1.Development of Surgical Robots in Recent Years.
Lixiao YANG ; Zhengsong HOU ; Wei TANG ; Sinan ZHU ; Qi BAO ; Jiabin TONG ; Xiuwen DING
Chinese Journal of Medical Instrumentation 2023;47(1):1-12
OBJECTIVE:
To study the development of surgical robots at home and abroad in recent years.
METHODS:
Through a large number of literature review and analysis, the qualification approval and technical function characteristics of domestic and foreign surgical robots from January 2019 to July 2022 were analyzed.
RESULTS:
The related situations of 39 surgical robots were analyzed and reported, and the shortcomings and future development direction of the current surgical robots were summarized.
CONCLUSIONS
The development of surgical robots in China is now in a rapid development stage. At present, surgical robots generally have the disadvantages of high cost, lack of tactile feedback (force feedback), large size, large space occupation and difficult to move. In the future, it will develop towards intelligent, miniaturized, remote, open and low-cost.
China
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Robotics
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Robotic Surgical Procedures
2.Expression and biological role of LncSox4 in non-small cell lung cancer
Sinan HOU ; Yanke CHEN ; Jianmei GU ; Xiaoge DING ; Jiayin ZHANG ; Hui QIAN ; Wenrong XU ; Xu ZHANG
Chinese Journal of Clinical Laboratory Science 2019;37(10):731-736
Objective:
To determine the changed expression levels, biological roles and underlying mechanism of LncSox4 in non-small cell lung cancer (NSCLC), providing novel biomarkers for NSCLC diagnosis and therapy.
Methods:
QRT-PCR was used to detect the expression of LncSox4 in the tumor tissues of NSCLC patients. Colony formation, cell growth curve, Transwell migration and invasion assays were used to determine the effects of LncSox4 knockdown on A549 cell function, respectively. Flow cytometry was used to determine the effects of LncSox4 on the progression of A549 cell cycle. QRT-PCR and western blot were used to explore the expressions of genes and proteins in epithelial-mesenchymal transition (EMT).
Results:
The expression of LncSox4 was upregulated significantly in carcinoma tissues of NSCLC compared to the para-carcinoma tissues (t=7.109,P<0.01). The growth rate of A549 cells slowed down in LncSox4 knockdown group and the number of formed cell colonies was less than that in control group(P<0.01). LncSox4 knockdown reduced the migration and invasion abilities of A549 cells (P<0.01) and induced cell cycle arrest at G1 phase(P<0.01). LncSox4 knockdown downregulated the protein expressions of Cyclin D1, c-Myc, N-cadherin, and Vimentin, while upregulated the expression of E-cadherin in A549 cells. LncSox4 knockdown also decreased the expressions of EMT-related transcription factors including snail, slug and twist.
Conclusion
The high expression of LncSox4 in NSCLC may promote malignant progression of NSCLC by enhancing cell proliferation, migration and invasion, suggesting that it should be a promising target for diagnosis and therapy of NSCLC.
3.Clinical value and biological role of LINC00978 in non-small cell lung cancer
Yan HU ; Xiaoge DING ; Jianmei GU ; Sinan HOU ; Yanke CHEN ; Xueyan ZANG ; Jiayin ZHANG ; Yu ZHANG ; Meng SHAO ; Zheying MAO ; Hui QIAN ; Wenrong XU ; Xu ZHANG
Chinese Journal of Clinical Laboratory Science 2019;37(8):596-602
Objective:
To investigate the expression change, biological role and action mechanism of long non-coding RNA (lncRNA) LINC00978 in non-small cell lung cancer (NSCLC).
Methods:
The expression levels of LINC00978 in tumor tissues and serum samples of NSCLC patients were detected by the qRT-PCR. The effects of knockdown and overexpression of LINC00978 on the biological function of A549 cells were determined by the CCK-8, colony formation, Transwell migration and invasion assays. The action mechanisms of LINC00978 in NSCLC were investigated by the flow cytometry, qRT-PCR and western blot, respectively.
Results:
The expression levels of LINC00978 in the tissues ( t =2.465, P <0.05) and serum samples ( t =8.781, P <0.01) of NSCLC patients increased. The knockdown of LINC00978 inhibited the proliferation, migration and invasion of A549 cells ( P <0.01) and induced cell cycle arrest at G1 phase and apoptosis of A549 cells ( P <0.01). The knockdown of LINC00978 downregulated the expression of Cyclin D1 and Bcl-2 , and upregulated the expression of Bax ( P <0.05). In addition, the knockdown of LINC00978 inhibited the expression of N-cadherin, Vimentin, Snail, Slug and Twist, and promoted the expression of E-cadherin ( P <0.05). The overexpression of LINC00978 had the opposite effect.
Conclusion
LINC00978 is highly expressed in NSCLC and can promote the occurrence and progression of NSCLC, which may serve as a potential target for the diagnosis and therapy of NSCLC.