Objective To study the clinical and imaging characteristics of cerebral venous sinus thrombosis(CVST).Methods Clinical data of 9 cases with CVST were retrospectively analyzed.Results All patients had headache,nausea and vomiting; 5 patients had epilepsy; 3 patients had focal neurological deficits; 3 patients had fever; 3 patients had palilledema; 3 patients had disturbance of consciousness. CSF examination showed prominent high intracranial pressure, but conventional and biochemical examinations were normal. 8 patients did CT scan, but the diagnosis was not clear. All patients first MRI showed venous sinus and related brain areas long T1 and T2 signal; MRV showed that the involved venoussinus had non-visualized signal. MRI in chronic phase showed slightly higher T1 and T2 signal; MRV showed sinus enhancement.The outline of uncomplete reconalzation was unclear. Conclusions The common high intracranial pressure is unspecific sign and symptom of patients with CVST. CSF examination show that the intracranial pressure is prominent high, but conventional and biochemical examination are normal. MRI can show that the normal flow void of the dural sinus is disappeared, instead of abnormal high or equality intensities. The characters of CVST in MRV are those the blood flow signal of involved venous sinus be disappeared or showed anormalism.

OBJECTIVE:To compare the in vitro antibacterial activity of azlocillin given alone with azlocillin plus tazobactam against168strains of clinically isolated pathogenic bacteria.METHODS:The antibacterial activities of two antibac_ terials against168strains of clinically isolated pathogenic bacteria in vitro were detected by two-fold dilution method.RE-SULTS:The MIC 50 and the MIC 90 of the combined therapy of azlocillin/tazobactam(4∶1)were1/32and1/64,respectively that of azlocillin given alone.CONCLUSION:The concomitant therapy of azlocillin with tazobactam improves the antibacterial activity.

Endothelialprogenitorcels(EPCs)arethepluripotentstemcelsofvascularendothelial cels. They have self-differentiation and proliferation ability. A large number of animal experiments and preliminary clinical studies have show n that EPCs have broad prospects of clinical application. This article review s the research status of EPCs and their application in the clinical treatment of ischemic stroke.

Background To investigate the expression of the early growth response gene-1 ( Egr-1 ) mRNA after focal cerebral ischemia / reperfusion in rats.Methods Ten healthy male SD rats weighing 200 ～ 250 g were used to create model of focal cerebral ischemia. The expression of Egr-1 after focal cerebral ischemia/reperfusion in rats was determined using in situ hybridization and RT-PCR.Results (1) The result of the in situ hybridization: A trace amount of Egr-1 mRNA expressed in the neurons and the glial cells in the sham operated group. The expression of Egr-1 mRNA at the ischemic side increased dramatically following ischemia and reached peaks after 4 hours' reperfusion. Egr-1 expression started to subside following 22 hours' reperfusion and further decreased following 166 hours' reperfusion, which was still significantly higher than that in the sham operated group. (2) The result of RT-PCR: The expression of Egr-1 mRNA at the ischemic side was significantly higher than that in the sham operated group at all time points after ischemia/reperfusion in the rats(P ＜0. 01). Expression of Egr-1 increased 2 h after ischemia and reached the peak 4 h following reperfusion, and then decreased dramatically at 46 h after reperfusion which was still higher than that in the sham operated group (P ＜ 0. 01). As the ischemia/reperfusion period prolonged, the expression of Egr-1 mRNA increased gradually, but still detectable even 166 h following reperfusion. The expression of Egr-1 was significantly higher than that in the sham operated group at all time points (P ＜0. 01).Conclusions The expression of Egr-1 mRNA increase in the neurons and the glial cells after ischemia/reperfusion, which may have protective effects on ischemic brain tissues.

OBJECTIVE:To observe the effects of clarithromycin and fleroxacin on Pseudomonas aeruginosa(PA) biofilm METHODS:Clinical isolates of 7 strains of PA from respiratory tract were cultured with modified plate culture method;bacterial biofilm model was identified by silver nitrate staining;MICs were determined by broth microdilution The number of viable bacteria in biofilm was measured by using MTT method and bacterial adherence was measured by crystal violet staining RESULTS:1/16MIC and 1/4MIC of clarithromycin could inhibit the adherence of PA to silica-gel film(P

AIM: To evaluate effects of diltiazem on platelet hyperreactivity in situations associated with endothelial injury and their possible relationship to cytosolic calcium concentration. METHODS: Blood samples were collected at 7 time points from 35 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) who received combined diltiazem and aspirin/ticlopidine therapy or aspirin/ticlopidine therapy alone. Platelet expression of glycoprotein Ⅱb/Ⅲa and cytosolic calcium concentration were measured, respectively, by whole blood flow cytometry and fluorospectrophotometry. The effects of diltiazem of different concentrations on expression of glycoprotein Ⅱb/Ⅲa were also studied in vitro in blood samples from patients with chronic stable angina. RESULTS: Of the two treatments, aspirin/ticlopidine therapy did not prevent an acute increase of expression of glycoprotein Ⅱb/Ⅲa 5 minutes and 10 minutes after first inflation and 10 minutes after PTCA, whereas combined diltiazem and aspirin/ticlopidine therapy had a significant inhibitory effect. In the group receiving aspirin/ticlopidine therapy, there was a short-term elevation of platelet [Ca~(2+)]i immediately following PTCA which was significantly reduced by diltiazem treatment. Expression of glycoprotein Ⅱb/Ⅲa was significantly inhibited in vitro by diltiazem in the concentration of 200 ?g/L or higher, but not 50 ?g/L. CONCLUSIONS: Combined diltiazem and aspirin/ticlopidine therapy significantly inhibited platelet activation that continued in the presence of conventional aspirin/ticlopidine treatment. Antiplatelet effects of diltiazem were probably a consequence of reduction of platelet [Ca~(2+)]i and may only be achieved in higher than therapeutic concentrations. [

Objective The aim of this study was to investigate the differences of the cell ultrastucture of normal mouse hatched blastocysts and their dormant ones cultured in vitro after freezing-thawing, and to explore whether the dor-mant embryos have a better anti-freezing shock property than the normal hatched mouse embryos .Methods By transmis-sion electron microscopy , the ultrastructure of these two types of mouse embryos was observed and analyzed .Results By comparative analysis of their ultrastructure , the results showed that the dormant embryos before freezing are being austerity and with lower energy metabolism at a ‘ground state ’ .After freezing-thawing and culture , their cellular structure seemed to be similar to that of the normal embryos cultured in vitro before freezing.However, after freezing-thawing and culture, the number of mitochondria decreased , the nuclei were loose , and their heterochromatin also increased .Conclusions From the ultrastructural observation , compared with the normal mouse hatched embryos , the cellular state of dormant mouse em-bryos after freezing-thawing is more favorable for material storage and energy metabolism , thus, indicating that they have a better anti-freezing property than normal hatched embryos .

Objective To detect the treatment effect of PC3 cells with triptolide on altering the expression of genes.Methods MTT assay was used to detec the inhibition of proliferation.Apoptosis was detected by Annexin-V/PI staining.RT-PCR was used to analyze the mRNA expressions of BCL-2,BAX,PIG3,P21,FAS,CASPASE3.Results Triptolide caused a time - and dose - dependent inhibition of cell proliferation,and IC50 of 24 h and 48 h were 18.3 ng/ml and 13.5 ng/ml,respectively.Compared with the 24 h group,the low concentration of triptolide(5 ng/ml,t =1.47,P ＞0.05)and the high concentration of triptolide ( 160 ng/ml,t =0.91,P ＞0.05)had no statistical significance in 48 h group,while 10 ng/ml( t =3.26,P ＜0.05),20 ng/ml( t =4.21,P ＜0.05),40 ng/ml( t =4.09,P ＜0.05),80 ng/ml( t =2.91,P ＜ 0.05 )had statistical significance.At the concentration of 18.3 ng/ml,triptolide induced PC3 cells apoptosis in a time - dependent manner.Compared with the control group,Anexin-V( + )/PI(-)was(5.42±2.21)％(t =3.52,P ＜0.05)in 6h,(13.51±3.37)％(t =6.53,P ＜0.01) 12h,(29.3 ±4.53)％ ( t =8.74,P ＜0.01) 24 h group separately,and it had statistical significance.RTPCR showed that 18.3 ng/ml triptolide up-regulated the mRNA expression of BAX and PIG3,down-regulated P21 and BCL-2.FAS and CASPASE3 did not show obvious changes.Conclusions Triptolide inhibits the proliferation of PC3 and induces apoptosis,and the changes of BCL-2,BAX,PIG3 and P21 may play an important role in the apoptosis of PC-3 cells.

Objective To evaluate anti-HEV IgG and IgM diagnostic kits with sera from convalescent hepatitis E patients and to establish the quantification method of detecting anti-HEV lgG.Methods Detect 42 convalescent serum samples of over 6 months after onset of hepatitis E patients from Jiangsu province with anti-HEV IgM and IgG diagnostic kits. Select and mix the anti-HEV IgG positive sera which were confirmed by Western blot with ORF2 and ORF3 antigen. The mixed serum was calibrated with a WHO anti-HEV Ig standard. A series quantitative linear standard was made for quantitative detection of anti-HEV IgG in hepatitis E vaccine clinical trials phase Ⅲ. Results The positive rates of the anti-HEV IgG di-agnose kits of G, K, MP, Wantai were 71.4%, 78.6%, 92.9% and 100% respectively. The positive rates of G was lower than that of MP (χ~2 = 5.19, P<0.05) and obviously lower than Wantai (χ~2 = 11.76,P<0.01). The positive rates of K was also obviously lower than that of Wantai (χ~2 =7.96, P <0.01).The positive rates of the anti-HEV IgM diagnose kits of MP, G, X, Wantai, K were 21.4%, 7.1%,21.4%, 64.3%, 78.6% respectively. The positive rate of both K and Wantai were obviously higher than that of MP(χ~2 = 15.75 ,P<0.01 ; X2 = 27.43 ,P< 0.01). With the Western blot confirmation test, 30 and 18 sera were reactive to ORF2 and ORF3 antigen separately. The anti-HEV IgG concentration of HEV-D01 mixed by 13 samples was 57.94 U/ml by the calibration. Prepare seven 1.5-fold dilution series of quantita-tive linear standard for HEV vaccine clinical trials phase Ⅲ, concentration range from 0.077 to 0.877 U/ml. The quantitive values of high, medium and low concentrations quality control samples lay in the range of average ± 2s, and the CV of quantitative values were 16%, 16%, 12% respectively. Conclusion The quality of different anti-HEY IgM and IgG diagnose kits were different. This study had set up a set of anti-HEV IgG linear quantitative standard, which fit for detecting anti-HEV IgG antibodies quantitatively in HEVvaccine clinical trial phase Ⅲ.

Objective To study the hepatocyte cells infected by hepatitis C virus (HCV) positive serum. Methods Human hepatocyte 7701 was incubated with HCV RNA-positive and HCV antibody(Ab) negative sera BP52. Then, the expression of HCV antigen and the presence of HCV-RNA in cell and supernatant were assayed by RT-PCR, sequence analysis, immunofluorescent staining, Western blot, confocal laser microscopy. The ultrastructural changes of infected cells were observed by electro-microscopy. Results Plus-strand RNA and minus-strand RNA were intermittently detected in cell and/or supernatant on day 7-45 after infection. Sequence analysis demonstrated that the positive DNA nucleic acids were identified with HCV 5′-non-coding region(NCR) sequence. HCV core and NS3 protein were expressed in cytoplasm of infected cells. After 2 or 3 weeks, obvious intracellular ultrastructural changes and virus-like particles were observed. Conclusion human hepatocyte 7701 could support replication of HCV in vitro, which could be a useful tool for setting up cell model of HCV infection and studying the mechanism of HCV infection.