Promotion of plasma membrane repair by vitamin E

Severe vitamin E deficiency results in lethal myopathy in animal models. Membrane repair is an important myocyte response to plasma membrane disruption injury as when repair fails, myocytes die and muscular dystrophy ensues. Here we show that supplementation of cultured cells with α-tocopherol, the most common form of vitamin E, promotes plasma membrane repair. Conversely, in the absence of α-tocopherol supplementation, exposure of cultured cells to an oxidant challenge strikingly inhibits repair. Comparative measurements reveal that, to promote repair, an anti-oxidant must associate with membranes, as α-tocopherol does, or be capable of α-tocopherol regeneration. Finally, we show that myocytes in intact muscle cannot repair membranes when exposed to an oxidant challenge, but show enhanced repair when supplemented with vitamin E. Our work suggests a novel biological function for vitamin E in promoting myocyte plasma membrane repair. We propose that this function is essential for maintenance of skeletal muscle homeostasis

Validating the model of predictors of academic self-handicapping behavior

The main aim of the present study is to validate the model of predictors of self-handicapping behavior (POASH) on the data derived from undergraduate students in an ongoing co-curriculum compulsory course. The study adapted and extended the original theory of reciprocal interaction of emotion, cognition and behavior by adding self-handicapping behavior component. In so doing, this study assessed the direct and indirect effects of emotion, cognition and behavior via student engagement on self-handicapping behavior. The second purpose of the study is to evaluate gender and nationality status invariants of the causal structure of POASH. This cross-validation procedure determined whether gender and nationality status moderated the causal structure of the model, and thus the generality of POASH. The data was collected from two self-reported questionnaires administered to 790 undergraduates of an International Islamic University in Malaysia. A confirmatory three-step approach theory testing and development using Maximum Likelihood method was applied. The results of structured equation modeling supported the adequacy of POASH and the causal structure of POASH proved to be applicable to both genders and nationality statuses

Transmission of Systemic AA Amyloidosis in Animals

Amyloidoses are a group of protein-misfolding disorders that are characterized by the deposition of amyloid fibrils in organs and/or tissues. In reactive amyloid A (AA) amyloidosis, serum AA (SAA) protein forms deposits in mice, domestic and wild animals, and humans that experience chronic inflammation. AA amyloid fibrils are abnormal beta-sheet-rich forms of the serum precursor SAA, with conformational changes that promote fibril formation. Extracellular deposition of amyloid fibrils causes disease in affected animals. Recent findings suggest that AA amyloidosis could be transmissible. Similar to the pathogenesis of transmissible prion diseases, amyloid fibrils induce a seeding-nucleation process that may lead to development of AA amyloidosis. We review studies of possible transmission in bovine, avian, mouse, and cheetah AA amyloidosis