Using heme oxygenase-1 expression as a model, we demonstrate diff

Using heme oxygenase-1 expression as a model, we demonstrate differential heme oxygenase-1 induction by atorvastatin in athero-resistant compared with atheroprone sites of the murine aorta. In vitro, exposure of human endothelial cells to laminar shear stress significantly reduced the statin concentration required to induce heme oxygenase-1 and protect against H(2)O(2)-mediated injury. Synergy

was observed between laminar shear stress and atorvastatin, resulting in optimal expression of heme oxygenase-1 and resistance to oxidative stress, a response inhibited by heme oxygenase-1 small interfering RNA. Moreover, treatment of laminar shear stress-exposed endothelial cells resulted in a significant fall in intracellular cholesterol. Mechanistically, synergy required Akt phosphorylation, activation of Kruppel-like factor 2, NF-E2-related factor-2 (Nrf2), Selleck AZD1208 increased nitric-oxide synthase activity, and enhanced HO-1 mRNA stability. In contrast, heme oxygenase-1 induction by atorvastatin in endothelial cells exposed to oscillatory flow was markedly attenuated. We have identified a novel relationship between laminar shear stress and statins, demonstrating that atorvastatin-mediated heme oxygenase-1-dependent antioxidant effects are laminar shear stress-dependent, proving the principle that biomechanical signaling contributes significantly to endothelial responsiveness

to pharmacological agents. Our findings suggest statin pleiotropy may be suboptimal at disturbed flow atherosusceptible sites, Selleck FG 4592 emphasizing the need for more specific U0126 therapeutic agents, such as those targeting Kruppel-like factor 2 or Nrf2.”
“We evaluated Verbal IQ (VIQ)-Performance IQ (PIQ) and Verbal Comprehension Index (VCI)-Perceptual Organization Index (POI) discrepancies among 16 patients with right-sided and 20 with left-sided cerebral lesions. Means for age and education among left hemisphere-damaged patients were 46.25 years (SD = 17.42)

and 12.17 years (SD = 2.87). Means and standard deviations for age and education were 47.86 years (SD = 16.83) and 12.27 years (SD = 2.46) for those with right-sided damage. Left hemisphere lesions produced nonsignificant VIQ < PIQ and VCI < POI means, whereas right hemisphere damage resulted in significant VIQ > PIQ and VCI > POI mean discrepancies. Additional analyses indicated that neither discrepancy score was effective in identifying lateralized brain damage.”
“The distribution of poly(acrylic acid) (PAA) in model laminates of nanocellulose and poly(vinyl alcohol) (PVOH) was investigated by FTIR chemical imaging. The method was effective in spatially discerning the three components of the composite. PAA can potentially improve the performance of nanocellulose reinforced PVOH by not only crosslinking the PVOH matrix but also improving the adhesion between PVOH and nanocellulose by forming ester linkages with both of them.

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