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• W2012105082 endingPage "147" @default.
• W2012105082 startingPage "140" @default.
• W2012105082 abstract "In 1967, Okamoto et al suggested that the absence of ganglion cells in Hirschsprung's disease (HD) was attributable to failure of migration of neural crest cells. The earlier the arrest of migration, the longer the aganglionic segment. Since then, this hypothesis generally has been accepted. However, subsequent experiments using mouse models of intestinal aganglionosis indicate that nerve cells may reach the correct position but then fail to develop or survive. An alternative hypothesis has been proposed that the aganglionosis may be caused by failure of differentiation as a result of microenvironmental changes after the migration has occurred. Extracellular matrix proteins are recognized as important microenvironmental factors. It has been shown that enteric neurogenesis is dependent on extracellular matrices, which provide a migration pathway for neural crest-derived cells and promote the maturation of settled neural crestderived cells. Altered distributions of extracellular matrices have been shown in human HD cases and murine HD models, suggesting the role of extracellular matrices in the pathogenesis of HD. Recent studies suggest that intestinal smooth muscle cells, target cells of enteric neurons, play an important role in guiding and influencing its own innervation. Normal maturation was inhibited in neurons cultured with smooth muscle cells of aganglionic colon in comparison to normal colon. Furthermore, it was demonstrated that levels of neurotrophic factors, crucial in the development and survival of enteric neurons, are decreased in circular muscle layers of aganglionic colon in comparison to normoganglionic colon. The smooth muscle cells of the aganglionic colon may represent an unfavorable microenvironment for neuronal development compared with the normally innervated region. Recently, markedly increased immunoreactivity of major histocompatibility complex (MHC) class II antigens and ICAM-1 was demonstrated in aganglionic bowel, suggesting the immunological mechanisms may be involved in the etiology of HD. Genetic factors have been implicated in the etiology of this condition because HD is known to occur in families and in association with some chromosomal abnormalities. Recent expansion of molecular genetics identified multiple susceptibility genes of HD, including the RET gene, the glial cell line-derived neurotrophic factor gene, the endothelin-B receptor gene, and endothelin-3 gene. Of these, inactivating mutations of the RET gene are the most frequent, occurring in 50% of familial and 15% to 20% of sporadic cases of HD. To date, despite extensive research, the exact etiology of this condition remains poorly understood. The present report describes the authors' current understanding of and recent progress in the etiology of HD." @default.
• W2012105082 created "2016-06-24" @default.
• W2012105082 creator A5022143556 @default.
• W2012105082 creator A5060652405 @default.
• W2012105082 creator A5066641863 @default.
• W2012105082 date "1998-08-01" @default.
• W2012105082 modified "2023-10-10" @default.
• W2012105082 title "Hirschsprung's Disease: A Search for Etiology" @default.
• W2012105082 cites W1511353372 @default.
• W2012105082 cites W1521180176 @default.
• W2012105082 cites W190302511 @default.
• W2012105082 cites W1916345350 @default.
• W2012105082 cites W1945199177 @default.
• W2012105082 cites W1965322478 @default.
• W2012105082 cites W1965540256 @default.
• W2012105082 cites W1966703550 @default.
• W2012105082 cites W1966742876 @default.
• W2012105082 cites W1969504371 @default.
• W2012105082 cites W1971238657 @default.
• W2012105082 cites W1972869928 @default.
• W2012105082 cites W1973224789 @default.
• W2012105082 cites W1974767821 @default.
• W2012105082 cites W1975063089 @default.
• W2012105082 cites W1983208899 @default.
• W2012105082 cites W1991038604 @default.
• W2012105082 cites W1993402913 @default.
• W2012105082 cites W1993525691 @default.
• W2012105082 cites W1994452959 @default.
• W2012105082 cites W1995175291 @default.
• W2012105082 cites W1995401716 @default.
• W2012105082 cites W1996360049 @default.
• W2012105082 cites W1999693507 @default.
• W2012105082 cites W2008714651 @default.
• W2012105082 cites W2010740233 @default.
• W2012105082 cites W2013452292 @default.
• W2012105082 cites W2014078232 @default.
• W2012105082 cites W2015615691 @default.
• W2012105082 cites W2023142792 @default.
• W2012105082 cites W2023200495 @default.
• W2012105082 cites W2023525449 @default.
• W2012105082 cites W2030996806 @default.
• W2012105082 cites W2032489620 @default.
• W2012105082 cites W2032544809 @default.
• W2012105082 cites W2037025785 @default.
• W2012105082 cites W2037050570 @default.
• W2012105082 cites W2037550327 @default.
• W2012105082 cites W2039865408 @default.
• W2012105082 cites W2040345915 @default.
• W2012105082 cites W2044591984 @default.
• W2012105082 cites W2046670624 @default.
• W2012105082 cites W2048760424 @default.
• W2012105082 cites W2051998916 @default.
• W2012105082 cites W2054191157 @default.
• W2012105082 cites W2054633430 @default.
• W2012105082 cites W2054810445 @default.
• W2012105082 cites W2057720341 @default.
• W2012105082 cites W2060833848 @default.
• W2012105082 cites W2062010832 @default.
• W2012105082 cites W2065855600 @default.
• W2012105082 cites W2067436010 @default.
• W2012105082 cites W2067741077 @default.
• W2012105082 cites W2071895580 @default.
• W2012105082 cites W2074185366 @default.
• W2012105082 cites W2075441122 @default.
• W2012105082 cites W2077844716 @default.
• W2012105082 cites W2078970989 @default.
• W2012105082 cites W2082754954 @default.
• W2012105082 cites W2083967663 @default.
• W2012105082 cites W2084117694 @default.
• W2012105082 cites W2084219905 @default.
• W2012105082 cites W2085477806 @default.
• W2012105082 cites W2085591362 @default.
• W2012105082 cites W2089348287 @default.
• W2012105082 cites W2089855907 @default.
• W2012105082 cites W2090310439 @default.
• W2012105082 cites W2100870243 @default.
• W2012105082 cites W2105165426 @default.
• W2012105082 cites W2133802016 @default.
• W2012105082 cites W2134254169 @default.
• W2012105082 cites W2134679933 @default.
• W2012105082 cites W2134894529 @default.
• W2012105082 cites W2135454969 @default.
• W2012105082 cites W2142680440 @default.
• W2012105082 cites W2148057917 @default.
• W2012105082 cites W2148060680 @default.
• W2012105082 cites W2148252815 @default.
• W2012105082 cites W2155013075 @default.
• W2012105082 cites W2164942430 @default.
• W2012105082 cites W2179076164 @default.
• W2012105082 cites W2192523766 @default.
• W2012105082 cites W2215211951 @default.
• W2012105082 cites W2221784365 @default.
• W2012105082 cites W2316883228 @default.
• W2012105082 cites W2331562215 @default.
• W2012105082 cites W2342511806 @default.
• W2012105082 cites W3162973495 @default.
• W2012105082 cites W4252172071 @default.
• W2012105082 cites W51465864 @default.

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