Reepithelialization is the process responsible for restoring an intact epidermis following cutaneous injury. A change in the activity of keratinocytes is required for reepithelialization to occur, and this is likely to be regulated by the altered expression of effector genes, mediated by transcription factors. The injury itself provides a stimulus for transcription factor activation either directly due to mechanical stress, or via paracrine mechanisms such as the release of growth factors from damaged cells. Members of the activator protein-1 family, in particular c-fos and c-jun, have been the most widely studied wound-induced transcription factors. The signal transduction pathways linking cellular injury to activator protein-1 stimulation appear to involve an increase in intracellular Ca2+ and activation of mitogen-activated protein kinases. Given that a number of genes involved in the reepithelialization of wounds are regulated by activator protein-1, a distinct role for this transcription factor in reepithelialization is beginning to emerge. This article reviews the evidence for activator protein-1 involvement in reepithelialization, with particular focus on the activation of this transcription factor in response to wounding, the second messenger/kinase pathways involved, and the modulation of downstream genes that have the capacity to regulate keratinocyte function.

Rwanda demonstrates how a process of community consultation and participation is able to identify and rank community members according to 'social poverty', drawing on the Ubudehe tradition which is considered a strength of Rwanda's social fabric. However, with the Ubudehe categorisation now the basis for determining eligibility to a range of social benefits, the process has come under some strain. This article highlights two issues related to targeting and graduation: (1) the difficulty in identifying the poor/non-poor and ranking the population using community participatory techniques; and (2) the sensitivity of eligibility criteria and graduation thresholds to different targeting modalities. Our primary interest is to establish whether improvements for identifying the poor and non-poor can be made without undermining community ownership and what these improvements would look like. This will be useful for policymakers in Rwanda as the new five-year development strategy places importance on graduating households out of extreme poverty.

The rate of new human immunodeficiency virus (HIV) infections globally is alarming. Although antiretroviral therapy (ART) improves the quality of life among this group of patients, ARTs are associated with risk of cardiovascular diseases (CVD). Moreover, virally suppressed patients still experience immune activation associated with HIV migration from reservoir sites. Statins are widely recommended as therapeutic agents to control ART-related CVD; however, their impacts on the cluster of differentiation (CD)4 count and viral load are inconsistent. To assess the effect of statins on markers of HIV infections, immune activation and cholesterol, we thoroughly reviewed evidence from randomised controlled trials. We found 20 relevant trials from three databases with 1802 people living with HIV (PLHIV) on statin–placebo treatment. Our evidence showed no significant effect on CD4 T-cell count standardised mean difference (SMD): (−0.59, 95% confidence intervals (CI): (−1.38, 0.19), p = 0.14) following statin intervention in PLHIV on ART. We also found no significant difference in baseline CD4 T-cell count (SD: (−0.01, 95%CI: (−0.25, 0.23), p = 0.95). Our findings revealed no significant association between statins and risk of viral rebound in PLHIV with undetectable viral load risk ratio (RR): (1.01, 95% CI: (0.98, 1.04), p = 0.65). Additionally, we found a significant increase in CD8+CD38+HLA-DR+ T-cells (SMD (1.10, 95% CI: (0.93, 1.28), p < 0.00001) and CD4+CD38+HLA-DR+ T-cells (SMD (0.92, 95% CI: (0.32, 1.52), p = 0.003). Finally, compared to placebo, statins significantly reduced total cholesterol (SMD: (−2.87, 95% CI: (−4.08, −1.65), p < 0.0001)). Our results suggest that the statin lipid-lowering effect in PLHIV on ART may elevate immune activation without influencing the viral load and CD4 count. However, due to the limited evidence synthesised in this meta-analysis, we recommend that future powered trials with sufficient sample sizes evaluate statins’ effect on CD4 count and viral load, especially in virally suppressed patients.