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Pàgina 1 des de 45 resultats
Complement activation, circulating protease inhibitors and pregnancy-associated proteins in severe pre-eclampsia.
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Circulating protease inhibitors, pregnancy-associated proteins and the split product of complement factor 3 (C3d) were measured in 14 women with severe pre-eclampsia and their matched controls. Only the mean levels of antithrombin III were observed to be significantly lower in pre-eclampsia (P less
Correlation of Plasma Neutrophil Elastase Activity and Endogenous Protease Inhibitor Levels with the Severity of Pre-eclampsia.
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BACKGROUND
Pre-eclampsia (PE) is a common maternal syndrome characterized by severe systemic inflammatory response including neutrophil activation leading to uncontrolled activity of elastase. The excessive activity of elastase would lead to destroyal of the integrity of endothelial cells and could
Neutrophil CD11B expression and neutrophil activation in pre-eclampsia.
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1. Neutrophil activation was examined in 22 women with pre-eclampsia and 22 age- and gestation-matched control subjects using whole-blood flow cytometry to assess basal and platelet-activating factor stimulated CD11b and CD18. 2. Basal neutrophil CD11b expression was significantly increased in women
The importance of cysteine cathepsin proteases for placental development.
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The typically lysosomal family of cysteine cathepsin proteases has been implicated in the development of the placenta in particular, from studies in the mouse. Here, we analysed overall expression, regulation and presence of transcript isoforms of cysteine cathepsins during human extra-embryonic
Role of the IGF system in trophoblast invasion and pre-eclampsia.
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Insulin-like growth factor-II (IGF-II) and IGF binding protein-1 (IGFBP-1) appear to play an important role in paracrine interactions at the maternal-fetal interface in human pregnancy. Patterns of expression of IGF-II and IGFBP-1 at the decidual-trophoblast interface suggest paracrine interactions
Urinary tissue kallikrein excretion in black African women with severe pre-eclampsia.
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BACKGROUND
A study of tissue kallikrein excretion in African women with severe pre-eclampsia.
METHODS
Random untimed urine samples were collected from all women (n=198) recruited to this study; 66 women with severe pre-eclampsia, 66 normotensive pregnant women of similar length of gestation and 66
Decitabine Improves the Clinical Manifestations of Rats With l-NAME-Induced Pre-eclampsia: A Potential Approach to Studying Pre-eclampsia.
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OBJECTIVE
Pre-eclampsia is a major cause of maternal mortality and morbidity. Conditions with low oxygen tension are regarded as a key factor. Decitabine can partly attenuate the effects of hypoxia. This research was designed to investigate the effects of decitabine in rats with NG-Nitro-L-arginine
Lectin pathway proteins of the complement system in normotensive pregnancy and pre-eclampsia.
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Interaction between pregnancy-induced bioactive peptides and the placental proteases.
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Studies have shown that placental proteases metabolize vasoactive peptides, possibly derived from the fetus, and protect the exchange of peptide hormones across the placenta in order to maintain feto-placental homeostasis. Changes in maternal serum protease activities were useful for monitoring
A distinct concerted mechanism of structural dynamism defines activity of human serine protease HtrA3.
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Human HtrA3 (High temperature requirement protease A3) is a trimeric multitasking propapoptotic serine protease associated with critical cellular functions and pathogenicity. Implicated in diseases including cancer and pre-eclampsia, its role as a tumor suppressor and potential therapeutic target
Alternative forms of a novel aspartyl protease gene are differentially expressed in human gestational tissues.
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The aim of this study was to identify genes involved in human placentation. To do this, differential gene expression was assessed in the decidua (placental bed) from pre-eclamptic and normotensive pregnancies using the polymerase chain reaction (PCR)-based subtractive technique of representational
[Possible role of placental proteases via degradation of vasoactive peptides in the maternal and fetal blood pressure].
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Both fetal and maternal blood pressure is regulated mainly by the humoral factor, vasoactive peptides such as angiotensin II and vasopressin, but not by autoregulation and the autonomic nervous system. It is known that the normal musculoelastic tissue in the vessel wall of the coiled artery, which
Microarray analysis of differentially expressed genes in placental tissue of pre-eclampsia: up-regulation of obesity-related genes.
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Susceptibility genes present in both mother and fetus most likely contribute to the risk of pre-eclampsia. Placental biopsies were therefore investigated by high-density DNA microarray analysis to determine genes differentially regulated within chorionic villous tissue in pre-eclampsia and normal
Protease chymotrypsin mediates the endothelial expression of P- and E-selectin, but not ICAM and VCAM, induced by placental trophoblasts from pre-eclamptic pregnancies.
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OBJECTIVE
Soluble endothelial-cell adhesion molecules (ICAM, VCAM and PECAM) are markers of endothelial activation, and are elevated in the maternal circulation during pregnancy and even further increased in pregnancies complicated by pre-eclampsia (PE). To identify possible sources of endothelial
Matrix metalloprotease-9, placental syncytiotrophoblast and the endothelial dysfunction of pre-eclampsia.
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The maternal syndrome of pre-eclampsia is caused by generalized maternal endothelial cell dysfunction, arising directly or indirectly from factors of placental origin. Syncytiotrophoblast membrane microvesicular particles are shed from the placental surface into maternal blood in increased amounts
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