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10.1007/s00408-018-0154-2 http://scihub22266oqcxt.onion/10.1007/s00408-018-0154-2 C6283619!6283619!30167842     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Lung 2018 ; 196 (6): 737-43 Nephropedia Template TP {{tp|p=30167842|t=2018. TIMP-1 Promotes the Immune Response in Influenza Induced Acute Lung Injury |pdf=|usr=}}{{30167842}} gab.com Text TIMP-1 Promotes the Immune Response in Influenza Induced Acute Lung Injury JO: Lung http://www.kidney.de/pget.php?&tw=1&pmid=30167842 #FOAvip Introduction: Influenza infects millions of people each year causing respiratory distress and death in severe cases. On average, 200,000 people annually are hospitalized in the United States for influenza related complications. Tissue inhibitor of metalloproteinase-1 (TIMP-1), a secreted protein that inhibits MMPs, has been found to be involved in lung inflammation. Here, we evaluated the role of TIMP-1 in the host response to influenza-induced lung injury. Methods: Wild-type and Timp1-deficient (Timp1?/?) mice that were 8-12 weeks old were administered A/PR/8/34 (PR8), a murine adapted H1N1 influenza virus, and euthanized 6 days after influenza installation. Bronchoalveolar lavage fluid and lungs were harvested from each mouse for ELISA, protein assay, PCR, and histological analysis. Cytospins were executed on bronchoalveolar lavage fluid to identify immune cells based on morphology and cell count. Results: Wild-type mice experienced significantly more weight loss compared to Timp1?/? mice after influenza infection. Wild-type mice demonstrated more immune cell infiltrate and airway inflammation. Interestingly, PR8 levels were identical between the wild-type and Timp1?/? mice 6 days post-influenza infection. Conclusion: The data suggests that Timp1 promotes the immune response in the lungs after influenza infection facilitating an injurious phenotype as a result of influenza infection. Twit Text FOAVip TIMP-1 Promotes the Immune Response in Influenza Induced Acute Lung Injury ????Lung http://www.kidney.de/pget.php?&tw=1&pmid=30167842 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30167842 #FOAvip English Wikipedia <ref>{{Cite pmid|30167842}}</ref> TIMP-1 Promotes the Immune Response in Influenza Induced Acute Lung Injury #MMPMID30167842 Allen JR; Ge L; Huang Y; Brauer R; Parimon T; Cassel S; Sutterwala F; Peter C Lung 2018[Dec]; 196 (6): 737-43 PMID30167842show ga Introduction: Influenza infects millions of people each year causing respiratory distress and death in severe cases. On average, 200,000 people annually are hospitalized in the United States for influenza related complications. Tissue inhibitor of metalloproteinase-1 (TIMP-1), a secreted protein that inhibits MMPs, has been found to be involved in lung inflammation. Here, we evaluated the role of TIMP-1 in the host response to influenza-induced lung injury. Methods: Wild-type and Timp1-deficient (Timp1?/?) mice that were 8-12 weeks old were administered A/PR/8/34 (PR8), a murine adapted H1N1 influenza virus, and euthanized 6 days after influenza installation. Bronchoalveolar lavage fluid and lungs were harvested from each mouse for ELISA, protein assay, PCR, and histological analysis. Cytospins were executed on bronchoalveolar lavage fluid to identify immune cells based on morphology and cell count. Results: Wild-type mice experienced significantly more weight loss compared to Timp1?/? mice after influenza infection. Wild-type mice demonstrated more immune cell infiltrate and airway inflammation. Interestingly, PR8 levels were identical between the wild-type and Timp1?/? mice 6 days post-influenza infection. Conclusion: The data suggests that Timp1 promotes the immune response in the lungs after influenza infection facilitating an injurious phenotype as a result of influenza infection. äTIMP-1 Promotes the Immune Response in Influenza Induced Acute Lung In(epmc).pdf DeepDyve Pubget Overpricing