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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prematurity remains the major cause of perinatal mortality and morbidity in Singapore. Prevention of prematurity is therefore of vital importance. Epidemiological methods using historical variables have been superseded by ongoing pregnancy factors including work, exercise and cervical dilatation. PGF levels bear a positive correlation to duration and cervical dilatation but are not elevated at onset. PGE production is high in ruptured membranes. Progesterone and relaxin are potent inhibitors before labour. Infection must play an important role in developing countries as organisms not thought of to be pathogenic produce phospholipase A2. For prediction, cervical assessment and topography are proving important. In view of the dangerous side effects of tocolytic drugs and the difficulty in diagnosis of preterm labour, absence of fetal breathing is a useful index of progressive labour. In those labours that are advanced, whether to allow vaginal delivery or not will be determined by the presentation and condition of the fetus. The complementary role of other drugs to reduce morbidity from hyaline membrane disease and intraventricular haemorrhage is being studied. Fetal acidosis should be avoided and the infant delivered without trauma under optimal circumstances. In utero transfer to a facility with neonatal intensive care carries a better prognosis for the baby.
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PMID:Current concepts in the management of preterm labour. 269 76

A number of organisms, including Mycoplasma, group B Streptococcus, Bacteroides, Neisseria gonorrhoeae and Chlamydia trachomatis, have been isolated more frequently from patients in premature labor than from controls. Prophylactic antibiotic treatment in some studies lowered the incidence of prematurity. Silent chorioamnionitis has been noted in 15% of patients in premature labor. Untreated pyelonephritis is clearly associated with premature labor; however, the association of asymptomatic bacteriuria, appropriately treated pyelonephritis and premature labor is less clear. Some microorganisms have been demonstrated to produce phospholipase A2 and possibly prostaglandins, which might be the mechanism for some of the associations between premature labor and bacteria.
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PMID:Microorganisms and premature labor. 327 13

The results of recent studies support the concept that Ureaplasma urealyticum may be a major cause of perinatal infection in both term and preterm infants. It has been postulated that phospholipase degradation of placental phospholipids by microorganisms triggers the onset of premature labor. Since the presence of ureaplasmas in placentas is associated with pregnancy loss, prematurity, and neonatal morbidity, we assayed U. urealyticum for the presence of phospholipase A1, A2, and C activities. Phospholipase A1 activity was low in lysates of exponential-phase cells of U. urealyticum. Phospholipase A2 activity was present and was 100-fold higher than the activity of phospholipase A1 in serotypes 3,4, and 8. The total activity and specific activity of phospholipase A2 in serotype 8 were nearly threefold higher than the activities in serotypes 3 and 4. Cell lysates of all three serotypes showed the presence of phospholipase C activity during the exponential phase of growth, and no significant difference in activity was observed among the three serotypes. In stationary-phase cells the phospholipase C activity was 10-fold lower than the activity in exponential-phase cells. Our results demonstrate that phospholipase activities are present in U. urealyticum cells and that the specific activities of phospholipase A2 differed among the three serotypes tested, while the activities of phospholipases A1 and C were similar.
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PMID:Endogenous activity of phospholipases A and C in Ureaplasma urealyticum. 370 Jun 18

The clinical relevance of vaginal colonization with Mycoplasma hominis (M hominis) as a cause of prematurity is doubtful. One of the possible pathways which could explain the role of M hominis in the induction of preterm labour is an increased synthesis of prostaglandins by a phospholipase A2 activity. The aim of this study was to prove whether M hominis secrets proteins with a PLA2 activity and to test whether there are strain differences in the enzyme activity between M hominis isolated from women with normal pregnancy and those with preterm labour. Using specific radio-immunoassay we could not measure any PLA2 activity in the supernatant of all investigated M hominis strains. We exclude the mechanism of induction of preterm labour by M hominis via an increased prostaglandin synthesis. Our findings make a relation between vaginal colonization with M hominis and prematurity unlikely.
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PMID:Absence of phospholipase A2 activity in genital Mycoplasma hominis. 977 81

Prematurity is one of the leading causes of infant mortality. It may result from intrauterine infection, which mediates premature labor by stimulating the production of inflammatory lipid mediators such as prostaglandin F2alpha (PGF2alpha). The biological effects of PGF2alpha are mediated via the G protein-coupled receptor FP; however, the molecular mechanism(s) of FP signaling that mediates inflammatory lipid mediator production remains unclear. We reported previously that in the human uterus, a composite organ in which fibroblast, epithelial, and smooth muscle cells are the major constituents, an inverse relationship exists between the levels of PGF2alpha and a steroid-inducible anti-inflammatory protein, uteroglobin. Here we report that, in NIH 3T3 fibroblasts and human uterine smooth muscle cells, FP signaling is mediated via multi-kinase pathways in a cell type-specific manner to activate NF-kappaB, thus stimulating the expression of cyclooxygenase-2. Cyclooxygenase-2 is a critical enzyme for the production of prostaglandins from arachidonic acid, which is released from membrane phospholipids by phospholipase A2, the expression of which is also stimulated by PGF2alpha. Most importantly, uteroglobin inhibits FP-mediated NF-kappaB activation and cyclooxygenase-2 gene expression by binding and most likely by sequestering PGF2alpha into its central hydrophobic cavity, thereby preventing FP-PGF2alpha interaction and suppressing the production of inflammatory lipid mediators. We propose that uteroglobin plays important roles in maintaining homeostasis in organs that are vulnerable to inadvertent stimulation of FP-mediated inflammatory response.
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PMID:Uteroglobin inhibits prostaglandin F2alpha receptor-mediated expression of genes critical for the production of pro-inflammatory lipid mediators. 1606 84