Objectives To investigate the effect of bladder function and behavior change training on urinary retention after epidural anesthesia and the method to decrease it. Methods 265 patients receiv-ing operation under epidural anesthesia were divided into two groups, the experimental group (132 cases) and the control group (133 cases). The experimental group was further divided into 3 groups: one to two days of training, 3 to 4 days of training and above 5 days of training preoperation. The experimental group carried out bladder function and behavior change training, but the control group never undertook any train-ing. After operation the data were analyzed. Results The incidence of urinary retention was significantly different between the experimental group and the control group (P<0.01);The time length of the training before operation aorrelated with incidence of urinary retention(P<0.05). Conclusions Bladder function and behavior change training contributed to decrease urinary retention after epidural anesthesia.The training time and incidence of urinary retention showed inverse proportion. This could decrease the opportunity of suffering from urethral catheterization and urinary tract infection.

Objective To determine whether p38 mitogen-activated protein kinase (p38MAPK) signaling pathway is involved in cerebral fractalkine-induced hyperalgesia in mice.Methods Two hundred and twenty-five male Kunming mice weighing 30-40 g were randomly divided into 4 groups:group control ( group C,n =55 ) ;group fractalkine (group F,n =60); group anti-CX3CR1 + fractalkine (group CF,n =55) and group SB203580 (p38MAPK inhibitor) + fractalkine (group SF,n =55).Fractalkine 100 ng was injected into cerebral lateral ventricle (i.c.v.) in groups F,CF and SF.Anti-CX3CR1 1 μg and SB203580 1 μg were injected i.c.v.at 1 h before fractalkine injection in groups CF and SF respectively.Paw withdrawal latency to a thermal nociceptive stimulus (PWL) was measured at 30 min before the drugs were injected into cerebral lateral ventricle and 30,60,120 and 240 min after fractalkine injection.Five animals were sacrificed after PWL measurement at each time point and their brains were removed for determination of phosphorylated p38MAPK protein expression (by Western blot analysis).Five animals were sacrificed at 30 min before the drugs were injected into cerebral lateral ventricle and 6,12 and 24 h after fractalkine injection for determination of IL-1β and TNF-α contents in the brain (by ELISA) in all the 4 groups.In group F 5 animals were sacrificed at 4 h after fractalkine injection for determination of action of fractalkine on microglia or astrocyte (by immunofluorescence).Results Fractalkine i.c.v.injection significantly reduced PWL and increased phosphorylated 38MAPK,IL-1β and TNF-α levels in group F as compared with group C.Pretreatment with anti-CX3CR1 or SB203580 significantly decreased fractalkine-induced hyperalgesia and phosphorylated-p38MAPK,IL-1β and TNF-α levels in groups CF and SF as compared with group F.Fractalkine was localized at microglia.Conclusion p38MAPK signal transduction pathway is involved in cerebral fractalkine-induced hyperalgesia in mice.

Objective To evaluate the role of inositol triphosphate receptor (IP3 R) in the fractalkine-induced activation of p38MAPK signaling pathway in BV-2 microglial cells.Methods BV-2 microglial cells were seeded in 3.5 cm diameter dishes (5 ml/dish),50 ml culture flasks (8 ml/flask) or 24-well plates (1 ml/hole) with a density of 1 × 105/ml and randomly divided into 5 groups (n =25 each) ∶ control group (group C),fractalkinegroup (group F),CX3C chemokine receptor 1 (CX3CR1) antibody anti-CX3CR1 + fractalkine group (group CF),IP3R antagonist 2-APB + fractalkine group (group AF) and p38 mitogen-activated protease (p38MAPK) inhibitor SB203580 + fractalkine group (group SF).Fractalkine 10 nmol/L was added to the culture medium in groups F,CF,AF and SF.The anti-CX3CR1 15 μmol/L,2-APB 50 μmol/L and SB203580 10 μmol/L were added to the culture medium in groups CF,AF and SF,respectively,1 h before addition of fractalkine.The cells were then cultured for 24 h.The intracellular Ca2+ concentration ([Ca2+]i) was measured during the 10 min incubation with fractalkine.The phosphorylation of p38MAPK was measured at 0,30,60,120 and 240 min of incubation with fractalkine.The concentrations of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in theculture medium were determined at 24 h of incubation with fractalkine.Results Compared with group C,[Ca2+]i,and the phosphorylation of p38MAPK and concentrations of IL-1β and TNF-α were significantly increased in groups F,CF,AF and SF (P ＜ 0.05).[Ca2+]i was significant lower in groups AF and CF and phosphorylation of p38MAPK and concentrations of IL-1β and TNF-α were significantly lower in groups CF,AF and SF than in group F (P ＜ 0.05).Conclusion IP3 R is involve in the fractalkine-induced activation of p38MAPK signaling pathway in BV-2 microglial cells.

OBJECTIVETo study the effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance ApoE -/- mice.

METHODEight male C57BL/6J mice were selected in the normal group (NF), 40 male ApoE -/- mice were fed for 16 weeks, divided into the model group (HF), the rosiglitazone group ( LGLT), the Jinlida low-dose group (JLDL), the Jinlida medium-dose group (JLDM), the Jinlida high-dose group (JLDH) and then orally given drugs for 8 weeks. The organization free fatty acids, BCA protein concentration determination methods were used to determine the skeletal muscle FFA content. The Real-time fluorescent quantitative reverse transcription PCR ( RT-PCR) and Western blot method were adopted to determine mRNA and protein expressions of mice fatty acids transposition enzyme (FAT/CD36), carnitine palm acyltransferase 1 (CPT1), peroxide proliferators-activated receptor α( PPAR α).

RESULTJinlida could decrease fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG), free fatty acid (FFA) and fasting insulin (FIns) and raise insulin sensitive index (ISI) in mice to varying degrees. It could also up-regulate mRNA and protein expressions of CPT1 and PPARα, and down-regulate mRNA and protein levels of FAT/CD36.

CONCLUSIONJinlida can improve fat-induced insulin resistance ApoE -/- in mice by adjusting the changes in expression of skeletal muscle lipid transport enzymes.

Animals ; Apolipoproteins E ; deficiency ; genetics ; Blood Glucose ; metabolism ; CD36 Antigens ; genetics ; metabolism ; Carnitine O-Palmitoyltransferase ; genetics ; metabolism ; Dietary Fats ; adverse effects ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Hypoglycemic Agents ; administration & dosage ; Insulin ; metabolism ; Insulin Resistance ; Lipid Metabolism ; drug effects ; Male ; Metabolic Diseases ; drug therapy ; enzymology ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal ; drug effects ; metabolism

OBJECTIVETo explore the relationship between quinone oxidoreductase1 (NQO1) gene nonsynonymous cSNP and the genetic susceptibility of esophageal cancer.

METHODSPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and Allele-Specific PCR (AS-PCR) were employed to assess the polymorphism of NQO1 genes both in 106 patients with esophageal cancer and control subjects matched by age, gender and origin.

RESULTSIt was shown that no C/C genotype was found at 406 of NQO1. The allelic frequency of NQO1 609T was significantly higher in patients with esophageal cancer than in the control subjects (P < 0.005) and the individuals with 609T allelic genotype of NQO1 gene were at greater risk to develop esophageal cancer (OR = 4.76, 95% CI = 1.064 - 3.397). But Individuals with mutant allele of NQO1 465 genotype did not show the rising risk of esophageal cancer.

CONCLUSIONSThe NQO1 C609T polymorphisms should likely be associated with the genetic susceptibility of esophageal cancer.

Alleles ; China ; Esophageal Neoplasms ; ethnology ; genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; Polymorphism, Single Nucleotide

OBJECTIVETo understand the clinical characteristics and outcome associated with respiratory syncytial virus (RSV) infection in hematopoietic stem cell transplantation (HSCT) recipients with primary immunodeficiencies (PIDs).

METHODNasopharyngeal aspirate samples were collected consecutively before and after HSCT from 9 recipients from Apr. 2009 to Sep. 2010 and analyzed for the presence of RSV using real-time polymerase chain reaction assay. To further verify the presence of the virus, positive samples for PCR were isolated for RSV. RSV G gene was amplified, sequenced and used for phylogenetic analysis.

RESULTThe presence of RSV was detected in 3 out of 9 children. The viral replication in all the patients was prolonged for months. All the 3 patients with RSV infection were treated with intravenous immune globulin (IVIG) and one was treated with antiviral medication. All patients survived and achieved successful immune reconstitution.

CONCLUSIONThis study indicates that the HSCT recipients with PID are at increased risk for RSV infection. RSV can shed for months after the initial infection and the patients recover with the course of immune reconstitution.

Child, Preschool ; Female ; Hematopoietic Stem Cell Transplantation ; adverse effects ; Humans ; Immunologic Deficiency Syndromes ; surgery ; virology ; Infant ; Prognosis ; Respiratory Syncytial Virus Infections ; diagnosis ; drug therapy ; Respiratory Syncytial Viruses ; genetics ; isolation & purification ; physiology ; Virus Replication ; Virus Shedding

Objective To investigate the expression level and promoter methylation of SOX17 gene and the clinical correlations in Chinese patients with chronic myeloid leukemia ( CML ) . Methods The levels of SOX17 expression and methylation were detected by RQ-PCR and RQ-MSP. Results SOX17 expression level was significantly lower in CML compared with 30 controls (P=0.001). The area under the receiver operating characteristic (ROC) curve (AUC) was 0.748 to differentiate CML from control (P=0.001). There was a trend of correlation between SOX17 expression and bcr/abl transcript (r = 0.439,P = 0.068) in CML patients. Hypermethylation of SOX17 promoter was detected in 3 (4%) CML patients, however, there was no difference as compared with 32 controls. In our study, SOX17 hypermethylation was not corrected with its expression. Conclusion Decreased SOX17 expression is a common molecular event in CML and may be considered as an available biomarker to diagnose CML. Dysregulated SOX17 is not caused by promoter hypermethylation in CML.

Aim To screen novel NS5 inhibitors a-gainst dengue virus ( DENV) replication. Methods His-tagged DENV2 NS5 RNA-dependent polymerase ( NS5 RdRp ) was expressed and purified in BL21 cells. The binding ability of the small molecules to NS5 polymerase was determined by SPR assay. The activity of dengue inhibition by Z1 was determined by CPE, LDH and plaque assay. RNA synthesis was as-sessed by Real-time PCR. The dsRNA synthesis and viral proteins were detected by immunofluorescence as-say. The level of viral proteins was examined by West-ern blot. The stage of DENV life cycle was evaluated by time of drug-addition assay. Results A small mo-lecular Z1 was discovered, which could bind to NS5 RdRp. Z1 inhibited DENV2 RNA replication, synthe-sis of dsRNA and protein synthesis in post-entry stage of dengue life-cycle. Cell based assay confirmed that Z1 inhibited DENV-induced cell death with EC50 val-ues of 4. 75μmol·L-1 . Conclusions The novel NS5 inhibitor Z1, inhibits DENV2 RNA replication, protein synthesis and release of progeny virus, which may be severed as an anti-DENV2 antiviral drug for further de-velopment.

OBJECTIVETo explore the effect of p38MAPK signaling pathway in interleukin-18-induced transdifferentiation in renal proximal tubular cells.

METHODSHuman proximal tubular epithelial cell line (HK-2 cells) was cultured in vitro. After preincubated with SB203580 (0, 5, 10, 20 micromol/L) for 30 minutes, cells were exposed to IL-18 (100 ng/ml) for 24, 48 and 72 hours respectively. The expressions of a-smooth actin (alpha-SMA) in cultured HK-2 cells were assessed by RT-PCR and ELISA.

RESULTSIL-18-induced expressions of a-SMA mRNA and protein were inhibited obviously by a dose-dependent manner when HK-2 cells were incubated with SB203580 (0, 5, 10, 20 micromol/L) and IL-18 (100 ng/ml) for different time (P < 0.05).

CONCLUSIONIL-18-induced transdifferentiation of renal tubular epithelial cells (RTECs) is suppressed obviously by blocking p38MAPK signaling pathways. IL-18-induced transdifferentiation of RTECs is probably mediated, at least in part, through the activation of p38MAPK signaling pathways.

Cell Line ; Cell Transdifferentiation ; drug effects ; Enzyme Inhibitors ; pharmacology ; Epithelial Cells ; cytology ; Fibrosis ; physiopathology ; Humans ; Imidazoles ; pharmacology ; Interleukin-18 ; pharmacology ; Kidney ; pathology ; Kidney Tubules, Proximal ; cytology ; MAP Kinase Signaling System ; Myofibroblasts ; cytology ; Pyridines ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo observe the effect of three Chinese medical formulae (Zhifei Mixture I , Zhfei Mixture II, and Zhifei Mixture II) on main and secondary symptoms and signs of children with Totally 70 mycoplasma pneumonia in treating three types of children mycoplasma pneumonia.

METHODSchildren with mycoplasma pneumonia were assigned to the control group (38 cases) and the treatment group (32 case). All patients were intravenously injected with Azithromycin and took Ambroxol Hydrochloride and Clenbuterol Hydrochloride Oral Solution. Those in the treatment group additionally took Zhifei Mixture I , Zhfei Mixture II, and Zhifei Mixture Ill by syndrome typing. Their main and secondary symptoms and signs were observed before and after treatment (main symptoms and signs covered fever, cough, abundant sputum, short breath, and anoxia; secondary symptoms and signs covered aversion to cold, heart rate, facial complexion, spirit, appetite, and sweating).

RESULTSSeven patients were lost in this study. Compared with before treatment in the same group, scores for main and secondary symptoms and signs decreased in the treatment group (P <0.01). The therapeutic effect on fever and cough was obviously better in the control group (P <0.01). The main and secondary symptoms and signs were more obviously improved in the treatment group than in the control group (P <0.01). Commpared with the control group, scores for main and secondary symptoms and signs decreased more in the treatment group (P <0.01). Patients' main and secondary symptoms and signs were more obviously improved (P <0.05).

CONCLUSIONSZhifei Mixture combined Western drugs could significantly improve main and secondary symptoms and signs of mycoplasma pneumonia children patients. Its efficacy was superior to that of using Western medicine alone.

Ambroxol ; administration & dosage ; therapeutic use ; Anti-Bacterial Agents ; administration & dosage ; therapeutic use ; Azithromycin ; administration & dosage ; therapeutic use ; Bronchodilator Agents ; administration & dosage ; therapeutic use ; Child ; Clenbuterol ; administration & dosage ; therapeutic use ; Drugs, Chinese Herbal ; therapeutic use ; Expectorants ; administration & dosage ; therapeutic use ; Fever ; Humans ; Pneumonia, Mycoplasma ; drug therapy ; Syndrome