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EFFECTS OF PURSED LIP BREATHING AND BILATERAL CHEST WALL AUGMENTATION ON SLOWING RESPIRATORY RATES.Fassett, Ann Carleton. January 1983 (has links)
No description available.
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Hsp90 and hsp70 genes of Theileria annulata : structure, regulation and molecular phylogenySmith, David January 1998 (has links)
No description available.
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Studies on DNA binding and the activation of transcription by the cyclic AMP receptor protein of Escherichia coliBrierley, I. January 1986 (has links)
No description available.
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The role of nitric oxide in the cardiovascular systemRees, Daryl David January 1991 (has links)
Nitric oxide is generated by the vascular endothelium from L-arginine by a constitutive, Ca2+-dependent, NO synthase. Analogues of L-arginine were characterised as inhibitors of NO synthase to investigate the biological significance of the L-arginine-NO pathway in the vessel wall and its role in the cardiovascular system. These inhibitors attenuate the endothelium-dependent vasorelaxation and hypotension induced by various agents, produce an increase in vascular tone and an increase in blood pressure. This suggests that NO is involved in endothelium-dependent relaxation and its continuous release maintains a vasodilator tone and plays a fundamental role in the regulation of blood flow and blood pressure. The removal of the NO-dependent vasodilator tone, results in an `upregulation' of its intracellular receptor, the soluble guanylate cyclase and an increased sensitivity to those vasodilators which act by stimulating this enzyme. This phenomenon of `supersensitivity' to nitrovasodilators may be an important component of their therapeutic action in certain cardiovasulcar disorders. Vascular tissue also expresses an inducible, Ca2+-independent, NO-synthase after activation by lipopolysaccharide (LPS) which results in the generation of large quantities of NO, predominantly from the smooth muscle layer, with a consequent loss of vascular tone and a hyporeactivity to the vasoconstrictor action of phenylephrine. Induction of NO synthase in the vasculature may therefore be responsible for the hypotension and hyporesponsiveness to pressor agents characteristic of endotoxin shock. The glucocorticoid, dexamethasone inhibits the expression of this enzyme but not its activity, which may explain why steroids are more effective at preventing rather than treating this condition. These results suggest that in the cardiovascular system, NO can be considered to have both a protective and a pathological role. The release of small amounts of NO from the constitutive, Ca2+-dependent NO synthase, acts as an adaptive mechanism whereby the vascular endothelium responds to changes in its environment and regulates blood flow and blood pressure to maintain organ perfusion. In contrast, following the induction of the Ca2+-independent NO synthase, after immunological stimulation, NO is released in large quantities from vascular tissue, which may result in pathological vasodilation and tissue damage.
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Regulation of the human tissue factor gene in human umbilical vein endothelial cellsNathwani, Amit Chunilal January 1997 (has links)
No description available.
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Regulation of transcriptional elongation by RNA polymerase IIYankulov, Krassimir Yankov January 1994 (has links)
No description available.
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Recovery of spatial vision following intense light adaptationMargrain, Thomas Hengist January 1997 (has links)
No description available.
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Hypothalamic catecholamines in the regulation of LH secretion in the domestic fowl (Gallus domesticus)Harbuz, M. S. January 1988 (has links)
No description available.
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Characterisation of the rat phenylalanine hydroxylase gene promotorRees, D. January 2000 (has links)
No description available.
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An analysis of Antirrhinum majus cyclin A20 and cyclin D1 function in Arabidopsis thalianaParinyapong, Piyarat January 2002 (has links)
No description available.
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