Graduate Institute of Transition and Leisure Education for Individuals with Disabilities

Taipei, Taiwan

Graduate Institute of Transition and Leisure Education for Individuals with Disabilities

Taipei, Taiwan
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Kau M.-M.,National Taipei University of Nursing and Health Sciences | Wang J.-R.,Shin Kong Wu Ho Su Memorial Hospital | Tsai S.-C.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | Yu C.-H.,Chung Shan Medical University | Wang P.S.,National Yang Ming University
British Journal of Pharmacology | Year: 2012

Background and purpose: Bufalin and cinobufagin exhibit cardiotonic and natriuretic activities. The aim of this study was to evaluate the effects of bufalin and cinobufagin on aldosterone and cortisol secretion and their mechanisms of action in human adrenocortical cells (NCI-H295). Experimental approach: H295 cells were incubated with bufalin or cinobufagin in the presence or absence of angiotensin II (Ang II), forskolin, 8-Br-cAMP, corticosterone or deoxycortisol. The role of ERK1/2 was studied by use of the inhibitor of MEK (U0126). The binding of transcription factor steroidogenic factor 1 (SF-1) to steroidogenic acute regulatory (StAR) gene promoter was analysed by EMSA. Key results: Bufalin and cinobufagin markedly inhibited basal, Ang II-, forskolin- or 8-Br-cAMP-stimulated aldosterone and cortisol secretion, and the conversions of corticosterone to aldosterone and deoxycortisol to cortisol. Bufalin and cinobufagin also inhibited StAR protein expression and SF-1 binding to StAR gene promoter. They both increased phosphorylation of ERK1/2, and U0126 fully abolished these effects on ERK1/2 in H295 cells. Furthermore, U0126 reversed the inhibitory effects of bufalin and cinobufagin on StAR protein expression and the binding of SF-1 to StAR gene promoter. However, U0126 did not completely reverse their inhibitory effects on aldosterone and cortisol release. Conclusions and implications: The inhibitory effects of bufalin and cinobufagin on steroidogenesis of aldosterone and cortisol were associated with inhibition of aldosterone synthase and 11β-hydroxylase, as well as the suppression of StAR protein expression and SF-1 binding to StAR promoter via the phosphorylation of ERK1/2 in H295 cells. © 2011 The British Pharmacological Society.

Su C.-T.,Fu Jen Catholic University | Wu M.-Y.,National Chung Cheng University | Yang A.-L.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | Chen-Sea M.-J.,National Cheng Kung University | Hwang I.-S.,National Cheng Kung University
American Journal of Occupational Therapy | Year: 2010

OBJECTIVE. To compare stance control between children with sensory modulation disorder (SMD) and typically developing children in various visual and somatosensory conditions. METHOD. Thirty-one children participated in this study, including 17 children with SMD and 14 matched typically developing children. The Sensory Profile was used to screen for sensory modulation problems, which were further confirmed by measures of electrodermal response and the Evaluation of Sensory Processing. Stance parameters for an assessment of postural stability were obtained with a dual-axis accelerometer on the lumbar area. RESULTS. The children with SMD presented atypical sensory responses in terms of both electrophysiological and behavioral measures. The results for stance showed a greater body sway in the SMD group than in the control group (p < .05). However, the group difference was not always significant under the conditions of reliable somatosensory input and sway-referenced vision. CONCLUSION. Our findings first confirmed impaired stance control in children with SMD.

Lephart S.M.,University of Pittsburgh | Tsai Y.-S.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | Sell T.C.,University of Pittsburgh | Smoliga J.M.,Marywood University | And 2 more authors.
Journal of Orthopaedic and Sports Physical Therapy | Year: 2010

Study Design: Controlled laboratory study using a cross-sectional design. OBJECTiVES: To examine the kinematics and kinetics of the trunk and the physical characteristics of trunk and hip in golfers with and without a history of low back pain (LBP). Background: Modified swing patterns and general exercises have been suggested for golfers with back pain. Yet we do not know what contributes to LBP in golfers. To create and validate a low back-specific exercise program to help prevent and improve back injuries in golfers, it may be valuable to understand the differences in biomechanical and physical characteristics of golfers with and without a history of LBP. Methods: Sixteen male golfers with a history of LBP were matched by age and handicap with 16 male golfers without a history of LBP. All golfers underwent a biomechanical swing analysis, trunk and hip strength and flexibility assessment, spinal proprioception testing, and postural stability testing. Results: The group with a history of LBP demonstrated significantly less trunk extension strength at 60°/s and left hip adduction strength, as well as limited trunk rotation angle toward the nonlead side. No significant differences were found in postural stability, trunk kinematics, and maximum spinal moments during the golf swing. Conclusion: Deficits observed in this study may affect a golfer's ability to overcome the spinal loads generated during the golf swing over time. Exercises for improving these physical deficits can be considered, although the cause-effect of LBP in golfers still cannot be determined.

Chou C.-C.,Chang Gung Memorial Hospital | Bai C.-H.,Taipei Medical University | Bai C.-H.,Shin Kong Wu Ho Su Memorial Hospital | Tsai S.-C.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | And 2 more authors.
Internal Medicine | Year: 2010

Background Ghrelin has a protective effect on endothelial cells. Endothelial cell dysfunction is associated with cardiovascular disease (CVD) and CVD remains the leading cause of morbidity in hemodialysis (HD) patients. Acylated ghrelin (A-Ghr) is the functional form of ghrelin, so we hypothesized that A-Ghr is associated with the occurrence of CVD in HD patients. Methods We conducted a prospective cohort study in 412 HD patients. The cohort was sub-grouped into low and high A-Ghr groups according to the median A-Ghr level of 4.88 pg/mL. The association between the low/high A-Ghr groups and the incidence of CVD were analyzed. Results The HD patients in a low A-Ghr group had a greater risk of incidental CVD than those in a high A-Ghr ghrelin. This association remained significant after the adjustment for possible confounding factors, including age, gender, HD duration, BMI, diabetes, albumin, nPCR and Charlson's comorbidity index score. Conclusion It appears that a low serum A-Ghr level is associated with the development of CVD in HD patients. © 2010 The Japanese Society of Internal Medicine.

Tsai Y.-L.,Taipei Veterans General Hospital | Tsai S.-C.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | Yen S.-H.,Taipei Veterans General Hospital | Yen S.-H.,National Yang Ming University | And 11 more authors.
Child's Nervous System | Year: 2013

Objective: External beam radiotherapy (EBRT) is frequently used to improve disease control for pediatric brain tumor patients. However, to facilitate the radiotherapy (RT) procedure, "forced" type interventions including conscious sedation or general anesthesia are frequently used to manage patients' fear and anxiety. The aim of this study was to investigate the effects of therapeutic play (TP) in reducing anxiety for pediatric brain tumor patients treated by EBRT. Methods: Between April 1st and September 30th, 2009, 19 young brain tumor patients, aged 3-15 years and recommended for RT, were recruited: ten to a control group and nine to the study intervention group. The study group was introduced with TP during EBRT. The Beck Youth Anxiety Inventory and the Faces Anxiety Scale were used to evaluate patients' psychological levels of anxiety. The heart rate variability and salivary cortisol concentrations were used to indicate the patients' physical levels of anxiety. Both the psychological and physiological tests were administered to all subjects before and after the RT procedure. Results: The study group had significantly lower anxiety scores and expressed fewer negative emotions than did the control group before EBRT. Conclusions: TP can not only improve the quality of medical services but can also reduce costs and staffing demands. In addition, it can help lower young patients' anxiety and fear during medical procedures. As a result, it further decreases the potential negative impacts of hospitalization on these young patients. © 2013 Springer-Verlag Berlin Heidelberg.

Yang A.-L.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | Yeh C.-K.,National Cheng Kung University | Su C.-T.,Fu Jen Catholic University | Lo C.-W.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | And 3 more authors.
Experimental Physiology | Year: 2010

Limited information is available concerning the effects of aerobic exercise on vasorelaxation in hypertension. The aim of this study was to investigate the effects of a single bout of aerobic exercise on insulin- and insulin-like growth factor-1 (IGF-1)-induced vasorelaxation in hypertensive rats. Four-month-old spontaneously hypertensive rats were randomly divided into a sedentary group (SHR) and an exercise group (SHR+Ex) subjected to a single bout of aerobic exercise conducted by treadmill running at 21 m min-1 for 1 h. Age-matched Wistar-Kyoto rats were used as a normotensive control group (WKY). Insulin- and IGF-1-induced vasorelaxant responses in the three groups were evaluated by using isolated aortic rings, with or without endothelial denudation, in organ baths. Possible roles of phosphatidylinositol 3-kinase (PI3K) and nitric oxide synthase (NOS) involved in the NO-dependent vasorelaxation were examined by adding selective inhibitors. The role of superoxide was also clarified by adding superoxide dismutase (SOD). In addition, the endothelium-independent vascular responses to sodium nitroprusside (SNP), a NO donor, were examined. The insulin- and IGF-1-induced vasorelaxation was significantly (P < 0.05) decreased in the SHR group compared with the WKY group. This decreased response in SHR was improved by exercise. These vasorelaxant responses among the three groups became similar after endothelial denudation and pretreatment with the PI3K inhibitor, NOS inhibitor or SOD. Also, no difference among groups was found in the SNP-induced vasorelaxation. We concluded that a single bout of aerobic exercise acutely improves insulin- and IGF-1-mediated vasorelaxation in an endothelium-dependent manner in hypertensive rats. © 2010 The Physiological Society.

Liou C.-M.,Chung Shan Medical University | Yang A.-L.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities | Kuo C.-H.,Taipei Physical Education College | Tin H.,Chung Shan Medical University | And 4 more authors.
Cell Biochemistry and Function | Year: 2010

Objectives Cardiac apoptosis was found in ovariectomized rats without ischemia. Limited information regarding the protective effects of 17β-estradiol (E2) on cardiac Fas-dependent and mitochondria-dependent apoptotic pathways after post-menopause or bilateral oophorectomy in women was available. Methods Forty-eight female Wistar rats at 6-7 months of age were divided into sham-operated group (Sham, n=16) and bilateral ovariectomized group (n=32). After 4 weeks of operation, rats in ovariectomized group were injected intraperitoneally with either saline (OVX, n=16) or 10≤g/kg/day 17β-estradiol (E2) for 10 weeks (OVX-E2, n=16). The excised hearts were measured by Hematoxylin-eosin staining, DAPI staining, positive TUNEL assays, and Western Blotting. Results 17β-estradiol (E2) decreased OVX-induced cardiac widely dispersed TUNEL-positive apoptotic cells. 17β-estradiol (E2) decreased OVX-induced TNF-alpha, Fas ligand (Fas L), Fas death receptors (Fas), Fas-associated death domain (FADD), activated caspase 8, and activated caspase 3 (Fas pathways). 17β-estradiol (E2) decreased OVX-induced proapoptotic t-Bid, Bax, Bax-to-Bcl2 ratio, Bax-to- BclXL ratio, activated caspase 9, and activated caspase 3 as well as increased anti-apoptotic Bcl2 and Bcl-XL relative to OVX (mitochondria pathway). Conclusions Our findings suggest that chronic 17β-estradiol (E2) treatment can prevent ovariectomy-induced cardiac Fas-dependent and mitochondria-dependent apoptotic pathways in rat models. The findings may provide one of possible mechenisms of 17β-estradiol (E2) for potentially preventing cardiac apoptosis after bilateral ovariectomy or menopause. Copyright © 2010 John Wiley & Sons, Ltd.

Lu C.-C.,Nursing and Management College | Lu C.-C.,Mackay Memorial Hospital | Tsai S.-C.,Graduate Institute of Transition and Leisure Education for Individuals with Disabilities
Hormone and Metabolic Research | Year: 2011

Previous studies have demonstrated that plasma calcitonin is lower in hypothyroid patients and that thyroxine stimulates the human thyroid to release calcitonin. Therefore, thyroid hormones may regulate the secretion of calcitonin, but further work is needed to address this possibility in more detail. TT cells, a model of human thyroid C cells, were incubated in a medium containing vehicle, thyroxine, or thyroxine methyl-hemisuccinate-bovine serum albumin (BSA-L-T4, thyroxine was immobilized and linked to BSA); then, the levels of secreted calcitonin (hCT), calcitonin mRNA, and cAMP were measured. To study links that connect the cAMP-dependent protein kinase A (PKA) pathway to the observed thyroxine effects, cells were treated with either vehicle or thyroxine plus SQ22536 [an adenylyl cyclase (AC) inhibitor], KT5720 (a PKA inhibitor), or 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor). The activity levels of AC and PKA, and secreted calcitonin were then measured. The results indicate that thyroxine increases calcitonin secretion, cellular cAMP accumulation, and the activities of AC and PKA, but does not increase hCT mRNA levels in TT cells. BSA-L-T4 also increases calcitonin secretion. These effects are inhibited by SQ22536, and KT5720 and suggest that the nongenomic thyroxine effects that stimulate calcitonin secretion from TT cells involve the cAMP-dependent PKA pathway. © Georg Thieme Verlag KG Stuttgart - New York.

PubMed | Graduate Institute of Transition and Leisure Education for Individuals with Disabilities
Type: Journal Article | Journal: The Chinese journal of physiology | Year: 2011

Ovarian failure is commonly caused by aging, autoimmune disease, menopause and cancer therapy. We used an ischemic model in the ovary to test the hypothesis that stem cells are helpful for ovarian regeneration after injury. Three treatment regimes were employed: sham-operated control, ligation plus PBS, and ligation plus immortalized human bone marrow stromal cells (stem cells) groups. After ligation-induced ischemia, stem cells or PBS were injected into rat ovaries. Then, pregnant mare serum gonadotropin was given intra-peritoneally to initiate folliculogenesis. The animals were then sacrificed. The ovary gland was weighed, and ovarian folliculogenesis, stem cell differentiation and vascular neogenesis were evaluated. In order to study improvement of folliculogenesis after ovarian ischemia, steroidogenic acute regulatory protein (StAR), p44/p42 MAPK (T-ERK1/2), and phospho-p44/ p42 MAPK (P-ERK1/2) expression were specifically evaluated. Results indicated that ovarian size was smaller and that the rate of folliculogenesis was lower in ovarian ischemic-reperfusion animals, but both recovered after stem cell treatment. The stem cells migrated into the ovary and differentiated into theca cells, granulosa cells, corona radiata cells and vascular endothelial cells. In addition, von Willebrand factor (vWF) expression was increased; 17beta-estradiol (E2), progesterone (P4), P-ERK1/2 and StAR protein expression was recovered by stem cells treatment in the ischemic ovaries. The serum LH was significantly increased in ovaries of ischemia-reperfusion animals, but the stem cell treatment restored the effects. These results suggest that stem cells might be helpful for ovarian regeneration after injuries by promoting vascular neogenesis and steroidogenesis through the MAPK pathway.

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