Clinical Laboratory Techniques ; Drug Resistance, Bacterial ; Humans ; Microbial Sensitivity Tests ; Mycobacterium tuberculosis ; drug effects ; Tuberculosis ; diagnosis

Antitubercular Agents ; pharmacology ; Drug Resistance, Bacterial ; Humans ; Microbial Sensitivity Tests ; Mycobacterium tuberculosis ; drug effects ; isolation & purification ; Tuberculosis, Multidrug-Resistant ; diagnosis ; microbiology

Humans ; Recurrence ; Respiratory Tract Infections

AIM: To investigate the role of NF-κB in diabetic neuropathy.METHODS: The diabetic rats were induced by intraperitoneal injection of streptozocin ( STZ) .The pain behavior test was used to detect the mechanical and thermal withdraw threshold of the rats’ bilateral hind paws.The protein levels of p-NF-κB and t-NF-κB in the rats’ L4 and L5 dorsal root ganglions ( DRG) were determined by Western blotting.The expression of Nav1.7 in DRG of diabetic neuropathy rats with or without NF-κB inhibitor PDTC was detected by the method of immunohistochemistry.RESULTS:The mechanical and thermal withdraw threshold of bilateral hind paws in the diabetic rats was decreased from 4 weeks to 12 weeks after injection of STZ.The protein levels of p-NF-κB in L4 and L5 DRG were significantly increased in the rats with diabetic neuropathy.Intrathecal administration of NF-κB inhibitor PDTC attenuated the increase in p-NF-κB and Nav1.7 in L4 and L5 DRG.Pain behaviors were also alleviated by PDTC.CONCLUSION:The increase in p-NF-κB is closely rela-ted to the generation of diabetic neuropathy.Inhibition of NF-κB blocks pain behaviors and the over-expression of Nav1.7 in DRG.

Objective To observe the clinical efficacy of Qingjinchangfei drink for treating AECOPD.Methods We Used random number table to separate 84 patients in to two groups:treatment group and control group.The treatment group used western medicine conventional treatment and Chinese medicine decoction Qingjinchangfei drink.The control group used western medicine conventional treatment.Both two groups were 14 days treatment.We recorded the improvement of symptoms and signs everyday.We compared the lung function,inflammatory cytokines,such as IL-8、IL-2 before and after treatment in the two groups.Results The total efficient in treatment group was obviously better than that in control group.The indicators such as clinical symptoms,signs,pulmonary function indicators were obviously better than that in control group.Compared with before treatment,IL-8,ET,MDA and TNF-? in sputum and blood were obviously lower but IL-2 was obviously higher.Conclusion Qingjinchangfei drink plus western medicine conventional treatment for treating AECOPD was obviously better than western medicine conventional treatment.

Objective To identify a unique protein as a novel genetic marker for rapid molecular typing of Mycobacteriutn tuberculosis Beijing genotype strains by comparing the proteome of Beijing genotype strains with non-Beijing strains.Methods Fifty-six clinical isolates of Mycobacterium tuber- culosis were analyzed by spoligotyping to determine genotypes.The two-dimensional electrophoresis (2 DE)was used to compare the global protein patterns between Beijing genotype strains and non Bei jing strains.Differential expressed proteins were measured by matrix assisted laser desorption ioniza tion lime of flight mass spectrometry(MALDI-TOF-MS).The data obtained from peptide mass fingerprinting were compared in protein database.The genes encoding differential expressed proteins and their upstream were sequenced.Results Forty nine of the 56 isolates were Beijing genotype strains and 7 isolates were non-Beijing strains.A unique protein Rv0927c was identified,which is absent in Beijing genotype strains compared with 7 non Beijing strains and H37Rv.There were two characteristic mutations in Beijing genotype strains,a deletion of AGC at nucleotide position 421 of Rv0927c and a 127 G→A muta- tion in the upstream of Rv0927c.but not in non Beijing strains and H37Rv.Conclusion Characteris tic mutations of Rv0927c in Beijing genotype strains can be used as a novel genetic marker for rapid molecular typing of Mycobacteriuln tuberculosis Beijing genotype strains and non Beijing strains.

Hemolysins of Leptospira interragans have been shown to be the virulence factor in the pathogenesis of leptospirosis and 10 potential hemolysin genes were charecterized by genomic annotation of L.interrogans serovar.Lai strain 56601. In the present study, the LA0202 gene supposed to encode one of the new potential hemolysin was cloned and the protein encoded was purified. The purified protein was shown to have highly hemolytic activity as demonstrated on the sheep blood agar plate. It was also confirmed that the LA0202 protein-mediated hemolysis on sheep erythrocytes was osmotically protected by PEG6000. Meanwhile, this protein could induce pore formation on sheep erythrocytes and cause damages on the membrane of human L-02 liver cells. In addition, it could induce apoptosis of human L-02 liver cells after treatment of cells with this protein for 24 hours. It is evident that LA0202 protein acting as a pore-formong hemolysin can induce cytotoxic damage on mammalian cells.

Objective To investigate the protective effects of elctroacupuncture(EA)at Zusanli(ST36) points on intestinal villas damage and mucosal permeability induced by small intestine pro-inflammatory factors in rats with intestinal ischemia/reperfusion(I/R). Methods 30 Sprague-Dawley(SD)rats were randomly divided into three groups(each,n=10):intestinal I/R group(model group),intestinal I/R+EA ST36 group(EA group)and intestinal I/R+sham EA group(SEA group). Rats were subjected to superior mesenteric artery(SMA)clamping at its root part to occlude the vessel for 30 minutes,followed by reperfusion for 60 minutes to form intestinal I/R models. Rats in EA group received EA at the bilateral ST36 points(2-3 mA,2-100 Hz)for 30 minutes immediately after ischemia,those in SEA group received EA at bilateral sham points(the point was located at 0.5 cm away from ST36 point in its lateral side)with the same frequency and intensity of stimulation as EA group for 30 minutes,and those in model group received no treatment. Animals were sacrificed 60 minutes after reperfusion and segments of distal part of ileum were harvested,then the levels of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in intestinal tissue were measured. Histopathologic changes were viewed and graded via light microscopy. A solution of fluorescein isothiocyanate(FITC)-dextran was injected into the lumen of the segment of intestine 30 minutes after reperfusion,systemic blood was drawn via abdominal aorta puncture at 60 minutes after reperfusion,and then the level of FITC-dextran in blood was measured to determine the changes in intestinal permeability. Results Compared to the model group and SEA group,EA ST36 significantly attenuated intestine TNF-α(pg/mg:3.01±0.50 vs. 8.65±1.02,8.42±1.41,both P<0.05)and IL-6 levels(pg/mg:2.51±0.15 vs. 6.34±0.86,6.13±1.12,both P<0.05),successfully maintained low gut injury scores(1.50±0.33 vs. 3.18±0.39,3.04±0.37,both P<0.05), and significantly reduced permeability of the distal ileum and the content of FITC-dextran(μg/L:282.42±73.92 vs. 856.22±229.47,844.22±239.47,both P<0.05). However,there were no significant differences in all above variables between SEA and model group(all P>0.05). Sections of distal ileum from animals in the model group and SEA group showed no obvious difference histologically,and the pathological manifestations were villous tip necrosis, blunt-shaped and collapse. Compared to the model group and SEA group,the intestinal villous injury in animals of EA group was much milder. Conclusion In rats with intestinal I/R injury,EA ST36 points has protective effect on the gut that is possibly due to the fact it may obviously lower the levels of the pro-inflammatory factors of small intestinal tissue,alleviate mucosal insult of gut and reduce the mucosal permeability.

Adult ; Fracture Fixation, Internal ; Fractures, Ununited ; surgery ; Humans ; Male ; Scaphoid Bone ; injuries ; surgery

Objective To investigate the increased expression of microRNA-146a(miR-146a) in peripheral blood mononuclear cells (PBMC) of patients with chronic immune thrombocytopenic purpura (ITP) and its clinical significance. Methods Twenty-eight patients with chronic ITP and 28 healthy controls matched with age and gender were enrolled in this study. Fluorescent quantitative PCR reaction was used to detect the relative expression of miR-146a in their PBMC. The serum concentration of TNF-α, IL-2,IL-1 β and IFN-γ were measured by ELISA. CCK-8 method was used to detect the proliferation ability of PBMC , which transfected with miR-146a mimics or inhibitor and then stimulated with platelet . Results The relative expression of miR-146a in ITP patients was higher than that of healthy controls. The increased expression of miR-146a was negatively correlated with the serum TNF-α, IL-2 and IFN-γ. The PBMC transfected with miR-146a mimics had reduced expression of IL-2 and proliferation when stimulated with platelet.In contrast, the opposite effect was observed with the miR-146a inhibitors transfection. Conclusion MiR146a was involved in the pathogenesis of chronic ITP by controlling IL-2 production and PBMC proliferation.Thus, it may be a potential therapy target for chronic ITP.