Objective:To observe the difference of results of treadmill exercise test (TET) between male smokers and non-smokers .Methods:A total of 200 men with long-term smoking ≥20 cigarette per day were screened from outpatients and treated as smoking group .Another 200 men with similar age ,who didn’ t smoke at all ,were regarded as non-smoking control group (control group) .There were no medical history for hypertension ,hyperlipidemia ,diabetes ,and were nega-tive for electrocardiography and color echocardiography (exclude left ventricular hypertrophy etc .organic heart disease) in two groups .TET results and incidence rate of acute myocardial infarction (AMI) within two years were compared between two groups .Results:Compared with control group ,there were significant rise in TET positive rate (37. 5% vs .57. 5% , P<0.001) and incidence rate of AMI (8.5% vs .17.5% ,P=0.007) within two years in smoking group .Conclusion:Risk of suffering from coronary artery disease is more high in smokers among men .

OBJECTIVE To explore the infection rate with identifying test of vancomycin-resistant enterococci(VRE) from clinical samples,that is 3.7 percent and to genotype VRE. METHODS vanA,vanB and vanC were detected by PCR in six isolates of VRE which were identified by the broth microdilution susceptibility test and Etest.The one of vanB was further analyzed with DNA sequence and ermB,qacE△1-sul1 gentypes were detected. RESULTS Seventeen isolates of enterococci(MIC≥4 ?g/ml) were obtained of 160 isolates of enterococci which came from Jiangxi Children′s Hospital by microdilution methods.while 6 isolates were gotten by Etest.It demonstrated that susceptibilities of VRE were different in four in vitro susceptibility testing methods.VRE showed resistance to erythromycin(10/17),disinfectant/sulfanilamide(0/17). CONCLUSIONS VRE screening test and the determination of MIC are reliable in finding VRE.VRE genotype is valuable on further research and epidemiological survey of our province.

Brain Diseases ; etiology ; therapy ; Heat Stroke ; complications ; therapy ; Humans ; Hyperbaric Oxygenation ; Male ; Middle Aged ; Occupational Diseases ; complications ; therapy

ObjectiveTo determine whether the inhibition of caveolin-1 tyrosine residues 14 (Cav-1-Y14) phosphorylation with protein tyrosine kinase inhibitors (PP2) will upregulate heme oxygenase-1 (HO-1) activity to protect against ventilation induced lung injury in vivo of an animal model.Methods Fifty-four male Sprague-Dawley (SD) rats were randomly divided into nine groups (eachn = 6). Group A served as normal control group, in which rats did not receive ventilation but tracheotomy. Groups B1 and B2 received lung protective ventilation respectively for 1 hour or 2 hours. Groups C1 and C2 received high tidal volume (40 mL/kg) ventilation for 1 hour or 2 hours, respectively. The group D1 or D2 also received high tidal volume ventilation for 1 hour or 2 hour respectively, but they were given PP2 1 hour before high tidal volume ventilation. The groups E1 and E2 also received high tidal volume ventilation respectively for 1 hour or 2 hours, but tyrosine kinase inhibitor PP2 and HO-1 inhibitor zinc protoporphyrinⅨ(ZnPPⅨ) were given to animals 18 hours before high tidal volume ventilation. All the animals were sacrificed after ventilation, and the specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Then the changes in pathology of lung tissue was observed, and diffuse alveolar damage scores (DAD) were calculated, myeloperoxidase (MPO) activity was measured by colorimetric analysis, lung wet/dry ratio (W/D) was estimated. The expressions of phosphorylated caveolin-1 (P-Cav-1-Y14), caveolin-1 (Cav-1) and HO-1 were determined by Western Blot. The expressions of high mobility group B1 (HMGB1) and advanced glycation end product receptor (RAGE) in lung tissues were assayed with immunohistochemistry staining. The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA).Results There was no significant difference in all the parameters between group A and groups B. Compared with group B1, DAD score, W/D ratio, the activity of MPO and the concentration of TNF-α in BALF in group C1 were significantly increased [DAD score:7.97±0.59 vs. 0.55±0.13, W/D ratio: 5.70±1.61 vs. 5.04±0.63, MPO (U/g): 1.82±0.14 vs. 0.77±0.26, TNF-α(ng/L): 370.10±29.61 vs. 54.38±8.18, allP< 0.05], and the injury in ventilation 2 hours group was more serious than that in ventilation 1 hour group. Compared with groups C, all the parameters in groups D were significantly decreased. The parameters in groups E were significantly higher than those in groups A, B, and D, but no significant difference was found as compared with groups C. Compared with groups B, the protein expressions of Cav-1 and P-Cav-1-Y14 (gray value) in groups C were significantly increased (1 hour: 1.49±0.02 vs. 1.26±0.13, 1.34±0.02 vs. 0.87±0.04;2 hours: 1.58±0.02 vs. 1.27±0.27, 1.31±0.01 vs. 0.95±0.02, allP< 0.05), and the expression of HO-1 protein (gray value) was significantly decreased (1 hour: 0.59±0.02 vs. 1.10±0.01, 2 hours: 0.49±0.01 vs. 1.20±0.02, both P< 0.05). No significant difference in Cav-1 protein expression between groups D as well as groups E and groups C. The protein expression of P-Cav-1-Y14 in groups D and E was significantly lower than that in groups C. The protein expression of HO-1 in groups D was significantly higher than that in groups C, but the phenomenon was not found in groups E as compared with groups C. Compared with group A, the positive expression of HMGB1 and RAGE in lung tissue in groups C and E was significantly increased, but no significant difference was found between groups B as well as groups D and group A.Conclusion Cav-1-Y14 phosphorylation is the key factor for ventilator induced lung injury, which can not only lead to a decrease in vascular barrier function, but also inhibit the activity of HO-1 enzyme, thus further aggravates inflammatory injury of the lung as induced by mechanical ventilation.

Objective To investigate whether the inhibition of caveolin-1 (Cav-1) phosphorylation will regulate effectively nuclear factor-erythroid 2-related factor (Nrf2) signal pathway and downstream effector molecules and protest against ventilation induced lung injury (VILI) in an animal model in vivo. Methods Ninety male Sprague-Dawley (SD) rats were randomly divided into nine groups (each n = 10): sham group in which rats did not receive ventilation but received tracheotomy; lung protective ventilation (PV) for 1 hour or 2 hours group; mechanical ventilation (MV) at high volume tidal (VT, 40 mL/kg) for 1 hour or 2 hours group; protein tyrosine kinase inhibitor PP2 or rosiglitazone (Rsg) pretreatment + high VT ventilation for 1 hour or 2 hours groups. The two pretreatment groups were given intraperitoneal injection PP2 15 mg/kg or intragastric administration of Rsg 5 mg/kg 1 hour before ventilation respectively. The rats were sacrificed after model reproduction, and bronchoalveolar lavage fluid (BALF) was collected. Pulmonary vascular permeability was measured by Evans blue (EB). The levels of tumor necrosis factor-α (TNF-α), activator protein-1 (AP-1), nuclear factor-κB (NF-κB), and interleukin-8 (IL-8) in BALF were determined by enzyme linked immunosorbent assay (ELISA). Then the lung tissues were collected, the lung wet/dry ratio (W/D) was calculated, the changes in pathology was observed with light microscope, and myeloperoxidase (MPO) activity was determined by colorimetric analysis. Nrf2 mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of Cav-1 tyrosine residues 14 phosphorylation (pCav-1-Y14), Cav-1, peroxisome proliferators-activated receptor γ (PPARγ) and claudin-5 as well as Nrf2 in cytoplasm and nucleus were determined by Western Blot. The positive expressions of PPARγ and claudin-5 in lung tissues were assayed with immunohistochemistry staining. Results There were no obvious pathological changes in the lung tissue in sham group and PV groups, and there were no significant differences in all the parameters between the two groups either. However, the injury in lung tissue was severe in the high VT groups in which W/D ratio, EB contents, MPO activity, and TNF-α, AP-1, IL-8, NF-κB levels in BALF as well as the protein expressions of Cav-1 and pCav-1-Y14 were significantly higher than those of sham group and PV groups, and the protein expressions of PPARγ and claudin-5 were significant lower than those of sham group and PV groups with a dose-dependent manner; but Nrf2 expressions in cytoplasm and nucleus did not show a statistical increase. After pretreatment of PP2 or Rsg, W/D ratio, MPO activity, EB contents, TNF-α, AP-1, IL-8, and NF-κB in BALF were significantly decreased as compared with those of high VT group, and RT-PCR showed significant up-regulation of Nrf2 mRNA in lung tissues too. Moreover, there was a statistically significant increase in expressed Nrf2 proteins in nucleus in PP2 or Rsg groups as compared with those of high VT groups [Nrf2 in nucleus (gray value): 0.61±0.06, 0.56±0.06 vs. 0.31±0.02 at 1 hour, 0.38±0.06, 0.43±0.07 vs. 0.22±0.03 at 2 hours; all P < 0.05], but no significant difference was found in the expression of Nrf2 protein in the cytoplasm among all groups. The protein expressions of pCav-1-Y14 in PP2 pretreatment groups were significantly lower than those of high VT groups (gray value: 0.89±0.04 vs. 1.48±0.02 at 1 hour, 0.86±0.02 vs. 1.31±0.01 at 2 hours; both P < 0.05); but expressed PPARγ proteins and expressed claudin-5 proteins in PP2 or Rsg pretreatment groups were significantly higher than those of high VT groups [PPARγ (gray value): 0.34±0.07, 0.42±0.13 vs. 0.17±0.07 at 1 hour, 0.38±0.09, 0.33±0.07 vs. 0.16±0.03 at 2 hours; claudin-5 (gray value): 0.33±0.05, 0.38±0.07 vs. 0.14±0.03 at 1 hour; 0.30±0.06, 0.31±0.04 vs. 0.17±0.04 at 2 hours; all P < 0.05]. Conclusions The inhibition of Cav-1-Y14 phosphorylation can increase the expression of Nrf2 in the nucleus, then result in an increase in the protein expressions of PPARγ and claudin-5 of its effector molecules. This effect can reduce the inflammation and capillary permeability of lung tissue in the model of VILI.

Objective CD4+ T lymphocytes have been shown to play an important role in the pathogenesis of systemic lupus erythematosus (SLE). To identify the commonly accumulated T cell clones and to investigate its role in murine lupus models, it was analyzed that the T cell clonality infiltrating in different tissues derived from (NZB?NZW)F1 as well as MRL/lpr mice. Methods The expressions of T cell receptor (TCR) V? gene were analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) combined with single-strand conformation polymorphism (SSCP) study. The phenotype of T cells expanded in different organs was determined by magnetic cell sorting (MACS). Results RT-PCR and SSCP study of TCR V? chain demonstrated that there were some identical T cell clonotypes expanded and accumulated in different organs in aged diseased mice. Most of these identical clonotypes were CD4+ T cells in both of the two strains. In contrast, young mice exhibited little accumulation of common clone in different organs. The TCR V? usage of these identical clonotypes was limited in V?2, V?6, V?8.1, V?10, V?16, V?18 in MRL/lpr mice and V?6, V?7 in (NZB?NZW)F1 mice respectively. Conclusion The results suggest that activated and clonally expanded CD4+ T cells commonly accumulated in different tissues in aged murine lupus models. These CD4+ T cell clonotypes may be involved in specific immune responses of SLE, thus playing a pathogenic role in these lupus mice.

Objective There were some identical T cell clonotypes expanded and accumulated in different organs in aged diseased (NZB?NZW)F1 and MRL/lpr mice. The amino acid motifs in the third complementarity determining region (CDR3) from the T cell receptor (TCR) V? chain was analyzed to demonstrate the antigenic specificity of these identical clones. Methods The TCR V?6 gene in kidneys and brains from different individuals of aged diseased lupus mice were amplified by reverse transcriptase polymerase chain reaction (RT-PCR) respectively. The amino acid motifs in CDR3 loops of TCR V?6 chain were demonstrated by DNA cloning and DNA sequence analysis. The amino acid motifs from the identical T cell clones accumulated in different organs were identified by single-strand conformation polymorphism (SSCP). Results Some conserved amino acid motifs such as isoleucine (I) and aspartic acid (D) were observed in CDR3 loops of TCR V?6 from these identical T cell clones in different individuals of aged diseased (NZB?NZW)F1 mice. Likewise, I, glycine (G) and D or glutamic acid (E) were also found in MRL/lpr mice. Conclusion These identical T cell clones may recognize restricted T cell epitopes on autoantigens and are involved in specific immune responses in SLE.

Objective To explore the risk factors for asthma in children.Methods A 1:1 matched and hospital-based case-control study was conducted to analyses risk factors for asthma in 300 pairs of children by logistic regression analysis. Results The result of univariate Logistic regression analysis showed that there were 17 related factors for children asthma, including disease history of parents in respiratory system,family income,atopie character,history of acute respiratory infections, eating habit,the amount of sea foods intakes,foam plastics,family decoration,the way of exhaust fume in kitchen,the exhaust effectiveness,raising pet in house,family history of asthma,family history of allergic rhinitis,family history of food allergy,dust allergy of parents,systemic therapy after the first attack.With multivariate Logistic regression analysis,7 factors were entered the model,6 risk factors including father's history of respiratory diseases(OR 3.771,95%CI 1.533～9.278),low family income(OR 1.503, 95%CI 1.258～1.795),atopy(OR 3.788,95%CI 2.368～6.058),meat-eating habit(OR 2.042,95%CI 1.481～2.815),asthma history of family members(OR 1.710,95%CI 0.988～2.958),the family history of allergic rhinitis(OR 1.991,95%CI 1.234～3.211), and 1 protective factor of raising pet in house(OR 0.443,95%CI 0.265～0.739).The coefficients of these factors in multivariate logistic regression model were 1.327、0.407、1.322、0.714、0.536、0.689、and-0.814 respectively.Conclusion Children asthma was a multi-factorial complex disease,and the interaction of environmental and genetic risk factors played an important role in the onset of this disease.

Objective To observe the effects of dexamethasone (DEX) therapy on the clinical outcome and changes of lymphocyte subsets in children with mild and severe encephalitis.Methods Eighty-two children with mild and severe viral encephalitis were randomly divided into two groups: with DEX treatment (n=46) or without(n=36).The clinical efficacy was evaluated 3 weeks later, and the clinical manifestation were also observed. The changes of CD4~+,CD8~+ T lymphocyte percentage were determined by flow cytometry on admission and at 1 week,4 weeks after treatment.Another group of 20 cases was enrolled as control group.Results Compared with the control group,both the DEX treatment group and non-DEX treatment group showed a reduced CD4~+ lymphocyte count, an increased CD8~+ lymphocyte count(P

Objective To explore the risk factors in children with epilepsy and their effects on attack rate of epilepsy.Methods One hundred and sixty epilepsy patients(patient group,88 boys and 72 girls)and 150 healthy children(control group,72 boys and 78 girls)were selected.All children conformed epilepsy at the west China second hospital were consecutively included in the study for 6 months period.The range of age was from 1 month to 16 years[(7.0?4.7)years old] of patient group children.All children with epilepsy had no-causation seizure for more than twice time and were diagnosed by electroencephalogram.Neurologically normal children in same period,matched for age and sex,visiting the health care clinic were selected as controls.The range of age was from 2 month to 16 years [(6.3?4.5)years old] of control group children.The risk factors examined were febrile convulsions,head trauma,central nervous system infections,abnormal perinatal history,family history of epilepsy and parental consanguinity.The data of patients and controls were obtained from a questionnaire through personal interviews.Details on the patient,family history,and parental age at the time of childbirth were included.Medical records were then reviewed.According to the data type,the statistics were performed with ?2 test and the significance level was the P