0.05).The iris diaphragm was flat to mild concave which lead the width of anterior chamber angle increased postoperation, no peripheral synechia was found. Conclusion: Phacoemulsification and foldable posterior chamber intraocular lens implantation through clear corneal incision had no significant influence on the long term intraocular pressure in simple senile cataract patients, the width of anterior chamber angle increased postoperation.

AIM:To detect the existence of signal joint T-cell receptor excision DNA circles(sjTRECs)of 23 TCR V? subfamilies in mononuclear cells of patients with multiple myeloma(MM),and to evaluate the recent thymic emigrants of corresponding V? subfamily nave T cells in MM patients.METHODS:23 TCR V? subfamily sjTRECs were amplified in genomic DNA from 5?104 PBMCs of 12 cases in MM patients by using semi-nest PCR.10 normal individuals served as controls.RESULTS:The number of detectable V? subfamily sjTRECs was 5.00?2.45 from MM patients,as compared with 9.60?5.48 from normal individuals,the difference was significant(P

AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h，the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia.

Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.

Objective: To investigate whether insulin stimulates the translocation of glucose transporter-4 (GLUT4) and glucose uptak e in ischemic myocardium. Methods: Plasma concentration of gluc ose, lactate, free fatty acid and insulin were determined by autoanalyser, and G LUT4 was studied by Western blotting analysis. Results: Insulin increased GLUT4 significantly in sarcolemma of ischemic myocardium ［(25±4)% vs (40±6)%］, and GLUT4 content in intracellular membrane decreased proporti onally. The glucose uptake increased significantly in insulin-ischemic myocardi um. The uptake of insulin-ischemic myocardium was almost 2 times that of ischem ic myocardium. Conclusion: Insulin stimulation results in GLUT4 translocation and increases glucose uptake in ischemic myocardium. When myocardi al ischemia occurs, insulin is helpful in increasing myocardial glucose uptake a nd utilization.

Objective　To investigate the mechanism for that insulin facilitates increase of glucose uptake. Methods　The expression of myocardial GLUT4 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT4 mRNA was determined by semiquantitative Northern blotting. Results　After infusing insulin for 8　hours，the　expression　of　GLUT4 mRNA and GLUT4 polypeptide was significantly higher in canine myocardium than in　those　found normal ones. The glucose uptake was upregulated at　the　same　time．Conclusions　Our findings suggest that insulin facilitates the expression of GLUT4 mRNA and GLUT4 polypeptide in canine hearts. Enhanced GLUT4 expression is one of the important molecular mechanism by which myocardial cells enhance glucose uptake by insulin stimulation.

AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h,the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia. [

Exhalation ; Humans ; Nitric Oxide ; analysis ; Nose

Objective To evaluate the relationship between the change of the aortomitral angle (AMA) with left ventricular systolic function in patients with ischemic cardiomyopathy (ICM) by echocardiography.Methods Thirty-one patients were enrolled in the ICM group,and 59 healthy subjects were selected as the control group.On the parasternal left ventricular long axis plane,AMA were measured at the R wave apex (R-AMA),J-point(J-AMA),ST-segment midpoint(ST-AMA),T-final wave (T-AMA)and P-final wave (P-AMA).The angle difference(⊿ θ) =AMAmax-AMAmin,the angle changing rate =⊿ θ/AMAmax.The global left ventricular longitudinal strain (GLS) and global circumferential strain (GCS) were obtained by 2D-speckle tracking echocardiography.Left ventricular ejection fraction(LVEF),left ventricular end-diastolic volume(LVEDV) and left ventricular end-systolic volume(LVESV) were measured using Simpson biplane method.Results The J-AMA was the largest in the control group,while the ST-AMA was the largest in the ICM group.The levels of LVEDV,LVESV and AMA in ICM group were significantly higher than those in control group,while LVEF,GLS,GCS,⊿ θ/AMAmax and ⊿ θ were decreased (P ＜0.05).In the control group,there was a correlation between T-AMA and LVEF (r =-0.349,P =0.007),and ⊿ θ was negatively correlated with GLS (r =-0.372,P =0.004).In the ICM group,⊿1 θ/AMAmax and ⊿ θ were correlated with LVEF (r =0.424,P =0.018;r =0.490,P =0.005).Conclusions AMA in ICM patients is significantly increased.The angle difference and the rate of its change are closely related to the LVEF,which is a manifestation of three-dimensional structure change of the myocardial.

Objective:To investigate the gene expression of TCR V? subfamily T cells and clonality in peripheral blood CD4+ and CD8+ cells from patients with chronic myelogenous leukemia-chronic phase(CML-CP).Methods:The complementarity determining region 3(CDR3)of TCR V? subfamily genes in peripheral blood mononuclear cells(PBMCs),sorted CD4+ and CD8+ cells from 19 CML-CP patients were amplified using RT-PCR,the products were further by genescan analysis to identify the clonality of T cells.Results:Only 1 to 21 V? subfamilies were detected in peripheral blood CD4+ and CD8+ cells from patients with CML.The most frequent expression of V? subfamily was V?13 followed by V?9.Clonal expanded T cells in some V? subfamilies could be identified in both CD4+ and CD8+ cells,especially in CD8+ cells.The clonal expanded of V?21 subfamily in CD4+ cells and V?11 subfamily in CD8+ cells were identified most frequently.Conclusion:The restricted distribution of TCR V? repertoire has been found in CD4+ and CD8+ cells in patients with CML.Clonal expanded CD4+ cells and CD8+ cells have been identified which may relate to host immune response to CML antigen and may play a important role in anti-CML effect.