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• W2110100816 abstract "Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology?I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it benign intimal hyperplasia. However, normal or benign intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates early in life to form a multi-layer intimal hyperplasia and then continues to self-renew in a controlled manner throughout life, relatively rarely compromising the blood supply to the heart, causing complications requiring intervention only in a small fraction of the population, while all humans are carriers of benign hyperplasia. Unfortunately, this fundamental fact has not been widely appreciated in arteriosclerosis research and medical education, which continue to operate on the assumption that the normal arterial intima is always an ideal single-layer endothelium. As a result, the disease is perceived and studied as a new pathological event caused by new mechanisms. The discovery that normal coronary arteries are morphologically indistinguishable from deadly coronary arteriosclerosis continues to elicit surprise.Two questions should inform the priorities of our research: (1) what controls switch the single cell-layer intimal phenotype into normal hyperplasia? (2) how is normal (benign) hyperplasia maintained? We would be hard-pressed to gain practical insights without scrutinizing our premises." @default.
• W2110100816 created "2016-06-24" @default.
• W2110100816 creator A5055497627 @default.
• W2110100816 date "2007-10-31" @default.
• W2110100816 modified "2023-10-16" @default.
• W2110100816 title "Analysis of arterial intimal hyperplasia: review and hypothesis" @default.
• W2110100816 cites W1521680442 @default.
• W2110100816 cites W18752242 @default.
• W2110100816 cites W1887126031 @default.
• W2110100816 cites W1904595997 @default.
• W2110100816 cites W1963840048 @default.
• W2110100816 cites W1965157322 @default.
• W2110100816 cites W1966036045 @default.
• W2110100816 cites W1966431818 @default.
• W2110100816 cites W1967443574 @default.
• W2110100816 cites W1967711309 @default.
• W2110100816 cites W1968640534 @default.
• W2110100816 cites W1972582706 @default.
• W2110100816 cites W1972789975 @default.
• W2110100816 cites W1973355122 @default.
• W2110100816 cites W1974072658 @default.
• W2110100816 cites W1974539982 @default.
• W2110100816 cites W1974708001 @default.
• W2110100816 cites W1975280036 @default.
• W2110100816 cites W1977236267 @default.
• W2110100816 cites W1977427723 @default.
• W2110100816 cites W1977777509 @default.
• W2110100816 cites W1977905404 @default.
• W2110100816 cites W1978794285 @default.
• W2110100816 cites W1980735554 @default.
• W2110100816 cites W1981926053 @default.
• W2110100816 cites W1982051099 @default.
• W2110100816 cites W1984099405 @default.
• W2110100816 cites W1985542535 @default.
• W2110100816 cites W1985826092 @default.
• W2110100816 cites W1986321752 @default.
• W2110100816 cites W1986953318 @default.
• W2110100816 cites W1987232206 @default.
• W2110100816 cites W1987616522 @default.
• W2110100816 cites W1990298004 @default.
• W2110100816 cites W1991237283 @default.
• W2110100816 cites W1991549598 @default.
• W2110100816 cites W1992787068 @default.
• W2110100816 cites W1993205016 @default.
• W2110100816 cites W1993997290 @default.
• W2110100816 cites W1994425929 @default.
• W2110100816 cites W1995739525 @default.
• W2110100816 cites W1997221488 @default.
• W2110100816 cites W1999400534 @default.
• W2110100816 cites W2000111545 @default.
• W2110100816 cites W2000568229 @default.
• W2110100816 cites W2001793664 @default.
• W2110100816 cites W2001822903 @default.
• W2110100816 cites W2001835838 @default.
• W2110100816 cites W2004850519 @default.
• W2110100816 cites W2005120629 @default.
• W2110100816 cites W2008427272 @default.
• W2110100816 cites W2009158881 @default.
• W2110100816 cites W2009983186 @default.
• W2110100816 cites W2010407587 @default.
• W2110100816 cites W2011634677 @default.
• W2110100816 cites W2012447761 @default.
• W2110100816 cites W2012861732 @default.
• W2110100816 cites W2013329210 @default.
• W2110100816 cites W2014106235 @default.
• W2110100816 cites W2014319474 @default.
• W2110100816 cites W2014958065 @default.
• W2110100816 cites W2015219342 @default.
• W2110100816 cites W2016279534 @default.
• W2110100816 cites W2016691951 @default.
• W2110100816 cites W2017506108 @default.
• W2110100816 cites W2020048566 @default.
• W2110100816 cites W2020206633 @default.
• W2110100816 cites W2021152913 @default.
• W2110100816 cites W2021320440 @default.
• W2110100816 cites W2021588424 @default.
• W2110100816 cites W2022017539 @default.
• W2110100816 cites W2023730546 @default.
• W2110100816 cites W2025166762 @default.
• W2110100816 cites W2026459254 @default.
• W2110100816 cites W2026487217 @default.
• W2110100816 cites W2028116439 @default.
• W2110100816 cites W2029073666 @default.
• W2110100816 cites W2029205132 @default.
• W2110100816 cites W2029331845 @default.
• W2110100816 cites W2030537932 @default.
• W2110100816 cites W2030603652 @default.
• W2110100816 cites W2032274464 @default.
• W2110100816 cites W2032931290 @default.
• W2110100816 cites W2033390204 @default.
• W2110100816 cites W2034404961 @default.
• W2110100816 cites W2036375988 @default.
• W2110100816 cites W2037238128 @default.
• W2110100816 cites W2038890085 @default.
• W2110100816 cites W2039968877 @default.
• W2110100816 cites W2040863716 @default.
• W2110100816 cites W2043645992 @default.
• W2110100816 cites W2046286846 @default.
• W2110100816 cites W2046469019 @default.
• W2110100816 cites W2046815543 @default.

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