Shigakkan University
Obu, Japan

Shigakkan University is a private university in Ōbu, Aichi, Japan. Until the school renamed itself to Shigakkan in 2010, the school was known as Chukyo Women's University. The school was founded in 1905.Despite that the name contained the word "women," the school had accepted male students since 1998. Wikipedia.

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Background: Basketball is one of the most popular sports in the world. However, men’s national teams of Asian countries have not performed well at world-level competitions such as Olympic and world cup games. Clarifying the feature of Asian basketball games would be some help to improve the competitiveness of Asian teams. Objectives: This study aimed to identify game-related statistics which discriminate between winning and losing teams in Asian men’s basketball competitions. In addition, European competitions were also analyzed and the results were compared between Asian and European competitions. Methods: A total of 179 games from the 2011, 2013 and 2015 FIBA Asia Championships were analyzed for Asian competitions, and a total of 259 games from the 2011, 2013 and 2015 FIBA EuroBasket were analyzed for European competitions. All games were classified into three types (balanced, unbalancedandvery unbalanced) according to point differential. Adiscriminant analysiswasperformed to identify game-related statistics which discriminate between winning and losing teams. Results: In European competitions, 76% of the games were classified into balanced games and none of the games was classified into very unbalanced games. In Asian competitions, on the other hand, only 48% of the games were classified into balanced games and 15% of the games were classified into very unbalanced games. In balanced games, defensive rebounds and assists discriminated between winning and losing teams in Asian competitions whereas defensive rebounds did so in European competitions. In unbalanced games, successful 2-point field goals, defensive rebounds and assists discriminated between winning and losing teams in both Asian and European competitions. Conclusions: Asian competitions had higher proportions of unbalanced and very unbalanced games than European competitions. However, a discriminant analysis, which was performed independently for each type of game, showed similar results between Asian and European competitions. The only difference was observed in balanced games’ assists which discriminated between winning and losing teams in Asian competitions but not in European competitions. © 2017, Sports Medicine Research Center.

Kaida S.,Kamagaya General Hospital | Imai Y.,Health Science University | Ohashi K.,Health Science University | Kitagawa A.,Shigakkan University
Cell Biochemistry and Function | Year: 2013

We examined whether water-immersion restraint stress (WIRS) disrupts nonenzymatic antioxidant defense systems through ascorbic acid depletion in the adrenal gland of rats. Rats were exposed to WIRS for 0.5, 1.5, 3 or 6h. WIRS increased serum adrenocorticotropic hormone, corticosterone and glucose concentrations and adrenal corticosterone content at each time point. WIRS increased adrenal lipid peroxide content at 3 and 6h, and the increase was twofold higher than the unstressed level at 6h. WIRS decreased adrenal ascorbic acid content at each time point, and the decrease reached one-third of the unstressed level at 6h. WIRS increased adrenal reduced glutathione content at 0.5 and 6h but reduced that content to half of the unstressed level at 6h. WIRS increased adrenal α-tocopherol content at 1.5h but returned that content to the unstressed level thereafter. When rats with 6h of WIRS was orally preadministered with l-ascorbic acid (250mg/kg), WIRS-induced changes in adrenal lipid peroxide, ascorbic acid and reduced glutathione contents were attenuated without any change in stress response. These results indicate that WIRS disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats. © 2012 John Wiley & Sons, Ltd.

PubMed | Nagoya Gakuin University, Aiche Medical College for Physical and Occupational Therapy, Shigakkan University and Nagoya University
Type: | Journal: Muscle & nerve | Year: 2016

Resistance training promotes recovery from muscle atrophy, but optimum training programs have not been established. We aimed to determine the optimum training intensity for muscle atrophy.Mice recovering from atrophied muscles following 2 weeks of tail suspension underwent repeated isometric training with varying joint torques 50 times per day.Muscle recovery assessed by maximal isometric contraction and myofiber CSAs were facilitated at 40% and 60% maximum contraction strength (MC), but at not at 10% and 90% MC. At 60% and 90% MC, damaged and contained smaller diameter fibers were observed. Activation of myogenic satellite cells and a marked increase in myonuclei were observed at 40%, 60%, and 90% MC.The increases in myofiber CSAs were likely caused by increased myonuclei formed through fusion of resistance-induced myofibers with myogenic satellite cells. These data indicate that resistance training without muscle damage facilitates efficient recovery from atrophy. This article is protected by copyright. All rights reserved.

Tomori K.,Kanagawa University of Human Services | Ohta Y.,Kanagawa University of Human Services | Nishizawa T.,Shigakkan University | Tamaki H.,Niigata University of Health and Welfare | Takekura H.,National Institute of Fitness and Sports in Kanoya
Journal of Muscle Research and Cell Motility | Year: 2010

We determine the effects of direct electrical stimulation (ES) on the histological profiles in atrophied skeletal muscle fibers after denervation caused by nerve freezing. Direct ES was performed on the tibialis anterior (TA) muscle after denervation in 7-week-old rats divided into groups as follows: control (CON), denervation (DN), or denervation with direct ES (subdivided into a 4 mA (ES4), an 8 mA (ES8), or a 16 mA stimulus (ES16). The stimulation frequency was set at 10 Hz, and the voltage was set at 40 V (30 min/day, 6 days/week, for 3 weeks). Ultrastructural profiles of the membrane systems involved in excitation-contraction coupling, and four kinds of mRNA expression profiles were evaluated. Morphological disruptions occurred in transverse (t)-tubule networks following denervation: an apparent disruption of the transverse networks, and an increase in the longitudinal t-tubules spanning the gap between the two transverse networks, with the appearance of pentads and heptads. These membrane disruptions seemed to be ameliorated by relatively low intensity ES (4 mA and 8 mA), and the area of longitudinally oriented t-tubules and the number of pentads and heptads decreased significantly (P < 0.01) in ES4 and ES8 compared to the DN. The highest intensity (16 mA) did not improve the disruption of membrane systems. There were no significant differences in the α1sDHPR and RyR1 mRNA expression among CON, DN, and all ES groups. After 3 weeks of denervation all nerve terminals had disappeared from the neuromuscular junctions (NMJs) in the CON and ES16 groups. However, in the ES4 and ES8 groups, modified nerve terminals were seen in the NMJs. The relatively low-intensity ES ameliorates disruption of membrane system architecture in denervated skeletal muscle fibers, but that it is necessary to select the optimal stimulus intensities to preserve the structural integrity of denervated muscle fibers. © 2010 Springer Science+Business Media B.V.

PubMed | University of Shizuoka, Osaka University, Matsumoto University, Nagoya University and 3 more.
Type: | Journal: Scientific reports | Year: 2017

Branched-chain amino acids (BCAAs) are essential amino acids for mammals and play key roles in the regulation of protein metabolism. However, the effect of BCAA deficiency on protein metabolism in skeletal muscle in vivo remains unclear. Here we generated mice with lower BCAA concentrations by specifically accelerating BCAA catabolism in skeletal muscle and heart (BDK-mKO mice). The mice appeared to be healthy without any obvious defects when fed a protein-rich diet; however, bolus ingestion of BCAAs showed that mTORC1 sensitivity in skeletal muscle was enhanced in BDK-mKO mice compared to the corresponding control mice. When these mice were fed a low protein diet, the concentration of myofibrillar protein was significantly decreased (but not soluble protein) and mTORC1 activity was reduced without significant change in autophagy. BCAA supplementation in drinking water attenuated the decreases in myofibrillar protein levels and mTORC1 activity. These results suggest that BCAAs are essential for maintaining myofibrillar proteins during protein undernutrition by keeping mTORC1 activity rather than by inhibiting autophagy and translation. This is the first report to reveal the importance of BCAAs for protein metabolism of skeletal muscle in vivo.

PubMed | University of Miyazaki, National Center for Global Health and Medicine, Kobe University, National Health Research Institute and 3 more.
Type: Journal Article | Journal: Cell reports | Year: 2016

Central insulin action activates hepatic IL-6/STAT3 signaling, which suppresses the gene expression of hepatic gluconeogenic enzymes. The vagus nerve plays an important role in this centrally mediated hepatic response; however, the precise mechanism underlying this brain-liver interaction is unclear. Here, we present our findings that the vagus nerve suppresses hepatic IL-6/STAT3 signaling via 7-nicotinic acetylcholine receptors (7-nAchR) on Kupffer cells, and that central insulin action activates hepatic IL-6/STAT3 signaling by suppressing vagal activity. Indeed, central insulin-mediated hepatic IL-6/STAT3 activation and gluconeogenic gene suppression were impeded in mice with hepatic vagotomy, pharmacological cholinergic blockade, or 7-nAchR deficiency. In high-fat diet-induced obese and insulin-resistant mice, control of the vagus nerve by central insulin action was disturbed, inducing a persistent increase of inflammatory cytokines. These findings suggest that dysregulation of the 7-nAchR-mediated control of Kupffer cells by central insulin action may affect the pathogenesis of chronic hepatic inflammation in obesity.

Kitagawa A.,Shigakkan University | Ohta Y.,Aichi University | Ohashi K.,Health Science University
Journal of Pineal Research | Year: 2012

In this study, we examined whether melatonin improves metabolic syndrome induced by high fructose intake in male Wistar rats. Feeding of a diet containing 60% fructose (HFD) for 4 or 6 wk caused increased serum insulin, triglyceride, total cholesterol, free fatty acids, uric acid, leptin, and lipid peroxide concentrations as well as hepatic triglyceride and cholesterol concentrations, and relative intra-abdominal fat and liver weights. The 4- or 6-wk HFD feeding reduced serum high-density lipoprotein cholesterol and adiponectin concentrations. The 6-wk HFD feeding increased serum tumor necrosis factor-α concentration and hepatic lipid peroxide concentration and lowered hepatic reduced glutathione concentration. Daily intraperitoneal administration of melatonin (1 or 10 mg/kg body weight), starting at 4-wk HFD feeding, attenuated these changes at 6-wk HFD feeding more effectively at its higher dose than at its lower dose. In an oral glucose tolerance test, rats with 4- or 6-wk HFD feeding showed higher serum insulin response curve and normal serum glucose response curve when compared with the corresponding animals that received the control diet. The 4- or 6-wk HFD feeding caused insulin resistance, judging from the scores of HOMR-IR and QUICKI, which are indices of insulin resistance. The daily administered melatonin (1 or 10 mg/kg body weight) ameliorated the higher serum insulin response curve in the oral glucose tolerance test and insulin resistance at 6-wk HFD feeding more effectively at its higher dose than at its lower dose. These results indicate that melatonin improves metabolic syndrome induced by high fructose intake in rats. © 2011 John Wiley & Sons A/S.

Naznin F.,University of Miyazaki | Toshinai K.,University of Miyazaki | Toshinai K.,Shigakkan University | Waise T.M.Z.,University of Miyazaki | And 5 more authors.
Journal of Endocrinology | Year: 2015

Ghrelin, a stomach-derived orexigenic peptide, transmits starvation signals to the hypothalamus via the vagus afferent nerve. Peripheral administration of ghrelin does not induce food intake in high fat diet (HFD)-induced obese mice. We investigated whether this ghrelin resistance was caused by dysfunction of the vagus afferent pathway. Administration (s.c.) of ghrelin did not induce food intake, suppression of oxygen consumption, electrical activity of the vagal afferent nerve, phosphorylation of ERK2 and AMP-activated protein kinase alpha in the nodose ganglion, or Fos expression in hypothalamic arcuate nucleus of mice fed a HFD for 12 weeks. Administration of anti-ghrelin IgG did not induce suppression of food intake in HFD-fed mice. Expression levels of ghrelin receptor mRNA in the nodose ganglion and hypothalamus of HFD-fed mice were reduced. Inflammatory responses, including upregulation of macrophage/microglia markers and inflammatory cytokines, occurred in the nodose ganglion and hypothalamus of HFD-fed mice. A HFD blunted ghrelin signaling in the nodose ganglion via a mechanism involving in situ activation of inflammation. These results indicate that ghrelin resistance in the obese state may be caused by dysregulation of ghrelin signaling via the vagal afferent. © 2015 The authors.

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