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chorioamnionitis/glutatió
L'enllaç es desa al porta-retalls
12 resultats
Lipopolysaccharide-induced chorioamnionitis causes acute inflammatory changes in the ovine central nervous system.
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OBJECTIVE
To better understand the inflammatory response in the central nervous system (CNS) after lipopolysaccharide (LPS)-induced chorioamnionitis.
METHODS
Fetal sheep were exposed to intra-amniotic LPS 2 or 14 days before preterm delivery at 125 days of gestation. mRNA levels of cytokines, TLRs
Airway inflammatory cell responses to intra-amniotic lipopolysaccharide in a sheep model of chorioamnionitis.
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Chorioamnionitis, a risk factor for bronchopulmonary dysplasia in preterm infants, causes an influx of inflammatory cells into the fetal lung. Using a fetal sheep model, we evaluated the time course of activation, functional maturity, and apoptosis of the leukocytes recruited to the fetal air spaces
In Utero Exposure to Histological Chorioamnionitis Primes the Exometabolomic Profiles of Preterm CD4+ T Lymphocytes.
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Histological chorioamnionitis (HCA) is an intrauterine inflammatory condition that increases the risk for preterm birth, death, and disability because of persistent systemic and localized inflammation. The immunological mechanisms sustaining this response in the preterm newborn remain unclear. We
Maternal plasma prolidase, matrix metalloproteinases 1 and 13, and oxidative stress levels in pregnancies complicated by preterm premature rupture of the membranes and chorioamnionitis.
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OBJECTIVE
This study aimed to investigate the role of various biochemical markers in preterm premature rupture of membranes (PPROM) and in prediction of chorioamnionitis in patients with PPROM.
METHODS
This case-control study included a total of 100 pregnant women at 26-34 gestational weeks. Of
Antenatal N-acetylcysteine to improve outcomes of premature infants with intra-amniotic infection and inflammation (Triple I): randomized clinical trial
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Background: Intrauterine infection and/or inflammation (Triple I) is an important cause of preterm birth (PTB) and adverse newborn outcomes. N-acetylcysteine (NAC) is a Food and Drug Administration (FDA)-approved drug safely administered
Effect of Fine Particulate Matter (PM2.5) on Rat Placenta Pathology and Perinatal Outcomes.
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BACKGROUND Fine particulate matter with aerodynamic diameters smaller than 2.5 μm (PM2.5) has been reported to cause adverse effects on human health. Evidence has shown the association between PM2.5 exposure and adverse perinatal outcomes, and the most common method is epidemiological investigation.
Novel biomarkers in amniotic fluid for early assessment of intraamniotic infection.
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Intra-amniotic infection/inflammation (IAI) is associated with preterm birth, short and long-term adverse clinical outcomes and oxidative stress. The diagnosis of IAI is based on histological and clinical findings; however, often these results are unspecific. Therefore, efforts have been directed
Oxidative stress in infants born to preeclamptic mothers.
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BACKGROUND
Oxidative stress may play an important role in the pathophysiology of preeclampsia. An increase in lipid peroxidation products and a decrease in antioxidant activity in preeclamptic women have been reported in many papers. The objective of this study was to evaluate oxidative stress in
Assessment of oxidative damage and enzymatic antioxidant system activity on the umbilical cord blood and saliva from preterm newborns with risk factors for early-onset neonatal sepsis.
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Interleukin-1 receptor antagonist protects against lipopolysaccharide induced diaphragm weakness in preterm lambs.
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Chorioamnionitis (inflammation of the fetal membranes) is strongly associated with preterm birth and in utero exposure to inflammation significantly impairs contractile function in the preterm lamb diaphragm. The fetal inflammatory response to intra-amniotic (IA) lipopolysaccharide (LPS) is
Lipopolysaccharide-induced weakness in the preterm diaphragm is associated with mitochondrial electron transport chain dysfunction and oxidative stress.
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Diaphragmatic contractility is reduced in preterm lambs after lipopolysaccharide (LPS) exposure in utero. The mechanism of impaired fetal diaphragm contractility after LPS exposure is unknown. We hypothesise that in utero exposure to LPS induces a deficiency of mitochondrial complex activity and
Reduction-oxidation (redox) state regulation of matrix metalloproteinase activity in human fetal membranes.
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OBJECTIVE
The mechanisms underlying membrane rupture at term and preterm are obscure. Collagenolytic activity of matrix metalloproteinases in amniochorionic membranes increases during spontaneous term and preterm labor associated with intra-amniotic infection. We sought to test the hypothesis that
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