Objective To investigate the clinical distribution characteristics and trend in antibacterial resistance of Acinetobacter baumannii in Pudong Hospital Affiliated to Fudan University,so as to provide the guidance for clinical rational use of antibacterial agents and infection control.Methods SPSS 1 9.0 statistical software was adopted to retrospectively analyze the specimen source, department distribution and antibacterial resistance change of the 1 678 strains of Acinetobacter baumannii in this hospital from Jan-uary 2010 to October 2014.Results Clinical isolates of Acinetobacter baumannii mainly came from respiratory tract specimens(ac-counted for 79.1%).The intensive care unit(21.1%),department of neurosurgery(1 7.7%)and department of cardiology(1 7.6%) were the top three departments from which the strains were isolated.The isolates of Acinetobacter baumannii were highly resistant to the first and second generation of cephalosporins,cephamycin,ampicillin and nitrofurantoin,and the resistance rates reached a-bove 90%.The resistance rates of these isolates against carbapenems,aztreonam,cefperazone-sulbactam and ampicillin-salbactam showed obviously uptrends,but the resistance rates of these isolates against amikacin and cotrimoxazole showed downtrends.And the resistance rates of these isolates against other antibacterial agents stayed between 30% and 50%.During the five years,the de-tection rates of multi-drug resistant strains steadied around 35.0%.Though the detection rates of pan-drug resistant strains de-clined year by year,the strains were isolated each year.Conclusion The antibacterial resistance of Acinetobacter baumannii is seri-ous in this hospital,with multi-drug and pan-drug resistance persisting.It is necessary to enhance monitoring antibacterial resist-ance,ensure rational use of antibacterial agents,and promote implementation of disinfection and isolation,so as to prevent the spread and popularity of Acinetobacter baumannii resistance in hospital.

Humans ; Medicine, Chinese Traditional ; Nephrotic Syndrome ; diagnosis ; therapy

Objective:To find the threshold value concentration of cobalt causing myocardium cell damage.Methods:Cobalt in different concentrations (10 μg/ml,20 μg/ml,40 μg/ml,80 μg/ml) were added into the medium of cultured myocardium cell of rat (1～3 days old) in vitro.Then the activities of GOT,CK,LDH,HBDH in the medium were measured.Results:The results showed that when cobalt concentration was 10～20 μg/ml,the activity of GOT,CK,LDH,HBDH did not change markedly.But when cobalt concentration was more than 40 μg/ml,the activities of those enzymes increased significantly.Conclusion:The studies demonstrated that the activities of enzymes in the medium of cultured myocardium cell could increase with the difference of coblat concentrations.The threshold value concentration of cobalt which could cause myocardium cell damage is 40 μg/ml.

Objective To investigate the risk factor for new-onset diabetes after transplantation (NODAT) and the relationship between NODAT and arterial stiffness. Methods Oral glucose tolerance test (OGTT) was performed on 195 patients with renal transplantation. The degree of arterial stiffness, which was determined by brachial ankle pulse wave velocity (baPWV), anklebrachial blood pressure index (ABPI) and intima-media thickness (IMT) of the carotid artery, was evaluated. Results Twenty-nine patients diagnosed as NODAT had significantly higher fasting plasma glucose before transplantation, blood pressure and incidence of hepatitis C virus (HCV) infection than in patients without NODAT. Multivariate regression analysis revealed that the risk factor of NODAT was fasting plasma glucose pre-transplantation, HCV infection and systolic blood pressure.The independent determinant of the advanced arterial stiffness on NODAT was the statement of hypertension and age. Conclusions High fasting plasma glucose prior to transplantation, HCV infection and high blood pressure are risk factors for NODAT in patients after renal transplantation.Strict control of blood pressure is the key way to prevent the NODAT and atherosclerosis.

To develop a method for the determination of residual solvents inα-ketophenylalanine calcium by capillary gas chromatography. Methods:The residual solvents were separated on a DB-624(30 m × 0. 32 mm, 0. 25 μm) capillary chromato-graphic column with temperature programming. The column temperature was maintained at 40℃ for 1 min,and then raised to 180℃at a rate of 10℃·min-1 and maintained for 2 min. N2 was used as the carrier gas, and FID was used as the detector with temperature of 250 ℃. The injector temperature was 200 ℃ and the split ratio was 10∶1, and direct injection was adopted. Methanol, ethanol, ethyl acetate and tetrahydrofuran in α-ketoleucine calcium were detected using an external standard method. Results:The four solvents were separated completely. There was a good linear relationship between the peak area and the concentration of each solvent ( r=0. 997 2-0. 999 5). The average recovery of the four solvents was 95. 47%-100. 26%(RSD≤4. 7%, n=9). Conclusion:The method is rap-id, simple, accurate and sensitive, and can be used in the determination of residual solvents in α-ketophenylalanine calcium.

Objective To investigate the dynamic change of T-lymphocyte subpopulations in the patients with SARS to understand the pathogenesis of SARS,and to find the specific early diagnostic and warning indexes for SARS.Methods T-lymphocytes in the peripheral blood were labelled by specific fluorescein antibodies and examined by flow cytometry in 252 cases of patients with SARS.The relationship between the dynamic change of T-lymphocyte subpopulations and the clinical progression was analyzed.Results The CD 3 +,CD 4 + and CD 8 + T cells,especially CD 4 + T cells decreased at the fist two-week of the disease course and reached to the lowest level at the second week,and began to increase from the third week in all patients.The change pattern of CD 3 +,CD 4 + and CD 8 + T cells in the severe type of SARS was the same as that of the mild type of SARS,but with more serious extent and longer time.The CD 4 + cell amount of the first,second and third weeks in the mild type of SARS was 515?444/?l,421?350/?l and 600?389/?l respectively,and was up to normal level at the fourth week.The CD 4 + cell amount of the first,second,third and fourth weeks in the severe type of SARS was 312?158/?l,255?187/?l,435?343/?l and 539?394/?l respectively,and still lower than normal level at the fourth week.There was a significant difference in the CD 3 +,CD 4 + and CD 8 + cell amount among the different weeks of disease course in both types.NK cell amount also decreased during the course of disease.The CD 4 +/CD 8 + ratio did not change much and was within the normal range.Conclusions The decrease of CD 3 +,CD 4 + and CD 8 + T cells is a sensitive index for early diagnosis of SARS.The continuous decrease of them may indicate the severe condition of the patients with SARS.

Objective To observe the effect of cytokine-induced killer (CIK) cells on the apoptosis of human leukemia cells,and explore the role of miR-155 in this process.Methods The cytotoxicity of CIK cells against a variety of leukemic cell lines (NALM-6,Jurkat) was investigated by MTT technique,miR-155 was determined by real time quantitative PCR,and the apoptosis was detected by flow cytometry in NALM-6 and Jurkat cells induced by CIK cells.Psi CHECK2-CEBP/β 3'-UTR containing the binding site of miR-155 was constructed,and then it was transfected into NALM-6 and Jurkat cells.Luciferase activity of CEBP/β (CCAAT/enhancer binding protein beta) was determined with the assistance of dual luciferase report system.Results CIK cells possessed strong cytotoxicity against NALM-6 and Jurkat cells,which was time-dependent and dose-dependent (P ＜ 0.05).CIK cells could increase the expression of miR-155 in NALM-6 cells by (2.87±0.19) fold (t =2.787,P ＜ 0.05),and in Jurkat cells by (1.98±0.25) fold (t =3.513,P ＜ 0.05).Moreover,miR-155 mimics could promote the apoptosis of NALM-6 and Jurkat cells induced by CIK cells (t =4.239,P ＜ 0.05;t =3.565,P ＜ 0.05).However,miR-155 inhibitor might block this process (t =3.772,P ＜ 0.05;t =4.017,P ＜ 0.05).MiR-155 targeted at the site of CEBP/β3'-UTR,and CIK cells could decrease the luciferase activity of NALM-6 cells by (42.89±2.07) ％ (t =3.578,P ＜ 0.05),meanwhile,in Jurkat cells by (37.02±1.95) ％ (t =4.393,P ＜ 0.05).Conclusion CIK cells could enhance human leukemia NALM-6 and Jurkat cells apoptosis by upregulating miR-155,which may provide a new database to elucidate leukemia cell therapy using CIK cells.

Objective To investigate the effect of Atorvastatin on the proliferation and apoptosis of leukemic HL-60-cell line,and to explore the possible role of phosphatidylinositol 3-kinase/serine/threonine protein kinase /mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway in this process.Methods HL-60 cells were incubated with different concentrations of Atorvastatin (1,5,10 μmol/L),and HL-60 cells without any treatment were used as controls.The proliferation of HL-60 which was investigated by four methyl thiazolyl tetrazolium assay when cells were cultured for 12,24,48 hours.The apoptosis was detected by flow cytometry after cells were incubated for 48 hours.The mRNA and protein expressions of AKT,PI3K and mTOR were detected by reverse transcription-polymerase chain reaction and Western blot methods,respectively.Results The results indicated that Atorvastatin could inhibit the proliferation and induce the apoptosis of HL-60 cells.When treated with 10 μmol/L Atorvastatin after 48 h,the proliferation inhibition of HL-60 was observed most obviously,with a high rate of (39.77 ± 3.01) ％,compared with the control group,it had statistical significance (t =4.016,P ＜ 0.01),meanwhile,the apoptosis of HL-60 was most notable,at a rate of (43.29 ±3.91)％,compared with the control group,it had statistical significance (t =3.625,P ＜ 0.05).There were basal expression of AKT,PI3K and mTOR in the control group.When treated with 10 μmol/L Atorvastatin after 48 h,the mRNA expression of PI3K,AKT and mTOR were down-regulated most obviously,at a decrease of (37.05 ± 4.11) ％,(53.79 ± 3.27) ％,(40.63 ± 2.42) ％ (t =4.805,3.799,4.312,all P ＜ 0.05),respectively,in comparison with the control group.At the same condition,the protein expression of PI3K,AKT and mTOR were decreased most visibly,with a decline of (41.09 ± 3.17) ％,(45.67 ± 2.92) ％,(63.41 ± 3.59) ％ (t =3.576,4.727,4.902,all P ＜ 0.05) respectively in comparison with the control group.Conclusions Atorvastatin can inhibit the proliferation and induce the apoptosis of leukemic cell HL-60,and the mechanism may be associated with the PI3K/ AKT/mTOR signal pathway.

China ; Health Knowledge, Attitudes, Practice ; Humans ; Occupational Diseases ; prevention & control ; Occupational Exposure ; prevention & control ; Occupational Health ; statistics & numerical data ; Rural Population ; statistics & numerical data