This study empirically tested the DeLone and McLean model of information systems success model (the DM model) in a university e-learning context using structural equation modeling. The results indicated that system quality, information quality, all affected the two mediating constructs, system use and user satisfaction, which in turn, influences the e-learning systems success. The nature of e-learning systems is fundamentally different from the environment in which the DeLone and McLean model is developed and tested, either voluntary or quasi-voluntary environments. However, e-learning systems are to be used in a mandatory environment. For that reason, the DeLone and McLean model has a limited explanatory power for explaining the role of e-learning systems on the outcomes of e-learning. Consequently, we conclude that the primary focus of the e-learning system empirical research should shift from the system factor toward human and design factors. E-learning systems empirical research is focusing on the critical success factors of e-learning outcomes that are comparable to or superior than traditional face-to-face learning system.

The cytotoxic potential of an antipyretic and analgesic drug, acetaminophen (APAP), was evaluated in mouse J774.2 monocyte macrophages. The cytotoxicity of APAP was evaluated by MTT cell viability and apoptosis assays. Based on the cell viability and apoptosis assays, further experiments were designed with a low (1 µmol/ml) and a high (10 µmol/ml) dose treatment of APAP in J774.2 cells. Mitochondrial oxidative stress, reactive oxygen species (ROS), mitochondrial glutathione (GSH) metabolism, lipid and protein peroxidation were measured in the drug treated cells. An increase in mitochondrial oxidative stress and ROS production was observed. A decrease in the mitochondrial GSH pool, accompanied by an increase in lipid and protein peroxidation appeared to be the main cause of mitochondrial oxidative stress. GSH pool and GSH metabolizing enzymes were differentially affected in the mitochondria and extramitochondrial compartments. Increased nuclear translocation of NF-kB-p65, a marker of redox metabolism was also observed in the drug treated cells. In addition, we have demonstrated, for the first time that the mitochondrial aconitase enzyme is a potential ROS-sensitive target in J774.2 cells, which might be used as a marker for APAP-induced cytotoxicity. These results have clearly suggested that APAP induced cytotoxicity in macrophages is mediated by increased mitochondrial oxidative stress and altered redox metabolism. This might have implications in determining the role of circulating macrophages against APAP induced toxicity and cellular defenses in tissues.

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Diabetic nephropathy has become the leading cause of end-stage kidney disease worldwide and is associated with an increased cardiovascular risk. The earliest clinical manifestation is microalbuminuria. Tight blood glucose and blood pressure control reduce the risk of microalbuminuria. Once microalbuminuria is present, the rate of progression to end stage kidney disease and cardiovascular disease can be delayed by aggressive management of blood pressure, glucose, and lipids. Inhibition of the reninangiotensin system is important in reducing intraglomerular pressure but other classes of antihypertensive agents may also be needed to obtain adequate control of systemic blood pressure. Such measures can at least reduce by half the rate of progression of nephropathy and cardiovascular disease.

PBL does not require an increase in number of faculty. The time spent by faculty on educational activities was similar in the two curriculum models. Although the cost of two strategies was similar, but the educational roles and the faculty engagement in education in a PBL curriculum is broader than in the traditional curriculum.