1.Flap fenestration in treatment of mis-deployment of stent-graft in false lumen of aortic dissection
Ye PAN ; Jun ZHAO ; Weiguo FU ; Jiacai MEI ; Mingzhe SHAO ; Jian ZHANG
Chinese Journal of Trauma 2013;(3):216-220
Objective To evaluate feasibility of flap fenestration in management of the condition that a stent-graft is wrongly deployed in false lumen of aortic dissection.Methods A retrospective analysis was conducted on a case of Stanford type B aortic dissection who was confirmed that the stent-graft had been wrongly deployed in false lumen of aortic dissection by CT angiography (CTA) after endovascular repair.Thereafter,an additional surgical management was carried out.At length,flap fenestration at 2 cm below pre-deployed stent-graft was performed using an Outback catheter so as to link false and true lumens.Successively,another stent-graft was placed via the access to draw blood flow from false lumen back to true lumen and then coil embolization was performed for distal breach of the dissection.Results Surgery was carried out under local anesthesia,with operation duration of 170 minutes and intraoperative blood loss of 350 ml.The chest and back pain disappeared after operation.The patient commenced to take food and take off-bed activity at the very day of operation in absence of paraplegia,visceral ischemia,or other complications.Aortic CTA at postoperative one week showed ideal positioning of stent-graft,fluent blood flow of aorta and major visceral artery,and vanishing of false lumen.Conclusions Flap fenestration at far-end of pre-deployed stent-graft so as to draw blood flow back to true lumen by connecting the new placed stent graft to pre-deployed stent-graft is an effective treatment for mis-deployment of stentgraft in false lumen of aortic dissection.Outback catheter for flap fenestration is characterized by accurate location and high safety.
2.Inhibitory effect of Schisandrin B on proliferation of pancreatic cancer Pan02 cells and its mechanism
Jiacai FU ; Lingsha QING ; Lu YANG ; Meihui SONG ; Xianying ZHANG ; Xiaocui LIU ; Fengjin LI ; Ling QI
Journal of Jilin University(Medicine Edition) 2024;50(3):638-646
Objective:To discuss the inhibitory effect of Schisandrin B on the proliferation of pancreatic cancer Pan02 cells,and to clarify the mechanism.Methods:CCK-8 method was used to detect the proliferation rates of the Pan02 cells after treated with different concentrations(0,0.78,1.56,3.12,6.25,12.50,and 25.00 mg·L-1)of Schisandrin B to select the optimal concentration and treatment time of Schisandrin B.The mouse pancreatic cancer Pan02 cells were divided into control group(0 mg·L-1 Schisandrin B),2.5 mg·L-1 Schisandrin B group,5.0 mg·L-1 Schisandrin B group,and 10.0 mg·L-1 Schisandrin B group.The morpholoy of Pan02 cells invarious groups was observed with light microscope;5-ethynyl-2'-deoxyuridine(EdU)staining assay was used to detect the positive expression rates of the Pan02 cells in various groups;flow cytometry was used to detect the percentages of the Pan02 cells at different cell cycles and the apoptotic rates of the cells in various groups;Western blotting method was used to detect the expression levels of cell cycle and apoptosis-related proteins in the cells in various groups.Results:The CCK-8 method results showed that after treated with Schisandrin B for 48 and 72 h,compared with 0 mg·L-1 Schisandrin B,the proliferation rates of the Pan02 cells after treated with different concentrations of Schisandrin B were decreased(P<0.01),especially at 72 h.0.25,5.0,and 10.0 mg·L-1 Schisandrin B were selected to treat the Pan02 cells,and 72 h was the treatment time.In control group,the Pan02 cells had a spindle shape,with good condition,and grew closely adhered to the wall with normal organelles and cytoplasm,in 2.5 and 5.0 mg·L-1 Schisandrin B groups,the cell volume was decreased,the intercellular adhesion was disappeared,and the cell membrane was intact but more permeable;the cytoplasm shrank and vacuolar structures appeared inside the cells,with some fragmented and floating on the surface of the solution;in 10.0 mg·L-1 Schisandrin B group,the Pan02 cells exhibited notable apoptotic bodies,indicating an apoptotic state.The EdU staining results showed that compared with control group,the rates of EdU positive cells in 2.5,5.0,and 10.0 mg·L-1 Schisandrin B groups were significantly decreased(P<0.01).The flow cytometry results showed that compared with control group,the percentages of the cells at S phase in 2.5,5.0,and 10.0 mg·L-1 Schisandrin B groups were significantly increased(P<0.01),while the percentages of the cells at G2/M phase were significantly decreased(P<0.01),and the percentages of the cells at G0/G1 phase in 5.0 amd 1.0 mg·L-1 Schisandrin groups were decreased(P<0.01);compared with control group,the apoptotic rates of the cells in 2.5,5.0,and 10.0 mg·L-1 Schisandrin B groups were significantly increased(P<0.01).The Western blotting results showed that compared with control group,the expression levels of p27,B-cell lymphoma 2(Bcl-2)associated X protein(Bax),cleaved cysteine aspartic acid protease-3(cleaved Caspase-3),and cleaved poly adenosine diphosphate(ADP)ribose polymerase(cleaved PARP)proteins in the cells in 2.5 mg·L-1 Schisandrin B group were significantly increased(P<0.05 or P<0.01),the expression levels of cyclin A2,cyclin E2,and Bcl-2 proteins in the cells in 5.0 and 10.0 mg·L-1 Schisandrin B groups were significantly decreased(P<0.05 or P<0.01),while the expression levels of p27,Bax,cleaved Caspase-3,and cleaved PARP proteins in the cells in 5.0 and 10.0 mg·L-1 Schisandrin B groups were significantly increased(P<0.01).Conclusion:Schisandrin B has an inhibitory effect on proliferation of the pancreatic cancer Pan02 cells,and its mechanism may be related to the activation of the cysteine aspartic acid protease-3(Caspase-3)pathway to induce the apoptosis and activating p27 protein to induce the arrest of cell cycle at S phase.
3.Advances in the bioaugmentation-assisted remediation of petroleum contaminated soil.
Jin ZHENG ; Yali FU ; Quanwei SONG ; Jiacai XIE ; Shuangjun LIN ; Rubing LIANG
Chinese Journal of Biotechnology 2021;37(10):3622-3635
Bioremediation is considered as a cost-effective, efficient and free-of-secondary-pollution technology for petroleum pollution remediation. Due to the limitation of soil environmental conditions and the nature of petroleum pollutants, the insufficient number and the low growth rate of indigenous petroleum-degrading microorganisms in soil lead to long remediation cycle and poor remediation efficiency. Bioaugmentation can effectively improve the biodegradation efficiency. By supplying functional microbes or microbial consortia, immobilized microbes, surfactants and growth substrates, the remediation effect of indigenous microorganisms on petroleum pollutants in soil can be boosted. This article summarizes the reported petroleum-degrading microbes and the main factors influencing microbial remediation of petroleum contaminated soil. Moreover, this article discusses a variety of effective strategies to enhance the bioremediation efficiency, as well as future directions of bioaugmentation strategies.
Biodegradation, Environmental
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Petroleum
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Soil
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Soil Microbiology
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Soil Pollutants