巻号一覧
56 巻, 1 号
選択された号の論文の4件中1～4を表示しています
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REVIEWS
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4. A "global" dimension to reform at Keio UniversityR Harsha Rao2007 年 56 巻 1 号 p. 1-13
発行日: 2007年
公開日: 2007/04/11
ジャーナル フリーKeio University School of Medicine is awakening to the realization that it will achieve international recognition as a center of excellence in medical education and healthcare only by inculcating clinical skills and critical thinking in its medical graduates. A new "global" perspective identifies the traditional failure of Japanese medical education to provide its graduates with clinical skills training as the root cause of a number of deficiencies. These include (i) the reluctance of Japanese medical graduates to seek global experience; (ii) the absence of interest in the global healthcare marketplace for Japanese medical graduates as potential recruits; (iii) the failure to incorporate globally accepted innovations, like problem-based learning, in Japanese medical education; (iv) the failure to follow globally accepted standards of clinical practice in Japan; (v) the lack of instruction in general internal medicine in Japan; and (vi) the neglect of evidence-based medicine in Japanese healthcare practice. Keio University is embarking on an ambitious effort that commits both the will and resources necessary to reform medical education at Keio in accordance with global norms. The initiatives currently underway include (i) incorporating PBL into the curriculum to foster active learning, (ii) implementing measures to promote interactive teaching techniques among the faculty, and (iii) granting recognition to teachers through new promotion policies. Wider implementation of these initiatives across the country will enable Japanese healthcare and Japanese physicians to occupy their rightful place of respect in the global healthcare market, comparable to the widespread international recognition given to Japanese medical researchers.抄録全体を表示PDF形式でダウンロード (408K) -
Nicholas O. Davidson2007 年 56 巻 1 号 p. 14-20
発行日: 2007年
公開日: 2007/04/11
ジャーナル フリーColorectal cancer (CRC) is among the most prevalent and preventable forms of cancer worldwide, accounting for over 600,000 deaths in 2005. Both genetic and environmental factors contribute to cancer etiology and estimates suggest that at least one third of CRC has a familial component. There is increased awareness of a strong genetic component to CRC risk, with the identification of several high penetrance alleles that predict increased CRC susceptibility. These include familial adenomatous polyposis (FAP), linked to mutations or deletions of the APC tumor suppressor gene, as well as Lynch syndrome (formerly known as hereditary non-polyposis colorectal cancer or HNPCC), which is linked to mutations or deletions of one or more mismatch repair genes including MLH1, MSH2 and MSH6. In addition, mutations in genes encoding key signaling molecules have been linked to autosomal dominant hamartomatous syndromes that are associated with increased susceptibility to CRC. These include Peutz-Jeghers syndrome, which is linked to mutations in STK11/LKB and Juvenile polyposis, which is linked to mutations in the genes encoding SMAD4 and BMPR1A. In addition to these high penetrance autosomal dominant alleles, recessive mutations in the MYH mismatch repair gene are associated with a phenotype similar to FAP. With the widespread availability of genetic testing for these alleles, physicians will be faced with a complex array of choices in terms of advocating who should be tested, when should such testing take place, how it should be conducted and interpreted and why it changes the management and outcomes for the patient and his or her family.抄録全体を表示PDF形式でダウンロード (333K) -
Mayumi Kawada, Yuriko Hachiya, Atsuko Arihiro, Emiko Mizoguchi2007 年 56 巻 1 号 p. 21-27
発行日: 2007年
公開日: 2007/04/11
ジャーナル フリーIt has been hypothesized that dysregulated host/microbial interactions play a pivotal role in the pathogenesis of inflammatory bowel disease. However, the exact mechanisms underlying the induction and perpetuation of the intestinal disorder are unclear. Recently, we unexpectedly discovered significantly upregulated gene expression of chitinase 3-like-1 in inflamed colon of the dextran sulfate sodium-induced colitis model by employing the DNA-microarray analysis. Chitinase 3-like-1 has a chitin binding ability, but lacks the enzymatic activity of lysing microbial cell wall. Chitinase 3-like-1 protein is mainly expressed in colonic epithelial cells and macrophages in the inflamed colon of dextran sulfate sodium-induced colitis. Chitinase 3-like-1, which can be upregulated after pro-inflammatory cytokine stimulation, possesses an ability to enhance the adhesion and internalization of intracellular bacteria into colonic epithelial cells. Most importantly, in vivo neutralization of chitinase 3-like-1 significantly suppressed the development of dextran sulfate sodium-induced colitis by dramatically decreasing the bacterial adhesion and invasion into colonic epithelial cells. Furthermore, anti-chitinase 3-like-1 antibody-treated mice exhibited a significantly lower load of Salmonella typhimurium in peripheral organs as compared to control rabbit IgG-treated mice. Recently, it has been reported that acidic mammalian chitinase is expressed in the setting of T helper-2-associated inflammation and subsequently induces airway hyperresponsiveness in allergic asthma patients. In addition, pan-chitinase inhibitor significantly ameliorates T helper-2-mediated inflammation and airway hypersensitivity. These studies provide to be a novel insight into the physiological role of mammalian chitinases in host/microbial interactions, and inhibition of chitinase activity would be considered a novel therapeutic strategy of allergic and inflammatory disorders.抄録全体を表示PDF形式でダウンロード (654K)
ORIGINAL ARTICLE
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Kazuhiro Kawanabe, Akira Kawashima, Issei Sashimoto, Tsuyoshi Takeda, ...2007 年 56 巻 1 号 p. 28-33
発行日: 2007年
公開日: 2007/04/11
ジャーナル フリーThe present study was conducted to determine the beneficial effect of whole-body vibration (WBV) exercise in addition to muscle strengthening, balance, and walking exercises on the walking ability in the elderly. Sixty-seven elderly participants were divided into two groups; the WBV exercise plus routine exercises group (n=40) and the routine exercises alone group (n=27). WBV exercise was performed on a Galileo machine (Novotec, Pforzheim, Germany) at an intensity of 12-20 Hz, for a duration of 4 minutes, once every week. All the participants in both the groups were similarly instructed to undergo routine exercises such as balance and muscle strengthening trainings, and take walking exercise twice a week. The period of this study was 2 months to evaluate the acute effects of WBV exercise. The mean age of the participants was 72.0 years (range, 59-86 years). At baseline, there were significant negative correlations between age and the walking speed, step length, and maximum standing time on one leg. After the 2-month exercise program, the walking speed, step length, and the maximum standing time on one leg were significantly improved in the WBV exercise plus routine exercises group, while no significant changes in these parameters were observed in the routine exercises alone group. Thus, the present study showed the beneficial effect of WBV exercise in addition to muscle strengthening, balance, and walking exercises in improving the walking ability in the elderly. WBV exercise was safe and well tolerated in the elderly.抄録全体を表示PDF形式でダウンロード (560K)
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