Objective To find out the present situation of hepatitis B infection or immunity in Tianjin city,and to provide the scientific basis for the hepatitis B control and prevention.Methods 2 594 samples were selected with the methods of different proportionate stratified and cluster sampling,and the hepatitis B infection markers were detected by ELISA.Results The positive rates of HBsAg,anti-HBs,anti-HBc and HBV were 2.62％,46.72％,10.60％ and 51.54％.Conclusion Compared with the results in 1992,the positive rates of HBsAg,anti-HBc and HBV were decreased significantly,while the positive rate of anti-HBs increased significandy,which ascribed to the comprehensive measure with the vaccination against hepatitis B as a main strategy for control hepatitis B.

BACKGROUND:Previous studies have indicated that resistin stimulates a large set of chemokines in chondrocytes that are known to be important in inflammatory joint lesions.
OBJECTIVE:To further investigate the mechanism of co-regulation roles of transcription and post-transcription in the up-regulation of two chemokine genes CCL3 and CCL4 in chondrocytes in response to resistin.
METHODS:Human chondrocytes, T/C-28a2 and ATDC5 cels were cultured. The function of resistin on the chemokine genes, and the expression of C/EBPβ, nuclear factor-κB isoforms and chondrogenic specific miRNAs were tested by qPCR. The co-regulation of C/EBPβ and nuclear factor-κB was investigated by nuclear factor-κB inhibitor (IKK-NBD) and C/EBPβ inhibitor (SB303580) treatments, and subcelular localization was detected with or without resistin stimulation.
RESULTS AND CONCLUSION:Resistin could increase the expression of chemokine genes independently. Chondrocytes reacted in a non-restrictedly cel-specific manner to resistin; C/EBPβ inhibitor, nuclear factor-κB and some chondrogenic specific miRNAs in a combinatorial manner regulated chemokine gene expression. The activity of C/EBPβ was augmented by a transient increase in activity of nuclear factor-κB, and both transcription factors acted independently on the chemokine genes, CCL3 and CCL4.