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1.
Cancer Research and Clinic ; (6): 760-762, 2021.
Artículo en Chino | WPRIM | ID: wpr-912963

RESUMEN

Objective:To explore the safety and feasibility of Da Vinci robotic-assisted laparoscopic resection in treatment of liver benign tumors.Methods:The clinical data of 62 patients with liver benign tumors admitted to Fujian Medical University Union Hospital from January 2016 to December 2019 were retrospectively analyzed. All patients were divided into 2 groups: 25 cases undergoing Da Vinci robotic-assisted laparoscopic resection (the robotic group) and 37 cases undergoing conventional laparoscopic resection for liver benign tumors (the laparoscopic group). The operation duration, intraoperative blood loss, postoperative abdominal drainage tube removal time, incidence of postoperative complications, postoperative hospital stay time of both groups were compared.Results:Operations of all 62 patients were successfully completed. The operation time of the robotic group was longer than that of the laparoscopic group [(192±52) min vs. (158±41) min], intraoperative blood loss of the robotic group was less than that of the laparoscopic group [(159±67) ml vs.(213±59) ml], and differences were statistically significant between the two groups (both P < 0.05). The postoperative abdominal drainage tube removal time of the robotic group and the laparoscopic group was (7.0±1.5) d and (7.2±1.3) d, the incidence of postoperative complications was 8.0% (2/25) and 5.4% (2/37), and the postoperative hospital stay time was (7.0±2.4) d and (7.3±2.2) d, respectively; and differences were statistically significant between both groups (all P > 0.05). Conclusion:Da Vinci robotic-assisted laparoscopic resection is a safe and effective operation method in treatment of liver benign tumors with advantages of small wound and less blood loss.

2.
Chinese Journal of Biochemical Pharmaceutics ; (6): 34-36,40, 2016.
Artículo en Chino | WPRIM | ID: wpr-603392

RESUMEN

Objective To identify the factors those regulate CCCP-induced non-canonical autophagy.Methods Different cells expressing GFP-LC3 were treated with or without CCCP (30μM) for 6 h.Fluorescent images were taken and cell lysates were analyzed by western blot assay.Real-time PCR was used to measure the mRNA levels of LC3B.FIP200-KO MEF cells were cultured and treated by 30 μM CCCP with or without water channel inhibitors, for 6 h.Cell lysates were analyzed by Western blot assay.Results CCCP could not induced autophagy in Atg5-KO MEF cells.CCCP could induce non-canonical autophagy in ULK1-KO MEF, FIP200-KO MEF, and Beclin1-KD U251.CCCP treatment in FIP200-KO MEF cells had no effect on the expression level of LC3B mRNA.We also found two distinct aquaporin water channel inhibitors could inhibit the generation of LC3 which was induced by CCCP.Conclusion CCCP induced non-canonical autophagy was Atg5-dependent, but Beclin1-, ULK1-and FIP200-independent.Osmotic imbalance could regulate CCCP-induce non-canonical autophagy.

3.
Journal of Clinical Hepatology ; (12): 244-2015.
Artículo en Chino | WPRIM | ID: wpr-778022

RESUMEN

ObjectiveTo investigate the effect of NOTCH4 expression on vasculogenic mimicry (VM) formation in hepatocellular carcinoma (HCC). MethodsTumor tissues were collected from 85 patients diagnosed with HCC. The relationship between NOTCH4 expression and VM was examined using immunohistochemical staining and PAS/CD31 double staining. The influence of siRNA-mediated NOTCH4 silencing on VM network formation in HCC was observed in the 3D cell culture system in vitro. Experimental data were assessed with Mann-Whitney U test and one-way analysis of variance. ResultsNOTCH4 had significantly higher expression in VM-positive HCC tissues than in VM-negative HCC tissues (P=0.019). In siRNA-treated cells, NOTCH4 mRNA and protein expression was significantly down-regulated compared with those in mock-treated cells (P=0.007; P=0.003) and untreated cells (P=0.000; P=0.000). VM network formation was impaired by inhibition of NOTCH4 expression in the 3D cell culture system. ConclusionNOTCH4 plays an important role in VM formation in HCC and may provide a novel molecular target for anti-angiogenesis therapy for HCC.

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