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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to analyse the relationship between the ovarian response to stimulation in in-vitro fertilization (IVF) treatment cycles and relaxin concentrations during subsequent pregnancies, 31 healthy women pregnant after IVF treatment were studied prospectively. The maximum number of follicles observed from day -4 to day -2 in relation to ovum retrieval and the number of oocytes recovered were recorded. In addition, blood samples were drawn in the follicular phase, the luteal phase, early pregnancy and at gestational weeks 12, 16, 20, 27 and 35 to assess oestradiol, progesterone, human chorionic gonadotrophin and relaxin. The maximum numbers (mean +/- SEM) of follicles observed and oocytes recovered were 9.0 +/- 0.6 and 6.1 +/- 0.5 respectively. The supraphysiological mean relaxin values were strongly correlated to the maximum number of follicles observed (r = 0.72, P < 0.0001) and the number of oocytes recovered (r = 0.64, P < 0.0001), indicating that the source of increased relaxin production during IVF pregnancy might be the ovary. These results are supported by experimental data. In the present study, the occurrence of multiple pregnancy was not associated with higher relaxin concentrations, which is further support for the hypothesis that the ovary is the main source of serum relaxin.
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PMID:Supraphysiological serum relaxin concentration during pregnancy achieved by in-vitro fertilization is strongly correlated to the number of growing follicles in the treatment cycle. 892 Oct 86

CG produced by fetal tissues extends the functional lifespan of the primate corpus luteum during early pregnancy. Previous studies showed that urinary hCG administered to monkeys to simulate the rising CG levels associated with early pregnancy enhanced both progesterone (P) and relaxin (RLX) production by the corpus luteum. The current study was designed: 1) to compare the ability of recombinant (r) and urinary (u) hCG to stimulate luteal function, and 2) to assess the role of P in the regulation of luteal RLX secretion during simulated early pregnancy by concomitant administration of hCG and the 3 beta-hydroxysteroid dehydrogenase inhibitor trilostane to reduce P production. Rhesus monkeys received injections of either r-hCG or u-hCG (Ares Serono) in increasing doses (15-2880 IU/dose, twice daily) for 9 days beginning on day 9 of the luteal phase (n = 5/group). An additional group (n = 4) received r-hCG as described above, with concomitant oral administration of trilostane (500 mg/dose twice daily; Sanofi Winthrop). Daily serum samples were assayed for hCG by immunoradiometric assay, steroid hormones by RIA, and RLX by enzyme-linked immunosorbent assay. Serum hCG levels typically were not different between the r-HCG and u-hCG groups during or after treatment. Concentrations of hCG peaked 1 day after the final injection in monkeys receiving r-hCG (mean +/- SEM. 2759 +/- 120 mIU/mL) and u-hCG (2120 +/- 60 mIU/mL) and dropped below 5 mIU/mL by 10 days after the final treatment in all groups. Both r-hCG and u-hCG stimulated luteal P and RLX production. Progesterone levels rose rapidly after the initiation of hCG treatment and peaked in animals receiving r-hCG (14.4 +/- 2.8 ng/mL) and u-hCG (11.9 +/- 1.4 ng/mL) 4 days after initial administration. RLX levels peaked in the r-hCG (400 +/- pg/mL) and u-hCG (323 +/- 85 pg/mL) groups within 4 days of the final hCG treatment. Trilostane with r-hCG reduced P concentrations to very low levels (< 0.5 ng/mL; P < 0.01) within 1 day of administration compared to those in animals receiving r-hCG only and maintained these low levels for the entire treatment interval. Nevertheless, trilostane administration did not alter luteal RLX production, with serum levels peaking at 377 +/- 76 pg/mL. These data indicate that r-hCG and u-hCG were equally efficacious in stimulating the steroidogenic and peptidergic activities of the corpus luteum during simulated early pregnancy. In addition, P deprivation during r-hCG administration did not alter circulating RLX levels, suggesting that P is not a major regulator of RLX production by the primate corpus luteum during early pregnancy.
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PMID:Stimulation of primate luteal function by recombinant human chorionic gonadotropin and modulation of steroid, but not relaxin, production by an inhibitor of 3 beta-hydroxysteroid dehydrogenase during simulated early pregnancy. 896 69

To elucidate the mechanism of relaxin action, we studied the binding characteristics of human relaxin and its effects on intracellular concentrations of cAMP and tyrosine phosphorylation of cellular proteins in a model system of human cervix, human lower uterine segment fibroblasts. Human relaxin labeled with 125I bound specifically to a single class of high-affinity relaxin binding sites, distinct from insulin receptors, with a mean (+/-SEM) dissociation constant (Kd) of 4.36 +/- 1.7 x 10(-9) M and a mean of 3220 +/- 557 binding sites per cell in human lower uterine segment fibroblasts. Relaxin, in quantities that were shown previously to stimulate intracellular levels of cAMP in other cell types, had no effect on intracellular levels of cAMP in human lower uterine segment fibroblasts even in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine (IBMX). Incubation of the cells with relaxin caused a significant increase in tyrosine phosphorylation of a protein with an apparent Mr of approximately 220 kDa in these cells. In concert with results of recent studies that demonstrated that the Mr of the relaxin receptor is approximately 220 kDa, our data suggest that the phosphorylated protein is likely to be the relaxin receptor.
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PMID:Demonstration of a relaxin receptor and relaxin-stimulated tyrosine phosphorylation in human lower uterine segment fibroblasts. 949 55

Experiments were done to examine whether rat relaxin is dipsogenic and whether such dipsogenic effects of rat relaxin are related to time of injection during the light-dark cycle. Female rats were fitted with a chronic intra-cerebro-ventricular (i.c.v.) cannula. Rat relaxin (2.5, 5, 10, 25, 50, or 100 ng/2 microl in 0.9% saline) was injected into the right lateral ventricle at either morning (0800-1000 h), afternoon (1400-1600 h), or night (2200-2400 h), and water consumption was measured. Relaxin caused a dose-dependent dipsogenesis at doses > or = 5 ng, but the sensitivity and magnitude of the response varied with the photoperiod. Water consumption was smallest (3.5 +/- 0.7 ml at 50 ng) and least sensitive (minimal effective dose at 25 ng) in the afternoon and maximal (17.7 +/- 2.3 ml at 50 ng) and most sensitive (minimal effective dose 5 ng) at night. The latency from injection to drinking was 55.8 +/- 10.4 sec (mean +/- SEM) and did not vary significantly with either the dose or time of day. A second set of experiments was done to examine the effects of neutralizing the central actions of relaxin on drinking behavior in pregnancy. Pregnant rats were injected daily, through a chronically implanted i.c.v. cannula, with either a specific monoclonal antibody raised against rat relaxin from day 12 to day 22 of gestation or with saline as a control. Drinking and eating behavior and weight gain were monitored every 12 h during pregnancy. There was a significant decrease in water consumed at night, but no effect on drinking during the day in relaxin-neutralized rats. These animals also showed a decrease in weight gain during pregnancy compared with controls and gave birth to lighter-weight litters. These data provide evidence that the dipsogenic response to exogenous rat relaxin in female rats varies with time of injection during the light-dark cycle and suggest that relaxin in the brain may have a role in nighttime drinking behavior during the second half of pregnancy.
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PMID:The dipsogenic effects of rat relaxin: The effect of photoperiod and the potential role of relaxin on drinking in pregnancy. 956 40


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