HIV-Risk Behaviors and Intimate Partner Violence in Urban, Adolescent Girls: Impact of Sexual Relationship Power and Partner Age Differential

Thesis (Ph.D.)--University of Rochester. School of Nursing. Dept. of Health Practice Research, 2010.Purpose: Adolescent girls with older male sexual partners are more likely than their peers dating similar-aged partners to engage in high-risk sexual behaviors, including unprotected vaginal intercourse. It has been proposed that a power differential explains this relationship; however, this has yet to be empirically supported. Low relationship power has been associated with intimate partner violence (IPV) and high-risk sexual behaviors. A proposed framework of gender power depicts relationships between individuals, dyadic characteristics, sexual relationship power, intimate partner violence, and reproductive health outcomes. The purpose of this study was to determine if sexual relationship power mediated the relationship between: (1) partner age discordance and high-risk sexual behaviors and (2) partner age discordance and IPV in a sample of vulnerable adolescent girls. Additionally, this study’s purpose was to determine if IPV mediated the relationship between: (1) partner age discordance and high-risk sexual behaviors and (2) sexual relationship power and IPV in the same sample. Methods: An anonymous, cross-sectional, computer-assisted survey was conducted with sexually active girls (ages 14-18) in an urban school-based health center, in a midsize city in upstate New York. Multiple regressions were conducted to examine sexual relationship power and IPV as mediators of the relationships among variables (partner age difference, IPV, and high-risk behaviors). Results: The sample (N=146) was predominantly black, non-Hispanic, and low-income. Mean age was 16 years and mean partner age difference was 1.6 years. Controlling for demographic risk covariates, partner age difference was significantly related to frequency of unprotected vaginal intercourse (p< .05). However, neither sexual relationship power nor IPV mediated this relationship. High rates of physical, psychological, and sexual violence (by respondent and partner) were reported by this sample. Low sexual relationship power was significantly related to IPV [physical assault (p<.001, psychological aggression, p<.001 and sexual coercion, p< .001]; but IPV was not related to high-risk sexual behavior or partner age differential. Conclusions: Adolescent girls having an older male partner are more likely to engage in higher-risk sexual behaviors; however, neither sexual relationship power nor IPV explain this relationship. There was no relationship between partner age differential and (1) sexual relationship power or (2) IPV. Additional research is needed targeting adolescent girls with older male partners and exploring factors that impact sexual risk behaviors, sexual relationship power and IPV

Apolipoprotein A-I mimetics mitigate intestinal inflammation in COX2-dependent inflammatory bowel disease model

Cyclooxygenase 2 (Cox2) total knockout and myeloid knockout (MKO) mice develop Crohn's-like intestinal inflammation when fed cholate-containing high fat diet (CCHF). We demonstrated that CCHF impaired intestinal barrier function and increased translocation of endotoxin, initiating TLR/MyD88-dependent inflammation in Cox2 KO but not WT mice. Cox2 MKO increased pro-inflammatory mediators in LPS-activated macrophages, and in the intestinal tissue and plasma upon CCHF challenge. Cox2 MKO also reduced inflammation resolving lipoxin A4 (LXA4) in intestinal tissue, while administration of an LXA4 analog rescued disease in Cox2 MKO mice fed CCHF. The apolipoprotein A-I (APOA1) mimetic 4F mitigated disease in both the Cox2 MKO/CCHF and piroxicam-accelerated Il10-/- models of inflammatory bowel disease (IBD) and reduced elevated levels of pro-inflammatory mediators in tissue and plasma. APOA1 mimetic Tg6F therapy was also effective in reducing intestinal inflammation in the Cox2 MKO/CCHF model. We further demonstrated that APOA1 mimetic peptides: i) inhibited LPS and oxidized 1-palmitoyl-2-arachidonoyl-sn-phosphatidylcholine (oxPAPC) dependent pro-inflammatory responses in human macrophages and intestinal epithelium; and ii) directly cleared pro-inflammatory lipids from mouse intestinal tissue and plasma. Our results support a causal role for pro-inflammatory and inflammation resolving lipids in IBD pathology and a translational potential for APOA1 mimetic peptides for the treatment of IBD