FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2016210008> ?p ?o ?g. }

• W2016210008 endingPage "85" @default.
• W2016210008 startingPage "77" @default.
• W2016210008 abstract "to investigate the role of apoptosis, expression of death-promoting molecules and mediators of apoptosis in the development of popliteal artery aneurysms.ten popliteal artery aneurysm (PAA) specimens were obtained from patients undergoing elective surgical repair. Normal controls were popliteal arteries obtained from patients without PAA undergoing infrainguinal bypass surgery (n=8). Standard histochemistry techniques were used to assess elastic lamellae fragmentation and inflammatory infiltrate in PAA. Vascular smooth muscle cells (VSMC), macrophages, T lymphocytes, death-promoting molecules, CPP-32, Fas, p53, perforin, apoptosis-mediating Bcl-2 family proteins and apoptotic death substrate, poly(ADP-ribose) polymerase (PARP) were detected immunohistochemically. Detection of apoptosis was by TUNEL assay. Proteolytic activity was determined by 10% gelatin gel zymography.there is a conspicuous disruption and fragmentation of elastic lamellae in PAA as compared to normal arteries. Increased gelatinolytic activity was observed at 92, 84, 72 and 67 kDa in PAA tissues. There is a significant decrease of VSMCs in the PAA walls (p=0.02). The control arteries had fewer CD68+ macrophages and CD3+ T cells in their media (p<0.01). There was a significant increase in the number of cells undergoing apoptosis in aneurysmal tissue than in the normal vessels, (p<0.02) as well as an increased expression of Bax, CPP-32, Fas, p53 and perforin.the data confirm the architectural disruption of the PAA wall and illustrate an apparent biological response involving inflammatory infiltrate, apoptosis and signalling molecules capable of initiating cell death. In addition to compromising the mechanical integrity of the vessel wall, VSMC loss may contribute to imbalance in the protein profile, accelerating extracellular matrix degradation that could favour PAA development." @default.
• W2016210008 created "2016-06-24" @default.
• W2016210008 creator A5026274935 @default.
• W2016210008 creator A5029324729 @default.
• W2016210008 creator A5088996870 @default.
• W2016210008 date "2001-07-01" @default.
• W2016210008 modified "2023-09-25" @default.
• W2016210008 title "Examination of the Apoptotic Pathway and Proteolysis in the Pathogenesis of Popliteal Artery Aneurysms" @default.
• W2016210008 cites W1970184435 @default.
• W2016210008 cites W1981920986 @default.
• W2016210008 cites W1996180957 @default.
• W2016210008 cites W2001374505 @default.
• W2016210008 cites W2006721089 @default.
• W2016210008 cites W2008032729 @default.
• W2016210008 cites W2019190889 @default.
• W2016210008 cites W2025599602 @default.
• W2016210008 cites W2029080338 @default.
• W2016210008 cites W2030010731 @default.
• W2016210008 cites W2030585342 @default.
• W2016210008 cites W2049057533 @default.
• W2016210008 cites W2051070266 @default.
• W2016210008 cites W2052730870 @default.
• W2016210008 cites W2058863239 @default.
• W2016210008 cites W2061091803 @default.
• W2016210008 cites W2066620120 @default.
• W2016210008 cites W2075357422 @default.
• W2016210008 cites W2077987011 @default.
• W2016210008 cites W2081145901 @default.
• W2016210008 cites W2084468122 @default.
• W2016210008 cites W2091637617 @default.
• W2016210008 cites W2128313579 @default.
• W2016210008 cites W2134979684 @default.
• W2016210008 cites W2136298958 @default.
• W2016210008 cites W2151455800 @default.
• W2016210008 cites W2158326731 @default.
• W2016210008 cites W2167973356 @default.
• W2016210008 cites W2470035890 @default.
• W2016210008 cites W3143448550 @default.
• W2016210008 cites W4293247451 @default.
• W2016210008 cites W4376567326 @default.
• W2016210008 doi "https://doi.org/10.1053/ejvs.2001.1344" @default.
• W2016210008 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11461108" @default.
• W2016210008 hasPublicationYear "2001" @default.
• W2016210008 type Work @default.
• W2016210008 sameAs 2016210008 @default.
• W2016210008 citedByCount "20" @default.
• W2016210008 countsByYear W20162100082012 @default.
• W2016210008 countsByYear W20162100082013 @default.
• W2016210008 countsByYear W20162100082014 @default.
• W2016210008 countsByYear W20162100082019 @default.
• W2016210008 countsByYear W20162100082020 @default.
• W2016210008 countsByYear W20162100082021 @default.
• W2016210008 countsByYear W20162100082023 @default.
• W2016210008 crossrefType "journal-article" @default.
• W2016210008 hasAuthorship W2016210008A5026274935 @default.
• W2016210008 hasAuthorship W2016210008A5029324729 @default.
• W2016210008 hasAuthorship W2016210008A5088996870 @default.
• W2016210008 hasBestOaLocation W20162100081 @default.
• W2016210008 hasConcept C142724271 @default.
• W2016210008 hasConcept C18903297 @default.
• W2016210008 hasConcept C190283241 @default.
• W2016210008 hasConcept C191015642 @default.
• W2016210008 hasConcept C196795494 @default.
• W2016210008 hasConcept C204232928 @default.
• W2016210008 hasConcept C31573885 @default.
• W2016210008 hasConcept C43759708 @default.
• W2016210008 hasConcept C55493867 @default.
• W2016210008 hasConcept C71924100 @default.
• W2016210008 hasConcept C86803240 @default.
• W2016210008 hasConceptScore W2016210008C142724271 @default.
• W2016210008 hasConceptScore W2016210008C18903297 @default.
• W2016210008 hasConceptScore W2016210008C190283241 @default.
• W2016210008 hasConceptScore W2016210008C191015642 @default.
• W2016210008 hasConceptScore W2016210008C196795494 @default.
• W2016210008 hasConceptScore W2016210008C204232928 @default.
• W2016210008 hasConceptScore W2016210008C31573885 @default.
• W2016210008 hasConceptScore W2016210008C43759708 @default.
• W2016210008 hasConceptScore W2016210008C55493867 @default.
• W2016210008 hasConceptScore W2016210008C71924100 @default.
• W2016210008 hasConceptScore W2016210008C86803240 @default.
• W2016210008 hasIssue "1" @default.
• W2016210008 hasLocation W20162100081 @default.
• W2016210008 hasLocation W20162100082 @default.
• W2016210008 hasOpenAccess W2016210008 @default.
• W2016210008 hasPrimaryLocation W20162100081 @default.
• W2016210008 hasRelatedWork W1618068833 @default.
• W2016210008 hasRelatedWork W1987693880 @default.
• W2016210008 hasRelatedWork W2033514966 @default.
• W2016210008 hasRelatedWork W2117519097 @default.
• W2016210008 hasRelatedWork W2161791039 @default.
• W2016210008 hasRelatedWork W2437448382 @default.
• W2016210008 hasRelatedWork W2753668566 @default.
• W2016210008 hasRelatedWork W4200546529 @default.
• W2016210008 hasRelatedWork W4238435355 @default.
• W2016210008 hasRelatedWork W4283693058 @default.
• W2016210008 hasVolume "22" @default.
• W2016210008 isParatext "false" @default.
• W2016210008 isRetracted "false" @default.

• next