医学部

Hidemi Teramoto

  (寺本 英已)

Profile Information

Affiliation
School of Medicine, Fujita Health University
Degree
医学博士

J-GLOBAL ID
200901094089601510
researchmap Member ID
6000019626

Papers

 30
  • Hidemi Teramoto, Kazuya Shiogama, Yasuyoshi Mizutani, Ken-ichi Inada, Toshio Kamahora, Masanao Makino, Yutaka Tsutsumi
    JOURNAL OF CLINICAL MICROBIOLOGY, 49(9) 3358-3360, Sep, 2011  Peer-reviewed
    The hepatitis C virus (HCV) outbreak that occurred between 1940 and 1999 in a closed leprosy sanatorium located on a small island in Japan was analyzed. The analysis of 318 nucleotides in the NS5B region of HCV allowed us to establish the existence of at least three different HCV strains in this sanatorium.
  • Kazuya Shiogama, Hidemi Teramoto, Yukiko Morita, Yasuyoshi Mizutani, Ryoichi Shimomura, Ken-ichi Inada, Toshio Kamahora, Masanao Makino, Yutaka Tsutsumi
    JOURNAL OF MEDICAL VIROLOGY, 82(4) 556-561, Apr, 2010  Peer-reviewed
    Oku-Komyo-En is one of the national leprosy sanatoria, located on a small island in Setouchi city, Okayama prefecture of Japan since 1938. Since autopsies were carried out routinely on almost all patients who had died in the sanatorium up to 1980, approximately 1,000 formalin-fixed autopsy tissue samples were available for analysis. When these samples were reviewed, the pathological data indicated a sharp rise in the death rate caused by cirrhosis of the liver and hepatocellular carcinoma (HCC) since 1960 and 1970, respectively. Hepatitis C virus (HCV) infection is a common cause of HCC in Japan. The presence of HCV RNA was demonstrated in paraffin sections prepared from the autopsied liver tissue fixed in formalin for a prolonged period of time, by employing nested RT-PCR using type-specific primers. The data showed that HCV RNA was detectable in samples of the liver archived as early as 1940, representing the liver tissues kept in formalin for up to 67 years. HCV genotypes 1b and 2a were found by RT-PCR at 85.7% and 14.3%, respectively, in patients with leprosy. J. Med. Virol. 82:556-561,2010. (C) 2010 Wiley-Liss, Inc.
  • Hidemi Teramoto, Hiroaki Mizuno, Hideto Yogo, Shinji Hori, Shinsuke Nakayama
    JOURNAL OF THE AMERICAN GERIATRICS SOCIETY, 57(10) 1965-1966, Oct, 2009  Peer-reviewed
  • H. Teramoto, H. Miwa, V. Patel, N. Letwin, M. D. Castellone, N. Imai, M. Shikami, A. Imamura, J. S. Gutkind, M. Nitta, N. H. Lee
    CLINICAL AND LABORATORY HAEMATOLOGY, 28(4) 262-266, Aug, 2006  
    This is a case report of granulocytic sarcoma occurring as a nasal lesion prior to the onset of acute myelogenous leukaemia (AML). To understand this case in more detail, we used 40 000 human cDNA microarray to identify the gene expression patterns of nonleukaemic stage bone marrow (BM), AML stage BM and AML stage peripheral blood cells and subsequently define the molecular basis of this disease progression. Of significance, we have tracked the expression profile of BM samples during the course of nonleukaemic to leukaemic progression, and identified a number of genes that may account for the growth potential of leukaemia cells and indicate poor prognosis of this case.
  • MD Castellone, H Teramoto, BO Williams, KM Druey, JS Gutkind
    SCIENCE, 310(5753) 1504-1510, Dec, 2005  Peer-reviewed
    How cyclooxygenase-2 (COX-2) and its proinflammatory metabolite prostaglandin E2 (PGE2) enhance colon cancer progression remains poorly understood. We show that PGE2 stimulates colon cancer cell growth through its heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor, EP2, by a signaling route that involves the activation of phosphoinositide 3-kinase and the protein kinase Akt by free G protein beta gamma subunits and the direct association of the G protein a. subunit with the regulator of G protein signaling (RGS) domain of axin. This leads to the inactivation and release of glycogen synthase kinase 3 beta from its complex with axin, thereby relieving the inhibitory phosphorytation of beta-catenin and activating its signaling pathway. These findings may provide a molecular framework for the future evaluation of chemopreventive strategies for colorectal cancer.

Misc.

 2
  • Maria Domenica Castellone, Hidemi Teramoto, J. Silvio Gutkind
    CANCER RESEARCH, 66(23) 11085-11088, Dec, 2006  
    Colorectal cancer poses a major clinical challenge in the developed world where this disease is common. Recent findings suggest that the prostaglandin E-2, the proinflammatory product of elevated cyclooxygenase-2 activity in colon cancer, stimulates cancer cell growth through a G protein-dependent signaling pathway coupling the prostaglandin EP2 receptor to beta-catenin control. These findings provide new insights into the molecular framework needed to evaluate chemopreventive strategies for colorectal cancer.
  • JS Gutkind, P Crespo, NZ Xu, H Teramoto, OA Coso
    LIFE SCIENCES, 60(13-14) 999-1006, Feb, 1997  
    m1 and m2 receptors are traditionally linked to tissue specific functions performed by fully differentiated cells. However, these receptors have been also implicated in growth stimulation. The mechanisms whereby these receptors regulate proliferative signaling pathways are still poorly understood. Furthermore, pharmacological evidence suggest that many growth promoting agents act on G(i) coupled receptors, but there is no formal proof that induction of DNA-synthesis results from decreased intracellular levels of cAMP. In our laboratory, we have used the expression of m1 and m2 receptors as a model for studying proliferative signaling through G protein-coupled receptors. Currently available evidence suggest that these receptors signal to distinct members of the MAP kinase superfamily, MAP kinase and JNK, through beta gamma subunits of heterotrimeric G proteins acting, respectively, on a Ras and Rac1 dependent pathway.