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10.1093/toxsci/kfq155 http://scihub22266oqcxt.onion/10.1093/toxsci/kfq155 20511350!2905409!20511350     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Toxicol+Sci 2010 ; 116 (2): 673-81 Nephropedia Template TP {{tp|p=20511350|t=2010. Acute cobalt-induced lung injury and the role of hypoxia-inducible factor 1alpha in modulating inflammation |pdf=|usr=}}{{20511350}} gab.com Text Acute cobalt-induced lung injury and the role of hypoxia-inducible factor 1alpha in modulating inflammation JO: Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=20511350 #FOAvip Air pollution is a critical factor in the development and exacerbation of pulmonary diseases. Ozone, automobile exhaust, cigarette smoke, and metallic dust are among the potentially harmful pollution components that are linked to disease progression. Transition metals, such as cobalt, have been identified at significant levels in air pollution. Cobalt exerts numerous biological effects, including mimicking hypoxia. Similar to hypoxia, cobalt exposure results in the stabilization of hypoxia-inducible factors (HIFs), a family of proteins that regulate the cellular response to oxygen deficit. HIFs also play an important role in innate immunity and inflammatory processes. To characterize the role of HIF1alpha, the most ubiquitously expressed HIF, in the early events during cobalt-induced lung inflammation, an inducible lung-specific HIF1alpha deletion model was employed. Control mice showed classical signs of metal-induced injury following cobalt exposure, including neutrophilic infiltration and induction of Th1 cytokines. In contrast, HIF1alpha-deficient mice exhibited pronounced eosinophil counts in bronchoalveolar lavage fluid and lung tissue complemented with Th2 cytokine induction. The timing of these results suggests that the loss of epithelial-derived HIF1alpha alters the lung's innate immune response and biases the tissue toward a Th2-mediated inflammation. Twit Text FOAVip Acute cobalt-induced lung injury and the role of hypoxia-inducible factor 1alpha in modulating inflammation ????Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=20511350 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20511350 #FOAvip English Wikipedia <ref>{{Cite pmid|20511350}}</ref> Acute cobalt-induced lung injury and the role of hypoxia-inducible factor 1alpha in modulating inflammation #MMPMID20511350 Saini Y; Greenwood KK; Merrill C; Kim KY; Patial S; Parameswaran N; Harkema JR; LaPres JJ Toxicol Sci 2010[Aug]; 116 (2): 673-81 PMID20511350show ga Air pollution is a critical factor in the development and exacerbation of pulmonary diseases. Ozone, automobile exhaust, cigarette smoke, and metallic dust are among the potentially harmful pollution components that are linked to disease progression. Transition metals, such as cobalt, have been identified at significant levels in air pollution. Cobalt exerts numerous biological effects, including mimicking hypoxia. Similar to hypoxia, cobalt exposure results in the stabilization of hypoxia-inducible factors (HIFs), a family of proteins that regulate the cellular response to oxygen deficit. HIFs also play an important role in innate immunity and inflammatory processes. To characterize the role of HIF1alpha, the most ubiquitously expressed HIF, in the early events during cobalt-induced lung inflammation, an inducible lung-specific HIF1alpha deletion model was employed. Control mice showed classical signs of metal-induced injury following cobalt exposure, including neutrophilic infiltration and induction of Th1 cytokines. In contrast, HIF1alpha-deficient mice exhibited pronounced eosinophil counts in bronchoalveolar lavage fluid and lung tissue complemented with Th2 cytokine induction. The timing of these results suggests that the loss of epithelial-derived HIF1alpha alters the lung's innate immune response and biases the tissue toward a Th2-mediated inflammation. |Animals[MESH] |Bronchoalveolar Lavage Fluid/chemistry/cytology[MESH] |Cobalt/*toxicity[MESH] |Cytokines/genetics[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*physiology[MESH] |Immunity, Innate/drug effects[MESH] |Inflammation/*etiology[MESH] |Lung/*drug effects/immunology/pathology[MESH] |Mice[MESH]Acute cobalt-induced lung injury and the role of hypoxia-inducible fac(epmc).pdf DeepDyve Pubget Overpricing