Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/cddiscovery.2017.56 http://scihub22266oqcxt.onion/10.1038/cddiscovery.2017.56 C5611684!5611684!28955505     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Discov 2017 ; 3 (ä): 17056- Nephropedia Template TP {{tp|p=28955505|t=2017. Necroptotic debris including damaged mitochondria elicits sepsis-like syndrome during late-phase tularemia |pdf=|usr=}}{{28955505}} gab.com Text Necroptotic debris including damaged mitochondria elicits sepsis-like syndrome during late-phase tularemia JO: Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=28955505 #FOAvip Infection with Francisella tularensis ssp. tularensis (Ft) strain SchuS4 causes an often lethal disease known as tularemia in rodents, non-human primates, and humans. Ft subverts host cell death programs to facilitate their exponential replication within macrophages and other cell types during early respiratory infection (?72?h). The mechanism(s) by which cell death is triggered remains incompletely defined, as does the impact of Ft on mitochondria, the host cell?s organellar ?canary in a coal mine?. Herein, we reveal that Ft infection of host cells, particularly macrophages and polymorphonuclear leukocytes, drives necroptosis via a receptor-interacting protein kinase 1/3-mediated mechanism. During necroptosis mitochondria and other organelles become damaged. Ft-induced mitochondrial damage is characterized by: (i) a decrease in membrane potential and consequent mitochondrial oncosis or swelling, (ii) increased generation of superoxide radicals, and (iii) release of intact or damaged mitochondria into the lung parenchyma. Host cell recognition of and response to released mitochondria and other damage-associated molecular patterns engenders a sepsis-like syndrome typified by production of TNF, IL-1?, IL-6, IL-12p70, and IFN-? during late-phase tularemia (?72?h), but are absent early during infection. Twit Text FOAVip Necroptotic debris including damaged mitochondria elicits sepsis-like syndrome during late-phase tularemia ????Cell Death Discov http://www.kidney.de/pget.php?&tw=1&pmid=28955505 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28955505 #FOAvip English Wikipedia <ref>{{Cite pmid|28955505}}</ref> Necroptotic debris including damaged mitochondria elicits sepsis-like syndrome during late-phase tularemia #MMPMID28955505 Singh A; Periasamy S; Malik M; Bakshi CS; Stephen L; Ault JG; Mannella CA; Sellati TJ Cell Death Discov 2017[]; 3 (ä): 17056- PMID28955505show ga Infection with Francisella tularensis ssp. tularensis (Ft) strain SchuS4 causes an often lethal disease known as tularemia in rodents, non-human primates, and humans. Ft subverts host cell death programs to facilitate their exponential replication within macrophages and other cell types during early respiratory infection (?72?h). The mechanism(s) by which cell death is triggered remains incompletely defined, as does the impact of Ft on mitochondria, the host cell?s organellar ?canary in a coal mine?. Herein, we reveal that Ft infection of host cells, particularly macrophages and polymorphonuclear leukocytes, drives necroptosis via a receptor-interacting protein kinase 1/3-mediated mechanism. During necroptosis mitochondria and other organelles become damaged. Ft-induced mitochondrial damage is characterized by: (i) a decrease in membrane potential and consequent mitochondrial oncosis or swelling, (ii) increased generation of superoxide radicals, and (iii) release of intact or damaged mitochondria into the lung parenchyma. Host cell recognition of and response to released mitochondria and other damage-associated molecular patterns engenders a sepsis-like syndrome typified by production of TNF, IL-1?, IL-6, IL-12p70, and IFN-? during late-phase tularemia (?72?h), but are absent early during infection. äNecroptotic debris including damaged mitochondria elicits sepsis-like (epmc).pdf DeepDyve Pubget Overpricing