Objective To investigate the role of β-arrestin2 in intestinal inflammation and illustrate the mechanisms from the perspective of epithelial barrier function. Methods Dextran sodium sulfate(DSS)is used to induce acute intestinal colitis in mice. The experiment groups are designed as the wild type control(WT),the wild type colitis (WT+DSS) and the β-arrestin2- knockout colitis (KO+DSS). The expression of β-arrestin2 gene by mRNA and protein level is compared between the WT and WT + DSS groups. The difference of weight loss , disease activity index(DAI),spleen weight,colon length,histological score,intestinal permeability and important tight junction proteins (occludin ,claudin1 and ZO-1) were detected in the WT+DSS and KO+DSS groups. Results Compared with the WT group,the expression of β-arrestin2 was significantly higher in the colon of the WT+DSS group. Compared with the WT+DSS group,the KO+DSS group had less weight loss(P < 0.05),lower DAI(P<0.05),smaller spleen,longer colon and lower histological score(P=0.002). The KO+DSS group had a lower intestinal permeability(P = 0.009)and higher protein level of occludin and claudin1.There was no signifi-cant difference of ZO-1 in the two groups. Conclusion β-arrestin2 may promote mouse colitis through impairment of epithelial barrier function.

Objectives To identify ABO blood type from a child having discrepant results in forward and reverse ABO blood grouping by serological identification and genetic testing.Methods After routine serological detection with ABO blood group,the ABO gene and ABO blood group-A subgroup genotype were tested by PCR-SSP method.Results The Serological results showed that the specimen was positive type A (anti-A:1 +w),the reverse type is O type (Ac:2 +,Bc:4 +);PCRSSP A-subtype typing showed that the genotype of the child was Ax14/O2.Conclusion Difficult blood type identification sometimes need to combine serology and molecular biology methods to confirm.In this case,the phenotype of the child was Ax,and the genotype was Ax14/O2.