Paramagnetic structural defects and conductivity in hydrogenated nanocrystalline carbon-doped silicon films

The behavior of paramagnetic defects and dark conductivity in heterogeneous samples of hydrogenated nanocrystalline carbon-containing silicon (nc-SiC:H) prepared by the photo-CVD method is studied. It is shown that, with increasing carbon content in nc-SiC:H, a phase transition from a nanocrystalline to an amorphous structure occurs, producing a reduction in paramagnetic defect density and a significant decrease in the dark conductivity.     

Capabilities of MS for analytical quantitative determination of the ratio of α- and βAsp7 isoforms of the amyloid-β peptide in binary mixtures

There is strong evidence that the amyloid-β peptide (Aβ) plays a crucial role in the pathogenesis of Alzheimer's disease (AD), a lethal neurodegenerative disorder of the elderly. During pathology development, the peptide as well as its various chemically modified isoforms is accumulated in specific brain tissues as characteristic proteinaceous deposits, the so-called amyloid plaques, which are the pathomorphological mark of AD, although the level of Αβ in the blood is the same for healthy individuals and for AD patients. Earlier, it has been shown that isomerization of aspartate 7, the most abundant post-translational modification of the Αβ peptide, is tightly involved in a set of molecular processes associated with AD progression. Therefore, the isoAsp 7-containing Αβ isomer (isoAβ) is assumed to be a potential biomarker of AD that can be identified in the blood. Here, we present an analytical mass spectrometric method for quantitative determination of the ratio of normal and isomerized Αβ fragments 1-16 in their binary mixtures, and all analytical capabilities, such as accuracy, detection limits, and sensitivity of the presented method, are determined and thoroughly discussed. On the basis of this method, an analytical approach for quantitative determination of this modification in the blood will be developed in further studies.     

Using Ultrahigh-Molecular-Weight Polyethylene in Hydraulic Drives

Russian Engineering Research - The use of ultrahigh-molecular-weight polyethylene (UHMWPE) in manufacturing is proposed—in particular, for the cuffs of hydraulic drives. The properties of...     

In Vivo Inhibition of TRPC6 by SH045 Attenuates Renal Fibrosis in a New Zealand Obese (NZO) Mouse Model of Metabolic Syndrome

Metabolic syndrome is a significant worldwide public health challenge and is inextricably linked to adverse renal and cardiovascular outcomes. The inhibition of the transient receptor potential cation channel subfamily C member 6 (TRPC6) has been found to ameliorate renal outcomes in the unilateral ureteral obstruction (UUO) of accelerated renal fibrosis. Therefore, the pharmacological inhibition of TPRC6 could be a promising therapeutic intervention in the progressive tubulo-interstitial fibrosis in hypertension and metabolic syndrome. In the present study, we hypothesized that the novel selective TRPC6 inhibitor SH045 (larixyl N-methylcarbamate) ameliorates UUO-accelerated renal fibrosis in a New Zealand obese (NZO) mouse model, which is a polygenic model of metabolic syndrome. The in vivo inhibition of TRPC6 by SH045 markedly decreased the mRNA expression of pro-fibrotic markers (Col1α1, Col3α1, Col4α1, Acta2, Ccn2, Fn1) and chemokines (Cxcl1, Ccl5, Ccr2) in UUO kidneys of NZO mice compared to kidneys of vehicle-treated animals. Renal expressions of intercellular adhesion molecule 1 (ICAM-1) and α-smooth muscle actin (α-SMA) were diminished in SH045- versus vehicle-treated UUO mice. Furthermore, renal inflammatory cell infiltration (F4/80+ and CD4+) and tubulointerstitial fibrosis (Sirius red and fibronectin staining) were ameliorated in SH045-treated NZO mice. We conclude that the pharmacological inhibition of TRPC6 might be a promising antifibrotic therapeutic method to treat progressive tubulo-interstitial fibrosis in hypertension and metabolic syndrome.