In vitro sealing of punctured fetal membranes: Potential treatment for midtrimester premature rupture of membranes

2001 ◽  
Vol 185 (5) ◽  
pp. 1090-1093 ◽  
Author(s):  
Uma M. Reddy ◽  
Shailen S. Shah ◽  
Richard L. Nemiroff ◽  
Samir K. Ballas ◽  
Terry Hyslop ◽  
...  
2005 ◽  
Vol 58 (7-8) ◽  
pp. 375-379 ◽  
Author(s):  
Dunja Tabs ◽  
Tihomir Vejnovic ◽  
Nebojsa Radunovic

Women conceiving by assisted reproduction are at higher risk for preterm and premature rupture of membranes. The aim of our study was to estimate and compare incidence of preterm premature rupture of membranes in singleton pregnancies of women who conceived by intrauterine insemination and in vitro fertilization, from 1999 to 2003. We investigated 87 women from the intrauterine insemination, and 102 from the in vitro fertilization program. There were no statistically significant differences in regard to preterm and premature rupture of membranes: p>0.75 in two groups. The incidence of premature rupture of membranes was 2.30% (after intrauterine insemination) and 2.94% (after in vitro fertilization). There was no statistically significant differences in regard to preterm and premature rupture of membranes in women who conceived by insemination and in vitro fertilization. Estimated incidence of preterm and premature rupture of membranes was similar to the literature data and also similar to incidence after natural conception.


Reproduction ◽  
2011 ◽  
Vol 142 (1) ◽  
pp. 183-194 ◽  
Author(s):  
Megan L Calmus ◽  
Elyse E Macksoud ◽  
Richard Tucker ◽  
Renato V Iozzo ◽  
Beatrice E Lechner

Preterm premature rupture of membranes is responsible for one-third of preterm births. Ehlers–Danlos syndrome (EDS) is associated with preterm premature rupture of membranes in humans. In particular, an EDS variant is caused by a genetic mutation resulting in abnormal secretion of biglycan and decorin, two small leucine-rich proteoglycans highly expressed in reproductive tissues. Because biglycan/decorin null mutant (Bgn−/−Dcn−/−) mice demonstrate phenotypic changes similar to EDS, we used this model to test whether either biglycan or decorin or both play a role in the attainment of successful term gestation. Wild-type biglycan null mutant, decorin null mutant, and biglycan/decorin null mutant pregnancies were assessed for the length of gestation, pup and placenta weight, and litter size. Quantitative real-time PCR was performed to measure biglycan and decorin gene expression, and immunohistochemistry was performed to assess protein expression in placenta and fetal membranes at embryonic days E12, E15, and E18.Bgn−/−Dcn−/−dams displayed preterm birth, whereas the possession of at least two biglycan or decorin wild-type alleles was protective of preterm birth. The number ofBgn−/−Dcn−/−pups was decreased at postnatal day P1 but not at E18. Biglycan and decorin were upregulated in the placenta in the absence of each other and were developmentally regulated in fetal membranes, suggesting that these two proteoglycans demonstrate genetic complementation and contribute to gestational success in a dose-dependent manner. Thus, the biglycan/decorin null mutant mouse is a model of genetically induced preterm birth and perinatal loss. This model presents novel targets for preventive or therapeutic manipulation of preterm birth.


2021 ◽  
Vol 22 (19) ◽  
pp. 10584
Author(s):  
Chidambra D. Halari ◽  
Michael Zheng ◽  
Peeyush K. Lala

Two small leucine-rich proteoglycans (SLRP), decorin and biglycan, play important roles in structural–functional integrity of the placenta and fetal membranes, and their alterations can result in several pregnancy-associated diseases. In this review, we briefly discuss normal placental structure and functions, define and classify SLRPs, and then focus on two SLRPs, decorin (DCN) and biglycan (BGN). We discuss the consequences of deletions/mutations of DCN and BGN. We then summarize DCN and BGN expression in the pregnant uterus, myometrium, decidua, placenta, and fetal membranes. Actions of these SLRPs as ligands are then discussed in the context of multiple binding partners in the extracellular matrix and cell surface (receptors), as well as their alterations in pathological pregnancies, such as preeclampsia, fetal growth restriction, and preterm premature rupture of membranes. Lastly, we raise some unanswered questions as food for thought.


2021 ◽  
Author(s):  
Corinne Belville ◽  
Flora Ponelle-Chachuat ◽  
Marion Rouzaire ◽  
Christelle Gross ◽  
Bruno Pereira ◽  
...  

The integrity of human fetal membranes is crucial for harmonious fetal development throughout pregnancy. Their premature rupture is often the consequence of a physiological phenomenon previously exacerbated. Beyond all biological processes implied, inflammation is of primary importance and is qualified as sterile at the end of pregnancy. Complementary methylomic and transcriptomic strategies on amnion and choriodecidua explants taken from the altered (cervix zone) and intact fetal membranes at term and before labor were used in this study. By cross-analyzing genome-wide studies strengthened by in vitro experiments, we deciphered how the expression of Toll-like receptor 4 (TLR4), a well-known actor of pathological fetal membrane rupture, is controlled. Indeed, it is differentially regulated in the altered zone and between both layers by a dual mechanism: 1) the methylation of TLR4 and miRNA promoters and 2) targeting by miRNA (let-7a-2 and miR-125b-1) acting on the 3-UTR of TLR4. Consequently, this study demonstrates that a fine regulation of TLR4 is required for sterile inflammation establishment at the end of pregnancy and that it may be dysregulated in the pathological premature rupture of membranes.


2008 ◽  
Vol 25 (1) ◽  
pp. 029-032 ◽  
Author(s):  
Ronald George ◽  
Jennifer Kalich ◽  
Bryan Yonish ◽  
Amy Murtha

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