徳島大学 / 教育研究者総覧 --- 上番増喬

専門分野

研究テーマ

著書・論文

著書:

1.	Takashi Uebanso, Takaaki Shimohata, Kazuaki Mawatari and Akira Takahashi : Glycolate as a Biological Marker of B Vitamins, Springer, 2022. (キーワード) Glycolate / B-vitamins / Glyoxylate / Glycolate oxidase
2.	池原敏孝, 勢井宏義, 田中弘之, 上番増喬, 北岡和義, 髙橋章, 中橋睦美, 中屋豊, 藤原広明 : 人体生理学の基礎改訂第2版, 医学出版社, 2016年8月. (キーワード) 生理学 (physiology)

学術論文(審査論文):

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. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.heliyon.2024.e27456 (文献検索サイトへのリンク) ● 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. (徳島大学機関リポジトリ) ● Metadata: 119259 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.71.102 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.71.102 (徳島大学機関リポジトリ: 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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.3390/biology12121467 (文献検索サイトへのリンク) ● 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.	Naoko Oda, Kohei Sugihara, Takashi Uebanso, Hirokazu Ohminami, Kohta Ohnishi, Masashi Masuda, Hisami Yamanaka-Okumura and Yutaka Taketani : Dietary phosphate disturbs of gut microbiome in mice., Journal of Clinical Biochemistry and Nutrition, Vol.73, No.3, 221-227, 2023. (要約) were observed in high phosphate diet group. Furthermore, high phosphate diet induced reduction of microbial diversity and decreased mRNA levels of colonic tight junction markers. These results suggest that the excessive intake of dietary phosphate disturbs gut microbiota and affects intestinal barrier function. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.23-9 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37970557 ● Search Scopus @ Elsevier (PMID): 37970557 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.23-9 (DOI: 10.3164/jcbn.23-9, PubMed: 37970557)
5.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.12938/bmfh.2022-093 (文献検索サイトへのリンク) ● 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)
6.	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. (要約) 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. (キーワード) Humans / Bacterial Toxins / Vibrio Infections / Virulence Factors / Muscle, Skeletal (徳島大学機関リポジトリ) ● Metadata: 118290 (出版サイトへのリンク) ● Publication site (DOI): 10.1128/msystems.00682-22 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 118290, DOI: 10.1128/msystems.00682-22, PubMed: 36939368)
7.	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. (要約) 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. (キーワード) Mice / Animals / Circadian Clocks / ARNTL Transcription Factors / フラボノイド (flavonoids) / Liver / サーカディアン・リズム (circadian rhythm) / CLOCK Proteins (徳島大学機関リポジトリ) ● Metadata: 118294 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/mnfr.202200270 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36829302 ● CiNii @ 国立情報学研究所 (CRID): 1360579929468635008 ● Summary page in Scopus @ Elsevier: 2-s2.0-85150827501 (徳島大学機関リポジトリ: 118294, DOI: 10.1002/mnfr.202200270, PubMed: 36829302, CiNii: 1360579929468635008, Elsevier: Scopus)
8.	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. (要約) 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. (キーワード) 細菌 (bacteria) / Campylobacter Infections / Campylobacter jejuni / Epithelial Cells / Humans / Microtubule-Associated Proteins / シグナル伝達 (signal transduction) / Virulence / rac1 GTP-Binding Protein (徳島大学機関リポジトリ) ● Metadata: 117002 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fcimb.2022.829682 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 117002, DOI: 10.3389/fcimb.2022.829682, PubMed: 35310852)
9.	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. (要約) 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. (キーワード) Disinfection / Herpesvirus 1, Human / Humans / Ultraviolet Rays / Viral Structures / Virus Inactivation / Water Purification (徳島大学機関リポジトリ) ● Metadata: 117004 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jphotobiol.2022.112410 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 117004, DOI: 10.1016/j.jphotobiol.2022.112410, PubMed: 35193038)
10.	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. (要約) 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. (キーワード) Animals / Colitis / Colon / Dextran Sulfate / Disease Models, Animal / Gene Deletion / 炎症 (inflammation) / Mice / Mice, Inbred C57BL / ノックアウトマウス (knockout mice) / RNA, Messenger / Taste (出版サイトへのリンク) ● Publication site (DOI): 10.3177/jnsv.68.204 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35768251 ● CiNii @ 国立情報学研究所 (CRID): 1390011097096971008 ● Summary page in Scopus @ Elsevier: 2-s2.0-85133147656 (DOI: 10.3177/jnsv.68.204, PubMed: 35768251, CiNii: 1390011097096971008, Elsevier: Scopus)
11.	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. (要約) Together these results suggest that VB2 restriction could be a new dietary approach to improve hyperoxaluria when endogenous production of oxalate is increased. (キーワード) Alcohol Oxidoreductases / Animals / Creatinine / Diet / Hydroxyproline / Hyperoxaluria / Kidney / 男性 (male) / Mice, Inbred C57BL / Mice, Obese / 肥満症 (obesity) / Oxalates / Riboflavin / Riboflavin Deficiency (出版サイトへのリンク) ● Publication site (DOI): 10.1002/mnfr.202100226 (文献検索サイトへのリンク) ● 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)
12.	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. (要約) 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. (キーワード) Animals / Cystic Fibrosis Transmembrane Conductance Regulator / Diarrhea / Gastroenteritis / 炎症 (inflammation) / Mice / Vibrio parahaemolyticus (徳島大学機関リポジトリ) ● Metadata: 115628 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.68.59 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 115628, DOI: 10.2152/jmi.68.59, PubMed: 33994481)
13.	Kensuke Horiyama, Takahiro Emoto, Takeyuki Haraguchi, Takashi Uebanso, Yuki Naito, Takuma Gyobu, Kenta Kanemoto, Junichi Inobe, Ayumi Sano, Masatake Akutagawa and Akira Takahashi : Bowel sound-based features to investigate the effect of coffee and soda on gastrointestinal motility, Biomedical Signal Processing and Control, Vol.66, 102425, 2021. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bspc.2021.102425 (文献検索サイトへのリンク) ● Summary page in Scopus @ Elsevier: 2-s2.0-85101785195 (DOI: 10.1016/j.bspc.2021.102425, Elsevier: Scopus)
14.	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. (徳島大学機関リポジトリ) ● Metadata: 115319 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/app10165549 (文献検索サイトへのリンク) ● Search Scopus @ Elsevier (DOI): 10.3390/app10165549 (徳島大学機関リポジトリ: 115319, DOI: 10.3390/app10165549)
15.	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. (要約) infection. (徳島大学機関リポジトリ) ● Metadata: 114634 (出版サイトへのリンク) ● Publication site (DOI): 10.1128/mSphere.00960-19 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 114634, DOI: 10.1128/mSphere.00960-19, PubMed: 32188755)
16.	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. (要約) (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. (徳島大学機関リポジトリ) ● Metadata: 115656 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/nu12030736 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32168816 ● Search Scopus @ Elsevier (PMID): 32168816 ● Search Scopus @ Elsevier (DOI): 10.3390/nu12030736 (徳島大学機関リポジトリ: 115656, DOI: 10.3390/nu12030736, PubMed: 32168816)
17.	Haruhide Udagawa, Masaki Hiramoto, Miho Kawaguchi, Takashi Uebanso, Mica Ohara-Imaizumi, Takao Nammo, Wataru Nishimura and Kazuki Yasuda : Characterization of the taste receptor-related G-protein, α-gustducin, in pancreatic β-cells., Journal of Diabetes Investigation, Vol.xxx, No.xxx, xxx, 2020. (要約) α-Gustducin is involved in the regulation of cyclic adenosine monophosphate, intracellular calcium levels and insulin secretion in pancreatic β-cells in a manner independent of taste receptor signaling. α-Gustducin might play a novel role in β-cell physiology and the development of type 2 diabetes. (徳島大学機関リポジトリ) ● Metadata: 115503 (出版サイトへのリンク) ● Publication site (DOI): 10.1111/jdi.13214 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31957256 ● Search Scopus @ Elsevier (PMID): 31957256 ● Search Scopus @ Elsevier (DOI): 10.1111/jdi.13214 (徳島大学機関リポジトリ: 115503, DOI: 10.1111/jdi.13214, PubMed: 31957256)
18.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114642 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.67.163 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32378601 ● Summary page in Scopus @ Elsevier: 2-s2.0-85084329310 (徳島大学機関リポジトリ: 114642, DOI: 10.2152/jmi.67.163, PubMed: 32378601, Elsevier: Scopus)
19.	Hiromichi Yumoto, Takashi Uebanso, Takaaki Shimohata and Akira Takahashi : Current understanding of the gut microflora in subjects with nutrition-associated metabolic disorder such as obesity and/or diabetes: Is there any relevance with oral microflora?, Current Oral Health Reports, Vol.6, No.2, 100-109, 2019. (徳島大学機関リポジトリ) ● Metadata: 113630 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s40496-019-0221-7 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1572261552667553664 ● Search Scopus @ Elsevier (DOI): 10.1007/s40496-019-0221-7 (徳島大学機関リポジトリ: 113630, DOI: 10.1007/s40496-019-0221-7, CiNii: 1572261552667553664)
20.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 113411 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.66.148 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 113411, DOI: 10.2152/jmi.66.148, PubMed: 31064928)
21.	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. (要約) 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. (キーワード) Caco-2 Cells / Campylobacter jejuni / Endoplasmic Reticulum Stress / Thapsigargin / Transcription Factor CHOP / Tunicamycin / Unfolded Protein Response (徳島大学機関リポジトリ) ● Metadata: 114338 (出版サイトへのリンク) ● Publication site (DOI): 10.1371/journal.pone.0205865 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 114338, DOI: 10.1371/journal.pone.0205865, PubMed: 30321237)
22.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 111607 (出版サイトへのリンク) ● Publication site (DOI): 10.3389/fcimb.2018.00015 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 111607, DOI: 10.3389/fcimb.2018.00015, PubMed: 29441328)
23.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114647 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.17-53 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 114647, DOI: 10.3164/jcbn.17-53, PubMed: 29610555)
24.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 114676 (出版サイトへのリンク) ● Publication site (DOI): 10.1128/IAI.00311-17 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 114676, DOI: 10.1128/IAI.00311-17, PubMed: 28784926)
25.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 115660 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/nu9070756 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28708089 ● Summary page in Scopus @ Elsevier: 2-s2.0-85025080133 (徳島大学機関リポジトリ: 115660, DOI: 10.3390/nu9070756, PubMed: 28708089, Elsevier: Scopus)
26.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 115661 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/nu9060560 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28587159 ● Search Scopus @ Elsevier (PMID): 28587159 ● Search Scopus @ Elsevier (DOI): 10.3390/nu9060560 (徳島大学機関リポジトリ: 115661, DOI: 10.3390/nu9060560, PubMed: 28587159)
27.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 111155 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.63.63 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 111155, DOI: 10.2152/jmi.63.63, PubMed: 27040055)
28.	Kosuke Saito, Takashi Uebanso, Keiko Maekawa, Masaki Ishikawa, Ryo Taguchi, Takao Nammo, Tomoko Nishimaki-Mogami, Haruhide Udagawa, Masato Fujii, Yuichiro Shibazaki, Hiroyuki Yoneyama, Kazuki Yasuda and Yoshiro Saito : Characterization of hepatic lipid profiles in a mouse model with nonalcoholic steatohepatitis and subsequent fibrosis., Scientific Reports, Vol.5, 12466, 2015. (要約) Nonalcoholic steatohepatitis (NASH) is a major health problem since it often leads to hepatocellular carcinoma. However, the underlying mechanisms of NASH development and subsequent fibrosis have yet to be clarified. We compared comprehensive lipidomic profiles between mice with high fat diet (HFD)-induced steatosis and STAM mice with NASH and subsequent fibrosis. The STAM mouse is a model that demonstrates NASH progression resembling the disease in humans: STAM mice manifest NASH at 8 weeks, which progresses to fibrosis at 12 weeks, and finally develop hepatocellular carcinoma. Overall, 250 lipid molecules were detected in the liver using liquid chromatography-mass spectrometry. We found that STAM mice with NASH presented a significantly higher abundance of sphingolipids and lower levels of triacylglycerols than the HFD-fed control mice. The abundance of certain fatty acids in phospholipid side chains was also significantly different between STAM and control mice, although global levels of phosphatidylcholines and phosphatidylethanolamines were comparable. Finally, increase in levels of acylcarnitines and some diacylglycerols was observed in STAM mice toward the fibrosis stage, but not in age-matched control mice. Our study provides insights into the lipid status of the steatotic, NASH, and fibrotic liver that would help elucidate the molecular pathophysiology of NASH progression. (出版サイトへのリンク) ● Publication site (DOI): 10.1038/srep12466 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26289793 ● Summary page in Scopus @ Elsevier: 2-s2.0-84939639945 (DOI: 10.1038/srep12466, PubMed: 26289793, Elsevier: Scopus)
29.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 109503 (出版サイトへのリンク) ● Publication site (DOI): 10.1128/JB.00306-15 (文献検索サイトへのリンク) ● 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 (徳島大学機関リポジトリ: 109503, DOI: 10.1128/JB.00306-15, PubMed: 26148713)
30.	Masaki Hiramoto, Haruhide Udagawa, Atsushi Watanabe, Keisuke Miyazawa, Naoko Ishibashi, Miho Kawaguchi, Takashi Uebanso, Wataru Nishimura, Takao Nammo and Kazuki Yasuda : Comparative analysis of type 2 diabetes-associated SNP alleles identifies allele-specific DNA-binding proteins for the KCNQ1 locus., International Journal of Molecular Medicine, Vol.36, No.1, 222-230, 2015. (要約) Although recent genome-wide association studies (GWAS) have been extremely successful, it remains a big challenge to functionally annotate disease‑associated single nucleotide polymorphisms (SNPs), as the majority of these SNPs are located in non‑coding regions of the genome. In this study, we described a novel strategy for identifying the proteins that bind to the SNP‑containing locus in an allele‑specific manner and successfully applied this method to SNPs in the type 2 diabetes mellitus susceptibility gene, potassium voltage‑gated channel, KQT‑like subfamily Q, member 1 (KCNQ1). DNA fragments encompassing SNPs, and risk or non‑risk alleles were immobilized onto the novel nanobeads and DNA‑binding proteins were purified from the nuclear extracts of pancreatic β cells using these DNA‑immobilized nanobeads. Comparative analysis of the allele-specific DNA-binding proteins indicated that the affinities of several proteins for the examined SNPs differed between the alleles. Nuclear transcription factor Y (NF‑Y) specifically bound the non‑risk allele of the SNP rs2074196 region and stimulated the transcriptional activity of an artificial promoter containing SNP rs2074196 in an allele‑specific manner. These results suggest that SNP rs2074196 modulates the affinity of the locus for NF‑Y and possibly induces subsequent changes in gene expression. The findings of this study indicate that our comparative method using novel nanobeads is effective for the identification of allele‑specific DNA‑binding proteins, which may provide important clues for the functional impact of disease‑associated non‑coding SNPs. (出版サイトへのリンク) ● Publication site (DOI): 10.3892/ijmm.2015.2203 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25955334 ● Summary page in Scopus @ Elsevier: 2-s2.0-84930325829 (DOI: 10.3892/ijmm.2015.2203, PubMed: 25955334, Elsevier: Scopus)
31.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 110108 (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jiac.2014.07.007 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25107576 ● Summary page in Scopus @ Elsevier: 2-s2.0-84908232552 (徳島大学機関リポジトリ: 110108, DOI: 10.1016/j.jiac.2014.07.007, PubMed: 25107576, Elsevier: Scopus)
32.	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. (要約) 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. (出版サイトへのリンク) ● Publication site (DOI): 10.1111/php.12309 (文献検索サイトへのリンク) ● 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)
33.	Hirokazu Ohminami, Kikuko Amou, Yutaka Taketani, Kazusa Sato, Makiko Fukaya, Takashi Uebanso, Hidekazu Arai, Megumi Koganei, Hajime Sasaki, Hisami Okumura, Hironori Yamamoto and Eiji Takeda : Dietary combination of sucrose and linoleic acid causes skeletal muscle metabolic abnormalities in Zucker fatty rats through specific modification of fatty acid composition., Journal of Clinical Biochemistry and Nutrition, Vol.55, No.1, 15-25, 2014. (要約) A dietary combination of sucrose and linoleic acid strongly contributes to the development of metabolic disorders in Zucker fatty rats. However, the underlying mechanisms of the metabolic disorders are poorly understood. We hypothesized that the metabolic disorders were triggered at a stage earlier than the 8 weeks we had previously reported. In this study, we investigated early molecular events induced by the sucrose and linoleic acid diet in Zucker fatty rats by comparison with other combinations of carbohydrate (sucrose or palatinose) and fat (linoleic acid or oleic acid). Skeletal muscle arachidonic acid levels were significantly increased in the sucrose and linoleic acid group compared to the other dietary groups at 4 weeks, while there were no obvious differences in the metabolic phenotype between the groups. Expression of genes related to arachidonic acid synthesis was induced in skeletal muscle but not in liver and adipose tissue in sucrose and linoleic acid group rats. In addition, the sucrose and linoleic acid group exhibited a rapid induction in endoplasmic reticulum stress and abnormal lipid metabolism in skeletal muscle. We concluded that the dietary combination of sucrose and linoleic acid primarily induces metabolic disorders in skeletal muscle through increases in arachidonic acid and endoplasmic reticulum stress, in advance of systemic metabolic disorders. (徳島大学機関リポジトリ) ● Metadata: 106169 (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.14-11 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25147427 ● Search Scopus @ Elsevier (PMID): 25147427 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.14-11 (徳島大学機関リポジトリ: 106169, DOI: 10.3164/jcbn.14-11, PubMed: 25147427)
34.	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. (要約) 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. (徳島大学機関リポジトリ) ● Metadata: 109573 (出版サイトへのリンク) ● Publication site (DOI): 10.2152/jmi.61.285 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25264046 ● Summary page in Scopus @ Elsevier: 2-s2.0-84907509465 (徳島大学機関リポジトリ: 109573, DOI: 10.2152/jmi.61.285, PubMed: 25264046, Elsevier: Scopus)
35.	Takehiro Sugiyama, Misao Nakanishi, Kazufusa Hoshimoto, Takashi Uebanso, Kaori Inoue, Hisako Endo, Shigeki Minoura, Kazuki Yasuda and Mitsuhiko Noda : Severely fluctuating blood glucose levels associated with a somatostatin-producing ovarian neuroendocrine tumor., The Journal of Clinical Endocrinology and Metabolism, Vol.97, No.11, 3845-3850, 2012. (要約) Somatostatin-producing tumors are a rare type of neuroendocrine tumor. Their effects on blood glucose levels have been variously reported, and detailed reports have been scarce. The aim of this study was to identify the reasons for the extraordinary blood glucose fluctuations in a case with no previous history of diabetes. A 68-yr-old nondiabetic woman with an ovarian tumor was suffering from hyper- and hypoglycemia. Based on the results of an oral glucose tolerance test and continuous glucose monitoring, we speculated that the fluctuating blood glucose level was accompanied not only by a low insulin level but also by low counter-regulatory hormones levels, and that those broad hormonal suppressions were caused by a high somatostatin level produced in the ovarian tumor. We performed an oophorectomy and assessed the pathology of the tumor and changes in the blood glucose profile as well as hormonal levels postoperatively. The blood glucose level was completely normalized after the oophorectomy. Insulin secretion was also normalized. Histological examination showed that the tumor comprised a mature cystic teratoma and a stromal carcinoid. Immunohistochemically, the stromal carcinoid component was positive for somatostatin. The somatostatin level was 8505 pmol/liter preoperatively, which dropped down to 71.5 pmol/liter postoperatively. We found two previous reports of somatostatin-producing ovarian neuroendocrine tumors. Somatostatin levels among cases of ovarian origin were much higher than those among cases of gastrointestinal origins, and cases of ovarian origin all experienced blood glucose fluctuations. Extremely high somatostatin levels and blood glucose fluctuations may be characteristics of somatostatin-producing ovarian neuroendocrine tumors. (キーワード) Aged / Blood Glucose / Female / Glucose Tolerance Test / Humans / Hyperglycemia / Hypoglycemia / Ovarian Neoplasms / Ovariectomy / Somatostatinoma (出版サイトへのリンク) ● Publication site (DOI): 10.1210/jc.2012-2091 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22962430 ● Search Scopus @ Elsevier (PMID): 22962430 ● Search Scopus @ Elsevier (DOI): 10.1210/jc.2012-2091 (DOI: 10.1210/jc.2012-2091, PubMed: 22962430)
36.	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. (要約) The V. parahaemolyticus FeSOD VP2118 may enhance ROS resistance and could promote its survival in the intestinal tract to facilitate host tissue infection. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.bbagen.2012.06.019 (文献検索サイトへのリンク) ● 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)
37.	Takashi Uebanso, Yutaka Taketani, Hironori Yamamoto, Kikuko Amou, Sarasa Tanaka, Hidekazu Arai, Yuichiro Takei, Masashi Masuda, Hisami Yamanaka-Okumura and Eiji Takeda : Liver X receptor negatively regulates fibroblast growth factor 21 in the fatty liver induced by cholesterol-enriched diet., The Journal of Nutritional Biochemistry, Vol.23, No.7, 785-790, 2011. (要約) Cholesterol homeostasis is regulated by the liver X receptor (LXR) at the transcriptional level, but it remains unknown whether LXR can affect expression levels of intrahepatic lipolysis related gene. Recent evidence has demonstrated that fibroblast growth factor 21 (FGF21) regulates hepatic lipolysis and fatty acid utilization. In the present study, we examined the role of LXR in FGF21 gene expression associated with regulation of cross-talk signals between cholesterol and triglyceride metabolism in the liver. An in vivo cholesterol feeding test revealed that intake of excess cholesterol increased cholesterol catabolism related gene expression as well as fatty-acid biosynthesis related gene expression. Moreover, the accumulated cholesterol suppressed FGF21 and hormone-sensitive lipase (HSL) gene expression. After 15-day cholesterol feeding, hepatic triglyceride concentrations were negatively correlated with expression levels of the FGF21 and HSL genes in the liver. An LXR agonist (TO-901317) repressed the FGF21 gene expression in mouse primary hepatocytes and HepG2 cells. A promoter deletion study and electrophoretic mobility shift assay revealed that the human FGF21 promoter has at least one LXR response element located from -37 to -22 bp. In summary, LXR represses FGF21 gene expression at the transcription level and might suppress lipolysis and lipid utilization to protect the liver from excess accumulation of toxic cholesterol. (出版サイトへのリンク) ● Publication site (DOI): 10.1016/j.jnutbio.2011.03.023 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21889884 ● Search Scopus @ Elsevier (PMID): 21889884 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2011.03.023 (DOI: 10.1016/j.jnutbio.2011.03.023, PubMed: 21889884)
38.	Kikuko Amou, Hidekazu Arai, Takashi Uebanso, Makiko Fukaya, Megumi Koganei, Hajime Sasaki, Hironori Yamamoto, Yutaka Taketani and Eiji Takeda : Effects of xylitol on metabolic parameters and visceral fat accumulation., Journal of Clinical Biochemistry and Nutrition, Vol.49, No.1, 1-7, 2011. (要約) Xylitol is widely used as a sweetener in foods and medications. Xylitol ingestion causes a small blood glucose rise, and it is commonly used as an alternative to high-energy supplements in diabetics. In previous studies, a xylitol metabolite, xylulose-5-phosphate, was shown to activate carbohydrate response element binding protein, and to promote lipogenic enzyme gene transcription in vitro; however, the effects of xylitol in vivo are not understood. Here we investigated the effects of dietary xylitol on lipid metabolism and visceral fat accumulation in rats fed a high-fat diet. Sprague-Dawley rats were fed a high-fat diet containing 0g (control), 1.0g/100kcal (X1) or 2.0g/100kcal (X2) of xylitol. After the 8-week feeding period, visceral fat mass and plasma insulin and lipid concentrations were significantly lower in xylitol-fed rats than those in high-fat diet rats. Gene expression levels of ChREBP and lipogenic enzymes were higher, whereas the expression of sterol regulatory-element binding protein 1c was lower and fatty acid oxidation-related genes were significantly higher in the liver of xylitol-fed rats as compared with high-fat diet rats. In conclusion, intake of xylitol may be beneficial in preventing the development of obesity and metabolic abnormalities in rats with diet-induced obesity. (出版サイトへのリンク) ● Publication site (DOI): 10.3164/jcbn.10-111 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21765599 ● Search Scopus @ Elsevier (PMID): 21765599 ● Search Scopus @ Elsevier (DOI): 10.3164/jcbn.10-111 (DOI: 10.3164/jcbn.10-111, PubMed: 21765599)

国際会議:

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.	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.
3.	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.
4.	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.
5.	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.
6.	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.
7.	Oda Naoko, Sugihara Kohei, Miho Ikeda, Yuho Higashimura, Takashi Uebanso, Kohta Ohnishi, Hirokazu Ohminami, Masashi Masuda, Hisami Okumura and Yutaka Taketani : Dietary phosphate disturbs of gut microbiome in mice., American Society of Nephrolody Kidney Week 2019, Washington, D.C., Nov. 2019.
8.	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.
9.	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.
10.	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.
11.	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.
12.	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.
13.	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.
14.	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.
15.	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.
16.	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.
17.	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.
18.	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.
19.	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.
20.	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.
21.	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.
22.	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.
23.	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.
24.	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.
25.	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.
26.	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.
27.	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.
28.	Masaki Hiramoto, Wataru Nishimura, Miho Kawaguchi, Haruhide Udagawa, Takashi Uebanso, Eri Takahashi, Keiko Kano, Yasushi Kaburagi, Naoko Ishibashi, Koki Etoh, Takao Nammo and Kazuki Yasuda : Nicotinamide regulates gene expression in post-transcriptional mechanisms in pancreatic beta cells, Key stone symposia on Molecular and Cellular Biology, santa fe, Feb. 2013.
29.	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.
30.	Takashi Uebanso, Hitomi Iba, Shoko Asada, Takaaki Shimohata and Akira Takahashi : REGULATION AND EFFECTS OF VP1671(VSCQ) ON VIRULENCE Of VIBRIO PARAHAEMOLYTICUS, International Symposium on Single cell Analysis, Kyoto, Nov. 2012.
31.	Masaki Hiramoto, Wataru Nishimura, Miho Kawaguchi, Haruhide Udagawa, Takashi Uebanso, Eri Takahashi, Keiko Kano, Yasushi Kaburagi, Naoko Ishibashi, Koki Etoh, Takao Nammo and Kazuki Yasuda : New insights into nicotinamide signaling associated with insulin production in pancreatic beta cells, American Society for Cell Biology, San Francisco, Nov. 2012.
32.	W Nishimura, M Kawaguchi, K Eto, T Nammo, H Udagawa, Takashi Uebanso, M Hiramoto, M Goto, Y Shimizu, T Okamura and K Yasuda : Generation and Characterization of Pdx1-Gaussia Luciferase Mouse., American Diabetes Association's 72nd Scientific Sessions, Philadelphia, Jun. 2012.

国内講演発表:

1.	白山優斗, 栗本一輝, 渡辺智貴, 岡本敏弘, 山口堅三, 上番増喬, 馬渡一諭, 髙橋章, 原口雅宣 : 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, 2024年3月.
2.	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.
3.	松岡実花, 武野香澄, 井上詩央里, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2023年12月.
4.	小野実優, 石田快, 牧本真奈, 下畑隆明, 上番増喬, 粟飯原睦美, 芥川正武, 榎本崇宏, 馬渡一諭, 岩田剛敏, 髙橋章 : 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, 2023年12月.
5.	馬渡一諭, 戸田沙慧, 平野希美, 結城史音, 上番増喬, 髙橋章 : 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, 2023年10月.
6.	戸田沙慧, 馬渡一諭, 殿脇壱成, 平野希美, 山口ももか, Bui Thi Kim Ngan, 石川寧子, 篠田浩一, 上番増喬, 髙橋章 : 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, 2023年10月.
7.	相澤心太, 小井優萌那, 山下路代, 白石志帆, 宮脇克行, 粟飯原睦美, 二川健, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2023年10月.
8.	牧本真奈, 福島志帆, 山中咲季, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2023年9月.
9.	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.
10.	斧田優志, 石田快, 石川寧子, 田中佐保, 山下路代, 福島志帆, 相澤俊彦, 山内繁晴, 藤川康夫, 田中智毅, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2023年8月.
11.	石田快, 斧田優志, 石川寧子, 田中佐保, 山下路代, 福島志帆, 相澤俊彦, 山内繁晴, 藤川康夫, 田中智毅, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2023年8月.
12.	馬渡一諭, 小池宣也, 野原一成, 敷島康普, 三浦宏之, 新居佳孝, 上番増喬, 下畑隆明, 八木田和弘, 髙橋章, Yoo Seung-Hee, 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, 2023年8月.
13.	上番増喬 : 鉄恒常性維持に対する腸内細菌叢の役割の解析, 2023年度中四国乳酸菌研究会, 2023年6月.
14.	馬渡一諭, 小池宣也, 野原一成, 敷島康普, 三浦宏之, 新居佳孝, 上番増喬, 下畑隆明, 八木田和弘, 髙橋章, Seung-Hee Yoo, 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, 2023年5月.
15.	武野香澄, 上番増喬, 相澤心太, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2023年5月.
16.	戸田沙慧, 馬渡一諭, 古家光二, 殿脇壱成, BUI THI KIM NGAN, 石川寧子, 篠田浩一, 上番増喬, 髙橋章 : 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, 2023年5月.
17.	山野恵理華, 伊藤千菜美, 松木大揮, 鴻野まどか, ウラアナイツト, 内田貴之, 上番増喬, 高木均, 二川健 : セルロースナノファイバーの栄養学的機能性の検討, 第77回日本栄養・食糧学会大会, 2023年5月.
18.	戸田沙慧, 馬渡一諭, 殿脇壱成, 平野希美, 山口ももか, Bui Thi Kim Ngan, 石川寧子, 篠田浩一, 上番増喬, 髙橋章 : 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」, 2023年2月.
19.	福島志帆, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2022年11月.
20.	石田快, 粟飯原睦美, 下畑隆明, 北山栞里, 勢川玲花, 上番増喬, 馬渡一諭, 鈴木浩司, 芥川正武, 榎本崇宏, 山本光生, 富久章子, 和田敬宏, 岡本雅之, 伊藤浩, 安野卓, 木内陽介, 髙橋章 : 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, 2022年9月.
21.	石田快, 粟飯原睦美, 下畑隆明, 北山栞里, 勢川玲花, 上番増喬, 馬渡一諭, 鈴木浩司, 芥川正武, 榎本崇宏, 山本光生, 富久章子, 和田敬宏, 岡本雅之, 伊藤浩, 安野卓, 木内陽介, 髙橋章 : 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, 2022年9月.
22.	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.
23.	石田快, 下畑隆明, 佐野真梨奈, 射場仁美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2022年6月.
24.	射場仁美, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2022年6月.
25.	上番増喬, 相澤心太, 中村真彩, 須山真衣, 吉本亜由美, 増田瑠見子, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2022年6月.
26.	北山栞里, 下畑隆明, 白石志帆, 石田快, 緒方美裕起, 上番増喬, 馬渡一諭, 粟飯原睦美, 芥川正武, 榎本崇宏, 鈴木浩司, 安野卓, 伊藤浩, 和田敬宏, 岡本雅之, 富久章子, 髙橋章, 木内陽介 : 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, 2022年1月.
27.	石田快, 下畑隆明, 神田結奈, 増田瑠見子, 上番増喬, 馬渡一諭, 柏本孝茂, 髙橋章 : Metabolism changing of Vibrio vulnificus infected tissue in wound infection model mouse, 第93回日本細菌学会総会, 2020年2月.
28.	近藤翼, 荒尾菜月, 上番増喬, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2020年2月.
29.	福島志帆, 下畑隆明, 木戸純子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2020年2月.
30.	下畑隆明, 木戸純子, 鳴滝涼香, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2020年2月.
31.	池田美萌, 織田奈央子, 上番増喬, 大南博和, 大西康太, 増田真志, 奥村仙示, 竹谷豊 : 高リン食が腸内環境を介して慢性腎臓病に与える影響, 第23回日本病態栄養学会年次集会, 2020年1月.
32.	相澤心太, 上番増喬, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2019年11月.
33.	下畑隆明, 木戸純子, 福島志帆, 天宅あや, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2019年9月.
34.	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.
35.	福島志帆, 下畑隆明, 木戸純子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2019年8月.
36.	福井萌加, 上番増喬, 内藤千里, 増田瑠見子, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2019年5月.
37.	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.
38.	石田快, 下畑隆明, 畑山翔, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : Effect of cholesterol on Campylobacter jejuni survival in host intestinal epithelial cells, 第92回日本細菌学会総会, 2019年4月.
39.	福島志帆, 下畑隆明, 木戸純子, 石田快, 上番増喬, 馬渡一諭, 髙橋章 : オートファジーの誘導はCampylobacter jejuniの宿主細胞への侵入過程を促進する, 第92回日本細菌学会総会, 2019年4月.
40.	福島志帆, 下畑隆明, 木戸純子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年10月.
41.	神田結奈, 東山諒, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 福島志帆, 石田快, 上番増喬, 馬渡一諭, 柏本孝茂, 髙橋章 : 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, 2018年10月.
42.	天宅あや, 下畑隆明, 畑山翔, NGUYEN QUOC ANH, 木戸純子, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年9月.
43.	畑山翔, 下畑隆明, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 中橋睦美, 中本晶子, 首藤恵泉, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年9月.
44.	神田結奈, 東山諒, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 福島志帆, 石田快, 上番増喬, 馬渡一諭, 柏本孝茂, 髙橋章 : 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, 2018年9月.
45.	福島志帆, 下畑隆明, 木戸純子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年9月.
46.	下畑隆明, 畑山翔, 木戸純子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年9月.
47.	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.
48.	天宅あや, 下畑隆明, NGUYEN QUOC ANH, 畑山翔, 木戸純子, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年8月.
49.	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.
50.	石田快, 下畑隆明, 木戸純子, 天宅あや, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年5月.
51.	福島志帆, 下畑隆明, 木戸純子, 天宅あや, 石田快, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年5月.
52.	天宅あや, 下畑隆明, 畑山翔, NGUYEN QUOC ANH, 木戸純子, 福島志帆, 石田快, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年5月.
53.	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.
54.	天宅あや, 下畑隆明, 畑山翔, NGUYEN QUOC ANH, 木戸純子, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年3月.
55.	福島志帆, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 神田結奈, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年3月.
56.	福島志帆, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年2月.
57.	木戸純子, 下畑隆明, 天野幸恵, 畑山翔, 天宅あや, 福島志帆, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : CFTR発現はCampylobacter jejuniの微小管を介した輸送を抑制する, 2017年度生命科学系学会合同年次大会, 2017年12月.
58.	天宅あや, 下畑隆明, 畑山翔, NGUYEN QUOC ANH, 木戸純子, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年度生命科学系学会合同年次大会, 2017年12月.
59.	福島志帆, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年度生命科学系学会合同年次大会, 2017年12月.
60.	下畑隆明, 木戸純子, 畑山翔, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年10月.
61.	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.
62.	天宅あや, 下畑隆明, 畑山翔, NGUYEN QUOC ANH, 木戸純子, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年10月.
63.	畑山翔, 下畑隆明, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年10月.
64.	福島志帆, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 神田結奈, 鳴滝涼香, 石田快, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年10月.
65.	木戸純子, 下畑隆明, 天野幸恵, 畑山翔, 佐藤優里, 神田結奈, 天宅あや, 福島志帆, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年8月.
66.	織田奈央子, 杉原康平, 吉本亜由美, 上番増喬, 増田真志, 奥村仙示, 竹谷豊 : 高リン食摂取は腸内環境を変化させる, 日本栄養食糧学会, 322, 2017年5月.
67.	上番増喬, 大西愛, 北山礼子, 吉本亜由美, 中橋睦美, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2017年5月.
68.	畑山翔, 下畑隆明, 天野幸恵, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年5月.
69.	天宅あや, 下畑隆明, 木戸純子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年4月.
70.	畑山翔, 下畑隆明, 天野幸恵, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年3月.
71.	下畑隆明, 木戸純子, 佐藤優里, 畑山翔, 神田結奈, 福島志帆, 天宅あや, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年3月.
72.	馬渡一諭, 安井実希, 本庄アイリ, 西坂理沙, 枝川美幸, 岩本夏美, 渡邊瞳, 下畑隆明, 上番増喬, 髙橋章 : Screening of genes related with ultraviolet A-sensitivity by transposon mutagenesis in Vibrio parahaemolyticus, 90th Annual Meeting of Japanese Society of bacteriology, 46, 2017年3月.
73.	上番増喬, 吉本亜由美, 下畑隆明, 中橋睦美, 馬渡一諭, 髙橋章 : 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, 2017年3月.
74.	宇山真由, 曽我部正弘, 平田光里, 中川忠彦, 福家慧, 寺前智史, 藤本大策, 田中宏典, 三井康裕, 北村晋志, 岡本耕一, 高山哲治, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 榎本崇宏, 芥川正武, 片島るみ, 岡久稔也 : 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, 2016年11月.
75.	玉井瑠人, 笠井嘉人, 田中大基, 谷直也, 平田光里, 中川忠彦, 友成哲, 谷口達哉, 岡本耕一, 宮本弘志, 高山哲治, 榎本崇宏, 芥川正武, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 宇山真由, 曽我部正弘, 岡久稔也 : 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, 2016年11月.
76.	渡邊瞳, 馬渡一諭, 西坂理沙, 中橋睦美, 常冨愛香里, 下畑隆明, 上番増喬, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 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, 2016年10月.
77.	下畑隆明, 福島志帆, 佐藤優里, 扶川留音, 木戸純子, 神田結奈, 天宅あや, 畑山翔, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2016年10月.
78.	木戸純子, 下畑隆明, 天野幸恵, 畑山翔, 天宅あや, 福島志帆, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2016年10月.
79.	中橋睦美, 常冨愛香里, 上番増喬, 下畑隆明, 馬渡一諭, 芥川正武, 木内陽介, 髙橋章 : 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, 2016年9月.
80.	髙橋章, 下畑隆明, 馬渡一諭, 上番増喬, 常冨愛香里, 中橋睦美, 芥川正武, 木内陽介 : 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, 2016年9月.
81.	常冨愛香里, 下畑隆明, 永田早紀恵, 天野幸恵, 中橋睦美, 原田優美, 上番増喬, 馬渡一諭, 宮脇克行, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 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, 2016年9月.
82.	下畑隆明, 福島志帆, 佐藤優里, 扶川留音, 木戸純子, 神田結奈, 天宅あや, 畑山翔, 中橋睦美, 上番増喬, 原田永勝, 馬渡一諭, 髙橋章 : 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, 2016年9月.
83.	畑山翔, 下畑隆明, 根来幸恵, 木戸純子, 射場仁美, 上番増喬, 馬渡一諭, 髙橋章 : 腸管上皮細胞におけるtight junctionsの破綻は細胞側面からの脂質ラフトを介したCampylobacter jejuniの侵入を促進する, 日米医学協力研究会コレラ・細菌性腸管感染症専門部会, 2016年8月.
84.	西坂理沙, 渡邊瞳, 馬渡一諭, 中橋睦美, 常冨愛香里, 下畑隆明, 上番増喬, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 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, 2016年7月.
85.	木戸純子, 下畑隆明, 根来幸恵, 畑山翔, 天宅あや, 福島志帆, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2016年7月.
86.	吉本亜由美, 上番増喬, 下畑隆明, 中橋睦美, 馬渡一諭, 髙橋章 : 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, 2016年7月.
87.	畑山翔, 下畑隆明, 吉兼道子, 天野幸恵, 佐藤優里, 木戸純子, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2016年5月.
88.	常冨愛香里, 下畑隆明, 後藤茉凜, 天野幸恵, 中橋睦美, 原田優美, 上番増喬, 馬渡一諭, 宮脇克行, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 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, 2016年5月.
89.	宇山真由, 曽我部正弘, 平田光里, 中川忠彦, 高岡慶史, 谷口達哉, 高山哲治, 榎本崇宏, 芥川正武, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 岡久稔也 : 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, 2016年5月. (キーワード) 胸腹水濾過濃縮再静注法
90.	常冨愛香里, 木戸純子, 上番増喬, 下畑隆明, 馬渡一諭, 髙橋章 : 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, 2016年4月.
91.	西坂理沙, 馬渡一諭, 山下智子, 木戸純子, 常冨愛香里, 下畑隆明, 上番増喬, 髙橋章 : 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, 2016年4月.
92.	木戸純子, 下畑隆明, 根来幸恵, 畑山翔, 佐藤優里, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : Campylobacter jejuniの細胞侵入は細胞膜表面CFTRにより調節される, 第89回日本細菌学会総会, 2016年3月.
93.	下畑隆明, 佐藤優里, 扶川留音, 木戸純子, 天野幸恵, 畑山翔, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 代謝解析で明らかとなったCampylobacter jejuni感染による宿主細胞での特徴的なアミノ酸変動について, 第89回日本細菌学会総会, 2016年3月.
94.	吉本亜由美, 上番増喬, 中橋睦美, 下畑隆明, 馬渡一諭, 髙橋章 : Effect of low dose antibiotics administration during prenatal period on newborns postnatal health, 第89回日本細菌学会総会, 2016年3月.
95.	馬渡一諭, 枝川美幸, 岩本夏実, 前谷実希, 本庄アイリ, 西坂理沙, 渡邊瞳, 下畑隆明, 上番増喬, 髙橋章 : Identification of genes associated with ultraviolet-A sensitivity in Vibrio parahaemolyticus, 第89回日本細菌学会総会, 2016年3月.
96.	西坂理沙, 馬渡一諭, 常冨愛香里, 渡邊瞳, 上番増明子, 下畑隆明, 上番増喬, 金本優杞, 村上明男, 髙橋章 : Ultraviolet-A (UVA) irradiation by light emitting diode (LED) inhibits growth of cyanobacteria, 第89回日本細菌学会総会, 2016年3月.
97.	谷直也, 田中大基, 末内辰尚, 高岡慶史, 中川忠彦, 高山哲治, 河野正樹, 榎本崇宏, 芥川正武, 木内陽介, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 宇山真由, 曽我部正弘, 岡久稔也 : 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, 2015年11月.
98.	田中大基, 谷直也, 武原正典, 田中宏典, 田中貴大, 友成哲, 谷口達哉, 中川忠彦, 高山哲治, 河野正樹, 榎本崇宏, 芥川正武, 木内陽介, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 宇山真由, 曽我部正弘, 岡久稔也 : 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, 2015年11月.
99.	河野正樹, 榎本崇宏, 芥川正武, 宇山真由, 曽我部正弘, 中川忠彦, 高山哲治, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 村島徹, 出口喜宏, 荒巻広至, 岡久稔也 : 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, 2015年10月.
100.	木戸純子, 下畑隆明, 根来幸恵, 畑山翔, 佐藤優里, 扶川留音, 吉兼道子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2015年8月.
101.	常冨愛香里, 正村彰規, 中橋睦美, 西坂理沙, 後藤茉凛, 馬渡一諭, 下畑隆明, 上番増喬, 宮脇克行, 芥川正武, 木内陽介, 髙橋章 : 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, 2015年8月.
102.	西坂理沙, 馬渡一諭, 常冨愛香里, 後藤茉凛, 上番増明子, 下畑隆明, 上番増喬, 榎本崇宏, 芥川正武, 木内陽介, 金本優杞, 村上明男, 髙橋章 : 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, 2015年8月.
103.	畑山翔, 下畑隆明, 吉兼道子, 根来幸恵, 佐藤優里, 木戸純子, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2015年8月.
104.	下畑隆明, 木戸純子, 根来幸恵, 畑山翔, 佐藤優里, 射場仁美, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2015年7月.
105.	木戸純子, 下畑隆明, 根来幸恵, 畑山翔, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2015年4月.
106.	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.
107.	畑山翔, 下畑隆明, 根来幸恵, 佐藤優里, 木戸純子, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2015年3月.
108.	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.
109.	常冨愛香里, 中橋睦美, 西坂理沙, 馬渡一諭, 下畑隆明, 上番増喬, 宮脇克行, 芥川正武, 木内陽介, 髙橋章 : 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, 2014年10月.
110.	木戸純子, 下畑隆明, 根来幸恵, 畑山翔, 佐藤優里, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2014年10月.
111.	本庄アイリ, 馬渡一諭, 前谷実希, 岩本夏実, 山下智子, 中橋睦美, 下畑隆明, 上番増喬, 髙橋章 : 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, 2014年7月.
112.	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.
113.	畑山翔, 下畑隆明, 根来幸恵, 佐藤優里, 木戸純子, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2014年7月.
114.	常冨愛香里, 正村彰規, 粟飯原睦美, 馬渡一諭, 下畑隆明, 上番増喬, 石崎仁愛, 芥川正武, 木内陽介, 髙橋章 : 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, 2014年5月.
115.	本庄アイリ, 馬渡一諭, 前谷実希, 常冨愛香里, 畑山翔, 粟飯原睦美, 下畑隆明, 上番増喬, 髙橋章 : Vibrio parahaemolyticusのkatGgene, VPA0768発現上昇は近紫外線(UVA)耐性獲得に関与する, 第68回日本栄養・食糧学会大会, 2014年5月.
116.	根耒幸恵, 下畑隆明, 畑山翔, 松本麻里, 佐藤優里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : Campylobacter jejuni 感染はCFTR機能を抑制する, 第68回日本栄養・食糧学会大会, 2014年5月.
117.	馬渡一諭, 本庄アイリ, 常冨愛香里, 畑山翔, 粟飯原睦美, 下畑隆明, 上番増喬, 髙橋章 : 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, 2014年3月.
118.	下畑隆明, 根耒幸恵, 畑山翔, 佐藤優里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : Campylobacter jejuni感染はT84細胞におけるCl-分泌を抑制する, 第87回日本細菌学会総会, 2014年3月.
119.	Takao Nammo, haruhide Udagawa, Miho Kawaguchi, Nobuaki Hunahashi, 上番増喬, Masaki Hiramoto, Wataru Nishimura, Kazuki Yasuda : 膵島のゲノム網羅的解析による糖尿病発症機序の考察, Journal of the Japan Diabtes Society, Vol.57, No.suppl1, s404, 2014年.
120.	林田麻里王, 粟飯原睦美, 上番増喬, 下畑隆明, 馬渡一諭, 髙橋章, 星山哲平, 芥川正武, 榎本崇宏, 木内陽介 : 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, 2013年10月.
121.	本庄アイリ, 枝川美幸, 馬渡一諭, 前谷実希, 粟飯原睦美, 下畑隆明, 上番増喬, 上手麻希, 間世田英明, 髙橋章 : 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, 2013年10月.
122.	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.
123.	林田麻里王, 粟飯原睦美, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章, 星山哲平, 榎本崇宏, 芥川正武, 木内陽介 : 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, 2013年8月.
124.	常冨愛香里, 粟飯原睦美, 石崎仁愛, 上番増喬, 下畑隆明, 芥川正武, 馬渡一諭, 髙橋章, 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, 2013年8月.
125.	浅田翔子, 射場仁美, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年8月.
126.	本庄アイリ, 馬渡一諭, 粟飯原睦美, 下畑隆明, 上番増喬, 髙橋章 : 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, 2013年8月.
127.	根来幸恵, 下畑隆明, 畑山翔, 松本麻里, 佐藤優里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年8月.
128.	畑山翔, 下畑隆明, 根来幸恵, 松本麻里, 佐藤優里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年8月.
129.	根来幸恵, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年6月.
130.	下畑隆明, 根来幸恵, 畑山翔, 松本麻里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年3月.
131.	浅田翔子, 射場仁美, 下畑隆明, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2012年10月.
132.	馬渡一諭, 黒川香菜, 本庄アイリ, 藤井麻未, 山本智実, 前谷実希, 粟飯原睦美, 下畑隆明, 上番増喬, 髙橋章 : 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, 2012年10月.
133.	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.
134.	平本正樹, 宇田川陽秀, 渡辺淳, 上番増喬, 川口美穂, 石橋奈緒子, 南茂隆生, 西村渉, 安田和基 : KCNQ1遺伝子イントロンのSNP領域においてアリル特異的に結合する因子の単離・同定・解析, 日本糖尿病学会, 2012年5月.
135.	上番増喬, 宇田川陽秀, 西村渉, 平本正樹, 川口美穂, 南茂隆生, 安田和基 : 膵β細胞株における，ケトン体代謝酵素BDH2の新規機能の解析, 日本糖尿病学会, 2012年5月.
136.	南茂隆生, 上番増喬, 宇田川陽, 衛藤弘城, 川口美穂, 西村渉, 平本正樹, 安田和基 : 膵β細胞株を用いた，分泌刺激による遺伝子発現変化とFAIREによるクロマチン状態の評価, 日本糖尿病学会, 2012年5月.
137.	宇田川陽秀, 平本正樹, 上番増喬, 川口美穂, 南茂隆生, 西村渉, 安田和基 : 膵β細胞株INS-1における糖尿病遺伝因子KCNQ1の機能解析, 日本糖尿病学会, 2012年5月.
138.	竹谷豊, 上番増喬, 大南博和, 武田英二 : ヒトFGF21は絶食・飽食シグナルを感知する栄養代謝の変化に応答する因子である, 第32回日本肥満学会, 2011年9月.

その他・研究会:

1.	石田快, 下畑隆明, 神田結奈, 増田瑠見子, 山﨑浩平, 上番増喬, 馬渡一諭, 柏本孝茂, 髙橋章 : 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, 2022年8月.
2.	下畑隆明, 木戸純子, 鳴滝涼香, 佐藤優里, 扶川留音, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2019年9月.
3.	福島志帆, 下畑隆明, 木戸純子, 辻口舞, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2019年9月.
4.	辻口舞, 下畑隆明, 木戸純子, 福島志帆, 石田快, 吉本亜由美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2019年9月.
5.	畑山翔, 下畑隆明, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 中橋睦美, 中本晶子, 首藤恵泉, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年12月.
6.	石田快, 下畑隆明, 畑山翔, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年12月.
7.	辻口舞, 下畑隆明, 福島志帆, 畑山翔, 木戸純子, 石田快, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年12月.
8.	天宅あや, 下畑隆明, 畑山翔, NGUYEN QUOC ANH, 木戸純子, 福島志帆, 石田快, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2018年8月.
9.	常冨愛香里, 畑山翔, 下畑隆明, 木戸純子, 天野幸恵, 中橋睦美, 上番増喬, 馬渡一諭, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 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, 2017年12月.
10.	福島志帆, 下畑隆明, 畑山翔, 木戸純子, 天宅あや, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2017年12月.
11.	馬渡一諭, 渡邊瞳, 西坂理沙, 中橋睦美, 常冨愛香里, 児島瑞基, 野上夏希, 牧野美鈴, 増田瑠見子, 下畑隆明, 上番増喬, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 透析液の細菌汚染調査と近紫外発光ダイオードによる殺菌効果の評価, 電子情報通信学会技術研究報告(MEとバイオサイバネティックス), Vol.117, No.165, 13-16, 2017年7月. (キーワード) 人工透析 / 細菌汚染 / 近紫外線 / 発光ダイオード (LED) / 殺菌
12.	畑山翔, 下畑隆明, 天野幸恵, 木戸純子, 神田結奈, 天宅あや, 福島志帆, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2016年11月.
13.	木戸純子, 下畑隆明, 佐藤優里, 畑山翔, 神田結奈, 天宅あや, 福島志帆, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2016年11月.
14.	天宅あや, 下畑隆明, 畑山翔, 木戸純子, 上番増喬, 馬渡一諭, 原田永勝, 髙橋章 : 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, 2016年11月.
15.	上番増喬 : 「博士課程に未来はあるのか?(あるといいけど)」, 生化学若い研究者の会中四国支部初夏セミナー, 4-6, 2016年6月.
16.	佐藤優里, 下畑隆明, 扶川留音, 根来幸恵, 畑山翔, 木戸純子, 上番増喬, 原田永勝, 馬渡一諭, 髙橋章 : 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, 2015年12月.
17.	常冨愛香里, 下畑隆明, 後藤茉凜, 天野幸恵, 中橋睦美, 上番増喬, 馬渡一諭, 宮脇克行, 榎本崇宏, 芥川正武, 木内陽介, 髙橋章 : 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, 2015年12月.
18.	木戸純子, 下畑隆明, 根来幸恵, 畑山翔, 佐藤優里, 扶川留音, 吉兼道子, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2015年12月.
19.	下畑隆明, 木戸純子, 根来幸恵, 畑山翔, 佐藤優里, 中橋睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2014年12月.
20.	佐藤優里, 下畑隆明, 根来幸恵, 畑山翔, 木戸純子, 中橋睦美, 上番増喬, 原田永勝, 馬渡一諭, 髙橋章 : 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, 2014年12月.
21.	根来幸恵, 下畑隆明, 畑山翔, 松本麻里, 佐藤優里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年7月.
22.	畑山翔, 下畑隆明, 根来幸恵, 松本麻里, 佐藤優里, 粟飯原睦美, 上番増喬, 馬渡一諭, 髙橋章 : 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, 2013年7月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

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 (研究課題/領域番号: 23K18578 )
組織特異的な栄養代謝の変化がエピゲノム修飾と生活習慣病発症に及ぼす影響の解明 (研究課題/領域番号: 23K28018 )
便秘の客観的評価のための腸音解析システムの開発 (研究課題/領域番号: 20K12755 )
ケトン体代謝の流れがエピゲノム修飾と細胞機能、代謝疾患発症に及ぼす影響の解明 (研究課題/領域番号: 20K11624 )
癌患者の栄養指標としてのBIA-位相角の可能性　～赤血球膜脂肪酸との関連性探索～ (研究課題/領域番号: 20K11530 )
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 (研究課題/領域番号: 18KK0274 )
生体内・外の代謝情報を統合したハイブリッド栄養学の創出 (研究課題/領域番号: 18K19746 )
腸内複合環境制御による次世代栄養療法の確立 (研究課題/領域番号: 16K15191 )
代謝シグナルの流れにより変化するエピゲノムと生活習慣病の関連性の解明 (研究課題/領域番号: 15H05647 )
「ケトン体代謝により制御されるエピゲノム修飾と糖尿病の関連性の解明」 (研究課題/領域番号: 24790244 )
糖尿病の成因となるエピゲノム修飾の網羅的解析-栄養応答システムとの関連性の解明- (研究課題/領域番号: 22890244 )
研究者番号（10581829）による検索

助教 : 上番増喬

研究活動

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

国際会議:

国内講演発表:

その他・研究会:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

助教 : 上番増 喬

研究活動

専門分野

研究テーマ

著書・論文

著書:

学術論文(審査論文):

国際会議:

国内講演発表:

その他・研究会:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

助教 : 上番増喬