Objective To analyze the epitopes of anti-hepatitis C virus(HCV)antibodies by peptide library biopanning. Methods Phage random peptide library of 12 amino acids was immunoscreened with purified IgG from the sera of hepatitis C patients. Positive clones which were obtained after 3 rounds of biopanning were detected by ELISA and 4 of them were sequenced. Results After 3 rounds of screening, the radio of output to input increased from (4.6×10~(-4))% to (5.3×10~(-2))%, meaning the enrichment was effective. At the third round of screening, all the selected clones proved to specifically react with the sera for immunoscreening. Four positive phage clones were sequenced, which shared a very conservative sequence and was named as C1. Its inserting sequence in the coat protein III was deduced to be GSMSPYVRWYTP, and the positive rate of C1 reacted with 20 cases of HCV patients was 85%.Conclusion The antigen-mimic peptide C1 is successfully screened from 12 random phage peptide library and it has some diagnostic value.

Objective To explore the relationship between Helicobacter pylori(Hp) infection and serum homocysteine(Hcy) level ,carotid intima-media thickness and plaque stability in carotid atherosclerosis cases .Methods 206 carotid atherosclerosis pa-tients were collected between March 2012 and January 2013 in our hospital .According to the results of 14C urea breath test ,all the subjects were divided into Hp infection group and non-Hp infection group .And according to the degree of carotid artery atheroscle-rosis ,patients with Hp infection were divided into carotid intima-media thickness thickening group ,stable plaque group and unstable plaque group .The serum Hcy level was detected by enzymatic cycling method ,and the relationship between Hp infection and serum Hcy level ,carotid intima-media thickness and plaque stability in carotid atherosclerosis cases were analyzed .Results Serum Hcy level and carotid carotid intima-media thickness of patients with carotid atherosclerosis in Hp infection group were higher than those in non-Hp infection group(P<0 .01) .The differences in constitution ratio of patients with different types of carotid atherosclerosis in Hp infection group and non-Hp infection group was statistically significant(χ2 =15 .939 ,P=0 .000 3) .In Hp infection group , there were statistically of serum Hcy levels among carotid intima-media thickness thickening group ,stable plaque group and unsta-ble plaque group(P<0 .01) .Linear correlation analysis showed that the serum Hcy level and carotid intima-media thickness were positively correlated in Hp infection group(r=0 .731 ,P<0 .01) .Conclusion Hp infection is likely to promote the development and progression of atherosclerosis through influencing Hcy metabolism and increasing carotid intima-media thickness and instability of carotid atherosclerotic plaque .

Objective To investigate the infection of Helicobacter pylori infection on the serum concentration of homocysteine (Hcy) and its relationship with coronary heart disease (CHD) .Methods 159 cases of patients with CHD were selected as the re‐search subjects .They were divided into two groups :infection group and non‐infection group ,according to the results of 14 C‐urea breathe test .And they were also divided into three groups :negative group ,mild infection group and severe infestation group ,accord‐ing to the severity of infection .The CHD patients infected Helicobacter pylori were divided into three groups:low risk group ,mod‐erate risk group and high risk group ,according to SYNTAX scores .The serum Hcy concentration was determined by cyclic enzy‐matic method .Results Comparing with non‐infection group ,the serum Hcy concentration significantly increased in infection group (P<0 .01) .With the aggravation of Helicobacter pylori infection ,the serum Hcy concentration increased .There were significant difference among negative group ,mild infection group and severe infestation group (P<0 .01) .In the CHD patients infected Heli‐cobacter pylori ,the serum Hcy concentration also increased with the aggravation of the severity of coronary lesion .And there were significant difference among low risk group ,moderate risk group and high risk group (P<0 .01) .Conclusion Helicobacter pylori plays a role in the incidence and development of CHD through increasing the serum Hcy concentration .

Objective To explore the influence of Helicobacter pylori (Hp) infection in serum lipoprotein associated phospholipase A2 (Lp-PLA2), carotid intima-media thickness and stability of atherosclerotic plaques in atherosclerosis patients.Methods A total of 393 cases of patients with carotid artery arteriosclerosis confirmed by carotid color uhrasonography, who are informed consent, was selected as objects.The14C urea breath test was used to determine the infection situation of selected objects of helicobacter pylori.Meanwhile, enzyme-linked immunosorbent assay (ELISA) was used to determine the level of serum lipoprotein associated phospholipase A2 (Lp-PLA2).Results Serum Lp-PLA2 levels and carotid intimamedia thickness (IMT) of patients with carotid artery atherosclerosis in Hp infection group were higher than that of Hp non-infection group, and with the degree of Hp infection aggravating in the patients of carotid artery atherosclerosis, their serum Lp-PLA2 levels and carotid IMT were also increased accordingly.F test showed that the differences of serum Lp-PLA2 levels and carotid IMT in different degree of carotid artery atherosclerosis group were statistically significant (P ＜0.01).The incidence of unstable plaque of Hp infection group was obviously higher than that of the Hp non-infection group in the carotid atherosclerosis with plaques with statistical significance (chi square value =4.744, P =0.029).Multivariate linear regression analysis showed that the possibility of complication of unstable plaques in Hp infection group of carotid artery atherosclerosis was 1.82 times than that of non-infection group.With serum Lp-PLA2 every increasing 1 μg/L, the possibility of instability plaque increased by 2％.Conclusions Hp infection may promote the occurrence and development of carotid artery atherosclerosis by increasing serum level of Lp-PLA2 and changing the stability of atherosclerotic plaques.