The Keio Journal of Medicine
Online ISSN : 1880-1293
Print ISSN : 0022-9717
ISSN-L : 0022-9717
55 巻, 2 号
選択された号の論文の4件中1~4を表示しています
REVIEWS
  • 1. Reflections on the state of medical education in Japan
    R Harsha Rao
    2006 年 55 巻 2 号 p. 41-51
    発行日: 2006年
    公開日: 2006/07/14
    ジャーナル フリー
    The current shortcomings in Japanese medical education are highlighted by identifying four major areas of concern, based on the author’s personal observations at Keio University Hospital. The first of these is a woeful lack of clinical skills among Japanese medical students and residents. This lack springs directly from the complete absence of any bedside clinical instruction, which constitutes the second area of concern. The third is the attitude of faculty towards teaching as a burden that detracts and diverts them from their primary goal of academic advancement through research. Finally, there is no recognition of the value of a problem-based approach to teaching clinical medicine, so that clinical problem-solving skills have atrophied to the point of near-extinction in the current generation of Japanese physicians. The promise of problem-based learning (PBL) provides a crucial starting point for efforts to change the system. PBL emphasizes the importance of an integrated approach to clinical problems, and a reliance on critical thinking — the basis of primary care. This contrasts with the selective and highly specialized approach to disease, and reliance on sophisticated technology, which are hallmarks of specialty care. The effort to reform medical education will fail without visionary leadership and without the willingness to confront the truth, as unpleasant as it may seem to be. Both these crucial elements exist at Keio University at this critical juncture. It is this happy confluence that emboldens the author to hope that the future of reform is in good hands at this august institution.
  • Yuichi Hirose, Kazunari Yoshida
    2006 年 55 巻 2 号 p. 52-58
    発行日: 2006年
    公開日: 2006/07/14
    ジャーナル フリー
    Gliomas are the most common primary brain tumor, and are histopathologically classified according to their cell type and the degree of malignancy. However, sometimes diagnosis can be controversial, and tumors of the same entity possibly have a wide range of survival. Genetic analysis of these tumors is considered to have great importance in terms that it can provide clinically relevant classification of the tumors and compensate for the limitation of the histological classification. Previous studies using comparative genomic hybridization (CGH) demonstrated that copy number aberrations (CNAs) were frequently recognized in these tumors, and revealed that a gain on chromosomal arm 7q was the most common CNA in diffuse astrocytomas, whereas a small population of the tumor showed losses on 1p/19q which characterizes oligodendrogliomas with good responsiveness to chemotherapeutic regime using procarbazine, nitrosourea and vincristine. High grade (malignant) gliomas (i.e. anaplastic astrocytomas, anaplastic oligodendrogliomas and glioblastomas) have been reported to have a gain on 7p and losses on 9p and 10q. In case of ependymomas, frequent chromosomal aberrations in intracranial tumors were a gain on 1q and losses on 6q, and, on the other hand, a gain on chromosome 7 was recognized almost exclusively in spinal cord tumors. These data suggest that intracranial and spinal cord ependymomas are different genetic diseases and comprise different subgroups within one histological entity. In conclusion, genetic analysis of gliomas may help to classify these tumors and provide leads concerning their initiation and progression. The relationship of these aberrations to patient outcome needs to be addressed.
  • Eva Carro, Ignacio Torres-Aleman
    2006 年 55 巻 2 号 p. 59-63
    発行日: 2006年
    公開日: 2006/07/14
    ジャーナル フリー
    Insulin-like growth factor I (IGF-I) is present at high concentrations in the circulation. Tissue-specific genetic ablation has shown that the majority of serum IGF-I is secreted by liver cells, although all major organs synthesize it. IGF-I is an important signal during development, including brain growth. Although the biological role of IGF-I in organs such as muscle or ovary is reasonably well established, its biological significance in the adult brain is far from clear. In this regard, while local IGF-I synthesis decreases during brain development, protein levels remain relatively constant throughout life until old age, where a decline is found, not only in the brain but also in the blood-stream. This mismatch between declining local synthesis early after birth and steady protein levels may be explained by the ability of serum IGF-I to access the brain across the blood-brain-barrier. This peripheral IGF-I input to the brain is a physiologically meaningful process of potential impact in brain diseases. Numerous brain mechanisms are regulated by serum IGF-I. Many of these, such as cell energy modulation or growth and survival are common to other IGF-I target tissues but there are also a number of brain-specific mechanisms regulated by IGF-I which likely underlie the ability of serum IGF-I to modulate the major function of the brain: cognition. We propose that serum IGF-I forms part of the mechanisms involved in the “cognitive reserve” concept of brain responses to homeostasis breakdown. Based on IGF-I pleiotropy not only in brain but elsewhere, we consider that loss of IGF-I function is an important step towards disease.
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