Gender‐Equitable Parental Decision Making and Intimate Partner Violence Perpetration in Bangladesh

Objective This article examines the relationship between the exposure of men as children to gender‐equitable parental decision making and the potential for subsequent later life engagement in intimate partner violence (IPV) in Bangladesh. Background Although researchers have recently begun to explore multilevel influences on IPV perpetration, no studies have examined how decision making between parents at home and within the community relates to IPV perpetration in low-income settings. Drawing on a theoretical framework of gendered social learning, gender-equitable parental decision making may be an important protective factor against IPV. Method This study uses a random probability sample of 1,499 married men in Bangladesh. The main outcome is physical IPV perpetration in adulthood, whereas two exposure variables measure the equity of parental decision making in the man's childhood home and his current community. A series of two-level negative binomial models, controlling for pertinent individual- and community-level factors, are estimated. Results Exposure in childhood to more equitable decision making between parents is negatively associated with a man's physical IPV perpetration in adulthood. Gender‐equitable parental decision making within one's current community is not significantly associated with IPV. Conclusion Boys who grow up exposed to more equitable decision making between parents in the home may be less likely to engage in physical IPV perpetration as an adult

c-Myc uses Cul4b to preserve genome integrity and promote antiviral CD8+ T cell immunity

Abstract During infection, virus-specific CD8+ T cells undergo rapid bursts of proliferation and differentiate into effector cells that kill virus-infected cells and reduce viral load. This rapid clonal expansion can put T cells at significant risk for replication-induced DNA damage. Here, we find that c-Myc links CD8+ T cell expansion to DNA damage response pathways though the E3 ubiquitin ligase, Cullin 4b (Cul4b). Following activation, c-Myc increases the levels of Cul4b and other members of the Cullin RING Ligase 4 (CRL4) complex. Despite expressing c-Myc at high levels, Cul4b-deficient CD8+ T cells do not expand and clear the Armstrong strain of lymphocytic choriomeningitis virus (LCMV) in vivo. Cul4b-deficient CD8+ T cells accrue DNA damage and succumb to proliferative catastrophe early after antigen encounter. Mechanistically, Cul4b knockout induces an accumulation of p21 and Cyclin E2, resulting in replication stress. Our data show that c-Myc supports cell proliferation by maintaining genome stability via Cul4b, thereby directly coupling these two interdependent pathways. These data clarify how CD8+ T cells use c-Myc and Cul4b to sustain their potential for extraordinary population expansion, longevity and antiviral responses