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Objective:To investigate the effects of heme oxygenase-1 (HO-1) on hepatic sinusoidal endothelial cells (LSECs) proliferation, migration, and hepatocyte proliferation.Methods:Eighteen male C57BL/6 mouse aged 6-8 weeks old were underwent partial hepatectomy. Cell proliferation and HO-1 expression in residual liver tissue were detected by immunofluorescence histochemistry at 0 d, 2 d and 4 d after operation. In vitro, LSECs were transfected with adenovirus carrying HO-1 gene (HO-1 group), and the cells were transfected with empty vector adenovirus and the non-transfected cells were used as control. In addition, LSECs from different transfection groups were co-cultured with hepatocyte without contact to evaluate the effect of HO-1 expression on promoting hepatocyte proliferation. Western Blotting and RT-PCR were used to detect the protein and mRNA expression of HO-1, inhibitor of DNA binding and or differentiation (Id1), hepatocyte growth factor (HGF) and Wnt2. Cell proliferation was detected by EdU. The ability of cell migration was detected by Transwell migration assay.Results:Compared with 0 d after hepatectomy, LSECs proliferation and HO-1 expression within LSECs were increased significantly at 4 d after surgery. EdU positive rate of LSECs in HO-1 group (27.20±4.80)% was higher than that in empty vector group (12.47±3.30)% and non-transfected group (15.97±2.50)%. The number of LSECs migration in HO-1 group (258.70±36.56) was higher than that in empty vector group (122.00±38.16) and non-transfected group (107.70±30.01). The protein and mRNA expression level of HO-1, Id1, HGF and Wnt2 in HO-1 group were higher than that in empty vector group and non-transfected group. EdU positive rate of hepatocytes that co-cultured with LSECs in HO-1 group (18.33±2.52) % was higher than that in empty vector group (11.33±1.53)% and non-transfected group (11.7±2.08)%. The differences were statistically significant (all P<0.05). Conclusion:Up-regulation of HO-1 promoted LSECs proliferation and migration of, as well as up-regulation of HO-1 in LSECs enhanced the capacity of LSECs to promote hepatocyte proliferation.
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Liver is the most important metastatic target organ of colorectal cancer. Nearly 50% of colorectal patients are found to have liver metastasis during the course of the disease, including 25% of colorectal patients undergoing simultaneous liver metastasis and the other 25% undergoing metachronous liver metastasis. Liver metastasis is the main cause of death for colorectal patients and the prevention and treatment of colorectal cancer liver metastasis is the top priority to overcome the disease. Active surgical treatment can bring survival benefits to colorectal patients. The authors analyze and summarize the multidisciplinary treatment of colorectal liver metastasis in the department of organ transplantation of First Affiliated Hospital of Kunming Medical University to discuss the hepatectomy strategy of colorectal liver metastasis.
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Liver sinusoidal endothelial cells (LSECs) play a positive role in maintaining microcirculation of the liver to achieve liver homeostasis, and they also mediate a balance between regeneration and fibrosis in the process repair of liver injury. After acute liver injury, LSECs are the regulators of liver regeneration, while in chronic injury, abnormally activated LSECs promote development of liver fibrosis. In this paper, we summarized the recent progress in research on the balance between LSECs-mediated liver regeneration and fibrosis, with the aim to provide new ideas in treating liver fibrosis and promoting liver regeneration by targeting LSECs.
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Hepatic ischemia-reperfusion injury is often occurred during the hepatobiliary surgery,and is closely correlated with postoperative of liver function recovery and prognosis.Although the mechanisms of hepatic ischemia-reperfusion injury are complex,mitochondrial structural dysfunction is an important event for hepatic ischemia-reperfusion injury.This review summarized the current mechanism of hepatic ischemia-reperfusion injury,and with a focus on mitigating its damage through the mitochondrial autophagy and apoptosis pathway.
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<p><b>OBJECTIVE</b>Osteosarcoma is the most common type of malignant bone tumor in children and adolescents. The role of E3 ligases in tumorigenesis is currently a focus in tumor research. In the present study, we investigated the role of the E3 ligase tripartite motif 21 (TRIM21) in osteosarcoma cell proliferation.</p><p><b>METHODS</b>3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays were used to assess osteosarcoma cell viability. U2-OS cells stably carrying a recombinant lentivirus expressing tetracycline-regulated TRIM21 were screened. Co-immunoprecipitation was coupled with LCMS/MS analysis to identify novel interacting partners of TRIM21. Co-immunoprecipitation and bimolecular fluorescence complementation (BIFC) were performed to validate the interactions between TRIM21 and its novel partner YWHAZ. A TRIM21-ΔRING construct was generated to test the effects of TRIM21 ligase activity on YWHAZ.</p><p><b>RESULTS</b>TRIM21 positively regulated osteosarcoma cell proliferation. Overexpression of TRIM21 enhanced osteosarcoma cell tolerance toward various stresses. YWHAZ protein was identified as a novel interacting partner of TRIM21 and its expression levels were negatively regulated by TRIM21. The RING domain of TRIM21 was required for TRIM21 negative regulation of YWHAZ expression. However, overexpression of YWHAZ did not affect positive regulation of osteosarcoma cell proliferation by TRIM21.</p><p><b>CONCLUSION</b>Our results further clarify the molecular mechanisms underlying the pathogenesis of osteosarcoma.</p>
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Humans , 14-3-3 Proteins , Genetics , Metabolism , Cell Proliferation , Genetics , Osteosarcoma , Genetics , Ribonucleoproteins , Genetics , Metabolism , Tumor Cells, CulturedABSTRACT
Objective To investigate the protective effect of gastrodin (Gas) on the hepatic ischemia-reperfusion injury (HIRI) in mice,and study possible mechanisms.Methods Forty male C57BL/6 mice were randomly divided into sham-operated group (Sham),HIRI group,gastrodin-treated groups with low and high does (Gas-L,Gas-H,respectively),and cobalt protoporphyrin(CoPP) group(n =8).Mice in Gas-L,Gas-H,and CoPP groups were injected intraperitoneally with individual drugs and dose before operation.Except for Sham group,an 70％ volume HIRI model was established by means of 60 minutes ischemia and then 6 hours reperfusion in the other groups.The levels of serum AST and ALT in each group were compared.The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the liver tissue were measured;The level of TNF-αt,IL-6,IL-10 and heme oxygenase-I (HO-1) mRNA level were detected by real time quantitative PCR.Liver tissue was stained with H&E.The hepatocyte apoptosis was studied by TUNEL.Results Respectively,the serum ALT level in the HIRI,Gas-L,Gas-H and CoPP groups was (5 057.34±290.80)U/L,(3 917.49±198.10) U/L,(3 645.63± 171.10) U/L,(2 977.78± 179.00) U/L,and the ALT level was (5 871.25 ± 819.01) U/L,(4 660.88 ± 505.96) U/L,(4 182.00 ± 507.51) U/L,(3 788.65±462.14)U/L.The serum level of ALT and AST in Gas-L,Gas-H and CoPP groups was lower than HIRI group (P＜ 0.05).The apoptotic index in Gas-L,Gas-H and CoPP groups respectively was (37.89±4.27)％,(32.59±3.78)％,(20.45-±2.49)％,which was lower than group (58.92±3.32)％ (P＜ 0.05).Compared with HIRI group,the TNF-α and IL-6 mRNA level in Gas-L,Gas-H and CoPP groups were decreased,and the levels of IL-10 and HO-1 mRNA were increased.Simultaneously,the activity of SOD was promoted,whereas the levels of MDA was reduced (P＜0.05).Conclusions Gastrodin shows an protective function aganist liver ischemia-reperfusion injury in mice by inhibiting inflammation,oxidative stress and cell apoptosis.The up-regulation of HO-1 by gastrodin may be the possible mechanism.
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Objective:To explore effect of walking on rehabilitation in aged patients with hypertension complicated anxiety.Methods:A total of 160 aged patients with hypertension complicated anxiety were enrolled,randomly divided into medica-tion group (n＝80,received routine medication ) and exercise group (n＝80,received walking exercise based on routine medication),both groups were treated for four months.Carotid intima-media thickness (IMT) and ZUNG self-rating anxi-ety scale (SAS) score before and after treatment,incidence rate of cardiovascular events after one-year follow-up were compared between two groups.Results:Compared with before treatment,there were significant reductions in IMT and SAS score in two groups after treatment,P＝0.001 all;compared with medication group after treatment,there were significant reductions in IMT [ (1.05 ± 0.26) mm vs.(0.90 ± 0.46) mm] and SAS [ (38.07 ± 0.25) scores vs.(23.02 ± 0.46) scores] in exercise group,P＜0.01 both.During one-year follow-up,total incidence rate of cardiovascular events in exer-cise group was significantly lower than that of medication group (30.67% vs.69.74%,P＝0.001).Conclusion:Walking helps to improve anxiety,reduce incidence of adverse cardiovascular events in aged patients with hypertension complicated anxiety.It’ s safe and reliable,which is worth extending.
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Objective To explore whether CD4 +T cells in mice can secrete exosomes and the possibility of exosomes to participate in the inflammation and immune response process. Methods Spleen samples were taken from mice, and CD4 +T cells were isolated from the spleen tissue using magnetic bead separation method. Exosomes of CD4 + T cells were extracted from the supernatant and observed under transmission electron microscope. PCR assay was used to detect the expression of miR-23a and miR-214. Results Exosomes were observed under elecron microscope, and the expression of miR-23a and miR-214 were detected by PCR assay. Conclusions CD4 + T cells in mice can secrete exosomes,which offer possibility to participate in the inflammation and immune response.
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Objective To explore whether CD4 +T cells in mice can secrete exosomes and the possibility of exosomes to participate in the inflammation and immune response process. Methods Spleen samples were taken from mice, and CD4 +T cells were isolated from the spleen tissue using magnetic bead separation method. Exosomes of CD4 + T cells were extracted from the supernatant and observed under transmission electron microscope. PCR assay was used to detect the expression of miR-23a and miR-214. Results Exosomes were observed under elecron microscope, and the expression of miR-23a and miR-214 were detected by PCR assay. Conclusions CD4 + T cells in mice can secrete exosomes,which offer possibility to participate in the inflammation and immune response.
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Objective To explore the effectivity and feasibility of uindirectional barbed suture for primary closure of common bile duct on Laparoscopic Exploration of Common Bile Duct Stones, Methods From January 2013 to August 2015,109 cases of primary closure of common bile duct after Laparoscopic Exploration of Common Bile Duct Stones were performed in this hospital.The characteristics of these cases were retrospectively comparatively analyzed.Results Conventional braided Sutures in 68 cases(group A),barbed Suture Devices in 41 cases (group B).There was no difference in postoperative hospital stay,intraoperative blood loss and complication rate between the two groups.Differences in bile duct incision suture time and operative time between the two groups were significantly different.Conclusion The application of uindirectional barbed suture for primary closure of common bile duct using barbed suture after Laparoscopic Exploration is a safe and effective way after treatment of choledocholithiasis.This method cuold reduce the difficulty of operation,and shorten the operation time and the learning curve.
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Objective To explore the effect of heme oxygenase-1 (HO-1) on expressions of hypoxia inducing factor 1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF)and regeneration of hepatic vascular plexus after orthotopic liver transplantation ischemia-reperfusion injury in rats.Methods Theexperimental study was conducted.According to the random number table,240 SD rats were divided into the 3 groups,80 rats in each group.Empty virus group:rats were transfected with the empty virus.Induced group:rats were transfected with HO-1 overexpression adenovirus.Inhibited group:rats were transfected with HO-1 RNAi adenovirus.Rats were made pairs (1 ∶ 1) and established rat liver transplantation model according to two cuffs method.Rats with less weight and with heavier weight were respectively chosen as donor rats and recipient rats,and then recieved tail intravenous injection of adenovirus at 24 hours before operation.(1) Detection of transfection efficiency of adenovirus before operation:HO-1 expression of liver tissue of rats in each group was detected by Western blot at 12 and 24 hours after injection of adenovirus.(2) Liver function test of recipient rats after liver transplantation:liver functions of recipient rats [alanine transaminase (ALT),aspartate transaminase (AST),alkaline phosphatase (ALP),gamma-glutamyl transferase (GGT)] were detected at l,3,7 and 14 days postoperatively.(3) Pathological histology of liver tissue and injury scores of recipient rats in the 3 groups after liver transplantation:paraffin sections of recipient rats in the 3 groups at postoperative 1 and 14 days were stained by HE staining and observed by light microscope,and were evaluated by Suzuki damage score standard.(4) Relative expressions of HIF-1α,VEGF and HO-1 in liver tissue of recipient rats were detected by Western blot.(5) Von Willebrand factor (vWF) in liver tissue of recipient rats at 14 days postoperatively was detected by immunofluorescence staining and small vessels were counted.Measurement data with normal distribution were represented as x ±s.Comparison between groups was analyzed by the independent-sample t test,comparison among groups was done using one-way ANOVA,and pairwise comparison was analyzed by the LSD test.Results (1) Detection of transfection efficiency of adenovirus before operation:the relative expression of HO-1 of liver tissue of rats at 12 and 24 hours preoperatively after injection of adenovirus was 1.08±0.16 and 1.08±0.26 in the empty virus group,1.18±0.21 and 1.39±0.19 in the induced group,0.87±0.26 and 0.57±0.12 in the inhibited group,respectively,with statistically significant differences in different time points (F =4.232,36.513,P＜ 0.05).(2) Liver function test of recipient rats after liver transplantation:level of ALT at 3 days postoperatively in the empty virus group,induced group and inhibited group was (504±67)U/L,(438±47)U/L and (490±39)U/L,with a statistically significant difference (F=3.517,P＜0.05).Levels of ALT,AST and ALP at 7 days posto-peratively were (443±49) U/L,(430± 34) U/L,(455± 38) U/L in the empty virus group and (382± 49) U/L,(372±50) U/L,(394±25) U/L in the induced group and (493±44) U/L,(455±62) U/L,(470±72) U/L in the inhibited group,respectively,with statistically significant differences (F =10.950,5.667,5.398,P＜0.05).Levels of ALT,AST,ALP and GGT at 14 days postoperatively were (394±46)U/L,(361 ±68)U/L,(417 ±17)U/L,(4.5±1.1)U/L in the empty virus group and (283±47) U/L,(288±60) U/L,(332±46) U/L,(2.5±0.5) U/L in the induced group and (446± 43) U/L,(422± 51) U/L,(423± 63) U/L,(4.3 ± 1.3) U/L in the inhibited group,respectively,with statistically significant differences (F=26.906,9.924,8.013,9.279,P＜ 0.05).(3) Pathological histology of liver tissue and injury scores of recipient rats in the 3 groups after liver transplantation:liver cell swelling,loose cytoplasm and a varying quantity of inflammatory cell infiltration in the portal regions in the liver tissue of 3 groups were observed at 1 day postoperatively.A few inflammatory cell infiltrations in the portal regions,basically normal liver cell arrangement and a slightly swelling of liver cell were found in the empty virus group at 14 days postoperatively.Reduced liver cell swelling and basically normal structure of liver lobule were observed in the induced group.There were small patchy or focal necrosis of liver cell,masses of inflammatory cell infiltration in the portal regions and damage of bile duct in the inhibited group.Suzuki score at 1 day postoperatively in the empty virus group,induced group and inhibited group were respectively 6.7± 1.7,6.1 ± 1.2 and 7.6± 1.3,with no statistically significant difference (F=2.257,P＞0.05).Suzuki score at 14day postoperatively in the empty virus group,induced group and inhibited group were respectively 4.0±0.8,2.9± 0.8 and 5.1± 1.4,with a statistically significant difference (F=9.776,P＜0.05).(4) Western blot results:the relative expressions of HIF-1α and VEGF (43 KD) in liver tissue of recipient rats at 1 day postoperatively were 0.21±0.10,0.30±0.12 in the empty virus group and 0.23±0.09,0.34±0.14 in the induced group and 0.17± 0.06,0.29±0.11 in the inhibited group,respectively,with no statistically significant difference (F =0.902,0.410,P＞0.05).The relative expressions of VEGF (24 KD) and HO-1 in liver tissue of recipient rats at 1 day postoperatively were 1.21 ±0.25,0.55±0.12 in the empty virus group and 2.13±0.40,0.72±0.12 in the induced group and 0.91±0.22,0.26±0.07 in the inhibited group,respectively,with statistically significant differences (F=35.158,39.082,P ＜ 0.05).The relative expressions of HIF-1α,VEGF (43 KD),VEGF (24 KD) and HO-1 in liver tissue of recipient rats at 7 days postoperatively were 0.49±0.22,0.46±0.13,0.98± 0.37,0.98±0.37 in the empty virus group and 0.83±0.26,0.63±0.19,1.60±0.33,1.49±0.46 in the induced group and 0.24±0.09,0.30±0.12,0.64±0.18,0.75±0.26 in the inhibited group,respectively,with statistically significant differences (F=16.853,10.021,20.756,8.156,P＜0.05).(5) Immunofluorescence staining results:number of small vessels at 14 days postoperatively in the empty virus group,induced group and inhibited group was respectively 7.9±2.0,10.6± 1.9 and 7.6 ± 1.9,with a statistically significant difference (F=5.921,P＜0.05).Conclusion HO-1 could promote expressions of HIF-1α and VEGF in liver tissue after liver transplantation ischemia-reperfusion injury and regeneration of intrahepatic vascular plexus,and it also alleviate bile duct ischemia-reperfusion injury after liver transplantation.
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<p><b>OBJECTIVE</b>Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance greatly limits the clinical therapeutic efficacy of TRAIL. Elucidating the molecular mechanism underlying TRAIL resistance will be fundamental to resolving this problem.</p><p><b>METHODS</b>Nuclear and cytoplasmic protein extraction and immuno？uorescence (IF) assay were used to detect changes in heterogeneous nuclear ribonucleoprotein K (hnRNPK) localization in H1299 cells. The evaluation of cell apoptosis in cells transfected with GFP-hnRNPK, GFP-hnRNPK S284/353A, or GFP-hnRNPK S284/353D mutant was performed using cleaved caspase-3 antibody. The gene expression of XIAP was tested by quantitative RT-PCR.</p><p><b>RESULTS</b>Previously, we reported that hnRNPK antagonized TRAIL-induced apoptosis through inhibition of PKC-mediated GSK3β phosphorylation. In this study, we further demonstrate that TRAIL treatment induces cytoplasmic accumulation of hnRNPK in H1299 cells. The hnRNPK localized in the cytoplasm has a higher capacity to antagonize TRAIL-induced apoptosis. Both ERK1/2 signaling inhibitor U0126 and ERK-phosphoacceptor-site mutant (GFP-hnRNPK S284/353A) diminish cytoplasmic accumulation of hnRNPK induced by TRAIL. Moreover, we show that XIAP is involved in hnRNPK-mediated TRAIL resistance in H1299 cells.</p><p><b>CONCLUSION</b>Taken together, these results give new insights into the understanding of the molecular mechanism associated with TRAIL resistance in lung adenocarcinoma.</p>
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Humans , Apoptosis , Physiology , Cell Line, Tumor , Gene Expression Regulation , Physiology , Heterogeneous-Nuclear Ribonucleoprotein K , Genetics , Metabolism , Mitogen-Activated Protein Kinase 1 , Genetics , Metabolism , Mitogen-Activated Protein Kinase 3 , Genetics , Metabolism , TNF-Related Apoptosis-Inducing Ligand , Genetics , Metabolism , Up-Regulation , Physiology , X-Linked Inhibitor of Apoptosis Protein , Genetics , MetabolismABSTRACT
Objective To investigate the influence of glomerular filtration rate (GFR)of living donor on recovery of graft function after transplantation.Methods Clinical data of 108 pairs of donors and recipients undergoing living donor renal transplantation at the Organ Transplantation Center of First Affiliated Hospital of Kunming Medical University from 2009 to 2013 were retrospectively studied.The objects were divided into G1 group (GFR <40 ml/min),G2 group(GFR 40 ~45 ml/min),G3 group(GFR 46 ~50 ml/min)and G4 group (GFR >50 ml/min)according to GFR of the donor kidneys.Changes in serum creatinine (Scr)at 1 week,2 weeks,3 weeks,1 month,3 months,6 months and 1 year after transplantation as well as survival conditions of patient and kidney within 1 year after transplantation of each group were compared.Results Compared with G1 group,Scr at 2 weeks,3 weeks,1 month after transplantation was lower in G2 group,G3 group and G4 group,and the difference had statistical significance (all in P <0.05).As for survival conditions of patient and kidney within 1 year after transplantation,one patient in G1 group developed graft failure due to hyperacute rejection and one patient in G1 group died of severe pulmonary infection.One patient in G2 group developed graft failure due to acute rejection.One patient in G3 group died of severe pulmonary infection.One patient in G4 group died of severe pulmonary infection. Other patients and grafts survived during the follow-up.Conclusions Low GFR of living kidney donor has certain influence on recovery of graft function in the early stage (within one month)after renal transplantation.
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Background and purpose: Because of the aggressive nature of hilar cholangiocarcinoma and the absence of effective adjuvant therapy, surgical radical resection offers hilar cholangiocarcinoma patients the only choice. Research focus include preoperative assessment, the use of preoperative biliary drainage, the range of hepatic resection, and the range of lymphadenectomy. To investigate the clinical experience and efifcacy of combined hepatectomy in the treatment of hilar cholangiocarcinoma. Methods: Two hundred and seven patients with hilar cholangiocarcinoma treated surgically in the First Afifliated Hospital of Kunming Medical University form Jan. 2007 to Oct. 2013 were retrospectively analyzed. Results:Of the 207 patients, 125 patients who received radical resection (R0 resection) and the curative resection rate was 60.4%. One hundred and iffty-six cases were treated in combined hepatectomy group, 51 cases in non-hepatectomy group, the rate of R0 resection was 70.5%in hepatectomy group and 29.4%in non-hepatectomy group, and the difference was signiifcant (P<0.01). Two patients died perioperatively, the main postoperative complications included hepatic function insufifciency and bile leakage. One hundred and seventy-two patients were followed up, the median survival time of the 102 patients who received R0 resection was 45 months, and the 1, 3, 5 year survival rates were 96.1%, 59.1%and 17.2%. The median survival time of the 70 patients who received R1-2 resection was 26 months, and the 1, 3 year survival rates were 81.3%and 19.2%, and none of the patient survived for over 5 years. The survival rate of patients who received R0 resection was signiifcantly higher than those who received R1-2 resection (χ2=39.121, P<0.01). In the hepatectomy group was awarded the R0 resection in patients with postoperative 1, 3, 5 year survival rate was 97.8%, 63.9% and 18.0%, in non-hepatectomy group received R0 resection in patients with postoperative 1, 3, 5 year survival rate was 83.3%, 20.8%and 8.3%. There were signiifcant differences in the postoperative survival rate between both group (χ2=5.988, P=0.014). Conclusion:Radical excision is the key to improve the long term survival. Combined hemihepatectomy and standardized lymph node resection has signiifcantly improved the radical resection rate and the efifcacy of treatment for hilar cholangiocarcinoma.
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Hepatic ischemia-reperfusion injury,a relatively common phenomenon in clinical pathophysiology, is one of the currently difficult and hot issues in liver surgery and liver transplantation clinical studies. p38 mitogen activated protein kinases are activated in a variety of diseases and stress conditions. p38 signaling pathway activation is one of the important mechanisms leading to hepatic ischemia-reperfusion injury. This article reviews the roles and mechanisms of P38 signaling pathway recently years in the liver ischemia reperfusion injury.
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<p><b>OBJECTIVE</b>To study the effect of heme oxygenase-1 (HO-1) on peribiliary vascular plexus (PVP) in rat bile duct ischemia/reperfusion injury.</p><p><b>METHODS</b>Total 128 male SD rats were randomly divided into saline group (Saline), empty virus group (Adv), induced group (Adv-HO-1) and suppressed group (HO-1 siRNA), and there were 32 rats in each group. Rats were injected using 0.5 ml of saline, empty adenovirus, HO-1 adenovirus and siRNA adenovirus (2×10(9) TU/rat) via the dorsal penile vein 24 hours before surgery. Liver function was analyzed at 1 hour and 1, 7, 14 days after reperfusion. HO-1, hypoxiainducible factor-1α (HIF-1α), stromal cell derived factor-1α (SDF-1α) and vascular endothelial growth factor (VEGF) protein content was analyzed by Western blot. The endothelial progenitor cells (EPCs) ratio in the liver and peripheral blood was detected by flow cytometry. Small vascular around the bile duct was observed by α-smooth muscle actin and von Willebrand factor double immunofluorescence staining.</p><p><b>RESULTS</b>Reduced liver injury and higher expression of HIF-1α, SDF-1α and VEGF in the induced group after surgery (q = 5.68-7.52, P < 0.01). EPCs ratio in the liver and peripheral blood was significantly higher in the induced group than saline group (q = 12.14 and 15.26, P < 0.01), and the suppressed group at 7 days after surgery were less than saline group significantly (q = 4.83 and 5.07, P < 0.01). In comparison to the suppressed group, higher density of small vascular around the bile duct was seen in the liver tissue of induced group.</p><p><b>CONCLUSIONS</b>HO-1 can induce the expression of HIF-1α, SDF-1α and VEGF, and mobilize the release of EPCs to the peripheral from the bone marrow. EPCs migrate to the liver and promote damaged PVP repair and regeneration.</p>
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Animals , Male , Rats , Bile Ducts , Chemokine CXCL12 , Metabolism , Endothelial Cells , Cell Biology , Heme Oxygenase (Decyclizing) , Physiology , Hypoxia-Inducible Factor 1, alpha Subunit , Metabolism , Neovascularization, Physiologic , RNA, Small Interfering , Rats, Sprague-Dawley , Reperfusion Injury , Stem Cells , Cell Biology , Vascular Endothelial Growth Factor A , MetabolismABSTRACT
Objective To evaluate upfront common bile duct suturing against T-tube drainage after exploration in the treatment of common bile duct stone.Methods 253 cases of extrahepatic bile duct stones treated at our department from 2008 June to 2012 January were randomly divided into primary suture group and T tube drainage group,by t test or analysis of variance independent sample comparison.Results All operations were successful.Postoperative bile leakage was observed in 2 patients in group A and 4 in group B respectively(P ＞ 0.05),there was no reoperations in the two groups.In group B retrograde biliary tract infection developed in one and was cured by biliary tract flush combined with antibiotics administration.The abdominal drainage was bile tainted fluid about 5-10 ml a day in bile leakage cases in both groups and healed itself in 3-4 days without fever,jaundice symptoms.There was no other severe complications such as pancreatitis.The postoperative biliary complication rate (P =0.802),operative time (P =0.137),intraoperative blood loss (P =0.069) and liver function recovery(ALT P =0.087,AST P =0.752,TBIL P =0.459,DBIL P =0.217,ALP P =0.576,GGT P =0.362) was not significantly different between the two groups.In group A postoperative flatus passing (P =0.037),postoperative fluid volume (P =0.008),postoperative hospital stay(P =0.015) were better than that in T-tube drainage group.At 3 to 12 months follow-up,no patients were found to have residual stones and biliary stricture in group A and group B.Conclusions With the definite indication and proficient surgical technology,primary suture of common bile duct after exploration is a safe and effective way after treatment of choledocholithiasis.
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Objective To investigate theeffect of ischemic postconditioning (IPO) on ischemia/reperfusion injury via mitochondrial pathway.Methods Male Sprague-Dawley rats were divided into three groups by means of random number table.Rats in IRI group and IPO group received liver transplantation.The portal vein in IRI group was opened immediately after liver implantation to restore the blood supply.The graft rats in IPO group received IPO before the portal vein was completely opened: 60-s ischemia and 60-s reperfusion of the portal vein,repeated 6 times).The rats in the sham-operation group were only subject to dissociation of the liver ligament.Six h after portal vein reperfusion,liver function was tested.The expression of Bcl-2 mRNA and Bax mRNA was detected by using real time-PCR.The protein expression of Cyt-c was detected by using Western blotting.The apoptosis and necrosis of liver tissue and the mitochondrial transmembrane potential were detected by using flow cytomertry.The changes of mitochondrial structure were observed under an electron microscope.Results The liver functions in IRI group and IPO group were significantly worse (P＜0.05),the levels of Bax mRNA were significantly higher (P＜0.05),the levels of Bcl-2 mRNA were significantly lower (P＜0.05),the levels of Cyt-c protein were significantly higher (P＜0.05),the levels of apoptosis and necrosis were significantly higher (P＜0.05),and mitochondrial transmembrane potential (MTP) of liver cells was significantly lower (P＜0.05) than in sham operation group.The changes of all the parameters in IRI group were more significant than in IPO group (P ＜ 0.05).The morphological changes of the liver mitochondria were also significantly aggravated in IRI group as compared with IPO group.Conclusion IPO reduced IRI by inhibiting the mitochondrial signaling pathway in rats undergoing liver transplantation.
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Functional insulinoma accounts for 85% of insulinoma, and it is evenly distributed in the head, body and tail of the pancreas. The main clinical manifestation of patients with functional insulinoma is endocrine disorder, and 92% of them presented with neurological symptoms. Preoperative localization of functional insulinoma is difficult because of the small size of the tumor. A 31-year-old male patient with the chief complaint of paroxysmal dizziness and confusion was admitted to the First Affiliated Hospital of Kunming Medical College on May 3,2010. The patient was preliminarily diagnosed with functional insulinoma by detecting the levels of fasting blood glucose,serum insulin and fasting serum C-peptide, as well as the presence of Whipple's triad. Ultrasonography and enhanced computed tomography demonstrated that a well-defined tumor of 13.0 mm ×13.0 mm in size was located in the pancreatic uncinate process.On May 27, 2010, the patient received surgical resection of the tumor, and histological examination of the resected specimen confirmed insulinoma.
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Objective To observe the effect of focal cerebral ischemic preconditioning on the expression of glial fibrillary acidic protein (GFAP) and to investigate the significance of astrocyte activation in cerebral ischemic tolerance.Methods Thirty-six healthy male SpragueDawley rats were randomly divided into reischenmic,ischemic and control groups (n = 12 in each group) after ischemic preconditioning.The former two groups received 10 minutes middle cerebral artery occlusion (MCAO) preconditioning or sham operation 3 days before the 2-hour MCAO.The rats were killed 24 hours after the second MCAO.The control group only receivedthe two sham operations with an interval of three days.The infarct volume,histopathological changes,and GFAP expression in each group were compared.Results The infarct volume after ischemic preconditioning in the reischenmic and ischemic groups was 136.85 ± 14.51 mm3and 281.37 ± 29.93 mm3 respectively.The former was significantly reduced 53.15%compared to the latter (P =0.007).At the same time,neuronal degeneration and necrosis was reduced significantly,and GFAP expression was upregulated significantly (the mean absorbance for immunohistochemical staining in both groups was 102.66 ± 8.39 and 86.28 ± 6.19respectively,P = 0.009) after ischemic preconditioning in the reischemic group.Conclusions Focal ischemic preconditioning may induce brain ischemic tolerance and promote GFAP expression.The activation of astrocytes may be one of the mechanisms of cerebral ischemic tolerance.