CHRONIC INFLAMMATION AT ORAL AND CERVICO-VAGINAL MUCOSA

口腔和宫颈阴道粘膜的慢性炎症

• 批准号: 8360730
• 负责人: KRISTIN ASHFORD
• 金额: $ 27.3万
• 依托单位: UNIVERSITY OF KENTUCKY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-08-01 至 2012-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8360730
• 关键词: African American; Anxiety; Biological Markers; Biological Markers; Birth; Caucasians; Caucasoid Race; Chronic; Cotinine; Coupled; Early treatment; Economics; Funding; Grant; Hispanics; Incidence; Inflammation; Inflammatory; Investigation; Latino; Link; Low Birth Weight Infant; Minority Groups; Mucous Membrane; National Center for Research Resources; Oral; Outcome; Patient Self-Report; Population; Population Heterogeneity; Predictive Value; Pregnancy; Pregnancy Outcome; Pregnant Women; Premature Birth; Principal Investigator; Process; Research; Research Infrastructure; Resources; Risk; Risk Factors; Rural; Saliva; Sampling; Serum; Source; Stress; Systemic disease; Testing; Underserved Population; United States National Institutes of Health; Urine; Vagina; Woman; base; biobehavior; cost; depressive symptoms; experience; inflammatory marker; prenatal; psychosocial; racial and ethnic; vaginal fluid

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Preterm birth (PTB; 37 weeks gestation) and low birthweight (LBW; 2,500 g) deliveries continue to increase in the U.S. resulting in substantial economic and societal costs. Adverse pregnancy outcomes are disproportionately expressed in ethnic and racial minority populations and historically underserved populations, particularly from rural regions of the nation. However, a substantial proportion of the general overall increase in incidence of PTB and LBW, including severe PTB (32 weeks) and very low birthweight (1,500 g), cannot be explained by classical risk factors for these negative birth outcomes. Thus, a broader view of the potential interrelationships leading to adverse pregnancy outcomes, including biologic markers or processes could provide some predictive value allowing earlier intervention to reduce this burden in the population. This investigation will test the General Hypothesis that "women who deliver preterm will have higher levels of prenatal inflammatory markers in whole saliva, serum and cervico-vaginal fluid (CVF), which are displayed earlier in pregnancy compared to women who deliver term". Three specific aims will be used to guide the study in testing this hypothesis: Specific Aim 1: To compare and contrast the expression of trimester-specific prenatal inflammatory markers in whole saliva, serum and CVF. Rationale: This aim will determine our ability of detect trimester-specific inflammatory markers in saliva, serum, and CVF. Specific Aim 2: To define the differences in the expression of trimester-specific prenatal inflammatory markers between women who do and do not experience preterm birth in a multi-racial/ethnic population. Rationale: This aim will establish PTB-specific risk factors based on prenatal inflammatory biomarker profiles in a racially/ethnically diverse population of Caucasian, African American and Hispanic/Latino women) and preterm birth (37 completed weeks of gestation). Specific Aim 3: To determine if trimester-specific prenatal inflammatory markers linked with psychosocial and biobehavioral variables pose a significant risk for preterm birth in a multi-racial/ethnic sample of pregnant women. Rationale: This aim will establish if trimester-specific systemic and local prenatal markers of inflammation coupled with psychosocial and biobehavioral variables impact preterm birth risk and self-reported levels of prenatal depressive symptoms; anxiety; stress, urine cotinine, and self-reported prenatal SHS exposure

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 早产（PTB;妊娠37周）和低出生体重（LBW; 2，500 g）的分娩在美国继续增加，导致巨大的经济和社会成本。 不良妊娠结局在少数民族和种族人口以及历史上得不到充分服务的人口中，特别是来自该国农村地区的人口中不成比例地表达。 然而，PTB和LBW发生率总体增加的很大一部分，包括重度PTB（32周）和极低出生体重（1，500 g），不能用这些负面出生结局的经典风险因素来解释。 因此，更广泛地了解导致不良妊娠结局的潜在相互关系，包括生物标志物或过程，可以提供一些预测价值，允许早期干预，以减少人群中的这种负担。 这项研究将测试一般假设，即“早产的妇女在整个唾液，血清和宫颈阴道液（CVF）中具有更高水平的产前炎症标记物，与足月分娩的妇女相比，这些标记物在妊娠早期显示”。具体目标1：比较和对比全唾液、血清和CVF中孕期特异性产前炎症标志物的表达。基本原理：该目标将确定我们检测唾液、血清和CVF中妊娠期特异性炎症标志物的能力。 具体目标二：在多种族/民族人群中，确定发生早产和未发生早产的妇女之间孕期特异性产前炎症标志物表达的差异。基本原理：这一目标将基于白人、非裔美国人和西班牙裔/拉丁裔妇女的种族/种族多样性人群中的产前炎症生物标志物特征和早产（妊娠37周）确定PTB特异性风险因素。具体目标3：在多种族/民族孕妇样本中，确定与心理社会和生物行为变量相关的三个月特异性产前炎症标志物是否对早产构成显著风险。基本原理：这一目标将确定是否孕期特异性全身和局部产前炎症标志物与心理社会和生物行为变量结合影响早产风险和自我报告的产前抑郁症状水平;焦虑;压力，尿可替宁和自我报告的产前SHS暴露