FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2044758098> ?p ?o ?g. }

• W2044758098 endingPage "825" @default.
• W2044758098 startingPage "819" @default.
• W2044758098 abstract "Hypertension, diabetes mellitus and chronic glomerular diseases reportedly cause in excess of 80% of the incident cases of end-stage renal disease (ESRD) in the U.S. The factors that initiate progressive renal failure in patients with these disorders remain unknown. Several investigators have reported enhanced synthesis and activity of cytokines in the kidneys of patients with renal failure. The ensuing inflammation and fibrosis have been postulated to contribute to the development of progressive renal failure. There is also abundant evidence supporting the contribution of genetic factors in ESRD susceptibility based upon the strong familial clustering of ESRD, particularly in African Americans. Therefore, genetic linkage analysis may be useful to evaluate the role of candidate genes in several cytokine cascades that could contribute to the pathogenesis of chronic renal failure. We tested for genetic linkage between eight cytokine candidate genes and chronic renal failure in a collection of African American sibling pairs concordant for ESRD. Epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) beta 1, TGF-beta 2 and TGF-beta 3, and tumor necrosis factor (TNF)-alpha and TNF-beta candidate genes were selected for analysis due to their putative roles in diabetic renal disease and chronic glomerulonephritis. The interleukin-1 receptor antagonist gene (IL1RN) was also genotyped due to its reported association with diabetic nephropathy. Non-parametric (genetic model independent) affected sib pair linkage analysis was used to evaluate evidence for linkage. In order to genotype TGF-beta 3, we identified four closely linked, previously unidentified, highly polymorphic microsatellite loci near the TGF-beta 3 gene. Linkage of ESRD and transforming growth factor beta 2 polymorphisms on human chromosome 1 approached significance for non-diabetic nephropathy (predominantly chronic glomerular disease, hypertensive nephrosclerosis and unknown etiology) (P = 0.08), but showed no linkage to diabetic nephropathy. The other candidate loci did not demonstrate linkage to ESRD in the total population or in the subgroups with diabetic or non-diabetic etiologies of ESRD. The IL1RN gene did not show significant evidence for linkage to ESRD; however, we did confirm an association between allele 2 of IL1RN and ESRD (as reported in diabetic nephropathy). Overall, these results suggest that these growth factor loci do not make major contributions to the pathogenesis of ESRD in African Americans." @default.
• W2044758098 created "2016-06-24" @default.
• W2044758098 creator A5006046269 @default.
• W2044758098 creator A5020768763 @default.
• W2044758098 creator A5059764563 @default.
• W2044758098 creator A5070735232 @default.
• W2044758098 creator A5078445383 @default.
• W2044758098 creator A5087036525 @default.
• W2044758098 date "1997-03-01" @default.
• W2044758098 modified "2023-09-23" @default.
• W2044758098 title "Genetic linkage analysis of growth factor loci and end-stage renal disease in African Americans" @default.
• W2044758098 cites W120968873 @default.
• W2044758098 cites W1981665521 @default.
• W2044758098 cites W1981667667 @default.
• W2044758098 cites W1983222975 @default.
• W2044758098 cites W1986499750 @default.
• W2044758098 cites W1996052299 @default.
• W2044758098 cites W1997895757 @default.
• W2044758098 cites W2014461731 @default.
• W2044758098 cites W2015197182 @default.
• W2044758098 cites W2023362855 @default.
• W2044758098 cites W2028156913 @default.
• W2044758098 cites W2029579765 @default.
• W2044758098 cites W2032997554 @default.
• W2044758098 cites W2045333999 @default.
• W2044758098 cites W2045493972 @default.
• W2044758098 cites W2051679072 @default.
• W2044758098 cites W2067679923 @default.
• W2044758098 cites W2073264424 @default.
• W2044758098 cites W2073414552 @default.
• W2044758098 cites W2074323470 @default.
• W2044758098 cites W2091852263 @default.
• W2044758098 cites W2092661802 @default.
• W2044758098 cites W2094695464 @default.
• W2044758098 cites W2097748223 @default.
• W2044758098 cites W2166713786 @default.
• W2044758098 cites W2340171512 @default.
• W2044758098 cites W4211252102 @default.
• W2044758098 doi "https://doi.org/10.1038/ki.1997.115" @default.
• W2044758098 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9067916" @default.
• W2044758098 hasPublicationYear "1997" @default.
• W2044758098 type Work @default.
• W2044758098 sameAs 2044758098 @default.
• W2044758098 citedByCount "73" @default.
• W2044758098 countsByYear W20447580982013 @default.
• W2044758098 countsByYear W20447580982014 @default.
• W2044758098 countsByYear W20447580982015 @default.
• W2044758098 countsByYear W20447580982017 @default.
• W2044758098 countsByYear W20447580982019 @default.
• W2044758098 crossrefType "journal-article" @default.
• W2044758098 hasAuthorship W2044758098A5006046269 @default.
• W2044758098 hasAuthorship W2044758098A5020768763 @default.
• W2044758098 hasAuthorship W2044758098A5059764563 @default.
• W2044758098 hasAuthorship W2044758098A5070735232 @default.
• W2044758098 hasAuthorship W2044758098A5078445383 @default.
• W2044758098 hasAuthorship W2044758098A5087036525 @default.
• W2044758098 hasBestOaLocation W20447580981 @default.
• W2044758098 hasConcept C104317684 @default.
• W2044758098 hasConcept C126322002 @default.
• W2044758098 hasConcept C134018914 @default.
• W2044758098 hasConcept C142870003 @default.
• W2044758098 hasConcept C203014093 @default.
• W2044758098 hasConcept C2778653478 @default.
• W2044758098 hasConcept C2779134260 @default.
• W2044758098 hasConcept C2779922275 @default.
• W2044758098 hasConcept C2780091579 @default.
• W2044758098 hasConcept C3019040382 @default.
• W2044758098 hasConcept C54355233 @default.
• W2044758098 hasConcept C67636389 @default.
• W2044758098 hasConcept C69991583 @default.
• W2044758098 hasConcept C71924100 @default.
• W2044758098 hasConcept C86803240 @default.
• W2044758098 hasConceptScore W2044758098C104317684 @default.
• W2044758098 hasConceptScore W2044758098C126322002 @default.
• W2044758098 hasConceptScore W2044758098C134018914 @default.
• W2044758098 hasConceptScore W2044758098C142870003 @default.
• W2044758098 hasConceptScore W2044758098C203014093 @default.
• W2044758098 hasConceptScore W2044758098C2778653478 @default.
• W2044758098 hasConceptScore W2044758098C2779134260 @default.
• W2044758098 hasConceptScore W2044758098C2779922275 @default.
• W2044758098 hasConceptScore W2044758098C2780091579 @default.
• W2044758098 hasConceptScore W2044758098C3019040382 @default.
• W2044758098 hasConceptScore W2044758098C54355233 @default.
• W2044758098 hasConceptScore W2044758098C67636389 @default.
• W2044758098 hasConceptScore W2044758098C69991583 @default.
• W2044758098 hasConceptScore W2044758098C71924100 @default.
• W2044758098 hasConceptScore W2044758098C86803240 @default.
• W2044758098 hasIssue "3" @default.
• W2044758098 hasLocation W20447580981 @default.
• W2044758098 hasLocation W20447580982 @default.
• W2044758098 hasOpenAccess W2044758098 @default.
• W2044758098 hasPrimaryLocation W20447580981 @default.
• W2044758098 hasRelatedWork W1512761412 @default.
• W2044758098 hasRelatedWork W2032111989 @default.
• W2044758098 hasRelatedWork W2038657938 @default.
• W2044758098 hasRelatedWork W2047956456 @default.
• W2044758098 hasRelatedWork W2104195310 @default.
• W2044758098 hasRelatedWork W2109026982 @default.

• next