Intensification of poverty and degradation of health infrastructure over recent decades in countries most affected by HIV/AIDS present formidable challenges to clinical research. This paper addresses theoverallstandard of health care (SOC) that should be provided to research participants in developing countries, rather than the narrow definition of SOC that has characterised the international debate on standards of health care. It argues that contributing to sustainable improvements in health by progressively ratcheting the standard of care upwards for research participants and their communities is an ethical obligation of those in resource-rich countries who sponsor and implement research in poorer ones.

Background: HIV prevention research in resource-limited countries is associated with a variety of ethical dilemmas. Key amongst these is the question of what constitutes an appropriate standard of health care (SoC) for participants in HIV prevention trials. This paper describes a communityfocused approach to develop a locally-appropriate SoC in the context of a phase III vaginal microbicide trial in Mwanza City, northwest Tanzania.

Background Arterial restenosis after vascular surgery is a common cause of midterm restenosis and treatment failure. Herein, we aim to investigate the role of microbe‐derived butyrate, FFAR2 (free fatty acid receptor 2), and FFAR3 (free fatty acid receptor 3) in mitigating neointimal hyperplasia development in remodeling murine arteries after injury. Methods and Results C57 BL /6 mice treated with oral vancomycin before unilateral femoral wire injury to deplete gut microbiota had significantly diminished serum and stool butyrate and more neointimal hyperplasia development after arterial injury, which was reversed by concomitant butyrate supplementation. Deficiency of FFAR 3 but not FFAR2, both receptors for butyrate, exacerbated neointimal hyperplasia development after injury. FFAR 3 deficiency was also associated with delayed recovery of the endothelial layer in vivo. FFAR 3 gene expression was observed in multiple peripheral arteries, and expression was increased after arterial injury. Treatment of endothelial but not vascular smooth muscle cells with the pharmacologic FFAR 3 agonist 1‐methylcyclopropane carboxylate stimulated cellular migration and proliferation in scratch assays. Conclusions Our results support a protective role for butyrate and FFAR 3 in the development of neointimal hyperplasia after arterial injury and delineate activation of the butyrate‐ FFAR 3 pathway as a valuable strategy for the prevention and treatment of neointimal hyperplasia.

Background The potential role of the gut microbiome in cardiovascular diseases is increasingly evident. Arterial restenosis attributable to neointimal hyperplasia after cardiovascular procedures such as balloon angioplasty, stenting, and bypass surgery is a common cause of treatment failure, yet whether gut microbiota participate in the development of neointimal hyperplasia remains largely unknown. Methods and Results We performed fecal microbial transplantation from conventionally raised male C57BL/6 mice to age‐, sex‐, and strain‐matched germ‐free mice. Five weeks after inoculation, all mice underwent unilateral carotid ligation. Neointimal hyperplasia development was quantified after 4 weeks. Conventionally raised and germ‐free cohorts served as comparison groups. Conclusions Germ‐free mice have significantly attenuated neointimal hyperplasia development compared with conventionally raised mice. The arterial remodeling response is restored by fecal transplantation. Our results describe a causative role of gut microbiota in contributing to the pathogenesis of neointimal hyperplasia.