Lake drying and livelihood dynamics in Lake Chad: unravelling the mechanisms, contexts and responses

This article examines lake drying and livelihood dynamics in the context of multiple stressors through a case study of the ‘‘Small Lake Chad’’ in the Republic of Chad. Livelihoods research in regions experiencing persistent lake water fluctuations has largely focused on the wellbeing and security of lakeshore dwellers. Little is known about the mechanisms through which lake drying shapes livelihood drawbacks and opportunities, and whether locally evolved responses are enhancing livelihoods. Here we address these gaps using empirical, mixed-methods field research couched within the framework of livelihoods and human well-being contexts. The analysis demonstrates that limited opportunities outside agriculture, the influx of mixed ethnic migrants and the increasing spate of violence all enhance livelihood challenges. Livelihood opportunities centre on the renewal effects of seasonal flood pulses on lake waters and the learning opportunities triggered by past droughts. Although drying has spurred new adaptive behaviours predicated on seasonality, traditional predictive factors and the availability of assets, responses have remained largely reactive. The article points to where lake drying fits amongst changes in the wider socioeconomic landscape in which people live, and suggests that awareness of the particularities of the mechanisms that connect lake drying to livelihoods can offer insights into the ways local people might be assisted by governments and development actors

Differential gene expression in mouse primary hepatocytes exposed to the peroxisome proliferator-activated receptor α agonists

BACKGROUND: Fibrates are a unique hypolipidemic drugs that lower plasma triglyceride and cholesterol levels through their action as peroxisome proliferator-activated receptor alpha (PPARα) agonists. The activation of PPARα leads to a cascade of events that result in the pharmacological (hypolipidemic) and adverse (carcinogenic) effects in rodent liver. RESULTS: To understand the molecular mechanisms responsible for the pleiotropic effects of PPARα agonists, we treated mouse primary hepatocytes with three PPARα agonists (bezafibrate, fenofibrate, and WY-14,643) at multiple concentrations (0, 10, 30, and 100 μM) for 24 hours. When primary hepatocytes were exposed to these agents, transactivation of PPARα was elevated as measured by luciferase assay. Global gene expression profiles in response to PPARα agonists were obtained by microarray analysis. Among differentially expressed genes (DEGs), there were 4, 8, and 21 genes commonly regulated by bezafibrate, fenofibrate, and WY-14,643 treatments across 3 doses, respectively, in a dose-dependent manner. Treatments with 100 μM of bezafibrate, fenofibrate, and WY-14,643 resulted in 151, 149, and 145 genes altered, respectively. Among them, 121 genes were commonly regulated by at least two drugs. Many genes are involved in fatty acid metabolism including oxidative reaction. Some of the gene changes were associated with production of reactive oxygen species, cell proliferation of peroxisomes, and hepatic disorders. In addition, 11 genes related to the development of liver cancer were observed. CONCLUSION: Our results suggest that treatment of PPARα agonists results in the production of oxidative stress and increased peroxisome proliferation, thus providing a better understanding of mechanisms underlying PPARα agonist-induced hepatic disorders and hepatocarcinomas