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- 저자 : Zan-Hong Wang (검색결과 2 건)
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Arjun Sinkemani,Xin Hong,Zeng-Xin Gao,Su-Yang Zhuang,Zan-Li Jiang,Shao-Dong Zhang,Jun-Ping Bao,Lei Zhu,Pei Zhang,Xin-Hui Xie,Feng Wang,Xiao-Tao Wu 대한척추외과학회 2015 Asian Spine Journal Vol.9 No.6
Study Design: Retrospective, case control evaluation of 86 patients who underwent microendoscopic discectomy (MED) and percutaneous transforaminal endoscopic discectomy (PTED) for the treatment of lumbar disc herniation (LDH). Purpose: To evaluate the safety and the outcomes of MED and PTED for the treatment of LDH. Overview of Literature: MED and PTED are minimally invasive surgical techniques for lower back pain. Studies to date have shown that MED and PTED are safe and effective treatment modalities for LDH. Methods: A retrospective study was performed in patients with LDH treated with MED (n=50) and transforaminal endoscopic discectomy (PTED; n=36) in our hospital. All patients were followed-up with self-evaluation questionnaires, Oswestry disability index (ODI), medical outcomes study 36-item short form health survey and MacNab criteria. All the patients in both groups were followed up to 12 months after the operation. Results: ODI questionnaire responses were not statistically different between the MED and PTED groups (53.00 vs. 48.72) before treatment. Average scores and minimal disability after 5 days to 12 months of follow-up were 4.96 in the MED group and 3.61 in the PTED group. According to MacNab criteria, 92.0% of the MED group and 94.4% of the PTED group had excellent or good results with no significant difference. Conclusions: There was no significant difference between MED and PTED outcomes. Further large-scale, randomized studies with long-term follow-up are needed.
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Li Xu,Jing-Hua Liu,Jing Zhang,Na Zhang,Zan-Hong Wang 대한암학회 2015 Cancer Research and Treatment Vol.47 No.2
Purpose Autophagy is one of the ways to degrade unfolded proteins after endoplasmic reticulum(ER) stress. The purpose of this study is to determine whether a blockade of autophagyleads to aggravated endoplasmic reticulum stress, which then induces cells apoptosis inHeLa cells treated with paclitaxel. Materials and MethodsAutophagy activation and the proapoptotic effects were characterized using monodansylcadaverinelabeling and Hoechest staining, respectively. A Western blot analysis was usedto detect the expression of apoptotic and autophagy-related genes. A flow cytometry wasused to assess the cell apoptosis ratio. ResultsPaclitaxel exposure induced the aggregation of autophagosomes in the cytoplasms ofcervical cancer HeLa cells. The expression of Beclin 1 and LC3 II were upregulated, but p62was downregulated, which suggests that autophagy was promoted by paclitaxel. On theother hand, the expression of GRP78 obviously increased, suggesting that ER stress wasinduced after paclitaxel treatment. The cell proliferation assay indicated that a knockdownof Beclin 1 sensitized HeLa cells to paclitaxel. Furthermore, paclitaxel-mediated apoptoticcell death was further potentiated by the pretreatment with autophagy inhibitor chloroquineor small interfering RNA against Beclin 1. These results suggest that an induction ofautophagy by paclitaxel may induce cell survival rather than cell death in HeLa cells;moreover, inhibition of autophagy led to an aggravated ER stress and an induction ofdownstream apoptosis. ConclusionOur results reveal autophagy induced by paclitaxel conferred protection of tumor cellsagainst apoptosis, and blockade of autophagy subsequently aggravated ER stress, enhancingthe apoptosis associated with paclitaxel treatment in HeLa cells.
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