RESUMO
OBJECTIVE: To assess the relationship of moderate and late preterm birth (320/7-366/7 weeks) to long-term educational outcomes. STUDY DESIGN: We hypothesized that moderate and late preterm birth would be associated with adverse outcomes in elementary school. To test this, we linked vital statistics patient discharge data from the Office of Statewide Health Planning and Development including birth outcomes, to the 2015-2016 school year administrative data of a large, urban school district (n = 72 316). We compared the relative risk of moderate and late preterm and term infants for later adverse neurocognitive and behavioral outcomes in kindergarten through the 12th grade. RESULTS: After adjusting for socioeconomic status, compared with term birth, moderate and late preterm birth was associated with an increased risk of low performance in mathematics and English language arts, chronic absenteeism, and suspension. These risks emerged in kindergarten through grade 2 and remained in grades 3-5, but seemed to wash out in later grades, with the exception of suspension, which remained through grades 9-12. CONCLUSIONS: Confirming our hypothesis, moderate and late preterm birth was associated with adverse educational outcomes in late elementary school, indicating that it is a significant risk factor that school districts could leverage when targeting early intervention. Future studies will need to test these relations in geographically and socioeconomically diverse school districts, include a wider variety of outcomes, and consider how early interventions moderate associations between birth outcomes and educational outcomes.
Assuntos
Escolaridade , Nascimento Prematuro , Absenteísmo , Adolescente , California/epidemiologia , Criança , Desenvolvimento Infantil , Pré-Escolar , Feminino , Idade Gestacional , Humanos , Lactente , Recém-Nascido , Estudos de Linguagem , Masculino , MatemáticaRESUMO
PBAF and BAF are two chromatin-remodeling complexes of the SWI/SNF family essential for mammalian transcription and development. Although these complexes share eight identical subunits, only PBAF can facilitate transcriptional activation by nuclear receptors in vitro. Here we show that these complexes have selectivity in mediating transcription of different interferon-responsive genes. The selectivity by PBAF requires a novel subunit, BAF200, but not the previously described PBAF-specificity subunit, BAF180 (Polybromo). Our study provides in vivo evidence that PBAF and BAF regulate expression of distinct genes, and suggests that BAF200 plays a key role in PBAF function.
Assuntos
Montagem e Desmontagem da Cromatina , Proteínas Cromossômicas não Histona/metabolismo , Fatores de Transcrição/metabolismo , Proteínas Cromossômicas não Histona/química , Proteínas Cromossômicas não Histona/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Células HeLa , Humanos , Técnicas In Vitro , Interferon Tipo I/farmacologia , Complexos Multiproteicos/química , Complexos Multiproteicos/metabolismo , Subunidades Proteicas , RNA Interferente Pequeno/genética , Proteínas Recombinantes , Fatores de Transcrição/química , Fatores de Transcrição/genéticaRESUMO
Genetic alterations serve as beacons for the involvement of specific pathways in tumorigenesis. It was previously shown that 5% of prostate tumors harbor CTNNB1 mutations, suggesting that this tumor type may involve a deregulated APC/CTNNB1 pathway. To explore this possibility further, we searched for mutations in genes implicated in this pathway in 22 samples that included cell lines, xenografts, and primary tumors. We identified seven alterations: two in CTNNB1, three in APC, and two in hTRCP1 (also known as BTRC) which controls the degradation of CTNNB1. Alterations in the CTNNB1 regulatory domain, APC, and hTRCP1 were mutually exclusive, consistent with their equivalent effects on CTNNB1 stability. These results suggest that CTNNB1 signaling plays a critical role in the development of a significant fraction of prostate cancers. Moreover, they provide the first evidence that hTRCP1 plays a role in human neoplasia.