ObjectiveTo investigate changes of sex hormone levels and sexual function in male patients after liver transplantation.MethodsBlood samples were taken from 69 male patients receiving liver transplantation pretransplantation and postoperative 3rd,7th,14th day,1st and 3rd month respectively.Serum estradiol and testosterone were measured by radioimmunoassay.Serum sex hormone binding globulin was measured by ELISA.Sixty-nine discharged adult male liver transplant recipients ( age ranging 24 -45 years) with a normally functioning allograft for at least 6 months were questioned on their pre-and post-operativesexualfunction compared with 23adulthealthy controls.ResultsPretransplantation serum estradiol and sex hormone binding globulin were significantly higher (87.56±31.21 vs.26.00 ±9.12,u=9.30,P＜0.0001,134.50±30.68 vs.51.04 ±12.05,u=12.69,P ＜ 0.0001,respectively),and testosterone was lower than normal controls (2.02 ± 1.28 vs.4.82 ± 1.48,u =-8.73,P ＜0.0001 ) and levels were correlated with MELD scores (r =0.80,P ＜0.0001,r =-0.77,P ＜0.0001,r =0.72,P ＜0.0001,respectively).Sex hormone levels were back to normal on postoperative 2nd week (serum estradiol) or 1st month (serum testosterone and sex hormone binding globulin).Compared with pretransplant status,sexual function improved significantly when evaluated on postoperative 6th month.ConclusionsLevels of serum sex hormone were correlated with MELD scores before liver transplant.After liver transplant,estradiol was back to normal level on postoperative 2nd week,testosterone and sex hormone binding globulin back to normal level on postoperative 1 st month.Sexual function significantly improves after liver transplantation.

Objective This study aimed to investigate the effects of angiotensin Ⅱ and Losartan pretreatment on regulating insulin secretion in human islet ? cells.Methods We measured changes in intracellular calcium by confocal laser scanning microscopy using Flou3-AM-loaded human islet cells.RT-PCR was used to measure changes in intracellular CaM.Dynamic insulin secretory responses were determined by chemiluminescence following perfusion of human islets.Results Exposure of the isolated islets to angiotensin Ⅱ induced glucose-stimulated insulin release coupled with intracellular calcium ascending in first phase and descending in second phase.Intracellular CaM concentration could not be affected by angiotensin Ⅱ.Conclusion The change of free Ca2+is induced by the combination of AngⅡ with ATI receptors of islet B cells,which results in the damage to islet B cells.Losartan pretreatment protects the islet B-cell function by inhibiting calcium overload.

Objective To examine the effects of mixed infusion of mesenchymal stem cells(MSCs) and bone marrow cells(BMCs) in the induction of chimerism and islet allograft tolerance.Methods BALB/C mouse was used as the recipient and C57BL/6 mouse was as the donor.BALB/C mice were rendered diabetic via injection of streptozotocin.The islet cells of donor mice were transplanted into the recipient mice under the capsule of kidney.Rat anti-mouse CD154 mAb was intraperitoneally injected to the recipient mice.All of recipient mice(n=25) were then randomly divided into five groups: A group(received nothing),B group(donor MSCs),C group(donor BMCs),D group(donor BMCs and MSCs) and E group(donor BMCs and the third strain-derived MSCs).The chimerism level of donor cells and the survival time of islet grafts were compared among these five groups on 7,30d and 60d after transplantation.Results On 30d and 60d after islet transplantation,the chimerism levels of donor cells in D and E groups,in which the recipient mice received the mixed infusion of MSCs and BMCs,were significantly higher than that in C group,in which the recipient mice received BMCs infusion only,and the survival time of islet graft prolonged from 53.0?16.4d to 77.0?7.7d and 61.0?2.2d,respectively(P

Objective To investigate the effects of injecting allogeneic mesenchymal stem cells(MSCs) on the cellular immunity in rat in vivo.Methods Bone marrow-derived MSCs were isolated from Wistar rats.The purity of MSCs was identified by morphological examination with microphotography,and the phenotypes were identified with flow cytometry.Twenty SD rats were randomly divided into 4 groups.Different concentrations of MSCs(5?106/ml for group A,5?105/ml for group B,and 5?104/ml for group C,respectively) and PBS(for group D) were given to allogeneic SD rats via intravenous infusions.The suppressive effect of MSCs on lymphocytes proliferation in recipient rat was analyzed using mixed lymphocyte cultures(MLR) 10 days after cultivation.At the same time,proportions of CD4+,CD8+ and CD4+CD25+/CD4+ T-lymphocytes in peripheral blood and spleen were analyzed with flow cytometry.Results Proliferation rate of splenic lymphocytes in group A(5?106/ml MSCs,8.58%?0.27%) was markedly lowered compared with that in group D(PBS,24.40%?5.21%,P

Objective To explore the changes in angiotensin Ⅱ(AngⅡ)produced by Langerhan islets of Syrian hamsters after blockage of renin-angiotensin system(RAS)by different inhibitors.Methods Islet cells from Syrian golden hamster were isolated and purified,and angiotensin Ⅰ was added.The experiment was then divided into six groups:control group(PBS was added),captopril group,chymostatin group,aprotinin group,?-antitrypsin group,and captopril+chymostatin group(according to inhibitors added).The content of AngⅡ in supernatant was detected by enzyme-linked immunosorbent assay(ELISA).Results Compared with control group,the AngⅡ content decreased by 42.50% and 50.94% in captopril group and chymostatin group,respectively(P

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.

OBJECTIVE: To optimize the microwave assisted extraction technology of icariin from Epimedii Folium. METHODS: The microwave assisted extraction technology of icariin from Epimedii Folium was optimized by L9(34)orthogonal design using extraction temperature, extraction time, alcohol concentration,ratio of solid and liquid with the content of icariin as index. RESULTS: The optimal extraction process of icariin was as follows: extraction temperature of 60 ℃,extraction time of 6 min, 30% alcohol and ratio of solid and liquid was 1 ∶ 20. CONCLUSION: The extraction technology is high efficiency and requires short period for extraction of icariin from Epimedii Folium with low cost.

The teacher training of medical colleges has become a pressing task force.Young doctors should systematically study the educational theory,make positive observation,conduct teaching rounds and share experience,use the Internet,read the literature and pay attention to academic practice to improve clinical teaching ability.

Objective To investigate the effect of intermittent high glucose on proliferation, apoptosis, and cell cycle progression of INS-1 cells, and the possible intracellular pathways activated by intermittent high glucose. Methods Cell viability was evaluated by cell counting kit, the cell cycle was determined by flow cytometry,Annexin-V/PI double-labeled cell apoptosis detection kit was used to monitor cell apoptosis. Cell cycle related protein Skp2 and p27 expressions were detected by Western blot. Results ( 1 ) Both intermittent and constant high glucose significantly inhibited the growth of INS-1 cells, and the former effect was more significant. ( 2 ) Intermittent and constant high glucose levels significantly increased apoptosis in INS-1 cells, and the former effect was more significant. (3) Intermittent and constant high glucose levels significantly inhibited the cell process, the G0/G1 cell cycle arrest also was induced by intermittent high glucose, resulting in lowered proportion of the G2/M phase and S phase of INS-1 cells. (4) Intermittent and constant high glucose significantly decreased the level of protein Skp2 and increased the level of cell cycle related protein p27. Conclusion Intermittent high glucose levels affect INS-1 cell growth and proliferation, as well as induce cell apoptosis, probably by decreasing the level of protein Skp2 and increasing the level of p27 in the cells, resulting in arrest of progression through the G1 phase to the S phase of INS1 cells, and thus impairment of cell proliferation.