Objective To explore the effects of H 2 S on neuronal injuries induced by oxygen glucose deprivation /reoxygenation ( OGD/R) in cortical neurons .Methods For OGD, the primary cultured cortical neurons were incubated with glucose-free EBSS media for 4h in N2/CO2/O2 (93%/5%/2%) atmosphere.Thereafter, the media were replaced by Neurobasal/B27 culture media and the neurons were incubated for 12 h in a 5%CO2 incubator at 37℃.NaHS was used as a H2S donor and cell survival rate was determined by cell counting kit 8(CCk-8).[Ca2+]i was determined using fura-2/AM and fluorescence microscopic imaging systems .The release rate of lactate dehydrogenase ( LDH) was determined by lactate dehydrogenase assay kit , and cell damage was analyzed by staining of propidium iodide ( PI ) .Results After pretreated with 200, 300 and 600μmol/L sodium hydrosulfide ( NaHS) for 30min before OGD/R, the cell survival rate of neurons significantly increased (n=4).[Ca2+]I(n=5), LDH release rate (n=4) and cell damage percentage (n=6) in the neuron pretreated with 300 μM NaHS were significantly lower than those in ODG/R cells.Treatment with 10μmol/L calcium chelator BAPTA also reduced the LDH release rate and cell damage percentage induced by ODG /R in neurons . Conclusion The results indicate that H 2 S may inhibit the OGD/R induced damage in cortical neurons via reducing calcium overload of neurons .

Objective To explore the potential value of tuberculosis protein chip for clinical diagnosis of tuberculosis.Methods The antibody level of tuberculosis protein ESAT-6,CFP10,16 KD,38 KD and LAM was determined in 4 093 patients,inclu-ding 441 tuberculosis and 3 652 non-tuberculosis cases by protein chip.Results The tuberculosis antibody was positive in 297 of the 441 tuberculosis cases and 647 of the 3 652 non-tuberculosis cases.Tuberculosis protein chip provided a sensitivity of 67.35% and specificity of 82.28% in the diagnosis of tuberculosis.Conclusions Tuberculosis protein chip test is a quick,easy and effective method for identifying potential tuberculosis patients with good specificity.

Ischemia and hypoxia cause functional damage to brain tissues during stroke， and when blood supply is restored to brain tissues after ischemia， a large number of free radicals and calcium overload cause cerebral ischemia-reperfusion injury， which further aggravates the condition. Autophagy is a self-protection mechanism that maintains the homeostasis of the intracellular environment， but excessive autophagy causes brain tissue damage. MiRNA is a small endogenous non-coding RNA molecule that regulate various physiological activities at the gene level by binding to complementary sequences in the 3 '- UTR of its target gene mRNA， leading to translation inhibition or mRNA degradation. MiRNA not only directly acts on autophagy related proteins， but also participates in autophagy regulation induced by ischemia/reperfusion through various signaling pathways. However， there is still a lack of systematic induction and analysis of miRNA regulation of autophagy signaling pathways induced by cerebral ischemia/reperfusion. This article reviews the regulation of cellular autophagy during cerebral ischemia/ reperfusion by miRNA-124， miRNA-298， miRNA-202-5p， miRNA-142， miRNA-26b and so on through different signaling pathways， providing a systematic and theoretical approach for the study of autophagy in stroke.