Expression and clinical significance of serum ubiquitin in esophageal squamous cell carcinoma / 医学研究生学报

Objective　Ubiquitin-proteasome system (UPS) plays a central role in the development of esophageal cancer. However, As the executor of UPS, the expression and clinical significance of detection of serum ubiquitin (UB) in Esophageal Squamous Cell Carcinoma(ESCC) patients have not been fully elucidated. The aim of this study was to investigate the expression and diagnostic value of serum ubiquitin (UB) in ESCC.　Methods　A total of eighty-eight ESCC patients and forty healthy controls from February 2018 to May 2019 at the Affiliated Jiangyin Hospital of Nantong University were enrolled. Serum UB was measured by ELISA, and serum squamous cell carcinoma antigen (SCC) and carcinoembryonic antigen (CEA) were determined by chemiluminescence method. The ROC curve was used to analyze the diagnostic value of each indicator. Besides, the correlation between serum UB and clinicopathological features of ESCC were analyzed.　Results　The level of serum UB in ESCC group was significantly higher than that in the control group[(41.96±3.273)ng/ml vs (80.86±7.993)ng/ml, P<0.05]. The level of serum UB in ESCC patients was related to lymphatic metastasis and tumor stage (P<0.05). The sensitivity of UB, SCC, CEA and the three combined diagnosis of ESCC were 65.9%, 52.3%, 51.1%, and 76.1%, respectively. The AUC under the ROC curve were 0.690, 0.677, 0.635, and 0.795, respectively.　Conclusion　Serum UB is highly expressed in ESCC and is closely related to tumor progression. Combined with SCC and CEA, UB can improve the sensitivity of diagnosis of ESCC and can be used as an effective serological screening biomarker.

Study on the role of Cathepsin B and JNK signaling pathway in the development of cerebral aneurysm

OBJECTIVE@#To investigate the correlation between JNK signal and the apoptosis of VSMC as well as the expression of Cathepsin B and to explore the role of JNK signal in the development of cerebral aneurysm.@*METHODS@#Rat models of cerebral aneurysm were established and histopathologic changes of cerebral aneurysm and the apoptosis of VSMC were analyzed. Rat models were respectively subject to subcutaneous injection of Cathepsin B siRNA and JNK inhibitor SP600125. Western blot technique was used to detect the expression of proteins like Cathepsin B, Caspase-3, and p-JNK. Spearman's rho was used to examine the correlation between p-JNK and Cathepsin B, as well as the expression of relevant proteins.@*RESULTS@#The success rate of modeling rats with cerebral aneurysm was 88.75%. After the respective injection of Cathepsin B siRNA, SP600125 and their combination, the cell densities of VSMC of rats with cerebral aneurysm all increased significantly (P < 0.05 or P < 0.01), but the apoptosis rate of VSMC decreased significantly (P < 0.01). Compared with normal rats, the expression of Cathepsin B, Caspase-3 and p-JNK in Cerebral aneurysm models increased significantly. Effectively intervening Cathepsin B genes with Cathepsin B siRNA could significantly inhibit the expression of Cathepsin B and Caspase-3, but hardly influence the expression of p-JNK. JNK inhibitor SP600125 had no influence on the expression of Cathepsin B and Caspase-3, but effectively inhibited the expression of p-JNK. In cerebral aneurysm tissues, positive correlation was observed between the expression of p-JNK and Cathepsin B, the correlation coefficient was r = 0.640.@*CONCLUSION@#After the attack of cerebral aneurysm, proteins like Cathepsin B, Caspase-3 and p-JNK are all involved in the apoptosis of VSMCs. This process may be realized by Cathepsin B which activates the apoptosis mechanism of Caspase-3 and mediate the apoptosis of VSMC through the JNK signaling pathway. Therefore, silencing Cathepsin B gene or inhibiting the conduction through JNK signaling pathway can mitigate the apoptosis of vascular smooth muscle cells in cerebral aneurysm.

Study on the role of Cathepsin B and JNK signaling pathway in the development of cerebral aneurysm

Objective To investigate the correlation between JNK signal and the apoptosis of VSMC as well as the expression of Cathepsin B and to explore the role of JNK signal in the development of cerebral aneurysm. Methods Rat models of cerebral aneurysm were established and histopathologic changes of cerebral aneurysm and the apoptosis of VSMC were analyzed. Rat models were respectively subject to subcutaneous injection of Cathepsin B siRNA and JNK inhibitor SP600125. Western blot technique was used to detect the expression of proteins like Cathepsin B, Caspase-3, and p-JNK. Spearman's rho was used to examine the correlation between p-JNK and Cathepsin B, as well as the expression of relevant proteins. Results The success rate of modeling rats with cerebral aneurysm was 88.75%. After the respective injection of Cathepsin B siRNA, SP600125 and their combination, the cell densities of VSMC of rats with cerebral aneurysm all increased significantly (P < 0.05 or P < 0.01), but the apoptosis rate of VSMC decreased significantly (P < 0.01). Compared with normal rats, the expression of Cathepsin B, Caspase-3 and p-JNK in Cerebral aneurysm models increased significantly. Effectively intervening Cathepsin B genes with Cathepsin B siRNA could significantly inhibit the expression of Cathepsin B and Caspase-3, but hardly influence the expression of p-JNK. JNK inhibitor SP600125 had no influence on the expression of Cathepsin B and Caspase-3, but effectively inhibited the expression of p-JNK. In cerebral aneurysm tissues, positive correlation was observed between the expression of p-JNK and Cathepsin B, the correlation coefficient was r = 0.640. Conclusion After the attack of cerebral aneurysm, proteins like Cathepsin B, Caspase-3 and p-JNK are all involved in the apoptosis of VSMCs. This process may be realized by Cathepsin B which activates the apoptosis mechanism of Caspase-3 and mediate the apoptosis of VSMC through the JNK signaling pathway. Therefore, silencing Cathepsin B gene or inhibiting the conduction through JNK signaling pathway can mitigate the apoptosis of vascular smooth muscle cells in cerebral aneurysm.

Clinical efficacy of malignant obstructive jaundice treated by domestic biliary metallic stent insertion / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To evaluate the clinical efficacy of implanted biliary metallic stents in the management of malignant obstructive jaundice (MOJ).</p><p><b>METHODS</b>Percutaneous transhepatic cholangiography and stent insertion were performed in 241 consecutive patients to treat malignant biliary obstruction between December 1998 and February 2009. The study end point was patient death. All patients were followed-up until death or until February 2010. The therapeutic efficacy was determined by statistical analysis of life span and pre- and post-operative laboratory indices.</p><p><b>RESULTS</b>All 241 patients were successfully stented. The level of bilirubin descended obviously within four weeks of implantation (P less than 0.05), and the early mortality rate was 4.56% (11/241). Two-hundred-and-two patients were followed-up (range: 8-193 weeks post-transplantation) and showed a median survival of 43.55 weeks. The survival rates at 13, 26, 39 and 52 weeks post-transplantation were 87%, 66%, 56%, and 41%, respectively. The stent patency rates at 13, 26, 39 and 52 weeks post-transplantation were 70%, 46%, 36% and 24%, respectively; the mean stent patency was 27.57 weeks. Cox regression analysis identified the strong predictors of improved survival as an initial bilirubin level of less than 221 mumol/L (P = 0.01) and a stent-induced bilirubin reduction of more than 50% (P = 0.002).</p><p><b>CONCLUSION</b>Transhepatic metallic biliary stenting is a safe and effective therapeutic intervention for malignant biliary obstruction. Significant periods of survival and palliation of jaundice can be achieved with this method. Hyperbilirubinemia and a stent-induced bilirubin reduction of less than 50% are independent predictive factors for the survival of MOJ patients.</p>