28 research outputs found

    Muscle-specific tyrosine kinase-antibody-positive myasthenic crisis with detailed electrophysiologic studies.

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    A 69-year-old male who presented in a coma due to sudden respiratory arrest was transferred to our hospital. After endotracheal intubation with manual ventilation, he became alert and his neurologic findings were within the normal range, except for palsy of the respiratory muscles. Biochemical analyses of the blood and brain computed tomography failed to indicate the cause of the respiratory arrest. An edrophonium test did not improve the respiratory arrest. An urgent electromyogram at the dorsal interossei, biceps, and sternocleidomastoideus muscle and a repetitive nerve stimulation test at the trapezius and deltoid muscle were also negative on the first hospital day. However, on the 16th day in the hospital, a repetitive nerve stimulation test at the levator labii superioris alaeque nasi showed a waning phenomenon. This result indicated a diagnosis of myasthenia gravis. Anti.muscle-specific tyrosine kinase antibody was found to be positive. After treatment with plasmapheresis and prednisolone, he regained normal respiratory function. Anti.muscle-specific tyrosine kinase (MuSK)-antibodypositive myasthenia gravis (MG) (MuSK-MG) tends to be associated with a lower incidence of a positive edrophonium test, a lower incidence of a positive electrophysiologic study excluding the face, and a higher incidence of respiratory failure in comparison to anti.acetylcholine receptors (AchR)-antibody-positive MG (AchR-MG). Respiratory failure is curable with treatment. Accordingly, in addition to obtaining a precise diagnosis, an emergency physician should recommend an electrophysiologic study including the face to make a differential diagnosis for respiratory arrest when biochemical and radiologic studies fail to indicate the cause of the respiratory arrest

    Results and Issues in Student Teaching Program for Freshman at Okayama University on 2011

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    本研究の目的は,岡山大学教育学部における1年次の教育実習プログラムの成果と課題の検討であった。そのため,平成23年度の教育実習Ⅰ受講生294名を対象に実習後に調査を行った。その結果,(1)教育実践力を構成する4つの力や附属学校園における実習目的の多くが達成されている,(2)4つの力のうち「コーディネート力」「生徒指導力」の達成度が特に高く,「学習指導力」の学校種ごとの学習指導の特徴や違いを説明することは達成度が低い,(3)附属学校園が掲げる目的のうち,観察して学ぶことの達成度が高いが,実際に児童生徒 と関わって学ぶことの達成度は低い傾向である,(4)実習中の実習生の取り組みに関しては,授業観察において事実を観察,記録することは取り組めているが,解釈的な授業観察や,協議会での発言は十分取り組めていない,の4点が主に示唆され,実習Ⅰの課題や不安に対する学生の自由記述と併せて結果が考察された

    Dietary Ceramide Prepared from Soy Sauce Lees Improves Skin Barrier Function in Hairless Mice

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    Dietary sphingolipids such as glucosylceramide and sphingomyelin are known to improve the skin barrier function of damaged skin. In this study, we focused on free-ceramide prepared from soy sauce lees, which is a byproduct of soy sauce production. The effects of dietary soy sauce lees ceramide on the skin of normal mice were evaluated and compared with those of dietary maize glucosylceramide. We found that transepidermal water loss value was significantly suppressed by dietary supplementation with soy sauce lees ceramide as effectively as or more effectively than maize glucosylceramide. Although the content of total and each subclass of ceramide in the epidermis was not significantly altered by dietary sphingolipids, that of 12 types of ceramide molecules, which were not present in dietary sources, was significantly increased upon ingestion of maize glucosylceramide and showed a tendency to increase with soy sauce lees ceramide intake. In addition, the mRNA expression of ceramide synthase 4 and involucrin in the skin was downregulated by sphingolipids. This study, for the first time, demonstrated that dietary soy sauce lees ceramide enhances skin barrier function in normal hairless mice, although further studies are needed to clarify the molecular mechanism

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    Haploinsufficiency of akt1 prolongs the lifespan of mice.

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    There is increasing evidence that nutrient-sensing machinery is critically involved in the regulation of aging. The insulin/insulin-like growth factor-1 signaling pathway is the best-characterized pathway with an influence on longevity in a variety of organisms, ranging from yeast to rodents. Reduced expression of the receptor for this pathway has been reported to prolong the lifespan; however, the underlying mechanisms are largely unknown. Here we show that haploinsufficiency of Akt1 leads to an increase of the lifespan in mice. Akt1 (+/-) mice had a lower body weight than their littermates with less fat mass and normal glucose metabolism. Ribosomal biogenesis and the mitochondrial DNA content were significantly reduced in these mice, along with a decrease of oxidative stress. Consistent with the results obtained in mice, inhibition of Akt-1 promoted longevity in nematodes (Caenorhabditis elegans), whereas activation of Akt-1 shortened the lifespan. Inhibition of Akt-1 led to a decrease of ribosomal gene expression and the mitochondrial DNA content in both human cells and nematodes. Moreover, deletion of ribosomal gene expression resulted in a decrease of the mitochondrial DNA content and normalized the lifespan shortened by Akt-1 activation in nematodes. These results suggest that an increase of mitochondrial amount and energy expenditure associated with enhanced protein synthesis accelerates both aging and the onset of age-associated diseases
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