Objective To understand the species,clinical distribution features and drug susceptibility situation of bloodstream infection pathogenic bacteria in this hospital to provide reference for clinical empirical treatment.Methods The retrospective analysis was performed on 1 938 strains of pathogenic bacteria isolated from blood culture in our hospital from January 2012 to August 2016,their species distribution,department distribution and drug sensitivity were analyzed.Results A total of 1 938 strain of bacteria were comprised of 56 kinds of bacteria and 8 kinds of fungi.Gram-negative bacteria had 1 216 strains,accounting for 64.2%,Gram-positive bacteria had 677 strains,accounting for 34.9%,Fungi had 45 strains,accounting for 2.4%.The top 5 of isolation rates were Escherichia coli(628 strains,32.4%),Klebsiella pneumoniae(230 strains,11.9%),Salmonella(143 strains,7.4%),Staphylococcus epidermidis(142 strains,7.3%) and Staphylococcus hominis (130 strains,6.7%).Enterobacteriaceae bacteria had 1 098 strains(58.0%),which was dominated by Escherichia coli and Klebsiella pneumoniae,in which 363 strains(57.8%) were Escherichia coli and 85 strains(37.0%) were extended spectrum β lactamases (ESBLs) producing Klebsiella pneumoniae.Nonfermenters had 118 strains(6.1%),Acinetobacter baumannii and Pseudomonas aeruginosa were predominant.Staphylococcus aureus had 75 strains (3.9%),the MRSA occurrence rate was 25.3%,coagulase-negative staphylococci (CoNS) had 401 strains (20.7%),the methicillin-resistant CoNS occurrence rate was 72.8%.Enterococcus had 85 strains(4.5%).The top 5 departments in positive rates were respiratory department,ICU,hepatobiliary department,gastroenterology department and hematology department.The other departments were consistent to the overall distribution except for ICU and pediatrics.The majority of Acinetobacter baumannii showed multi-drug resistant.Vancomycin-resistant Staphylococcus and Enterococcus did not be detected,Candida maintained good sensitivity to commonly used antifungal agents.Conclusion Bloodstream infection pathogenic bacteria in this hospital are widely distributed.Commonly used drug have different sensitivities,the overall drug resistance rate is higher,clinic may conduct early medication according to the pathogenic bacterial department distribution and drug sensitivity.

This paper deals with the analysis and discussion on how to harmonize the following three relations respectively between general objective and concrete objective, pertinence and systematicness as well as political nature and actualization in ideological and political theory education and teaching in higher institutions.

AIM To study the changes of IgE, IL-4 and IFN-y in serum and pulmonary tissue homogenate of asthmatic guinea pigs and the effects of scoparone on them. METHODS To divide animals into three groups: control, asthma and scoparone treatment groups. Choose the model guinea pigs of asthma sensitized with OA, and observe the changes of IgE, IL-4 and IFN-r in serum and pulmonary tissue homogenate of asthmatic guinea pigs and the effects of scoparone on them by means of chemolumi nescence, radio immunoassay, enzyme-linked immunoabsordent assay. RESULTS IgE and IL-4 in serum and pulmonary tissue homoge-nate of asthmatic guinea pigs obviously increase (P

Possessing ideological qualities is a gradual process. We should establish a multiplex, synthetical and entire assessment system for the ideological and political theory course exams in medical colleges. The innovation of exam mode can promote the diversification of teaching style.

Objective To investigate the mRNA and protein expression of GPX3 gene in non-small cell lung cancer (NSCLC) patients, and then discuss the clinical significance of GPX3 in NSCLC patients. Methods Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to detect the GPX3 mRNA and protein levels in NSCLC tissues and adjacent non-cancerous normal lung tissues from 60 patients undergoing surgical treatment. The correlation between the expression levels of GPX3 and clinicopathological features was analyzed. Results The relative expression value of GPX3 mRNA was higher in adjacent non-cancerous tissues than in non-small cell lung cancer tissue (P < 0.05). GPX3 mRNA expression was significantly correlated with TNM stage、differentiation and lymph node metastasis. The integral optical density value of GPX3 protein confirmed was lower in adjacent non-cancerous tissues than in non-small cell lung cancer tissues (P < 0.05). In additional, the expression of GPX3 was related to TNM stage and lymph node metastasis. Conclusion The expression of GPX3 gene may play an important role in the carcinogenesis and progression of NSCLC.

Objective To explore the effect of the DNA methyltransferase 5-aza-2'-deoxycytidine (5-aza-CdR)on human esophageal squamous cancer Ecal09 cells.nethods Human esophageal squamous cell cancer(ESCC)Eca109 cells were treated by 5-aza-CdR with 10-7,10-6,1O-5,10-4,0 mol/L. Respectively.Consequently,the growth rate of the cells was detected by MTT assay and morphological structure Was observed.Meanwhile,cell apoptosis and cell cycle were analyzed by flow cytometry method. (FCM).ResulIs The proliferation of Eea109 cells Was inhibited by 5-aza-CdR from 10-7 to 10-4 mol/L Moreover,the inhibition rate showed time-and-concentration-dependent manner(24～96 h,F=160.06,P=0.000,10-7～10-4 mol/L,F:60.95,P:0.000).The maximum rate of inhibitory was reached up to(15.70±0.75)% in the group treated by 10-4 mol/L 5-aza-CdR after 96 hours.An apoptosis peak appeared before diploid peak.The proportion of Go/G1 phase cells Was significantly increased(F=6479.46, P=0.000),especially up to(89.70±0.91)% in the group treated by 10-4 mo/L 5-aza-CdR after 96 h. However,the proportion of S phase cells Was obviously decreased(F=4222.26,P=0.000),especially down to(9.10±0.48)% in the group treated bv 10-4mol/L 5-aza-CdR after 96 h.Conclusions The proliferation of Eca109 cells is inhibited bv 5-aza-CdR in a time-and-concentration-dependent manner.Moreover,the 5-aza-CdR can inhibit cell growth by regulation of DNA cycle and apoptosis.

Objective To understand the clinical distribution characteristics of Acinetobacter baumannii in our hospital and the change situation of drug resistance rates to provide a basis for the clinical rational drug use and the nosocomial infection manage-ment.Methods The Acinetobacter baumannii strains isolated in our hospital from January 2005 to December 2013 were performed the retrospective analysis on its department distribution,specimen distribution and change of drug resistance rates.Results 964 strains of Acinetobacter baumannii were isolated during these 9 years,in which 713 strains were multi-drug resistant.The isolated strains were less during 2005 -2008,which were 30,26,22,19 strains respectively.The isolated strains began to increase during 2009-2010,which were 65,50 strains respectively.The detection rate began to enormously increase from 2011,which were 157, 229,366 strains respectively from 2011 to 2013.The top three departments of the highest isolation rates during these 9 years were ICU,neurosurgery department and respiratory department.The specimen source was always dominated by the respiratory tract specimens,followed by the secretion samples,in recent years,the detection rates of blood,urine and drainage specimens were in-creased to some extent.The drug resistance rates in 13 kinds of drugs totally showed the increasing trend,the resistance rate of par-tial drugs was decreased to some extent.Conclusion Acinetobacter baumannii easily cause nosocomial infections,which is difficult to be eliminated and has high occurrence in the departments centralized with critical patients.The respiratory infection is the main pathogenic type.Its drug resistance is serious,multi-drug resistant and pan-resistant strains have the higher proportion.Clinic should rationally use the drugs based on the drug susceptibility test results,coordinates with the infection control departments for doing disinfection and isolation well and prevent ing the outbreak of nosocomial infections.

Objective To investigate the effect of GH on proliferation of pancreatic cancer cells and observe the features of IGF-IGFBP3 pathway in the host after GH administration. Methods Pancreatic cancer cells (SW-1990,PANC-1 and P3) during exponential growth stage were harvested and cultured in medium containing growth hormone (50 ng/ml). After 24, 48 and 72 hours, cells were counted using a Coulter Counter. Thirty-five Athymic nude Balb/c mice were inoculated with SW-1990cells. When tumors became palpable after inoculation, animals were randomized to receive GH points (1 h, 2 h, 6 h, 24 after the last injection), plasma samples were gathered for subsequent ELISA determination and liver was rapidly incised for immune blotting analysis. Results The results revealed that GH stimulated cell growth in vitro. GH elevated levels of IGF-Ⅰ , Ⅱ at the 1st , 2nd , 6th hour after the last injection. GH augmented the expression of IGFBP3 in the liver of the host in vivo (1 h, 2 h, 6 h, 24 h, respectively). Conclusion Such proteins as IGF- Ⅰ and Ⅱ might be associated with mechanism of last effect of GH on tumor host. The up-regulation of IGFBP3 by GH administration in the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.

Objective To investigate the expression of pSTAT5 in 7 pancreatic carcinoma cell lines,and the change of expression of pSTAT5 in pancreatic carcinoma cells SW1990 after growth hormone (GH) treatment, and explore its molecular mechanism. Methods Human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, AsPc, P3, PANC1) were cultured in vitro, and Western blotting was used to detect the expression of pSTAT5 in these cell lines. SW1990 in exponential growth phase was collected and nude Balb/c mice were inoculated with SW1990 cells. When tumors became palpable after inoculation, mice (normal saline group). 1 h, 2 h and 24 h after the last dose of GH treatment, the mice were sacrificed.Western blotting was used to detect the expression of pSTAT5 in SW1990 and inoculation tumor cells after GH injection. Results Positive expression of pSTAT5 was observed in all human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, Aspc, P3, PANC1). 5 minutes after GH (50 ng/ml) stimulation, the expression of pSTAT5 in SW1990 was 0.57 ±0.05, which was significantly increased; and it reached 0.64 ±0.04 at 10 minutes, then decreased to 0.39 ±0.03 at 15 minutes, however, it remained higher than that in the control group at 1 h (0.33 ± 0.02 vs 0.25 ± 0.06), and its expression at 2 h was 0.26 ± 0.03 and returned to the normal level. The expression of pSTAT5 in xenograft was not significantly changed. Conclusions GH could rapidly up-regulate the expression of pSTAT5 in SW1990 but the effect lasted for a relatively short period. GH had no significant effect on the expression of pSTAT5 in xenograft.

Objective To study the impact of exogenous growth hormone (GH) on the levels of insulin-like growth factor-Ⅰ and -Ⅱ (IGF-Ⅰ, -Ⅱ) of the pancreatic cancer tissue and the small intestine mucosa of the host. Methods In situ hybridization was performed on pancreatic cancer cell lines (SW-1990) and inoculation tumor of the host to determine the location of the mRNA transcript encoding IGF R-Ⅰ,-Ⅱ. Athymic nude Balb/c mice were inoculated with SW-1990 cells. After inoculated tumors have become palpable, animals were randomized to receive GH (4 mg/kg once daily for 2 weeks) versus saline control. After the animals were killed at time point, tissues (tumor and small intestine) were rapidly incised for subsequent immune blotting analysis. Results Strong IGF R-Ⅰ,-Ⅱ mRNA hybridization signal could be detected in pancreatic cancer cell. There was no statistically significant difference between the level of IGF-Ⅰ, Ⅱ in the tumor of the GH and NS groups after 1 hours of GH injection (P>0.05). GH augmented the expression of IGF-Ⅰ(1 h : 0.33±0.05, P<0.05 ; 2 h : 0.34±0.04, P<0.05 ; 6 h:0.34±0.05, P<0.05), -Ⅱ(1 h : 0.36±0.05, P<0.05) in the small intestine mucosa of the host. Conclusions The expression of IGF-Ⅰ, Ⅱ in the small intestine mucosa of the host was elevated by GH, but not in the inoculation tumor in vivo. The discrepancy of GH-IGF pathway between inoculation tumor and small intestine of the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.