OBJECTIVE To investigate the distribution and characteristics of drug-resistance of Staphylococcus aureus (SAU) causing lower respiratory infection, for rational using of antibiotics in clinical practice. METHODS A retrospective analysis on S. aureus isolates and their drug-resistance characteristics were carried out. These strains were isolated from lower respiratory specimens in clinical laboratory of Renmin Hospital of Wuhan University from Jan 2007 to Dec 2007. RESULTS Among 94 strains, 69 were meticillin-resistant S. aureus(MRSA), accounting for 73.40%. All MRSA strains were resistant to penicillin G, while sensitive to vancomycin and teicoplanin. Resistant rate to chloramphenicol was 7.24 %. The average resistance rate of MRSA to quinolones, macrolides and aminoglycosides were relatively high (56.52-98.55%). And resistant rate of MRSA was higher than the meticillin-sensitive S. aureus (MSSA) in average level. CONCLUSIONS Hospitals at all levels are proposed to strengthen drug resistance supervising so as to prevent the infection breaks.

Objective To study the expressive levels of galectin-3 (gal-3) and sambucus nigra agglutinin(SNA) and to detect their clinicopathological significances in benign and malignant lesions of the gallbladder. Methods EnVisonTM Immunohistochemistry for assaying gal-3 expressive levels and ABC cytochemistry for determining SNA expressive levels were used in conventional paraffin-embedded sections from the specimens of adenocarcinoma (n = 108) , peritumoral tissues (n=46) . Adenomatous polyp (n=15), and chronic cholecystitis (n = 35). Results The positive rates of gal-3 and SNA were significantly higher in adenocarcinoma (62. 0%, 66. 7%) than in peritumoral tissues (39. 1%,45.6%), adenomatous polyp (26.7%, 33.3%) and chronic cholecystitis (11.4%, 11.4%)(P<0. 05 or P<0. 01). The positive gal-3 and SNA in benign cases showed atypical hyperplasia of the epthelium. The positive rates of gal-3 and SNA expression were significantly lower in well-differentiated adenocarcioma, mass with a maximal diameter of <2 cm, absence of lymph node metastasis,and absence of invasion to adjacent tissues than in poor-differentiated adenocarcinoma, mass with a maximal diameter of ≥2 cm, lymph node metastasis and invasion to adjacent tissues. (P<0. 05 or P<0. 01). There was a significant correlation between the expressive levels of gal-3 and SNA in gallbladder adenocarcinoma (x2=9. 51, P<0. 01). Conclusions The expressive levels of gal-3 and SNA lectins had important effects on carcinogenesis, progression and biologic behaviors of gallbladder cancer. Patients with positive gal-3 and /or SNA expressions had poor prognosis.

ObjectiveTo study the expression of ABCG2, SFRP2, BRMS1 and HPA and detect their clinicopathologicalsignificancesinthebenignandmalignatntlesionsofthegallbladder.MethodsEnVisiom immunohistochemical method for determining the expressions of ABCG2, SFRP2,BRMS1 and HPA was used in paraffin-embedded sections of surgical resected specimens from gallbladder adenocarcinoma (n =108), peritumoral tissues (n =46 ), adenomatous polyp (n =15 ), and chronic cholecystitis ( n =35 ).ResultsThe positive rates of ABCG2 and HPA expression were significantly higher in gallbladder adenocarcinoma than that in peritumoral tissues, adenomatous polyp and chronic cholecystitis (P ＜ 0. 05 or P ＜ 0. 01 ) ; The positive rates of SFRP2 and BRMS1 expression were significantly lower in gallbladder adenocarcinoma than that in peritumoral tissues, adenomatous polyp and chronic cholecystitis(P ＜0. 05 or P ＜0. 01 ). The positive cases of ABCG2 and/or HPA as well as negative ones of SFRP2 and/or BRMS1in the benign lesions showed moderately-or severely-atypical hyperplasia of gallbladder epithelium. The frequency of samples with positive staining for ABCG2 and/or HPA in cases with small tumor volume (diameter ＜ 2 cm), no lymph node metastasis, and no invasion into surrounding tissues was significantly lower than that in cases with larger tumor volume (diameter＞ 2 cm ), lymph node metastasis, and invasion into surrounding tissues ( P ＜ 0.05 or P ＜ 0. 01 ). However, compared with ABCG2 and/or HPA, the expression of SFRP2 and/or BRMS1 showed an opposite correlation in these cases ( P ＜ 0. 05 or P ＜0. 01 ). Unitivariate Kaplan-Meier analysis showed that increased expressions of ABCG2 (P =0. 019) and HPA ( P =0. 016) or decreased expression of SFRP2 ( P =0. 019) and BRMS1 ( P =0. 008 )were associated with poorer overall survival, respectively. Multivariate Cox regression analysis showed that increased expression of ABCG2 (P =0. 018 ) and HPA ( P =0. 019) and/or decreased expression of SFRP2 (P =0. 015 ) and BRMS1 ( P =0. 011 ) were independently poor-prognostic predictors in gallbladder adenocarcinoma.ConclusionsThe expression of ABCG2, SFRP2, BRMS1 or HPA might be closely related to the carcinogenesis, clinical biological behaviors, and prognosis of gallbladder adenocarcinoma.

Objective To establish a model of pancreatic cancer induced by 7,12-dimethylbenzathracene (DMBA) in SD rats, and to detect the expression levels of RAD51 and Myc-associated factor X (MAX) and their effect on carcinogenesis of rat pancreas. Methods Ninety SD rats were randomly divided into 3 groups: a model group, an intervention group, and a control group. DMBA was directly implanted into the parenchyma of rat pancreas (the model group and the intervention group). Rats in the intervention group were treated with 1 mL trichostatin A (TSA) saline solution (1 μg/mL) via ip weekly. Rats within 3～5 months in the model group and the intervention group were executed and observed by macrograph and under microscope. Meanwhile, the rats in the control group were executed at 5th month. The EnVision~(TM) immunohistochemistry to assay the expression levels of RAD51 and MAX was used in conventional paraffin-embedded sections from the above pancreatic specimens.Results The incidence of pancreatic cancer in the model group within 3-5 months was 48.7% (18/37), including 17 ductal adenocarcinomas and 1 fibrosarcoma. The incidence of pancreatic cancer in the intervention group within 3-5 months was 33.3%(12/36), including 11 ductal adenocarcinomas and 1 fibrosarcoma. The maximal diameter of mass in the model group was significantly higher than that in the intervention group (P＜0.05). No pathological changes were found in pancreas of the control group and other extra-pancreatic main organs of the model group and the intervention group (such as the liver, biliary tract, gastrointestine tract, kidney, and lung). The positive rate of RAD51 was significantly higher in ductal adenocarcinoma in the model group, the intervention group, and the model group +the intervention group than those in corresponding groups of non-cancerous pancreatic tissues (P＜0.01), but the positive rate of MAX expression was opposite to RAD51 expression(P＜0.01). The positive tissues of RAD51 expression and/or negative tissues of MAX expression in non-cancerous tissues showed atypical-hyperplasia of ductal epitheli. Pacncreas of the control group showed the negative expression of RAD51 and positive expression of MAX. Two cases of fibrosarcoma showed the negative expression of RAD51 and MAX.Conclusion DMBA directly implanted into the parenchyma of pancreas can obtain an ideal pancreatic cancer model with high incidence in a short time. The TSA might have an inhibitive effect on carcinogenesis and growth of rat pancreas. The over-expression of RAD51 and/or lose-expression might have important effect on carcinogenesis induced DMBA in rat pancreas.

Objective To study the expressive levels of EZH2 and PTEN in pancreatic cancer and non-cancerous tissue,and the effects on carcinogenesis of rat pancreas.Methods dimethylbenzathracene(DMBA) was directly implanted into the parenchyma of rat pancreas(group A,group B).The rats of group B were treated with 1 mL trichostatin A(TSA) solution(1?g/mL) intravenously per weer 1 week after the model were set up.The rats of group A,B were killed within 3-5 months and the rats in the control(C group) were executed at 5 months to observe the develope of pancreatic cancer by macrograph and microscopy,The EnVisionTM immunohistochemistry was used to assay the expression of EZH2 and PTEN in above pancreatic specimens.Results(1) The incidence of pancreatic cancer within 3-5 months in group A was 48.7%(18/37),including 17 cases of ductal adenocarcinoma and 1 case of fibrosarcoma.The incidence of pancreatic cancer in group B was 33.3%(12/36),including 11 cases of ductal adenocarcinoma and 1 cases of fibrosarcoma.The mean maximal diameter of mass was significantly higher in group A than that in group B(P 0.05).The non-cancerous pancreatic tissues with positive expression of EZH2 and/or negative expression of PTEN showed mild to severe atypical hyperplasia of ductal epithelium.An inconsistency was found between the expression of EZH2 and PTEN in ductal adenocarcinoma(P =0.045).Pancreas of group C showed negative expression of EZH2 and positive expression of PTEN.Two cases of fibrosarcoma showed negative expression of EZH2 and PTEN.Conclusions By use of higher dose of DMBA directly implanted into the parenchyma of pancreas,high incidence of pancreatic cancer can be obtained.TSA could have an inhibitive effect on carcinogenesis and growth of pancratic cancer.The activation of EZH2 gene and inactivation of PTEN gene might have Key effects on pancreas carcinogenesis induced by DMBA in rat.

Wavelet transform(WT) is a powerful technique in signal separation and can improve the signal-to-noise ratio by separating the white noise and useful signal.The method in the paper introduces the concepts of Wavelet transform.According to the analysis of Wavelet coefficients between the noise and signal at different levels,the appropriate filter is realized.The patch clamp experiment results demonstrate the feasibility of the method.

The roles of NF-kappaB (NF-kappaB) expression, Bax activity and cytochrome C (Cyt C) release, apoptosis of islet cells induced by high concentration glucose were explored in vitro. Pancreatic islet cells, which were isolated from Kunming mice, were cultured with different concentrations of glucose in DMEM, and divided into the following groups: G1, G2, G3, G4, G5, and G6 groups, corresponding to the glucose concentrations of 5.6, 7.8, 11.1, 16.7, 22.5, and 27.6 mmol/L, respectively. After culture for 120 h, insulin secretion was evaluated by radioimmunoassay, and the NF-kappaB expression was detected by immunocytochemistry. Bax activity and Cyt C release were measured by immunofluorescence, and apoptosis was examined by Hoechst33342 assay. The results showed that in G1, G2 and G3 groups, insulin secretion was enhanced with the increase of glucose concentration, and the NF-kappaB expression was also increased (P<0.05), but Bax activity, Cyt C release and apoptosis rate showed no significant difference among them. However, in G4, G5, and G6 groups, apoptosis rate of islet cells, NF-kappaB expression, Bax activity, and Cyt C release were all significantly increased, and insulin secretion was impaired as compared with G1, G2, and G3 groups (P<0.05). It was concluded that the exposure of islet cells to high glucose could induce islet cells apoptosis as well as impaired insulin secretion. The NF-kappaB signaling pathway and mitochondria pathway in islet cells might play some roles in the progressive loss of islet cells in diabetes. The inhibition of the NF-kappaB expression could be an effective strategy for protecting pancreatic islet cells.

Objective To analyze and verify the expression profiles of long non-coding RNAs (lncRNAs) in gastric cancer (GC) metastatic lymphonodus.Methods Microarray analysis was performed in 3 GC positive lymphonodus and 1 normal lymph node with Agilent Array platform to measure the expression levels of lncRNAs and mRNAs and to investigate the expression differences of lncRNAs in GC metastatic lymphonodus and normal lymphonodus, and hierarchical clustering used to screen out the differently expressed lncRNAs.15 up-regulated lncRNAs and 15 down-regulated lncRNAs were randomly chosen and RT-PCR was used to verify the expression differences.Results Comparing with normal lymphonodus, 353 lncRNAs and 547 mRNAs are up-regulated, but 464 lncRNAs and 562 mRNAs are down-regulated in GC metastatic lymphanodus as 6 times or more variation was found.The expressions of lncRNA OR3A4, LOC84740, FCGR1C and C21orf 96 were increased in GC metastatic lymphonodus, but lncRNA MSTO2P, LOC344595, TUG1, TYW3 and KRT8P10 decreased.Conclusions LncRNAs are aberrantly expressed in GC metastatic lymphonodus.

Objective To observe hibernation phenomena of Oncomelanai hupensis and explore the way of inducing the hibernation in laboratory. \ Methods\ Snails, O\^hupensis hupensis, were collected from marshland of Jiangsu. The snail hibernation was induced by the way of cultivation at a mimic natural environment in the laboratory with gradually changing temperature. The amount of oxygen consumed by snails was tested by iodine titration, and their hibernation was tested by pin puncture followed by warm water. \ Results \ There was no significant difference on the rate of snail \{hibernation\} when the temperature was reduced by 1 ℃ per 24 hrs and by 1 ℃ per 48 hrs. The hibernation rate \{increased\} with the decreasing temperature. There was a significant regression relationship between hibernation rate and temperature with R\+2=0\^967 (F=207\^72, P

Objective To explore the aestivation and lethal hyperthermy temperature of Oncomelania hupensis in summer,which is one of important ecology indexes,in order to understand the potential impact of global warming on the distribution of Oncomelania snail in mainland China. Methods Oncomelania hupensis hupensis snails were collected from the marshland region in Jiangsu Province and the aestivation and lethal hyperthermy temperature were examined by increasing temperature gradually in laboratory. Results The lethal hyperthermy temperatures of 50% Oncomelamia snails in dry and wet environment was 40.01℃ ( 95% of confidence interval from 39.76-40.27℃) and 42.13℃( 95% of confidence interval from 41.59-42.68℃), respectively. The logistic regression equations between temperature and mortality were d=101/(1+e 61.402269-1.535058X) (F=69.997,P