OBJECTIVE To investigate the drug resistance and the status of producing ESBLs and AmpC beta-lactamases of Klebsiella pneumoniae isolates from 2006 to 2007 in local district.METHODS From 2006 to 2007,110 strains of K.pneumoniae insensitive to cefoxitin were collected.The sensitiveness to 16 antibiotics were tested by K-B method and microdilution method.Genes of TEM,SHV,GES,PER,CTX-M-1,CTX-M-2,CTX-M-3,DHA and MIR-1/ACT-1 were tested by PCR.The gene transfer was detected by conjugation test.RESULTS The resistance rate of 110 K.pneumoniae strains to meropenem,imipenem,piperacillin/tazobactam,cefoperazone/sulbactam,ceftazidime and cefepime was 0-49.9%.The resistance rate to other antibiotics was 80-100%.And ESBLs production was the main result.Genes of ESBLs were CTX-M and SHV.Genes of AmpC beta-lactamases were ACT and DHA.They all could transfer the drug-resistance from plasmid to receptor bacteria.CONCLUSIONS Co-existing of ESBLs and AmpC beta-lactamases is the main reason of multi-drug resistance that K.pneumoniae.Transferring of drug-resistance gene leads to the spreading of drug-resistance.The drug-resistance rate of K.pneumoniae decreased during the last two years.

OBJECTIVE To investigate the resistance of Staphylococcus to erythromycin and clindamycin and detect the percentage and gene for inducible resistance in Tai'an.METHODS The susceptibilities of Staphylococcus to erythromycin and clindamycin were examined by Kirby-Bauer disc agar diffusion test and the inducible erythromycin resistance to clindamycin was checked by D-test according to the standards of NCCLS,and the resistance genes msrA,Vgb,sat4,ermA,ermB and ermC were detected by using PCR technology.RESULTS Among the 326 strains,162(44.12%)were all resistant to erythromycin and clindamycin;68(20.86%)were resistant to erythromycin and sensitive to clindamycin but they were positive in D-test;42(12.88%)were resistant to erythromycin and sensitive to clindamycin but they were negative in D-test.The rates of inducible resistance of MRSA,MSSA,MRCNS and MSCNS to clindamycin were 40.00%,56.25%,63.38% and 66.67%,respectively among the Staphylococcus which were resistant to erythromycin and sensitive to clindamycin.The gene ermC was the main one for inducible erythromycin resistance to clindamycin.The percentage of gene ermC was 85.29% and that of ermC and sat4 either was 7.35%;all the others were negative.CONCLUSIONS The rate of inducible erythromycin resistance to clindamycin in our area is relatively high,and D-test in clinical microbiology laboratory should be done so that the physicians can select the reasonable MLSB antimicrobial agents.

OBJECTIVE To sudy drug resistance related gene of carbopenem resistant Pseudomonas aeruginosa and type 1 integrating enzyme gene.METHODS With PCR method to detect and analyze carbopenem resistant P.aeruginosa pertinent metal ?-lactamase IMP,VIM,SPM,GIM genes and cell membrane protein oprD2 gene and six main drug resistance genes of type Ⅰ integrating enzyme gene and five others.RESULTS Fifty one strains of imipenem and meropenem resistant P.aeruginosa SPM,GIM metal enzyme genes were detected to be negative,16 strains of IMP and 5 strains of VIM type metal enzyme were all positive,14 strains of carbopenem resistant P.aeruginosa oprD2 gene were positive,other 37 strains of P.aeruginosa oprD2 gene were negative,7 strains produced metal enzyme and cell membrane protein oprD2 gene were deleted at the same time,49 strains with type Ⅰ integrating enzyme gene intⅠ1 were positive.CONCLUSIONS It is indicated the gene deletion of P.aeruginosa outer membrane protein OprD2 is important mechanism of carbopenem resistant P.aeruginosa,the second is metal enzyme,type Ⅰ integrating enzyme exists largely in P.aeruginosa.This hints the monitoring that drug resistance gene spreads and propagates in bacterium strain must be reinforced.

0.05). Conclusion:The excessive expression of Survivin in gallbladder cancer indicates that Survivin could be not only correlated with the occurrence of carcinoma but an early and common event in gallbladder carcinogenesis. Surviv in will promisingly become a novel tumor marker and can be applied in the clinic al practice for helping the early diagnosis as well as targeting gene therapy fo r gallbladder cancer.

BACKGROUND: Osteonecrosis of the femoral head (ONFH) following internal fixation of femoral neck fractures is difficult to be cured in clinic.OBJECTIVE: To analyze the literatures concerning ONFH in patients with femoral neck fractures treated with screw internal fixation in recent 15 years, and to summarize the research progress in views of epidemiology, etiology, diagnosis,treatment and rehabilitation.METHODS: Databases of CNKI, WanFang, CqVip, PubMed, Medline, Web of Science were searched with the keywords of femoral neck fracture, osteonecrosis of femoral head, osteonecrosis, internal fixation, internal fixation with screw in English and Chinese, respectively. Afterwards, the reviews and case reports were excluded. RESULTS AND CONCLUSION: (1) A total of 54 eligible articles addressing the ONFH following internal fixation for femoral neck fractures were included, and the incidence of ONFH varied from 8.1% to 37.2%, which was found at an average of 17 months after injury. (2) ONFH was found to be related to age, preoperative fracture displacement, preoperative traction,reduction condition, time from injury to operation, elderly patients companied with other diseases, older patients undergoing removal of the screws, closed or open internal fixation, restored time postoperatively, high body mass index, hyperlipidemia, season, and depression. (3) Early prevention and remedial surgery were used to treat ONFH. (4) The patients without weight-bearing activities at 3-6 months postoperatively could be beneficial for functional recovery. (5) These results suggest that choosing appropriate surgical programs and rehabilitation plan can reduce the incidence of ONFH and achieve good treatment outcomes, such as reasonable preoperative planning, standardized operation skills, correct diagnosis and treatment, proper postoperative rehabilitation and good doctor-patient cooperation.

Objective:To analyze the clinical features and genotypes of mitochondrial complex Ⅰ deficiency due to NDUFAF5 gene mutations.Methods:Clinical data of 2 cases with mitochondrial complex Ⅰ deficiency due to NDUFAF5 gene mutations admitted in the Department of Pediatrics, Peking University First Hospital from February 2015 to July 2018 were retrospectively reviewed and followed up.Reported cases of mitochondrial complex Ⅰ deficiency due to NDUFAF5 gene mutations were searched in online databases, including the PubMed, Wanfang, Chinese Journal Full-Text Database and VIP database from January 1975 to February 2020 with " NDUFAF5" as the key word.Through literature review, clinical features and genotypes of mitochondrial complex Ⅰ deficiency due to NDUFAF5 gene mutations were summarized.Results:Case 1 showed mentor and mental regression after infection at the age of 1 year and 4 months.The condition of case 1 remained stable at the age of 5 year and 6 months at the last follow-up.Brain magnetic resonance imaging (MRI) showed multiple lesions in the white matter of the frontal and parieto-occipital lobes, basal ganglia, thalamus, cerebellum, brain stem and corpus callosum.Case 2 showed rapidly bilateral visual impairment at the age of 7 years and 4 months.The patient′s vision moderately recovered at the age of 8 years and 8 months.Brain MRI showed midbrain, periaqueductal gray, medulla oblongata and putamen lesions.Spinal MRI showed continuous lesions in the cervical cord 1-4.Genetic test showed NDUFAF5 gene c. 764C>T (p.Ala255Val) and c. 508C>T (p.Arg170Trp), homozygous c. 836T>G (p.Met279Arg) mutations in case 1 and case 2 respectively.Through online searching, 6 reports involving 14 cases were retrieved.The most common clinical phenotype was Leigh syndrome.Two cases had disease onset during the neonatal period, and their disease progressed rapidly and died within 1 year old.Eleven cases had onset during the infantile period, and 72.7% (8/11 cases) of them had a normal development.The common initial symptoms were mental or motor regression, feeding difficulty and dystonia.Seventy-two point seven percent (8/11 cases) had acute/subacute onset after infection, showing paroxysmal deterioration, and died in infancy or childhood.One patient developed dystonia in childhood and visual impairment in adulthood.Conclusions:The onset age ranged from neonatal period to childhood in patients with NDUFAF5 gene mutations, and their clinical phenotypes vary a lot.The main clinical phenotype is Leigh syndrome.Disease onset during the infantile period is frequent, and mostly presents paroxysmal deterioration after infection, while disease onset in childhood is rare.