OBJECTIVE:To analyze bacteria distribution and drug resistance of pediatric severe sepsis in our hospital,and to provide reference for clinical rational use of antimicrobial agents. METHODS:57 pediatric severe sepsis patients were collected from pediatric intensive care unit of our hospital during Jan. 2014 to May 2015. The results of pathogen culture and drug sensitivity tests were analyzed retrospectively. RESULTS:Of 57 children,pathogen were detected in 18 cases(31.58%). A total of 91 pathogen were detected,of which there were 24 strains of Gram-positive(G+)bacteria(26.37%)mainly including Staphylococcus and Entero-coccus,60 strains of Gram-negative (G-) bacteria (65.93%) mainly including Klebsiella pneumoniae and Acinetobacter calco-acetcus-A. baumannii complex and 7 strains of fungus (7.69%) as Candida. 4 strains of methicillin-resistant Staphylococcus,22 strains of carbapenems-resistant K. pneumoniae,21 strains of multi-drug resistant K. pneumoniae and 7 strains of multi-drug resistant A. calcoacetcus-A. baumannii complex were all detected. Methicillin-resistant Staphylococcus,Staphylococcus aureus and Streptococ-cus pneumoniae were sensitive to vancomycin and linezolid,with resistant rate of 0. K. pneumoniae was completely resistant to ampi-cillin sodium and sulbactam sodium,piperacillin sodium and tazobactam sodium,imipenem and cephalosporin,with resistant rate of 100%. Resistant rate of A. calcoacetcus-A. baumannii complex to major common antimicrobial agents was higher than 50%. Esche-richia coli was resistant to cefotaxime,and resistant rates of other antimicrobial agents were lower than 40%. CONCLUSIONS:Main pathogen of pediatric severe sepsis is G- bacteria in our hospital,and carbapenems-resistant K. pneumoniae is detected,to which should be pay attention. The multiple drug-resistant treatment should be adopted for pediatric severe sepsis caused by multiple drug-re-sistant bacteria. Antimicrobial agents should be selected rationally according to pathogen type and the results of drug sensitivity test.

Adult ; Bronchoalveolar Lavage ; methods ; Female ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; therapy ; Respiration, Artificial ; Young Adult

Objective To systematically evaluate the association between protein C and Legg -Calve -Perthes disease.Methods A literature research was performed through PubMed,Embase,Cochrane library,Web of Science,Chinese Biomedical Literature Database(CBM),China National Knowledge Infrastructure(CNKI)and Wan-fang Database from inception to February 201 6 on the association between protein C and Legg -Calve -Perthes disease.According to the Newcastle -Ottawa Scale(NOS)criteria,the quality of studies was evaluated and data were extracted.Meta -analysis was performed with Stata 1 1 .0 software.Results A total of 1 4 articles were included.Twelve articles on protein C and Legg -Calve -Perthes disease in the study group and the control group were compared.The results of Meta -analysis showed that there was no significant difference in protein C levels between the study group and the control group[odds radio(OR)=1 .41 ,95% confidence interval(CI)(0.87,2.28),P =0.1 47];five articles on protein C and the white race of Legg -Calve -Perthes disease between the study group and the control group were com-pared,The results of Meta -analysis showed that there was no significant difference in protein C levels between the whiteskin patients′group and the control group[OR =0.61 2,95%CI(1 .83,7.29),P =0.61 2];three articles on pro-tein C and the yellow race of Legg -Calve -Perthes disease between the study group and the control group were com-pared,and the results of Meta -analysis showed that there was no significant difference in protein C levels between the yellow skin patients group and the control group[OR =0.59,95%CI(0.05,6.72),P =0.080].Conclusion There is no significant correlation between protein C and Legg -Calve -Perthes disease.

The Bcl-2 family of proteins play a central role in the control of apoptosis, a fundamental process for both human health and disease, by mitochondrial pathway. PUMA(p53 up-regulated modulator of apoptosis protein) is one of BH3-only members of Bcl-2 family , its function is to promote cell apoptosis. To obtain BH3 death domain peptide of PUMA and detect its biological activity, the synthesized double-stranded oligomeric nucleotide encoding PUMA-BH3 peptide was cloned into expression vector pTYB2,thus generating a construct of pTYB2-PUMA-BH3 which expressed PUMA-BH3-intein-chitin binding domain fusion protein. Then the recombinant plasmid was transformed into E.coli BL-21 (DE3) and fusion protein was expressed under induction by IPTG. The soluble PUMA-BH3 peptide was purified from chitin affinity chromatography by DTT reduction. Through measuring mitochondria viability(MTT),mitochondria permeability transition(MPT) and the translocation of cytochrome c(Cyt c ) assayed by western blotting, the biological pro-apoptotic activity of PUMA-BH3 peptide was studied. The PUMA-BH3 peptide has the effects on decreasing the mitochondria viability remarkably , inducing mitochondrial swelling and promoting Cyt c releasing from isolated mitochodria . Mitochondrial swelling and the release of Cyt c induced by PUMA-BH3 peptide concerned with the opening of MPT,which can be improved by cyclosporine A(CsA).These results indicated that recombinant PUMA-BH3 peptide might possess pro-apoptosis activity and paved a reasonable way for the study of new apoptosis regulators.

Steroidal saponins have a wide range of pharmacological effects and biological activities, such as anti-tumor, antifungal, hypoglycemic, immune regulation, insecticides, etc. In the last ten years, some new structures of steroidal saponins compounds were found from natural plants, they have some new and different activities. In order to accelerate the research on the drug innovation of steroidal saponins, we summarized the new progress of the research on such compounds.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Antifungal Agents ; pharmacology ; Antineoplastic Agents, Phytogenic ; pharmacology ; Humans ; Hypoglycemic Agents ; pharmacology ; Saponins ; pharmacology ; Steroids ; pharmacology

Bacterial disinfectant resistance is the phenomenon that minimal inhibitory concentration or minimal bactericidal concentration of a certain disinfectant increases after a certain bacterium contacts with it many times. It exists widespread. Many species of bacteria are may resistant to a certain disinfectant, and a species of bacterium is may resistant to many disinfectant Disinfectant selectivity pressure is the extrinsic agent of bacterial disinfectant resistance. Resistance mechanisms include bacterial biochemistry structure, genetics pathway and enzymology pathway. There is relationship in disinfectant resistance and drug resistance. We should strengthen study and monitoring, enact unified standard and application specification to reduce bacterial disinfectant resistance.

To determine the relationship between the intercellular adhesion operon (ica) and the biofilm production in Staphylococcus epidennidis isolates from nosocomial infection, and the affection of ica on the antibiotic susceptibility of the isolates, we collected 106 strains, epidermidis isolates from nosocomial infection specimen to detect their biofilm production by quantitative and qualitative method and investigate the existence of ica operon by PCR. The minimal inhibitory concentration (MIC) to erythromycin, ampicillin, cefoxitin, ceftriaxone, teco-planin, ciprofloxacin, tetracycline, trimethoprim-sulfamethoxazole and vancomycin were tested. Among the isolates, 33 (31. 1% ) of them were detected out carrying ica operon. The rate of biofilm production of the ica-posi-tive isolates was higher than that of the ica-negative (P =0. 001) . By adding glucose and NaCl into the culture the detection rate of biofilm production could be increased. The antibiotic susceptibility of the plankton cells of ica-positive isolates to erythromycin, cefoxitin and ceftriaxone , except ampicillin, ciprofloxacin, tetracycline and tremethoprim-sulfamethoxazole, were lower than those of ica-negative isolates. This study showed that the existence of ica operon was close related to the biofilm formation in 5. epidermidis isolates from nosocomial infection. However, the mechanism of antibiotic resistance of the strains inside the biofilm still needed to be illustrated.

Objective To determine the genotypes and their epidermiology of microlide, lincosamide and streptogramin B(MLS_B)resistant S.epidermidis isolates causing nosocomial infection.Method 126 isolates were collected from inpatients in three hospitals in Beijing from 2003-2004 for testing the antibiotic susceptibility to the macrolide erythromycin,the lincosamide clindamycin.The resistance phenotypes of erythromycin-resistant isolates were determined by the double-disc test with erythromycin and clindamycin.The presence of the relative genes(ermA,ermB,ermC and msrA)to MLS_B resistance was identified by PCR and the similarity of the isolates was analyzed by PFGE.Result The isolates were mostly resistant to macrolide and lincosamide.In the constitutive phenotype cMLS_B isolates,the methicillin resistant S.epidermidis(MRSE)proportion appeared high(78.5%),whereas high methicillin susceptible S.epidermidis(MSSE)proportion was found in the inducible MLS_B phenotype(iMLS_B) (69.2%).ermC was shown as the most frequent determinant to the resistance,not only in MRSE and MSSE (70.8% and 6.8%),but also in iMLS_B and cMLS_B(76.9% and 90.3%).No specific endemic strain was found by PFGE analysis.The same resistance phenotype pattern was not clustered together and distributed into type A～F at the similarity of 60%.Among the phenotypes(cMLS_B,iMLS_B and MS phenotype),no significant difference was shown in the PFGE genotype distribution.Conclusion Our results indicate that the MLS_B resistance in S.epidermidis causing nosocomial infection is prevalent in the hospital and MLS_B antibiotics should be used iudiciously,ermC was shown as the most frequent determinant to the resistance.

Objective To estimate prenatal diagnoses strategy with abnormal results of non-invasive prenatal testing (NIPT) based on a case of mosaic for trisomy 22.Methods The pregnanct woman was recruited from Department of Prenatal Diagnosis Center of Xinhua Hospital.Ultrasound scans suggested fetal nuchal translucency was 3.5 mm.Peripheral venous blood was drawn from the pregnant woman for NIPT at 12+2 weeks gestation.For further prenatal diagnosis, amniocentesis was conducted at 16+2 weeks gestation, and karyotype analysis combination with chromosome microarray analysis (CMA) was executed to analysis amniocytes.Results NIPT results suggested that chromosome 21, 18 and 13 were normal and supplementary reports suggested that chromosome 22 were slightly above the normal range.Karyotype analyzed 35 cultured cells.Each of them revealed a normal female karyotype.However, CMA results suggested that chromosome 22 gain mosaic and its copy number was 2.26.The fetus was diagnosed as high possibility of mosaic for trisomy 22.Conclusions Combined with the NIPT results, which was slightly gain mosaic of chromosome 22, a prenatal diagnosis strategy were proposed.When NIPT results suggest chromosomal abnormities, karyotype analysis combination with CMA to diagnose were recommended.

OBJECTIVETo explore the feasibility of inducing human umbilical cord mesenchymal stem cells (HuMSCs) to differentiate into Leydig cells through conditioned medium derived from Leydig cells.

METHODSHuMSCs and Leydig cells were obtained by tissue blocks culture attachment and enzymatic digestion respectively. HuMSCs were induced by conditioned medium of Leydig cells as an experiment group while those before induction were cultured as a control group. The expressions of LHR, 3β-HSD and StAR in the induced HuMSCs were determined by RT-PCR after 3, 7 and 10 days of culture; those of CYP11A1, CYP17A1 and 3β-HSD measured by immunofluorescence staining after 2 weeks; and that of 3β-HSD detected by Western blot after 4 weeks.

RESULTSThe experimental group showed positively expressed LHR, 3β-HSD and StAR at 3, 7 and 10 days, CYP11A1, CYP17A1 and 3β-HSD at 2 weeks, and 3β-HSD at 4 weeks, while the control group revealed negative expressions at all the time points.

CONCLUSIONInduced with conditioned culture medium derived from Leydig cells, HuMSCs are likely to differentiate into steroidogenic cells and eventually into Leydig cells.

Cell Differentiation ; Culture Media, Conditioned ; Humans ; Leydig Cells ; cytology ; Male ; Mesenchymal Stromal Cells ; cytology ; Umbilical Cord ; cytology