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1 further prostaglandin production and further uterine contraction.
2 ate of the myometrium, and PGR-A facilitates uterine contraction.
3 hin the trophoblast as well as a trigger for uterine contraction.
4 s and calcium entry, which may contribute to uterine contraction.
5 ace electrodes has been attempted to monitor uterine contraction.
6 nd METx (100 nM) had no effect on OT induced uterine contractions.
7 tocia), suggesting that it is detrimental to uterine contractions.
8 tal membrane rupture, cervical ripening, and uterine contractions.
12 noid receptor agonist WIN 55,212-2 (WIN2) on uterine contractions (amplitude and rate) and micturitio
15 METx (41 nM) had no effect on spontaneous uterine contractions and METx (100 nM) had no effect on
17 ezo1 and Piezo2 in mice resulted in weakened uterine contractions and severe parturition defects.
18 onapeptide hormone used in labor to initiate uterine contractions and to prevent and treat postpartum
19 lular factors, targeted by drugs to regulate uterine contractions, and tissue level electromechanical
20 eight, frequency of prenatal visits, preterm uterine contractions, antepartum hemorrhages, placenta p
23 ide detailed 3D images and quantification of uterine contractions as well as novel insights into the
25 re monitoring of the fetal condition and the uterine contractions can be guaranteed, routine disconti
26 ic signals mediated by OT and PGs to promote uterine contractions, cervix softening, and membrane rup
36 targeting uterine cells in-vitro, inhibiting uterine contractions ex-vivo, while doubling uterine dru
42 preterm labour, but their ability to repress uterine contractions lasts </= 48 h and their use does n
43 ery increases with an increased frequency of uterine contractions, measurement of this frequency is n
45 ng of the heart rate well after the onset of uterine contractions (odds ratio, 3.9; 95 percent confid
48 ceptor agonists that act via cAMP can reduce uterine contractions to delay preterm labour, but their