Objectiye To explore the diagnostic and therapeutic methods of anastomotic leakage after low anterior resection of rectal cancer. Methods The clinical data of 16 cases with anastomotic leakage after sphincter saving operation which was performed through anterior resection for patients with lower rectal cancer were retrospectively analyzed. Results Among the 186 cases of low anterior resection of rectal cancer,16 cases occurred anastomotic leakage,incidence rate was 8.6% ;14 cases healed through local douche and drainage; 1 case healed by emergency operation and upper colostomy after bacterial peritonitis;only one elderly patient died for infectious shock. Conclusion Anastomotic leakage was the severe complication of low anterior resection,and timely correct treatment and doing well safety precautionary measures before operation could reduce the incidence rate of anastomotic leakage.

BACKGROUND:Researchers suggest that thermal damage happens when the temperature of biological tissues is over 44℃. Accurate analysis of burn range wil facilitate diagnosis and therapy of skin burns. OBJECTIVE: To establish the mathematical model of the skin tissues subjected to high temperature and to analyze heat transfer process, and then to predict the burn range of the skin. METHODS:A finite element method was used to simulate the temperature field when the skin tissue was burned. And the relevant animal experiment was conducted to identify the mathematical model. RESULTS AND CONCLUSION:The temperature field was obtained by using the finite element method and the variation tendency between the theoretical data and the experimental data were agreed, but they did not fuly coincide. The scope of skin burn can be predicted by the present finite element method, and help to research the process of heat transfer.

Objective To evaluate the efficiency and safety of transurethral plasmakinetic enucleation of prostate(PKEP) in the treatment of patients with benign prostate hyperplasia(BPH) after transrectal prostate biopsy(TRPB).Methods A total of 88 BPH patients who underwent PKEP in our hospital during Jan.2012 to May 2015 were retrospectively analyzed and followedup.38 patients underwent TRPB before PKEP were defined as TRPB group,and 50 patients underwent PKEP with no TRPB were defined as control group.The baseline data,perioperative data and postoperative follow-up outcomes were recorded and compared between the two groups.Results The mean age of the 88 patients were 69.7 years.Compared with control group,TRPB group showed that age was younger(t=2.62,P＜ 0.05)and prostate specific antigen(PSA) level was higher(t=13.64,P＜0.01).Operation duration was longer in TRPB group than in control group (93.6 ± 31.0) min vs.(77.9 ± 17.3) min (t =2.6 4,P ＜ 0.05).There were no significant differences in the preoperative data,blood loss,continuous bladder irrigation duration after operation and period of catheterization between two groups (all P ＞ 0.05).Trans-operative time was significantly shortened when the time interval between TRPB and PKEP is more than 4 weeks(P＜ 0.01),while blood loss was similar in the two groups(P＞ 0.0 5).There were no adverse events of blood transfusion,transurethral resection syndrome and injury of bladder or rectal in both two groups.There were no significant differences in maximum flow rate(Qmax),international prostate symptom score(IPSS) or quality of life(QOL) scores between the two groups at 3,6 and 12 months of follow up(all P＞ 0.05).Conclusions PKEP after TRPB is a safe and effective treatment for BPH patient.When the time interval between TRPB and PKEP is more than 4 weeks,the performing of PKEP operation would reduce the difficulty of operative procedure and increase the safety.

Objective To evaluated the risk factors of urethral recurrence ( UR) following radical cystectomy ( RC) in patients with bladder urothelial carcinoma.Methods The clinical data of 350 male patients who underwent RC between January 2005 and January 2013 were retrospectively analyzed.The mean age was 63 years (rang 46-76) years.176 cases had the history of non-muscle-invasive bladder cancer.15 cases were were found the tumor invasion into the prostatic urethral.The way of urinary diversion after RC included 172 cases were orthotopic neobladder, 90 cases were cutaneous diversion and 88 cases were ileal couduitin.331 cases underwent preoperation intravesical instillation.36 cases underwent systemic chemotherapy after operation.148 cases were found the multiple tumor lesions, which was more than 2 sites. The pathological stage was more than T2 satge in 189 cases.And 177 cases were diagnosed as high-grade urothelial carcinoma.Multivariate Cox regression analyses were used to evaluate the risk factors associated with the UR.Results There were 350 cases in this study, UR was observed in 28 cases ( 8%).On multivariate Cox regression analyses, previous history of NMIBC (HR=15.205,95%CI 3.718-62.180,P<0.001), prostate urethral involvement(HR=5.233,95%CI 1.106-24.754,P=0.037) and Non-orthotopic neobladder(HR=6.656,95%CI 1.840-24.077,P=0.004)which the operation of cutaneous diversion and ileal couduit , were independent risk factors of UR following RC.Intravesical instillation before operation ( HR =0.470, 95%CI 0.010-0.217, P <0.001 ) was the protective factor of the UR.Conclusions Previous history of NMIBC, prostatic urethral involvement and Non-orthotopic neobladder were independent risk factors of UR.Intravesical instillation before operation was protective factor of UR.Urethrectomy for patients with high risk factors and intravesical instillation before operation were important.

BACKGROUND:Reperfusion injury salvage kinase (RISK) pathway plays an important role in protective mechanism against ischemia reperfusion injury (IRI) induced by both ischemic pre-and post-conditioning. Many researches have been carried out on RISK pathway mechanism underlying ischemic post-conditioning conferring cardioprotection against IRI;however, there is less research about its effect on IRI in the skeletal muscle.
OBJECTIVE:To investigate the protective effect of an optimized protocol of ischemic post-conditioning on IRI in rat skeletal muscle and its underlying mechanism.
METHODS:Eighteen male Sprague-Dawley rats were equivalently randomized into IRI, ischemic post-conditioning and control groups. Rats were given occlusion or disocclusion of the right femoral artery of the right lower limb. Subsequently, the IRI group rats were subjected to 24 hours of reperfusion;the ischemic post-conditioning group immediately given 4 cycles of 30 seconds reperfusion/30 seconds ischemia, followed by 24 hours of reperfusion;the control group given no intervention.
RESULTS AND CONCLUSION:Hematoxylin-eosin staining showed that in the ischemic post-conditioning group, the morphology of muscle fibers changed little, with fewer inflammatory lesions and milder edema compared with the IRI group. The infarct size with TTC staining in the ischemic post-conditioning group was smaller than that in the IRI group. Western blot analysis revealed that the expressions of phospho-Akt and phosphorylated endothelial nitric oxide synthase-S1177 were significantly increased, but the expression of phosphorylated type endothelial nitric oxide synthase-Thr495 was much decreased in the ischemic post-conditioning group compared with the IRI group. The measurement of mitochondrial permeability transition pore opening with Ca2+induction showed that the absorbance values in the ischemic post-conditioning group were significantly lower than those in the IRI group (P<0.05). These results indicate that ischemia-reperfusion injury can be improved by applying an optimal protocol of ischemic post-conditioning in rat skeletal muscle. The underlying mechanism may be associated with the activation of RISK signaling pathway to inhibit opening of mitochondrial permeability transition pore, thereby contributing to the enhanced tolerance to IRI in rat skeletal muscle.

We analyzed the binding of P.rβ₂-GPI-DV with ox-LDL by fluorescence, molecular simulation and circular dichroism. We used SDS-PAGE and Western blotting to identify the purity of P.rβ₂-GPI-DV, fluorescence, circular dichroism spectroscopy and molecular docking simulation to analyze the binding between P.rβ₂-GPI-DV and oxLDL. P.rβ₂-GPI-DV was specifically recognized by anti-His antibody at 12 kDa position. The chromophoric groups, the changes of secondary structure and the molecular docking simulations revealed that the active pocket formed by Cys281-Lys-Asn-Lys-Glu-Lys-Lys287 and Leu313-Ala-Phe-Trp316 of P.rβ₂-GPI-DV and the -COOH carboxyl of oxLig-1 were the key for binding. P.rβ₂-GPI combined with ox-LDL via the fifth functional domain and the -COOH group. Our findings provide theoretical basis to further study the binding between β₂-GPI and ox-LDL in serum.

CD36, the major scavenger receptor, is intimately involved in the uptake of oxLDL in macrophages. To further study the function of CD36 in macrophages, we constructed CD36 gene silence cell lines (J774A.1) by lentivirus-mediated RNA interference technique, and analyzed the effect of CD36 in caveolin-1 protein expression. At first, 5 shRNA fragments were designed and synthesized according to the coding sequence (CDS) region of CD36 gene. Next, the CD36-shRNA was inserted into lentiviral vector to yield pLKO.1-CD36-shRNA plasmid. After DNA sequencing, the pLKO.1-CD36-shRNA plasmid and psiCHECK-II-CD36 were co-transfected into the 293T cells to screen the efficient CD36-shRNA. The efficient CD36-shRNA plasmid and the helper plasmid were co-transfected into the 293T cells to package the lentivirus, and then infected the J774A.1 cells. After screening by puromycin, CD36 gene silence cell lines (J774A.1) was established. Western blotting and confocal fluorescence microscopy results showed that the CD36 silencing efficiency in the gene silence cell line was 90%. Accompanied by a decrease in CD36 protein on cell surface, oxLDL binding to CD36 was significantly inhibited, indicating that the CD36 gene silence cell line is successfully established. Finally, the oxLDL stimulation and inhibitor experiments results showed that the CD36 knockdown significantly suppresses the phosphorylation of JNK and ERK, thereby inhibiting the oxLDL-induced caveolin-1 protein expression, demonstrating that CD36 modulates the caveolin-1 protein expression through the JNK/ERK-mediated signaling transduction.