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10.1038/s41598-019-53293-0 http://scihub22266oqcxt.onion/10.1038/s41598-019-53293-0 31727956!6856518!31727956     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31727956&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Sci+Rep 2019 ; 9 (1): 16774 Nephropedia Template TP {{tp|p=31727956|t=2019. Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis |pdf=|usr=}}{{31727956}} gab.com Text Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=31727956 #FOAvip Acute pancreatitis is characterized by an early intracellular protease activation and invasion of leukocytes into the pancreas. Cathepsins constitute a large group of lysosomal enzymes, that have been shown to modulate trypsinogen activation and neutrophil infiltration. Cathepsin G (CTSG) is a neutrophil serine protease of the chymotrypsin C family known to degrade extracellular matrix components and to have regulatory functions in inflammatory disorders. The aim of this study was to investigate the role of CTSG in pancreatitis. Isolated acinar cells were exposed to recombinant CTSG and supramaximal cholezystokinin stimulation. In CTSG(-/-) mice and corresponding controls acute experimental pancreatitis was induced by serial caerulein injections. Severity was assessed by histology, serum enzyme levels and zymogen activation. Neutrophil infiltration was quantified by chloro-acetate ersterase staining and myeloperoxidase measurement. CTSG was expessed in inflammatory cells but not in pancreatic acinar cells. CTSG had no effect on intra-acinar-cell trypsinogen activation. In CTSG(-/-) mice a transient decrease of neutrophil infiltration into the pancreas and lungs was found during acute pancreatitis while the disease severity remained largely unchanged. CTSG is involved in pancreatic neutrophil infiltration during pancreatitis, albeit to a lesser degree than the related neutrophil (PMN) elastase. Its absence therefore leaves pancreatitis severity essentially unaffected. Twit Text FOAVip Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=31727956 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31727956 #FOAvip English Wikipedia <ref>{{Cite pmid|31727956}}</ref> Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis #MMPMID31727956 Aghdassi AA; John DS; Sendler M; Storck C; van den Brandt C; Kruger B; Weiss FU; Mayerle J; Lerch MM Sci Rep 2019[Nov]; 9 (1): 16774 PMID31727956show ga Acute pancreatitis is characterized by an early intracellular protease activation and invasion of leukocytes into the pancreas. Cathepsins constitute a large group of lysosomal enzymes, that have been shown to modulate trypsinogen activation and neutrophil infiltration. Cathepsin G (CTSG) is a neutrophil serine protease of the chymotrypsin C family known to degrade extracellular matrix components and to have regulatory functions in inflammatory disorders. The aim of this study was to investigate the role of CTSG in pancreatitis. Isolated acinar cells were exposed to recombinant CTSG and supramaximal cholezystokinin stimulation. In CTSG(-/-) mice and corresponding controls acute experimental pancreatitis was induced by serial caerulein injections. Severity was assessed by histology, serum enzyme levels and zymogen activation. Neutrophil infiltration was quantified by chloro-acetate ersterase staining and myeloperoxidase measurement. CTSG was expessed in inflammatory cells but not in pancreatic acinar cells. CTSG had no effect on intra-acinar-cell trypsinogen activation. In CTSG(-/-) mice a transient decrease of neutrophil infiltration into the pancreas and lungs was found during acute pancreatitis while the disease severity remained largely unchanged. CTSG is involved in pancreatic neutrophil infiltration during pancreatitis, albeit to a lesser degree than the related neutrophil (PMN) elastase. Its absence therefore leaves pancreatitis severity essentially unaffected. |Acinar Cells/*cytology/drug effects/immunology[MESH] |Animals[MESH] |Cathepsin G/*genetics[MESH] |Cells, Cultured[MESH] |Ceruletide/*adverse effects[MESH] |Disease Models, Animal[MESH] |Gene Knockout Techniques[MESH] |Granulocytes/metabolism[MESH] |Male[MESH] |Mice[MESH] |Neutrophil Infiltration[MESH] |Neutrophils/*metabolism[MESH] |Pancreatitis/chemically induced/genetics/*immunology[MESH]Absence of the neutrophil serine protease cathepsin G decreases neutro(epmc).pdf DeepDyve Pubget Overpricing