The Keio Journal of Medicine
Online ISSN : 1880-1293
Print ISSN : 0022-9717
ISSN-L : 0022-9717
Volume 62, Issue 3
Displaying 1-3 of 3 articles from this issue
REVIEW
  • Geoffrey Burnstock
    2013 Volume 62 Issue 3 Pages 63-73
    Published: 2013
    Released on J-STAGE: September 25, 2013
    JOURNAL FREE ACCESS
    The article begins with a review of the main conceptual steps involved in the development of our understanding of purinergic signalling, including non-adrenergic, non-cholinergic (NANC) neurotransmission; identification of ATP as a NANC transmitter; purinergic cotransmission; recognition of two families of purinoceptors [P1 (adenosine) and P2 (ATP/ADP)]; and, later, cloning and characterisation of P1 (G protein-coupled), P2X (ion channel) and P2Y (G protein-coupled) receptor subtypes. Further studies have established the involvement of ATP in synaptic neurotransmission in both ganglia and in the central nervous system; long-term (trophic) purinergic signalling in cell proliferation, differentiation and death occurring in development and regeneration; and short-term purinergic signalling in neurotransmission, neuromodulation and secretion. ATP is released from most cell types in response to gentle mechanical stimulation and is rapidly degraded to adenosine by ecto-nucleotidases. This review then focuses on the pathophysiology of purinergic signalling in a wide variety of systems, including urinogenital, cardiovascular, airway, musculoskeletal and gastrointestinal. Consideration is also given to the involvement of purinoceptors in pain, cancer and diseases of the central nervous system. Purinergic therapeutic approaches for the treatment of some of these diseases are discussed.
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  • Masaki Ieda
    2013 Volume 62 Issue 3 Pages 74-82
    Published: 2013
    Released on J-STAGE: September 25, 2013
    Advance online publication: June 21, 2013
    JOURNAL FREE ACCESS
    In the field of developmental biology, the concept that cells, once terminally differentiated, are fixed in their cell fate was long believed to be true. However, Dr. Gurdon and colleagues challenged this fundamental doctrine and demonstrated that cellular reprogramming and cell fate conversion are possible by somatic nuclear transfer and cell fusion. The Weintraub laboratory discovered in the 1980s that a single transcription factor, MyoD, can convert fibroblasts into skeletal muscle cells, and subsequent studies also demonstrated that several transcription factors are lineage converting factors within the blood cell lineage. In 2006, Takahashi and Yamanaka discovered that transduction of the four stem cell-specific transcription factors Oct4, Sox2, Klf4, and c-Myc can reprogram mouse fibroblast cells into a pluripotent state. In 2007, they demonstrated that the same four factors similarly reprogram human somatic cells into pluripotent stem cells. These discoveries by Dr. Yamanaka and colleagues fundamentally changed research in the fields of disease modeling and regenerative medicine and also inspired the next stage of cellular reprogramming, i.e., the generation of desired cell types without reverting to stem cells by overexpression of lineage-specific transcription factors. Recent studies demonstrated that a diverse range of cell types, such as pancreatic β cells, neurons, neural progenitors, cardiomyocytes, and hepatocytes, can be directly induced from somatic cells by combinations of specific factors. In this article, I review the pioneering works of cellular reprogramming and discuss the recent progress and future perspectives of direct reprogramming technology.
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ORIGINAL ARTICLE
  • Atsuhiko Murata, Kohji Okamoto, Shinya Matsuda, Kazuaki Kuwabara, Yuka ...
    2013 Volume 62 Issue 3 Pages 83-94
    Published: 2013
    Released on J-STAGE: September 25, 2013
    Advance online publication: August 05, 2013
    JOURNAL FREE ACCESS
    Little information is available on the factors influencing length of stay (LOS) in hospital and medical costs during hospitalization associated with cholecystectomy for acute cholecystitis. We determined the independent factors affecting LOS and medical costs of patients who underwent cholecystectomy for acute cholecystitis based on data from the Diagnosis Procedure Combination (DPC) database. In 2008, a total of 2176 patients with acute cholecystitis were referred for cholecystectomy to 624 hospitals in Japan. We collected patient characteristics and data on treatments for acute cholecystitis using the DPC database and identified independent factors affecting LOS and medical costs during hospitalization using multiple linear regression models. Analysis revealed that early cholecystectomy was significantly associated with a decrease in LOS, whereas longer preoperative antimicrobial therapy was significantly associated with an increase of LOS: the standardized coefficient for early cholecystectomy was −0.372 and that for preoperative antimicrobial therapy was 0.353 (P < 0.001). These procedures were also significant independent factors with regard to medical costs during hospitalization: the standardized coefficient for early cholecystectomy was −0.391 and that for preoperative antimicrobial therapy was 0.335 (P < 0.001). Early cholecystectomy significantly reduces the LOS and medical costs of cholecystectomy for acute cholecystitis, while preoperative antimicrobial therapy increases LOS and medical costs during hospitalization. These results highlight the need for health care implementations such as promotion of early cholecystectomy, appropriate use of antimicrobial drugs, and centralization of patients with cholecystectomy for acute cholecystitis in Japan.
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