Journal of The Society of Japanese Women Scientists
Online ISSN : 2186-3776
Print ISSN : 1349-4449
ISSN-L : 1349-4449
Volume 12, Issue 1
Displaying 1-5 of 5 articles from this issue
Review
  • Miwa Sugiura
    Article type: Review
    2012 Volume 12 Issue 1 Pages 1-10
    Published: 2012
    Released on J-STAGE: July 03, 2012
    JOURNAL FREE ACCESS
    Photosynthetic organisms such as plants and cyanobacteria convert light energy to chemical energy efficiently by photosynthetic electron transfer accompanied by water oxidation. Elucidation of their molecular mechanisms must be a very important subject not only for general scientific interest but also for helping to find solutions to energy and environmental problems. However, molecular mechanisms of photosynthesis, especially water oxidation for electron donation and regulation mechanisms of cofactors relating to the electron transfer in Photosystem II, are not yet clear. In this review, we interpret the structure of Photosystem II and the electron transfer system based on the redox potential of cofactors and water oxidation mechanisms. Furthermore, we introduce application research for energy reproduction by using Photosystem II.
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  • Miki Nagase
    Article type: Review
    2012 Volume 12 Issue 1 Pages 11-21
    Published: 2012
    Released on J-STAGE: July 03, 2012
    JOURNAL FREE ACCESS
    Aldosterone is traditionally viewed as a hormone regulating the homeostasis of electrolytes, body fluid volume, and blood pressure. Recently, aldosterone emerged as a deleterious hormone in the cardiovascular and renal system. We examined whether the aldosterone/mineralocorticoid receptor (MR) system is involved in the process leading from metabolic syndrome to kidney disease. We demonstrated that SHR/cp, a rat model of metabolic syndrome, was susceptible to podocyte injury, proteinuria, and chronic kidney disease. Aldosterone excess caused by adipocyte-derived aldosterone releasing factors was suggested to underlie the nephropathy, and MR antagonist ameliorated the injury. High salt reduced plasma aldosterone, but paradoxically augmented MR activation and exacerbated cardiac and renal injury, which was mitigated by MR antagonist. These findings corroborate our hypothesis that obesity and salt, two cardinal features of modern society, cause MR overactivation and cardiorenal diseases. Furthermore, we identified an alternative pathway of MR activation by Rac1 GTPase. RhoGDIα knockout mice, a kidney-specific Rac1 activation model, developed albuminuria, podocyte damage, and glomerulosclerosis. The knockout mice exhibited enhanced MR signaling despite normoaldosteronemia, and MR antagonist dramatically abrogated renal impairment. Importantly, Rac-sepcific inhibitor substantially ameliorated renal injury, concomitantly with repression of Rac1 and MR activity.
    In vitro transfection studies provided direct evidence of Rac1-mediated MR activation. The “Rac1-mediated MR activation” was also critically involved in angiotensin II/salt-induced nephropathy, Dahl salt-sensitive hypertension, and oxidative stress-evoked cardiac injury. In conclusion, our findings suggest that MR activation plays a pivotal role in the pathogenesis of chronic kidney disease in metabolic syndrome, and that MR may be activated both aldosterone dependently (via aldosterone releasing factors) and independently (via Rac1). MR antagonists, or agents that modulate MR activity such as Rac inhibitors, are promising renoprotective drugs in metabolic syndrome, although long-term effects
    on renal outcomes, mortality, and safety need to be established.
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  • Misao Owada, Teruo Kitagawa
    Article type: Review
    2012 Volume 12 Issue 1 Pages 22-31
    Published: 2012
    Released on J-STAGE: July 03, 2012
    JOURNAL FREE ACCESS
    Type 1 diabetes mellitus (insulin dependent diabetes mellitus,IDDM) occurs mainly in childhood, however, the management of type 1 diabetes had been poor in Japan until the 1980s because of a low incidence of this disease and a subsequent lack of medical knowledge about it. In 1979, the international pediatric association for diabetes mellitus named ISGD (international study group on diabetes in children and adolescents) invited Dr. Teruo Kitagwa a Japanese pediatrician who works in this field to join them. He explained about diabetes in Japanese children. After international communication became common in Japanese pediatricians who were interested in diabetes, Japanese pediatricians were able to get new and useful information about type 1 diabetes from Western countries where type 1 diabetes is common. As a result, the prognosis of type 1 diabetes in children started getting better in the late 1990s in Japan. However, from a urine screening program , we found that the incidence of type 2 diabetes, one of the most common metabolic disorders usually appearing in the 4th or 5th decade of life, is not unusual in Japanese children. Patients with type 2 diabetes are detected by a urine glucose test of asymptomatic school children. This screening was started in the Tokyo area in 1974 and from 1992, the Ministry of Education made this screening mandatory for all school children. Currently in Japan the incidence of childhood type 2 diabetes is higher than type 1 diabetes. In this paper we describe the development of the clinical studies of both type 1 and type 2 diabetes in Japanese children during past 40 years in Japan
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Original Paper
  • Mikiko Abe, Eriko Oshima, Shota Sakai, Yoshio Hirabayashi, Tetsuya Tsu ...
    Article type: Original Paper
    2012 Volume 12 Issue 1 Pages 32-43
    Published: 2012
    Released on J-STAGE: July 03, 2012
    Advance online publication: February 28, 2012
    JOURNAL FREE ACCESS
    We analyzed hair lipids focusing on sphingolipids of murine hair. Murine hair contains ceramides (Cer), glucosylceramides (GlcCer) and sphingomyelins (SM). Composition and structure of murine hair sphingolipids are different from those of epidermal sphingolipids. Cer of murine hair has little acylCer, which is a key molecule of the epidermal barrier, and a small amount of Cer with -hydroxy acids (OH) which are rich in the epidermis. The major molecule of murine hair Cer was C20:0/d18:0. Both whole hairs (including follicles) and hair shafts have GlcCer but little or no acylGlcCer. The major FA of hair GlcCer were C18 molecules. GlcCer carrying long chain OHFA (chain length more than 20) were detected in whole hairs, whereas these OHGlcCer were rarely in the shaft. Whole hairs have SM, but hair shafts have little SM, indicating that SM is a component of hair follicular cells in the wild mice. The major FA of hair SM were C16:0, C18:0, C24:0 and C16h:0. In hairs, the metabolic pathways and functions of Cer, GlcCer and SM may be different from each other.
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