Objective To detect the expression of SSX and to correlate it with clinical indicators of primary hepatocellular carcinoma (HCC).Methods The expression of SSX1-5 mRNA and SSX1 protein were respectively detected by RT-PCR and Western blot and immunohistochemistry staining.The relation between the expression of SSX mRNA and SSX1 protein with clinical indicators were analysed.Results SSX1,SSX2,and SSX3 mRNA were expressed in hepatocellular carcinoma cell lines BEL-7404,Hep G2,and SMMC-7721.In 26 HCC samples,SSX1-SSX5 mRNA was detectable in 53.8％,42.3％,50.0％,46.2％ and 26.9％.The expression of SSX1 mRNA was not related to serum AFP levels (P ＞0.05).Specific expression was both found in the normal group and the high value group.The expression rate of SSX1 mRNA was 85.7％ in the older group,which was higher than in the younger group (16.7％,P ＜ 0.05).The expression rate of SSX1 protein was 50％ in HCC tissues,which was not seen in the caner-adjacent or cirrhosis tissues.In 49 HCC paraffin tissue section samples,the expression rate of SSX1 protein was higher than that in caner-adjacent tissues (46.9％ vs 18.4％,P ＜ 0.05).The expression rate of SSX1 protein was 68.3％ in the large hepatocellular carcinoma group,which was higher than in the small hepatocellular carcinoma group (29.6％),(P ＜ 0.05).Conclusions SSX1 mRNA is expressed with a high percentage and specificity in HCC and their products are new potential promising targets for antigen-specific immunotherapy of HCC.The detection of SSX1 expression has the potential value for auxiliary diagnosis of HCC.

The prevalence of acute flaccid paralysis (AFP) associated with EV71 and the genetic variation in Fujian , China from 2003 to 2012 was investigated in this study .Descriptive epidemiology was used to analyze the epidemiologic and clinical features of AFP cases associated with EV 71 .Phylogenetic analysis was performed to explore the genetical characteris-tics of EV71 based on the complete VP1 nucleotide and amino acid sequences .Results showed that the mean incidence of EV71-associated AFP in children under 15 years old was 2 .24/10 000 000 in Fujian Province during 2003 and 2012 ,based on the number of EV71 isolates and the reported AFP cases .And the incidence has increased since 2008 .The EV71 strains isolated from the AFP cases or from the healthy contacts were distributed in 9 prefectures of Fujian Province ,most in the months of May and June .Of 76 .0% (19/25) of AFP cases associated with EV 71 were the children under 3 years and the male-to-female ratio was 1 .5 :1 .Twenty out of twenty-two cases (90 .91% ) had fevers before the onset of paralysis .Most cases had unilater-al limb paralysis (14/22 ,63 .6% ) .Typical manifestations of hand-foot-and-mouth disease (HFMD) were observed in five cases before the onset of paralysis .Residual paralysis was observed in two cases during the follow-up visits .The strains isolated from 25 cases belonged to genotype C4 .All other strains belonged to subtype C4a except the subtype C4b strains isolated in 2003 .The homology among the strains was high in 2009-2011 ,and the homology among these strains and the representative strains in Fuyang ,Anhui Province was also in the high level .Therefore ,it was possible that the isolated strains had the same origin and might cause the epidemic .In conclusion ,an AFP surveillance system could be developed for analyzing the incidence of AFP associated with EV71 ,determining the features of the isolates ,and describing the intensity and trends of EV71 epidem-ics .

To investigate the effects of CD14 on nuclear transcription factorκB (NF-κB) was activated by lipid-associated membrane proteins (LAMPs) of Mycoplasma genitalium (Mg) ,THP-1 cells were pretreated with serum human or CD14 neu-tralizing antibody ,and then were stimulated by LAMPs .The activation of NF-κBp65 was detected by ELISA .After LAMPs was pretreated with sCD14 stimulated Hela cells with the co-transfection ,the activity of NF-κB luciferase were detected by the dual-luciferase reporter gene to analyze the role of CD14-mediated NF-κB activation by LAMPs .The activation of NF-κBp65 was significantly up-regulated in LAMPs activated THP-1 cells by human serum .It’s suggested that CD14 neutralizing anti-body could inhibit the activation of NF-κBp65 in LAMPs stimulated THP-1 .The activation of NF-κB was significantly up-regu-lated in LAMPs activated Hela cells by mCD14 or sCD14 .CD14 could augment the activation of NF-κB by Mg LAMPs .

Objective To analyze the correlation between apolipoprotein E(ApoE) gene polymorphisms and the incidence rate of chronic cardiovascular disease as well as the blood lipid levels of patients.Methods ApoE gene polymorphism and lipid levels were measured by suing gene chip analysis system and biochemical analyze in 1 414 cases of chronic cardiovascular disease patients(experimental groups) and 374 cases of healthy subjects(control group).Results Compared with control group,E3/4 genotype frequency was increased in experimental group,while E2/E3 genotype frequency decreased(P<0.05).Compared with control group,the levels of total cholesterol(TC),triglyceride(TG),low density lipoprotein-cholesterol(LDL-C) were obviously increased and the level of HDL-C was decreased in experimental group(P<0.05).Compared with patients with E2/E3 genotype,the level of HDL-C in patients with E3/E4 genotype was decreased and the levels of TC,LDL-C were increased significantly(P<0.05).Proportions of different ApoE genotypes in patients with cerebral infarction,cerebral hemorrhage,hypertension,coronary heart disease,type-2 diabete and fatty liver were different.Compared with the E2/E3 genotype,the proportion of the E3/E4 genotype in patients with cerebral infarction,cerebral hemorrhage,hypertension,coronary heart disease,type-2 diabete and fatty liver were increased(P<0.05).Conclusion ApoE gene polymorphism might be important cause of the individual difference of lipid levels and a risk factor for the occurrence and development of chronic cardiovascular diseases.

Objective To analyze the genetic characteristics of VP1-VP4 genes carried by cox-sackievirus A6 (CVA6) strains isolated from severe cases of hand, foot, and mouth disease (HFMD) in Shenzhen during 2012 to 2015. -ethods The VP1-VP4 genes of CVA6 strains isolated from severe HFMD cases in Shenzhen during 2012 to 2015 were amplified and sequenced. Phylogenetic analysis was performed to analyze the VP1-VP4 genes of CVA6 isolates and sequences downloaded from GenBank by using DNASTAR6. 0 and MEGA6. 02 software packages. Results Four cases of severe HFMD were caused by CVA6 in Shenzhen during 2012 to 2015. All of the patients had the symptom of fever, skin rash and aseptic encephalitis. The CVA6 strain causing severe HFMD in 2013 shared 98. 8％-98. 9％ homology in nucleotide sequences and 99. 3％-99. 8％ in amino acid sequences with the strains isolated in 2012. Two amino acid mutations were found in the CVA6 strain isolated in 2013, which were G73E in VP2 region and S13G in VP1 region. However, the CVA6 strain isolated in 2015 only shared 95. 0％ homology in nucleotide sequences and 99. 3％ homology in amino acid sequences with the strain isolated in 2013. Six amino acid mutations were identified including E73G in VP2 region and T5A, S27N, A30V, N137S and V242I in VP1 region. The phylogenetic analysis revealed that the four CVA6 strains belong to D3 sub-genotype. The CVA6 strains causing severe cases in 2012 had the nearest genetic relationship with the strain isolated in Changsha in 2012 (KJ156349). The CVA6 strain isolated in Shenzhen in 2013 had the nearest genetic relationship with the strain isolated in Shanghai in 2013 (KJ612513). The Shenzhen CVA6 isolate in 2015 showed high similarity to Weifang CVA6 isolate in 2014 (KX752785). Conclusions All CVA6 strains causing severe HFMD ca-ses in Shenzhen during 2012 to 2015 belongs to D3 sub-genotype. Mutations of S27N and A30V in the VP1 region of the CVA6 isolate in 2015 are located in the B cell epitopes. In addition, the VP1-V242I mutation in the CVA6 strain isolated in 2015 is located in the binding site of PSGL-1 receptor. These mutations may affect the binding of CVA6 strains to the cellular receptors and their infectivity to people.