Objective: To study the correlation of apoptosis inducer TWEAK and extracellular matrix protein Del-1 with pancreatic cancer malignancy. Methods: A total of 54 patients with pancreatic cancer who received radical rese...Objective: To study the correlation of apoptosis inducer TWEAK and extracellular matrix protein Del-1 with pancreatic cancer malignancy. Methods: A total of 54 patients with pancreatic cancer who received radical resection and 32 patients with pancreatic trauma who received partial resection in Tianyou Hospital Affiliated to Wuhan University of Science &Technology between May 2014 and March 2017 were selected, proper amount of pancreatic cancer tissue and normal pancreatic tissue were collected respectively, RNA was extracted and synthesized into cDNA by reverse transcription, and then fluorescence quantitative PCR kits were used to determine TWEAK, Del-1, Survivin, USP9X, DPF2, Stathmin, CD44v9, GPSM2, MMP9, Snail and Vimentin mRNA expression. Results: TWEAK, Del-1, Survivin, USP9X, DPF2, Stathmin, CD44v9, GPSM2, MMP9, Snail and Vimentin mRNA expression in pancreatic cancer tissue were significantly higher than those in normal pancreatic tissue;Survivin, USP9X, DPF2 and Stathmin mRNA expression in pancreatic cancer tissue with high TWEAK expression were significantly higher than those in pancreatic cancer tissue with low TWEAK expression;CD44v9, GPSM2, MMP9, Snail and Vimentin mRNA expression in pancreatic cancer tissue with high Del-1 expression were significantly higher than those in pancreatic cancer tissue with low Del-1 expression. Conclusion: The high expression of TWEAK and Del-1 in pancreatic cancer tissue can promote the proliferation and invasion of pancreatic cancer cells respectively.展开更多
应用移动1/N展开方法,计算Van del pol振子方程的本征值。对v=0,且应用SUSY—QM计算其本征值。当光泵参数g远低于阈值或在阈值附近,所有本征值都能和数值计算结果相吻合。当g远高于阈值时,基态和第一激发态本征值亦能和数值计算结果相...应用移动1/N展开方法,计算Van del pol振子方程的本征值。对v=0,且应用SUSY—QM计算其本征值。当光泵参数g远低于阈值或在阈值附近,所有本征值都能和数值计算结果相吻合。当g远高于阈值时,基态和第一激发态本征值亦能和数值计算结果相吻合。展开更多
This study aimed to investigate the impact of developmental endothelial locus-1(Del-1)on sarcoplasmic reticulum Ca^(2+)ATPase 2(SERCA2)and its potential effects on spinal cord injury(SCI).A total of 48 mice were rando...This study aimed to investigate the impact of developmental endothelial locus-1(Del-1)on sarcoplasmic reticulum Ca^(2+)ATPase 2(SERCA2)and its potential effects on spinal cord injury(SCI).A total of 48 mice were randomly assigned to the sham group,SCI group,and SCI+CE group.Each group was further divided into two subgroups.The Del treatment subgroup received tail-vein injections of Del-1(1μg/d)for a consecutive week,while the other group was injected with an equivalent volume of normal saline.After 1 week of experimentation,the mice were euthanized,and the spinal cord was extracted for further analysis.Initially,the impact of Del-1 on SERCA2 in the spinal cord was assessed using western blotting analysis.Subsequently,the effects of Del-1 on stress,inflammation,and apoptosis in the endoplasmic reticulum(ER)of SCI mice were analyzed through Western blotting analysis and fluorescent TUNEL.Finally,the study utilized Western blotting analysis and fluorescent TUNEL analysis to examine the consequences of Del-1 blocking SERCA2 on ER stress,inflammation,and apoptosis in mice.The results revealed that Del-1 treatment significantly increased the expression of SERCA2 in the spinal cord(P<0.01)and mitigated SCI-induced ER stress,inflammation,and neuronal apoptosis(P<0.01).Blocking SERCA2 expression in the spinal cord of SCI mice promoted ER stress,inflammatory response,and neuronal cell apoptosis(P<0.01).However,Del-1 treatment did not alleviate the effects of blocking SERCA2 on ER stress,inflammatory response,and neuronal cell apoptosis(P>0.05).In conclusion,this study proposed that Del-1 could reduce ER stress,inflammatory response,and nerve cell apoptosis in spinal cord injury by enhancing the expression of SERCA2.展开更多
文摘Objective: To study the correlation of apoptosis inducer TWEAK and extracellular matrix protein Del-1 with pancreatic cancer malignancy. Methods: A total of 54 patients with pancreatic cancer who received radical resection and 32 patients with pancreatic trauma who received partial resection in Tianyou Hospital Affiliated to Wuhan University of Science &Technology between May 2014 and March 2017 were selected, proper amount of pancreatic cancer tissue and normal pancreatic tissue were collected respectively, RNA was extracted and synthesized into cDNA by reverse transcription, and then fluorescence quantitative PCR kits were used to determine TWEAK, Del-1, Survivin, USP9X, DPF2, Stathmin, CD44v9, GPSM2, MMP9, Snail and Vimentin mRNA expression. Results: TWEAK, Del-1, Survivin, USP9X, DPF2, Stathmin, CD44v9, GPSM2, MMP9, Snail and Vimentin mRNA expression in pancreatic cancer tissue were significantly higher than those in normal pancreatic tissue;Survivin, USP9X, DPF2 and Stathmin mRNA expression in pancreatic cancer tissue with high TWEAK expression were significantly higher than those in pancreatic cancer tissue with low TWEAK expression;CD44v9, GPSM2, MMP9, Snail and Vimentin mRNA expression in pancreatic cancer tissue with high Del-1 expression were significantly higher than those in pancreatic cancer tissue with low Del-1 expression. Conclusion: The high expression of TWEAK and Del-1 in pancreatic cancer tissue can promote the proliferation and invasion of pancreatic cancer cells respectively.
基金National Key Research and Development Plan of China(Grant No.2016YFC1101503)。
文摘This study aimed to investigate the impact of developmental endothelial locus-1(Del-1)on sarcoplasmic reticulum Ca^(2+)ATPase 2(SERCA2)and its potential effects on spinal cord injury(SCI).A total of 48 mice were randomly assigned to the sham group,SCI group,and SCI+CE group.Each group was further divided into two subgroups.The Del treatment subgroup received tail-vein injections of Del-1(1μg/d)for a consecutive week,while the other group was injected with an equivalent volume of normal saline.After 1 week of experimentation,the mice were euthanized,and the spinal cord was extracted for further analysis.Initially,the impact of Del-1 on SERCA2 in the spinal cord was assessed using western blotting analysis.Subsequently,the effects of Del-1 on stress,inflammation,and apoptosis in the endoplasmic reticulum(ER)of SCI mice were analyzed through Western blotting analysis and fluorescent TUNEL.Finally,the study utilized Western blotting analysis and fluorescent TUNEL analysis to examine the consequences of Del-1 blocking SERCA2 on ER stress,inflammation,and apoptosis in mice.The results revealed that Del-1 treatment significantly increased the expression of SERCA2 in the spinal cord(P<0.01)and mitigated SCI-induced ER stress,inflammation,and neuronal apoptosis(P<0.01).Blocking SERCA2 expression in the spinal cord of SCI mice promoted ER stress,inflammatory response,and neuronal cell apoptosis(P<0.01).However,Del-1 treatment did not alleviate the effects of blocking SERCA2 on ER stress,inflammatory response,and neuronal cell apoptosis(P>0.05).In conclusion,this study proposed that Del-1 could reduce ER stress,inflammatory response,and nerve cell apoptosis in spinal cord injury by enhancing the expression of SERCA2.
