ENVIRONMENTAL INFLUENCES ON THE PERINATAL LUNG DEVELOPMENT

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 该项目的目标是： 1.描述猴在发育关键窗口期（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）的条件，这些条件与母亲和/或婴儿的超声检查、羊水和血液样本的测量值相关。 2.确定在关键围产期发育期（从妊娠早期到出生后13个月）暴露于ETS对恒河猴免疫发育的影响。 3.确定相同的围产期ETS暴露是否会增强肺中神经营养因子的产生，并与C纤维中P物质的产生增加相关，从而导致CNS呼吸反应过度。 4.确定围产期后停止暴露于ETS是否会改善影响或与肺及其神经控制的持续变化有关。 5.确定ETS对NF-κ B信号传导的影响，以增加幼猴肺中的细胞凋亡。 6.评价围产期暴露于ETS对新生恒河猴脑发育和认知功能的影响。 7.研究吸烟和饮酒对线粒体损伤和动脉粥样硬化形成的相互作用。

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. The Objectives of this project are: 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 apoptosis in infant monkey lungs. 6. To evaluate the impact of perinatal exposure to ETS on brain development and cognitive function in the neonatal Rhesus monkey. 7. To examine the potential for interaction between tobacco smoke and alcohol on mitochondrial damage and atherogenesis.