RHEUMATOID ARTHRITIS MULTIDIMENSIONAL PROJECT (RAMP)

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。 对压力的情绪反应与免疫和炎症变化有关，例如炎性细胞因子谱的变化，新的研究表明，这种变化与长期疼痛的加重有关。我们的总体目标是研究情绪对疼痛和对疼痛的炎症反应的影响，以及炎症和其他生理因素在多大程度上解释情绪、感知到的压力和疼痛之间的联系。这将在类风湿性关节炎患者中进行检查，对他们来说，非常需要额外的疼痛管理策略，对他们来说，情绪调节可能特别重要。 在每一次建议的3次“情绪”访问中，间隔约1个月，40名受试者将完成集中情绪的练习，以引发愤怒、抑郁情绪或积极情绪；这些访问将与不引发情绪的基线对照访问形成对比。在每次就诊期间，将在基线以及痛阈值测试之前、期间和30分钟后抽取血液。将对血液进行C反应蛋白(仅基线)、促炎细胞因子TNF-a、IL-1、IL-6、抗炎细胞因子IL-10、皮质醇和儿茶酚胺的检测。 我们预计(1)状态愤怒和消极情绪都会增加RA疼痛的严重程度，并且在对急性疼痛的反应中，会增加皮质醇和促炎细胞因子的反应。积极情绪会起到相反的作用；(2)细胞因子的变化会解释状态情绪对RA疼痛程度和痛阈值的影响。

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. Emotional responses to stress are linked with immune and inflammatory changes, such as changes to inflammatory cytokine profiles, and new research suggests that such changes are implicated in the aggravation of long-term pain. Our overall objective is to examine the impact of emotion on pain and inflammatory responses to pain, as well as the degree to which inflammation and other physiological factors explain associations between emotion, perceived stress, and pain. This will be examined among individuals with rheumatoid arthritis, for whom additional strategies to manage pain are greatly needed and for whom emotional regulation may be particularly important. During each of 3 proposed "emotion" visits, spaced about 1 month apart, 40 individuals will complete emotion-focusing exercises to elicit either anger, depressed mood, or positive emotion; these visits will be contrasted with a baseline control visit during which emotion is not elicited. During each visit, blood will be drawn at baseline and just before, during, and 30 minutes after a pain threshold test. Blood will be assayed for C-reactive protein (baseline only), and proinflammatory cytokines TNF-a, IL-1, IL-6, anti-inflammatory cytokine interleukin-10 (IL-10), cortisol, and catecholamines. We expect that (1) both state anger and negative mood will increase RA pain severity and, in response to acute pain, will increase cortisol and proinflammatory cytokine responses. Positive emotion will have the opposite effects; (2) Cytokine changes will account for the effects of state emotion on both pain severity from RA and pain threshold.