AIM:To compare the influence of anterior chamber maintainer and viscoelastic agent on corneal astigmatism and endothelial cells after phacoemulsification.METHODS:Totally 70 patients(70 eyes) of cataract from April 2013 to April 2015 were randomly divided into the study group and the control group, with 35 cases in each group.The study group were treated with anterior chamber maintainer during phacoemulsification with support system approach, and the control group were treated with phacoemulsification under viscoelastic agent.RESULTS:The age (t=0.215, P=0.831), the density of corneal endothelial cells (t=-0.352, P=0.726) and corneal luminosity (t=-0.162, P=0.872) of two groups had no significant difference before surgery;there were no significant difference in preoperative visual acuity (t=0.463, P=0.599) and visual acuity (t=1.616, P=0.124) at 1mo after operation.And patients in the study group (t=-21.129, P<0.01) and the control group (t=-12.780, P<0.01) before surgery and 1mo postoperative when compared with the naked eye eyesight showed significant difference.The visual acuity after operations improved significantly.There were significant differences of corneal endothelial cells density (t=8.489, P< 0.01) and corneal astigmatism (t=-2.032, P=0.046) in the study group before surgery and 1mo after surgery;corneal endothelial cell density (t=8.999, P<0.01) and corneal astigmatism (t=-2.167, P=0.034) in the control group before surgery and 1mo after surgery also had significant differences.There was no significant difference in the rate of corneal endothelial cell loss between the two groups (t=0.410, P=0.683).CONCLUSION:Compared with viscoelastic agent, anterior chamber maintainer during phacoemulsification in patients with cataract won't increase the damage of postoperative surgically induced astigmatism and corneal endothelial cells, which mean the method of anterior chamber maintainer during phacoemulsification in the treatment of cataract is safe and effective.

BACKGROUND:Mesenchymal stem cells(MSCs) have immunoregulation,can reduce the occurrence rate of graft versus host disease following transplantation,and treat autoimmune disease. OBJECTIVE:To observe the immunoregulation of human umbilical cord(UC) -MSCs on bone marrow T-lymphocyte of patients with aplastic anemia. DESIGN,TIME AND SETTING:A randomized grouping design,in vitro cytological controlled study. Cases were obtained from the Department of Hematology,First Hospital and Second Hospital Affiliated to Nanchang University. Experiments were conducted at the Institute of Hematology,Second Hospital Affiliated to Nanchang University from September 2007 to November 2008. PARTICIPANTS/MATERIALS:A total of 22 patients with aplastic anemia were enrolled at the Department of Hematology,First Hospital and Second Hospital Affiliated to Nanchang University. There were 6 cases of severe aplastic anemia(3 males and 3 females) ,with a median age of 38(16-68) years;16 cases of chronic aplastic anemia(9 males and 7 females) ,with a median age of 41(25-59) years. Umbilical cord was obtained from healthy full-term fetus by normal uterine-incision delivery for isolation,culture and determination of human UC-MSCs. METHODS:MSCs were extracted from human umbilical cord. T-lymphocytes were isolated from bone marrow of patients with aplastic anemia by density gradient centrifugation. MSCs were cocultured with T-lymphocytes. In the control group,T-lymphocytes were incubated at 1?105/well. In the UC-MSCs group,human UC-MSCs were incubated at various densities of 1?105/well,0.5?105/well,0.1?105/well and 0.05?105/well. In the experimental group,T-lymphocytes were cocultured with UC-MSCs at 1:1,1:0.5,1:0.1,1:0.05. MAIN OUTCOME MEASURES:Inhibitory rate of human UC-MSCs at various concentrations on T-lymphocytes of aplastic anemia patients was measured by MTT assay. CD4+/CD8+ changes of the T cells were analyzed by flow cytometry. Expression of the two marrow hematopoietic factors(interleukin-2 and ?-interferon) in the supernatant was evaluated by ELISA. RESULTS:The second passage of MSCs had typical morphology of fibroblast,and highly expressed CD166,CD29,CD54,but lowly expressed CD13,CD34,CD45. MSCs could be induced into adipocytes. UC-MSCs showed inhibitory effect on lymphocyte proliferation of aplastic anemia patients when UC-MSCs and lymphocytes mixed at the ratio of 1:1,0.5:1,0.1:1,and their inhibitory rate were(56.2?12.1) %,(43.7?10.4) %,(28.6?8.9) %. The effect was the strongest at the ratio of 1:1. UC-MSCs adjusted the proportion of CD4+ and CD8+,inhibited the secretion of interleukin-2 and ?-interferon by T cells of aplastic anemia patients. CONCLUSION:Human UC-MSCs can mediate an immunoregulation effect on T lymphocytes of aplastic anemia patients in vitro and the inhibitory effects are dependent on the amount of UC-MSCs.

Objective To investigate the influence of the aberrant protein expression and mRNA transcription of transforming growth factor ? 1(TGF? 1) on the biological behavior of human bladder transitional cell carcinomas. Methods The expression of TGF? 1 was investigated in 74 specimens of TCCs by SP immunohistochemistry staining, and the level of TGF? 1 mRNA were determined in 43 cases of TCCs by the method of quantitative RT PCR. Results The positives expression rate of TGF? 1 was 89.2%. Superficial tumors had lower overexpressive rate of TGF? 1(33.3%) than the invasive TCCs(83.8%), P

OBJECTIVETo investigate the association of A260G and A386G polymorphisms of the DAZL gene with male infertility caused by oligozoospermia or azoospermia.

METHODSWe searched the PubMed, Science Direct, Wiley Online Library, CNKI, VIP, and CDDB databases up to November 30, 2013 for case-control studies evaluating the relationship of SNP260 and SNP386 polymorphisms of the DAZL gene with male infertility, and meanwhile conducted manual sourcing of the references in the identified studies and relevant articles. Two reviewers independently screened the title, abstract and keywords of each article retrieved. The StataSE12. 0 software was used for meta-analysis and other statistical analyses.

RESULTSTotally, 13 case-control studies were included (10 about A260G and 11 about A386G), involving 2 715 infertile patients (2 500 with oligozoospermia or azoospermia) and 1 835 normozoospermic men. DAZL A260G showed no statistical significance in the allele, dominant, recessive, co-dominant, or super-dominant gene model (P >0. 05). DAZL A386G exhibited a strong correlation with oligozoospermia or azoospermia in Asians in the allele gene model (OR = 0. 15, 95% CI 0.07 -0.34, P <0.05), dominant gene model (OR =0. 16, 95% CI 0.07 - 0. 35, P <0.05), co-dominant gene model (AA/AG) (OR = 0. 15, 95% CI 0. 06 - 0. 33, P < 0. 05), and super-dominant gene model (OR = 0. 15 (95% CI 0.06 - 0.33, P <0.05) , and so did it in Chinese in the four gene models ( OR = 0. 11, 95% CI 0.04 - 0. 28, P <0.05; OR =0. 11, 95% CI 0.04 - 0.28, P<0.05; OR = 0.09, 95% CI 0.03 - 0.26, P<0.05; OR = 0.09, 95% CI 0.03 - 0.26, P< 0.05).

CONCLUSIONOur study manifested that the DAZL polymorphism A386G, but not A260G, was correlated with reduced sper- matogenesis or sperm count specifically in Chinese males. More high-quality trials are required for a deeper insight into the exact relationship of DAZL A260G and A386G polymorphisms with oligozoospermia- or azoospermia-induced male infertility.

Alleles ; Asian Continental Ancestry Group ; Azoospermia ; genetics ; Case-Control Studies ; Humans ; Infertility, Male ; genetics ; Male ; Oligospermia ; genetics ; Polymorphism, Genetic ; RNA-Binding Proteins ; genetics ; Spermatozoa

Objective To study the expression of human kallikrein gene(KLK) 4 and KLK5 in ovarian cancers,and to investigate the pathogenesis in malignant tumors. Methods Fifty specimens of ovarian cancers were divided into three groups: malignant tumor group(n=23),borderline tumor group(n=6) and control group(normal or benign tumor,n=21).Fluorescent quantitative RT-PCR was employed to determine the expression of KLK4 and KLK5 in these specimens. Results The expression of KLK4 in ovarian cancers was significantly higher than that of the control group(P

Objective To explore the effect of sodium butyrate(NaB) on phosphorylation/ acetylation of histone H3(ph/acH3) at G?-globin gene and A?-globin gene promoter regions in K562 cells.Methods K562 cells were devided into 2 groups:K562 cells were grown in the presence or absence of 0.5 mmol?L-1NaB for 48 h [K562(NaB) group] and untreated K562 cells group(K562 group).Semi-quantitative RT-PCR was employed to measure the levels of G?-globin mRNA and A?-globin mRNA.The real time PCR-based chromatin immunoprecipitation(ChIP) was used to detect the levels of ph/acH3 at G?-globin gene and A?-globin gene promoter regions.Results Compared with the K562 group,there was a 1.4-fold(t=-149.022,P=0.000) and 1.2-fold(t=-13.363,P=0.000) increase in G?-globin mRNA and A?-globin mRNA,respectively,in K562(NaB) group.The level of ph/acH3 at G?-globin gene and A?-globin gene promoter region increased by 2.9-fold(t=-12.833,P=0.006) and 3.2-fold(t=-10.484,P=0.000),respectively,in K562(NaB) group,compared with the K562 group.The %Input value of G?-globin and A?-globin promoter fragment was 10.0-fold(P=0.000) and 9.5-fold(P=0.000) higher than that value of Necdin gene promoter fragment in the K562(NaB) group,while the %Input value of G?-globin and A?-globin promoter fragment was 3.2-fold(P=0.000) and 2.7-fold(P=0.000) higher than that value of necdin gene promoter fragment in K562 group.Conclusions NaB improves the phosphorylation and acetylation of H3 at ?-globin gene promoter regions,and this may be one of the mechanisms of expression of ?-globin genes induced by NaB.

Objective To compare the bone mineral density of the regions of femoral and tibial tunnels for anterior cruciate ligament(ACL)reconstruction in order to provide reference for the choice of optimal screw diameter for interference fixation.Methods Thirty healthy volunteers aged from 18 to 35 years were enrolled in our study,and the dual-energy X-ray absorptiometry(DEXA)was used to measure the bone mineral density of femoral and tibial tunnel regions of the right knee.All the right knees of the volunteers were also scanned by spiral CT and three-dimensional reconstruction technique was utilized to determine the circular sections that pass through the longitudinal axis of the femoral and tibial tunnels separately.The CT gray scale values of the Sections were measured.From August to October 2010,9 patients who had been diagnosed as ACL rupture underwent the operation of ACL reconstruction,and cylindrical cancellous bone peg was removed from the femoral and tibial tunnel respectively during the operation.Volumetric bone mineral density of the bone pegs were measured by using a standardized immersion technique according to Archimedes’ principle.Results Measured by DEXA,bone density of the femoral tunnel region arid tibial tunnel region were(1.162±0.034)g/cm2 and(0.814±0.038)g/cm2 respectively.The difference was significant between the femoral and tibial tunnel region(t=9.11,P=0.000).The CT gray scale value of the section for femoral tunnel region was(211.7±11.5)Hu,while that of the tibial tunnel region was(104.9±7.4)Hu.There was statistically significant difference between them(t=10.15,P=0.000).The volumetric bone mineral density of the bone peg from femoral tunnel and tibial tunnel were(2.80±0.88)g/cm3 and(1.88±0.59)g/cm3 respectively.The difference was statistically significant(t=4.32,P=0.002).Conclusion For ACL reconstruction,bone mineral density of femoral tunnel region is higher than that of the tibial tunnel.

Objective To investigate the effect of angiotensin Ⅱ(AngⅡ) and losartan on ? cells,and its related molecular mechanisms.Methods Normally cultured RIN-m cells were divided into three groups:control group(cultured with RPMI 1640 medium),AngⅡ group(treated with 100 nmol/L AngⅡ),losartan group(treated with 1 ?mol/L losartan 15min before addition of 100nmol/L AngⅡ).After incubation for another 48h,the apoptosis rate of RIN-m cells was quantified by flow cytometry(FCM) with Annexin-V FITC/PI dual staining.The expressions of Bcl-2 and Bax mRNA and protein were determined by RT-PCR and Western blotting,and the activities of Caspase 3 and Caspase 9 were detected by spectrophotometry.Results The apoptosis rate of RIN-m cells was significantly higher in AngⅡgroup than in both control and losartan group(P0.05).In comparison to the control group,the expressions of Bcl-2 mRNA and protein significantly declined,while of Bax mRNA and protein increased obviously in AngⅡ group(P0.05),but the expressions of Bcl-2 mRNA and protein were significantly higher(P0.05).Conclusion AngⅡ may induce the apoptosis of ? cells through mitochondrial pathway,and pre-intervention with losartan,which partly reverses the effect of AngⅡ,may play a protective effect on ? cells.

Objective To investigate the effect of angiotenisn ⅡI (Ang Ⅱ) on RIN-m β-cell,and to explore the mechanism of β-cell function impairment caused by Ang Ⅱ.Methods RIN-m cells were cultured with various concentrations of AngⅡ (0.1,1,10,100 nmol/L).After incubation for 24 hours,the basal(3.3 mmol/L) and glucose-stimulated(16.7 mmol/L) insulin secretion(GSIS)were detected by radioimmunoassay,mRNA and protein expressions of uncoupling protein 2(UCP2)were determined by RT-PCR and Western blot,respectively.The intracellular ATP content was measured by luciferase bioluminescence.The mitochondrial membrane potential and cellular Ca~(2+) concentration were detected by flow cytometry.Results (1) Various concentrations of Ang Ⅱ had no significant influence on the basal insulin secrection of RIN-m cell(F=0.644,P = 0.634).Except for 0.1 nmol/L AngⅡ,the other concentrations of Ang Ⅱ markedly reduced GSIS of RIN-m cells(F= 118.528,P = 0.000).(2) Compared with the control group,Ang Ⅱ significantly increased mRNA and protein expression of UCP2(F= 1 370,P = 0.000;F=675.175,P = 0.000).(3)Except for 0.1 nmol/L Ang Ⅱ,the other concentrations of Ang Ⅱ significantly decreased the mitochondrial membrane potential,cellular ATP content,and cellular Ca2+ concentration of RIN-m cell(F=4.035,P=0.008;F=3.353,P = 0.013;F=5.867,P = 0.001).Conclusion Ang Ⅱ impairs GSIS of p-cell,the mechanism of impairment may be interpreted that Ang Ⅱ can increase the expression of UCP2,furthermore,it can reduce mitochondrial membrane potential,decrease the content of cellular ATP and the concentration of cellular Ca~(2+),can finally impair the function of β-cell.