Objective:To investigate the effects of the psychological stress on peripheral blood lymphocytes apoptosis and Bax,Bcl-2 gene expression in rats after being given different intensity of noise stress.Methods:All 24 SD rats were divided into three groups:control,high intensity of the noise stress,middle intensity of the noise stress. The apoptosis in peripheral blood lymphocytes(PBL)of rats was demonstrated with the flow cytometer to determine the percentages of apoptosis in rat PBL,and the expression changes of related Bcl-2,Bax genes were observed by us- ing immunohistochemical method.Results:1)After high intensity of the noise stress for three weeks,the apoptosis in rat PBL increased significantly compared with the control.2)After high intensity of the noise stress for three weeks, Bcl-2 expression as down-regulation in PBL,but the B ax expression remained obviously high.Conclusion:It indi- cates that apoptosis exists in the immunocytes of rats in the course of high intensity of the psychological stress and it consists with the expression of the related regulatory genes.

The normal growth of blood vessels is the result of dynamic balance of angiogenic factor and inhibitory factor in vascular tissue.However, when the balance is broken, the growth of new blood vessels will be induced.Endogenous angiogenesis inhibitory factor, is a group of negative feedback molecules produced by the body itself that inhibit angiogenesis.Its function of inhibiting angiogenesis is mainly realized by promoting the binding of angiogenic factor to its receptor, or its downstream angiogenesis signal, or promoting vascular endothelial apoptosis.The study of angiogenesis inhibitory factor has potential clinical significance for the prevention and treatment of retinal neovascularization.Recent studies on retinal neovascularization inhibitory factor are reviewed in this paper.

Objective To explore the change of serum level of neuron specific enolase (NSE) in neonates with asphyxia before and after head mild hypothermia.Methods Eighty-two asphyxial neonates were selected,including 39 mild asphyxial neonates and 43 severe asphy-xial neonates,and 29 healthy neonates were selected as control group.Forty-three severe asphyxial neonates were randomly assigned into mild hypothermia treatment group and traditional treatment group.Neonates in traditional treatment group were just given traditional treatment.While neonates in mild hypothermia treatment group received head mild hypothermia therapy and their nasopharyngeal temperature were maintained at(34.0 ? 0.5) ℃ for 72 h.Before treatment and 72 h after treatment,2 mL blood was collected,and the serum NSE was determined by radio immunoassay.Results NSE levels in mild asphyxial neonates group[(34.83?6.17) ?g/L] and severe asphyxial group[(59.58?8.87) ?g/L] were significantly higher than that of control group[(30.57?4.88) ?g/L](t=3.07 P0.05).The level of NSE at 72 h in severe asphyxial neonates with head mild hypothermia therapy[(40.97?6.55) ?g/L] was significantly lower than that of traditional treatment group [(48.15?5.57) ?g/L](t=3.86 P

Objective To construct a luciferase gene expression vector containing full-length 3' untranslated region(3'UTR)of mouse vascular endothelial growth factor-C(VEGF-C)gene,and to observe the effects of VEGF-C 3'UTR on luciferase gene expression by a double-fluorescence report system.Methods Polymerase chain reaction(PCR)was used to amplify VEGF-C 3'UTR and a 312bp VEGF-C coding region(CR)fragment from full-length VEGF-C cDNA in mouse Lewis lung cancer cells.The luciferase expression vectors containing VEGF-C 3'UTR or VEGF-C CR were constructed by subcloning the PCR products to luciferase reporter vector pGL3-Promoter using gene engineering technology,and then they were transfected to mouse Lewis lung carcinoma cells by LipofectamineTM 2000.The activities and mRNA expression of luciferase were detected by Dual-Luciferase Reporter System and quantitative RT-PCR,respectively.Results Mouse VEGF-C 3'UTR(429bp)and VEGF-C CR(312bp)were successfully amplified by PCR.The VEGF-C 3'UTR and VEGF-C CR fragments were successfully inserted into pTA2 vector,and then subcloned to pGL3-Promoter vector at Xba Ⅰ site by using restriction endonucleases analysis.The DNA sequences and insertion orientation of PCR products were all correct by sequencing analysis.The resulted luciferase expression plasmids were named pGL3-VEGF-C 3'UTR and pGL3-VEGF-C CR,respectively.Dual-Luciferase Reporter System detection and quantitative RT-PCR showed that in Lewis lung carcinoma cells,the activities of luciferase and expression of luciferase mRNA in the pGL3-Promoter group were higher than that in the pGL3-VEGF-C 3'UTR group,and there was no significant difference between pGL3-VEGF-C CR group and pGL3-Promoter group.Conclusion VEGF-C 3'UTR can inhibit luciferase gene expression.

OBJECTIVE To investigate the clinical character of patients with severe acute pancreatitis(SAP)(infected) with deep fungal organisms and its prevention and treatment with fluconazole.METHODS Among 256(patients) with SAP,46 cases with SAP and deep fungal infection treated by fluconazole were selected as(fluconazole) treatment group,66 patients with suspicious deep fungal infection were randomized into 2 groups: fluconazole(prevention) group(42 cases) and control group(24 cases).RESULTS There were lower incidences of deep fungal(infection) in fluconazole prevention group than that in control one(P

Objective To explore the clinical value of real time contrast-enhanced ultrasound in diagnosis of liver localized fatty deletion and fatty infiltration which couldn't be confirmed by conventional ultrasonography. Methods Contrast-enhanced ultrasound was performed on 94 patients with liver localized diseases confirmed by baseline sonography, among them 34 patients with liver localized fatty deletion and fatty infiltration were enrolled. Results Contrast-enhanced ultrasonography didn't show apparent occupancy nidus in 34 patients. Enhancement mode of lesions was the same as liver parenchyma, which was distinctly different from liver occupancy diseases. Conclusion Real time contrast-enhanced ultrasound can display typical signs of liver localized fatty deletion and fatty infiltration and has significant value in diagnosis and differentiating diagnosis of them.

Objective To study the therapeutical effect of glutathione(GL),a powerful antioxidant on the symptoms and ECG in patients with coronary heart disease and its mechanisms.Methods Eighty-five subjects with coronary heart disease were recruited(45 male and 40 female).The patients were randomized to receive GL (240 mg,ivgtt,qd,for 14 days,n=44)on the top of conventional treatment(aspirin+?-blocks+ACEI)or conven- tional treatement alone(control,n=41).The serum MDA,SOD,NO levels were determined.Electrocardio- graphy(ST stage,T wave)was examined.Results GL significantly improved clinical symptoms scores(2.0+0.5 vs control:1.5+0.5,P

Objective To investigate the transactivating effect of hepatitis C virus(HCV)core protein on inducible nitric oxide synthase(iNOS)gene promoter and the molecular biological mecha- nisms of HCV pathogenesis.Methods Polymerase chain reaction(PCR)technique was employed to amplify the sequence of iNOS promoter by using HepG2 genomic DNA as template,and the product was cloned into pGEM-T vector.The iNOSp gene was cut from T-iNOSp by KpnⅠand XhoⅠ,and then was cloned into pCAT3-Basic,the constructed vector was named as pCAT3-iNOSp,pCAT3-iN- OSp was transfected into the LO_2 cell line.LO_2 cell was also cotransfected with pcDNA3.1(-)-core and pCAT3-iNOSp by FuGENE 6 transfection reagents.The LO_2 cells transfected with pCAT3-Basic was used as negative control.The activity of CAT in LO_2 cells was detected by an ELISA kit after 48 hours,which reflected the transactivating function of HCV core protein to iNOS gene promoter.Re- sults The expressive vector pcDNA3.1(-)-core and report vector pCAT3-iNOSp had been construc- ted and confirmed by restriction enzyme digestion and sequencing.The expression of CAT in LO_2 cells transfected with pCAT3-iNOSp and peDNA3,1(-)-core was 11 times as higher as that of pCAT3-bas- ic,and 6 times as higher as that of pCAT3-iNOSp.Conclusion It is suggested that HCV core protein can transactivate iNOS gene promoter.

Adult ; Aged ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; pathology ; physiopathology ; Respiratory Function Tests

Adolescent ; Adult ; Ankylosis ; complications ; surgery ; Female ; Humans ; Imaging, Three-Dimensional ; Male ; Micrognathism ; complications ; surgery ; Models, Anatomic ; Skull ; anatomy & histology ; Temporomandibular Joint Disorders ; complications ; surgery ; Young Adult