Objective:To evaluate the diagnostic value of rifampin resistance real-time fluorescent quantitative nucleic acid amplification technology (GeneXpert) combined with T cell spot test of tuberculosis infection (T-SPOT.TB) in tuberculous meningitis (TBM).Methods:The clinical data of 70 TBM patients (TBM group) and 30 non-TBM patients (non-TBM group) in Shenyang Chest Hospital from March 2017 to December 2019 were retrospectively analyzed. All patients were detected by GeneXpert and T-SPOT.TB. The results of MGIT960 liquid culture of cerebrospinal fluid were used as the gold standard to evaluate the diagnosis of TBM by GeneXpert and T-SPOT.TB.Results:The positive rates of GeneXpert and T-SPOT.TB in parallel and in series in TBM group were significantly higher than those in non-TBM group: 27.14% (19/70) vs. 0, 72.86% (51/70) vs. 46.67% (14/30), 78.57% (55/70) vs. 46.67% (14/30) and 21.43% (15/70) vs. 0, and there were statistical differences ( P<0.01 or <0.05). The sensitivity and accuracy of two methods in parallel in TBM diagnosis were 78.57% and 71.00% respectively. The specificity and misdiagnosis rate of two methods in series in TBM diagnosis were 100.00% and 0 respectively. Conclusions:The sensitivity of GeneXpert and T-SPOT.TB in parallel is the highest in TBM diagnosis. The specificity of the two methods in series and GeneXpert alone is as high as 100.00%. The two methods can reduce the misdiagnosis rate of TBM in series and reduce the rate of missed diagnosis in parallel.

Objective To examine the effect and mechanism of sodium ferulate inhibiting P38 MAPK in macrophage on neurotoxicity which was mediated by fribrilar-amyloid-induced.Methods The isolated peritoneal macropohages were cultured.P38 MAPK protein in nuclear extracts was analyzed by Western blot and production of tumor necrosis factor-?(TNF-?) was detected by ELISA.For neuron-macrophage co-cultures,Microtubute-associated protein-2(MAP-2) expression was detected by immunocytochemical technique.The level of LDH in the medium was measured.Results The production of TNF-? and P38 MAPK protein in nuclear extracts increased significantly by incubation with A?25-35.LDH efflux in neuron-macrophage co-culture medium increased and MAP-2 expression decreased significantly(P

AIM: To investigate effect of sodium ferulate on A?25-35-mediated signaling pathway. METHODS: The isolated peritoneal macrophages from mice were cultured. p38 MAPK protein kinase in nuclear extracts was analyzed by Western blotting. The concentration of TNF-? and NO in supernatant were measured by ELISA and Griess reaction technique. The expression of iNOS protein was detected by immunochemical technique. RESULTS: A?25-35 significantly increased the concentrations of TNF-? and NO in supernatant, expression of iNOS in macrophages and p38 MAPK protein kinase in nuclear extracts, which were blocked by sodium ferulate. CONCLUSION: Sodium ferulate inhibits p38 MAPK activation triggered by A?25-35.

Objective To explore the safety of the human bone marrow‐derived mesenchymal stem cells (hBMSCs) after silencing of human leukocyte antigen A2 expression .Methods We divided the cells into three groups:normal cultured cells of the 8th passage served as control group , and hBMSCs after HLA A2 silencing expression of the 5th and 15th passage as experimental groups 1 and 2 ,respectively .The hBMSCs were recultured by sterile methods .The growth curve ,telomerase activation ,and expressions of P27 ,cyclin D2 and cyclin‐dependent kinase 4 (CDK4) were utilized to explore the safety of the hBMSCs induced by LV‐siRNA‐HLA A2 .The BMSCs were transplanted to the subcutaneous layer of nude mice .Tissue types were detected 24 weeks after transplantation . Results The cell curves had no obvious left or right shift in all the groups . The telomerease activation in experimental groups 1 and 2 did not significantly differ from those in control group . The expressions of anti‐oncogene P27 ,cyclin D2 and CDK4 had no obvious difference between the two experimental groups and control group , either . There was only ectopic osteogenesis 24 weeks after the BMSCs (HLA A2 gene silenced ) were transplanted to the subcutaneous layer of the nude mice .Conclusion There was no obvious evidence to support that hBMSCs had undergone change in safety after the silencing of HLA A 2 expression .

AIM To investigate the neuroprotective effects and possible mechanisms of saponins from Anemarrhena asphodeloides Bge. (SAaB) on neuronal damage induced by amyloid β-protein fragments 25-35 (Aβ25-35). METHODS Cultured mouse peritoneal macrophages were stimulated with Aβ25-35 (20 μmol·L-1) for 0.5, 1, 2 and 6 h or preincubated with SAaB (10, 30 and 100 μmol·L-1)for 10 min or mitogen-activated protein kinase (MAPK) specific inhibitors (p38 MAPK inhibitor SB 203580 and MEK specific inhibitor PD98059) for 30 min prior to the addition of Aβ25-35(20 μmol·L-1). After stimulation with Aβ25-35 for the indicated times, total cellular extracts were prepared for Western blotting of extracellular signal-regulated kinase (ERK) and p38 MAPK. After stimulation with Aβ25-35 for 48 h, the supernatants of cultured macrophages were collected for quantification of tumor necrosis factor-α (TNF-α) and nitric oxide (NO) and protein expression of inducible nitric oxide synthase (iNOS) in macrophages was determined by immunocytochemical staining. To determine whether SAaB has protective effect against neuronal apoptosis mediated by Aβ25-35-induced macrophages activation, macrophages were stimulated with Aβ25-35 in the presence or absence of SAaB (10, 30 and 100 μmol·L-1) for 48 h and then the cell-free supernatant of Aβ25-35-stimulated macrophages was transferred to the culture of cerebellar granule neurons for 72 h. Neuronal apoptosis was quantitated by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. RESULTS Aβ25-35(20 μmol·L-1) significantly induced increase in phospho-ERK1/2 and phospho-p38 MAPK protein expression without affecting total protein levels and in the production of TNF-α and NO in cultured macrophages. Aβ25-35-induced increase of TNF-α production in macrophages involved activation of ERK1/2 signal pathway. Importantly, TNF-α and NO generated by cultured macrophages after Aβ25-35 stimulation may be responsible for the majority of the neuronal apoptosis. SAaB (30 and 100 μmol·L-1) significantly suppressed Aβ25-35-induced increase in phospho-ERK1/2 and phospho-p38 MAPK protein. In addition, SAaB (10, 30 and 100 μmol·L-1) also decreased the level of TNF-α and NO in supernatants of cultured macrophage and inhibited Aβ25-35-induced increase in iNOS protein expression of macrophages. Neuronal apoptosis mediated by Aβ25-35-induced macrophage activation was also significantly attenuated by treatment with SAaB (10, 30 and 100 μmol·L-1). CONCLUSION SAaB protects neurons against the neuronal cell death induced by Aβ25-35. The beneficial effects of SAaB may be related to the reduction of TNF-α and NO from activated macrophage induced by Aβ25-35.

Collaborative development among medical practice, education and research is a strategic decision of the country in disciplinary development guided by the innovation-driven strategy. In October 2017, Beijing Hospitals Authority organized 18 tertiary hospitals with pediatrics discipline and founded a collaborative development center for pediatrics. This center operated in a model featuring both leadership of due authorities and autonomous administration. Two of the specialized pediatrics hospitals work as leading units, and existing high quality pediatrics resources of the member hospitals were pooled to establish an academics committee and an executive committee. A development system was established with disciplinary construction as the focus, collaborative development as the goal and horizontal collaboration as the means. It was designed to explore a new model featuring overall planning and standardized management of the discipline, building of a shared platform for clinical capacity development, joint development of continued medical education and talent cultivation, as well as diversified and multi-centered research and platform resources sharing. This model can effectively promote the overall development level of pediatrics in Beijing municipal hospitals.