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

Public Health ; economics ; Social Support

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.

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

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

BacKground:Fanconi anemia( FA)pathway as a DNA crossIink damage repair pathway pIays an important roIe in maintaining genome stabiIity. In recent years,FA pathway was wideIy studied in DNA damage and cancer pathogenesis. Aims:To investigate the interaction between RAD18 and FANCD2 protein in human coIorectaI cancer ceII Iine SW480. Methods:Antigen-antibody compIex was co-precipitated by immunoprecipitation. Expressions of rabbit anti-human FANCD2 and RAD18 protein in antigen-antibody compIexes were detected by Western bIotting. The pIasmids of GST-RAD18 and GST were transferred into BL21 ceIIs and induced to express the target proteins. TotaI proteins of the ceII was extracted and GST-beads were used to conjugate the GST-RAD18 protein,and then incubated with the SW480 ceII Iysates, and Western bIotting was performed with the addition of rabbit anti-human FANCD2 antibodies. Results:RAD18 protein was detected in the antigen-antibody compIex from immunoprecipitation by using anti-FANCD2 antibody,and FANCD2 protein was detected by using anti-RAD18 antibody. FANCD2 protein was aIso detected by using anti-GST-RAD18 antibody. GST-RAD18 protein used as bait protein couId capture the FANCD2 protein in SW480 ceIIs. Conclusions:There is an interaction between RAD18 and FANCD2 protein in SW480 ceIIs,and aIso an interaction between GST-RAD18 and FANCD2 protein.

Objective To explore the prognosis of elderly patients suffered from hospital-acquired pneumonia (HAP) by T cell subsets and clinical pulmonary infection score (CPIS).Methods A cohort of 125 elderly patients admitted in ICU & ED (Emergency Department) from Aug,2012 to Jul,2013 were enrolled for a prospective and observational study.The patients were divided into 3 groups:HAP survival group (n =50,group A),HAP death group (n =40,group B) and non-HAP group (n =35,control group).The criteria of exclusion were patients with auto-immune diseases,immunodeficiency,allergic disorders,malignancies,diabetes,trauma,surgical diseases,or patients with recent use of immunosuppressive agents or cyclooxygenase-inhibitors (Aspirin etc.).In the control group,patients with nosocomial pneumonia and other diseases afecting the CPIS were excluded.APACHE Ⅱ scores of all patients were recorded.Blood T cell subsets (including values of CD3,CD4 +,CD8 +,and CD4 +/CD8 +)were measured on the admission day,the 1st day of HAP onset and the 5th day after onset of HAP in HAP patients whereas these measurements were tested only on the admission day in controls.Meanwhile,the CPISs were recorded on the admission day,the 1st day of HAP onset and the 5th day after onset of HAP in HAP patients.Flow cytometer (FCM) was used to detect T cell subsets.Data of statistical analysis were represented as Mean ± SD.The significant differences in T cell subsets and CPIS between survival group and death group were analyzed by independent t test.The paired samples t test was employed in survival group and death group.Linear correlation analysis was made between CD4 +/CD8 + ratio and CPIS in survival and death groups,respectively.Results There were no significant differences in demographics and clinical features (including age,sex,length of stay,APACHE Ⅱ scores) of patients in survivors and non-survivors (P ＞ 0.05).The values of CDs (CD3,CD4 + and CD4 +/CD8 + ratio) between patients of control group and patients of HAP groups were not significantly different on the admission day (P ＞ 0.05).The values of CDs on the admission day were much lower than those on the 1 st day of HAP onset in both survivors and nonsurvivors (P ＜ 0.05).The values of CDs on the 5th day after onset of HAP were higher than those on the 1 st day of HAP onset in the survival group (P ＜ 0.05),while there were no significant differences in CDs between different intervals after HAP onset in the death group (P ＞ 0.05).There were no significant changes in values of CD8 + in any group (P ＞ 0.05).Both survivors and non-survivors had much higher CPIS values on the 1st day of HAP onset than those on the admission day (P ＜0.01).The survival group had higher CPIS on the 5th day after onset of HAP compared to the 1st day of HAP onset (P ＜0.01),while there was no significant change in the death group.Linear correlation analysis showed negative correlation between CD4 +/CD8 + ratio and CPIS on both the 1 st day of HAP onset (survival group:R =-0.740,P =0.004 ; death group:R =-0.613,P =0.035) and the 5th day after onset of HAP (survival group:R =-0.639,P =0.009; death group:R=-0.686,P=0.021).Conclusions The hospital-acquired pneumonia appears as an immune imbalance disorder.The difference in CDs is a promising objective tool,aiding in prediction of prognosis of HAP in the elderly,the lower the CDs,the higher severity.The CD4 + / CD8 + ratio showed a negative correlation with CPIS.Monitoring of T cell subsets and CPIS may provide clinical value for the treatment of hospital-acquired pneumonia in the elderly.

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.