Adolescent ; Adult ; Female ; Humans ; Male ; Middle Aged ; Occupational Diseases ; diagnosis ; etiology ; Ulna ; injuries ; Wrist Injuries ; diagnosis ; etiology ; Young Adult

Background and purpose:Ara-C is one of the most effective and common agents in the treatment of acute nonlyphocytic leukemia. Telomerase is a unique complex of ribonucleoprotein. It plays an important role in the pathogenesis and development of cancer. In this study, we investigate the changes of mRNA expression of telomerase subunits in HL-60 cells induced by Ara-c and try to come up with a theory that could help to assess the efficacy of Ara-C. Methods:The combinations of various Ara-C concentration and the incubation time were used to treat HL-60. The ratios of apoptotic cell to necrosis cell were determined by flow cytometry and the expressions of telomerase subunits mRNA were evaluated by RT-PCR.Results:① There was no influence on transcription of telomerase subunits gene after HL-60 cells was cultured with 0~0.2ug/ml Ara-C for 12 hours;② 2ug/ml and 10ug/ml of Ara-C could down regulate the expression of hTERT from 0.80+0.07 to 0.50+0.04 and 0.39+0.03, not hTR and hTP1;③ with longer incubation with 10ug/ml of Ara-C, the percentage of apoptosis could be increased. The maximal induction of apoptosis (18.16+4.25%) could be reached at 12hrs treatment of Ara-C, then gradually decreased later on. The rate of necrosis increased with time, the maximal percentage(57.94+12.03%) of necrosis was observed at 48hrs of incubation time with drug. The mRNA level of hTERT gene also decreased along with the cultured time , the lowest value (0.18+0.03) has been documented at 48hrs time point, but not hTR、TP1.Conclusions:① Ara-C could down-regulate the expression of hTERT mRNA in a dose-and time-dependent manner, but not hTR、hTP1;② There might be no relationship between the percentage of apoptosis induced by Ara-C apoptosis and the expression of telomerase hTERT gene mRNA, but a close relationship between necrosis and the expression of hTERT mRNA has been found.

Animals ; Disease Models, Animal ; Graft vs Host Reaction ; Liver Cirrhosis, Biliary ; Mice

Adult ; Ascorbic Acid ; administration & dosage ; analysis ; Humans ; Male ; Nutrition Surveys ; Occupational Health ; Riboflavin ; administration & dosage ; analysis ; Thiamine ; administration & dosage ; analysis ; Vitamins ; administration & dosage ; analysis

Na+/H+ antiporter plays an important role in mechanisms of the plant salt tolerance, it extrudes Na+ from cell energized by the proton gradient generated by the plasm membrane H(+)-ATPase and/or compartmentalizes Na+ in vacuole energized by the proton gradient generated by the vacuolar membrane H(+)-ATPase and H(+)-PPiase. This review mainly discusses the latest progress in the study of Na+/H+ antiporter in plant and yeast at molecular level.
Phylogeny ; Plants ; metabolism ; Salts ; metabolism ; Sodium ; metabolism ; Sodium-Hydrogen Exchangers ; classification ; metabolism ; Vacuoles ; physiology

Objective:To evaluate the clinical outcome of botulinum A toxin(BTX-A)injection into external sphincter combined with oral baclofen in treatment of detrusor-external sphincter dyssynergia(DESD)after spinal cord injury(SCI). Methods:A total of 38 urodynamic examination-confirmed DESD patients,male 31 and female 7,with an average age of (36.5?17.8)years old,were included in this study.200 U of BTX-A toxin was dissolved in 8 ml of normal saline and the solution was injected at 8 different sites(1 ml per site)of the external sphincter via a 5F flexible cystoscopic needle.On the second day,9 patients(BTX-A+baclofen group)were randomly selected for baclofen oral administration,3/d for 3 months; the other 26 patients were taken as control.Urodynamic examination was repeated in all patients 4 weeks later;the voiding diary and urodynamic outcomes were compared before and after treatment.The adverse and toxic effects were observed in the patients who were followed up for 2-9 months.Results:One month after treatment the voiding and storing functions of bladder were improved to different degrees,with the mean maximum uroflow rate(Qmax),the mean urine volume,the mean maximal cystometric capacity and the bladder compliance increased significantly and the mean postvoid residual urine volume and the mean maximal voiding pressure decreased significantly(all P

OBJECTIVETo explore whether daunorubicin (DNR) combined with cytosine arabinoside (Ara-C) and DNR alone have similar effect on acute promyelocytic leukemia (APL) cell line NB4 and acute myeloblastic leukemia cell line HL-60 in vitro.

METHODSCell morphology, cells viability, and cell apoptosis (Annexin-V by flow cytometry assay) were analysed.

RESULTSAfter incubation with DNR plus Ara-C for 24 hours,NB4 cell viability [(36.75 +/- 3.82)%] (n = 6) and cell apoptosis rate [(21.24 +/- 5.82)%] (n = 3) did not change significantly compared to that treated with DNR alone for 24 hours [(35.73 + 6.28 )%, (22.55 +/- 3.26)%, respectively] (P > 0.05). However, HL-60 cell viability [(67.17 +/- 2.07)%] and cell apoptosis rate [(48.05 +/- 0.92)%] changed significantly in DNR plus Ara-C group compared with DNR alone [(63.31 +/- 1.80)% ,(41.51 +/- 0.89)%, respectively] (P < 0.01 and < 0.05, respectively).

CONCLUSIONDNR plus Ara-C and DNR alone have similar effect on NB4 cells, but have different effect on HL-60 cells.

Apoptosis ; drug effects ; Cytarabine ; pharmacology ; Daunorubicin ; pharmacology ; HL-60 Cells ; drug effects ; Humans ; Leukemia, Promyelocytic, Acute ; pathology

Objective To observe the effects of chloroquine phosphate on apoptosis of leukemic cell line U937, and investigate whether chloroquine phosphate induces leukemic cell apoptosis by normalizing protein PNAS-2's abnormal subcellular location. Methods Chloroquine phosphate of different concentrations were added into culture fluid of leukemic cell line U937 at logarithmic phase. MTr was used to measure cell proliferation, flow cytometry and laser confocal microscopy were applied to detect cell apoptosis, and immunofluorescence technology was employed to observe the effects of chloroquine phosphate on the changes of subcellular location of protein PNAS-2. Results Apoptosis of leukemic cell line U937 was significantly induced by 50 μg/mL chloroquine phosphate, and subcellular location of protein PNAS-2 was changed. Conclusion Chlorequine phosphate can induce apoptosis of leukemic cell line U937, and the mechanism may be related to the normalization of PNAS-2's abnormal subcellular location in U937 cell line. Chloroquine phosphate has the potential to be used in leukemic therapy.

OBJECTIVETo investigate the role of the key intracellular signaling molecule glycogen synthase kinase-3 beta in the mechanism of liver ischemia reperfusion (IR).

METHODSC57BL/6 mice were subjected to 90 min warm liver cephalad lobe ischemia, followed by various length of reperfusion. Experiment groups included sham control group, liver IRI model group and glycogen synthase kinase-3 beta inhibitor-treated group (SB216763 in DMSO, 25 g/kg, i.p, 2 hour prior to the onset of liver ischemia). The expression of glycogen synthase kinase-3 beta protein was analysed by Western blotting. The serum ALT levels were determined to reflect the function of liver. The affected liver lobes were harvested for histology analysis. The inflammatory gene expression was detected by Quantitative PCR.

RESULTSBy western blot analysis, we found that ischemia itself activated glycogen synthase kinase-3 beta by a significant decrease of its phosphorylation. Glycogen synthase kinase-3 beta inhibitor SB216763-pretreatment ameliorated the liver damages significantly as compared to the controls (sALT: 2046+/-513 U/L vs 5809+/-1689 U/L, P = 0.0153), and suppressed the gene expressions of IL-12, TNFa, IL-1b and IL-6.

CONCLUSIONSThis study demonstrated that the ischemia process modulated liver innate immune activation via a GSK-3-dependent mechanism which favored the development of a pro-inflammation response and lead to liver tissue damages. GSK-3b may be a new therapeutic target to ameliorate liver IRI in transplant patients.

Animals ; Glycogen Synthase Kinase 3 ; metabolism ; Glycogen Synthase Kinase 3 beta ; Inflammation ; metabolism ; Liver ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury ; metabolism ; pathology

BACKGROUNDLiver transplantation is the most effective treatment for patients with end-stage liver failure, however infection after transplantation is a serious clinical complication. The purpose of this research was to investigate the molecular epidemiology and the influence of multidrug-resistant Gram-positive infection in patients, following liver transplantation, to provide reference for clinical treatment and prevention of Gram-positive bacterial infection.

METHODSWe isolated and detected bacteria from phlegm, throat swabs, urine, wound or wound secretions, blood, and fecal samples from 221 liver transplant patients in our hospital from January 2007 to April 2010. All isolated bacterial strains were identified and tested by minimal inhibitory concentration (MIC) drug-sensitive detection using the BioMerieux ATB bacterial identification instrument and repetitive extragenic palindromic-polymerase chain reaction (REP-PCR) detection of bacterial homology. Risk factors were calculated by multivariate Logistic regression analysis.

RESULTSWe collected 250 specimens from 221 patients hospitalized following liver transplantation surgery, of which 29 patients developed multiple infections. Sixty-five Gram-positive bacterial strains were isolated from different specimens from 53 infectious patients. We detected 29 multidrug-resistant Gram-positive strains from 29 patients (44.62%), including 20 Staphylococcus aureus (S. aureus) strains (68.97%) and nine Enterococcus strains (31.03%). All 20 S. aureus strains were highly resistant to aminoglycosides (gentamicin), cephalosporins (cefoxitin), quinolones (ciprofloxacin and levofloxacin), lincomycins (clindamycin), penicillin, and erythromycin. The resistance rate reached 100% in some cases. The S. aureus strains were highly sensitive to vancomycin and oxazolidinone (linezolid), with MIC50 < 2 µg/ml for both. The nine Enterococci strains were also highly resistant to aminoglycosides, quinolones, and penicillins, and highly sensitive to vancomycin (MIC50 < 2 µg/ml) and oxazolidinone (MIC50 < 1 µg/ml). Using REP-PCR detection, S. aureus was divided into five genotypes with 14 B-type strains. Enterococcus was divided into 11 genotypes, with two D-type strains, two G-type strains, and two K-type strains. The risk factors for Gram-positive bacterial infection in patients following liver transplantation were preoperative use of antibiotics (OR = 3.949, P = 0.004), high intra-operative blood input (OR = 1.071, P = 0.005), and postoperative renal failure (OR = 5.427, P = 0.043).

CONCLUSIONSS. aureus and Enterococcus were the main pathogens causing infection following liver transplantation in patients with drug-resistant Gram-positive bacterial infection. The isolated strains were resistant to multiple antibiotics. B-type S. aureus strains were predominant. Reasonable use of antibiotics, decreasing intra-operative blood input, and preventing post-operative renal failure may reduce Gram-positive bacterial infections and the appearance of drug-resistant strains following liver transplantation.

Adult ; Anti-Bacterial Agents ; pharmacology ; Drug Resistance, Multiple, Bacterial ; genetics ; Female ; Gram-Positive Bacteria ; drug effects ; genetics ; pathogenicity ; Gram-Positive Bacterial Infections ; epidemiology ; etiology ; microbiology ; Humans ; Liver Transplantation ; adverse effects ; Male ; Microbial Sensitivity Tests ; Middle Aged ; Molecular Epidemiology