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cholestasis/hypoxia
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 63 rezultatus
Early cholestasis in premature infants receiving total parenteral nutrition: a possible consequence of shock and hypoxia.
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We report 18 premature infants (gestational age: 31.1 weeks +/- 2.6 [mean +/- SD] (range: 28-36]) with necrotizing enterocolitis (NEC) who developed total parenteral nutrition (TPN) associated cholestasis. Liver function tests were performed at the start of TPN (D1) and repeated once a week.
Ursodeoxycholyl lysophosphatidylethanolamide inhibits cholestasis- and hypoxia-induced apoptosis by upregulating antiapoptosis proteins.
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An increase of toxic bile acids such as glycochenodeoxycholic acid occurs during warm ischemia reperfusion causing cholestasis and damage in hepatocytes and intrahepatic biliary epithelial cells. We aim to test antiapoptosis effects of ursodeoxycholyl lysophosphatidylethanolamide under cholestatic
Hypoxia-induced regulation of placental REDD1 and mTOR was impaired in a rat model of estrogen-induced cholestasis.
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Hypoxia inducible factor-1α (HIF-1α), regulated in development and DNA damage response-1 (REDD1), and mammalian target of rapamycin (mTOR) play distinct roles in response to hypoxia. The aim of this study was to evaluate whether the HIF-1α-REDD1-mTOR-mediated hypoxic stress response also operates
Hypoxia-inducible factor-2α promotes hepatocyte apoptosis during cholestasis.
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OBJECTIVE
Hypoxia-inducible factor-2α (HIF-2α) has been reported to play an important role in a host of pathophysiological processes, including cellular survival. This study explores the role of HIF-2α in cholestasis-mediated hepatocyte apoptosis.
METHODS
Hypoxia-inducible factor-2α expression was
[Study on fetal hypoxia in intrahepatic cholestasis of pregnancy].
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OBJECTIVE
To investigate the mechanism and the related factors of fetal hypoxia in intrahepatic cholestasis of pregnancy (ICP).
METHODS
Cord blood total bile acids(TBA), hypoxanthine (HX), and endothelin (ET) concentrations were measured in 30 newborns of mothers with ICP and 30 infants of normal
Expression of vascular endothelial growth factor (VEGF) under hypoxia in placenta with intrahepatic cholestasis of pregnancy and its clinically pathological significance.
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The expression of vascular endothelial growth factor (VEGF) under hypoxia in the placenta with intrahepatic cholestasis of pregnancy (ICP) was observed, and mechanisms of ICP fetal distress were discussed.
METHODS
Different culturing times were established in hypoxia incubator, and protein
[The relationship between P53 and hypoxia-inducible transcription factor-1alpha in the placenta of patient with intrahepatic cholestasis of pregnancy under acute hypoxic condition].
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OBJECTIVE
Owing to the molecular mechanisms unexplored yet to fetal hypoxia signaling in the intrahepatic cholestasis of pregnancy (ICP), and therefore we intend to investigate the significant expression of the hypoxia-inducible transcription factor-1alpha (HIF-1alpha) in placenta of pregnant women
Expression of hypoxia-regulated genes and glycometabolic genes in placenta from patients with intrahepatic cholestasis of pregnancy.
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BACKGROUND
Intrahepatic cholestasis of pregnancy (ICP) is a liver disorder unique to pregnancy that is associated with increased rates of fetal distress and demise. While acute hypoxia is believed to cause the pathophysiology of ICP, direct molecular evidence for this is lacking. Here, we analyzed
Transient neonatal cholestasis: origin and outcome.
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We studied, retrospectively, 92 children who were first seen with neonatal cholestasis and who were followed up until liver test results normalized. Among the 92 children, 81 displayed factors responsible for chronic and/or acute perinatal distress. Onset of jaundice was recorded at a mean age of 7
Assessment of selected parameters of placental microstructure in patients with intrahepatic cholestasis of pregnancy.
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[Intrahepatic cholestasis of pregnancy and fetal injury].
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Intrahepatic cholestasis of pregnancy (ICP) is an unique complication in pregnancy, which usually manifests in the second or third trimester, and mainly harms the fetus. Its pathogenesis is not yet clear, and placental pathological changes are insufficient to explain the clinical phenomenon.Recent
Acidosis: A potential explanation for adverse fetal outcome in intrahepatic cholestasis of pregnancy. A case report.
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BACKGROUND
Intrahepatic cholestasis of pregnancy is a cholestatic disorder with an increased risk for adverse perinatal outcome. The mechanism underlying intrauterine demise is poorly understood.
METHODS
A nulliparous woman with gestational age of 36 plus 6 weeks presented with suspected
Total parenteral nutrition-related cholestasis in infants.
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An epidemiological study was conducted to estimate the proportion of infants on total parenteral nutrition (TPN) who developed cholestasis and to identify risk factors associated with the development of this disease. Data were abstracted from medical records of 624 infants less than or equal to 30
[Intrahepatic cholestasis of pregnancy: review].
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The etiology of intrahepatic cholestasis of pregnancy includes genetic and environmental factors. Bile acids elevation in maternal and fetal blood is the main fact of its physiopathology, causing maternal itching and high perinatal morbidity and mortality. High levels of maternal blood bile acids
[Perinatal monitoring in intrahepatic cholestasis of pregnancy].
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The sensitivity of meconium stain in amniotic fluid for prediction of fetal well-being in intrahepatic cholestasis of pregnancy(ICP) was evaluated. The study consisted of an ICP group(n = 30), and a control group (n = 30) and the umbilical arterial pH value(< 7.2) was used as a standard. The
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