PRIMATE DECIDUA AND FETAL MEMBRANES AS A PARACRINE SYSTEM

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 在没有感染的情况下，胎膜局部的低水平炎症反应可能与足月儿和早产儿的胎膜早破(PROM)有关。这与感染介导的早产的华丽炎症反应特征形成了鲜明的对比。胎膜早破和早产患者蜕膜松弛素表达增加。本研究的目的是确定在妊娠的非人灵长类动物模型中，羊膜内注射人重组松弛素是否会导致关键途径(发育生长调节剂、细胞外基质调节剂和/或促炎介质)的改变，这些途径可能是早产儿胎膜早破(PPROM)的先兆。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In the absence of infection, a localized low-level inflammatory response in the fetal membrane may be associated with premature rupture of membranes (PROM) in both term and preterm birth. This contrasts with the florid inflammatory response characteristic of infection-mediated preterm parturition. Decidual relaxin expression is increased in patients with PROM and preterm birth. The objective of this research is to ascertain whether intraamniotic administration of human recombinant relaxin in a pregnant nonhuman primate model causes changes in key pathways (developmental growth regulators, extracellular matrix modulators, and/or proinflammatory mediators) which may precede preterm premature rupture of the fetal membranes (PPROM).