Publications

BACKGROUND

Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States yet is one of the least recognized among the general public. HPV awareness may be relatively low among minority women. Because HPV awareness is associated with uptake of the HPV vaccine, it is critical to assess HPV awareness in the population and identify any racial/ethnic gaps.

METHODS

This study used nationally representative data collected by the National Survey of Family Growth between July 2007 and December 2008. A multivariable logistic regression model was used to determine the independent effect of race/ethnicity on HPV awareness while controlling for sociodemographic and clinical confounders in a sample of 4088 women. Stratified multivariable analysis was also conducted to assess the relationship between race/ethnicity and HPV awareness among women in different age groups.

RESULTS

After adjusting for confounders, Hispanic and black women overall were significantly less likely to have heard of HPV compared to white women (odds ratio [OR] 0.39, 95% confidence interval [CI] 0.29-0.54 and OR 0.39, 95% CI 0.29-0.54, respectively). Black women aged 15-18 and Hispanic women aged 19-26 had particularly low rates of HPV awareness (OR 0.17, 95% CI 0.07-0.43 and OR 0.18, 95% CI 0.11-0.30, respectively) compared to white women of the same ages.

CONCLUSIONS

Hispanic and black women have significantly lower levels of HPV awareness than white women. Targeted educational efforts will be important to improve HPV awareness and associated preventive health measures to avoid HPV-related morbidity and mortality.

Both the aa(3)-type cytochrome c oxidase from Rhodobacter sphaeroides (RsCcO(aa3)) and the closely related bo(3)-type ubiquinol oxidase from Escherichia coli (EcQO(bo3)) possess a proton-conducting D-channel that terminates at a glutamic acid, E286, which is critical for controlling proton transfer to the active site for oxygen chemistry and to a proton loading site for proton pumping. E286 mutations in each enzyme block proton flux and, therefore, inhibit oxidase function. In the current work, resonance Raman spectroscopy was used to show that the E286A and E286C mutations in RsCcO(aa3) result in long range conformational changes that influence the protein interactions with both heme a and heme a(3). Therefore, the severe reduction of the steady-state activity of the E286 mutants in RsCcO(aa3) to ~0.05% is not simply a result of the direct blockage of the D-channel, but it is also a consequence of the conformational changes induced by the mutations to heme a and to the heme a(3)-Cu(B) active site. In contrast, the E286C mutation of EcQO(bo3) exhibits no evidence of conformational changes at the two heme sites, indicating that its reduced activity (3%) is exclusively a result of the inhibition of proton transfer from the D-channel. We propose that in RsCcO(aa3), the E286 mutations severely perturb the active site through a close interaction with F282, which lies between E286 and the heme-copper active site. The local structure around E286 in EcQO(bo3) is different, providing a rationale for the very different effects of E286 mutations in the two enzymes. This article is part of a Special Issue entitled: Allosteric cooperativity in respiratory proteins.

OBJECTIVES

The aim of this study was to evaluate the effect of statin treatment in primary prevention of cardiovascular events in different race/ethnic groups.

BACKGROUND

Clinical trial evidence about the efficacy of statins in the primary prevention of cardiovascular events among nonwhites is uncertain.

METHODS

JUPITER trial, a randomized, double-blind, placebo-controlled evaluation of rosuvastatin 20 mg in the primary prevention of myocardial infarction (MI), stroke, arterial revascularization, hospitalization for unstable angina, and cardiovascular death included 12,683 whites and 5,117 nonwhites with low-density lipoprotein levels <130 mg/dL and high-sensitivity C-reactive protein levels ≥2.0 mg/L.

RESULTS

Random allocation to rosuvastatin resulted in a 45% reduction in the primary end point among whites (hazard ratio [HR] 0.55, 95% CI 0.43-0.69) and a 37% reduction among nonwhites (HR 0.63, 95% CI 0.41-0.99). Blacks (HR 0.65, 95% CI 0.35-1.22) and Hispanics (HR 0.58, 95% CI 0.25-1.39) had similar risk reductions. Among nonwhites in the placebo group, the stroke rate exceeded the MI rate (0.44 vs 0.20 per 100 person-years); an opposite pattern was observed among whites (0.31 vs 0.42 per 100 person-years). Nonwhites had higher death rates than whites (2.25 vs 0.93 per 100 person-years); however, all-cause mortality was similar at 20% with rosuvastatin treatment in both participant groups.

CONCLUSIONS

When used in primary prevention among individuals with low-density lipoprotein <130 mg/dL and high-sensitivity C-reactive protein ≥2 mg/L, rosuvastatin significantly reduced first MI, stroke, arterial revascularization, hospitalization for unstable angina, and cardiovascular death among whites and nonwhites.