Objective To investigate whether the expression of sterile alpha motif and histidine/aspartic acid domain containing protein 1 ( SAMHD1 ) could be induced by IFN-α and mediated by microRNA-181a (miR-181a). Methods THP-1 and Jurkat cells were treated with different doses of IFN-α(200 IU/ml and 1 000 IU/ml) for 24 h. The expression of miR-181a and SAMHD1 at mRNA level were de-tected by quantitative PCR. Western blot assay was performed to measure the expression of SAMHD1 at pro-tein level. THP-1 and Jurkat cells were transfected with p-181a, an over-expression vector of miR-181a, and then treated with 200 IU/ml of IFN-α. Changes in the expression of SAMHD1 in those cells were analyzed. Results IFN-α significantly enhanced the expression of SAMHD1 at mRNA and protein levels, but inhibi-ted the expression of miR-181a, especially in Jurkat cells. The expression of SAMHD induced by IFN-αwas inhibited in cells over-expressing miR-181a. Conclusion This study suggests that IFN-α could induce the expression of SAMHD1 by down-regulating the level of miR-181a.

Objective To investigate the effect of different HAART regimens on liver function,viral load and CD4+T cells of HIV infected children with HCV co-infection.Methods A total of 40 patients were divided into 4 groups:13 cases in AZT+3TC+NVP group(group A),16 cases in AZT+3TC+EFV group(group B),5 cases in D4T+3TC+EFV group(group C)and 6 cases in D4T+3TC+NVP group(group D).Liver function,viral load and CD4+T cells of patients in 4 groups were compared between before and after HAART.Results Eight patients(20％)had abnormal liver function before HAART treatment,and all of them had 1 level of liver damage.After receiving HAART,levels of ALT and AST were increased in group A and B(P<0.01);AST levels were increased in group C(P<0.01).CD4+T counts were all increased and HIV viral loads were decreased in 4 groups(P<0.01).There was no significant difference in RNA HCV load before and after HAART treatment(P>0.05).Conclusion Different HAART regimens can increase the liver damage in HIV infected children co-infected with HCV,but have little effect on the treatment efficiency of HAART regimens.

Objective To investigate the antimicrobial resistance profile of the clinical isolates collected from selected hospitals across China. Methods Twenty-nine general hospitals and five children's hospitals were involved in this program. Antimicrobial susceptibility testing was carried out according to a unified protocol using Kirby-Bauer method or automated systems. Results were interpreted according to CLSI 2017 breakpoints. Results A total of 190 610 clinical isolates were collected from January to December 2017, of which gram negative organisms accounted for 70.8％ (134 951/190 610) and gram positive cocci 29.2％ (55 649/190 610). The prevalence of methicillin-resistant strains was 35.3％ in S. aureus (MRSA) and 80.3％ in coagulase negative Staphylococcus (MRCNS) on average. MR strains showed much higher resistance rates to most of the other antimicrobial agents than MS strains. However, 91.6％ of MRSA strains were still susceptible to trimethoprim-sulfamethoxazole, while 86.2％ of MRCNS strains were susceptible to rifampin. No staphylococcal strains were found resistant to vancomycin. E. faecalis strains showed much lower resistance rates to most of the drugs tested (except chloramphenicol) than E. faecium. Vancomycin-resistant Enterococcus (VRE) was identified in both E. faecalis and E. faecium. The identified VRE strains were mainly vanA, vanB or vanM type based on phenotype or genotype. The proportion of PSSP or PRSP strains in the non-meningitis S.pneumoniae strains isolated from children decreased but the proportion of PISP strains increased when compared to the data of 2016. Enterobacteriaceae strains were still highly susceptible to carbapenems. Overall, less than 10％ of these strains (excluding Klebsiella spp.) were resistant to carbapenems. The prevalence of imipenem-resistant K. pneumoniae increased from 3.0％ in 2005 to 20.9％ in 2017, and meropenem-resistant K. pneumoniae increased from 2.9％ in 2005 to 24.0％ in 2017, more than 8-fold increase. About 66.7％ and 69.3％ of Acinetobacter (A. baumannii accounts for 91.5％) strains were resistant to imipenem and meropenem, respectively. Compared with the data of year 2016, P. aeruginosa strains showed decreasing resistance rate to carbapenems. Conclusions Bacterial resistance is still on the rise. It is necessary to strengthen hospital infection control and stewardship of antimicrobial agents. The communication between laboratorians and clinicians should be further improved in addition to surveillance of bacterial resistance.