Low-cost flexible supercapacitors with high-energy density based on nanostructured MnO2 and Fe2O3 thin films directly fabricated onto stainless steel.

The facile and economical electrochemical and successive ionic layer adsorption and reaction (SILAR) methods have been employed in order to prepare manganese oxide (MnO2) and iron oxide (Fe2O3) thin films, respectively with the fine optimized nanostructures on highly flexible stainless steel sheet. The symmetric and asymmetric flexible-solid-state supercapacitors (FSS-SCs) of nanostructured (nanosheets for MnO2 and nanoparticles for Fe2O3) electrodes with Na2SO4/Carboxymethyl cellulose (CMC) gel as a separator and electrolyte were assembled. MnO2 as positive and negative electrodes were used to fabricate symmetric SC, while the asymmetric SC was assembled by employing MnO2 as positive and Fe2O3 as negative electrode. Furthermore, the electrochemical features of symmetric and asymmetric SCs are systematically investigated. The results verify that the fabricated symmetric and asymmetric FSS-SCs present excellent reversibility (within the voltage window of 0-1 V and 0-2 V, respectively) and good cycling stability (83 and 91%, respectively for 3000 of CV cycles). Additionally, the asymmetric SC shows maximum specific capacitance of 92 Fg(-1), about 2-fold of higher energy density (41.8 Wh kg(-1)) than symmetric SC and excellent mechanical flexibility. Furthermore, the "real-life" demonstration of fabricated SCs to the panel of SUK confirms that asymmetric SC has 2-fold higher energy density compare to symmetric SC.

Use of NSE/PS2m-transgenic mice in the study of the protective effect of exercise on Alzheimer's disease.

In its late stage, Alzheimer's disease results in progressive muscle weakness in the arms and legs. The aim of this study was to determine whether mice expressing the skeletal muscle-specific mutant PS2 gene (a model of Alzheimer's disease) are a useful experimental system to study the protective effect of exercise on A beta-42 reduction, improvement of behavioural function and changes in metabolic parameters. With this aim in mind, the transgenic mice were subjected to treadmill exercise for 3 months. The results showed that in transgenic mice, but not in normal mice, treadmill exercise resulted in a reduction of A beta-42 deposits and an improvement in behavioural function, thereby restoring normal concentrations of total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and triglyceride. Thus, exercise may represent a practical therapeutic strategy for use with human patients with Alzheimer's disease.

Alterations in behavior, amyloid beta-42, caspase-3, and Cox-2 in mutant PS2 transgenic mouse model of Alzheimer's disease.

Alzheimer's disease (AD) occurs when neurons in the memory and cognition regions of the brain are accompanied by an accumulation of the long amyloid beta-proteins of the 39 to 43 amino acids derived from the amyloid precursor protein (APP) by cleavage with beta- and gamma-secretase. An increased production of Abeta-42 by mutation of PS2 genes promotes caspase expression and is associated with the Cox-2 found in the brain of AD patients. To address this question in vivo, we expressed the human mutant PS2 (hPS2m) (N141I) as well as wild PS2 (hPS2w) as a control in transgenic (Tg) mice under control of the neuron-specific enolase (NSE) promoter. Water maze tests were used to demonstrate the behavioral defect; dot blot, Western blot, and immunohistochemical analyses were performed on the brain with the hPS2, Abeta-42, caspase-3, and Cox-2 antibody. We concluded that 1) Tg mice showed a behavioral dysfunction in the water maze test, 2) levels of hPS2, Abeta-42, caspase-3, and Cox-2 expression were modulated in the brains of both Tg mice, 3) dense staining with antibody to hPS2, Abeta-42, caspase-3, and Cox-2 was visible in the brains of Tg mice compared with age-matched control mice, and 4) distinguishable AD phenotypes between hPS2w- and hPS2m-Tg mice did not appear. These results suggest that an elevation of Abeta-42 by overexpression of hPS2 and mutation of hPS2m might induce the behavioral deficit and caspase-3 and Cox-2 induction, which could be useful in the therapeutic testing of compounds to have considerable clinical effects.