Disaster Preparedness in a Resettled Refugee Community: Qualitative Findings.

INTRODUCTION: Under-resourced communities face disaster preparedness challenges. Research is limited for resettled refugee communities, which have unique preparedness needs. STUDY OBJECTIVE: This study aims to assess disaster preparedness among the refugee community in Clarkston, GA. METHODS: Twenty-five semi-structured interviews were completed with community stakeholders. Convenience sampling using the snowball method was utilized until thematic saturation was reached. Thematic analysis of interviews was conducted through an inductive, iterative approach by a multidisciplinary team using manual coding and MAXQDA. RESULTS: Three themes were identified: First, prioritization of routine daily needs took precedence for families over disaster preparedness. Second, communication impacts preparedness. Community members speak different languages and often do not have proficiency in English. Access to resources in native languages and creative communication tactics are important tools. Finally, the study revealed a unique interplay between government, community-based organizations, and the refugee community. A web of formal and informal responses is vital to helping this community in times of need. CONCLUSION: The refugee community in Clarkston, GA faces challenges, and disaster preparedness may not be top of mind for them. However, clear communication, disaster preparedness planning, and collaboration between government, community-based organizations, and the community are possible areas to focus on to bolster readiness.

Tetrasubstituted imidazoles as incognito Toll-like receptor 8 a(nta)gonists.

Small-molecule modulators of TLR8 have drawn much interests as it plays pivotal roles in the innate immune response to single-stranded RNAs (ssRNAs) derived from viruses. However, their clinical uses are limited because they can invoke an uncontrolled, global inflammatory response. The efforts described herein culminate in the fortuitous discovery of a tetrasubstituted imidazole CU-CPD107 which inhibits R848-induced TLR8 signaling. In stark contrast, CU-CPD107 shows unexpected synergistic agonist activities in the presence of ssRNA, while CU-CPD107 alone is unable to influence TLR8 signaling. CU-CPD107's unique, dichotomous behavior sheds light on a way to approach TLR agonists. CU-CPD107 offers the opportunity to avoid the undesired, global inflammation side effects that have rendered imidazoquinolines clinically irrelevant, providing an insight for the development of antiviral drugs.

NAFLD and HIV: Do Sex, Race, and Ethnicity Explain HIV-Related Risk?

PURPOSE OF REVIEW: Here, we review the epidemiology, diagnosis, and management of non-alcoholic fatty liver disease (NAFLD) in the general population, discuss HIV-specific differences in NAFLD pathogenesis, and summarize what is known regarding differences in NAFLD by race/ethnicity and sex. RECENT FINDINGS: The reported prevalence of NAFLD among people living with HIV varies by age, body mass index, comorbidity, and method of NAFLD diagnosis, but is generally thought to be greater among HIV-infected compared to HIV-uninfected populations. Minorities and women tend to experience poorer HIV treatment outcomes (Meditz et al. J Infect Dis. 203(4):442-51, 2011; Beer et al. Medicine (Baltimore). 95(13):e 3171, 2016; Gant et al. MMWR Morb Mortal Wkly Rep. 66(40):1065-72, 2017; Millett et al. Lancet. 380(9839):341-8, 2012; Wejnert et al. J Infect Dis. 213(5):776-83, 2016), and are at the greatest risk for significant weight gain with HIV treatment (Erlandson et al. Medicine (Baltimore). 95(46):e 5399, 2016). Thus, women and minorities living with HIV may be at a higher risk of developing NAFLD and progressive liver disease. Disparities in the diagnosis, progression, and prognosis of NAFLD and HIV-associated NAFLD may be, in part, explained by genetic and sex differences; however, data is limited.

Non-steroidal Anti-inflammatory Drugs Are Caspase Inhibitors.

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used drugs in the world. While the role of NSAIDs as cyclooxygenase (COX) inhibitors is well established, other targets may contribute to anti-inflammation. Here we report caspases as a new pharmacological target for NSAID family drugs such as ibuprofen, naproxen, and ketorolac at physiologic concentrations both in vitro and in vivo. We characterize caspase activity in both in vitro and in cell culture, and combine computational modeling and biophysical analysis to determine the mechanism of action. We observe that inhibition of caspase catalysis reduces cell death and the generation of pro-inflammatory cytokines. Further, NSAID inhibition of caspases is COX independent, representing a new anti-inflammatory mechanism. This finding expands upon existing NSAID anti-inflammatory behaviors, with implications for patient safety and next-generation drug design.