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.

10.3389/fphys.2018.00708 http://scihub22266oqcxt.onion/10.3389/fphys.2018.00708 C6018413!6018413 !29971011     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29971011 &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       Front+Physiol 2018 ; 9 (?): 708 Nephropedia Template TP {{tp|p=29971011 |t=2018. Osteoarthritis-Like Changes in Bardet-Biedl Syndrome Mutant Ciliopathy Mice (Bbs1(M390R/M390R)): Evidence for a Role of Primary Cilia in Cartilage Homeostasis and Regulation of Inflammation |pdf=|usr=}}{{29971011 }} gab.com Text Osteoarthritis-Like Changes in Bardet-Biedl Syndrome Mutant Ciliopathy Mice (Bbs1(M390R/M390R)): Evidence for a Role of Primary Cilia in Cartilage Homeostasis and Regulation of Inflammation JO: Front Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29971011 #FOAvip Osteoarthritis (OA) is a debilitating inflammation related disease characterized by joint pain and effusion, loss of mobility, and deformity that may result in functional joint failure and significant impact on quality of life. Once thought of as a simple "wear and tear" disease, it is now widely recognized that OA has a considerable metabolic component and is related to chronic inflammation. Defects associated with primary cilia have been shown to be cause OA-like changes in Bardet-Biedl mice. We examined the role of dysfunctional primary cilia in OA in mice through the regulation of the previously identified degradative and pro-inflammatory molecular pathways common to OA. We observed an increase in the presence of pro-inflammatory markers TGF?-1 and HTRA1 as well as cartilage destructive protease MMP-13 but a decrease in DDR-2. We observed a morphological difference in cartilage thickness in Bbs1 (M390R/M390R) mice compared to wild type (WT). We did not observe any difference in OARSI or Mankin scores between WT and Bbs1(M390R/M390R) mice. Primary cilia appear to be involved in the upregulation of biomarkers, including pro-inflammatory markers common to OA. Twit Text FOAVip Osteoarthritis-Like Changes in Bardet-Biedl Syndrome Mutant Ciliopathy Mice (Bbs1(M390R/M390R)): Evidence for a Role of Primary Cilia in Cartilage Homeostasis and Regulation of Inflammation ????Front Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29971011 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29971011 #FOAvip English Wikipedia <ref>{{Cite pmid|29971011 }}</ref> Osteoarthritis-Like Changes in Bardet-Biedl Syndrome Mutant Ciliopathy Mice (Bbs1(M390R/M390R)): Evidence for a Role of Primary Cilia in Cartilage Homeostasis and Regulation of Inflammation #MMPMID29971011 Sheffield ID ; McGee MA ; Glenn SJ ; Baek DY ; Coleman JM ; Dorius BK ; Williams C ; Rose BJ ; Sanchez AE ; Goodman MA ; Daines JM ; Eggett DL ; Sheffield VC ; Suli A ; Kooyman DL Front Physiol 2018[]; 9 (?): 708 PMID29971011 show ga Osteoarthritis (OA) is a debilitating inflammation related disease characterized by joint pain and effusion, loss of mobility, and deformity that may result in functional joint failure and significant impact on quality of life. Once thought of as a simple "wear and tear" disease, it is now widely recognized that OA has a considerable metabolic component and is related to chronic inflammation. Defects associated with primary cilia have been shown to be cause OA-like changes in Bardet-Biedl mice. We examined the role of dysfunctional primary cilia in OA in mice through the regulation of the previously identified degradative and pro-inflammatory molecular pathways common to OA. We observed an increase in the presence of pro-inflammatory markers TGF?-1 and HTRA1 as well as cartilage destructive protease MMP-13 but a decrease in DDR-2. We observed a morphological difference in cartilage thickness in Bbs1 (M390R/M390R) mice compared to wild type (WT). We did not observe any difference in OARSI or Mankin scores between WT and Bbs1(M390R/M390R) mice. Primary cilia appear to be involved in the upregulation of biomarkers, including pro-inflammatory markers common to OA. ?Osteoarthritis-Like Changes in Bardet-Biedl Syndrome Mutant Ciliopathy(epmc).pdf DeepDyve Pubget Overpricing