% of bulk mechanically alloyed n-type Pb1-xSnxTe (when x = 7% and 27%) significantly increase the electrical power produced Ricolinostat by the material when it is doped above 10(19) cm(-3) range. The experimentally measured temperature dependence of the electrical conductivity and Seebeck coefficient of Pb0.93Sn0.07Te
doped to 1.2 x 10(19) cm(-3) and Pb0.73Sn0.27Te doped to 3.8 x 10(18) cm(-3) are shown to be consistent with those calculated in the framework of the Boltzmann transport equations using the relaxation time approximation and a three-band model for which the materials-specific constants are taken from published literature. The SnO2 inclusions are shown to impact the transport coefficients by changing the energy dependence and SNX-5422 in vivo magnitude of the relaxation time due to the charge carrier scattering by a collection of inclusions in a geometry consistent with analysis of the x-ray diffraction data. Analysis of the experimental data shows that Pb0.93Sn0.07Te doped to 1.2 x 10(19) cm(-3) generates more power than would a material without the 2 vol. % of 15 nm SnO2 inclusions. Calculations using the experimentally validated model show that for carrier concentrations greater than 1 x 10(19) cm(-3), the presence
of these inclusions increases the power factor of both alloys in the 300-700 K temperature range. (C) 2011 American Institute of Physics. [doi:10.1063/1.3651173]“
“Nephrotoxicity is a major problem of Cyclosporine A (CsA) treatment, despite its beneficial role in organ transplantation and in a variety of immunologic disorders. This study was undertaken to investigate the potential renoprotective role of telmisartan in amelioration of chronic CsA induced nephrotoxicity. The rats were randomized into 4 equal groups. Group 1 received normal saline (control), group 2 received Cremophor EL and ethanol (CsA vehicle), group 3 received CsA 25 mg/kg/day s.c and group 4 received telmisartan
3 mg/kg/day orally in addition to CsA. The rats were pair fed with a standard chow diet throughout the experiment period (8 weeks). CsA nephrotoxicity NU7441 in vitro was assessed in terms of increased S.Cr (from 0.52 +/- 0.16 to 1.29 +/- 0.20 mg/ml), blood urea (from 24.69 +/- 1.89 to 75.88 +/- 2.33 mg/ml) and serum K (from 3.43 +/- 0.18 to 5.23 +/- 0.43 meq/l). CsA also caused significant increase (p<0.01) in MDA (from 0.74 +/- 0.13 to 2.96 +/- 0.43 nmol/mg protein) and significant decrease (p<0.01) in GSH and catalase in renal tissue. Telmisartan failed to restore the altered renal functions. On the other hand, it causes a significant improvement in the histological changes including the tubulointerstitial fibrosis and arteriolopathy (p<0.01). It also caused significant reduction (p<0.01) in CsA-induced oxidative stress. These findings suggested that telmisartan has a promising renoprotective effect against chronic CsA induced nephrotoxicity.