In contrast, the less weak proximal weakness patients demonstrated unstable trunk and ankle movements

only for backward directed balance perturbations. Both patient groups used arm movements to compensate for their instability. We conclude that primarily distal but also proximal muscle weakness leads to significant postural instability. This observation, together with the retained ability of patients to use compensatory arm movements, provides targets that may be amenable to improvement with therapeutic intervention. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Alport syndrome (AS) click here is a hereditary glomerulopathy due to abnormal composition of the glomerular basement membrane, leading to end-stage renal disease ( ESRD). Studies of animal models of AS have suggested a variety of potentially effective therapies, but none of these has been definitely shown to prevent or delay ESRD in human AS. Studies in Alport mice suggest that angiotensin inhibition not only has antiproteinuric effects but suppresses cytokine and collagen production as well as tubulointerstitial selleck fibrogenesis and inflammation. For these reasons, many Alport patients are treated

empirically with angiotensin antagonists. Cyclosporine may reduce proteinuria in AS, but the risk of nephrotoxic side effects complicates long-term therapy in children. Current data on the role of HMG-CoA reductase inhibition are sparse, so therapy should be limited to adults with dyslipoproteinemia. Results of some, but not all, studies suggest that bone marrow-derived cells may ameliorate disease in Alport mice. However, until experimental doubts concerning the superiority of bone-marrow transplantation over other treatments are resolved by additional investigation, human research subjects should not be exposed to cell-based therapies that may carry substantial risks. In summary, all potential

therapies are off-label use in children. As a consequence, initial therapeutic trials should focus on the safety and efficiency of medical treatment, as well as the optimal timing of therapy.”
“In the present study, we hypothesized that thymosin beta 4 (Tbeta4) is a potential therapy of multiple sclerosis (MS). To test this out hypothesis, SJL/J mice (n=21) were subjected to experimental autoimmune encephalomyelitis (EAE), an animal model of MS. EAE mice were treated with saline or Tbeta4 (6 mg/kg, n=10) every 3 days starting on the day of myelin proteolipid protein (PLP) immunization for total five doses. Neurological function, inflammatory infiltration, oligodendrocyte progenitor cells (OPCs) and mature oligodendrocytes were measured in the brain of EAE mice. Double immunohistochemical staining was used to detect proliferation and differentiation of OPCs. Tbeta4 was used to treat N20.1 cells (premature oligodendrocyte cell line) in vitro, and proliferation of N20.