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This paper demonstrates the application of hybrid energy system (HES) that comprises of photovoltaic (PV) array, battery storage system (BSS) and stand-by diesel generator (DGen) to mitigate the problem of load shedding. The main work involves techno-economic modelling to optimize the size of HES such that the levelized cost of electricity (LCOE) is minimized. The particle swarm optimization (PSO) algorithm is used to determine the optimum size of the components (PV, BSS). Simulations are performed in MATLAB using real dataset of irradiance, temperature and load shedding schedule of the small residential community situated in the city of Quetta, Pakistan. The LCOE for the HES system under study is 8.32 cents/kWh—which is lower than the conventional load shedding solution, namely the uninterruptable power supply (UPS) (13.06 cents/kWh) and diesel and generator system (29.19 cents/kWh). In fact, the LCOE of the HRES is lower than the grid electricity price of Pakistan (9.3 cents/kWh). Besides that, the HES alleviates the grid burden by 47.9% and 13.1% compared to the solution using the UPS and generator, respectively. The outcomes of the study suggests that HES is able to improve reliability and availability of electric power for regions that is affected by the load shedding issue. [ABSTRACT FROM AUTHOR]

Background: Methylation at C-5 (5-mdC) of CpG base pairs, the most abundant epigenetic modification of DNA, is catalyzed by 3 essential DNA methyltransferases (Dnmt1, Dnmt3a and Dnmt3b). Aberrations in DNA methylation and Dnmts are linked to different diseases including cancer. However, their role in alcoholic liver disease (ALD) has not been elucidated. Methodology/Principal Findings: Dnmtl wild type (Dnmt1+/+) and hypomorphic (Dnmt1N/+) male mice that express reduced level of Dnmt1 were fed Lieber-DeCarli liquid diet containing ethanol for 6 weeks. Control mice were pair-fed calorie-matched alcohol-free liquid diet, and Dnmtase activity, 5-mdC content, gene expression profile and liver histopathology were evaluated. Ethanol feeding caused pronounced decrease in hepatic Dnmtase activity in Dnmt1+/+ mice due to decrease in Dnmt1 and Dnmt3b protein levels and upregulation of miR-148 and miR-152 that target both Dnmt1 and Dnmt3b. Microarray and qPCR analysis showed that the genes involved in lipid, xenobiotic and glutathione metabolism, mitochondrial function and cell proliferation were dysregulated in the wild type mice fed alcohol. Surprisingly, Dnmt1N/+ mice were less susceptible to alcoholic steatosis compared to Dnmt1+/+ mice. Expression of several key genes involved in alcohol (Aldh3b1), lipid (Ppara, Lepr, Vldlr, Agpat9) and xenobiotic (Cyp39a1) metabolism, and oxidative stress (Mr-1, Fmo3) were significantly (P<0.05) altered in Dnmt1N/+ mice relative to the wild type mice fed alcohol diet. However, CpG islands encompassing the promoter regions of Agpat9, Lepr, Mr1 and Ppara were methylation-free in both genotypes irrespective of the diet, suggesting that promoter methylation does not regulate their expression. Similarly, 5-mdC content of the liver genome, as measured by LC-MS/MS analysis, was not affected by alcohol diet in the wild type or hypomorphic mice. Conclusions/Significance: Although feeding alcohol diet reduced Dnmtase activity, the loss of one copy of Dnmt1 protected mice from alcoholic hepatosteatosis by dysregulating genes involved in lipid metabolism and oxidative stress. [ABSTRACT FROM AUTHOR]