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Kinesio tape and proprioceptive exercises are both used for increasing balance in dancers. The purposes of this study were to: a) determine the acute effect of kinesio tape (KT) application on the ankle joint on balance performance, b) investigate the effects of an 8-week proprioceptive-neuromuscular (PN) training program on balance performance, and c) compare their effects vs modern dance technique classes alone. Thirty-three trained, university-level modern dance students (9 male, 24 female) were divided randomly into three groups: kinesio tape (KT, n=11), proprioceptive-neuromuscular (PN, n=11), or control (n=11). Static (turn-out passé-opened eyes/relevé and turn-out passé-closed eyes/flat foot), semi-dynamic (airplane), and dynamic balance (monopodalic-straight and -transverse in a turn-out passé-eyes opened/flat foot) tests were performed before and after the intervention. One day after pre-tests, KT mechanical correction technique was applied to the left ankle joint (supporting leg) in the KT group, and tests were repeated to determine the acute effect of KT. The PN group participated in an 8-week balance training program (2 days/wk, 60 min/day) involving exercises using stable and unstable surfaces. Significant improvements were observed for all static and dynamic balance tests in the PN group; semi-dynamic airplane and dynamic monopodalic-straight and transverse tests improved in the KT group; and only semi-dynamic airplane test scores changed significantly for the control group (p

Hearing loss is the most common sensory deficit in humans with causative variants in over 140 genes. With few exceptions, however, the population-specific distribution for many of the identified variants/genes is unclear. Until recently, the extensive genetic and clinical heterogeneity of deafness precluded comprehensive genetic analysis. Here, using a custom capture panel (MiamiOtoGenes), we undertook a targeted sequencing of 180 genes in a multi-ethnic cohort of 342 GJB2 mutation-negative deaf probands from South Africa, Nigeria, Tunisia, Turkey, Iran, India, Guatemala, and the United States (South Florida). We detected causative DNA variants in 25% of multiplex and 7% of simplex families. The detection rate varied between 0 and 57% based on ethnicity, with Guatemala and Iran at the lower and higher end of the spectrum, respectively. We detected causative variants within 27 genes without predominant recurring pathogenic variants. The most commonly implicated genes include MYO15A, SLC26A4, USH2A, MYO7A, MYO6, and TRIOBP. Overall, our study highlights the importance of family history and generation of databases for multiple ethnically discrete populations to improve our ability to detect and accurately interpret genetic variants for pathogenicity.

Objective High altitude and hypoxic preconditioning have cardioprotective effects by increasing coronary vascularity, reducing post-ischemic injury, and improving cardiac function. Our purpose was to examine if intermittent hypoxia treatment has any restoring effects related to the possible role of the HIF-1/VEGF pathway on diabetic cardiomyopathy. Methods Wistar Albino male rats (n=34) were divided into four groups: control (C), intermittent hypoxia (IH), diabetes mellitus (DM), and diabetes mellitus plus intermittent hypoxia (DM+IH). Following a streptozotocin (STZ) injection (50 mg/kg, i.p.), blood glucose levels of 250 mg/dL and above were considered as DM. IH and DM+IH groups were exposed to hypoxia 6 h/day for 42 days at a pressure corresponding to 3000 m altitude. Twenty-four hours after the IH protocol, hearts were excised. Hematoxylin and eosin-stained apical parts of the left ventricles were evaluated. Hypoxia inducible factor-1 (HIF-1), vascular endothelial growth factor 164 (VEGF164), and VEGF188 polymerase chain reaction products were run in agarose gel electrophoresis. Band density analysis of UV camera images was performed using Image J. The data were compared by one-way ANOVA, repeated measures two-way ANOVA, and the Kruskal-Wallis test. Results The percent weight change was lower in the DM group than in the controls (p=0.004). The tissue injury was the highest in the DM group and the least in the IH group. Diabetes decreased, whereas the IH treatment increased the vascularity. A decrease was observed in the VEGF188 mRNA levels in the DM+IH group compared with the C group, but there were no difference in HIF-1α and VEGF164 mRNA levels between the groups. Conclusion The IH treatment restored the diabetic effects on the heart by reducing tissue injury and increasing the capillarity without transcriptional changes in HIF-1/VEGF correspondingly.

Spirometric obstruction is a prevalent problem in older adults and related to life-style risk factors. Symptoms related to chronic-obstructive-pulmonary-disease (COPD) are also prevalent symptoms with diverse etiologies - not limited to pulmonary obstruction. Older adults may have unrecognized airway obstruction due to functional limitations or symptoms mis-attributed to age/other co-morbidities. Therefore, spirometric obstruction may clinically be over/under diagnosed. Over last few decades, the burden of smoking-related diseases has increased in older adults. Additional evidence regarding older adults is required. We aimed to study frequency of spirometric obstruction, its over/under diagnosis and tobacco exposure in a group of male nursing-home residents. For spirometric obstruction diagnosis, two different thresholds [(fixed value: 0.70) versus (age-corrected value: 0.65 in residents65 years of age)] were compared for better clinical practice. One hundred and three residents with 71.4 ± 6.3 years-of-age included. Spirometric obstruction prevalences were 39.8 and 29.1% with fixed and age-corrected FEV1/FVC thresholds, respectively. Age-corrected FEV1/FVC threshold underdiagnosed COPD in 1.9% while fixed threshold overdiagnosed spirometric obstruction in 8.7%. Active smokers were 64.1%, ex-smokers 23.3% and non-smokers 12.6%. Our study suggests high prevalences of spirometric obstruction and smoking in male nursing-home residents in Turkey. We suggest the use of age-corrected FEV1/FVC threshold practicing better than the use of fixed FEV1/FVC threshold in this patient group.

Objective: The objective was to determine whether knee osteoarthritis (OA) reduces exercise ambulatory capacity and impairs quality of life (QOL) in obese individuals. Research Methods and Procedures: There were 56 subjects, with and without knee OA, who were obese. The subjects were evaluated with anthropometric measurements, a body composition assessment, maximal cardiopulmonary exercise test, 6-minute walk test (6-MWT), perceived exertion (RPE), self-reported disability [Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC)], and the Medical Outcomes Study Short Form 36 (SF-36). Results: VO2peak was significantly higher in the controls when compared with the patients (mean ± standard deviation, 1.584 ± 0.23 L/kg per min vs. 0.986 ± 0.20 L/kg per min; p < 0.001). Obese subjects without knee OA walked a significantly longer distance in the 6-MWT than obese patients with knee OA (p < 0.001). We also observed significant negative correlation between Vo2max and RPE, WOMAC pain and physical limitation, and bodily pain and general health domains of short-form 36. Discussion: Knee OA reduces exercise and ambulatory capacity and impairs QOL in obese individuals. RPE, WOMAC pain, and SF-36 items might provide information about exercise capacity in the obese subjects with knee OA. Our study confirms that exercise capacity and QOL might be improved by energetic and intensive treatment of pain resulting from knee OA.

Apoptosis has been shown in cardiac cells under divergent physiological and pathological conditions. However, there has been an ongoing debate upon the relative contribution of cardiomyocyte apoptosis to the myocardial infarct size after ischemia-reperfusion (I-R) injury. We tested the hypothesis that blocking the death receptor pathway of apoptosis through genetic deletion of Fas receptors or Fas ligands would reduce myocardial infarct size caused by acute I-R injury. The hearts isolated from Fas receptor or Fas ligand knockout (KO) mice as well as the C57BL/6J wild-type control mice (N = 6-8 per group) were subjected to 20 min of global ischemia and 30 min of reperfusion in Langendorff mode. Our results show that the infarct size, determined with triphenyltetrazolium chloride staining, was not significantly different between the three groups (i.e., 30.2 +/- 3.9% for wild-type controls, 30.0 +/- 2.1% for Fas ligand KOs, and 23.8 +/- 3.6% for Fas receptor KOs; mean +/- SEM, p > 0.05). Postischemic leakage of lactate dehydrogenase, another marker of necrotic cellular injury, also was not significantly different between these groups (p > 0.05). In addition, postischemic ventricular contractile function as well as coronary flow were similar for all the experimental groups (p > 0.05). In conclusion, contrary to our original hypothesis, the present study in the gene KO mice suggests that the Fas ligand- and Fas receptor-mediated death receptor pathway of apoptosis is not the primary determinant of myocardial infarct size and ventricular dysfunction caused by acute global I-R injury in the isolated perfused mouse heart.

The pivotal role of platelets in the pathogenesis of atherosclerosis and cardiovascular diseases prompted considerable interest on the effect of physical exercise on platelets. The results about the platelet response to exercise are conflicting. The discrepancies may be attributed to the differences in the intensity and the duration of the exercise protocols and in the methodologies employed [1–3]. The exact mechanisms concerned in exercise-induced platelet responses are not completely understood. On the other hand, physical exercise is characterized by an increase in metabolic activity and oxygen consumption. This increase in oxygen uptake is associated with a substantial rise in the production of reactive oxygen species (ROS). The high production of ROS may be responsible for serious physiological and biochemical changes that occur during exercise [4–7]. To minimize free radical damage, there is a complex antioxidant defense system, which includes antioxidants within cells, cell membranes and extracellular fluids [5,8–10]. Within the strategy to maintain redox balance against oxidant conditions, blood has a central role because it transports and redistributes antioxidants to every part of the body. Measurement of total

Chronic systemic hypoxia (SH) enhances myocardial ischemic tolerance in mammals. We studied the delayed cardioprotection caused by acute SH and associated signaling mechanism. Conscious adult male mice were exposed to one or two cycles of hypoxia (H; 10% O2) or normoxia (21% O2) for various durations (30 min, 2 h, 4 h) followed by 24 h of reoxygenation. Hearts were isolated 24 h later and subjected to ischemia-reperfusion in a Langendorff model. Infarct size was reduced in mice pretreated with one (H4h) or two cycles (H4hx2) of 4 h SH compared with normoxia mice ( P < 0.05), which was abolished by an inducible nitric oxide synthase (NOS2) inhibitor ( S-methylisothiourea, 3 mg/kg) given before SH or ischemia. H4hx2 also failed to reduce infarct size in NOS2 knockout mice. Cyclooxygenase-2 (COX-2) inhibitor (NS-398, 10 mg/kg) did not block the protection given either before H4hx2 or ischemia. A two- to three fold increase in myocardial NOS2 expression was observed in H4h, H2hx2, and H4hx2 ( P < 0.05), whereas endothelial NOS (NOS3) or COX-2 remained unchanged. We conclude that acute SH induces delayed cardioprotection, which is triggered and mediated by NOS2, but not by NOS3 or COX-2.

OBJECTIVE Hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) are involved in signaling mechanisms of cellular responses to hypoxia. These factors have been investigated in tissue samples by simulating different altitudes by changing the percentage of oxygen. We aimed first to evaluate the effect of normobaric, systemic hypoxia (11% O2) on HIF-1α and VEGF mRNA levels in the heart muscle; secondly, to compare the levels of HIF-1α and VEGF mRNA in the left and right ventricle muscles. METHODS In this experimental study, 33 New Zealand male rabbits were assigned to control, acute hypoxia (4 hours) and intermittent hypoxia (4 hours/day for 14 days) groups (n=11/group). Total RNA was isolated from right and left ventricles of the heart. The expressions of HIF-1α and VEGF mRNAs were investigated by using Reverse Transcription Polymerase Chain Reaction (RT-PCR) method. The obtained data were compared by using ANOVA and paired t-test. RESULTS The results indicated that left ventricle VEGF mRNA expressions in both acute and intermittent hypoxia groups (1.08 ± 0.15 and 1.03 ± 0.19, respectively) were higher than that in the control group (0.88 ± 0.15) (p=0.03). Hypoxia treatments did not significantly alter HIF-1α mRNA in both ventricles (p=0.60 and p=0.51 for left and right ventricles, respectively). CONCLUSION Since systemic hypoxia results in induction of VEGF mRNA up-regulation only in left ventricle, it could be related to its higher metabolic activity and oxygen utilization. Hypoxia induced changes in the expression of HIF-1α mRNA may not be the only determining factor for HIF-1/VEGF pathway induction or the observed VEGF induction could be through other hypoxia sensitive pathways.

Asthma is a disease characterized by chronic airway inflammation. Generation of oxygen free radicals by activated inflammatory cells produces many of the pathophysiologic changes associated with asthma and may contribute to its pathogenesis. However, the activities of antioxidant enzymes and their relation with asthma have not been well defined. This study was performed to examine the activities of major intracellular antioxidants in mild asthmatic patients. Twelve asymptomatic mild asthmatic patients who never used any antiasthma medication and 13 age- and sex-matched healthy control subjects were selected. The activities of erythrocyte antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione-peroxidase (GSH-Px) were measured spectrophotometrically. The mean SOD activity of asthmatic patients was found to be significantly lower than that of the controls (p0.05). There was no significant difference in CAT and GSH-Px activities between patients and controls (p0.05). Although the mechanisms underlying the association between asthma and antioxidant system are unclear, according to our findings, decreased antioxidant protection may contribute to the pathogenesis of mild asthma.