Objective To assess the methodology of papers on systematic reviews and meta-analysis of interventions published in Journal of Evidence-Based Medicine .Methods Basic data were extracted from 70 papers on systematic reviews and meta-analysis of interventions published in Journal of Evidence-Based Medicinefrom 2001 to 2011 .Methodology used in these papers was assessed according to the AMSTAR Scale.The data were input into the Excelland analyzed using the SPSS7.0 and Meta-Analyst software.Results The methodology used in 34 papers (48.6%) was assessed using the Cochrane bias risk assessment tools.Fund support, number of authors and their affiliated institutions did not sig-nificantly affect the total score of methodology used in the 70 papers .Conclusion The methodology used in papers on systematic reviews and meta-analysis of interventions published in Journal of Evidence-Based Medicine is not quite valid as its early design program and retrieval strategies are imperfect , and it does not provide the excluded literature list and the interest conflict.

Objective To assess the effect of PRISMA statement on intervention-related systematic reviews and meta-analyses published in Evidence-based medicine .Methods Intervention-related systematic reviews and meta-analyses published in Evidence-based medicine from 2001 to 2011 were assessed according to the PRISMA scale and analyzed by Meta Analysist software.Results Seventy intervention-related systematic reviews and meta-analyses involving 14-disease spectra were included in this study.PRISMA statement and systematic reviews and meta-analysespublished by au-thors in colleges and universities could improve their academic level (P<0.05), fund support and the number of authors showed no significant effect on their academic level.Conclusion Literature retrieval methods,literature screening methods,bias assessment methods, and other analyzing methods used systematic reviews and meta-analyses published in Evidence-based medicine and their academic level can be improved by PRISMA statement.

Tuberculosis(TB) caused by the Mycobacterium tuberculosis(Mtb) is a worldwide public health threat.Microbiota in body affects human health and is involved in human diseases, and its clinical importance is begi-nning to be understood.In this review, studies on the relationship between the establishment of Mtb infection and microbiota as well as the development and antibiotic treatment of Mtb infection were discussed.Studies have shown that: (1) microbiota influences the establishment of Mtb infection; (2) co-infection of Helicobacter pylori alters susceptibility to Mtb infection and progression of active TB; (3) microbiota influences the progression of TB by regulating the nutritio-nal, metabolic and immune status of the host; (4) susceptibility to reinfection increases in TB patients treated with antibiotics, possibly due to T-cell epitope depletion of common intestinal non-Mtb Mycobacterium, the effects of antibio-tics are long-term in patients; (5) the occurrence of childhood TB is age-related and many factors such as co-infection and vaccine inoculation increase risk.An in-depth study of the relationship between the microbiota and TB will provide a new perspective on the prevention of TB.

Objective To study the cognitive impairment in SD rats after intermittent hypoxia (IH),and explore the relation of miR-26b up-regulated expression and neuron apoptosis in the hippocampus of SD rats after IH.Methods Eight-week-old male SD rats (n=20,each weighing approximately 300±10 g) were randomly divided into normal oxygen control group,IH 1-week group,IH 2-weeks group and IH 4-weeks group (n=5).Rats in the later three groups were given IH for different times,and rats in the normal oxygen control group were given normal oxygen.The spatial learning and memory abilities were detected by Morris Water Maze (MWM) in the normal oxygen control group and IH 4-weeks group.The levels of apoptosis proteins Caspase3 and Bax and anti-apoptosis protein Bcl-2 in the hippocampus of 4 groups were detected by Western blotting.The miR-26b expression level in the 4 groups was detected by real time-PCR.Results (1) The results of MWM revealed that the mean escape latency in the IH 4-weeks group was significantly prolonged as compared with that in the normal oxygen control group (P＜0.05);the time entering into the target quadrant in the IH 4-weeks group ([22.0±6.7] s) was significantly shorter than that in the normal oxygen control group ([39.8±8.8] s,P＜0.05).(2) Western blotting indicated that up-regulated expressions of apoptosis proteins Bax and Casepase3 and down-regulated expression of anti-apoptosis protein Bcl-2 in the IH 1-week group,IH 2-weeks group and IH 4-weeks group were noted as compared with those in the control group,with significant differences (P＜0.05);significantly higher apoptosis protein Bax and Casepase3 expressions in the IH 1-week group were noted as compared with those in the IH 2-weeks group and IH 4-weeks group (P＜0.05),while significantly decreased Bcl-2 expression in the IH 1-week group was noted as compared with that in the IH 2-weeks group and IH 4-weeks group (P＜0.05).(3) The results of real time-PCR revealed that the miR-26b expression level in the hippocampus was up-regulated in the IH 1-week group,IH 2-weeks group and IH 4-weeks group as compared with that in the control group,with significant differences (P＜0.05);miR-26b expression level in the IH 1-week group was significantly higher as compared with that in the IH 2-weeks group and IH 4-weeks group (P＜0.05).Conclusion The miR-26b up-regulated expression in the hippocampus might refer to Bax /Bcl-2-related mitochondrial apoptotic signaling pathway after IH brain injury;miR-26b could be a potential mean ofgene therapy after IH brain injury.

Objective To investigate the changes of microglia cell phenotypes in the injured brains of rats following repetitive mild traumatic brain injury (rmTBI).Methods Sixty male SD rats were randomly divided into sham-operated group,injury of one-week group,injury of two-week group,injury of four-week group,and injury of six-week group (n=12).Rats in the injury groups were induced rmTBI models by controlled cortical impact (CCI),and rats in the sham-operated group were only performed bone window opening without hitting.Six rats from each group were sacrificed;immunofluorescent staining was used to detect the Iba-1 positive microglial cells in the injured cortex and changes ofmicroglia subsets in the injured brain after rmTBI were analyzed by flow cytometry.Results As compared with the sham-operated group,the injury of one-week group and injury of six-week group had significantly increased percentages of Iba-1 positive microglial cells in the injured cortex (19％ and 12％,P＜0.05).flow cytometry indicated that CD451ow/CD11b+ cells were the microglial cells,accountting for 90％ ofCD11b+ cells;as compared with the sham-operated group,the injury of one-week group,injury of two-week group,injury of four-week group,and injury of six-week group had significantly increased M1 type microglial cells (P＜0.06),with injury of six-week group enjoying the highest level;as compared with the sham-operated group,the injury of one-week group,injury of two-week group and injury of four-week group had significantly increased M2 type microglial cells (P＜0.06),with injury of two-week group enjoying the highest level.Conclusion Dynamic changes ofmicroglia subsets after rmTBI are noted,which reveals that different subsets of microglia phenotypes might play their unique roles in the acute or chronic phases after rmTBI.