Bangladesh is one of the poorest and most disaster-prone countries in the world. To address both problems simultaneously, sustainable livelihoods (SL) could be better connected with disaster risk reduction (DRR). For this purpose, one initiative implemented in Bangladesh is called the Vulnerability to Resilience (V2R) programme which ran from 2013 to 2016. This programme was primarily initiated and funded by the British Red Cross in a consortium with the Swedish Red Cross and the German Red Cross. This article presents the first evaluation of the V2R programme with three objectives. The first objective was to measure whether the selected communities have achieved community resilience characteristics as defined by the programme. The second objective was to conduct a cost-benefit analysis for the intervention. The third objective was to analyse V2R's impact on the communities in terms of DRR and SL. Community-based focus group discussions and household-based surveys were conducted before and after the intervention (2013)(2014)(2015)(2016) in two coastal communities in Patuakhali district, Nowapara and Pashurbunia. The analysis found that community members are now engaged with many hazard-resilient and vulnerability-reducing livelihood activities, using SL to implement DRR, yet these approaches were almost absent prior to V2R. Consequently, the communities have achieved resilience characteristics, being more well-organized and better connected; having better access to infrastructure, services, and economic opportunities; are more knowledgeable and healthier; and are better managing their available resources. Critiques of the concepts are discussed, although in this case, DRR based on SL has shown positive results, exactly as development theory suggests.

The emergence of antimony (Sb) resistance has jeopardized the treatment of visceral leishmaniasis in various countries. Previous studies have considered the part played by leishmanial parasites in antimony resistance, but the involvement of host factors in the clinical scenario remained to be investigated. Here we show that unlike infection with Sb-sensitive (Sb s ) Leishmania donovani, infection with Sb-resistant (Sb r ) L. donovani induces the upregulation of multidrug resistance-associated protein 1 (MRP1) and permeability glycoprotein (P-gp) in host cells, resulting in a nonaccumulation of intracellular Sb following treatment with sodium antimony gluconate (SAG) favoring parasite replication. The inhibition of MRP1 and P-gp with resistance-modifying agents such as lovastatin allows Sb accumulation and parasite killing within macrophages and offers protection in an animal model in which infection with Sb r L. donovani is otherwise lethal. The occurrence of a similar scenario in clinical cases is supported by the findings that unlike monocytes from SAG-sensitive kala-azar (KA) patients, monocytes from SAG-unresponsive KA patients overexpress P-gp and MRP1 and fail to accumulate Sb following in vitro SAG treatment unless pretreated with inhibitors of ABC transporters. Thus, the expression status of MRP1 and P-gp in blood monocytes may be used as a diagnostic marker for Sb resistance and the treatment strategy can be designed accordingly. Our results also indicate that lovastatin, which can inhibit both P-gp and MRP1, might be beneficial for reverting Sb resistance in leishmaniasis as well as drug resistance in other clinical situations, including cancer.The emergence of antimony-resistant (Sb r ) visceral leishmaniasis (VL) in various parts of the world (1,8,17,48) has severely compromised control of the disease. Among alternative drugs, pentamidine is toxic; amphotericin B is both expensive and toxic, with reported cases of resistance (8, 48); and oral miltefosine is limited by cost, contraindications, and emerging resistance (1,8,41,53). Therefore, an understanding of the mode of resistance and an identification of cost-effective therapeutic combinations have become major issues.ATP binding cassette (ABC) transporters have been widely reported to export xenobiotics (24, 55) and cause drug resistance in various diseases such as cancer (23). Earlier studies have reported the expression of analogs of ABC transporters on the surfaces of Sb r strains of Leishmania promastigotes (27, 35, 41), believed to efflux antimonials. However, the demonstration of these transporters in promastigotes may not be very relevant to clinical situations. There are a few reports available on the expression of similar transporters in laboratory isolates of in vitro-developed Sb r strains of leishmanial amastigotes (15) or on amastigotes from field isolates of Sb r L. donovani (10, 51). Although sodium antimony gluconate (SAG) kills leishmanial amastigotes directly at higher doses in vitro as reported previously (54), a much lower dose...

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