Titlebook: Cell Signaling in Vascular Inflammation; Jahar Bhattacharya (Professor of Physiology and Ce Book 2005 Humana Press 2005 biology.calcium.ci

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1 Quantifying global climate systems,ossesses a wide range of chemical reactivity and multiple potential reactive targets. Three basic biochemical pathways—interaction with metal centers, reaction with reduced thiols, and production of nitrogen oxides—will be considered and discussed in terms of modulating the biological function of proteins by nitric oxide.

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Heme Oxygenase-1 and Carbon Monoxide in Vascular Regulation,de synthase (NOS) systems, respectively, play significant roles in the regulation of vascular function. The HO enzymes exist in both constitutive (HO-2, HO-3) and inducible (HO-1) isoforms, the latter identified as a component of the cellular stress response. HO converts heme to CO, biliverdin, and

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,Tumor Necrosis Factor-α/Receptor Signaling Through the Akt Kinase,pe in the body. TNF promotes immunity, but its expression is also associated with pathologies, such as rheumatoid arthritis, type II diabetes, and cachexia. Two distinct cell-surface receptors bind TNF, the type I receptor (TNFR1), which contains a conserved motif called a “death domain“ in its C-te

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cGMP-Dependent Protein Kinase in Regulation of the Perinatal Pulmonary Circulation,ation and a fall in pulmonary vascular resistance. In the perinatal period, both cAMP and cyclic guanosine monophosphate (cGMP) act via cGMP-dependent protein kinase (PKG) in mediating relaxation of the pulmonary circulation, with cGMP working predominantly via PKG. Oxygen exposure results in an inc

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Glutamate Receptor Activation in the Pathogenesis of Acute Lung Injury,em. But overactivation of these receptors can produce neuronal cell injury and death. Recent studies show that the glutamate agonist N-methyl-D-aspartate (NMDA) can trigger acute lung injury (ALI), manifested by high-permeability pulmonary edema, and that NMDA receptor subtypes are expressed in norm

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Pressure-Induced Inflammatory Signaling in Lung Endothelial Cells,t only of pulmonary edema, but also of inflammatory reactions in the lung. These processes are largely attributable to mechano-induced second-messenger responses in lung capillary endothelial cells. Pressure- and stretch-induced mobilization of intra- and extracellular calcium mediates an increase i