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http://scihub22266oqcxt.onion/ C4769347!4769347!27069753     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 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 Deprecated: Implicit conversion from float 267.2 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 Deprecated: Implicit conversion from float 267.2 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 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27069753.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Blood+Res 2015 ; 5 (2): 34-61 Nephropedia Template TP {{tp|p=27069753|t=2015. A novel interaction between megakaryocytes and activated fibrocytes increases TGF-? bioavailability in the Gata1low mouse model of myelofibrosis |pdf=|usr=}}{{27069753}} gab.com Text A novel interaction between megakaryocytes and activated fibrocytes increases TGF- bioavailability in the Gata1low mouse model of myelofibrosis JO: Am J Blood Res http://www.kidney.de/pget.php?&tw=1&pmid=27069753 #FOAvip Despite numerous circumstantial evidences, the pathogenic role of TGF-? in primary myelofibrosis (PMF), the most severe of the Philadelphia-negative myeloproliferative neoplasms, is still unclear because of the modest (2-fold) increases in its plasma levels observed in PMF patients and in the Gata1low mouse model. Whether myelofibrosis is associated with increased bioavailability of TGF-? bound to fibrotic fibres is unknown. Transmission electron-microscopy (TEM) observations identified that spleen from PMF patients and Gata1low mice contained megakaryocytes with abnormally high levels of TGF-? and collagen fibres embedded in their cytoplasm. Additional immuno-TEM observations of spleen from Gata1low mice revealed the presence of numerous activated fibrocytes establishing with their protrusions a novel cellular interaction, defined as peripolesis, with megakaryocytes. These protrusions infiltrated the megakaryocyte cytoplasm releasing collagen that was eventually detected in its mature polymerized form. Megakaryocytes, engulfed with mature collagen fibres, acquired the morphology of para-apoptotic cells and, in the most advanced cases, were recognized as polylobated heterochromatic nuclei surrounded by collagen fibres strictly associated with TGF-?. These areas contained concentrations of TGF-?-gold particles ~1000-fold greater than normal and numerous myofibroblasts, an indication that TGF-? was bioactive. Loss-of-function studies indicated that peripolesis between megakaryocytes and fibrocytes required both TGF-?, possibly for inducing fibrocyte activation, and P-selectin, possibly for mediating interaction between the two cell types. Loss-of-function of TGF-? and P-selectin also prevented fibrosis. These observations identify that myelofibrosis is associated with pathological increases of TGF-? bioavailability and suggest a novel megakaryocyte-mediated mechanism that may increase TGF-? bioavailability in chronic inflammation. Twit Text FOAVip A novel interaction between megakaryocytes and activated fibrocytes increases TGF- bioavailability in the Gata1low mouse model of myelofibrosis ????Am J Blood Res http://www.kidney.de/pget.php?&tw=1&pmid=27069753 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27069753 #FOAvip English Wikipedia <ref>{{Cite pmid|27069753}}</ref> A novel interaction between megakaryocytes and activated fibrocytes increases TGF-? bioavailability in the Gata1low mouse model of myelofibrosis #MMPMID27069753 Zingariello M; Ruggeri A; Martelli F; Marra M; Sancillo L; Ceglia I; Rana RA; Migliaccio AR Am J Blood Res 2015[]; 5 (2): 34-61 PMID27069753show ga Despite numerous circumstantial evidences, the pathogenic role of TGF-? in primary myelofibrosis (PMF), the most severe of the Philadelphia-negative myeloproliferative neoplasms, is still unclear because of the modest (2-fold) increases in its plasma levels observed in PMF patients and in the Gata1low mouse model. Whether myelofibrosis is associated with increased bioavailability of TGF-? bound to fibrotic fibres is unknown. Transmission electron-microscopy (TEM) observations identified that spleen from PMF patients and Gata1low mice contained megakaryocytes with abnormally high levels of TGF-? and collagen fibres embedded in their cytoplasm. Additional immuno-TEM observations of spleen from Gata1low mice revealed the presence of numerous activated fibrocytes establishing with their protrusions a novel cellular interaction, defined as peripolesis, with megakaryocytes. These protrusions infiltrated the megakaryocyte cytoplasm releasing collagen that was eventually detected in its mature polymerized form. Megakaryocytes, engulfed with mature collagen fibres, acquired the morphology of para-apoptotic cells and, in the most advanced cases, were recognized as polylobated heterochromatic nuclei surrounded by collagen fibres strictly associated with TGF-?. These areas contained concentrations of TGF-?-gold particles ~1000-fold greater than normal and numerous myofibroblasts, an indication that TGF-? was bioactive. Loss-of-function studies indicated that peripolesis between megakaryocytes and fibrocytes required both TGF-?, possibly for inducing fibrocyte activation, and P-selectin, possibly for mediating interaction between the two cell types. Loss-of-function of TGF-? and P-selectin also prevented fibrosis. These observations identify that myelofibrosis is associated with pathological increases of TGF-? bioavailability and suggest a novel megakaryocyte-mediated mechanism that may increase TGF-? bioavailability in chronic inflammation. äA novel interaction between megakaryocytes and activated fibrocytes in(epmc).pdf DeepDyve Pubget Overpricing