ObjectiveTo study B-cell activating factor(BAFF)/a proliferation inducing ligand (APRIL)protein and mRNA expression levels in patients with primary Sj(o)gren's syndrome(pSS)and its contribution to the pathogenesis of pSS.Methotis The levels of serum BAFF and APRIL were tested by ELISA method in 32 pSS patients and compared with 23 healthy control sabjects.BAFF/APRIL protein levels of labial salivary glands were examined in 17 pSS patients by immunohistochemical staining and compared with 8 healthy controls.BAFF/APRIL mRNA expression relative levels to GAPDH of PBMC were also detected in 18 pSS patients by real time RT-PCR and compared with 20 healthy controls.The relationship between BAFF/APRIL levels and several clinical manifestations in pSS patients were analyzed.Results The median level of serum BAFF in pSS were markedly higher than that in healthy controls[(7.4±3.9)ng/ml vs(3.7±1.1)ng/ml,P＜0.01].Serum APRIL levels were also significantly elevated compared to healthy controls[(26±15)ng/ml vs(16±15)ng/ml,P=0.039].The higher levels of BAFF were associated with higher levels of IgG,ESR.total globulin and the titer of ANA(P＜0.05).There was a positive correlation between serum APRIL levels and ESR and labial salivary gland lymphocyte focus scores(P＜0.05).The two cytokines levels inversely correlated with the count of peripheral white blood cells and platelets in pSS(P＜0.05).When comparing serum Ievels of APRIL and BAFF in patients with pSS,a positive correlation could be found(r=0.534,P=0.002).The BAFF/APRIL protein levels were higher in infiltrating lymphocytes of labial salivary glands from pSS patients than from the controls(P＜0.05).The BAFF mRNA[(0.023±0.024)vs(0.245±0.188),P＜0.01]and APRIL mRNA[(0.047±0.035)vs(0.130±0.097),P=0.002]levels of PBMC were significantly lower in pSS patients than in the normal controls.Conclusion The BAFF/APRIL levels of serum and labial salivary glands are significantly elevated in patients with pSS and correlate with clinical parameters.These indicate that BAFF and APRIL may be involved in the pathogenesis of pSS.The low BAFF mRNA and APRIL mRNA levels of PBMC in pSS may reveal that the production and regulation of this system is complicated.

Objective To investigate the relationship between genetic polymorphism of methylenetetrahydrofolate reductase (MTHFR) and the risk of acute lymphocytic leukemia (ALL). Methods Eighty-three patients with ALL and a cohort of 83 matched healthy objects were included, and DNA was extracted from their peripheral blood. PCR-RFLP was used to determine the genotypes of MTHFR C677T and A1298C. The adjusted odds ratio (OR) and 95% confidence interval (CI) were calculated using unconditional logistic regression model. Results It was found that the frequency of the MTHFR C677T TT genotype among patients was significantly different from that among control objects (P=0.008). The MTHFR C677T TT genotype had an increased risk of ALL compared with that of 677CC genotype (OR=3.229, 95%CI: 1.328-7.847, P=0.01). No significant association between the MTHFR C677T CT genotype or A1298C polymorphism and the risk of leukemia. Conclusion The present findings suggest that 677C→T polymorphism in MTHFR may be a genetic susceptibility factor for acute lymphocytic leukemia.

Objective To investigate the effects of EGB on hepatic fibrosis and expression of Activin A in rats with fibrosis.Methods From Oct.2004 to Apr.2005,the study was conducted in 30 adult male rats in the pepartment of Gastroenterology,the people's Hospital of Wuhan University.The rats were randomized into 3 groups:control group,model group and treatment group.Except the rats in the control group,others were induced to hepatic fibrosis by intraperitoneal injection of CCl_4 twice a week for 8 weeks.Those rats in the treatment group were intragastrically administered with EGB establish model of everyday.At the end of the 8th week,all rats were sacrificed.The samples of liver was staining with HE.The expression of Activin A was determined by immunohistochemistry and RT-PCR.Results The grade of fibrosis in EGB-treated groups were lower than that in the model group(P

Objective To study effects of hFRNK gene on phosphorylated p190RhoGAP expression and RhoA activation by mediated adenoviral vector in colorectal carcinoma cell Colo320WT stimulated with extrinsic gastrin17 in vitro.Methods AdEasyTMsystem was used to construct pAdhFRNK expressing human FRNK gene by recombination in E.coli.BJ5283.pCR3.1/GR plasmid expressing gastrin receptor CCK-2 was transfected into colonic carcinoma cell line Colo320 cells by LipofectamineTM2000 and expression stably CCK-2R clones was selected by G418(500 ?g/mL).The expression levels of gastrin receptor of Colo320 cells and the transfected cells Colo320WT were assayed by RT-PCR.Colo320WT cells were treated by 10～8 mol/L Gastrin17 for 0h and 12 h;and after Colo320WT cells were infected by pAdhFRNK(MOI:100)for 2 d,the cells were treated by Gastrin17 for 12 h again.The expression levels of phosphorylated p190RhoGAP of Colo320WT cells were assayed by immuniprecipation and western blot.RhoA activation was assayed by pull-down.using GST-Rhotekin-RBD followed by RhoA blotting.Results When 10～8 mol/L Gastrin17 stimulated Colo320WT cells for 12 h,the expression levels of phosphorylated p190RhoGAP increased apparently and RhoA activation diminished.When pAdhFRNK infected Colo320WT cells for 2 d and 10～8 mol/L Gastrin17 treated the cells for 12 h,the expression levels of phosphorylated p190RhoGAP decreased apparently and RhoA activity was elevated.Conclusion hFRNK can inhibit expression of phosphorylated p190RhoGAP and enhanced RhoA activity in the cells stimulated with Gastrin17,and its mechanism is probably that hFRNK can block FAK phosphorylation and FAK pathway.

The studies have demonstrated that arsenic trioxide (ATO) in combination with all-trans retinoic acid (ATRA) takes effects in treatment of acute promyelocytic leukemia (APL) through different underlying mechanisms. This has established the molecular foundation of ATO plus ATRA therapy. Currently, ATO plus ATRA has also been widely used in clinical practice.

Objective: To systematically review the efficacy and safety of arsenic trioxide (ATO) in treatment of acute promyelocytic leukemia (APL). Methods: The Cochrane Library (Issue 1, 2009), Cochrane Central Register of Controlled Trials (from 1970 to January 2009), MEDLINE (from 1978 to October 2008), EMBASE (from 1950 to March 2009), Chinese Biological Medical Literature Database (from 1978 to December 2008), China National Knowledge Infrastructure (CNKI, from 1994 to December 2008), and China Medical Academic Conference Database (from 1994 to December 2008) were electronically searched. We also searched the Meta-Register of controlled trials, Conference Proceedings of American Society of Hematology (from 1946 to December 2008) and Conference Proceedings of American Society of Clinical Oncology (from 1946 to December 2008) on the internet for grey literature. The related journals in the library of Third Military Medical University were hand-searched. The randomized controlled trials (RCTs) of ATO in treatment of APL were included. We adopted complete remission, overall survival rate, disease free survival rate, time to complete remission, relapse rate, mortality and adverse reactions as outcome indicators. Data were entered and analyzed with the Cochrane review manager software 5.0 (RevMan 5.0). Results: After merger of the included trials, five eligible RCTs with 328 cases were included. All the RCTs focused on the comparison of all-trans retinoic acid (ATRA) plus ATO regimen with ATRA monotherapy. Meta-analysis showed that the effect indexes for time to complete remission, two-year disease free survival rate, relapse rate, incidence of edema and incidence rate of QT interval prolongation were -1.20 [-1.68, -0.72], 8.64 [1.66,45.00], 0.21 [0.09,0.47], 4.16 [1.46,11.79] and 22.10 [2.75,177.49], respectively. The influences on other outcome indicators such as complete remission and leukocytosis were statistically non-significant. Conclusion: ATO can prolong disease free survival and reduce the time to complete remission and relapse rate of newly diagnosed APL patients, and increase the incidence of edema and prolongation of corrected QT interval during the treatment. Due to limitation of the included trials, this conclusion needs to be validated by further studies.

Objective To investigate the effect of methylation of the APC gene on expression and the correlation with clinical data in pancreatic cancer.Methods Sixty postoperative tissue samples with pancreatic cancer were collected in the First Affiliated Hospital of Zhengzhou University from August 2010 to January 2011,20 benign pancreatic disease tissues were collected as control groups.APC promoter methylation and gene expression levels were detected by Methylation Specific PCR (MSP),Real Time PCR (RT-PCR) and Western blot in 60 pancreatic carcinoma,42 metastasis and 20 benign pancreatic disease tissues,then analyze the relation between methylation of the APC gene and the clinical data.Results APC promoter methlation was observed 48.53％,46.67％ and 1.16％ in pancreatic carcinoma,metastasis and benign pancreatic disease tissue,respectively.Methylation of APC in pancreatic carcinoma and metastasis increased significantly compared with control tissues (x2 =12.903,14.402; P ＜ 0.05).There were no statistically significant differences of APC expression in these tissues (P ＞ 0.05).There was a significant correlation between methylation of APC and clinicopathological stage (x2 =6.801,P ＜ 0.05),but no correlation with gender,age,tumor size,histological grade and metastasis (x2 =0.727,1.311,0.372,0.148,0.017 ; P ＞ 0.05).Conclusion The methylation of APC gene is closely related with pancreatic carcinoma inogenesis and the clinicopathological stage,but do not effect the expression of APC in tissues.

Astrocytes play a major role in the reactive processes in response to neuronal injuries in the brain. Excessive gliosis is detrimental and can contribute to neuronal damage. CD81 (TAPA), a member of the tetraspanin family of proteins, is upregulated by astrocytes after traumatic injury to the rat central nervous system (CNS). To further understand the role of CD81 in the inhibition of astrocytes, we analyzed the effects of a CD81 antibody, on cultured rat astrocytes. The results indicated that the effect worked in a dose-dependent manner with certain dosage range. It, however, reached a dosage equilibrium at a high dosage. Furthermore, anti-CD81 antibody remarkably inhibited the proliferation of astrocytes after incubation with astrocytes for different periods of time and the effect presented a time-dependent fashion. However, anti-CD81 antibody substantially inhibited the proliferation of astrocytes at low density and middle density but slightly inhibited the proliferation of astrocytes at high density, suggesting that the effect was positively correlated with the proliferative ability of astrocytes. Finally, the cell cycle of astrocytes exposured to anti-CD81 antibody was arrested in S phase at the initial stage and at G(0)/G(1) phase over time. These findings indicated that CD81 exert significant inhibitory effect, dose-dependently and time-dependently, on the proliferation of astrocytes and the effect is positively correlated with the proliferative capability of astrocytes.

Objective To compare the efficacy and safety of arsenic trioxide ( ATO) with all-trans retinoic acid ( ATRA) for the treatment of acute promyelocytic leukemia ( APL) . Methods We searched the database of Cochrane Library ( Issue 1,2009) ,CENTRAL ( 1970 to 2009) ,Medline ( 1978 to 2008) ,EMBASE ( 1950 to 2009) ,CBM ( 1978 to 2008) ,CNKI ( 1994 to 2008) and CMAC ( 1994 to 2008) . We also searched the Meta register,Conference Proceedings of American Society of Hematology ( 1946 to 2008) and American Society of Clinical Oncology ( 2004 to 2008) on the internet for grey literature. We had searched the related journals in the library of Third Military Medical University,too. We included randomized controlled trials which compared ATO with ATRA for the treatment of APL. We adopt complete remission rate,overall survival rate, disease-free survival rate,time to complete remission,relapse rate,mortality and adverse reactions as result indicators. Data were entered and analyzed with the Cochrane review manager software ( Revman 5. 0) . Results Four eligible randomized controlled trials ( RCTs) were included ( n =243) . All the RCTs were methodologically graded as B. They all are focusing on the comparison of ATO monotherapy with ATRA monotherapy in treating newly diagnosed APL patients. Meta analysis showed that effect index for complete remission,2-year disease-free survival,time to complete remission,relapse rate and mortality was 0. 96 ( 0. 50,1. 86) ,2. 76 ( 0.71,10.66) ,-1.30 d ( -1.83,-0.78) ,0.86 ( 0.45,1.63) ,and 1.15 ( 0.45,2.95) ,respectively. All indicated no statistically significant difference. Effect index for incidence of liver dysfunction was 3. 03 ( 1. 25, 7. 37) ,which showed statistically significant difference between ATO group and ATRA group. Conclusion ATO is not superior to ATRA in treating newly diagnosed APL patients regarding complete remission,diseasefree survival rate,time to complete remission,relapse rate and mortality. What is worse,it will increase the incidence of liver dysfunction during treatment. Due to limitation of included trials,this conclusion need to be validated by further studies.

Objective To investigate the effect of anti-CD81(antibodys against CD81) on the proliferation of astrocytes. Methods Purified astrocytes from newborn rats' cerebral cortex were divided into 6 groups and added with anti-CD81 different concentrations(0,0.1,0.5,1,5,10?mg/L).The activity of astrocytes was tested by methyl thiazolyl terazolium(MTT).Three significative groups were chosen based on MTT result and added with anti-CD81 of different concentrations(0,0.5,5mg/L).After administration for 24 hours,the cell cycle of the astrocytes was measured by flow cytometer.The corresponding data were analyzed with SPSS statistical software. Results 1.By MTT,the average optical density(AOD) values of astrocytes were reduced after administration with anti-CD81 of different concentrations for 24 hours,that is,the number of astrocytes was reduced,which indicated anti-CD81 inhibited the proliferation of astrocytes and the effect showed a dose-dependent pattern.2.By cell cycle analysis,a progressive dose-dependent decrease was found in the index of cells in G-0/G-1 phase and an increase in S phase.Such as,the index of cells in G-0/G-1 phase,was 82.73 in 0,is 82.16 in 0.5?mg/L,was 78.58 in 5?mg/L.Conclusion Anti-CD81 inhibits the proliferation of astrocytes and the number of astrocytes is reduced.Further more,the index of cells decreases in G-0/G-1 phase and increases in phase S after administration with anti-CD81.This study shows that anti-CD81 doesn't restrain the cells from G-1 phase to S phase but the cells are arrested in S phase.