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Roberto Romero

Researcher at National Institutes of Health

Publications -  1622
Citations -  121818

Roberto Romero is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Amniotic fluid & Pregnancy. The author has an hindex of 151, co-authored 1516 publications receiving 108321 citations. Previous affiliations of Roberto Romero include University of Michigan & Weizmann Institute of Science.

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Abnormal concentration of maternal serum activin-A in gestational diseases

TL;DR: It is shown that preterm labor is associated with increased concentrations of activin-A in the maternal circulation and cord serum, and Hypersecretion of activIn-A is also shown in same patients with gestation diabetes; this reverts to normal after insulin treatment.
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Progesterone receptor isoform (A/B) ratio of human fetal membranes increases during term parturition

TL;DR: Human parturition at term is associated with changes in PR isoforms in the fetal membranes and, thus, a local 'functional progesterone withdrawal' may operate in human parturitions through this mechanism.
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Intraamniotic infection with genital mycoplasmas exhibits a more intense inflammatory response than intraamniotic infection with other microorganisms in patients with preterm premature rupture of membranes

TL;DR: Intraamniotic and maternal inflammatory responses are more intense in intraamniotic infection with genital mycoplasmas than in intraamiotics infection with other microorganisms in patients with preterm premature rupture of membranes.
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Recurrent Preterm Birth

TL;DR: The body of literature describing the risk of recurrence of spontaneous and indicated preterm birth is reviewed and the factors which modify the risk are discussed (a short sonographic cervical length and a positive cervicovaginal fetal fibronectin test).
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A role for the 72 kDa gelatinase (MMP-2) and its inhibitor (TIMP-2) in human parturition, premature rupture of membranes and intraamniotic infection.

TL;DR: Human parturition (preterm and term), rupture of fetal membranes (term and preterm) and intraamniotic infection are associated with a significant decrease in amniotic fluid TIMP-2 concentrations.