Background: Sex-race stratification may lead to identification of risk factors for low antihypertensive medication adherence that are not apparent when assessing risk factors in women and men without race stratification. We examined risk factors associated with low pharmacy refill adherence across sex-race subgroups (white women, black women, white men, black men) within the Cohort Study of Medication Adherence among Older Adults (n=2,122). Methods: Pharmacy refill adherence was calculated as proportion of days covered (PDC) using all antihypertensive prescriptions filled in the year prior to a baseline risk factor survey. Sex- and sex-race-stratified multivariable Poisson regression models with robust standard errors were used to estimate adjusted prevalence ratios and 95% confidence intervals for associations between participant characteristics and low adherence. Results: Prevalence of low adherence was 22.9% versus 40.7% in white versus black women (p<0.001) and 26.3% versus 37.2% in white versus black men (p=0.003). In multivariable models, reducing antihypertensive medication due to cost was associated with low adherence within each sex-race subgroup. Additional factors associated with low adherence included shorter hypertension duration and comorbidities in white women; not being married and depressive symptoms in white men; and ≥6 primary care visits/year and complementary and alternative medicine use in black men. Among men, not being married and reporting depressive symptoms were associated with low adherence for whites, but not blacks. Conclusions: Identification of sex-race-specific risk factors for low antihypertensive medication adherence may guide development and implementation of tailored interventions to increase antihypertensive medication adherence and blood pressure control among older patients.

Estrogen receptors (ERα and ERβ) are members of the nuclear receptor superfamily. They regulate the transcription of estrogen-responsive genes and mediate numerous estrogen related diseases (i.e., fertility, osteoporosis, cancer, etc.). As such, ERs are potentially useful targets for developing therapies and diagnostic tools for hormonally responsive human breast cancers. In this work, two benzimidazole-based sulphonamides originally designed to reduce proliferation in prostate cancer, have been evaluated for their ability to modulate growth in estrogen dependent and independent cell lines (MCF-7 and MDA-MB 231) using cell viability assays. The molecules reduced growth in MCF-7 cells, but differed in their impact on the growth of MDA-MB 231 cells. Although both molecules reduced estrogen response element (ERE) transcriptional activity in a dose dependent manner, the contrasting activity in the MDA-MB-231 cells seems to suggest that the molecules may act through alternate ER-mediated pathways. Further, the methyl analog showed modest selectivity for the ERβ receptor in an ER gene expression array panel. However, the napthyl analog diminished gene expression. The molecules were docked in the ligand binding domains of the ERα-antagonist and ERβ-agonist crystal structures to evaluate the potential of the molecules to interact with the receptors. The computational analysis complimented the results obtained in the assay of transcriptional activity and gene expression suggesting that the molecules upregulate ERβ activity while down regulating that of ERα.

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