Rehab Centers: Prophylactic Effects of Swimming Exercise on Autophagy-Induced Muscle Atrophy in Diabetic Rats.

Prophylactic effects of swimming exercise on autophagy-induced muscle atrophy in diabetic rats.

Filed under: Rehab Centers

Lab Anim Res. 2012 Sep; 28(3): 171-9
Lee Y, Kim JH, Hong Y, Lee SR, Chang KT, Hong Y

Diabetes decreases skeletal muscle mass and induces atrophy. However, the mechanisms by which hyperglycemia and insulin deficiency modify muscle mass are not well defined. In this study, we evaluated the effects of swimming exercise on muscle mass and intracellular protein degradation in diabetic rats, and proposed that autophagy inhibition induced by swimming exercise serves as a hypercatabolic mechanism in the skeletal muscles of diabetic rats, supporting a notion that swimming exercise could efficiently reverse the reduced skeletal muscle mass caused by diabetes. Adult male Sprague-Dawley rats were injected intraperitoneally with streptozotocin (60 mg/kg body weight) to induce diabetes and then submitted to 1 hr per day of forced swimming exercise, 5 days per week for 4 weeks. We conducted an intraperitoneal glucose tolerance test on the animals and measured body weight, skeletal muscle mass, and protein degradation and examined the level of autophagy in the isolated extensor digitorum longus, plantaris, and soleus muscles. Body weight and muscle tissue mass were higher in the exercising diabetic rats than in control diabetic rats that remained sedentary. Compared to control rats, exercising diabetic rats had lower blood glucose levels, increased intracellular contractile protein expression, and decreased autophagic protein expression. We conclude that swimming exercise improves muscle mass in diabetes-induced skeletal muscle atrophy, suggesting the activation of autophagy in diabetes contributes to muscle atrophy through hypercatabolic metabolism and that aerobic exercise, by suppressing autophagy, may modify or reverse skeletal muscle wasting in diabetic patients.
HubMed – rehab


Comparison of alpha-synuclein immunoreactivity in the spinal cord between the adult and aged beagle dog.

Filed under: Rehab Centers

Lab Anim Res. 2012 Sep; 28(3): 165-70
Ahn JH, Choi JH, Park JH, Yan BC, Kim IH, Lee JC, Lee DH, Kim JS, Shin HC, Won MH

Alpha-synuclein (?-syn) is a presynaptic protein that is richly expressed in the central and peripheral nervous systems of mammals, and it is related to the pathogenesis of Parkinson’s disease and other neurodegenerative disorders. In the present study, we compared the distribution of the immunoreactivity of ?-syn and its related gliosis in the spinal cord of young adult (2-3 years) and aged (10-12 years) beagle dogs. We discovered that ?-syn immunoreactivity was present in many neurons in the thoracic level of the aged spinal cord, however, its protein level was not distinct inform that of the adult spinal cord. In addition, ionized calcium-binding adapter molecule-1 (a marker for microglia) immunoreactivity, and not glial fibrillary acidic protein (a marker for astrocytes) immunoreactivity, was somewhat increased in the aged group compared to the adult group. These results indicate that ?-syn immunoreactivity was not dramatically changed in the dog spinal cord during aging.
HubMed – rehab


On the Kinematic Motion Primitives (kMPs) – Theory and Application.

Filed under: Rehab Centers

Front Neurorobot. 2012; 6: 10
Moro FL, Tsagarakis NG, Caldwell DG

Human neuromotor capabilities guarantee a wide variety of motions. A full understanding of human motion can be beneficial for rehabilitation or performance enhancement purposes, or for its reproduction on artificial systems like robots. This work aims at describing the complexity of human motion in a reduced dimensionality, by means of kinematic Motion Primitives (kMPs). A set of five invariant kMPs are identified for periodic motions, and a set of two kMPs for discrete motions. It is shown how these two sets of kMPs can be combined to synthesize more complex motion as the simultaneous execution of the periodic and the discrete motions. The results reported are an evidence of the theory of Central Pattern Generators (CPG), showing its effects on the kinematics, and are related to what presented in the literature on the Motor Primitives extracted from EMG signals. Experimental tests with the COmpliant huMANoid (COMAN) were performed to show that the kMPs extracted from human subjects can be used to transfer the features of human locomotion to the gait of a robot.
HubMed – rehab


Medical Director Responsibilities for Outpatient Cardiac Rehabilitation/Secondary Prevention Programs: 2012 Update: A Statement for Health Care Professionals From the American Association for Cardiovascular and Pulmonary Rehabilitation and the American Heart Association.

Filed under: Rehab Centers

Circulation. 2012 Oct 22;
King M, Bittner V, Josephson R, Lui K, Thomas RJ, Williams MA

Medical directors of cardiac rehabilitation/secondary prevention (CR/SP) programs are responsible for the safe and effective delivery of high-quality CR/SP services to eligible patients. Yet, the training and resources for CR/SP medical directors are limited. As a result, there appears to be considerable variability throughout CR/SP programs in the United States in the roles, responsibilities, and engagement of CR/SP medical directors. Since the publication of the 2005 scientific statement from the American Heart Association and American Association of Cardiovascular and Pulmonary Rehabilitation regarding medical director responsibilities for outpatient CR/SP programs, significant changes have occurred. This statement updates the responsibilities of CR/SP medical directors, in view of changes in federal legislation and regulations and changes in health care delivery and clinical practice that impact the roles and responsibilities of CR/SP medical directors.
HubMed – rehab


Neuroprotective Effect of Atorvastatin Involves Suppression of TNF-? and Upregulation of IL-10 in a Rat Model of Intracerebral Hemorrhage.

Filed under: Rehab Centers

Cell Biochem Biophys. 2012 Oct 23;
Ewen T, Qiuting L, Chaogang T, Tao T, Jun W, Liming T, Guanghong X

We evaluated the neuroprotective effects of atorvastatin (2, 5, and 10 mg/kg) on experimentally induced intracerebral hemorrhage (ICH) in adult rats; controls were administered PBS. Plasma TNF-? and IL-10 levels before and after ICH were analyzed at various time points by enzyme-linked immunosorbent assay (ELISA) and neurological behavior of rats was assessed by climbing scores. At 3-days postoperatively, brain water contents and TNF-?/IL-10 expression in brain tissue were determined. Histopathological changes and microglial cells in the brain tissue were evaluated by light-microscopy. Post-ICH neurological deficits differed significantly between sham-operated group A and experimental-ICH group B (P < 0.05). Brain water contents were significantly less in group A than in group B (P < 0.05). Significant differences (P < 0.05) between two groups were observed regarding activated microglia, TNF-? and IL-10 levels. Compared with group B, neurological deficits, brain water contents, pathological changes, and activated microglia were reduced (P < 0.05) in groups C (Experimental-ICH + atorvastatin 2 mg/kg), D (Experimental-ICH + atorvastatin 5 mg/kg) and E (Experimental-ICH + atorvastatin 10 mg/kg). Atorvastatin-induced a dose-dependent reduction of TNF-? and increase of IL-10 levels (P < 0.05). Therefore, it was concluded that atorvastatin improved neurofunctional rehabilitation in rats through the suppression of cytokines-mediated inflammatory response and attenuation of brain damage following intracerebral hemorrhage. HubMed – rehab



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