Objective To investigate the effects of acidic reperfusion on ischemia-reperfusion injury in isolated rat heart and the role of PI3K/Akt signaling pathway.Methods Seventy adult SD rats weishing 450-550 g were randomly divided into 7 groups(n=10 each):group Ⅰ ischemia-repedusion injury(X/R);groupⅡ ischemic post eonfioning(IPC);group Ⅲ acidic reperfusion(H+);group Ⅳ ischemie postconditioning+alkalotic nsperfusion(IPC+OH-);group Ⅴ alkalotic reperfusion(OH-);group Ⅵ acidic repeffusion+wortmannin (H+wort)and group ⅦVl wortmannin(wort).The animals were anesthetized with intraperitoneal(IP)urethane. Their chests were opened and hearts were excised and passively perfused in a Lsngendorff apparatus with KrebsHenseleit buffer(KHB)saturated with 95%O2-5%O2 at 37℃.The isolated hearts were made globally ischemic for 30 min followed by 120 rain reperfusion.Group II (IPC)WaS subjected to 6 cycles of 15 rain reperfusion and 15 min ischemia at the beginning of reperfusion. In group H+ and OH- (group Ⅲ ,Ⅴ ) the isolated hearts were perfused with KHB of pH 6.9 and 7.8 for 3 rain respectively at the beginning of reperfusion. In group IPC + OH( Ⅳ ) the isolated hearts were perfused with KHB of pH 7.8 for 3 rain followed by IPC. In group H + wort and wort ( Ⅵ,Ⅶ ) the isolated hearts were perfused with wortmannin 100 nmol/L in KHB of pH 6.9 and 7.4 for 3 min respectively at the beginning of reperfusion. LVEDP and ± dp/dtmax were measured before ischemia and at 30 min of reperfusion. Coronary effluent was collected for determination of NO concentration at 30 min of reperfusion. Lnfart size was measured at 120 rain of reperfusion. Results The LVEDP was decreased, ±dp/dt was increased, the infarct size was smaller and the NO concentration in coronary effluent was higher in group IPO and H+ compared with group I/R. Wortmannin abolished the protective effect of acidic reperfusion on isolated rat heart. Conclusion PI3K/Akt signaling pathway may be involved in the protective effects of acidic reperfusion on myocardium against ischemia-reperfusion injury.

Objective To explore the instruction value of the color Doppler ultrasonography for the diagnosis and treatment of the pediatric intussusceptions .Methods Retrospective study the color Doppler ultrasonographic performance of 114 patients with diagnosis of pediatric intussusception in the affiliated hospital of Zunyi medical college ,from October 2009 to June 2012 ,reviewed the case ,groups were compared according to the ways of therapeutic methods .Results All the 114 cases of children of the intus-susception are subject to air enema reset or surgery cured confirmed .Age younger than 12 months intussusception children ,air ene-ma reset were more likely to success ;the diameter of concentric circles levy,the length of sleeve for and the thickness of bowel wall were smaller ,the more suitable for outsiders air enema reset .The blood supply of scabbard of bowel wall and the mesenteric was rich ,the air enema reset had a higher success rate ,blood supply was poor and the success rate was lower .The success rate of air enema reset was influenced by the part of intussusception .Conclusion Combined use of conventional color ultrasonic and high fre-quency probe checking ,can raise the diagnosis rate of pediatric intussusception ,the primary lesion confirmed and the detection rate in the position of the disease ,provide guidance for clinical choice reduction treatment .

Objective:The treatment of late pregnancy complicated with utedne leiomyoma was investigated.Methods:193 Cases of Iate pregnancy complicated with uterine leiomyoma from January 2003 to August 2008 were recruited in our hospital.According to the delivery route,size and subtype of fibroid,blood loss,operation hours and postoperative inpatient period were compared.Results:104 cases of pregnancy complicated with uterine leiomyoma were diagnosed before cesarean section(CS).No significant differences on blood losses and operation hours were found between CS group and CS+myomectomy group(P>0.05).The operation heurs of leiomyoma in corpus uteri was significantly shorter than leiomyoma in lower uterine segment and cervix(P=0.007).Leiomyoma bigger than 8 cm needed significantly Ionger operative hours and lose more blood than the smaller leiomyoma.Operation hours,blood loss and postoperative inpatient period were significantly different between submucous leiomyoma and subserosal leiomyoma(P<0.05).Conclusions:Pregnancy complicated with uterine leiomyoma should be diagnosed as early as possible.During cesarean section on when leiomyoma is bigger than 8 cm,locating at lower uterine segment or cervix or submucous,the treatment should be cautious.

ObjectiveTo investigate whether neuronal intermediate filament protein(NF-66) could be used as a molecular marker for the determination of malignancy of insulinoma.MethodsThe expression of NF-66 protein was detected in insulinoma and pana - cancerous tissues and 3 insulinoma cell lines by immunohistochemistry staining. The relationship between the expression of NF-66 protein and the clinicopathological characteristics,survival was analyzed by univariate and multivariate statistical analysis.ResultsExpression of NF-66 was found in 102(77％ ) out of 132 insulinomas and none of 98 paired control (P =4.86 × 10-31 ).NF-66 was highly expressed in 3 insulinoma cell lines.The expression of NF-66 was found in 96 (81％) out of 118 benign tumors (P =0.003),while out of 14 malignant insulinomas,6(43％ ) were found to express NF-66 ( P =0.003 ).The expression of NF-66 was significantly associated with tumor size (3 cm as the cut-off point),distant metastasis (38％ vs 81％,P =0.013) and distant plus lymph node metastasis (46％ vs 81％,P =0.009),respectively.The expression of NF-66 was not correlated with age,gender,recurrence and overall survival.ConclusionsDown-regulation of NF-66 was significantly associated with tumor malignancy,suggesting that NF-66 could be a potentially novel molecular bionarker to distinguish malignancy from benign insulinoma.

The mechanism of injury on the human glomerular endothelial cells (ciGENC) induced by preeclampsia serum was investigated. Concentration of maternal serum sFlt-1 protein was detected by ELISA. Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader. Morphologic change of ciGENC was observed under inverted phase contrast microscope. The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group (P<0.01). Permeability in preeclampsia groups was significantly increased as compared with control group (P<0.01). By contrast with severe preeclampsia group, the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P<0.05). Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups. It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.

This study examined the effect of over-expression of sFlt-1 by trophoblasts on the barrier function of glomerular endothelial cells and the role of VEGF in this process in order to explore the pathogenesis of glomerular disease in preeclampsia. SFlt-1 expression in the human trophoblasts (TEV-1 cells) was enhanced by transfecting sFlt-1 plasmid DNA into TEV-1 cells. The monolayer barrier function of glomerular endothelial cells (ciGEnCs) was determined by measuring the fluorescence intensity of bovine serum albumin (BSA) that crossed the monolayer of glomerular endothelial cells. The results showed that the over-expression of sFlt-1 by TEV-1 cells led to the barrier dysfunction of ciGEnCs, and the exogenous VEGF could alleviate the ciGEnCs dysfunction resulting from the over-expression of sFlt-1 to a certain extent. It was concluded that the dysregulation of sFlt-1 and VEGF in preeclamptic pregnancy may contribute to the barrier dysfunction of glomerular endothelial cells, and VEGF may play an important role in maintaining the barrier function of glomerular endothelial cells, but it may not be the sole factor.

This study investigated the effect of epigenetic modification of maspin on extravillous trophoblastic function. The mRNA expression of maspin in placentae from normotensive and preeclamptic pregnant women was detected by RT-PCR. TEV-1 cells, a human first-trimester extravillous trophoblast cell line, were cultured and treated with CoCl(2) (300 μmol/L) to induce chemical hypoxia and with 5-aza (500 nmol/L) to induce demethylation. The mRNA expression of maspin in TEV-1 cells subjected to different treatments was determined by RT-PCR, and the proliferative and migratory abilities of TEV-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assays. Our results showed that the maspin mRNA expression level in placentae from preeclamptic women was much higher than that from normotensive women. CoCl(2) or 5-aza could up-regulate the mRNA expression of maspin and significantly suppress the proliferation and migration of TEV-1 cells. It was concluded that the epigenetic modification in promoter region of maspin contributes to incomplete trophoblast invasion, which offers a novel approach for predicting and treating placental dysfunction.

This study examined the effect of over-expression of sFlt-1 by trophoblasts on the barrier function of glomerular endothelial cells and the role of VEGF in this process in order to explore the pathogenesis of glomerular disease in preeclampsia.SFlt-1 expression in the human trophoblasts (TEV-1 cells) was enhanced by transfecting sFlt-1 plasmid DNA into TEV-1 cells.The monolayer barrier function of glomerular endothelial cells (ciGEnCs) was determined by measuring the fluorescence intensity of bovine serum albumin (BSA) that crossed the monolayer of glomerular endothelial cells.The results showed that the over-expression of sFlt-1 by TEV-1 cells led to the barrier dysfunction of ciGEnCs,and the exogenous VEGF could alleviate the ciGEnCs dysfunction resulting from the over-expression of sFlt-1 to a certain extent.It was concluded that the dysregulation of sFlt-1 and VEGF in preeclamptic pregnancy may contribute to the barrier dysfunction of glomerular endothelial cells,and VEGF may play an important role in maintaining the barrier function of glomerular endothelial cells,but it may not be the sole factor.

This study investigated the effect of epigenetic modification of maspin on extravillous trophoblastic function. The mRNA expression of maspin in placentae from normotensive and preeclamptic pregnant women was detected by RT-PCR. TEV-1 cells, a human first-trimester extravillous trophoblast cell line, were cultured and treated with CoCl(2) (300 μmol/L) to induce chemical hypoxia and with 5-aza (500 nmol/L) to induce demethylation. The mRNA expression of maspin in TEV-1 cells subjected to different treatments was determined by RT-PCR, and the proliferative and migratory abilities of TEV-1 cells were assessed by cell counting kit-8 (CCK-8) and Transwell assays. Our results showed that the maspin mRNA expression level in placentae from preeclamptic women was much higher than that from normotensive women. CoCl(2) or 5-aza could up-regulate the mRNA expression of maspin and significantly suppress the proliferation and migration of TEV-1 cells. It was concluded that the epigenetic modification in promoter region of maspin contributes to incomplete trophoblast invasion, which offers a novel approach for predicting and treating placental dysfunction.
Adult ; Chorionic Villi ; physiology ; Epigenesis, Genetic ; genetics ; Female ; Humans ; Pregnancy ; Serpins ; genetics ; Trophoblasts ; physiology

The mechanism of injury on the human glomerular endothelial cells (ciGENC) induced by preeclampsia serum was investigated.Concentration of maternal serum sFlt-1 protein was detected by ELISA.Fluorescently-labeled bovine serum albumin infiltrating through lower chamber of Transwell was measured by multifunction microplate reader.Morphologic change of ciGENC was observed under inverted phase contrast microscope.The concentration of sflt-1 in preeclampsia groups was significantly increased as compared with control group (P＜0.01).Permeability in preeclampsia groups was significantly increased as compared with control group (P＜0.01).By contrast with severe preeclampsia group,the permeability of ciGENC monolayer in mild preeclampsia group was decreased significantly (P＜0.05).Intervention of exogenous VEGF significantly decreased permeability of ciGENC in preeclampsia groups.It was concluded that sFlt-1 increased ciGENC permeability by damaging integrity of endothelial barrier function.