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.

10.1084/jem.20130295 http://scihub22266oqcxt.onion/10.1084/jem.20130295 24395887!3892976!24395887     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24395887&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       J+Exp+Med 2014 ; 211 (1): 165-79 Nephropedia Template TP {{tp|p=24395887|t=2014. Inflammation in rat pregnancy inhibits spiral artery remodeling leading to fetal growth restriction and features of preeclampsia |pdf=|usr=}}{{24395887}} gab.com Text Inflammation in rat pregnancy inhibits spiral artery remodeling leading to fetal growth restriction and features of preeclampsia JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=24395887 #FOAvip Fetal growth restriction (FGR) and preeclampsia (PE) are often associated with abnormal maternal inflammation, deficient spiral artery (SA) remodeling, and altered uteroplacental perfusion. Here, we provide evidence of a novel mechanistic link between abnormal maternal inflammation and the development of FGR with features of PE. Using a model in which pregnant rats are administered low-dose lipopolysaccharide (LPS) on gestational days 13.5-16.5, we show that abnormal inflammation resulted in FGR mediated by tumor necrosis factor-alpha (TNF). Inflammation was also associated with deficient trophoblast invasion and SA remodeling, as well as with altered uteroplacental hemodynamics and placental nitrosative stress. Moreover, inflammation increased maternal mean arterial pressure (MAP) and was associated with renal structural alterations and proteinuria characteristic of PE. Finally, transdermal administration of the nitric oxide (NO) mimetic glyceryl trinitrate prevented altered uteroplacental perfusion, LPS-induced inflammation, placental nitrosative stress, renal structural and functional alterations, increase in MAP, and FGR. These findings demonstrate that maternal inflammation can lead to severe pregnancy complications via a mechanism that involves increased maternal levels of TNF. Our study provides a rationale for the use of antiinflammatory agents or NO-mimetics in the treatment and/or prevention of inflammation-associated pregnancy complications. Twit Text FOAVip Inflammation in rat pregnancy inhibits spiral artery remodeling leading to fetal growth restriction and features of preeclampsia ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=24395887 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24395887 #FOAvip English Wikipedia <ref>{{Cite pmid|24395887}}</ref> Inflammation in rat pregnancy inhibits spiral artery remodeling leading to fetal growth restriction and features of preeclampsia #MMPMID24395887 Cotechini T; Komisarenko M; Sperou A; Macdonald-Goodfellow S; Adams MA; Graham CH J Exp Med 2014[Jan]; 211 (1): 165-79 PMID24395887show ga Fetal growth restriction (FGR) and preeclampsia (PE) are often associated with abnormal maternal inflammation, deficient spiral artery (SA) remodeling, and altered uteroplacental perfusion. Here, we provide evidence of a novel mechanistic link between abnormal maternal inflammation and the development of FGR with features of PE. Using a model in which pregnant rats are administered low-dose lipopolysaccharide (LPS) on gestational days 13.5-16.5, we show that abnormal inflammation resulted in FGR mediated by tumor necrosis factor-alpha (TNF). Inflammation was also associated with deficient trophoblast invasion and SA remodeling, as well as with altered uteroplacental hemodynamics and placental nitrosative stress. Moreover, inflammation increased maternal mean arterial pressure (MAP) and was associated with renal structural alterations and proteinuria characteristic of PE. Finally, transdermal administration of the nitric oxide (NO) mimetic glyceryl trinitrate prevented altered uteroplacental perfusion, LPS-induced inflammation, placental nitrosative stress, renal structural and functional alterations, increase in MAP, and FGR. These findings demonstrate that maternal inflammation can lead to severe pregnancy complications via a mechanism that involves increased maternal levels of TNF. Our study provides a rationale for the use of antiinflammatory agents or NO-mimetics in the treatment and/or prevention of inflammation-associated pregnancy complications. |Analysis of Variance[MESH] |Animals[MESH] |Blood Cell Count[MESH] |Blood Pressure/physiology[MESH] |Creatinine/urine[MESH] |Endometrium/*blood supply[MESH] |Female[MESH] |Fetal Growth Retardation/*etiology[MESH] |Image Processing, Computer-Assisted[MESH] |Immunohistochemistry[MESH] |Inflammation/chemically induced/*complications[MESH] |Kidney/ultrastructure[MESH] |Lipopolysaccharides/administration & dosage/toxicity[MESH] |Myocytes, Smooth Muscle/metabolism[MESH] |Pre-Eclampsia/*etiology[MESH] |Pregnancy[MESH] |Proteinuria/physiopathology[MESH] |Rats[MESH] |Telemetry[MESH] |Trophoblasts/metabolism[MESH] |Tumor Necrosis Factor-alpha/metabolism[MESH] |Ultrasonography, Doppler[MESH]Inflammation in rat pregnancy inhibits spiral artery remodeling leadin(epmc).pdf DeepDyve Pubget Overpricing