05) Conclusions: In a porcine model of ischemic HF, acute SCS im

05). Conclusions: In a porcine model of ischemic HF, acute SCS improved global and regional LV contractile function and intraventricular dyssynchrony, and decreased myocardial oxygen consumption without elevation of norepinephrine level. (J Cardiovasc Electrophysiol, Vol. 23, pp. 534-540, May 2012)”
“Context: Glucocorticoids are crucial in fetal lung

function. The amount of cortisol available to its receptors is increased by 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1). Glucocorticoids and IL-1 beta are known to induce 11 beta-HSD1 expression in a number of tissues, but controversial results were obtained with regard to 11 beta-HSD1 expression in human fetal lung.\n\nObjective: We examined the expression of 11 beta-HSD1 and its regulation by cortisol and IL-1 beta in human fetal lung.\n\nResults: Immunohistochemistry revealed 11 Adriamycin beta-HSD1 expression in the epithelium and mesenchymal layer of the small bronchus and bronchiole of human fetal lung at 8 months but not at 4 months gestation, which

was confirmed by PCR revealing 11 beta-HSD1 mRNA expression in the fetal lung tissue. By using a cell line derived from human fetal lung fibroblasts, we demonstrated that cortisol (10(-5) to 10(-3) mmol/liter) or IL-1 beta (0.1 to 10 ng/ml) induced 11 beta-HSD1 mRNA expression in a concentration-dependent manner. The induction of 11 beta-HSD1 by IL-1 beta was further increased Fosbretabulin manufacturer by cortisol, whereas the induction of cyclooxygenase 2 by IL-1 beta was inhibited by cortisol. Nuclear factor kappa B activation MDV3100 mouse inhibitor could only block the induction of cyclooxygenase 2 but not 11 beta-HSD1 by IL-1 beta, suggesting that different mechanisms were utilized by IL-1 beta in the regulation of 11 beta-HSD1 versus proinflammatory mediators. Global inhibition of CCAAT-enhancer-binding proteins (C/EBPs) with transfection of C/EBP-specific dominant-negative expression plasmid could attenuate the induction of 11

beta-HSD1 by IL-1 beta, suggesting that C/EBPs may mediate the induction of 11 beta-HSD1 by IL-1 beta.\n\nConclusions: 11 beta-HSD1 is expressed in human fetal lung; cortisol and IL-1 beta could synergistically induce its expression. (J Clin Endocrinol Metab 94: 306-313, 2009)”
“Background: Little is known about the potential of Brachypodium distachyon as a model for low temperature stress responses in Pooideae. The ice recrystallization inhibition protein (IRIP) genes, fructosyltransferase (FST) genes, and many C-repeat binding factor (CBF) genes are Pooideae specific and important in low temperature responses. Here we used comparative analyses to study conservation and evolution of these gene families in B. distachyon to better understand its potential as a model species for agriculturally important temperate grasses.

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