Public Health ; economics ; Social Support

Endothelium, Vascular ; cytology ; Humans ; Mucocutaneous Lymph Node Syndrome ; complications ; pathology ; Neovascularization, Pathologic ; Stem Cells ; cytology

Objective To investigate antimicrobial resistance of clinical isolates from 15 hospitals submitted to Guangzhou Surveillance of Antimicrobial Resistance (GSAR) in 2007,and to learn the feature of bacterial resistance in Guangzhou.Methods Disc diffusion test (K-B methods) was employed to study the antimicrobial resistance.Results Of 18 500 clinical isolates,Gram negative bacilli and Gram positive cocci accounted for 68.4% and 31.6%,respectively,and 45.7% isolates in Gram negative bacilli belonged to non-fermentative bacilli.The detection rotes of methiciHin-resistant strains was 55.9% in Staphylococcus aureus and 75.9% in coagulase negative Staphylococcus.All of the Staphylococcus pneumoniae isolates were penicillin-susceptible (PSSP) according to 2008 CLSI criterion.One strains of Enterobacter faecium were identified as vancomycin-resistance (VRE).The resistant rates of Enterobacter to imipenem and merpenem were the lowest.The prevalence of ESBLs-producing strains in Enterobacter coli and Klebsiella spp.isolates was 43.8% and 39.8%,respectively.Against all the ESBLs strains in Enterobacter coli and Klebsiella spp,meropenem,imipenem,cefoperazone/sulbactam,and piperacillin/tazobactam showed the lowest resistant rates,ranging from 0 to 14.1%,20.4%,24.4% and 25.4% isolates of Pseudomonas aernginosa were resistant to efoperazone/sulbactam,piperacillin/tazobactam and meropenem,while 75.6%,72.4% and 63.2% isolates of Pseudomonas aeruginosa were susceptible to piperacillin/tazobactam,meropenem and cefoperazone/sulbactam,respectively.The resistance rates of Acinetobacter spp.to cefoperazone/sulbactam and meropenem were 2.6% and 5.1%,respectively.Some panresistant isolates of Pseudomonas aeruginosa (5.5%) and Ac/naobacter baumannii (1.5%) emerged.The resistance of Pseudomonas aeruginosa and Aeinetobacter baumannii isolated from sputum sample was higher than those from blood sample.Conclusions The increase of isolated rates of non-fermentative Gram-negative bacilli and the emerging bacterial resistance and oandrug resistance in Pseudomonas aeruginosa and Acinetobacter baumannii warrants further enbancing the local surveillance of bacterial resistance and characterization of panresistance mechanism to inform the rational use of anfimicrobial agents and containment of bacterial resistance.

Objective To investigate the myocardial protective effect of isehemic post-conditioning in total repair for tetralogy of fallot,in order to improve short-term prognosis of infant patients.Methods 64 cases of TOF infant patients were randomly divided into two groups,32 cases in the control group:conventional surgery without ischemic post-conditioning,and other 32 cases in the experimental group:given three cycles of ischemic post-conditioning.Then the clinical indieators:cardiopulmonary bypass time,aortic cross-clamping time,automatic re-jump rate,the latter parallel to the off-line time,the off-line blood pressure,the offline dopamine usage,extubation time,ICU stay time,postoperative complications,and the testing laboratory indicators:the cTnI and CK-MB levels in plasma after anesthesia induction,10min after aortic cross-clamping,10min after aortic opening,ICU1h,1d after surgery,and 2d after surgery were observed.Results Two patients were died and,mortality rate was 3.1%.The remaining patients were discharged from hospital.Laboratory indicators of the control group and the experimental group had significant differences (all P＜0.05),while the clinical indicators of the two groups had no significant differences(all P＞0.05).But for the sub-group which the aortic cross-clamping time were more than 60min,the clinical indicators were significantly different(all P＜0.05).Conclusion Ischemic post-conditioning could enhance myocardial protection in total repair for tetralogy,of fallot.for the cases aortic cross-clamping time was more than 60min,their clinical meanings were more obvious.

Adult ; Aged ; Carcinoma, Hepatocellular ; surgery ; virology ; Female ; Follow-Up Studies ; Glutathione ; therapeutic use ; Hepatectomy ; methods ; Hepatitis B ; blood ; drug therapy ; Hepatitis B Surface Antigens ; blood ; Hepatitis C ; drug therapy ; Humans ; Liver Neoplasms ; surgery ; virology ; Male ; Middle Aged ; Prognosis

Aged ; Aortic Valve Insufficiency ; diagnostic imaging ; Echocardiography ; Humans ; Male

Aim To study the role of TNF-α/NF-κB signaling in matrix metalloproteinase ( MMP)-9 expres-sion induced by lipopolysaccharide ( LPS ) in airway epithelial cells, and to investigate the effects of lenti-virus mediated RNAi targeting a disintegrin and metal-loproteinase 17 ( ADAM17 ) gene on MMP-9 expression induced by LPS. Methods The ADAM17 siRNA ex-pression vector was constructed, and packaged to re-combinant lentivirus in 293T cells. The HBE4-E6/E7 cells were pretreated for 30 min by NF-κB inhibitor ( PDTC) and a recombinant human TNFR p75-Fc fu-sion protein ( Etanercept) , or infected by the recombi-nant lentivirus for 72 h, and then stimulated for 24 h by LPS or TNF-α. The release of TNF-α was detected by ELISA. The mRNA and protein levels of MMP-9 were analyzed respectively by RT-PCR and Western blot. NF-κB activity was detected by electrophoretic mobility shift assay. Results LPS and TNF-α signifi-cantly increased MMP-9 mRNA and protein expressions and the activation of NF-κB in HBE4-E6/E7 cells ( P<0. 05 ) . Etanercept and PDTC significantly inhibited MMP-9 expression and the activation of NF-κB induced by LPS ( P<0. 05 ) . Lentivirus mediated RNAi targe-ting ADAM17 significantly decreased TNF-α produc-tion, inhibited MMP-9 mRNA and protein expressions and the activation of NF-κB induced by LPS in HBE4-E6/E7 cells ( P <0. 05 ) . Lentivirus mediated RNAi targeting ADAM17 did not inhibit MMP-9 mRNA and protein expressions and the activation of NF-κB in-duced by TNF-α ( P>0. 05 ) . And PDTC significantly inhibited MMP-9 mRNA and protein expressions and the activation of NF-κB induced by TNF-α ( P <0. 05 ) . Conclusions TNF-α/NF-κB signaling partic-ipates in the regulation of MMP-9 expression induced by LPS in airway epithelial cells, and lentivirus-media-ted RNAi targeting ADAM17 plays an important role in that signaling pathway upstream by regulating TNF-αrelease.

Objective To evaluate the bedside index for severity in acute pancreatitis (BISAP) and harmless acute pancreatitis (HAP) scoring system in predicting prognosis of acute pancreatitis (AP).Methods A total of 442 AP patients,who were admitted to The First Affiliated Hospital of Sun Yat-sen University from January 2003 to December 2010,were retrospectively studied.BISAP and HAP scores were evaluated respectively.The value of BISAP and HAP scores in predicting severity,local complications,organ failure and mortality were measured by the area under the curve (AUC) of receiver operator characteristic curve (ROC),and it was compared with that of traditional Ranson's score.Results Among 442 patients,73 patients (16.5％) were diagnosed to have severe acute pancreatitis (SAP).AUC for BISAP score in predicting SAP,local complications,organ failure and mortality were 0.90 (95％ CI:0.86 ～ 0.93),0.82(95％ CI:0.76 ～ 0.89),0.93 (95％ CI:0.89 ～ 0.96),0.93 (95％ CI:0.87 ～ 0.98).There were no statistically significant differences in AUCs of the four prognostic parameters between BISAP and Ranson's score.The specificity,positive predictive value (PPV),and AUC of HAP score in predicting mild AP were 85％,95％ and 0.73 (95％ CI:0.67 ～ 0.79).The risk of dismal prognosis increased when both BISAP and HAP score were abnormal.Conclusions BISAP and Ranson's score have comparable ability in predicting prognosis of patients with AP.However,BISAP score is simpler.HAP score is a simple and accurate method for predicting prognosis of patients with mild AP.Combination of BISAP score with HAP score can better help predict the prognosis of AP patients.

This study is to establish a cell-based model targeting to neuraminidase (NA) of the 2009 H1N1 influenza A virus. NA is an influenza virus structural protein with enzymatic activity of the cleavage of HA-sialic acid interaction to release new viral particles from cells. A model of HIV-1 (pNL4-3.Luc.R(-)E(-)) based pseudovirions packed with HA [hemagglutinin, A/VietNam/1203/2004 (H5N1)] and NA [A/California/04/2009 (H1N1)] was established to evaluate compounds activities on NA function. The viral release can be blocked by neuraminidase inhibitors, oseltamivir and oseltamivir carboxylate, with IC50 of (61 +/- 31) nmol L(-1) and (5.5 +/- 2.9) nmol L(-1) respectively. A point mutation of H275Y on NA leads oseltamivir-resistance. This corresponding mutation was introduced into the system which was also confirmed by oseltamivir and oseltamivir carboxylate.