Objective To evaluate the significance of p53,Cdk_4 and Survivin in gastric epithelial dysplasia with colonic and small intestinal metaplasia.Methods Immunohistochemical SP method was used to detect p53,Cdk_4,and Survivin in 44 cases of colonic intestinal metaplasia(27 low grade epithelial dysplasia,17 high grade epithelial dysplasia) and 51 cases of small intestinal metaplasia(42 low grade epithelial dysplasia,9 high grade epithelial dysplasia) by endoscope.Results The positive expression rates of p53 and Survivin had significant difference in two types of intestinal metaplasia and the difference was significant between low-grade and high-grade epithelial dysplasia.The expression of CDK_4 had significant difference in two types of intestinal metaplasia and had not difference between low-grade and high-grade epithelial dysplasia.Conclusion The expressions of p53,CdK_4 and Survivin are closely associated not only with the types of intestinal metaplasia but also with the different grades of epithelial dysplasia.The expression of p53,Cdk_4,and Survivin may be valuable markers in assessing the biological behavior of gastric epithelial dysplasia with intestinal metaplasia.

In recent years,a considerable number of epidemiological investigations and animal studies have confirmed that metabolic diseases, such as obesity,type 2 diabetes mellitus and metabolic syndrome, have adverse effects on brain functions,inducing mood disorders and cognition impairment. Brain dysfunctions induced by obesity and related complications are associated with numerous central abnormalities,involving brain shrinkage and neurotrophic function impairment,brain insulin resistance, brain oxidative stress,and brain leptin resistance,as well as dysfunctioned dopamine motivation and the reward system. Moreover,these brain dysfunctions are mediated by several peripheral factors, such as triglycerides/free fatty acids,proinflammatory cytokines,and corticosterone/glucocorticoid. On the other hand,metabolic disturbances correlated with emotional-cognitive disorders are evident,but the mechanisms remain obscure. Because of the drawbacks of animal models, the majority of researches focus on the impact of mental stress on the metabolism of lipid and glucose. The interrela?tionship between metabolic diseases and brain functions has become one of the hot spots for research. In this review,we mainly discussed the potential mechanisms underlying mood disorders and cognition impairment induced by obesity and related complications.

Objective To investigate the expressions and effects of EGR-1, p53, p16, Cyclin D1 in Nasopharyngeal Carcinoma (NPC). Methods Expressions of EGR-1, p53, p16, and Cyclin D1 protein in paraffin-embedded specimens of 29 chronic nasopharyngitis, 45 NPC and 24 lymph-node metastasis were studied by immunohistochemical method (SABC). Results The positive rates of EGR-1, p16, and Cyclin D1 protein expressions in chronic nasopharyngitis were 44.83 %(13/29), 89.66 %(26/29) and 24.14 %(7/29) respectively, but no p53 protein expression. In NPC, the positive expression rates of the four proteins were 22.22 %(10/45), 91.11 %(41/45), 53.33 %(24/45) and 66.67 %(30/45), with significant difference compared with chronic nasopharyngitis respectively; and in lymph nodes metastasis were 16.67 %(4/24), 79.17 %(19/24), 70.83 %(17/24) and 75.00 %(18/24) with significant difference compared with those of chronic nasopharyngitis and NPC respectively except for p16 protein. Spearman correlation analysis showed that there were no significant correlation between the expression of EGR-1 and p53, p16, Cyclin D1 respectively both in NPC and in lymph nodes metastasis. In NPC, the expression of p53 showed a positive correlation with the expression of p16; and in lymph nodes metastasis the expression of Cyclin D1 showed positive correlation with the expressions of p16 and p53. Conclusions The expression of EGR-1 protein was significantly decreased both in NPC and in lymph-node metastasis, which suggested that Egr-1 gene may be a tumor suppressor gene and have an important effect in the pathogenesis and the progression of NPC. The overexpression of p53 and Cyclin D1 also have an important role in NPC, but p16 probably have no biological significance in NPC.