OBJECTIVE To investigate the flora distribution,enzyme producing and drug resistance of Citrobacter in our hospital,and analyzed multi drug resistance(MDR) character in order to guide the clinical medication.METHODS Totally 147 clinical isolates of Citrobacter were detected out ESBLs and AmpC ?-lactamases by three-dimensional test,MBL by the double-disk synergy test.at the same time,drug resistance to fifteen antibiotics was also detected by K-B method.RESULTS Hospital infection caused by Citrobacter.most commonly by C.freundii and then C.amalonaticus.Respiratory tract and urinary tract were prone to be infected than other sites(P0.05).The rate of ESBLs,AmpC,ESBLs+AmpC and MBL which produced by Citrobacter were 36.05% 10.20%,7.48% and 2.72%.The Citrobacter were sensitive to imipenem and meropenem,and their resistance rates to imipenem and meropenem were 4.76% and 3.40%,respectively.The resistance rate to cefoperazone/tazobactam was 23.81%.Otherwise,the resistance rate to 12 kinds of other antibiotics were all higher than 40.0%.MDR strains in the ICU ward were 81.08%,while in other wards were 53.64%,with significant difference(P

Objective To investigate the clinical efficacy of mesalazine combined with bifico in the treatment of ulcerative co -litis (UC) and its effect on toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88).Methods A total of 86 cases of UC was randomly divided into the observation and control groups with 43 cases in each group .The observation group was given me-salazine combined bifico treatment , and the control group was given mesalazine , and eight weeks as a course of treatment .The clinical efficacy was observed .Serum TLR4 and MyD88 were tested.Adverse reaction in treatment was recorded .Results The total effective rate (95.35%) in observation group was significantly higher than that (81.40%) in control group( P <0.05).The serum TLR4 and MyD88 after treatment of two groups were significantly lower than that before treatment , respectively ( P <0.05 or P <0.01 ) , and the decline in TLR4 of observation group was superior to that of control group ( P <0.05 ) .The difference of adverse reaction rate in two groups was not significant ( P >0.05 ) .Conclusions Mesalazine combined with bifico in the treatment of UC is safe and effective . The effect may be related to regulation of peripheral blood TLR 4 and MyD88 content .

Objective To explore the effects of tumor necrosis factor-α stimulated gene-6 (TSG-6) on early inflammation and blood brain barrier (BBB) in mice after ischemic stroke (IS).Methods A total of 90 healthy male C57BL/6j mice were randomly divided into sham-operated group (n=30),vehicle group (n=30) and TSG-6 treatment group (n=30);the middle cerebral artery occlusion models (IS) in the later two groups were established with suture emboli method;50 μg TSG-6 or PBS was immediately injected into mice via tail vein after IS.Neurological function deficits were assessed by modified neurological severity scale (mNSS) one and three days after IS;infraction volume was examined by triphenyl tetrazolium chloride (TTC) staining,the changes of brain water content were examined by wet and dry weight method,evans blue (EB) extravasation was assessed by means of EB fluorescent quantitation,myeloperoxidase (MPO) activity was tested by ultraviolet specterphotometry,and Western blotting was used to detect the expressions of matrix metalloproteinase-9 (MMP-9),high-mobility group protein box 1 (HMGB1) and toll-like receptor 4 (TLR4) three days after IS.Results Three days after IS,the mNSS scores (5.253±1.712),infraction volume ([26.100±5.640]％),EB extravasation ([7.233± 3.434] μg/g),brainwater content ([71.667±6.518]％),MPO activity ([70.383±17.558] mU/g) and HMGB1,TLR4 and MMP-9 expressions (0.503±0.230,0.482±0.159 and 0.611±0.170) in the TSG-6 treatment group were significantly lower or smaller than those in the vehicle group ([7.923±2.138],([36.883±8.553]％),([11.867±4.135] μg/g),([80.467±7.045]％),([112.617±26.782] mU/g),[0.861± 0.137],[0.833 ±0.193] and [0.910 ±0.156]) three days after IS (P＜0.05);the expressions of MMP-9 (0.611±0.170),HMGB1 (0.503±0.230) and TLR4 (0.482±0.159) in mice of TSG-6 treatment group were significantly down-regulated as compared with those in vehicle group those days after IS (P＜0.05).Conclusion TSG-6 can exert neuroprotective effect by protecting BBB from damage and reducing brain edema by reduction of MMP-9 after stroke,which is mediated by downregulation of HMGB 1 and its receptor TLR4 and the infiltration ofneutrophile granulocytes.