22 research outputs found

    Effect of circumferential air-splint pressure on the soleus stretch reflex during a voluntary ramp plantar flexion

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    Circumferential pressure (CP) applied to the limb has been shown to decrease muscle activity in subjects without neuromuscular disorders and in individuals with a spinal cord injury and cerebrovascular accidents.Було показано, що круговий тиск (КТ), прикладений до кінцівки, зумовлює зменшення м’язової активності в осіб без нервово-м’язових розладів і у пацієнтів з пошкодженнями спинного мозку й цереброваскулярними патологіями

    Effect of air-splint pressure on the soleus stretch reflex during a voluntary ramp plantar flexion

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    Circumferential pressure (CP) applied to the limb has been shown to decrease muscle activity in subjects without neuromuscular disorders and in individuals with spinal cord injury and cerebrovascular accidents. Thus far, studies estimating the CP efficacy with respect to reflex excitability of motoneurons mainly used the H reflex technique on a resting muscle. The purpose of our study, therefore, was to investigate the effect that CP exerts on the soleus stretch reflex (SSR) when superimposed onto a voluntary ramp plantar flexion movement in subjects without neuromuscular disorders. Forty-eight subjects volunteered for this study. SSRs were investigated before, during, and after the application of pressure to the calf. An inflated air-splint connected to a pressure transducer was used to administer and measure the pressure set to 45-50 mm Hg. The SSRs were elicited by dorsiflexing the subject\u27s ankle by 10 deg at 180 deg/sec, while the subject plantarflexed against a moving footplate at 20% of the maximum voluntary contraction through a 30 deg arc at 90 deg/sec. Twenty-five SSRs were recorded and averaged for each experimental phase; peak-to-peak amplitudes were measured and normalized, and reflex latencies were also measured. Friedman Repeated Measures Analysis of Variance on Ranks was used to analyze the differences in the SSR latency and amplitude from the baseline values. No significant general difference in the SSR amplitude was found during pressure application, although individual responses varied widely. The post-pressure values returned to the baseline, and the differences were insignificant. The reflex latencies were also unchanged with respect to the baseline levels. Thus, the CP inhibitory effect on reflex excitability of motoneurons is mild, on average, and variable when a voluntary movement is a condition. The CP technique may not be as efficacious in reducing muscle hyperactivity as was previously thought. © 2010 Springer Science+Business Media, Inc

    Longitudinal markers of cerebral amyloid angiopathy and related inflammation in rTg-DI rats

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    Abstract Cerebral amyloid angiopathy (CAA) is a prevalent vascular dementia and common comorbidity of Alzheimer’s disease (AD). While it is known that vascular fibrillar amyloid β (Aβ) deposits leads to vascular deterioration and can drive parenchymal CAA related inflammation (CAA-ri), underlying mechanisms of CAA pathology remain poorly understood. Here, we conducted brain regional proteomic analysis of early and late disease stages in the rTg-DI CAA rat model to gain molecular insight to mechanisms of CAA/CAA-ri progression and identify potential brain protein markers of CAA/CAA-ri. Longitudinal brain regional proteomic analysis revealed increased differentially expressed proteins (DEP) including ANXA3, HTRA1, APOE, CST3, and CLU, shared between the cortex, hippocampus, and thalamus, at both stages of disease in rTg-DI rats. Subsequent pathway analysis indicated pathway enrichment and predicted activation of TGF-β1, which was confirmed by immunolabeling and ELISA. Further, we identified numerous CAA related DEPs associate with astrocytes (HSPB1 and MLC1) and microglia (ANXA3, SPARC, TGF-β1) not previously associated with astrocytes or microglia in other AD models, possibly indicating that they are specific to CAA-ri. Thus, the data presented here identify several potential brain protein biomarkers of CAA/CAA-ri while providing novel molecular and mechanistic insight to mechanisms of CAA and CAA-ri pathological progression and glial cell mediated responses

    Vitamin E and age alter liver mitochondrial morphometry

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    Oxidative damage to mitochondrial membranes caused by free radical production during respiration plays a major role in tissue dysfunction. It has been hypothesized that aging is associated with mitochondrial enlargement and elongation. These changes may be enhanced by deficiencies in vitamin E and selenium. Vitamin E supplementation minimizes the age-related mitochondrial enlargement and elongation in the mouse liver. This study investigated the effects of vitamin E supplementation (500 IU/kg) on old (760 days) and older (827 days) C57BL/6 mice liver mitochondrial (Mt) morphometry. Fixed mitochondria from homogenized liver samples taken from control and vitamin E-supplemented mice were examined by transmission electron microscopy and measured by image analysis. Morphometric measurements included Mt area, short and long axis, and size distributions. Old vitamin E-supplemented mice had significantly smaller (p \u3c 0.0001) liver mitochondria than age-matched controls. While age had no significant effect on Mt area and short axis in the vitamin E-supplemented mice, it had a significant effect (p \u3c 0.002) on the long axis. Analysis of the long axis to short axis ratio indicated that age had a significant effect of mitochondrial elongation in the vitamin E fed mice. Vitamin E supplementation results in smaller mouse liver mitochondria as compared to age-matched cohorts and aging results in elongation but does not alter the size of liver mitochondria in mice supplemented with vitamin E. These results suggest that vitamin E provides a protective effect against age-related mitochondrial enlargement

    Adipocyte specific HO-1 gene therapy is effective in antioxidant treatment of insulin resistance and vascular function in an obese mice model

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    Obesity is a risk factor for vascular dysfunction and insulin resistance. The study aim was to demonstrate that adipocyte-specific HO-1 (heme oxygenase-1) gene therapy is a therapeutic approach for preventing the development of obesity-induced metabolic disease in an obese-mice model. Specific expression of HO-1 in adipose tissue was achieved by using a lentiviral vector expressing HO-1 under the control of the adiponectin vector (Lnv-adipo-HO-1). Mice fed a high-fat diet (HFD) developed adipocyte hypertrophy, fibrosis, decreased mitochondrial respiration, increased levels of inflammatory adipokines, insulin resistance, vascular dysfunction, and impaired heart mitochondrial signaling. These detrimental effects were prevented by the selective expression of HO-1 in adipocytes. Lnv-adipo-HO-1-transfected mice on a HFD display increased cellular respiration, increased oxygen consumption, increased mitochondrial function, and decreased adipocyte size. Moreover, RNA arrays confirmed that targeting adipocytes with HO-1 overrides the genetic susceptibility of adiposopathy and correlated with restoration of the expression of anti-inflammatory, thermogenic, and mitochondrial genes. Our data demonstrate that HO-1 gene therapy improved adipose tissue function and had positive impact on distal organs, suggesting that specific targeting of HO-1 gene therapy is an attractive therapeutic approach for improving insulin sensitivity, metabolic activity, and vascular function in obesity
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