Human PGD2S(Prostaglandin D2 Synthase, Brain) ELISA Kit

Prostaglandin E2 (PGE2) is involved in numerous physiological and pathological processes of the kidney via its four receptors. A previous study has suggested that a defect in the PGE2 receptor 1 (EP1) gene markedly suppressed the transforming growth factor-beta 1 (TGF-beta 1)-induced mesangial cell (MC) proliferation and extracellular matrix aggregation. Therefore, the present study aimed to adopt a pharmacological method of specifically suppressing or activating the EP1 receptor to further verify and demonstrate these results. The EP1 receptor antagonist SC-19220 and EP1 receptor agonist 17-phenyl-trinor-PGE2 ethyl amide (17-pt-PGE2) were selectively used to treat five-sixths nephrectomy renal fibrosis model mice and TGF-beta 1-stimulated MCs. An Alpha screen PGE2 assay kit, flow cytometry, western blotting and immunohistochemical techniques were adopted to perform in vivo and in vitro experiments. The present results suggested that compared with the control group, the selective EP1 receptor antagonist SC-19220 improved renal function, markedly reduced the plasma blood urea nitrogen and creatinine levels (P<0.05) and alleviated glomerulosclerosis (P<0.05). By contrast, the EP1 receptor agonist 17-pt-PGE2 aggravated renal dysfunction and glomerulosclerosis (P<0.05). To verify the renal protection mechanisms mediated by suppression of the EP1 receptor, the expression levels of endoplasmic reticulum stress (ERS)-related proteins, including chaperone glucose-regulated protein 78 (GRP78), transient receptor potential channel 1 (TRPC1) and protein kinase R-like endoplasmic reticulum kinase (PERK), were further evaluated histologically. The expression of GRP78, TRPC1 and PERK in the antagonist treatment group were markedly downregulated (P<0.05), whereas those in the agonist treatment group were upregulated (P<0.05). The present in vitro experiments demonstrated that, compared with the control group, the EP1 receptor antagonist suppressed the expression of GRP78, TRPC1 and PERK (P<0.05), reduced the production of PGE2 (P<0.05) and decreased the MC apoptosis rate (P<0.05), thus alleviating TGF-beta 1-stimulated MC injury. Consequently, consistent with previous results, selectively antagonizing the EP1 receptor improved renal function and mitigated glomerulosclerosis, and its potential mechanism might be associated with the suppression of ERS.

Objective:To determine if differences exist among nulliparous overweight and obese gravidas undergoing cervical ripening employing three different agents (dinoprostone, misoprostol, or cervical catheter). Methods:A retrospective cohort study of nulliparous overweight and obese women who underwent induction of labor at two south-central Pennsylvania hospitals between January 2014 and December 2017. Nulliparous gravidas, >= 37 weeks' gestational age, with singleton pregnancies in the vertex presentation, were included in the study. We employed the following definitions: (1) overweight: BMI 25.0-29.9 kg/m(2); (2) class I obesity: BMI 30.0-34.9 kg/m(2); (3) class II obesity: BMI 35.0-39.9 kg/m(2); and (4) class III obesity: BMI >40.0 kg/m(2). The primary outcome measure was the mean difference in induction-to-birth time. A subanalysis was performed to assess the effect of BMI on the primary outcome. Secondary outcome measures included mode of delivery, induction-to-second-stage-of-labor time, estimated blood loss, neonatal feeding type, neonatal Apgar scores, and neonatal admission to triage or intensive care unit (ICU) after delivery.A prioripower calculation estimated that 156 patients would be needed using the medium effective size. Data analysis was performed using ANOVA for continuous variables and chi-square tests for categorical variables. Results:Among 192 nulliparous overweight and obese gravidas, 70 received dinoprostone, 72 were given misoprostol, and 50 had cervical ripening with cervical catheters. There were no significant differences in mean induction to birth times among overweight and obese women when comparing the three cervical ripening agents (dinoprostone 24.5 +/- 15.2 versus misoprostol 28.7 +/- 12.3 and catheters 25.1 +/- 12.9 hours), (p = .145, 95% CI -8.7 to 0.2 and -5.5 to 4.3, respectively). Overweight nulliparous women had shorter mean induction to birth time (22.9 +/- 11.4 versus 29.2 +/- 15.8 hours) as compared to class II obese women, (p = .037, 95% CI -12.0 to -0.38). When overweight women were compared to class III obese women, shorter mean induction to birth time (22.9 +/- 11.4 versus 30.9 +/- 13.9 hours) was also found, (p = .005, 95% CI -13.4 to -2.4). Conclusion:Among nulliparous overweight and obese gravidas, neither dinoprostone, misoprostol, or cervical catheter significantly impacted the induction to birth time. There was a longer induction to birth time for class II and class III obese women when compared to overweight women. Additional studies are warranted to improve cervical ripening in nulliparous overweight and obese women.