Objective To investigate the molecular mechanism how edaravone reduces cytotoxicity caused by hypoxia/reoxygenation-induced injury.Methods Ischemia model-hypoxia/ reoxygenation model which also called oxygen and glucose deprivation/reoxygenation model (OGD-R) was established.Cells were divided into control group,OGD-R group,OGD-R with edaravone of different concentration groups Cells of OGD-R model were pretreated with the appropriate concentration of edaravone or combine with the specific channel blockers LY294002 and MK2206 individually,the expression levels of ERK,AKT and Bcl-2 were detected with Western-blot,while the expression levels of BDNF and Bcl-2 mRNA detected with RT-PCR,the expression levels of BDNF protein detected with ELISIA,the levels of LDH releasing and Hoechst33258 staining used with homologue assay kit or regents.Results The pretreatment of cultured neurons with edaravone alleviated hypoxia/reoxygenation induced neuronal injury in a dose-dependent manner (LDH releasing reduced,Caspase-3 activity and ratio of nuclear pyknosis declined).The edaravone pretreatment did not increase significantly the p-ERK expression levels,but the amount of p AKT expression was significantly increased(P＜0.01).Pretreatment of edaravone(10 μmol/L) remarkably reduced the LDH release and declined the ratio of nuclear pyknosis after reoxygenation (P＜0.01),which was inhibited by MK2206.Compared to OGD-R,edaravone pretreatment markedly promoted BDNF and Bcl-2 mRNA expression at each time point,and the most pronounced effects occured at 8 h after OGDR.ELISIA analysis showed that BDNF protein level was significantly elevated after edaravone pretreatment at the same point.Western blot analysis indicted that edaravone pretreatment significantly enhanced Bcl-2 protein expression at 8 h after OGD-R,which was blocked by MK2206.Conclusions Edaravone may alleviate hypoxia/reoxygenation induced neuronal injury by enhancing BDNF and Bcl-2 expression and inhibiting Caspase-3 activity through activation of the PI3K/Akt pathway.

Objective To investigate the effect of short bowel syndrome treated with living-related small bowel transplantation(SBT).Methods A male patient with residual intestine 20cm in length,which resulted from subtotal small bowel resection and right hemi-colectomy owing to intestinal volvulus,received a living-related SBT.The donor was the patient′s mother.Donor specific blood transfusion,50mL/per week,was carried out for 8 weeks.Cytomegalovirus infection status in both donor and recipient was negative.A 160cm segment of intestine was transplanted.The graft ileocolic artery and vein was anastomosed to the recipient′s infrarenal aorta and inferior vena cava end-to-side,respectively.A distal ileostomy was performed.(Immunosuppression),anti-infection and anticoagulation therapy,and nutritional support were given(postoperatively).Results The donor had an uneventful recovery.No technical complications were observed.The recipient was alive and well 31 weeks after operation.No graft rejection or infection was found.The(patient) was taken off TPN 8 weeks after operation,and got a low-fat meal.The result of D-xylose test was near normal.Conclusions Living-related small intestine transplantation is an effective treatment for short bowel syndrome.

Objective To investigate the effect of endocrine gland-derived vascular endothelial growth factor(EG-VEGF) on the proliferation and apoptosis of pancreatic cancer cells and on the regulation of PI3K/AKT signaling pathway.Methords The expression of EG-VEGF and its receptor-VEGFR-2 in pancreatic cancer tissues and adjacent normal tissues was detected by PCR.The effect of EG-VEGF on proliferation of human pancreatic cancer cells was detected by MTT assay.The effect of EG-VEGF on the apoptosis of human pancreatic cancer cells was detected by flow cytometry.Western lot was used to detect the changes of related proteins expression in PI3K/AKT signaling pathway after EG-VEGF treatment.Results The expression (3.08±0.30,2.17±0.16 respectively) of EG-VEGF and VEGFR-2 in pancreatic cancer tissues was significantly higher than those (1.55±0.73,0.54±0.34 respectively) in adjacent tissues (both P＜ 0.05).MTT and flow cytometry data showed that EG-VEGF could promote the proliferation of pancreatic cancer cells and inhibit cell apoptosis.Western blot showed that EG-VEGF promoted AKT phosphorylation and activated PI3K/AKT signaling pathway.Conclusion EG-VEGF is highly expressed in pancreatic cancer tissue,and can activate PI3K/AKT signaling pathway to promote cell proliferation and inhibit cell apoptosis.

Objective:To investigate the application value of peri-gastric devasculariza-tion without dissociation of esophagus for portal hypertension.Methods:The retrospective and descriptive study was conducted. The clinical data of 94 patients with portal hypertension who were admitted to three medical centers, including 75 cases in the People′s Hospital of Ningxia Hui Autonomous Region, 12 cases in the People′s Hospital of Wuhai and 7 cases in the People′s Hospital of Wuzhong, from July 2018 to December 2022 were collected. There were 68 males and 26 females, aged 46(range, 21-70)years. All 94 patients underwent peri-gastric devascularization without dissociation of esophagus. Observation indicators: (1) intraoperative condition; (2) postoperative complications; (3) follow-up. Measurement data with normal distribution were represented as Mean± SD, and measure-ment data with skewed distribution were represented as M(range). Count data were described as absolute numbers, and comparison between groups was conducted using the chi-square test or Fisher exact probability. Results:(1) Intraoperative condition. All 94 patients underwent surgery success-fully without operation death, including 82 cases receiving open surgery and 12 cases receiving laparoscopic surgery. The operation time and volume of intraoperative blood loss were (183±85)minutes and 289(range, 158-560)mL, respectively, for the 94 patients. (2) Postoperative complications. Of 94 patients, early portal vein thrombosis occurred in 24 cases, intra-abdominal infection occurred in 2 cases, hepatic encephalopathy occurred in 1 case, pulmonary embolism occurred in 1 case, intra-abdominal hemorrhage requiring operation to stop bleeding occurred in 1 case and pleural effusion requiring drainage occurred in 1 case. All patients with postoperative complications were cured after treatment. None of the 94 patient had postoperative esophageal complications such as odynophagia or dysphagia. (3) Follow-up. All 94 patients were followed up for 38(range, 6-60)months. Of the 45 patients with paraesophageal vein, there were 36 cases of thinner and 9 cases of occlusion of the distal subphrenic paraesophageal vein after surgery, respectively. Cases with esophageal varices disappearance, cases with mild and moderate residual of esophageal varices, cases with severe residual of esophageal varices, cases with recurrence of esophageal varices, cases with esophageal varices bleeding were 7, 70, 9, 4, 4 in the 94 patients after surgery. Cases with esophageal varices disappearance was 7 in the 45 patients with paraesophageal vein, versus 0 in the 49 patients without paraesophageal vein, showing a significant difference between them ( P<0.05). Of 94 patients, 17 cases developed postoperative late portal vein thrombosis and cavernous transformation, 7 cases developed liver cancer, 1 case had hepatic encephalopathy, and 6 cases died. Conclusion:Peri-gastric devascularization without dissociation of esophagus is safe and feasible for the treatment of portal hypertension.