Development & Malleability from Childhood to Adulthood

摘要 这项研究的主要目的是对31-35岁的人进行一项正常和 病原体的发展和两种普遍的一级预防性干预措施对远端 目标：反社会行为，药物滥用/依赖，精神症状/障碍，高风险性行为 行为，并成功适应教育，工作，浪漫的相关发展需求 关系和家庭（包括生育家庭和出身/取向）社会领域/背景。本研究 利用以下科学价值：1）前瞻性、发展性流行病学预防试验， 城市人口（N = 798），主要是非洲裔美国年轻人，他们在秋季开始上一年级 1993年，在巴尔的摩主要是中低收入地区的9所小学中，参与者 教师们被随机分配到两个普遍的，以小学为基础的，预防性的 干预或控制条件。这两种干预措施-家庭学校伙伴关系和课堂- 中心（CC）-有针对性的攻击-胁迫行为和学业成绩差的前因， 上述远端结局。关于这些结果及其假设表型的年度数据 主持人和调解人，包括参与者，家庭，同龄人群体，学校和邻里特征， 都是从一年级到26岁收集的。DNA是在成年早期获得的，这使得 研究遗传和表型因素在解释发育变异中的相互作用 干预的结果。拟议的年度评估将有助于更准确地评估 表型和遗传影响相互作用的时间和顺序，包括干预措施， 成功适应31-35岁之间的相关发展挑战。同样，我们将 继续研究表型和遗传因素的作用以及干预措施对 物质使用/滥用/依赖的发展和过程，精神症状/障碍，反社会 行为/障碍，以及成年早期的高风险性行为。最后，我们还将评估 端粒长度和端粒酶活性的变化作为一个功能的潜在表观遗传效应 随着时间的推移累积的压力和干预作为压力/端粒关系的调节剂。的 在拟议的评估过程中积累的知识应有助于为评估的性质、目标 以及我们未来预防性干预工作的时间安排。

Abstract The central purpose of the proposed study is to extend through ages 31-35 an examination of normal and pathogenic development and the impact of two, universal, first grade, preventive interventions on the distal targets of: antisocial behavior, substance abuse/dependence, psychiatric symptoms/disorders, high risk sexual behavior, and successful adaptation to the relevant developmental demands of the educational, work, romantic relationships, and family (both family of procreation and origin/orientation) social fields/contexts. This study capitalizes on the scientific value of 1) a prospective, developmental epidemiological prevention trial involving a population (N = 798) of urban, predominately African-American young adults, who began first grade in the fall of 1993 in 9 elementary schools in predominantly low to lower middle-income Baltimore areas96. Participants and teachers were randomly assigned to one of two universal, elementary school-based, preventive interventions, or a control condition. Both interventions—the Family School Partnership (FSP) and Classroom- Centered (CC)--targeted aggressive-coercive behavior and poor academic achievement as antecedents of the distal outcomes elaborated above. Annual data on these outcomes and their hypothesized phenotypic moderators and mediators, including participant, family, peer group, school, and neighborhood characteristics, have been collected from 1st grade through age 26. DNA was obtained in early adulthood, which has allowed examination of the interplay between genetic and phenotypic factors in explaining variation in developmental and intervention outcomes. The proposed annual assessments will allow a more precise assessment of the timing and sequencing of the interplay of phenotypic and genetic influences, including the interventions, on successful adaptation to the relevant developmental challenges between the ages of 31-35. Similarly, we will continue to study the role of phenotypic and genetic factors and the impact of the interventions on the development and course of substance use/abuse/dependence, psychiatric symptoms/disorders, antisocial behavior/disorder, and high risk sexual behavior through young adulthood. Finally, we will also assess potential epigenetic effects in terms of change in telomere length and telomerase activity as a function of accumulative stress over time and the interventions as moderators of the stress/telomere relationship. The knowledge accrued over the course of the proposed assessments should serve to inform the nature, targets, and timing of our future preventive intervention efforts.