PrEP Eligibility and Interest Among Clinic- and Community-Recruited Young Black Women in Atlanta, Georgia, USA.

BACKGROUND: Atlanta has been identified as an HIV "hot spot" for Black women and ranks 5th in the US with new infections. Yet little is known about PrEP eligibility or interest among young Black women in Atlanta. METHODS: A convenience sample of 1,261 Black women (ages 14-24 years) were recruited from two settings: community venues and sexual health clinics. They provided self-reported sexual behavior data and specimens for laboratory testing for chlamydia (CT) and gonorrhea (GC) infections. For each woman, the number of key self-reported behavioral HIV risk factors was calculated (0-6 factors for the clinic sample, 0-3 factors for the community sample). A single item assessed PrEP interest in the community sample only. RESULTS: Bacterial STI positivity, an indicator for PrEP eligibility, was 20.5% (17.1% CT, 6.3% GC) and 20.9% (18.8% CT, 5.2% GC) for the clinic and community samples, respectively. Of the 144 STI positive women from the clinic sample, 20.1% reported no behavioral risk indicators and 47.2% reported > 2 behavioral indicators. Of the 117 STI positive women from the community sample, 21.4% reported no behavioral risk indicators. 60.7% of the community sample reported they would be likely or very likely to use PrEP if available. CONCLUSION: Young Black women in Atlanta, whether sampled from community or sexual health settings, are at substantial risk for HIV infection and meet several PrEP eligibility criteria. Scaling up PrEP among women in Atlanta could have significant implications for HIV in this high burden region.

Concurrent cellular output from two proliferative populations in the early embryonic mouse corpus striatum.

In mice, the striatal compartment of the forebrain is established by embryonic day 11 (E11, E0 = day of conception) when a lateral ganglionic eminence emerges surrounding the lateral and ventral margins of the forebrain ventricles. The inception of the striatal compartment is evidence of altered cell cycle kinetics, especially a rapid production of postmitotic cells, within a discrete portion of the telencephalic neuroepithelium. As a step toward understanding the mechanisms which contribute to the development of a cytokinetically distinct striatal compartment, we characterized the rate and pattern of cellular output in the lateral ganglionic neuroepithelium of mice on E11. The data show that the striatal compartment is distinguished by concurrent and equivalent levels of cell output from two proliferative populations: a dominant secondary proliferative population and a smaller, pseudostratified ventricular epithelium. In addition, although the ganglionic neuroepithelium is expanding on E11, 30-35% of the daughter cells produced leave the cell cycle and become postmitotic. These cytogenetic events, occurring in the lateral ganglionic progenitor population, may contribute to the development of a distinct striatal compartment within the telencephalon.

The sequence of formation and development of corticostriate connections in mice.

We examined the development of the corticostriate pathway in mice by labeling corticofugal axons with the carbocyanine dye 1, 1'-dioctadecyl-3,3,3'-3'-tetramethylindocarbocyanine perchlorate (DiI). Growth cones of corticofugal axons enter the developing striatum on embryonic day 12 (E12; conception is on E0). By E15 corticofugal axons pass through the developing striatum in the internal capsule but do not produce striatal collaterals. Corticostriate collaterals are seen for the first time on E18, 6 days after the earliest arriving axons enter the striatum. At that time, presumptive synaptic contacts form between cortical axons and striatal neurons. Corticostriate collaterals arise from corticofugal axon trunks at or near axonal varicosities. Primitive corticostriate arbors form by postnatal day 2 (P2; day of birth is P0) and develop further by P7. Thus, corticostriate connections develop in three morphologically defined stages: first cortical axons elongate through the striatum to other subcortical targets, next they produce striatal collaterals, and finally they elaborate terminal arbors. The transition from elongation to collateralization stage may be triggered, among other factors, by signals from striatal neurons relayed via the synaptic contacts.