Objective To investigate the prevalence of aminoglycoside resistance gene in multidrug-resistant Acinetobacter bau-mannii isolated in clinical at a certain time,and to provide the basis for the control of nosocomial infection.Methods 9 strains of multidrug-resistant Acinetobacter baumannii were isolated in First People′Hospital of Weifang from November 26,2013 to Decem-ber 12,2013.Identification of bacteria and susceptibility testing were conducted by VITEK2,and partial antimicrobial drug suscepti-bility tests were performed by the disk diffusion method.Aminoglycoside resistance genes were detected by PCR and the positive genes were partly sequenced.Results Among the 9 stains of multidrug-resistant Acinetobacter baumannii,2 strains carried aac(3)-Ⅰ gene,3 carried ant(3″)-Ⅰ gene,3 carried aac(6′)-Ⅰ gene.AndarmA gene was positive in 9 strains.All strains were resistant to aminoglycosides,such as amikacin,gentamicin and tobramycin.There were 5 specien issolated in ICU,while 3 specimens were isola-ted in neurosurgery ward.All specimens were separated from sputum.Conclusion Antimicrobial resistance to aminoglycosides of Acinetobacter baumannii isolated in the hospital during this time was related to aminoglycoside resistance gene.Nosocomial infec-tion caused by multidrug-resistant Acinetobacter baumanniiin,ICU and neurosurgery ward should be vigorously monitored.

OBJECTIVE To survey the patient with pulmonary infection induced by extended-spectrum ?-lactamases-producing bacteria and their Enterobacteriaceae clinical characteristics, drug-resistance and countermeasure. METHODS Isolation, cultivation, identification, drug-sensitivity tests and confirmation of ESBLs-producing bacteria were done for the bacteria of sputum specimens collected from our hospital from Feb 2001 to Sept 2004. Susceptibility testing was performed by disk diffusion(K-B)method. RESULTS Totally 541 strains of Enterobacteriaceae were cultivated altogether and ESBLs-producing bacteria were 135 strains. The ESBLs- producing strains were sensitive to imipenem, and the resistance rates to it were 0.00% . The resistance rates of ESBLs-producing strains to cefoperazone/sulbactam and piperacillin/tazobactam were 31.11% and 44.44%, respectively . The multi-drug-resistance (MDR) rate of ESBLs-producing strains was higher than that of strains no producing ESBLs (P

Objective To optimize the short tandem repeats(STR)which link closely to survival motor neuron(SMN)and have redundant polymorphism information contents,and to use these STR in the prenatal diagnosis of spinal muscular atrophy(SMA).Methods Eleven STR loci(D5S435,D5F153, DSF151,D5S637,D5S1413,D5S125,D5S464,D5S1556,DSF149,D5S351,MAP1B-5')were amplified by PCR.Then the PCR products were detected by polyacrylamide gel electrophoresis(PAGE)and analyzed by silver staining.STR loci were evaluated and optimized by their PIC values.PCR-PAGE and gene scan were combined to make genetic link analysis for SMA families based on the optimized STR.Results Three STR loci(D5S435,DSF149 and D5S351)were selected with 8,19 and 18 polymorphic fragments detected respectively in 100 normal individuals.Their PIC values were 0.84,0.91 and 0.92 respectively.Four carriers and 2 normal individuals were detected from 6 SMA families with linkage analysis by using the 3 STR.Conclusion This genetic diagnosis system based on the 3 STR loci can provide rapid prenatal diagnosis for SMA families,can eliminate maternal blood contamination,and also can discriminate carriers from normal individuals in the fetuses,which makes the prenatal diagnosis system of SMA perfect.

OBJECTIVETo examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment(25-35) (Abeta(25-35))-induced PC12 cells cytotoxicity, and to further explore its mechanism.

METHODSExperimental PC12 cells were divided into the Abeta group (treated by Abeta(25-35) 100 micromol/L), the blank group (untreated), the positive control group (treated by Vit E 100 micromol/L after induction) and the ECR treated groups (treated by ECR with different concentrations of 1, 50 and 100 micromol/L). The damaged and survival condition of PC12 cells in various groups was monitored by lactate dehydrogenase (LDH) release and MTT assay. The content of malondialdehyde (MDA) was measured by fluorometric assay to indicate the lipid peroxidation. And the antioxidant enzymes activities in PC12 cells, including superoxide dismutases (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), were detected respectively.

RESULTSAfter PC12 cells were treated with Abeta(25-35) (100 micromol/L) for 24 hrs, they revealed a great decrease in MTT absorbance and activity of antioxidant enzymes, including SOD, CAT and GSH-Px as well as a significant increase of LDH activity and MDA content in PC12 cells (P < 0.01). When the cells was pretreated with 1-100 micromol/L ECR for 24 hrs before Abeta(25-35) treatment, the above-mentioned cytotoxic effect of Abeta(25-35) could be significantly attenuated dose-dependently, for ECR 50 micromol/L, P < 0.05 and for ECR 100 micromol/L, P < 0.01. Moreover, ECR also showed significant inhibition on the Abeta(25-35) induced decrease of SOD and GSH-Px activity, but not on that of CAT.

CONCLUSIONECR could protect PC12 cells from cytotoxicity of Abeta(25-35), and the protective mechanism might be related to the increase of SOD and GSH-Px activities and the decrease of MDA resulting from the ECR-pretreatment.

Amyloid beta-Peptides ; toxicity ; Animals ; Catalase ; analysis ; Ecdysterone ; pharmacology ; Glutathione Peroxidase ; analysis ; L-Lactate Dehydrogenase ; analysis ; Malondialdehyde ; analysis ; PC12 Cells ; Peptide Fragments ; toxicity ; Rats

AIMTo observe the behavior in learning and memory and the expression of c-fos gene from the brain of rats induced by beta-AP25-35, and the intervention of ecdysterone, in order to explore the protective mechanism of ecdysterone on the dysfunction of learning and memory of the rat induced by beta-AP25-35.

METHODSMicroinjection of beta-AP25-35 into hippocampus induced learning and memory dysfunction of rats. The learning and memory of rats were observed by Morris Water Maze. The expression of c-fos gene in the brain was detected by immunohistochemistry.

RESULTSThe results of Morris Water Maze showed that after rats were microinjected beta-AP25-35 into hippocampus, the rats in model group took longer latency and searching distance compared with the ones in control group (P < 0.01), and the rats in treated group (ECR 4 mg x kg(-1), ECR 8 mg x kg(-1) and nimodipine 7.2 mg x kg(-1)) took shorter latency and searching distance, especially the ECR 8 mg kg(-1) group (P < 0.01). At the same time, after the 5 days training, there was a higher expression of c-fos in hippocampus and cortex from the rats in control group than that in model group (P < 0.01), but in the treated group, there was a relatively higher expression of c-fos, especially the ECR 8 mg x kg(-1) group (P < 0.01).

CONCLUSIONMicroinjection of beta-AP25-35 into the rat hippocampus resulted in dysfunction of learning and memory. Ecdysterone was shown to improve the learning and memory of the rats and increase the expression of c-fos. Increasing the expression of c-fos is probably one of the most molecular mechanism of its protection.

Amyloid beta-Peptides ; antagonists & inhibitors ; toxicity ; Animals ; Ecdysterone ; pharmacology ; Gene Expression ; Genes, fos ; Hippocampus ; metabolism ; Male ; Maze Learning ; drug effects ; Microinjections ; Peptide Fragments ; antagonists & inhibitors ; toxicity ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo compare the therapeutic effect of Compound Recipe Gengniankang ( GNK) with that of hormone replacement treatment (HRT) on climacteric female rats with osteoporosis, and to investigate the roles of estrogen and estrogen receptors in the mechanism of osteoporosis.

METHODSClimacteric female rats with osteoporosis were chosen and divided into three groups (GNK group, HRT group and control group). Apoptosis of ovarian granulose cells was measured by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) assay. Serum level of estradiol (E(2)), follicle stimulating hormone (FSH), luteinizing hormone (LH) were determined by the method of radioimmunoassay (RIA). Reverse transcriptase polymerase chain reaction (RT-PCT) technology was used to evaluate the expression of estrogen receptor (ER) in bone. Bone mineral density (BMD) was measured by double energy X-ray absorption (DEXA).

RESULTSIn the climacteric rats, BMD, serum E(2), ER mRNA expression in bone decreased remarkably, and serum FSH, LH and apoptosis of ovarian granulose cells increased obviously. After treating with GNK, all the indexes were reversed except serum E(2). The increase of E(2) was not significant.

CONCLUSIONGNK is effective on climacteric osteoporosis female rats. Its role is performed not by increasing serum E(2) but by enhancing ER in the bone and inhibiting apoptosis of ovarian granulose cells. GNK can deter further exhaustion of ovarian function.

Age Factors ; Animals ; Apoptosis ; Bone Density ; drug effects ; Bone and Bones ; drug effects ; metabolism ; Climacteric ; Drugs, Chinese Herbal ; pharmacology ; Estradiol ; blood ; Female ; Follicle Stimulating Hormone ; blood ; Hormone Replacement Therapy ; Hormones ; blood ; Luteinizing Hormone ; blood ; Osteoporosis ; metabolism ; Ovary ; drug effects ; physiology ; Rats ; Receptors, Estrogen ; biosynthesis

OBJECTIVETo investigate the distribution of burn pathogens and their antibiotic resistance in a burn unit, so as to provide reference for clinical practice.

METHODSThree hundred and forty-eight burn patients hospitalized in our department were enrolled in this study. The pathogens isolated from the wounds, blood, venous catheter, sputum, urine, purulent discharge of wounds in these patients, and their antibiotic resistance were surveyed by retrospective analysis from Jan, 2001 to Dec, 2006.

RESULTSTotal-ly 464 strains were isolated, among which Gram negative (G-) bacilli accounted for 52.6%, Gram positive microorganisms (G+) accounted for 40.5%, and fungi accounted for 6.9%. The main pathogens were Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter species and Escherichia coli, among which Staphylococcus aureus (MRSA) was predominant (93.5%). MRSA was 100% resistant to levofloxacin, penicillium, oxacillin, and it was also resistant to other antibiotics except Vancomycin. The resistance rate of Pseudomonas aeruginosa to Cefoperazone/Sulbactam, Imipenem and cefepime were 15.8%, 36.8%, 33.3%, respectively.

CONCLUSIONStaphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter species and Escherichia coli were predominant in the burn unit,among them Staphylococcus aureus and Acinetobacter were more resistant to antibiotics.

Acinetobacter baumannii ; drug effects ; isolation & purification ; Burn Units ; Burns ; microbiology ; Cross Infection ; microbiology ; Drug Resistance, Bacterial ; Escherichia coli ; drug effects ; isolation & purification ; Humans ; Pseudomonas aeruginosa ; drug effects ; isolation & purification ; Retrospective Studies ; Staphylococcus aureus ; drug effects ; isolation & purification

OBJECTIVETo investigate hereditary susceptibility to coronary heart disease (CHD) in apolipoprotein E(apo E) and apo B polymorphisms of youths.

METHODSPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to analyze apoE, apoB Xba I, apoB 3' variable number of tandem repeat (VNTR) genotypes for 244 healthy Han students (among them were 109 students with positive CHD family history).

RESULTSThe allele frequencies of apo e4, XbaI x(+), 3'VNTR-B(hypervariable element, HVE>38) in the positive group were obviously higher than those in the negative group(P<0.05), and were significantly correlated with the increase in TC, LDL-C, apoB100 levels (P<0.05).

CONCLUSIONThe alleles for apo e4, XbaI x(+), 3'VNTR-B may be the important genetic markers of Han CHD.

Adolescent ; Alleles ; Apolipoproteins B ; genetics ; Apolipoproteins E ; genetics ; Coronary Disease ; genetics ; Female ; Gene Frequency ; Humans ; Male ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Young Adult

OBJECTIVETo observe the effects of local co-transfection vascular endothelial growth factor165 (VEGF165) and tissue-type plasminogen activator genes on inhibiting intimal hyperplasia and restenosis in rabbits artery after operation injury and possible mechanisms.

METHODSMicrology operation injury was used to establish the model of intimal injury of right external iliac artery in rabbits. To select 120 male New Zealand rabbits and were randomly divided into 3 groups (n = 40, in each group): Group A (physiological brine control group), Group B (pBudCE4.1 group), Group C (pBudCE4.1/VEGF165-tPA group). The vas-wall of micrology operation injury were infused respectively physiological brine, pBudCE4.1 and pBudCE4.1/VEGF165-tPA transfection solution by micro-injector. Each group were divided into 5 subgroups (n = 8, in each subgroup) randomly according to the sacrifice times (2 d, 1 week, 2 week, 4 week and 8 week after operation). The injured vascular specimen were harvested for pathology test, electric microscopy study, reverse transcription-PCR examining and immunochemistry detecting.

RESULTSThe intimal area and narrow ratio of vases in Group C at every time point after operation were significantly lessened than that in Group A and Group B (P < 0.01). The narrow ratio of vases in Group C at 8 week after operation were decreased respectively by 57.9% and 59.0% than that in Group A and B. The expression of VEGF165 mRNA in Group C were increased significantly than that in Group A and B at every time point after operation (P < 0.01), the expression reached the peak at 1 week and continued to 4 week after operation. Immunohistochemical identified that tPA positive cell in Group C were significantly increased than that in Group A and B (P < 0.01) at every time point after operation.

CONCLUSIONLocal co-transfection VEGF165 and tPA genes could restrain intimal hyperplasia and restenosis of vas, which lay a foundation for future multi-gene therapy of vascular intimal hyperplasia.

Animals ; Arteries ; pathology ; Endothelial Cells ; cytology ; Hyperplasia ; prevention & control ; In Vitro Techniques ; Male ; Myocytes, Smooth Muscle ; cytology ; Plasmids ; Rabbits ; Random Allocation ; Tissue Plasminogen Activator ; biosynthesis ; genetics ; Transfection ; Tunica Intima ; pathology ; Vascular Endothelial Growth Factor A ; biosynthesis ; genetics

OBJECTIVEIt was reported previously that genistein could inhibit proliferation of human ovarian carcinoma cell line SKOV(3), but mechanism was not clear. There is a close relationship between EGFR mediated signal transduction pathway and the development of ovarian tumor. This study aimed to investigate the effects of genistein on the EGFR mediated signal transduction pathway and to clarify its mechanisms of proliferation inhibition on human ovarian carcinoma cell line SKOV(3) and its xenograft in nude mice.

METHODSThe expression of c-erbB-2 protein was determined using immunocytochemistry. The expressions of c-jun and c-fos protein were determined using Western blotting. The expression of c-erbB-2, c-raf-1, c-jun and c-fos mRNA were tested by reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSThe expression of c-erbB-2, c-raf-1 and its downstream gene c-jun and c-fos were decreased at mRNA level in the 20 micromol/L genistein group. The expression of c-erbB-2 protein were decreased, its average absorbency (A) were decreased after treatment of SKOV(3) with 20 micromol/L genistein for 48 h, reached at 0.42 +/- 0.02 (P < 0.05). Western blotting demonstrated that the expressions of c-jun and c-fos protein were decreased gradually after being treated with 20 micromol/L genistein for 12 - 72 h.

CONCLUSIONSGenistein could down-regulate the expression of two key genes, c-erbB-2 and c-raf-1 at mRNA and protein level in the EGFR mediated signal transduction pathway, and down-regulate the expression of its downstream nuclear transcription factors c-jun and c-fos at mRNA and protein level. It is suggested that interfering the expressions of some key signal molecules in EGFR mediated signal transduction system by genistein may account for its molecular foundation of proliferation inhibition in ovarian carcinoma.

Animals ; Antineoplastic Agents ; pharmacology ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Genes, fos ; Genes, jun ; Genistein ; pharmacology ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Ovarian Neoplasms ; metabolism ; pathology ; Proto-Oncogene Proteins c-fos ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-jun ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-raf ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Receptor, Epidermal Growth Factor ; metabolism ; Receptor, ErbB-2 ; biosynthesis ; genetics ; Signal Transduction ; drug effects