Objective To explore pathogenic bacteria distribution and drug susceptibility testing results in children with purulent meningitis in Jinan area. Methods A total of 54 children with purulent meningitis were selected from January 2010 to December 2014, the cerebrospinal fluid smear and culture, according to the national standard of clinical inspection technology for bacteria isolation and identification by disc diffusion method for drug sensitive test were retrospectively analyzed. Results A total of 54 strains of pathogenic bacteria including 36 strains of gram-positive coccus, and 17 strains of gram-negative bacillus and one strain of suspected Neisseria meningitides were found. A total of 31 strains gram positive coccus is Streptococcus pneumoniae, and most gram-negative bacilli is E. coli. In the Gram-positive coccus, 61.3% was sensitive to penicillin, and more than 90% was sensitive to ceftriaxone and cefepime, 83.3% was sensitive to meropenem, 94.7% resistant to azithromycin, and 58.1% resistant to oxazocilline. In Gram-negative bacilli, 60% was sensitive to ampicillin sulbactam 71.4% was sensitive to cephalosporin , 57.1% was sensitive to ceftriaxone , 66.6% was sensitive to cefepime. Conclusions From cerebrospinal fluid cultured of purulent meningitis, Streptococcus pneumoniae and E. coli were major pathogenic bacteria in children with purulent meningitis in Jinan area.

Nonalcoholic fatty liver disease (NAFLD) is considered the manifestation of metabolic syndrome (MS) in the liver. Besides glucose and lipid metabolic disorders, the level of serum uric acid (SUA) is also associated with the progression of NAFLD. This article reviews the research achievements in the association between SUA and NAFLD and points out that SUA can independently predict the risks of MS, type 2 diabetes, and cardiovascular disease in both healthy people and patients. Its mechanism may be that SUA increases the expression of reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) through inducing ROS, and then it activates the NLR pyrin domain containing 3 inflammasome and induces the secretion of interleukin. Both basic and clinical research show that the drugs reducing SUA can inhibit the TXNIP pathway, reduce the blood glucose level, and alleviate liver ROS, inflammation, steatosis, and fibrosis. This article suggests that SUA may be a promising therapeutic method for NAFLD and needs further basic and clinical research.

Objective:To study the astragalus polysaccharides ( APS) effect on immune induced by influenza A virus HA2 eu-karyotic expression vector.Methods: The HA2 encoded by the DNA vaccine vector was efficiently expressed in CHO cells, as determined by reverse transcription polymerase chain reaction ( RT-PCR) and fluorescence analysis.60 rats were divided into six groups randomly,which were immunized with normal saline,pEGFP-N1,pHA2/EGFP+different dose of APS by intramuscular injection.The control sera were collected before injection.After injected the 36th day, sera were collected to analyzing IFN-γ, IL-4 and IgG level.Results:IFN-γ,IL-4 and IgG level of pHA2/EGFP+mAPS group was different from that of pEGFP-N1 group or pHA2/EGFP+lAPS group( P<0.05 ).Conclusion: Middle dose of APS could increase immune induced by influenza A virus HA2 eukaryotic expression vector.

Objective:To study whether high dose astragalus polysaccharides( APS) could affect the expression of pNS1/EGFP that included influenza A virus(IAV) non-structure protein 1(NS1) gene in the tissue.Methods:pNS1/EGFP was constructured with NS1 of IAV.Sixty Kunming mice were divided into three groups randomly.Each group of mice was injected separately with one of the following:pEGFP-N1, pNS1/EGFP and pNS1/EGFP+APS in intraperitoneal injection.The mice were injected by intramuscular injection twice with a 3-week interval between injections.The serum samples and muscle samples were obtained on day 14 and day 28 after the booster injection.Sera IL-4,sera IFN-γ,muscle caspase-3 and muscle NS1 expression were measured in ELISA,Western blot or RT-PCR.Results:There were no significant difference among the different groups in day 14 expect that IFN-γof pNS1/EGFP+APS were lower(P<0.05).IFN-γlevel or IL-4 level of pNS1/EGFP+APS were lower compared with other groups in day 28.caspase-3 of pNS1/EGFP+APS were lower compared with other groups in day 28.Conclusion:APS could increase the expression of pNS1/EGFP by decreasing the inflammation and apoptosis.

Only a small number of people may develop severe alcoholic liver disease after continuous or excessive drinking, which is different from the harm caused by smoking, and some people may even develop alcoholic liver disease associated with inflammation, liver cirrhosis, or primary liver cancer. There are complex risk factors for liver injury in these people; besides ethnic and genetic factors, drinking volume, and drinking duration, more important factors are involved in the pathophysiological changes of the liver, such as the type and quality of alcohol, drinking pattern, socioeconomic status, and government public policy, which may be the determining factors for the development of alcoholic liver disease. On the basis of literature review, this article proposes the concept that "liquor does not equal to alcohol" , which has important guiding significance for healthy drinking and the prevention of alcoholic liver disease.

Abstrac:Aim To study the effect of hydroxysafflor yellow A ( HYSA ) on the proliferation of vascular smooth muscle cells ( VSMCs) and the related molecu-lar mechanism. Methods The inhibitory effects of hydroxysafflor yellow A on VSMC proliferation was de-tected using cell culture, MTT assay, Western blot and immunohistochemical staining. Results The results showed that HYSA inhibited cell proliferation induced by PDGF in a dose-dependent (5,10,20,40 μmol· L-1 ) manner, reduced proliferating cell nuclear anti-gen ( PCNA ) expression and blocked PDGFR-MEK-ERK1/2 signaling pathway activated by PDGF in VSMCs. Conclusion HYSA inhibits VSMCs prolifer-ation via reducing the expression of PCNA and blocking signal transduction of MEK-ERK1/2 in VSMCs.