http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Zong-Sheng Yin (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
-
Dan Zong,Li Yin,Qian Zhong,Wen-jie Guo,Jian-hua Xu,Ning Jiang,Zhi-rui Lin,Man-zhi Li,Ping Han,Lin Xu,Xia He,Mu-sheng Zeng 대한암학회 2016 Cancer Research and Treatment Vol.48 No.1
Purpose The purpose of this study was to investigate the function of Zinc finger protein 488 (ZNF488) in nasopharyngeal carcinoma (NPC). Materials and Methods The endogenous expression of ZNF488 in NPC tissues, normal nasopharyngeal epithelium tissues and NPC cell lines were detected by quantitative reverse transcription polymerase chain reaction. ZNF488 over-expressing and knock-down NPC cell line models were estab- lished through retroviral vector pMSCV mediated over-expression and small interfering RNA (siRNA) mediated knock-down. The invasion and migration capacities were evaluated by wound healing and transwell invasion assays in ZNF488 over-expressing and control cell lines. Soft-agar colony formation and a xenograft experiment were performed to study tumorigenic ability in vitro and in vivo. Immunofluorescence and western blotting analysis were used to examine protein changes followed by ZNF488 over-expression. Microarray analysis was performed to explore gene expression profilings, while luciferase reporter assay to evaluate the transcriptive activity of Tcf/Lef. Results ZNF488 was over-expressed in NPC tissues compared with normal tissues, especially higher in 5-8F and S18, which are well-established high metastatic NPC clones. Functional studies indicate that over-expression of ZNF488 provokes invasion, whereas knock-down of ZNF488 alleviates invasive capability. Moreover, over-expression of ZNF488 promotes NPC tumor growth both in vitro and in vivo. Our data further show that over-expression of ZNF488 induces epithelial mesenchymal transition (EMT) by activating the WNT/β -catenin signaling pathway. Conclusion Our data strongly suggest that ZNF488 acts as an oncogene, promoting invasion and tumorigenesis by activating the Wnt/β -catenin pathway to induce EMT in NPC.
-
Bo Zu,Hong Pan,Xiao-Jun Zhang,Zong-Sheng Yin 대한척추외과학회 2016 Asian Spine Journal Vol.10 No.5
Study Design: Cohort study. Purpose: This study primarily aimed to evaluate the serum levels of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-4 in patients with lumbar radiculopathy 1 and 12 months after microdiscectomy. Overview of Literature: Lumbar radiculopathy is possibly caused by inflammatory changes in the nerve root. The intraneural application of pro-inflammatory cytokines induces behavioral signs associated with pain. Anti-inflammatory cytokine treatment effectively reduces hyperalgesia. Methods: The role of TNF-α and IL-4 in long-lasting lumbar radiculopathy was addressed. A total of 262 patients were recruited from Anqing Hospital, Anhui Medical University. During inclusion at 1 and 12 months, serum concentrations of TNF-α and IL-4 were analyzed by enzyme-linked immunosorbent assay, and pain intensity was reported on a 0–10 cm visual analog scale (VAS). Results: Sixty six patients had VAS <3 and 196 patients had VAS ≥3. Serum concentrations of pro-inflammatory TNF-α and antiinflammatory IL-4 in patients with lumbar radiculopathy related to disc herniation were measured at 1- and 12-month follow-up. TNF-α decreased in both VAS groups with time. In contrast, IL-4 increased in both groups at 1 month and then decreased gradually until month 12. The changes in serum levels of TNF-α and IL-4 over time between the VAS ≥3 and VAS <3 groups were significantly different. Conclusions: Chronic lumbar radiculopathy may be associated with high level of pro-inflammatory substances, such as TNF-α, in serum after disc herniation, and elevated anti-inflammatory cytokine in patients with lumbar radiculopathy may indicate a favorable outcome.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
