ABSTRACT
A large body of research identifies the critical role of early-life social contexts such as neighborhoods and households in shaping life course trajectories of health. Less is known about whether and how school characteristics affect individual health and contribute to population health inequality. However, recent scholarship argues that some school environments are so stressful due to high levels of violence, disorder, and poverty that they may be "toxic" to student health, but this hypothesis has not been tested using population data. Integrating insights from the life course perspective and stress process model, we use rich longitudinal data from the National Longitudinal Study of Adolescent to Adult Health (n = 11,382), diverse markers of physiological functioning and psychological well-being, and multilevel regression models to examine whether and how school characteristics shape trajectories of physiological dysregulation and depressive risk from adolescence through early adulthood. Findings reveal that, across multiple measures of physiological functioning and psychological well-being, the social and structural characteristics of schools play an essential role in shaping health risk from adolescence through young adulthood-long after students left school. In particular, indicators of school-level violence and perceptions of safety and school social disconnectedness had especially strong associations with health risk in both the short- and long-term. School socioeconomic composition was also strongly associated with physiological dysregulation in young adulthood, net of individual and neighborhood socioeconomic exposures. Together, findings from this study suggest that school environments can serve as early-life stressors in the lives of young people that unequally shape health trajectories and contribute to broader patterns of health inequality.
ABSTRACT
OBJECTIVE: To increase the specificity in diagnosing cervical biopsies in adolescents, we evaluated the use of p16 immunohistochemistry (IHC) as an adjuvant test in addition to hematoxylin and eosin (H&E). MATERIALS AND METHODS: One hundred cervical histological tissues from adolescents were stained with routine H&E and monoclonal p16 (clone E6H4; dilution, 1:25; Dako). One gynecologic pathologist and 3 pediatric pathologists independently reviewed the cases, rendered diagnoses first by using H&E alone, and then added p16 IHC as an adjuvant marker. The interobserver agreement between the gynecologic pathologist and the pediatric pathologists was calculated using kappa statistics. RESULTS: The agreement rates between the gynecologic pathologist and all 3 pediatric pathologists were fair (kappa = 0.39, 0.36, and 0.37) when only H&E sections were used, and were improved to moderate (kappa = 0.53, 0.44, and 0.50) after using p16 IHC in addition to H&E. CONCLUSIONS: The evaluation of cervical intraepithelial neoplasia based solely on H&E-stained biopsies may lack interobserver reproducibility. The p16 IHC reduces the number of discrepancies and improves the rate of agreement among pathologists in diagnosing adolescent's cervical lesions. The improvement in the diagnosis of cervical biopsies has important implications in the treatment and follow-up of adolescent girls with abnormal cervical cytological diagnoses.
