ABSTRACT
We sought to determine impacts of a pediatric primary care intervention, the Video Interaction Project, on 3-year trajectories of parenting stress related to parent-child interactions in low socioeconomic status (SES) families. A randomized controlled trial (RCT) was conducted, with random assignment to one of two interventions (Video Interaction Project [VIP]; Building Blocks [BB]) or control (C). As part of VIP, dyads attended one-on-one sessions with an interventionist who facilitated interactions in play and shared reading through review of videotaped parent-child interactions made on primary care visit days; learning materials and parenting pamphlets were also provided to facilitate parent-child interactions at home. Parenting stress related to parent-child interactions was assessed for VIP and Control groups at 6, 14, 24, and 36 months using the Parent-Child Dysfunctional Interaction subscale of the Parenting Stress Index- Short Form, with 378 dyads (84%) assessed at least once. Group differences emerged at 6 months with VIP associated with lower parenting stress at 3 of 4 ages considered cross-sectionally and an 17.7% reduction in parenting stress overall during the study period based on multi-level modeling. No age by group interaction was observed, indicating persistence of early VIP impacts. Results indicated that VIP, a preventive intervention targeting parent-child interactions, is associated with decreased parenting stress. Results therefore support the expansion of pediatric interventions such as VIP as part of a broad public health strategy to address poverty-related disparities in school-readiness.
ABSTRACT
Most DNA double-strand breaks (DSBs) in S- and G2-phase cells are repaired accurately by Rad51-dependent sister chromatid recombination. However, a minority give rise to gross chromosome rearrangements (GCRs), which can result in disease/death. What determines whether a DSB is repaired accurately or inaccurately is currently unclear. We provide evidence that suggests that perturbing replication by a non-programmed protein-DNA replication fork barrier results in the persistence of replication intermediates (most likely regions of unreplicated DNA) into mitosis, which results in anaphase bridge formation and ultimately to DNA breakage. However, unlike previously characterised replication-associated DSBs, these breaks are repaired mainly by Rad51-independent processes such as single-strand annealing, and are therefore prone to generate GCRs. These data highlight how a replication-associated DSB can be predisposed to give rise to genome rearrangements in eukaryotes.
