OHTANI Naoko

写真a

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Title

Professor

Laboratory location

Abeno Campus

Degree 【 display / non-display

  • Kyoto Prefectural University of Medicine -  Doctor(Medicine)

Research Areas 【 display / non-display

Tumor biology, Pathological medical chemistry, Pathological medical chemistry, Experimental pathology

Research Interests 【 display / non-display

tumor microenvironment, cellular senescence, obesity-associated cancer, gut microbiota

Association Memberships 【 display / non-display

  • International Cell Senescence Association

Current Career 【 display / non-display

  • Osaka City University   Graduate School of Medicine   Basic Medicine Course   Professor  

Career 【 display / non-display

  • 1998.12
    -
    2003.08

    Cancer Research UK   Paterson Institute for Cancer Research, Cell Cycle Group  

  • 1990.04
    -
    1991.03

    Harvard Medical School/Massachusetts Eye and Ear Infirmary   Howe Laboratory, Dr Dryja's group   Research fellow

Graduate School 【 display / non-display

  • 1990.04
    -
    1995.03

    Kyoto Prefectural University of Medicine  Graduate School, Division of Medicine 

Graduating School 【 display / non-display

  • 1982.04
    -
    1988.03

    Kyoto Prefectural University of Medicine   Faculty of Medicine  

 

Published Papers 【 display / non-display

  • Visualization of quantitative lipid distribution in mouse liver through near-infrared hyperspectral imaging

    Okubo Kyohei, Kitagawa Yuichi, Hosokawa Naoki, Umezawa Masakazu, Kamimura Masao, Kamiya Tomonori, Ohtani Naoko, Soga Kohei

    BIOMEDICAL OPTICS EXPRESS  12 ( 2 ) 823 - 835 2021.02  [Refereed]

    DOI PubMed

  • The mechanism of SASP in obesity-associated liver tumor microenvironnment

    Yamagishi Ryota, Kamachi Fumitaka, Cheng Yi, Hara Eiji, Ohtani Naoko

    CANCER SCIENCE  112   488 - 488 2021.02  [Refereed]

  • Metabolism in Cancer

    Nakayama Keiichi, Ohtani Naoko

    CANCER SCIENCE  112   1030 - 1030 2021.02  [Refereed]  [Invited]

  • Gut microbial metabolite and obesity-associated liver cancer

    Ohtani Naoko, Kamiya Tomonori, Kamachi Fumitaka, Yamagishi Ryota

    CANCER SCIENCE  112   1031 - 1031 2021.02  [Refereed]

  • A selective BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells

    Wakita Masahiro, Takahashi Akiko, Ohtani Naoko, Hara Eiji

    CANCER SCIENCE  112   554 - 554 2021.02  [Refereed]

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Review Papers (Misc) 【 display / non-display

  • Obesity and intestinal microbiota

    250 ( 9 ) 871 - 873 2014.08

Conference Activities & Talks 【 display / non-display

  • Gut microbiota and Liver disease: Hepatic encephalopathy

    OHTANI Naoko  [Invited]

    Annual Meeting of the Japanese Society of Toxicology  2021  The Japanese Society of Toxicology

     View Summary

    <p>The gut microbiota influences liver function through intestinal absorption and the subsequent transfer of their metabolites to the liver. This relationship, called "gut-liver axis", is therefore important in liver diseases. Hepatic encephalopathy (HE) is an end-stage clinical feature of liver cirrhosis (LC) caused by hyperammonaemia and the resulting neuropsychiatric disorders. Ammonia, a neurotoxic substance that can cross the blood-brain barrier, is produced abundantly by gut microbiota. Excess ammonia is normally converted into urea in hepatocytes. However, liver malfunction and the portosystemic shunts in LC patients cause a direct influx of ammonia into the systemic circulation, resulting in hyperammonaemia and neuropsychiatric disorders. However, species causing hyperammonaemia in HE patients remain unknown. In this study, we aimed to identify specific gut microbial species responsible for hyperammonaemia in HE patients, focusing on the responses to a non-absorbable antibiotic, rifaximin (RFX). We compared the faecal gut microbial profiles of healthy control and HE patients by 16S rRNA gene amplicon sequencing. We used linear discriminant analysis effect size (LEfSe) to identify species, and verified their function in vivo in mouse LC model. We found that urease-positive gut bacterial species, which is known to originally reside in oral cavity, is responsible for hyperammonaemia in RFX-responders, suggesting that these bacterial species transfer to the intestine through breaking stomach acid barrier due to the medication of proton pump inhibitors.</p><p></p>

    CiNii

  • Gut-Liver axis-mediated mechanism of obesity-associated hepatocellular carcinoma development

    Fumitaka Kamachi1 Ryota Yamagishi1, Masaru Nakamura3, Shota Yamazaki3, Yoshiki Nonaka1, Wei-Yu Chen4, Yoshimi Yukawa1,2, Norifumi Kawada1,2, Susumu Nakae5, Eiji Hara6 and Naoko Ohtani1

    2019 Cold Spring Harbor Asia Conference LIVER, BIOLOGY, DISEASES & CANCER   2019.12 

  • The Mechanism of Obesity-associated Liver Cancer Progression

    Naoko Ohtani  [Invited]

    The 50th Commemorial International Symposium of The Princess Takamatsu Cancer Research Fund New Horizons for Cancer Research and Precision Medicine  2019.11 

  • The Role of Gut Microbiota in Anti-tumor Immunity in Liver Tumor Microenvironment

    Naoko Ohtani  [Invited]

    JSH International Liver Conference 2019 “Liver Cirrhosis and Portal Hypertension: Modern Pathophysiology and Emerging Therapies” Session V : Gut-Liver Axis in Cirrhosis and Portal Hypertension   2019.10 

  • The role of cellular senescence and SASP in tumor microenvironment ofobesity-associated liver cancer

    Naoko Ohtani  [Invited]

    The 19th Scientific meeting of the Japanese Society of Anti-Aging Medicine International Joint Symposium   2019.06 

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Other international activities 【 display / non-display

  • Period :

    1990.04
    -
    1991.03

    Contents of activities : I joined Prof. Thaddeus P. Dryja's lab as a research fellow. We found germ line mutations in the ATF and SP1 sites in the promoter region from the DNA of two RB family patients, where they have important promoter activity. We published these results in Nature.

    USA