AGING AND THE INFLAMMATORY, METABOLIC AND AUTONOMIC RESPONSE TO SLEEP LOSS

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。 该方案的目的是使用一小时守夜模型来研究失眠期间炎症增加的机制，因为这种效应受个体对失眠影响的抵抗力差异的影响较小。他们假设，睡眠不足本身会导致炎症稳态的改变，因为在自主神经系统正常下调的时候，它会对自主神经系统产生需求，导致血压升高，进而导致白细胞、内皮细胞和脂肪细胞释放的炎症介质增加。这项研究将是一项2x2x2的分组设计，包括年轻人(21-40岁)和老年人(50-75岁)、脂肪和苗条、睡眠和睡眠剥夺。受试者将被随机分配到睡眠或警戒状态，在这一状态下，他们将保持清醒长达小时。

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 purpose of this protocol is to investigate the mechanism of increases in inflammation during sleep loss using a 64-hour vigil model because the effects are less influenced by individual differences in resistance to the effects of sleep loss. They hypothesize that sleep loss itself leads to an altered inflammatory homeostasis by placing demands on the autonomic nervous system at a time when the system normally down-regulates, resulting in increased blood pressure, which in turn leads to elevated inflammatory mediators released from both white blood cells, endothelial cells and adipocytes. This study will be a 2x2x2 between groups design with younger (21-40 yrs) and older (50-75 yrs), adipose and lean, sleep versus sleep deprivation. Subjects will be randomly assigned to a sleep or vigilance condition, where they will remain awake for up to 64 hours.