OBJECTIVE To investigate the risk factors of postoperative nosocomial infection in esophageal cancer patients,and to provide evidences for controlling nosocomial infection.METHODS The data of 466 cases with esophageal cancer,from Jan 2002 to Dec 2005,were studied retrospectively.RESULTS The nosocomial infection rate of patients with esophageal cancer was 21.03%.The main locations of infection were operation incision,lower respiratory tract and thorax.The nosocomial infection rate had increasing trend as lengthening the hospitalization duration.CONCLUSIONS The nosocomial infection with esophageal cancer is related to age,hospitalization duration and postoperative time.To take measures for infective factors,for example,intraoperative aseptic operation,postoperative drainage tube unblocked and rational use of antibiotics,is important to control and decrease the nosocomial infection.

Multiple chromosomal aberrations, nucleotide substitutions, and epigenetic modifications may occur in human cancer cells, which drive malignant transformation. The Cancer Genome Atlas (TCGA) project aims to promote large-scale multi-dimensional analysis of these molecular characteristics in human cancer and rapidly provide data to researchers. In this study, we introduce four flow paths of the production of TCGA data, the collections of various cancer types, the data category and level, and the standardized pipeline of data analysis, as well as several existing data analytical tools. We used ovarian cancer as an example to introduce the application of the TCGA data in the analyses of mutation, copy number, analysis, and expression. We summarized the important findings of glioblasto-ma by TCGA teams.

Aim To study the effects of pyrrolidine dithiocarbamate(PDTC) on matrix metalloproteinase-9(MMP-9) expression in alveolar macrophages(AM) induced by TNF-?,and then to explore it's signal pathway.Methods AM were collected from bronchoalveolar lavage fluid in patients with chronic obstructive pulmonary disease.AM were pretreated with PDTC and then stimulated by TNF-? or IL-1.MMP-9 mRNA expression was detected by semi-quantitative reverse transcription-polymerase chain reaction and MMP-9 protein expression was detected by Western blot.Phospho-I?B? protein levels induced by TNF-? or IL-1 were detected by Western blot.NF-?B activity was detected by electrophoretic mobility shift assay.Results Both the mRNA and protein levels of MMP-9 induced by TNF-? in AM were significantly elevated in a dose dependent manner(P0.05).PDTC had distinct effect of inhibiting the activation of NF-?B induced by TNF-? or IL-1 in a dose-dependent manner(P0.05).Conclusions NF-?B plays an important role in MMP-9 expression induced by TNF-? in AM;PDTC can down-regulate MMP-9 expression induced by TNF? in AM possibly through preventing the degradation of I?B? via ubiquitylation-proteasome proteolytic pathway.

OBJECTIVE To observe bacterial distribution in urinary infection and trend of drug resistance in Shangdong Province.METHODS The patients with urinary infection monitored by Shandong Provincial Nosocomial Infection Surveillance System from Aug 2001 to Jul 2005 were analyzed and summarized.RESULTS Among 933 isolates,524 strains(56.16%) were Gram-negative bacilli,214(22.94%) were Gram-positive cocci and 195(20.90%) fungi.The most common pathogens were Escherichia coli(311),Candida albicans(74),and Enterococcus spp(62).Most of them were multidrug resistant.Most strains of Gram-negative bacilli were highly susceptible to imipenem,while most strains of Gram-positive cocci were highly susceptible to vancomycin.CONCLUSIONS Resistance detection of bacteria periodically has an important significance to clinical treatment with drugs.

Objective Chronic persistent infection following hydrophilic polyacrylamide gel (HPG) injection is one of serious complications in augmentation mammaplasty.It was to search for a perfect treatment for the infection.MethodsA total of 126 patients who accepted HPG injection appeared serious chronic infections.Operation was performed to cut out the HPG and necrotic tissues.The cavities were repeatly washed with negative pressure drainage to control the infection.ResultsAll the symptoms were relieved one to 3 weeks after the treatments in 126 cases.The examination showed that no visible HPG and infection remained in the cavity.No defects existed in the breast and chest wall.ConclusionsFor this infection,the best therapy is to remove the pathologic tissue by surgery and to efficiently control the infection with medication.

AIM:To evaluate the role of inhaling N 6-phenyl-2R-isopropyl-adenosine (R-PIA) on the airway resistance and pulmonary compliance of experimental asthmatic guinea-pigs. METHODS: Experimental model of asthmatic guinea-pigs were made. Inhaling R-PIA 5 mg/mL( 5 mg R-PIA in 1 mL 0.9% saline). The airway resistance, pulmonary compliance and NO- x, cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP),tumor necrosis factor (TNF) in bronchoalveolar lavage fluid (BALF) were observed. RESULTS: Compared with asthma group, after inhaling R-PIA, the airway resistance of experimental asthmatic guinea-pigs increased ( P 0 05). CONCLUSION: Inhaling R-PIA could constrict the airway of experimental asthmatic guinea-pigs.

Objective To explore the features of the airway inflammation in a rat model of chronic bronchitis and study the role of IL-8 in the pathogenesis of chronic bronchitis. Methods The rat model of chronic bronchitis was set up by injecting LPS into trachea. Cell count and cytological classification in BALF were performed in experimental group and control group. The level of IL-8 in both serum and lung tissues of the two groups rats was measured by ELISA. Results The levels of IL-8 in both serum and lung tissues in the rats with chronic bronchitis were significantly higher than those in healthy control rats.The number of neutrophil in BALF of the rats with chronic bronchitis was significantly more than that in healthy control rats. Conclusion Both IL-8 and neutrophil were involved in airway inflammation of chronic bronchitis, and might play an important role in the pathogenesis of chronic bronchitis.

AIM: To investigate the amiloride-sensitive Na~+ channel current (Iamil) in primary cultured human bronchial epithelium cells of chronic obstructive pulmonary disease (COPD) patients and the influence of interleukin 4 and interleukin 6. METHODS: Human bronchial epithelium cells were isolated and cultured from 18 patients undergone pueumonectomy in hospital. Interleukin 4 or interleukin 6 at concentration of 10 ?g/L was used to treat these cultured cells, and Iamil was measured by whole cell patch clamp techniques. RESULTS: There was no markedly difference among normal no-smoking group, normal smoking group and COPD group. Interleukin 4 down-regulated the Iamil in normal no-smoking group, normal smoking group and COPD group. The down-regulated percentages were 59.7%, 54.7% and 30.0%. Interleukin 4 down-regulated the Iamil in normal no-smoking group (44.8%) and normal smoking group (34.9%) but not in COPD group, and the current forms were not changed after IL-4 or IL-6 treatment. CONCLUSIONS: Interleukin 4 and interleukin 6 down-regulated the Iamil in primary cultured human bronchial epithelium cells. It may contribute to the hypersecretion of COPD, and the up-regulated interleukin 4 and interleukin 6 in COPD patients may cause them react weaker to the treatment of interleukin 4 and interleukin 6.

AIM: To study the effect of cigarette smoke extract (CSE) on adhesion and migration of human airway epithelial cells and it's mechanism. METHODS: After 24 h culture, the airway epithelial cells were treated with different concentrations of CSE. The rate of cell attachment and the velocity of cell migration were measured. The expression of FIP200 mRNA and protein were analyzed by RT-PCR and Western blotting. RESULTS: CSE inhibited the rate of cell attachment and the velocity of cell migration. Meanwhile CSE increased the expression level of FIP200 mRNA and FIP200 protein. The effects of CSE became more evident with increased concentration of CSE. Expression of FIP200 mRNA and FIP200 protein were positively correlated to the decreased rate of cell attachment and the velocity of cell migration. CONCLUSION: CSE inhibits the rate of cell attachment, the velocity of cell migration and increases the expression of FIP200.

AIM: To study the role of adrenomedullin(AM) in the pathogenesis of hypoxic pulmonary hypertension. METHODS: Rats were exposed to chronic hypoxia for 14 days. After the measurement of the right ventricular systolic pressure (RVSP), the rats were executed. The weight of the right ventricle (RV), the left ventricle(LV) and the ventricular septum(SP) were determined. The ration RV/(LV+SP) was used to express the thickness of RV. In situ hybridization was used for the detection of the expression of AM mRNA in the lung and RV. RESULTS: The RVSP in the hypoxic group was (63.63?3.42) mmHg,which was significantly higher than that in control group [(34.13?3.40) mmHg]. The RV/(LV+SP) in hypoxic group was 0.439?0.039,which was increased obviously when compared with that of control (0.230?0.025). The level of AM mRNA expressed in the RV in the hypoxia group was significantly higher than that in the control group. CONCLUSION: The expression of AM mRNA in RV increased in the hypoxic condition, which suggests that AM may attenuate the inappropriate increase in pulmonary artery pressure.