eclampsia/hypoxie

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Changes in the metabolic footprint of placental explant-conditioned culture medium identifies metabolic disturbances related to hypoxia and pre-eclampsia.

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Pre-eclampsia (PE) is a multi-system disorder thought to be mediated by circulating factors released from damaged placental villous trophoblast. There is extensive evidence of changes in the villous tissue in PE, some of which may be replicated by culturing villous tissue in hypoxic conditions.

Hypoxia alters expression and function of syncytin and its receptor during trophoblast cell fusion of human placental BeWo cells: implications for impaired trophoblast syncytialisation in pre-eclampsia.

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The fundamental process of placental trophoblast cell fusion (syncytiotrophoblast formation or syncytialisation) which is a characteristic of this tissue is poorly understood. Pre-eclampsia is associated with placental hypoxia and suppressed syncytiotrophoblast formation. We therefore have studied

Expression of placenta growth factor, soluble fms-like tyrosine kinase-1, metal-responsive transcription factor-1, heme oxygenase 1 and hypoxia inducible factor-1α mRNAs in pre-eclampsia placenta and the effect of pre-eclampsia sera on their expression of choriocarcinoma cells.

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OBJECTIVE We studied the effect of pre-eclampsia sera on the expression of placenta growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), metal-responsive transcription factor-1 (MTF-1), heme oxygenase 1 (HO-1) and hypoxia inducible factor-1α (HIF-1α) mRNAs in JEG-3 cells

Vasomotor collapse in eclampsia; anoxia as a possible etiologic factor; report of three cases.

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Altered interleukin-6 receptor, IL-6R and gp130, production and expression and decreased SOCS-3 expression in placentas from women with pre-eclampsia.

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Interleukin-6 (IL-6) and its receptor complex, IL-6 receptor (IL-6R) and gp130, are critical in induction of suppressor of cytokine signalling-3 (SOCS-3) protein, a negative cytokine regulator and anti-inflammatory mediator, in a biological system. Increased inflammatory response is believed to

[The pathogenesis of generalized suppurative-septic complications in patients with eclampsia and massive blood loss of obstetrical origin].

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Changes in immune status, central hemodynamics, oxygen regimen and endogenous intoxication indexes have been compared in patients with eclampsia combined with blood loss and in patients with isolated blood loss. It has been established that severe septic processes were 1.5 times and lethality was 4

[Eclampsia: analysis of a series of 18 clinical cases. Management in a severe crisis].

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On the basis of a series of 18 cases of severe eclampsia, the authors analyse the predisposing circumstances for these episodes and the method of delivery. Caesarian section is still the usual method of delivery in severe cases (12/18). There is a high perinatal mortality (4/18), which is

Assessment of in utero hypoxia and risk of sudden infant death syndrome.

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Few data are available on the role of hypoxia in sudden infant death syndrome (SIDS). The purpose of this study was to assess whether 10 antenatal factors consistent with in utero hypoxia were associated with an increased risk of SIDS. Cases and two sets of controls were chosen from the Upstate New

Low-dose aspirin reduces hypoxia-induced sFlt1 release via the JNK/AP-1 pathway in human trophoblast and endothelial cells.

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Pre-eclampsia (PE) is a serious hypertensive disorder of pregnancy that remains a leading cause of perinatal and maternal morbidity and mortality worldwide. Placental ischemia/hypoxia and the secretion of soluble fms-like tyrosine kinase 1 (sFlt1) into maternal circulation are involved in the

Early Gestational Hypoxia and Adverse Developmental Outcomes.

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Hypoxia is a normal and essential part of embryonic development. However, this state may leave the embryo vulnerable to damage when oxygen supply is disturbed. Embryofetal response to hypoxia is dependent on duration and depth of hypoxia, as well as developmental stage. Early postimplantation rat

Hypertension in pregnancy--2--eclampsia.

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Eclampsia is a grand mal convulsion associated with pregnancy-induced hypertension. It is caused by cerebral hypoxia from intense vasospasm combined with cerebral oedema. CT scans show cerebral ischaemia from thrombosis and oedema.

Carbohydrate metabolism in pre-eclampsia.

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Intravenous glucose tolerance tests were performed on 30 primigravidae with pre-eclampsia and 15 normal primigravidae in late pregnancy. The groups were matched for age, height and weight and had no stigmata of potential diabetes. Plasma glucose, plasma immunoreactive insulin and plasma placental

Non-synonymous sequence variants within the oxygen-dependent degradation domain of the HIF1A gene are not associated with pre-eclampsia in the Finnish population.

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BACKGROUND Reduced placental perfusion predisposes to the maternal syndrome pre-eclampsia characterized by systemically reduced perfusion. Considerable data support the role of angiogenic factors in the development of the maternal syndrome. Hypoxia-inducible factor (HIF-1) mediates the cellular

Effect of hypoxia, oxidative stress and lipopolysaccharides on the release of prostaglandins and cytokines from human term placental explants.

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Placental hypoxia, ischaemia, reperfusion and resultant oxidative stress, with the release of various factors into the maternal vasculature acting as mediators of endothelial cell dysfunction, play an important role in the development of pre-eclampsia. Human term placental tissue explants were

[Activity of nucleolar organizer regions in trophoblast as affected by hypoxia].

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The aim of this study was to investigate the influence of hypoxia on the activity of nucleolar organizer regions (AgNORs) in placentas obtained from healthy women and patients with late gestosis (pre-eclampsia). Chorionic villi from healthy and pre-eclamptic placentas were incubated in hypoxic

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