Therefore, it is difficult to conclude that the genetic enhancement of spatial working memory is due to NR2B overexpression in prefrontal DIM-C-pPhtBu cortex not in hippocampus. To further determine whether NR2B overexpresson in prefrontal cortex can enhance working memory, the odor span task, which is independent of hippocampus, was selected to evaluate the non-spatial cued working memory. NR2B transgenic mice also showed significantly enhanced nonspatial working memory as represented by an increased span length, higher percentage of accuracy and fewer errors. Therefore, it indicates that NR2B overexpression in prefrontal cortex may contribute to enhanced working memory. To establish the correlation of prefrontal NR2B overexpression with enhanced working memory, our future effort might be to overexpress NR2B subunit Methylhexanamine hydrochloride specifically in PFC or to perturb expression of NR2B specifically in PFC. In summary, prefrontal over-expression of NR2B subunit not only facilitates prefrontal cortex long-term potentiation but also enhances prefrontal cortex-related working memory, suggesting NR2B subunit may also be a crucial switch for prefrontal cortex LTP and prefrontal cortex-related working memory. Furthermore, a number of studies indicated that during the delay period of working memory tasks, neurons of the prefrontal cortex exhibited the elevated persistent firing activity. If the persistent activity is disrupted by stimulation during the delay period, the animal is highly likely to make an error. Thus, we hypothesize that during delay period of working memory task, the persistent neural activity of PFC in NR2B transgenic mice could be stronger than that of Wt mice. We will need to test our hypothesis in the future work. Non-alcoholic fatty liver disease is associated with the metabolic syndrome, a cluster of factors associated with the development of insulin resistance and atherosclerosis which has reached epidemic proportions in the developed world. NAFLD includes a range of disorders, from simple steatosis which may be benign to non-alcoholic steatohepatitis, in which fatty liver is associated with inflammation. Patients with NASH may in turn develop liver fibrosis which may progress to liver failure.