ENVIRONMENTAL INFLUENCES ON THE PERINATAL LUNG DEVELOPMENT

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。 目标： 1.描述猴子在发育的关键时期(从妊娠早期到出生后13个月)暴露于常见室内空气污染物(ETS)的情况与超声检查、羊水和母婴血液样本的相关性。 2.探讨围生期发育的关键时期(从早期妊娠到出生后13个月龄)暴露于ETS对恒河猴免疫发育的影响。 3.为了确定同样的围产期ETS暴露是否增加了肺中神经营养素的产生，并与C纤维中P物质的产生增加导致CNS呼吸反应夸大有关。 4.确定围产期后停止接触ETS是否会改善效果，或与肺部及其神经控制的持续变化有关。 5.探讨ETS对核因子-kappaB信号转导途径促进幼猴肺细胞凋亡的影响 6.探讨围产期ETS暴露对新生恒河猴脑发育和认知功能的影响。 7.研究烟草烟雾和酒精在线粒体损伤和动脉粥样硬化形成中的相互作用。

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. Objectives: 1. To characterize conditions of exposure to a common indoor air pollutant (ETS) in monkeys during critical windows of development (ranging from early gestation to 13 months postnatal age) correlated to measures from ultrasonography, amniotic fluid and blood samples of the mother and/or infant. 2. To determine the consequences in the lung of exposure to ETS in monkeys during critical perinatal periods of development (from early gestation to 13 months postnatal age) on immunological development of the Rhesus monkey. 3. To determine if the same perinatal ETS exposure enhances neurotrophin production in the lungs in association with increased production of substance P in C-fibers resulting in exaggerated CNS respiratory responses. 4. To determine if cessation of exposure to ETS after the perinatal period will ameliorate effects or be associated with persistent changes in the lung and its neural control. 5. To determine the effects of ETS on NF-kappaB signaling to increase apopotosis in infant monkey lungs 6. To evaluate the impact of perinatal exposure to ETS on brain development and cognitive function in the neonal Rhesus monkey. 7. To examine the potential for interaction between tobacco smoke and alcohol on mitochondrial damage and atherogenesis.