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Although zinc oxide (ZnO) has a high theoretical capacity for lithium (Li) storage, it has poor cyclability because of the huge volume changes during charge-discharge cycles resulting in particle pulverization and detachment from the current collector. In this paper, a novel anode architecture for Li-ion batteries fabricated by encapsulation of ZnO nanoparticles in the hollow core of glassy carbon-reduced graphene oxide (C-rGO) electrospun composite nanofibers, is described. A one-step, co-axial electrospinning method is used to synthesize a mat of core-shell structured composite nanofibers composed of rGO embedded in poly(acrylonitrile) (shell) and a ZnO nanoparticle precursor with a carrier polymer (core).Subsequent calcination and carbonization produce a mechanically stable anode material, which is used directly as a free-standing anode ($60 mm thick) without any binder and current collector, which are inactive materials that only add to the battery mass and volume. The ZnO-C-rGO nanofiber composite was characterized by scanning electron microscopy, transmission electron microscopy, Raman spectroscopy and X-ray diffraction. The electrochemical performance of the composite was studied by galvanostatic charge-discharge measurements at different current densities, slow scan cyclic voltammetry (CV) and impedance measurements. Incorporation of an rGO network in the glassy nanofiber shell enhances both the capacity and electrical conductivity of the mat electrode resulting in faster electron kinetics, and thus, an improved rate capability. The interior void spaces combined with the mechanical strength and flexibility of the C-rGO shell act as a structural buffer effectively relieving the volumetric stresses generated during charge-discharge cycles. The synergistic effect of the metal oxide, rGO and the core-shell design results in a high capacity of 815 mA h g À1 at a current density of 50 mA g À1 with capacity retention of almost 80% after 100 cycles, thus demonstrating significant potential as an anode substitute for next generation Li-ion batteries.

The role of defective mismatch repair (MMR) system in ovarian carcinoma is not well defined. The purpose of the study was to determine the relationship between microsatellite instability (MSI), promoter methylation and protein expression of MMR genes in epithelial ovarian carcinoma (EOC). MSI and promoter methylation of MLH1, MSH2 and PMS2 genes were studied using PCR methods in the study cohort. A small subset of samples was used to analyze the protein expression by immunohistochemistry (IHC). MSI was observed in >60% of tumor samples and 47% of normal ovaries. MLH1 was methylated in 37.5% and 64.3% EOCs and LMP tumors. The loss of immunoexpression of MMR genes was not seen in ovarian tumors. There was no correlation between MSI, promoter methylation and protein expression of the MMR genes suggesting that each may function independently. MSI is a common event in ovarian carcinoma and may increase the clinical awareness of the subset of tumors.

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Free standing hollow carbon nanofiber (CNF) mats with high graphitic content have been fabricated through co-axial electrospinning followed by high temperature pyrolysis.

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The aim of our study was to find out the antiproteinuric effect of enalapril angiotensin-converting enzyme (ACE inhibitor) alone or in combination with cilnidipine in patients with type-2 diabetes mellitus. The study was conducted on 71 patients with type-2 diabetes mellitus patients with hypertension and microalbuminuria. They were divided into two groups randomly as follows: Group I (enalaprilalone, n = 36) and Group II (enalapril with cilnidipine, n = 35). In both the groups, baseline 24 h urinary albumin was estimated and was repeated every 3 months upto 1-year. After 1-year follow-up, reduction in microalbuminuria was found to be greater in Group II. In Group I microalbuminuria came down by 25.68 ± 21.40 while in Group II it reduced by 54.88 ± 13.84 (P < 0.001). We conclude that in diabetic population, cilnidipine has an additive effect in microalbuminuria reduction over and above the well-proven effect of ACE inhibitors.