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10.1152/ajplung.00252.2009 http://scihub22266oqcxt.onion/10.1152/ajplung.00252.2009 19915160!2822559!19915160     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Lung+Cell+Mol+Physiol 2010 ; 298 (2): L139-47 Nephropedia Template TP {{tp|p=19915160|t=2010. Role of hypoxia-inducible factor 1alpha in modulating cobalt-induced lung inflammation |pdf=|usr=}}{{19915160}} gab.com Text Role of hypoxia-inducible factor 1alpha in modulating cobalt-induced lung inflammation JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=19915160 #FOAvip Hypoxia plays an important role in development, cellular homeostasis, and pathological conditions, such as cancer and stroke. There is also growing evidence that hypoxia is an important modulator of the inflammatory process. Hypoxia-inducible factors (HIFs) are a family of proteins that regulate the cellular response to oxygen deficit, and loss of HIFs impairs inflammatory cell function. There is little known, however, about the role of epithelial-derived HIF signaling in modulating inflammation. Cobalt is capable of eliciting an allergic response and promoting HIF signaling. To characterize the inflammatory function of epithelial-derived HIF in response to inhaled cobalt, a conditional lung-specific HIF1alpha, the most ubiquitously expressed HIF, deletion mouse, was created. Control mice showed classic signs of metal-induced injury following cobalt exposure, including fibrosis and neutrophil infiltration. In contrast, HIF1alpha-deficient mice displayed a Th2 response that resembled asthma, including increased eosinophilic infiltration, mucus cell metaplasia, and chitinase-like protein expression. The results suggest that epithelial-derived HIF signaling has a critical role in establishing a tissue's inflammatory response, and compromised HIF1alpha signaling biases the tissue towards a Th2-mediated reaction. Twit Text FOAVip Role of hypoxia-inducible factor 1alpha in modulating cobalt-induced lung inflammation ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=19915160 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19915160 #FOAvip English Wikipedia <ref>{{Cite pmid|19915160}}</ref> Role of hypoxia-inducible factor 1alpha in modulating cobalt-induced lung inflammation #MMPMID19915160 Saini Y; Kim KY; Lewandowski R; Bramble LA; Harkema JR; Lapres JJ Am J Physiol Lung Cell Mol Physiol 2010[Feb]; 298 (2): L139-47 PMID19915160show ga Hypoxia plays an important role in development, cellular homeostasis, and pathological conditions, such as cancer and stroke. There is also growing evidence that hypoxia is an important modulator of the inflammatory process. Hypoxia-inducible factors (HIFs) are a family of proteins that regulate the cellular response to oxygen deficit, and loss of HIFs impairs inflammatory cell function. There is little known, however, about the role of epithelial-derived HIF signaling in modulating inflammation. Cobalt is capable of eliciting an allergic response and promoting HIF signaling. To characterize the inflammatory function of epithelial-derived HIF in response to inhaled cobalt, a conditional lung-specific HIF1alpha, the most ubiquitously expressed HIF, deletion mouse, was created. Control mice showed classic signs of metal-induced injury following cobalt exposure, including fibrosis and neutrophil infiltration. In contrast, HIF1alpha-deficient mice displayed a Th2 response that resembled asthma, including increased eosinophilic infiltration, mucus cell metaplasia, and chitinase-like protein expression. The results suggest that epithelial-derived HIF signaling has a critical role in establishing a tissue's inflammatory response, and compromised HIF1alpha signaling biases the tissue towards a Th2-mediated reaction. |*Cobalt/immunology/pharmacology[MESH] |Animals[MESH] |Asthma/chemically induced/immunology[MESH] |Body Weight[MESH] |Bronchoalveolar Lavage Fluid/cytology[MESH] |Cytokines/immunology[MESH] |Gene Expression Profiling[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism[MESH] |Inflammation/*chemically induced/immunology[MESH] |Lung/cytology/*drug effects/*immunology/pathology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Mice, Transgenic[MESH]Role of hypoxia-inducible factor 1alpha in modulating cobalt-induced l(epmc).pdf DeepDyve Pubget Overpricing