Objective To determine the relationship between serum vitamin B_(12)(VB_(12))level and multiple sclerosis(MS).Methods The pertinent articles of the VB12 and the case control studies of MS were retrieved comprehensively by manual retrieval and computer retrieval.The methodology quality of the retrieved artilces were evaluated,and the arcb'cles were screened.Heterogeneity test was performed.The valid data was extracted and analyzed by Stata 10.1.Results In this study,9 studies were included.A total of 807 subjects were enrolled,including 414 patients and 393 controls.The Meta-analysis showed that the serum level of VB_(12) in patients with MS was lower than that in controls(standardized mean difference-0.24,95% CI-0.39 to-0.10).The sensitivity analysis indicated that the result of meta-analysis was reliable.Conclusion The serum level of VB_(12) might be associated with MS,and the deficiency of VB_(12) may contribute to the development of MS.

Positive selection and differential selective pressure analyses were carried out to study Haemagglutinin (HA) genes of H9N2 influenza viruses from different hosts in this paper. Results showed that, although most positions in HAs were under neutral or purifying evolution, a few positions located in the antigenic regions and receptor binding sites were subject to positive selection and some of them were even positively selected at the population level. In addition, there were always some positions differentially selected for viruses from different hosts. Both selection pressure working on HA codons and positions differentially selected might account for the extension of the host range and adaptations to different hosts of H9N2 influenza viruses.

Human enterovirus 71 viruses have been long circulating throughout the world. In this study, we performed a positive selection analysis of the VP1 genes of capsid proteins from Enterovirus 71 viruses. Our results showed that although most sites were under negative or neutral evolution, four positions of the VP1 genes were under positive selection pressure. This might account for the spread and frequent outbreaks of the viruses and the enhanced neurovirulence. In particular, position 98 might be involved in neutralizing antibodies, modulating the virus-receptor interaction and enhancing the virulence of the viruses. Moreover, both positions 145 and 241 might correlate to determine the receptor specificity. However, these positions did not display much difference in amino acid polymorphism. In addition, no position in the VP1 genes of viruses isolated from China was under positive selection.

Objective: Our purpose was to study the relationship between the Fas antigen expression and neuron apoptosis after cerebral ischemia. Methods: We detected the Fas antigen expression and neuron apoptosis dynamically in the animal models with cerebral ischemia by immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method. Results: Fas antigen was positive after 30 minutes of ischemia and reached peak at 60 minutes. At the 24th hour, it began to decrease, and negative on the 3th day. While the positive cell for TUNEL method appeared after 60 minutes of ischemia, reached peak on 3 day, and decreased on 7 day. Conclusion: Neuron apoptosis after cerebral ischemia is closely related to the over-expression of Fas antigen.

Background and objectives:Hepatic steatosis and inflammation are key characteristics of non-alcoholic fatty liver disease(NAFLD).However,whether and how hepatic steatosis and liver inflammation are differentially regulated remains to be elucidated.Considering that disruption of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3(Pfkfb3/iPfk2)dissociates fat deposition and inflammation,the present study examined a role for Pfkfb3/iPfk2 in hematopoietic cells in regulating hepatic steatosis and inflammation in mice. Methods:Pfkfb3-disrupted(Pfkfb3+-)mice and wild-type(WT)littermates were fed a high-fat diet(HFD)and examined for NAFLD phenotype.Also,bone marrow cells isolated from Pfkfb3+/-mice and WT mice were differentiated into macrophages for analysis of macrophage activation status and for bone marrow transplantation(BMT)to generate chimeric(WT/BMT-Pfkfb3+/-)mice in which Pfkfb3 was disrupted only in hematopoietic cells and control chimeric(WT/BMT-WT)mice.The latter were also fed an HFD and examined for NAFLD phenotype.In vitro,hepatocytes were co-cultured with bone marrow-derived macrophages and examined for hepatocyte fat deposition and proinflammatory responses.Results:After the feeding period,HFD-fed Pfkfb3+/-mice displayed increased severity of liver inflam-mation in the absence of hepatic steatosis compared with HFD-fed WT mice.When inflammatory activation was analyzed,Pfkfb3+/-macrophages revealed increased proinflammatory activation and decreased anti-proinflammatory activation.When NAFLD phenotype was analyzed in the chimeric mice,WT/BMT-Pfkfb3+/-mice displayed increases in the severity of HFD-induced hepatic steatosis and inflammation compared with WT/BMT-WT mice.At the cellular level,hepatocytes co-cultured with Pfkfb3+/-macrophages revealed increased fat deposition and proinflammatory responses compared with hepatocytes co-cultured with WT macrophages. Conclusions:Pfkfb3 disruption only in hematopoietic cells exacerbates HFD-induced hepatic steatosis and inflammation whereas the Pfkfb3/iPfk2 in nonhematopoietic cells appeared to be needed for HFD feeding to induce hepatic steatosis.As such,the Pfkfb3/iPfk2 plays a unique role in regulating NAFLD pathophysiology.