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001-es BibID:BIBFORM074861
Első szerző:Rigó János (szülész-nőgyógyász)
Cím:Maternal and neonatal outcome of preeclamptic pregnancies : the potential roles of factor V Leiden mutation and 5,10 methylenetetrahydrofolate reductase / Rigó J. Jr, Nagy B., Fintor L., Tanyi J., Beke A., Karádi I., Papp Z.
Dátum:2000
ISSN:1064-1955
Megjegyzések:OBJECTIVE:To investigate the potential perinatal effects of Factor V Leiden mutation and 5,10 methylenetetrahydrofolate reductase C677T polymorphism in preeclamptic women.STUDY DESIGN:One hundred twenty preeclamptic women (N = 120) and 101 healthy pregnant controls (N = 101) were recruited and evaluated for frequency of Leiden and 5,10 methylenetetrahydrofolate reductase (MTHFR) mutations using polymerase chain reaction (PCR). Perinatal outcomes were then recorded and analyzed for all study participants and their neonates.RESULTS:Laboratory analysis yielded 22 (18.33%) heterozygous carriers of Factor V Leiden mutation among preeclamptic women and 3 (2.97%) heterozygous carriers among the healthy controls; differences between the two groups were found to be statistically significant [p < 0.001, the relative risk (RR) = 6.17, 95% confidence interval (95% CI) = 1.90-20.02]. Homozygous MTHFR mutations were found in 8 of 120 (6.67%) preeclamptic women and in 6 of the 101 (5.94%) healthy controls evaluated. Among preeclamptic women, episodes of hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome were reported in 7 of 22 (31.81%) of those with Factor V Leiden mutation and in 11 of 98 (11.22%) of those who were negative for the mutation. Group differences were determined to be statistically significant (p < 0.015, RR = 2.83, 95% CI = 1.24-6. 48). Perinatal indicators collected from the two groups included frequency of intrauterine growth retardation, birth weight, and gestational age. No statistically different perinatal outcomes were found between Factor V Leiden positive and negative preeclamptic women. In addition, MTHFR gene polymorphism did not appear to be correlated with the development of preeclampsia.CONCLUSION:Although the frequency of Factor V Leiden mutation appears to be significantly higher among preeclamptic women, the mechanism of pathogenesis and potential influence on perinatal outcomes is not yet well understood. Relatively high rates of HELLP syndrome among those with Factor V Leiden mutation suggest that this thrombogene mutation may play a significant role in hemostatic system activation. Our results suggest that the role of MTHFR polymorphism and other factors such as folic acid supplementation will require more extensive analysis in controlling worldwide morbidity and mortality associated with this important maternal condition.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Leiden mutation
MTHFR
preeclampsia
Megjelenés:Hypertension In Pregnancy. - 19 : 2 (2000), p. 163-172. -
További szerzők:Nagy Bálint (1956-) (molekuláris genetikus) Fintor, Lou Tanyi János Beke Artúr (szülész-nőgyógyász) Karádi István (1952-) (belgyógyász, kardiológus) Papp Zoltán (1942-) (szülész-nőgyógyász, genetikus)
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001-es BibID:BIBFORM065358
Első szerző:Tanyi János
Cím:Evaluation of the tyrosine kinase domain of the Met proto-oncogene in sporadic ovarian carcinomas / János Tanyi, Kálmán Tory, János Rigó Jr., Bálint Nagy, Zoltán Papp
Dátum:1999
ISSN:1219-4956 1532-2807
Megjegyzések:Most of the ovarian cancers originate from the ovar-ian surface epithelium derived from the coelomicmesothelium. The Met proto-oncogene encodes atransmembrane tyrosine kinase receptor (Met) thathas the capacity to regulate cell proliferation anddifferentation and it is activated by hepatocytegrowth factor. Trisomy of chromosome 7 and Metprotein overexpression have been were observed inovarian carcinomas, the papillary renal cancers andother solid tumors. Frequent mutations of Metproto-oncogene have been found in hereditary pap-illary renal cancer (HPRC) and most of the muta-tions are located in the tyrosine kinase domain. Theaim of this study to perform a mutation analysis ofexons 17?19 of Met proto-oncogene in epithelialovarian tumors (EOTs). We have examined 24 tumorsamples from patients, operated with EOTs. Muta-tion was detected in exon 18 in only one sample of24 EOTs. Our results indicate that mutations locat-ed in the Met proto-oncogene is not a commonevent in EOT. It is not clear whether the mutationplays a role in the tumorigenesis or progression ofEOT or not.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény hazai lapban
tyrosine
kinase
MET
protooncogene
ovarian
carcinomas
Megjelenés:Pathology & Oncology Research. - 5 (1999), p. 187-191. -
További szerzők:Tory Kálmán Rigó János (1958-) (szülész-nőgyógyász) Nagy Bálint (1956-) (molekuláris genetikus) Papp Zoltán (1942-) (szülész-nőgyógyász, genetikus)
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