective in metabolic syndrome. Thus, when we chose antihypertensive drugs in treating patients with metabolic syndrome, we have to choose proper drugs in addition to modify life-style. (Keyword) hypertension / diabetes mellitus / metabolic syndrome / angiotensin / insulin resistance (Tokushima University Institutional Repository) ● Metadata: 110178 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050001337465066624 (Tokushima University Institutional Repository: 110178, CiNii: 1050001337465066624)
6.	Yutaka Nakaya, Kazuaki Mawatari, Akira Takahashi, Nagakatsu Harada, Hata Akiko and Yasui Sonoko : The phytoestrogen ginsensoside Re activates potassium channels of vascular smooth muscle cells through PI3K/Akt and nitric oxide pathways, The Journal of Medical Investigation : JMI, Vol.54, No.3,4, 381-384, Aug. 2007. (Summary) In vascular smooth muscle cells, large-conductance Ca(2+)-activated K(+) channels (K(Ca) channels) play a pivotal role in determining membrane potential, and thereby the vascular tone. Ginsenoside Re, a phytochemical from ginseng, is reported to activate this channel, but its precise mechanism is unsolved. Patch clamp studies showed that ginsenoside Re activates K(Ca) channels in the arterial smooth muscle cell line A10 in a dose-dependent manner. The channel-opening effect of ginsenoside Re was inhibited by 1 microM L-NIO, an inhibitor of eNOS, but not by 3 microM SMTC, an inhibitor of nNOS, indicating that ginsenoside Re activated K(Ca) channels through activation of eNOS. SH-6 (10 microM), an Akt inhibitor, and wortmannin, a PI3-kinase inhibitor, completely blocked activation of K(Ca) channels by ginsenoside Re, indicating that it activates eNOS via a c-Src/PI3-kinase/Akt-dependent mechanism. In addition, the ginsenoside Re-induced activation of eNOS and K(Ca) channel was blocked by 10 microM ICI 182, 780, an inhibitor of membrane estrogen receptor-alpha, suggesting that eNOS activation occurs via a non-genomic pathway of this receptor. In conclusion, ginsenoside Re releases NO via a membrane sex steroid receptors, resulting in K(Ca) channel activation in vascular smooth muscle cells, promoting vasodilation and preventing severe arterial contraction. (Keyword) Animals / Cell Line / Ginsenosides / Muscle, Smooth, Vascular / Myocytes, Smooth Muscle / Nitric Oxide / Nitric Oxide Synthase Type III / Phosphatidylinositol 3-Kinases / Phytoestrogens / Potassium Channels, Calcium-Activated / Proto-Oncogene Proteins c-akt / Rats / Vasodilation (Tokushima University Institutional Repository) ● Metadata: 111546 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.54.381 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17878692 ● Search Scopus @ Elsevier (PMID): 17878692 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.54.381 (Tokushima University Institutional Repository: 111546, DOI: 10.2152/jmi.54.381, PubMed: 17878692)
7.	Yutaka Nakaya and Kazuaki Mawatari : 筋肉をつけるための栄養学, The Journal of Therapy, Vol.85, No.11, 2993-2997, Nov. 2003.
8.	Yutaka Nakaya, Kazuaki Mawatari and Eiko Takishita : 肝疾患の病変と栄養管理-解決すべき問題点「肝硬変への分割食と就寝前軽食-その効果と課題」, 日本病態栄養学会誌, Vol.4, No.1, 1-5, Jun. 2001.

Proceeding of International Conference:

1.	Kai Ishida, Takaaki Shimohata, Kanda Yuna, Nguyen Quoc Anh, Masuda Rumiko, Yamazaki Kohei, Takashi Uebanso, Kazuaki Mawatari, Kashimoto Takashige and Akira Takahashi : Characteristic metabolic changes in the infected tissue due to Vibrio vulnificus in a wound infection model., 57th United States Japan Cooperative Medical Science Program Joint Panel Conference on Cholera and Other Bacterial Enteric Infections, Dec. 2023.
2.	SHINODA Koichi, Kazuaki Mawatari, Bui K. N. T., Hirakawa H., Awamoto K., Wakitani M, Shinoda T. and Akira Takahashi : Development of novel far-UVC light source for high germicidal effects and low human health risk., 2023 IEEE Photonics Conference, Orlando, Nov. 2023.
3.	Akira Takahashi, Katsuyuki Miyawaki, Kazuaki Mawatari, Takeshi Nikawa, Mutsumi Aihara, Fukushima Shiho, Akizawa Shinta, Yamashita Michiyo and Koi Yumena : Development of closed-circulation soybean cultivation system applicable to extreme environments, The 3rd Japan-France International Symposium on Space Nutrition/Medicine, Kyoto, Nov. 2023.
4.	Onoda Yushi, Kai Ishida, Kadomura-Ishikawa Yasuko, Nagahashi Miharu, Yamashita Michiyo, Fukushima Shiho, Aizawa Toshihiko, Yamauchi Shigeharu, Fujikawa Yasuo, Tanaka Tomotake, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Investigation of the wavelength dependence of fungal inactivation by standardized UV-LED irradiation device, The 10th Congress of European Microbiologists FEMS 2023, Hamburg, Jul. 2023.
5.	Kai Ishida, Takaaki Shimohata, Kanda Yuna, Nguyen Quoc Anh, Masuda Rumiko, Yamazaki Kohei, Takashi Uebanso, Kazuaki Mawatari, Kashimoto Takashige and Akira Takahashi : Characteristic metabolic changes in the infected tissue due to Vibrio vulnificus in a wound infection model, 日米コレラ部会(日米医学協力研究会コレラ・細菌性腸管感染症専門部会), Jul. 2023.
6.	SHINODA Koichi, NGAN THI KIM BUI, Kazuaki Mawatari, HIRAKAWA H., AWAMOTO K., Wakitani M., SHINODA T. and Akira Takahashi : Application Of Far-UVC Radiation For Sterilization Using New Strategies To Reduce Human Health Risks And Environmental Loads, ASM Microbe 2023, Houston, Jun. 2023.
7.	Kai Ishida, Onoda Yushi, Yasuko Ishikawa, Nagahashi Miharu, Yamashita Michiyo, Fukushima S., Aizawa T., Yamauchi S., Fujikawa Y., Tanaka T., Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Evaluation of wavelength dependent inactivation of bacteria, viruses, and fungi by originally developed light source with UV-LEDs, ASM Microbe 2023, Houston, Jun. 2023.
8.	NGAN THI KIM BUI, SHINODA Koichi, Kazuaki Mawatari, HIRAKAWA H., AWAMOTO K., Wakitani M., SHINODA T. and Akira Takahashi : Determination of Optimum Wavelength of Far-UVC for Virucidal and Bactericidal Effects Using Plasma Emission-Based Light Modules, ASM Microbe 2023, Houston, Jun. 2023.
9.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni induce autophagy for the bacterial invasion in the host epithelial cells, 54th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Dec. 2019.
10.	Ulfa Maria, Takaaki Shimohata, Momoyo Azuma, Masami Sato, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari, Masatake Akutagawa and Yohsuke Kinouchi : UVA-LED irradiation system as non-antibiotic approach to inactivation of pathogenic bacteria associated infectious disease, 54th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Dec. 2019.
11.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Junko Kido, Anh Quoc Nguyen, Yuna Kanda, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Role of host cellular unfolded protein response signaling during Campylobacter jejuni infection, 53th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Mar. 2019.
12.	Anh Quoc Nguyen, Takaaki Shimohata, Sho Hatayama, Aya Tentaku, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Metabolic changing in epithelial cell during Vibrio parahaemolyticus infection, 53th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Mar. 2019.
13.	Yukiko Tomioka, Hidehiro Umehara, Shinya Watanabe, Masahito Nakataki, Masuda Rumiko, Kazuaki Mawatari, Takeshi Nikawa, Akira Takahashi, Shusuke Numata and Tetsuro Ohmori : Altered plasma metabolites related to one-carbon metabolism in schizophrenia., WFSBP Asia Pacific Regional Congress of Biological Psychiatry, Kobe, Sep. 2018.
14.	Toshiya Okahisa, Masahiro Sogabe, Mayu Uyama, Tadahiko Nakagawa, Tetsu Tomonari, Tatsuya Taniguchi, Koichi Okamoto, Tetsuji Takayama, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Takahiro Emoto, Masatake Akutagawa, M Yamada and M Fukuhara : Development Of A Multi-Ring Type Roller Pump Unit Equipped To A Compact And Convenient Ascites Purification Machine For Cell-Free And Concentrated Ascites Reinfusion Therapy (CART)., ASAIO 64th Annual Conference, Washington, D.C., Jun. 2018.
15.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Anh Quoc Nguyen, Junko Kido, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Induction of the unfolded protein response (UPR) decreased Campylobacter jejunin invasion, 118th General Meeting of the American Society for Microbiology, Jun. 2018.
16.	Shiho Fukushima, Yuri Sato, Takaaki Shimohata, Junko Kido, Yuna Kanda, Aya Tentaku, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni Utilized Autophagy for the Bacterial Survival in the Host Epithelial Cells, 118th General Meeting of the American Society for Microbiology, Jun. 2018.
17.	Junko Kido, Takaaki Shimohata, sachie amano, sho hatayama, yuri sato, yuna kanda, aya tentaku, shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR reduced microtubule-mediated Campylobacter jejuni invasion, 52th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Feb. 2018.
18.	Syo Hatayama, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : The relation of cellular Tight Junctions formation and Campylobacter jejuni invasion in intestinal epithelial cells, 51th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Feb. 2017.
19.	Hiroshi Tatano, Hisami Okumura, Daisuke Kajiura, C Kondo, A Hirayama, Kazuaki Mawatari, Yoshichika Kawai, Masashi Masuda and Yutaka Taketani : Exploring the impact of consuming different types of meat on metabolome profiles using a GC-MS metabolomics approach, 11th Metabolomics Society Conference, Dublin, Jul. 2016.
20.	Tadahiko Nakagawa, Yoshifumi Takaoka, Hironori Tanaka, Kumiko Tanaka, Tetsuji Takayama, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Masatake Akutagawa, Takahiro Emoto, Yohsuke Kinouchi, Toru Murashima, Satoru Yamaji, Zenji Tanaka, Masahiro Sogabe and Toshiya Okahisa : Roller Pump Circulation System For Preventing Filter Clogging During Cell-free and Concentrated Ascites Reinfusion Therapy (cart)., The 61th Annual Conference of American Society for Artificial Internal Organs(ASAIO), Chicago, Jun. 2015.
21.	Tsunedomi Akari, Masamura Akinori, Mutsumi Nakahashi, Nishisaka Risa, Kazuaki Mawatari, Takaaki Shimohata, Takashi Uebanso, Katsuyuki Miyawaki, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Disinfection system with UVA-LED for hydroponic nutrient solution, 6th FEMS Microbiology Congress, Jun. 2015.
22.	Hatayama Sho, Takaaki Shimohata, Negoro Sachie, Sato Yuri, Kido Junko, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : The denudation of lateral part promote Campylobacter jejuni invasion in Caco-2 cells., 6th FEMS Microbiology Congress, Jun. 2015.
23.	Takashi Uebanso, Takaaki Shimohata, Iba Hitomi, Nishimura Kazuya, Taniguchi Yuichi, Kazuki Horikawa, Mutsumi Nakahashi, Kazuaki Mawatari and Akira Takahashi : COMBINATION BETWEEN A FEW T3SS INJECTISOME AND A LOT EFFECTOR FOR KILLING HOST CELLS ON VIBRIO PARAHAEMOLYTICUS, 6th FEMS Microbiology Congress, Jun. 2015.
24.	Takaaki Shimohata, Negoro Sachie, Kido Junko, Hatayama Sho, Sato Yuri, Iba Hitomi, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : INFECTION OF CAMPYLOBACTER JEJUNI REDUCES CFTR MEDIATED CL- SECRETION IN T-84, 6th FEMS Microbiology Congress, Jun. 2015.
25.	Ayumi Yoshimoto, Takashi Uebanso, Kazuaki Mawatari, Mutsumi Nakahashi, Takaaki Shimohata and Akira Takahashi : Low dose antibiotics treatment in the prenatal period affect newborns health in later life, 12th Asian Congress of Nutrition, 70, May 2015.
26.	Takashi Uebanso, Ai Ohnishi, Takaaki Shimohata, Mutsumi Nakahashi, Kazuaki Mawatari and Akira Takahashi : Acceptable daily intake levels of sucralose consumption reduces fecal Clostridium cluster 4 in mouse, 12th Asian Congress of Nutrition, 70, May 2015.
27.	Takaaki Shimohata, Sachie Negoro, Sho Hatayama, Yuri Sato, Hitomi Iba, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni Infection Reduces Cftr Mediated Cl- Secretion In T-84, American Society for Microbiology 114th General Meeting, May 2014.
28.	Mutsumi Aihara, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Simultaneous irradiation with different wavelengths of ultraviolet light has synergistic bactericidal effect on Vibrio parahaemolyticus, 48th US-Japan Cooperative Medical Sciences Program Conference on cholera and Other Bacterial Enteric Infections, Feb. 2014.
29.	Sachie Negoro, Takaaki Shimohata, Syo Hatayama, Mari Matsumoto, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Suppression of CFTR-mediated Cl- transport in Campylobacter jejuni infection, International Symposium Hannover - Tokushima Research Communication, Aug. 2013.
30.	Takashi Uebanso, Hitomi Iba, Shoko Asada, Takaaki Shimohata, Mutsumi Aihara, Kazuaki Mawatari and Akira Takahashi : Regulation and effects of VP1671 (VscQ) on virulence of Vibrio parahaemolyticus, 5th FEMS Microbiology Congress, Jul. 2013.
31.	Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Synergistic bactericidal effect of ultraviolet light with a combination of different wavelength, 5th FEMS Microbiology Congress, Jul. 2013.
32.	Kazuaki Mawatari, Tam Thanh Thi Le, Miki Maetani, Tomomi Yamamoto, Airi Honjo, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : VP2118 has major roles in Vibrio parahaemolyticus response to oxidative stress, 5th FEMS Microbiology Congress, Jul. 2013.
33.	Kazuaki Mawatari, Tam Thanh Thi Le, Miki Maetani, Tomomi Yamamoto, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : VP2118 has major roles in Vibrio parahaemolyticus response to oxidative stress, US-Japan Cooperative Medical Science Program, 47th Annual Joint Panel Meeting on Cholera and Other Bacterial Enteric Infections, Dec. 2012.
34.	Kazuaki Mawatari, Yuka Isumi, Minami Hirayama, Miki Maetani, Tomomi Yamamoto, Sayaka Hayashida, Hitomi Iba, Mutsumi Aihara, Takaaki Shimohata and Akira Takahashi : OtnA-OtnB modulate capsular polysaccharide and polymyxin B resistance in Vibrio parahaemolyticus, 112th General Meeting of the American Society for Microbiology, Jun. 2012.
35.	Mutsumi Aihara, Kazuaki Mawatari, Takaaki Shimohata and Akira Takahashi : Bactericidal Effect of Ultraviolet Light with a Combination of Different Wavelengths, 112th General Meeting of the American Society for Microbiology, Jun. 2012.
36.	Hitomi Iba, Takaaki Shimohata, Masayuki Yamato, Kazuaki Mawatari and Akira Takahashi : The effect of VP1671 (vscQ) on virulence of Vibrio parahaemolyticus, 4th FEMS Microbiology Congress, Jun. 2011.
37.	Kazuaki Mawatari, Yumi Yoneda, Manami Honda, Hitomi Iba, Mutsumi Aihara, Zehong Su, Takaaki Shimohata, Masayuki Yamato and Akira Takahashi : VPA1604, a protein containing phosphorylated tyrosine, modulates high molecular weight capsular polysaccharide in Vibrio parahaemolyticus, 4th FEMS Microbiology Congress, Jun. 2011.
38.	Kazuaki Mawatari, Yumi Yoneda, Manami Honda, Hitomi Iba, Mutsumi Aihara, Zehong Su, Takaaki Shimohata, Masayuki Yamato and Akira Takahashi : VPA1604, a protein tyrosine kinase, modulates high molecular weight capsular polysaccharide in Vibrio parahaemolyticus, US-Japan Cooperative Medical Science Program, 45th Annual Joint Panel Meeting on Cholera and Other Bacterial Enteric Infections Panel, Kyoto, Dec. 2010.
39.	Takaaki Shimohata, Masayuki Nakano, Lian Xin, Kazuaki Mawatari, Masayuki Yamato and Akira Takahashi : Vibrio parahaemolyticus modulate IL-8 secretion through dual pathway, 110th General Meeting of the American Society for Microbiology, San Diego, CA, U.S.A., Jun. 2010.
40.	Rie Tsutsumi, Kazuaki Mawatari, Katayama Erika, Yutaka Nakaya and Yasuo Tsutsumi : Compound K produces cardiac protection by activating Akt phosphorylation., Experimental Biology Annual Meeting, Anaheim, California, Apr. 2010.
41.	Akira Takahashi, M. Nakano, Kazuaki Mawatari, Nagakatsu Harada and Yutaka Nakaya : Vibrio cholerae El tor Hemolysin Activates Cyclic AMT Dependent Cl-Secretory Pathways which Xaused Diarrhea, 108th General Meeting of the American Society for Microbiology, Boston, Jun. 2008.

Proceeding of Domestic Conference:

1.	NAKAMURA Minami, HIROKI Matsuki, ANAYT ULLA, Takayuki Uchida, Kazuaki Mawatari, Akira Takahashi, Shoichiro Takao, Katsuyuki Miyawaki, Takahito Watanabe, Taro Mito, Takayoshi Kuriki, 片岡孝介, 葦苅晟矢 and Takeshi Nikawa : コオロギ摂食による栄養学的な機能性検討, 第78回日本栄養・食糧学会大会, May 2024.
2.	SHIROYAMA Yuto, KURIMOTO Kazuki, Tomoki Watanabe, Toshihiro Okamoto, Kenzo Yamaguchi, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi and Masanobu Haraguchi : ナノサイズ金属埋め込み円柱構造を大面積で作製する手法の検討, 第71回応用物理学会春季学術講演会, 22p-P06-5, Mar. 2024.
3.	Duc Quang Tran, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Unraveling the Capacity and Mechanism of Gut Microbiota in Enhancing Essential Amino Acid Provision to Juvenile Mice Under Essential Amino Acid-Deficient Diet, 第268回徳島医学会学術集会(令和5年度冬季), Mar. 2024.
4.	MATSUOKA Mika, KASUMI Buno, Shiori Inoue, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : ケトジェニック食摂取時の血糖維持機構の解析, 第8回メタボローム解析シンポジウム, Dec. 2023.
5.	ONO Miyu, Kai Ishida, MAKIMOTO Mana, Takaaki Shimohata, Takashi Uebanso, Mutsumi Aihara, Masatake Akutagawa, Takahiro Emoto, Kazuaki Mawatari, 岩田剛敏 and Akira Takahashi : UVA 照射による Campylobacter jejuni の上皮定着性に対する影響, 第16 回日本カンピロバクター研究会総会, Dec. 2023.
6.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, Yui Matsumoto, Tomohiro Yoshida, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Akira Takahashi, 岡本泰昌 and Shusuke Numata : 大うつ病性障害患者における治療前後の血中代謝物濃度の変化, 第45回日本生物学的精神医学会年会, Nov. 2023.
7.	Kazuaki Mawatari, TODA Sae, HIRANO Nozomi, Shion Yuki, Takashi Uebanso and Akira Takahashi : 概日リズムを調節可能な低分子化合物の同定とその応用, 「プレシジョン栄養学の研究基盤確立を目指す食と栄養研究クラスター」「合成生物学に基づく産官学連携バイオエコノミー創薬プラットフォームの構築」研究クラスター若手合同ミーティング, Oct. 2023.
8.	TODA Sae, Kazuaki Mawatari, Issei Tonowaki, HIRANO Nozomi, YAMAGUCHI Momoka, NGAN THI KIM BUI, Yasuko Ishikawa, SHINODA Koichi, Takashi Uebanso and Akira Takahashi : 柑橘由来ポリメトキシフラボンは新型コロナウイルスの宿主細胞内複製を抑制する, 第56回日本栄養·食糧学会中国·四国支部大会, Oct. 2023.
9.	AIZAWA Shinta, KOI Yumena, MICHIYO Yamashita, 白石志帆, Katsuyuki Miyawaki, Mutsumi Aihara, Takeshi Nikawa, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 極地環境での大豆栽培方法の確立, 第56回日本栄養·食糧学会中国·四国支部大会, Oct. 2023.
10.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, Yui Matsumoto, Tomohiro Yoshida, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Akira Takahashi, 岡本泰昌 and Shusuke Numata : 双極性障害における血中代謝物の変化, 第33回日本臨床精神神経薬理学会学術集会, Sep. 2023.
11.	MAKIMOTO Mana, Shiho Fukushima, Saki Yamanaka, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni病原性に対するコハク酸の影響, 第44回日本食品微生物学会学術総会, Sep. 2023.
12.	Duc Quang Tran, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Unraveling the Capacity and Mechanism of Gut Microbiota in Enhancing Essential Amino Acid Provision to Juvenile Mice Under Essential Amino Acid-Deficient Diet, 2023 Tokushima Bioscience Retreat, Sep. 2023.
13.	Kazuaki Mawatari and Akira Takahashi : 光殺菌の波長依存性, 日本防菌防黴学会第50回年次大会, Aug. 2023.
14.	Bui Kim Thi Ngan, Kazuaki Mawatari, SHINODA Koichi, 平川仁, 粟本健司, 脇谷正幸, 篠田傳 and Akira Takahashi : Determination of optimum wavelength of far-UVC for virucidal and bactericidal effects using plasma emission-based light modules, 日本防菌防黴学会第50回年次大会, Aug. 2023.
15.	SHINODA Koichi, Kazuaki Mawatari, Ngan Thi Kim Bui, 平川仁, 粟本健司, 脇谷正幸, 篠田傳 and Akira Takahashi : 人にも環境にもやさしい光殺菌を目指した波長制御型Far-UVC光源の開発, 日本防菌防黴学会第50回年次大会, Aug. 2023.
16.	ONODA Yushi, Kai Ishida, Yasuko Ishikawa, Saho Tanaka, MICHIYO Yamashita, Shiho Fukushima, 相澤俊彦, 山内繁晴, 藤川康夫, 田中智毅, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : UV-LEDの光学特性に適したUV感受性評価のための標準化光源の開発, 日本防菌防黴学会第50回年次大会, Aug. 2023.
17.	Kai Ishida, ONODA Yushi, Yasuko Ishikawa, Saho Tanaka, MICHIYO Yamashita, Shiho Fukushima, 相澤俊彦, 山内繁晴, 藤川康夫, 田中智毅, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : ウイルスに対する波長依存的不活化効果の評価, 日本防菌防黴学会第50回年次大会, Aug. 2023.
18.	Kazuaki Mawatari, 小池宣也, 野原一成, 敷島康普, 三浦宏之, 新居佳孝, Takashi Uebanso, Takaaki Shimohata, 八木田和弘, Akira Takahashi, Yoo Seung-Hee and Chen Zheng : スダチ果皮特有のフラボノイド・スダチチンの概日リズム調節作用と肝脂質代謝改善作用, 第267回徳島医学会学術集会, Aug. 2023.
19.	Kazuaki Mawatari, 小池宣也, 野原一成, 敷島康普, 三浦宏之, 新居佳孝, Takashi Uebanso, Takaaki Shimohata, 八木田和弘, Akira Takahashi, Seung-Hee Yoo and Zheng Chen : スダチ由来ポリメトキシフラボン・スダチチンの概日リズム調節作用と肝脂質代謝改善作用, 第77回日本栄養・食糧学会大会, May 2023.
20.	KASUMI Buno, Takashi Uebanso, AIZAWA Shinta, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : 母体のケトジェニック食摂取が仔の脂質代謝に与える影響, May 2023.
21.	TODA Sae, Kazuaki Mawatari, FURUYA Koji, Issei Tonowaki, Bui Kim Thi Ngan, Yasuko Ishikawa, SHINODA Koichi, Takashi Uebanso and Akira Takahashi : 概日リズムを調節可能な化合物によるヒトコロナウイルス複製抑制効果, 第77回日本栄養・食糧学会大会, May 2023.
22.	HIROKI Matsuki, MINORI Suzuki, KONO Madoka, ANAYT ULLA, Kazuaki Mawatari, Akira Takahashi, Katsuyuki Miyawaki, Takahito Watanabe, Taro Mito, Takayoshi Kuriki and Takeshi Nikawa : コオロギの抗筋萎縮作用について, 第77回日本栄養・食糧学会大会, May 2023.
23.	TODA Sae, Kazuaki Mawatari, Issei Tonowaki, HIRANO Nozomi, YAMAGUCHI Momoka, NGAN THI KIM BUI, Yasuko Ishikawa, SHINODA Koichi, Takashi Uebanso and Akira Takahashi : ポリメトキシフラボンのノビレチンはコロナウイルスの宿主細胞内複製を抑制する, 徳島大学大学院医歯薬学研究部 2023 感染・免疫クラスター・ミニリトリート「生命科学・医工連携リトリートならびに教育クラスターによる分野横断的大学院教育の促進」, Feb. 2023.
24.	Shiho Fukushima, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : リソソームはCampylobacter jejuniの宿主細胞内生存に寄与する, 第95回日本生化学会大会, Nov. 2022.
25.	Kai Ishida, Mutsumi Aihara, Takaaki Shimohata, Shiori Kitayama, 勢川玲花, Takashi Uebanso, Kazuaki Mawatari, Hiroshi Suzuki, Masatake Akutagawa, Takahiro Emoto, 山本光生, 富久章子, 和田敬宏, 岡本雅之, 伊藤浩, Takashi Yasuno, Yohsuke Kinouchi and Akira Takahashi : 鶏舎におけるUV-LED導入による衛生環境改善効果の検討, 第43回日本食品微生物学会学術総会, Sep. 2022.
26.	Kai Ishida, Mutsumi Aihara, Takaaki Shimohata, Shiori Kitayama, 勢川玲花, Takashi Uebanso, Kazuaki Mawatari, Hiroshi Suzuki, Masatake Akutagawa, Takahiro Emoto, 山本光生, 富久章子, 和田敬宏, 岡本雅之, 伊藤浩, Takashi Yasuno, Yohsuke Kinouchi and Akira Takahashi : 鶏舎内へのUV―LED導入による鶏の生育及び衛生環境の改善効果の検討, 日本家禽学会2022年度秋季大会, Sep. 2022.
27.	Bui Kim Thi Ngan, Kazuaki Mawatari, Takahiro Emoto, Shiho Fukushima, Takashi Uebanso, Takaaki Shimohata, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : UV-LED irradiation reduces the infectivity of herpes simplex virus type 1 by targeting different viral components depending on the peak, 第265回徳島医学会学術集会, Jul. 2022.
28.	ISHIDA Kai, Takaaki Shimohata, Marina Sano, Hitomi Iba, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 菌体外NaCl濃度変化に応答する，腸炎ビブリオの病原性解析, 第76回日本栄養・食糧学会大会, Jun. 2022.
29.	Hitomi Iba, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Vibrio parahaemolyticusの病原因子T3SS1遺伝子発現は宿主細胞接着によって誘導される, 第76回日本栄養・食糧学会大会, Jun. 2022.
30.	Takashi Uebanso, AIZAWA Shinta, Maya Nakamura, Mai Suyama, Ayumi Yoshimoto, 増田瑠見子, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : ビタミンB2の栄養状態と高シュウ酸尿症との関係, 第76回日本栄養・食糧学会大会, Jun. 2022.
31.	KITAYAMA Shiori, Takaaki Shimohata, 白石志帆, ISHIDA Kai, Miyuki Ogata, Takashi Uebanso, Kazuaki Mawatari, Mutsumi Aihara, Masatake Akutagawa, Takahiro Emoto, Hiroshi Suzuki, Takashi Yasuno, 伊藤浩, 和田敬宏, 岡本雅之, 富久章子, Akira Takahashi and Yohsuke Kinouchi : UV-LEDによる鶏舎内光環境の構築, LED総合フォーラム2022 in 徳島, 169-172, Jan. 2022.
32.	kai ishida, Takaaki Shimohata, yuna kanda, Rumiko Masuda, Takashi Uebanso, Kazuaki Mawatari, 柏本孝茂 and Akira Takahashi : Metabolism changing of Vibrio vulnificus infected tissue in wound infection model mouse, 第93回日本細菌学会総会, Feb. 2020.
33.	Tsubasa Kondo, Natsuki Arao, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : 炎症性腸疾患における味覚受容体T1R3の役割の解析, 第260回徳島医学会学術集会, Feb. 2020.
34.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : オートファジーを介したCampylobacter jejuni侵入機構へのRac GTPaseの関与, 第260回徳島医学会学術集会, Feb. 2020.
35.	Takaaki Shimohata, Junko Kido, Ryoka Narutaki, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 代謝産物の網羅的解析から紐解く，Campylobacter jejuniの生存戦略, 第260回徳島医学会学術集会, Feb. 2020.
36.	Shinta Aizawa, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : 母親の腸内細菌叢の変化が仔の食物アレルギー発症に与える影響, 第72回日本細菌学会中国・四国支部総会, Nov. 2019.
37.	Takaaki Shimohata, Junko Kido, Shiho Fukushima, Aya Tentaku, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染は宿主上皮細胞のアミノ酸取り込みを促進する, 第92回日本生化学会大会, Sep. 2019.
38.	Ulfa Maria, Takaaki Shimohata, Shiho Fukushima, Masami Sato, Momoyo Azuma, Takashi Uebanso, Kazuaki Mawatari, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Effect of 365 nm LED on the inactivation of ESBL producing Escherichia coli, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Aug. 2019.
39.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni induce autophagy for the bacterial invasion in the host epithelial cells, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Aug. 2019.
40.	Moeka Fukui, Takashi Uebanso, Chisato Naitoh, 増田瑠見子, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : 腸管上皮細胞におけるケトン体代謝調節機構, 第73回日本栄養・食糧学会大会, May 2019.
41.	Ulfa Maria, Takaaki Shimohata, Shiho Fukushima, Momoyo Azuma, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : The effectiveness of UVA-LED irradiation on ESBL producing Escherichia coli, 第92回日本細菌学会総会, Apr. 2019.
42.	kai Ishida, Takaaki Shimohata, sho Hatayama, Junko Kido, yuna Kanda, aya Tentaku, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Effect of cholesterol on Campylobacter jejuni survival in host intestinal epithelial cells, 第92回日本細菌学会総会, Apr. 2019.
43.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Host autophagy was exploited to Campylobacter jejuni invasion in the epithelial cells, 第92回日本細菌学会総会, Apr. 2019.
44.	Hiroki Mori, Yuji Morine, Noriko Yokota, Hiroki Ishibashi, Kazuaki Mawatari, Akira Takahashi and Mitsuo Shimada : 膵・胆管合流異常における発がんメカニズムに関する検討, 第80回日本臨床外科学会総会, Nov. 2018.
45.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染で誘導されるオートファジーは宿主細胞への菌の侵入および細胞内生存を促進する, 第71回日本細菌学会中国・四国支部総会, Oct. 2018.
46.	Yuna Kanda, Ryo Higashiyama, Takaaki Shimohata, Sho Hatayama, Junko Kido, Aya Tentaku, Shiho Fukushima, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari, 柏本孝茂 and Akira Takahashi : Vibrio Vulnificusが産生するOMVの機能解析, 第71回日本細菌学会中国・四国支部総会, Oct. 2018.
47.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Anh Quoc Nguyen, Junko Kido, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染によって誘導される小胞体ストレス応答は菌の細胞侵入を抑制する, 第39回日本食品微生物学会学術総会, Sep. 2018.
48.	Sho Hatayama, Takaaki Shimohata, Junko Kido, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Akiko Nakamoto, Emi Shuto, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni汚染調理器具に対するUVA-LED照射殺菌の有効性について, 第39回日本食品微生物学会学術総会, Sep. 2018.
49.	Yuna Kanda, Ryo Higashiyama, Takaaki Shimohata, Sho Hatayama, Junko Kido, Aya Tentaku, Shiho Fukushima, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari, 柏本孝茂 and Akira Takahashi : Vibrio Vulnificusが産生するOMVの機能解析, 第39回日本食品微生物学会学術総会, Sep. 2018.
50.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : オートファジーはCampylobacter jejuniの宿主細胞への侵入過程を促進する, 第91回日本生化学会大会, Sep. 2018.
51.	Takaaki Shimohata, Sho Hatayama, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniは宿主腸管上皮細胞の細胞側面から効率的に侵入する, 第91回日本生化学会大会, Sep. 2018.
52.	Anh Quoc Nguyen, Takaaki Shimohata, Anh Quoc Nguyen, Sho Hatayama, Aya Tentaku, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Metabolic changing in epithelial cell during Vibrio parahaemolyticus infection, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Aug. 2018.
53.	Aya Tentaku, Takaaki Shimohata, Anh Quoc Nguyen, Sho Hatayama, Junko Kido, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Unfolded Protein Response Suppressed Campylobacter jejuni-invasion in Epithelial Cells, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Aug. 2018.
54.	Ulfa Maria, Takaaki Shimohata, Shiho Fukushima, Momoyo Azuma, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Application of UVA-LED on Extended-Spectrumβ-Lactamase(ESBL) Producing Escherichia coli from Clinical Isolates, 第257回徳島医学会学術集会, Aug. 2018.
55.	Kai Ishida, Takaaki Shimohata, Junko Kido, Aya Tentaku, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniの宿主腸管上皮細胞での生存に対するコレステロールの影響, 第92回日本感染症学会学術講演会, May 2018.
56.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, Aya Tentaku, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染で誘導されるオートファジーは宿主細胞への侵入および細胞内生存を促進する, 第92回日本感染症学会学術講演会, May 2018.
57.	Hiroki Mori, Yuji Morine, Keigo Yada, Hiroki Ishibashi, Kazuaki Mawatari, Akira Takahashi and Mitsuo Shimada : メタボローム解析を用いた膵・胆管合流異常における胆汁発癌物質の検討, 第55回日本小児外科学会学術集会, May 2018.
58.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Anh Quoc Nguyen, Junko Kido, Shiho Fukushima, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 宿主細胞内での小胞体ストレス応答(UPR)はCampylobacter jejuni感染に対する防御機構として働く, 第72回日本栄養・食糧学会大会, May 2018.
59.	Hiroki Mori, Yuji Morine, Keigo Yada, Hiroki Ishibashi, Kazuaki Mawatari, Akira Takahashi and Mitsuo Shimada : メタボローム解析を用いた膵・胆管合流異常の胆汁中発癌物質の同定, 第118回日本外科学会定期学術集会, Apr. 2018.
60.	Quoc Nguyen anh, Takaaki Shimohata, sho Hatayama, aya Tentaku, Junko kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Metabolic analysis of epithelial cellular metabolism during Vibrio parahaemolyticus infection, 第91回日本細菌学会総会, Mar. 2018.
61.	aya tentaku, Takaaki Shimohata, sho Hatayama, Quoc Nguyen Anh, Junko kido, shiho fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染における小胞体ストレス応答は菌の侵入を抑制する, 第91回日本細菌学会総会, Mar. 2018.
62.	shiho Fukushima, Takaaki Shimohata, sho Hatayama, Junko KIdo, aya Tentaku, yuna kanda, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniは菌の宿主上皮細胞への侵入および生存過程にオートファジーを利用する, 第91回日本細菌学会総会, Mar. 2018.
63.	Shiho Fukushima, Takaaki Shimohata, Sho Hatayama, Junko Kido, Aya Tentaku, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染で誘導されるオートファジーは，宿主上皮細胞における菌の侵入および生存を促進する, 第256回徳島医学会学術集会, Feb. 2018.
64.	junko kido, Takaaki Shimohata, sachie amano, sho hatayama, aya Tentaku, shiho fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR発現はCampylobacter jejuniの微小管を介した輸送を抑制する, ConBio2017, Dec. 2017.
65.	aya Tentaku, Takaaki Shimohata, sho Hatayama, Quoc Nguyen Anh, junko kido, shiho fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染で誘導される小胞体ストレス応答は細胞内への菌の侵入を抑制する, ConBio2017, Dec. 2017.
66.	shiho Fukushima, Takaaki Shimohata, sho Hatayama, junko kido, aya Tentaku, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染で誘導されるオートファジーは，宿主上皮細胞における菌の侵入および生存を促進する, ConBio2017, Dec. 2017.
67.	Takaaki Shimohata, Junko Kido, Sho Hatayama, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 代謝産物の解析から紐解くCampylobacter jejuniの宿主細胞内生存戦略, 第70回日本細菌学会中国・四国支部総会, Oct. 2017.
68.	Anh Quoc Nguyen, Takaaki Shimohata, Sho Hatayama, Aya Tentaku, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Metabolic analysis of epithelial cellular metabolism during Vibrio parahaemolyticus infection, 第70回日本細菌学会中国・四国支部総会, Oct. 2017.
69.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Anh Quoc Nguyen, Junko Kido, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Cpylobacter jejuni感染によって誘導される小胞体ストレス応答が菌に与える影響, 第70回日本細菌学会中国・四国支部総会, Oct. 2017.
70.	Sho Hatayama, Takaaki Shimohata, Junko Kido, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 極性化腸管上皮細胞におけるタイトジャンクション形成はCampylobacter jejuniの細胞内侵入機構に影響する, 第38回日本食品微生物学会学術総会, Oct. 2017.
71.	Shiho Fukushima, Takaaki Shimohata, Sho Hatayama, Junko Kido, Aya Tentaku, Yuna Kanda, Ryoka Narutaki, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染で誘導されるオートファジーは菌のクリアランス機構として働くのか, 第38回日本食品微生物学会学術総会, Oct. 2017.
72.	Junko Kido, Takaaki Shimohata, Sachie Amano, Syo Hatayama, Yuri Sato, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR reduced microtubule-mediated Campylobacter jejuni invasion, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Aug. 2017.
73.	Takashi Uebanso, Ai Ohnishi, Reiko Kitayama, Ayumi Yoshimoto, Mutsumi Nakahashi, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : 許容上限量の甘味料の摂取が腸内細菌叢と宿主へ及ぼす影響の解析, 日本栄養食糧学会, 243, May 2017.
74.	Sho Hatayama, Takaaki Shimohata, Sachie Amano, Junko Kido, 神田結奈, Aya Tentaku, Shiho Fukushima, 中橋睦美, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 宿主腸管上皮細胞のTight Junction形成が食中毒原因菌Campylobacter jejuniの侵入機構に及ぼす影響について, 日本栄養食糧学会, 244, May 2017.
75.	Aya Tentaku, Takaaki Shimohata, Junko Kido, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染における小胞体ストレスの誘導, 第91回日本感染症学会総会・学術講演会, Apr. 2017.
76.	Sho Hatayama, Takaaki Shimohata, Sachie Amano, Junko Kido, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 極性化腸管上皮細胞でのタイトジャンクションによるCampylobaster Jejuniの侵入制御について, 日本細菌学会総会, 50, Mar. 2017.
77.	Takaaki Shimohata, Junko Kido, Yuri Sato, Sho Hatayama, Yuna Kanda, Shiho Fukushima, Aya Tentaku, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni 感染はHeLa細胞におけるアミノ酸取り込みを活性化する, 日本細菌学会総会, 50, Mar. 2017.
78.	Kazuaki Mawatari, Miki Yasui, Airi Honjoh, Risa Nishisaka, 枝川美幸, 岩本夏美, Hitomi Watanabe, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : Screening of genes related with ultraviolet A-sensitivity by transposon mutagenesis in Vibrio parahaemolyticus, 90th Annual Meeting of Japanese Society of bacteriology, 46, Mar. 2017.
79.	Takashi Uebanso, 吉本亜由美, Takaaki Shimohata, Mutsumi Nakahashi, Kazuaki Mawatari and Akira Takahashi : 食事成分の腸内細菌叢への影響を代謝産物から読み解けるか?, 日本細菌学会総会, 42, Mar. 2017.
80.	Mayu Uyama, Masahiro Sogabe, 平田光里, Tadahiko Nakagawa, Akira Fukuya, Satoshi Teramae, Daisaku Fujimoto, Hironori Tanaka, Yasuhiro Mitsui, Shinji Kitamura, Koichi Okamoto, Tetsuji Takayama, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Takahiro Emoto, Masatake Akutagawa, Rumi Katashima and Toshiya Okahisa : 模擬腹水による胸腹水濾過濃縮再静注法の教育体制の構築, 第37回日本アフェレシス学会学術大会, Nov. 2016.
81.	Ryuto Tamai, Hiroto Kasai, Daiki Tanaka, Naoya Tani, 平田光里, Tadahiko Nakagawa, Tetsu Tomonari, Tatsuya Taniguchi, Koichi Okamoto, Hiroshi Miyamoto, Tetsuji Takayama, Takahiro Emoto, Masatake Akutagawa, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Mayu Uyama, Masahiro Sogabe and Toshiya Okahisa : 胸腹水濾過濃縮再静注法のクロスフロー方式の腹水濾過時の物理的刺激が腹水に及ぼす影響に関する実験的検討., 第54回日本人工臓器学会大会, Nov. 2016.
82.	Hiroshi Tatano, Hisami Okumura, Daisuke Kajiura, 近藤千佳, 平山明由, Kazuaki Mawatari, Yoshichika Kawai, Masashi Masuda and Yutaka Taketani : GC-MSを用いた肉の種類別の摂取バイオマーカーの探索, 第10回メタボロームシンポジウム, Oct. 2016.
83.	Hitomi Watanabe, Kazuaki Mawatari, Risa Nishisaka, Mutsumi Nakahashi, Akari Tsunedomi, Takaaki Shimohata, Takashi Uebanso, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : 透析液の細菌汚染調査と近視外LEDによる殺菌効果の評価, 第69回日本細菌学会中国・四国支部総会, Oct. 2016.
84.	Takaaki Shimohata, Shiho Fukushima, Yuri Sato, Rune Fukawa, Junko Kido, Yuna Kanda, Aya Tentaku, Syo Hatayama, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniの宿主細胞内生存戦力に関する検討, 第69回日本細菌学会中国・四国支部総会, Oct. 2016.
85.	Junko Kido, Takaaki Shimohata, Sachie Amano, Syo Hatayama, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR発現によるCampylobacter jejuniの侵入抑制機序の解明, 第69回日本細菌学会中国・四国支部総会, Oct. 2016.
86.	Mutsumi Nakahashi, Akari Tsunedomi, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : 紫外線LEDと次亜塩素酸ナトリウムの併用による食品殺菌装置の開発, 第37回日本食品微生物学会学術総会, Sep. 2016.
87.	Akira Takahashi, Takaaki Shimohata, Kazuaki Mawatari, Takashi Uebanso, Akari Tsunedomi, Mutsumi Nakahashi, Masatake Akutagawa and Yohsuke Kinouchi : 飲料水の色が近紫外線殺菌にあたえる影響, 第37回日本食品微生物学会学術総会, Sep. 2016.
88.	Akari Tsunedomi, Takaaki Shimohata, Sakie Nagata, Sachie Amano, Mutsumi Nakahashi, Yumi Harada, Takashi Uebanso, Kazuaki Mawatari, Katsuyuki Miyawaki, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Campylobacter jejuni食中毒予防に対するUVA-LED照射殺菌の有用性について, 第37回日本食品微生物学会学術総会, Sep. 2016.
89.	Takaaki Shimohata, Shiho Fukushima, Yuri Sato, Rune Fukawa, Junko Kido, Kanda Yuna, Aya Tentaku, Syo Hatayama, Mutsumi Nakahashi, Takashi Uebanso, Nagakatsu Harada, Kazuaki Mawatari and Akira Takahashi : 上皮細胞に侵入したCampylobacter jejuniのエネルギー獲得機構について, 第37回日本食品微生物学会学術総会, Sep. 2016.
90.	Sho Hatayama, Takaaki Shimohata, Sachie Negoro, Junko Kido, Hitomi Iba, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Disruption of tight junctions promote lipid raft-mediated Campylobacter jejuni invasion at lateral part of the intestinal cells, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Aug. 2016.
91.	Risa Nishisaka, Hitomi Watanabe, Kazuaki Mawatari, Mutsumi Nakahashi, Akari Tsunedomi, Takaaki Shimohata, Takashi Uebanso, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : 県内医療施設の透析液細菌汚染調査と近紫外LEDによる殺菌効果の評価, 第253回徳島医学会学術集会, Jul. 2016.
92.	Junko Kido, Takaaki Shimohata, Sachie Negoro, Sho Hatayama, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR発現によりCampylobacter jejuniの微小管依存性侵入機構が抑制される, 第253回徳島医学会学術集会, Jul. 2016.
93.	Ayumi Yoshimoto, Takashi Uebanso, Takaaki Shimohata, Mutsumi Nakahashi, Kazuaki Mawatari and Akira Takahashi : 妊娠期の母親の低用量の抗菌薬摂取が子供の健康に及ぼす影響の解析, 第253回徳島医学会学術集会, 24, Jul. 2016.
94.	Sho Hatayama, Takaaki Shimohata, Michiko Yoshikane, Sachie Amano, Yuri Sato, Junko Kido, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 食中毒原因菌Campylobacter jejuniは腸管上皮細胞側面の露出により宿主内へ効率的に侵入する, 第70回日本栄養・食糧学会大会, May 2016.
95.	Akari Tsunedomi, Takaaki Shimohata, Marin Gotoh, Sachie Amano, Mutsumi Nakahashi, 原田優美, Takashi Uebanso, Kazuaki Mawatari, Katsuyuki Miyawaki, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : UVA-LED殺菌システムによるCampylobacter jejuni食中毒の予防, 第70回日本栄養・食糧学会大会, May 2016.
96.	Mayu Uyama, Masahiro Sogabe, Hirata Misato, Tadahiko Nakagawa, Takaoka Yoshifumi, Tatsuya Taniguchi, Tetsuji Takayama, Takahiro Emoto, Masatake Akutagawa, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi and Toshiya Okahisa : 胸腹水濾過濃縮再静注法の手技習得のための輸液製剤を用いた模擬腹水の作成, 第43回日本血液浄化技術学会学術大会, May 2016. (Keyword) 胸腹水濾過濃縮再静注法
97.	Akari Tsunedomi, Junko Kido, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : UVA殺菌技術を用いた植物工場における病原微生物の抑制検討, 第90回日本感染症学会総会・学術講演会, Apr. 2016.
98.	Risa Nishisaka, Kazuaki Mawatari, Tomoko Yamashita, Junko Kido, Akari Tsunedomi, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : 透析液の汚染細菌調査と近紫外発光ダイオードを用いた殺菌効果の評価, 第90回日本感染症学会総会・学術講演会, Apr. 2016.
99.	Kido Junko, Takaaki Shimohata, Negoro Sachie, Hatayama Sho, Sato Yuri, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : The entry of Campylobacter jejuni was regulated by cell surface CFTR, The 89th Annual Meeting of Japanese Society for Bacteriology, Mar. 2016.
100.	Takaaki Shimohata, Sato Yuri, Fukawa Rune, Kido Junko, Amano Sachie, Hatayama Sho, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Metabolic analysis leveled the unique amino acid metabolism in Campylobacter jejuni infected cell, The 89th Annual Meeting of Japanese Society for Bacteriology, Mar. 2016.
101.	Yoshimoto Ayumi, Takashi Uebanso, Mutsumi Nakahashi, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Effect of low dose antibiotics administration during prenatal period on newborns postnatal health, The 89th Annual Meeting of Japanese Society for Bacteriology, Mar. 2016.
102.	Kazuaki Mawatari, Miyuki Edagawa, Natsumi Iwamoto, Miki Maetani, Airi Honjo, Risa Nishisaka, Hitomi Watanabe, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : Identification of genes associated with ultraviolet-A sensitivity in Vibrio parahaemolyticus, The 89th Annual Meeting of Japanese Society for Bacteriology, Mar. 2016.
103.	Nishisaka Risa, Kazuaki Mawatari, Tsunedomi Akari, Watanabe Hitomi, Uebanso Akiko, Takaaki Shimohata, Takashi Uebanso, Kanemoto Yuki, Murakami Akio and Akira Takahashi : Ultraviolet-A (UVA) irradiation by light emitting diode (LED) inhibits growth of cyanobacteria, The 89th Annual Meeting of Japanese Society for Bacteriology, Mar. 2016.
104.	谷直也, Daiki Tanaka, Tatsunao Sueuchi, 高岡慶史, Tadahiko Nakagawa, Tetsuji Takayama, Masaki Kawano, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Mayu Uyama, Masahiro Sogabe and Toshiya Okahisa : イノベーション対話ツールを活用した腸蠕動音収集解析システムの開発, 第53回日本人工臓器学会大会, Nov. 2015.
105.	Daiki Tanaka, Naoya Tani, Masanori Takehara, Hironori Tanaka, Takahiro Tanaka, Tetsu Tomonari, Tatsuya Taniguchi, Tadahiko Nakagawa, Tetsuji Takayama, Masaki Kawano, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Mayu Uyama, Masahiro Sogabe and Toshiya Okahisa : 模擬腹水を用いた胸腹水濾過濃縮装置の評価・教育システムの構築, 第53回日本人工臓器学会大会, Nov. 2015.
106.	Masaki Kawano, Takahiro Emoto, Masatake Akutagawa, Mayu Uyama, Masahiro Sogabe, Tadahiko Nakagawa, Tetsuji Takayama, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, 村島徹, 出口喜宏, 荒巻広至 and Toshiya Okahisa : 腹水濾過濃縮法(CART)用装置の現状と今後, 第36回日本アフェレシス学会学術総会, Oct. 2015.
107.	Junko Kido, Takaaki Shimohata, Sachie Negoro, Syo Hatayama, Yuri Sato, Rune Fukawa, Michiko Yoshikane, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniの上皮細胞侵入性に対するCFTRの関与について, 第251回徳島医学会学術集会, Aug. 2015.
108.	Akari Tsunedomi, Akinori Masamura, Mutsumi Nakahashi, Risa Nishisaka, Marin Gotoh, Kazuaki Mawatari, Takaaki Shimohata, Takashi Uebanso, Katsuyuki Miyawaki, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : 植物工場の養液殺菌システムの開発, 第251回徳島医学会学術集会, Aug. 2015.
109.	Risa Nishisaka, Kazuaki Mawatari, Akari Tsunedomi, Marin Gotoh, Akiko Uebanso, Takaaki Shimohata, Takashi Uebanso, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi, Yuki Kanemoto, Akio Murakami and Akira Takahashi : 近紫外線(ultrviolet-A)照射によるシアノバクテリア増殖抑制効果の解明, 第251回徳島医学会学術集会, Aug. 2015.
110.	Syo Hatayama, Takaaki Shimohata, Michiko Yoshikane, Sachie Negoro, Yuri Sato, Junko Kido, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniの上皮細胞への侵入は細胞のラテラル面の露出により増加する, 第251回徳島医学会学術集会, Aug. 2015.
111.	Takaaki Shimohata, Kido Junko, Negoro Sachie, Hatayama Sho, Sato Yuri, Iba Hitomi, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR regulates Campylobacter jejuni invasion in cultured cells, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, Jul. 2015.
112.	Tomoko Yamashita, Kazuaki Mawatari, Junko Kido, Takaaki Shimohata and Akira Takahashi : 人口透析装置汚染防止を目的とした近紫外発光ダイオード(UVA-LED)による照射殺菌条件の検討, 第89回日本感染症学会総会・学術講演, Apr. 2015.
113.	Junko Kido, Takaaki Shimohata, Sachie Negoro, Syo Hatayama, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTRがCampylobacter jejuniの細胞侵入性へ与える影響, 第89回日本感染症学会総会・学術講演, Apr. 2015.
114.	Kazuaki Mawatari, Airi Honjyo, Miki Yasui, Syo Hatayama, Mutsumi Nakahashi, Takaaki Shimohata and Akira Takahashi : 腸炎ビブリオのVP2357遺伝子変異は近紫外線(UVA)照射耐性獲得に寄与する, 第88回日本細菌学会総会, Mar. 2015.
115.	Quang Ngoc Phan, Takashi Uebanso, Kazuaki Mawatari, Takaaki Shimohata, Mutsumi Nakahashi and Akira Takahashi : DNA-binding protein HU coordinates pathogenicity in Vibrio parahaemolyticus, 第88回日本細菌学会総会, Mar. 2015.
116.	Syo Hatayama, Takaaki Shimohata, Sachie Negoro, Yuri Sato, Junko Kido, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniは腸管上皮の側部より効率的に侵入する, 第88回日本細菌学会総会, Mar. 2015.
117.	Phan Quang Ngoc, Takashi Uebanso, Kazuaki Mawatari, Takaaki Shimohata, Mutsumi Nakahashi and Akira Takahashi : DNA-binding protein HU coordinate pathogenicity in Vibrio parahaemolyticus, 第67回日本細菌学会中国・四国支部総会, Oct. 2014.
118.	Akari Tsunedomi, Mutsumi Nakahashi, Risa Nishisaka, Kazuaki Mawatari, Takaaki Shimohata, Takashi Uebanso, Katsuyuki Miyawaki, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : 水耕栽培用養液の還流型殺菌システムの開発, 第67回日本細菌学会中国・四国支部総会, Oct. 2014.
119.	Junko Kido, Takaaki Shimohata, Sachie Negoro, Syo Hatayama, Yuri Sato, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniによる細胞侵入とCFTRの関連について, 第67回日本細菌学会中国・四国支部総会, Oct. 2014.
120.	Teppei Hoshiyama, Masatake Akutagawa, Takahiro Emoto, Mutsumi Nakahashi, Marhio Hayashida, Akira Takahashi, Kazuaki Mawatari, Toshitaka Ikehara, Shinsuke Konaka and Yohsuke Kinouchi : UV及び可視光照射に対する腸炎ビブリオの遺伝子発現解析, Journal of Shikoku-Section Joint Convention of the Institutes of Electrical and Related Engineers, No.14-1, 229, Sep. 2014. (Summary) 腸炎ビブリオを紫外線および可視光に曝露した際，遺伝子発現がどのように変化するかについて，遺伝子チップを用いて網羅的に実験・解析を行っている．その結果，UV-A領域の光を照射した際，酸化修復に関する遺伝子の働きが抑えられること，緑色の光を照射した際に鞭毛関連の遺伝子が活性化することなどが示された．
121.	Honjo Airi, Kazuaki Mawatari, Maetani Miki, Iwamoto Natsumi, Yamashita Tomoko, Mutsumi Nakahashi, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : Anti-sigma factor VP2357の遺伝子変異はVibrio parahaemolyticusの近紫外線(UVA)耐性獲得に関与する, 第249回徳島医学会学術集会, Jul. 2014.
122.	Phan Quang Ngoc, Takashi Uebanso, Kazuaki Mawatari, Takaaki Shimohata, Mutsumi Aihara and Akira Takahashi : DNA-binding protein HU coordinates pathogenicity in Vibrio parahaemolyticus., 第249回徳島医学会学術集会, Jul. 2014.
123.	Hatayama Syo, Takaaki Shimohata, Negoro Sachie, Sato Yuri, Kido Junko, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni 感染による腸管上皮細胞のイオン輸送に関する検討, 第249回徳島医学会学術集会, Jul. 2014.
124.	Teppei Hoshiyama, Masatake Akutagawa, Takahiro Emoto, Mutsumi Nakahashi, Marhio Hayashida, Akira Takahashi, Kazuaki Mawatari, Toshitaka Ikehara, Shinsuke Konaka and Yohsuke Kinouchi : Gene expression analysis of Vibrio parahaemolyticus for the light irradiation, IEICE Technical Report (MBE), Vol.114, No.154, 19-24, Jul. 2014. (Summary) Effect of the light irradiation brings to the bacteria has been reported. For example, the sterilizing effect is obtained by the ultraviolet (UV) irradiation. Bacteria is known that they have photoreceptors in the visible light irradiation. Thus, it seems that effect of light irradiation depends on their wavelength. In this study, gene expression analysis was performed against Vibrio parahaemolyticus in order to elucidate the effect of the difference in wavelengths. As a result of them, Flagellar migration function of Vibrio parahaemolyticus was activated when it was irradiated with light of 520nm in wavelength. (Keyword) Light irradiation / Wavelength dependency / Gene expression analysis / Vibrio parahaemolyticus
125.	Akari Tsunedomi, 正村彰規, Mutsumi Aihara, Kazuaki Mawatari, Takaaki Shimohata, Takashi Uebanso, Masachika Ishizaki, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : 近紫外線による水耕栽培用培養液の殺菌法の開発, 第68回日本栄養・食糧学会大会, May 2014.
126.	本庄アイリ, Kazuaki Mawatari, 前谷実希, 常冨愛香里, 畑山翔, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : Upregulation of katG gene, VPA0768, induces ultraviolet-A (UVA) resistance in Vibrio parahaemolyticus, 第68回日本栄養・食糧学会大会, May 2014.
127.	Sachie Negoro, Takaaki Shimohata, Sho Hatayama, Mari Matsumoto, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Suppression of CFTR-mediated Cl- transport in Campylobacter jejuni infection, 第68回日本栄養・食糧学会大会, May 2014.
128.	Kazuaki Mawatari, Airi Honjoh, Akari Tsunedomi, Sho Hatayama, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : 近紫外線(UVA)照射により酸化される腸炎ビブリオタンパク質の同定, 第87回日本細菌学会総会, Mar. 2014.
129.	Takaaki Shimohata, Sachie Negoro, Sho Hatayama, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni infection reduces Cl- secretion in T-84, 第87回日本細菌学会総会, Mar. 2014.
130.	Mario Hayashida, Mutsumi Aihara, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari, Akira Takahashi, Teppei Hoshiyama, Masatake Akutagawa, Takahiro Emoto and Yohsuke Kinouchi : 紫外線・可視光照射により変動する微生物遺伝子の網羅的解析, 第66回日本細菌学会中国・四国支部総会, Oct. 2013.
131.	Airi Honjoh, Miyuki Edagawa, Kazuaki Mawatari, Miki Maetani, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso, Maki Uwate, Hideaki Maseda and Akira Takahashi : トランスポゾン挿入変異ライブラリを用いた腸炎ビブリオの近紫外線関連遺伝子の探索, 第66回日本細菌学会中国・四国支部総会, Oct. 2013.
132.	Mutsumi Aihara, Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Synergistic bactercidal effect of Ultraviolet light with a combination of different, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会日本側総会, Aug. 2013.
133.	Mario Hayashida, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari, Akira Takahashi, Teppei Hoshiyama, Takahiro Emoto, Masatake Akutagawa and Yohsuke Kinouchi : DNA マイクロアレイを用いた微生物遺伝子の網羅的解析, 第247回徳島医学会学術集会, Aug. 2013.
134.	Akari Tsunedomi, Mutsumi Aihara, Masachika Ishizaki, Takashi Uebanso, Takaaki Shimohata, Masatake Akutagawa, Kazuaki Mawatari, Akira Takahashi and 正村彰規 : UVA-LED を用いた水耕栽培用養液の殺菌, 第247回徳島医学会学術集会, Aug. 2013.
135.	Shoko Asada, Hitomi Iba, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 腸炎ビブリオの3型分泌装置遺伝子発現は細胞接着により誘導される, 第247回徳島医学会学術集会, Aug. 2013.
136.	Airi Honjoh, Kazuaki Mawatari, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : VP0221とVPA1604は腸炎ビブリオの莢膜多糖類を調節し，抗菌ペプチドと補体耐性に働く, 第247回徳島医学会学術集会, Aug. 2013.
137.	根来幸恵, Takaaki Shimohata, Sho Hatayama, Mari Matsumoto, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni 感染によるCl‐輸送チャネルの活性変化, 第247回徳島医学会学術集会, Aug. 2013.
138.	Sho Hatayama, Takaaki Shimohata, 根来幸恵, Mari Matsumoto, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 食中毒起因菌カンピロバクターによる下痢の機序に関する研究, 第247回徳島医学会学術集会, Aug. 2013.
139.	根来幸恵, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni 感染とCl-輸送の変化, 第87回日本感染症学会総会・学術講演会, Jun. 2013.
140.	Takaaki Shimohata, 根来幸恵, Sho Hatayama, Mari Matsumoto, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染によるクロライド分泌の変化, 第86回日本細菌学会総会, Mar. 2013.
141.	Shoko Asada, Hitomi Iba, Takaaki Shimohata, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Vibrio parahaemolyticusの病原因子 TTSS1遺伝子発現は細胞接着によって誘導される, 第65回日本細菌学会・中国・四国支部総会, Oct. 2012.
142.	Kazuaki Mawatari, Kana Kurokawa, Airi Honjoh, Mami Fujii, Tomomi Yamamoto, Miki Maetani, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : Vibrio parahaemolyticusを用いたUVA紫外線照射による殺菌機構の解析, 第65回日本細菌学会・中国・四国支部総会, Oct. 2012.
143.	Tam Thanh Thi Le, Kazuaki Mawatari, Mutsumi Aihara, Takaaki Shimohata, Takashi Uebanso and Akira Takahashi : VP2118 has major roles in Vibrio parahaemolyticus response to oxidative stress, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会日本側総会, Aug. 2012.
144.	Sayaka Hayashida, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : UVA-LEDと塩素を併用した水殺菌法の開発, 第86回日本感染症学会総会・学術講演会, Apr. 2012.
145.	Tomomi Yamamoto, Kazuaki Mawatari, Sayaka Hayashida, Takaaki Shimohata and Akira Takahashi : 発光ダイオードによる近紫外線照射(UVA-LED)によるウイルスの不活化, 第86回日本感染症学会総会・学術講演会, Apr. 2012.
146.	Kazuaki Mawatari, 井角友香, 平山みなみ, 前谷実希, 山本智実, 林田沙也加, 射場仁美, Mutsumi Aihara, Takaaki Shimohata and Akira Takahashi : Vibrio parahaemolyticus capsular polysaccharide is modulated by two pathways, VP0220-1 and VPA1602-4, 第85回日本細菌学会総会, Mar. 2012.
147.	Takaaki Shimohata, 射場仁美, 根来幸恵, 浅田翔子, Mutsumi Aihara, Kazuaki Mawatari and Akira Takahashi : VP1680 induces IL-8 secretion in Vibrio parahaemolyticus infection, 第85回日本細菌学会総会, Mar. 2012.
148.	Takaaki Shimohata, 射場仁美, 根来幸恵, 浅田翔子, Mutsumi Aihara, Kazuaki Mawatari and Akira Takahashi : 腸炎ビブリオT3SS1におけるトランスロコンの解析, 第64回日本細菌学会中国・四国支部総会, Oct. 2011.
149.	林田沙也加, Mutsumi Aihara, Takaaki Shimohata, Kazuaki Mawatari, Masatake Akutagawa, 木ノ内陽介 and Akira Takahashi : 水中の細菌に対するUVA-LEDと塩素との併用殺菌効果, 第64回日本細菌学会中国・四国支部総会, Oct. 2011.
150.	Kazuaki Mawatari, Yuka Isumi, Minami Hirayama, Miki Maetani, Tomomi Yamamoto, Sayaka Hayashida, Hitomi Iba, Mutsumi Aihara, Takaaki Shimohata and Akira Takahashi : VP0220-0221 and VPA1602-1604 modulate capsular polysaccharides in Vibrio parahaemolyticus, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会日本側総会, Aug. 2011.
151.	Takaaki Shimohata, 廉馨, Kazuaki Mawatari and Akira Takahashi : 腸炎ビブリオ感染は腸管上皮細胞においてMAPKsを活性化しIL-8の分泌を誘発する, 第85回日本感染症学会総会・学術講演会, Apr. 2011.
152.	戸田聡美, Hiroshi Sakaue, 谷口康子, Nagakatsu Harada, Kazuaki Mawatari, Yutaka Nakaya, Tetsuya Shiuchi and 箕越靖彦 : 自発運動制御におけるGhrelinの役割, 第14回日本病態栄養学会，神奈川県横浜市, Jan. 2011.
153.	戸田聡美, Hiroshi Sakaue, 谷口康子, Nagakatsu Harada, Kazuaki Mawatari, Yutaka Nakaya and Tetsuya Shiuchi : 自発運動制御におけるGhrelinの役割, 第31回日本肥満学会, Oct. 2010.
154.	Kazuaki Mawatari, 米田由美, 本田真奈美, 射場仁美, Mutsumi Aihara, Takaaki Shimohata, 蘇澤紅, Masayuki Yamato and Akira Takahashi : Vibrio parahaemolyticus のチロシンキナーゼVPA1604 は高分子量型莢膜多糖類(HMW-CPS)形成を調節する, 第63回日本細菌学会・中国・四国支部総会, Oct. 2010.
155.	Mutsumi Aihara, Masayuki Yamato, Kazuaki Mawatari, Akira Takahashi, Masatake Akutagawa and Yohsuke Kinouchi : 異なる紫外線波長の併用による殺菌効果, 第63回日本細菌学会・中国・四国支部総会, Oct. 2010.
156.	Takaaki Shimohata, 中野政之, Kazuaki Mawatari, Masayuki Yamato and Akira Takahashi : 腸炎ビブリオエフェクタータンパク質VP1680 はIL-8 の分泌を誘発する, 第63回日本細菌学会・中国・四国支部総会, Oct. 2010.
157.	Kazuaki Mawatari, Yumi Yoneda, Manami Honda, Hitomi Iba, Mutsumi Aihara, Zehong Su, Takaaki Shimohata, Masayuki Yamato and Akira Takahashi : VPA1604, a protein tyrosine kinase, modulates high molecular weight capsular polysaccharide in Vibrio parahaemolyticus, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会日本側総会, Jul. 2010.
158.	戸田聡美, Hiroshi Sakaue, 谷口康子, Nagakatsu Harada, Kazuaki Mawatari, Yutaka Nakaya, Tetsuya Shiuchi and 箕越靖彦 : 自発運動制御におけるGhrelinの役割, 3回日本糖尿病学会総会年次学術集会, May 2010.
159.	戸田聡美, Hiroshi Sakaue, 谷口康子, Tetsuya Shiuchi, Nagakatsu Harada, Kazuaki Mawatari and Yutaka Nakaya : 自発運動制御におけるGhrelinの役割, 第64回日本栄養・食糧学会大会, May 2010.
160.	射場仁美, Takaaki Shimohata, Kazuaki Mawatari, Masayuki Yamato, Takamasa Ohnishi and Akira Takahashi : 腸管ループを用いた腸炎ビブリオ誘発下痢機構の検討, 第64回日本栄養・食糧学会大会, May 2010.
161.	Takaaki Shimohata, 中野政之, 廉馨, Kazuaki Mawatari, Masayuki Yamato and Akira Takahashi : 腸炎ビブリオはMAPKsを介したIL-8の分泌を誘発する, 第64回日本栄養・食糧学会大会, May 2010.
162.	Takaaki Shimohata, Masayuki Nakano, Lian Xin, Kazuaki Mawatari, Masayuki Yamato and Akira Takahashi : Vibrio parahaemolyticus modulate IL-8 secretion through dual pathway, 第83回日本細菌学会総会, Mar. 2010.
163.	Kazuaki Mawatari, Yukina Takahashi, Nami Morikawa, Takaaki Shimohata, Akiko Hamamoto, Zehong Su, Masayuki Yamato and Akira Takahashi : VPA1604, a protein tyrosine kinase, modulate HMW K6-polysaccharide in Vibrio parahaemolyticus, 第83回日本細菌学会総会, Mar. 2010.
164.	中川忠彦, Nagakatsu Harada, 吉田将紀, 宮本愛子, 川西由希子, Kazuaki Mawatari, Akira Takahashi, Hiroshi Sakaue and Yutaka Nakaya : 脂質合成律速酵素グリセロール-3-リン酸アシルトランスフェラーゼ2の膜トポロジー解析, 第240回徳島医学会学術集会, Feb. 2010.
165.	Qinkai Li, Kazuaki Mawatari, Nagakatsu Harada, 中野政之, Akira Takahashi, Yutaka Nakaya, Toshio Hosaka, Bayasgalan Jambaldorj, 大塚良 and Makoto Funaki : Chronic 5-Hydroxytryptamine Treatment Induces Insulin Resistance in 3T3-L1 Adipocytes by mTOR-dependent modification of IRS-1, 第238回徳島医学会学術集会, Feb. 2009.
166.	原口さやか, 下畑隆明, Kazuaki Mawatari, Nagakatsu Harada, Akira Takahashi, Toshikazu Takahashi, 中尾俊之, 水口潤, 炭谷晴雄, Toshio Doi and Yutaka Nakaya : 慢性腎不全患者における早期の飢餓状態に対する就寝前夜食の効果ー間接カロリーメーターを用いた検討, 第12回日本病態栄養学会学術集会, Jan. 2009.
167.	原口さやか, 下畑隆明, Kazuaki Mawatari, Nagakatsu Harada, Toshio Hosaka, Akira Takahashi, 中尾俊之, Toshio Doi and Yutaka Nakaya : 間接カロリーメーターを用いた，慢性腎不全患者における早朝空腹時の代謝状態の検討, 第62回日本栄養・食糧学会, May 2008.
168.	河野尚平, Katsuya Hirasaka, 加川祥子, 中尾玲子, Kazuaki Mawatari, Nagakatsu Harada, Yutaka Nakaya, 石堂一巳, Yousuke Ebina, Kyoichi Kishi and Takeshi Nikawa : Cbl-b遺伝子欠損によるマクロファージの活性化を介した耐糖能異常, 第19回分子糖尿病学シンポジウム, Dec. 2007.
169.	Yutaka Nakaya, 安井苑子, Kazuaki Mawatari, Akira Takahashi, Nagakatsu Harada, Hossein Nazari, Takashi Kawano, Shuzo Oshita and 古川哲史 : 機能性食品の心血管系イオンチャネルに対する作用-Phytoestrogenのgenomicおよびnongenomic action, 長井長義記念シンポジウム, Sep. 2006.

Et cetera, Workshop:

1.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Akira Takahashi, 岡本泰昌 and Shusuke Numata : 双極性障害における血中メタボローム解析, 第42回躁うつ病の薬理・生化学的研究懇話会, Oct. 2023.
2.	Kai Ishida, Takaaki Shimohata, Yuna Kanda, 増田瑠見子, 山﨑浩平, Takashi Uebanso, Kazuaki Mawatari, 柏本孝茂 and Akira Takahashi : Vibrio vulnificus創傷感染が引き起こす宿主骨格筋内代謝変化の解析, 第16回細菌学若手コロッセウム, Aug. 2022.
3.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Akira Takahashi, 岡本泰昌 and Shusuke Numata : 双極性障害における血中代謝物の変化, 第13回脳科学クラスターミニリトリート, Feb. 2022.
4.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Shusuke Numata, Akira Takahashi, 岡本泰昌 and Tetsuro Ohmori : うつ病におけるキヌレニン経路の変化, 第40回躁うつ病の薬理・生化学的研究懇話会, Oct. 2021.
5.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Shusuke Numata, Akira Takahashi, 岡本泰昌 and Tetsuro Ohmori : うつ病におけるキヌレニン経路の変化, 第12回脳科学クラスターミニリトリート, Feb. 2021.
6.	Tomohiko Nakayama, Hidehiro Umehara, Yukiko Tomioka, 上敷領俊晴, 淵上学, 岡田剛, 増田瑠見子, Kazuaki Mawatari, Masahito Nakataki, Shusuke Numata, Akira Takahashi, 岡本泰昌 and Tetsuro Ohmori : うつ病におけるキヌレニン経路の変化, 第5回メタボロームシンポジウム, Dec. 2020.
7.	Takaaki Shimohata, Junko Kido, Ryoka Narutaki, Yuri Sato, Rune Fukawa, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染による，上皮細胞のアミノ酸輸送変動に関する検討, 第12回日本カンピロバクター研究会総会, Sep. 2019.
8.	Shiho Fukushima, Takaaki Shimohata, Junko Kido, mai Tsujiguchi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染においてオートファジーは菌の侵入過程を促進する, 第12回日本カンピロバクター研究会総会, Sep. 2019.
9.	Mai Tsujiguchi, Takaaki Shimohata, Junko Kido, Shiho Fukushima, Kai Ishida, Ayumi Yoshimoto, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 抗菌薬投与マウスモデルを用いたCampylobacter jejuniの感染によるコレステロール代謝への影響, 第12回日本カンピロバクター研究会総会, Sep. 2019.
10.	Sho Hatayama, Takaaki Shimohata, Junko Kido, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Akiko Nakamoto, Emi Shuto, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : UVA-LED照射による調理器具汚染Campylobacter jejuniの殺菌効果について, 第11回日本カンピロバクター研究会総会, Dec. 2018.
11.	Kai Ishida, Takaaki Shimohata, Sho Hatayama, Junko Kido, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniの上皮細胞内生存とコレステロールの関連, 第11回日本カンピロバクター研究会総会, Dec. 2018.
12.	Mai Tsujiguchi, Takaaki Shimohata, Shiho Fukushima, Sho Hatayama, Junko Kido, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Microarrayの解析から導くCampylobacter jejuniの侵入による宿主腸管上皮細胞での脂質代謝への影響, 第11回日本カンピロバクター研究会総会, Dec. 2018.
13.	Aya Tentaku, Takaaki Shimohata, Sho Hatayama, Anh Quoc Nguyen, Junko Kido, Shiho Fukushima, Kai Ishida, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 宿主細胞における小胞体ストレス応答はCampylobacter jejuniの細胞内侵入を抑制する, 第257回徳島医学会学術集会, Aug. 2018.
14.	Akari Tsunedomi, Sho Hatayama, Takaaki Shimohata, Junko Kido, Sachie Amano, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Campylobacter jejuni汚染対策に向けたUVA-LEDの有用性について, 第10回日本カンピロバクター研究会総会, Dec. 2017.
15.	Shiho Fukushima, Takaaki Shimohata, Sho Hatayama, Junko Kido, Aya Tentaku, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniが誘導するオートファジーが菌の侵入および生存に与える影響について, 第10回日本カンピロバクター研究会総会, Dec. 2017.
16.	Kazuaki Mawatari, Hitomi Watanabe, Risa Nishisaka, Mutsumi Nakahashi, Akari Tsunedomi, Mizuki Kojima, Natsuki Nogami, Misuzu Makino, Rumiko Masuda, Takaaki Shimohata, Takashi Uebanso, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Bacterial contamination in dialysis fluid and bactericidal effects of near UV-light emitting diodes, IEICE Technical Report (MBE), Vol.117, No.165, 13-16, Jul. 2017. (Keyword) artificial dialysis / microbial contamination / near UV / LED / disinfection
17.	Syo Hatayama, Takaaki Shimohata, Sachie Amano, Junko Kido, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniの宿主腸管上皮細胞への侵入とTight Junctions形成の関連について, 第9回日本カンピロバクター研究会総会, Nov. 2016.
18.	Junko Kido, Takaaki Shimohata, Yuri Sato, Syo Hatayama, Yuna Kanda, Aya Tentaku, Shiho Fukushima, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : 宿主アミノ酸輸送の変化と宿主細胞内Campylobacter jejuni生存について, 第9回日本カンピロバクター研究会総会, Nov. 2016.
19.	Aya Tentaku, Takaaki Shimohata, Syo Hatayama, Junko Kido, Takashi Uebanso, Kazuaki Mawatari, Nagakatsu Harada and Akira Takahashi : Campylobacter jejuni感染で誘導される小胞体ストレスについて, 第9回日本カンピロバクター研究会総会, Nov. 2016.
20.	Sato Yuri, Takaaki Shimohata, Fukawa Rune, Negoro Sachie, Hatayama Syo, Kido Junko, Takashi Uebanso, Nagakatsu Harada, Kazuaki Mawatari and Akira Takahashi : メタボローム解析を用いた宿主細胞内のCampylobacter jejuniのエネルギー源獲得機構の検索, 第8回日本カンピロバクター研究会総会, Dec. 2015.
21.	Tsunedomi Akari, Takaaki Shimohata, Gotoh Marin, Amano Sachie, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari, Katsuyuki Miyawaki, Takahiro Emoto, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : Campylobacter jejuniに対するUVA-LEDの有効性, 第8回日本カンピロバクター研究会総会, Dec. 2015.
22.	Kido Junko, Takaaki Shimohata, Negoro Sachie, Hatayama Sho, Sato Yuri, Fukawa Rune, Yoshikane Michiko, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTR発現によるCampylobacter jejuniの上皮細胞侵入抑制機構について, 第8回日本カンピロバクター研究会総会, Dec. 2015.
23.	Takaaki Shimohata, Junko Kido, Sachie Negoro, Syo Hatayama, Yuri Sato, Mutsumi Nakahashi, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : CFTRはCampylobacter jejuniの侵入抑制に寄与する, 第7回日本カンピロバクター研究会総会, Dec. 2014.
24.	Yuri Sato, Takaaki Shimohata, Sachie Negoro, Syo Hatayama, Junko Kido, Mutsumi Nakahashi, Takashi Uebanso, Nagakatsu Harada, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染とAutophagyの関連について, 第7回日本カンピロバクター研究会総会, Dec. 2014.
25.	Kazuaki Mawatari, 吉岡愛美子, Satomi Toda, Takamasa Ohnishi, Nagakatsu Harada, Hiroshi Sakaue and Yutaka Nakaya : 高自発走行モデル動物SPORTS ratの左心房血栓形成と発症要因の解析, 第15回徳島臨床脈管研究会, Nov. 2013.
26.	根来幸恵, Takaaki Shimohata, Sho Hatayama, Mari Matsumoto, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuni感染はCFTR機能を抑制する, 第6回日本カンピロバクター研究会, Jul. 2013.
27.	Sho Hatayama, Takaaki Shimohata, 根来幸恵, Mari Matsumoto, Yuri Sato, Mutsumi Aihara, Takashi Uebanso, Kazuaki Mawatari and Akira Takahashi : Campylobacter jejuniによる下痢誘発機構の検討, 第6回日本カンピロバクター研究会, Jul. 2013.
28.	Mostafa Gadelmoula, Xin Lian, Akiko Hamamoto, Kazuaki Mawatari, Masayuki Yamato, Masatake Akutagawa, Yutaka Nakaya, Yohsuke Kinouchi and Akira Takahashi : UVA-LED suitability for air disinfection, LED総合フォーラム論文集, 85-86, Apr. 2010.
29.	Xin Lian, Miku Maeda, Masayuki Yamato, Kazuaki Mawatari, Masatake Akutagawa, Yutaka Nakaya, Yohsuke Kinouchi and Akira Takahashi : New UVA-LED surface sterilization system for vegetables, LED総合フォーラム論文集, 83-84, Apr. 2010.
30.	Mutsumi Aihara, Keiko Shintani, Xin Lian, Mostafa Gadelmoula, Masayuki Yamato, Kazuaki Mawatari, Masatake Akutagawa, Yohsuke Kinouchi and Akira Takahashi : UVA-LED装置を用いた水殺菌装置の開発, LED総合フォーラム論文集, 79-80, Apr. 2010.

Patent:

1.	三好仁志, Akira Takahashi, Kazuaki Mawatari, Shiho Fukushima, Mutsumi Aihara, Katsuyuki Miyawaki, Takeshi Nikawa and Misuzu Makino : (Mar. 2023), 2023-046795.

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

UV-LEDを用いた新規生活・食リズム制御法の開発 (Project/Area Number: 24K22251 )
非伝搬性のハイブリッド光を用いた環境や人にやさしい殺菌システム (Project/Area Number: 23K18578 )
Development of LED sterilization system for Campylobacter jejuni-contaminated raw chicken (Project/Area Number: 20K11647 )
光環境制御による住空間衛生管理の新機軸 (Project/Area Number: 20H01616 )
腸内細菌叢の活性で調節される食物由来の概日リズム振動化合物の同定及びヒトへの応用 (Project/Area Number: 18KK0274 )
A study on oxidative stress as bactericidal mechanism of antibacterial agents by metabolome analysis (Project/Area Number: 16K11446 )
Interaction between gut microbiota and food-derived compounds for prevention and control of cardiovascular endothelial dysfunction(Fostering Joint International Research) (Project/Area Number: 15KK0345 )
Interaction between gut microbiota and food-derived compounds for prevention and control of cardiovascular endothelial dysfunction (Project/Area Number: 15K01717 )
Development of new chicken store system focused on attenuation of Campylobacter jejuni invasion by UVA irradiation (Project/Area Number: 26560046 )
Prevention of atrial thrombosis by food-derived bioactive components which act cardiovascular endothelial cells (Project/Area Number: 24500857 )
Establishment of the eating-habits control method by light (Project/Area Number: 23650479 )
Research for the regulation of voluntary exercise and energy metabolism by appetite-regulating factors (Project/Area Number: 22700693 )
Investigation in the mechanism of regulation of voluntary exercise and abdominal visceral fat accumulation by monoamines. (Project/Area Number: 20700551 )
Regulatory mechanisms of production of virulence factor in Vibrio parahaemolyticus (Project/Area Number: 17590393 )
粥状動脈硬化病巣における新規エンドセリン発現上昇のメカニズム (Project/Area Number: 16790239 )
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Associate Professor : Mawatari, Kazuaki

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