0.05). But the incidence of rehospitalization in combination group because of adverse cardiovascular events wasn’t more two times than that of non-combination group (OR=2.07; 95% confidence interval ranged from 1.87 to 2.20). CONCLUSION: The results of study are similar to other studies of foreign countries. PPI can influent the anti-platelet effect of clopidogrel so as to increase the incidence of rehospitalization risk resulted from adverse cardiovascular events. Physicians should apply PPI with cautions.

Objective To investigate the level of serum retinol-binding protein 4 (RBP4) and related factors in chronic hepatitis C (CHC). Methods Fifty-six patients with CHC (CHC group) and 35 healthy volunteers (control group) were selected. Serum RBP4 level was measured by ELISA method.Fasting blood glucose ( FBG ), triglycerides (TG), total cholesterol ( TC ), alanine aminotransferase (ALT),γ-glutamyl transpeptidase (γ-GT) were measured, HCV-RNA level was tested by qualitative polymerase chain reaction(q-PCR). Results There were no significant difference in FBG, TC,TG, γ-GT between two groups (P ＞ 0.05 ). Serum RBP4 level in CHC group [(33.38 ± 6.43 ) mg/L] was higher than that in control group [(26.11 ± 3.35) mg/L](P＜ 0.01),the CHC patients with ALT normal (26 cases) had significantly higher RBP4 level [( 38.96 ± 4.09) mg/L] compared with ALT abnormal [30 cases, ( 28.53 ± 3.43 ) mg/L](P ＜ 0.01 ). ALT level was negative with RBP4 in CHC group (r = -0.6368, P ＜ 0.05 ). Conclusion Serum RBP4 level is significantly associated with CHC and negatively correlated with ALT level,but not associated with FBG, TC,TG, γ-GT and HCV-RNA.

The reversible and precise temporal and spatial regulation of histone lysine methyltransferases(KMTs)is essential for epigenome homeostasis.The dysregulation of KMTs is associated with tumor initiation,metastasis,chemoresistance,invasiveness,and the immune microenvironment.Therapeutically,their promising effects are being evaluated in diversified preclinical and clinical trials,demonstrating encouraging outcomes in multiple malignancies.In this review,we have updated recent understandings of KMTs'functions and the development of their targeted inhibitors.First,we provide an updated overview of the regulatory roles of several KMT activities in oncogenesis,tumor suppression,and im-mune regulation.In addition,we summarize the current targeting strategies in different cancer types and multiple ongoing clinical trials of combination therapies with KMT inhibitors.In summary,we endeavor to depict the regulation of KMT-mediated epigenetic landscape and provide potential epigenetic targets in the treatment of cancers.