OBJECTIVE To investigate the site of nosocomial infection in ICU,distribution and resistance of bacteria in order to make the intervention strategy.METHODS Antimicrobial susceptibility of pathogenic bacteria isolated from nosocomial infection patients in ICU from Jul 2006 to Jul 2008 was performed by Kirby-Bauer method.RESULTS The main pathogens of nosocomial infection in ICU were Gram-negative organisms(48.09%),Gram-positives(38.93%),and fungi(12.98%).The most common pathogens were Staphylococcus aureus,Acinetobacter baumannii,Pseudomonas aeruginosa,fungi,and S.haemolyticus.All strains of S.aureus and S.haemolyticas were antimicrobial sensitive to vancomycin,teicoplanin and linezolid.All A.baumannii strains were antimicrobial sensitive to cefoperazone/sulbactam.They were resistant to other antimicrobial agents.CONCLUSIONS Gram-negative organisms are the main pathogenic bacteria of nosocomial infection in ICU,but the percentage of Gram-positives and fungi is increasing,S.aureus is the most main pathogenic bacterium of nosocomial infection in ICU.S.haemolyticus is also a main pathogenic bacterium.The pathogenic bacteria of nosocomial infection in ICU are highly resistant to the most antimicrobial agents.

Objective To study the scan parameter of spiral CT angiography in aortic dissection.Methods 34 cases with aortic dissection successively underwent SCTA were studied retrospectively.The CT scan parameters,methods of posteriorimage treating were reviewed and analysed one by one.Results In 34 cases,32 cases were diagnosed as aortic dissection and classified correctly,in accordance with the result of operation and DSA,the quality of image was satisfied and the rate of success at least above 88.9%.The use of main scan parameters:(1)the ascend aortic dissection:slice thickness 4 mm,reconstruction interval 2 mm,pitch 1.25;tube current 175 mA;(2)involed in ascend,arch,descend and throacic aorta dissection:slice thickness 5 mm,reconstruction interval 2～3 mm,pitch 1.5;tube current 150 mA;(3)involved in abdominal aortic dissection:slice thickness 6～8 mm,reconstruction interval 2～3 mm,pitch 1.5 or 1.75;tube current 125 mA.The tube voltage all were 120 kV,the dosage of contrast media was 90～100 ml;the delayed scan time was choiced 20 second in throacic aortic and 25 second in abdominal aortic.The posterior image methods main used MPR,SSD,MIP and VR. Conclusion To set a sensible scaning plan,choose and match scan parameters properly according to the scaning length,can avoid the shortage of restrain SCTA scaning length and get satisfied image.

Objective To evaluate the damage to the brochial plexus produced by pulsed radiofrequency (PRF)and radiofrequency thermocoagulation(RFTC).Methods Fifty-five male Wistar rats weighing 250-300 g were randomly divided into 3 groups:groupⅠPRF(n=25):groupⅡRFTC(n=25)and groupⅢnormal control(n=5).The animals were anesthetized with intraperitoneal chloral hydrate.The left brochial plexus was exposed and PRF or RFTC was applied to the left brochial plexus.The voltage and current of the minimal stimulation which elecited muscle twitching and the impedance before and after operation were recorded in group PRF and RFTC.The nerve function was scored according to Tarloo(0=flaccid paresis,5=normal gait)before and at 3d after operation.The animals were killed and the left brachial plexus was removed immediately and at 1, 7,14,30 d after operation(n=5 at each time point)for determination of histopathological changes using microscope.Results The impedance and Tarlov score were significantly decreased after operation as compared to the baseline values before operation in group RFTC and were also significantly lower than in group PRF. Microscopic examination showed that the myelinated nerve fibers exhibited Wallerian degeneration and axon regeneration and the cytochondria in cylindraxile were severely injured or disappeared in group RFTC.The myelinated nerve fibers and the cytochondria in cylindraxile were significantly less injured after operation in group PRF than in group RFTC and returned to normal at 7 d and 30 d respectively.Conclusion The injury to brachial plexus produced by PRF is slighter than that produced by RFTC.

Keratinocyte growth factor 2 (KGF-2) is a member of the FGF family that is mainly synthesized by mesenchymal cells and acta predominantly on epithelial cells in a paracrine manner. It is known to play an important role in fetal limb and lung development; skin wound healing and prostatic epithelial cell growth. The KGF-2 coding sequence were isolated from human kidney cDNA library, revealing that the Kgf-2 gene is also expressed in the kidney apparatus. Purified from prokaryotic E. coli cells, the effects of the recombinant KGF-2 protein in cultured keratinocyte were analyzed by using MTT assay and in situ TUNEL assay. Interestingly, results revealed that KGF-2 promoted keratinocyte cell growth by stimulating cell proliferation and attenuating cell apoptosis. These findings supported a few evidences that KGF-2 could contribute to alveolar epithelial cells against apoptosis. Cell migration assays for the first time revealed that KGF-2 could stimulate keratinocyte cell migration in vitro. In addition, in the pilot animal test, recombinant KGF-2 incorporated within the hydrogel dressing exhibited significantly stimulatory effect on cutaneous wound healing. These combined effects implicate a potential therapeutic application of human recombinant KGF-2 in the future.

Aged ; Female ; Fibroma ; pathology ; Fibroma, Ossifying ; pathology ; Gingival Neoplasms ; pathology ; Humans

Adult ; Bile Duct Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Bile Ducts, Intrahepatic ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Carcinoma, Squamous Cell ; diagnosis ; metabolism ; pathology ; surgery ; Cholangiocarcinoma ; diagnosis ; metabolism ; pathology ; surgery ; Cholecystectomy ; methods ; Diagnosis, Differential ; Hepatectomy ; methods ; Humans ; In Situ Hybridization ; Keratin-19 ; metabolism ; Keratin-7 ; metabolism ; Keratin-8 ; metabolism ; Magnetic Resonance Imaging ; Male ; RNA, Viral ; metabolism ; Tomography, X-Ray Computed

Objective To investigate the value of 18 F-fluorodeoxyglucose FDG) positron emission tomography (PET)-computed tomography (CT) in predicting the progression-free survival (PFS)and overall survival (OS) of patients with esophageal squamous cell carcinoma (ESCC) after threedimensional (3D) radiotherapy.Methods A retrospective analysis was performed on 98 ESCC patients,who underwent FDG PET-CT before 3D radiotherapy from 2004 to 2010,to investigate their 1-,3-,and 5-year PFS and OS rates.The relationship of maximum standard uptake value (SUVmax),mean SUV (SUVmean),metabolic target volume (MTV),length of primary tumor on PET-CT before radiotherapy,and number of tumors on PET with PFS and OS were analyzed.The SUVs and clinical data were analysed by independent samples t-test or Hotelling T2 test; the Kaplan-Meier method was used for calculating PFS and OS rates,and the Logrank test was used for survival difference analysis;the prognostic factors were analysed using the Cox proportional hazard model.Results The follow-up rate was 100％ ;56 patients were followed up for at least 3 years,and 27 for at 5 years.The SUVmax SUVmean and MTV of primary tumor,length of primary tumor on PET-CT before radiotherapy,and number of tumors on PET were correlated with PFS and OS (x2 =8.99-41.82,all P ＜ 0.01).The Cox regression analysis showed that PFS could be well predicted based on SUVmean (x2 =4.41,P =0.036,RR =1.398) and number of tumors on PET (x2 =6.79,P =0.009,RR =3.650) and that OS could be well predicted based on number of tumors on PET (x2 =5.03,P =0.025,RR =3.740).Conclusions When estimating the long-term response to precise radiotherapy in patients with ESCC,SUV mean and number of tumors on PET may be used to predict PFS,and number of tumors on PET may be used to predict OS.

ObjectiveTo investigate the effects of protein phosphatase 2A (PP2A) inhibitors on the viability of pancreatic cancer cell line PANC-1 and its mechanism.MethodsPANC-1 cells were treated with PP2A inhibitors Cantharidin or Okadiac acid.The activity degree of NF-κB pathway was tested by Western blot.NF-κB pathway was blocked from all sectors by PP2Acα plamid transfection,NF-κB inhibition of protein kinase α (IKKα) and NF-κB inhibitor α (IκBα) dominant negative mutant and p65 interfering plasmid.Cell viability was determined by MTT.ResultsPP2A inhibitors could induce phosphorylation of IKKα,further phosphorylation of IκBα and degradation and followed by the release of p65 into nucleus.When PP2Acα,IKKα dominant negative mutant and IκBα dominant negative mutant were overexpressed,or p65 was interfered,the inhibition rate of Cantharidin on cell viability decreased (31.85±13.37) ％,(23.48±8.98)％,(22.63±5.81)％ and (20.88±3.24)％respectively,and the inhibition rate of Okadiac acid on cell viability decreased (40.17 ± 11.65)％,(27.34±14.28)％,(24.85±3.39)％ and (27.08±3.81)％ respectively.ConclusionsPP2Ainhibitors play a role in preventing pancreatic cancer through PP2Acα/IKKα/IκBα/p65 pathway.

Objective To observe the clinical effect of MC and LC in treatment of elderly patients with cholelithiasis and dise~s the best treatment in elderly patients with cholelithiasis.Methods Of 798 elderly patients with cholelithiasis,412 patients were divided into MC group with minilaparotomy cholecystectomy treatment,and 386 patients were divided into LC group with laparoseopic cholecystectomy treatment,then compare clinical effect and complications after operation.Results There was no significant differences in incision length,operative time,blood loss,bed time,hospital stay(all P＜0.05);There Was significant statistical significance in cost of treatment,complications after operation(all P＜0.05).Conclusion Minilaparotomy cholecystectomy was suitable for elderly patients with cholelithiasis,and it Was good at cost of treatment,complications after operation.

Obesity is an established risk factor for endometrial cancer. Leptin, a secreted protein of the ob gene by white adipose tissue, plays an important role in the regulation of food intake and energy consumption in the brain and acts as a potential growth stimulator in normal and neoplastic cancer cells. However, a direct role for leptin in endometrial cancer has not been demonstrated. In the present study, the effect of leptin on the proliferation of Ishikawa endometrial cancer cells was investigated as well as the possible mechanism(s) underlying this action in endometrial cancers which express both short and long isoforms of leptin receptors. The expression of leptin receptor (ObRb) in Ishikawa cells was detected by RT-PCR and Western blotting. The cells after serum starvation, were treated by leptin with various concentrations (0, 10, 50, 100, 150 ng/mL) for different durations (6, 12, 24 h). The effect of leptin treatment on cell proliferation was examined by MTT assay. Meanwhile, inhibitory effect of Janus tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) inhibitor AG490 or extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor PD98059 on the proliferation of Ishikawa cells induced by leptin was also studied. Ishikawa cells were treated with 100 ng/mL leptin for various periods (0, 20, 40, 60 min), and the levels of STAT3 phosphorylation and ERK1/2 phosphorylation were examined by Western blotting. The results showed that leptin induced the phosphorylation of STAT3 and the activation of ERK1/2 in a time- and dose-dependent manner in the Ishikawa endometrial cancer cells. Blocking STAT3 phosphorylation with the inhibitor AG490, or blocking ERK1/2 activation by the specific ERK1/2 kinase inhibitor, PD98059, abolished leptin-induced proliferation of Ishikawa cells. In addition, leptin was found to potently induce the invasion of endometrial cancer cells in a Matrigel invasion assay. Leptin-stimulated invasion was effectively blocked by pharmacological inhibitors of STAT3 (AG490) and ERK1/2 kinase (PD98059). These results suggested that leptin promotes endometrial cancer growth and invasiveness by activating STAT3 and ERK1/2 signaling pathways and therefore blocking its action at the receptor level can be a rational therapeutic strategy.