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Wei Zhu,Jiahong Liu,Kuanxiang Shi,Fei Qi,Huiping Shen,Zhu Xu,Zhilong Ma 대한기계학회 2022 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.36 No.9
This paper proposes a three degree-of-freedoms (DOFs) cable-driven parallel robot (CDPR), which is actuated by three groups of parallel cables and tensioned by an elastic telescopic rod with a passive spring. Firstly, the architecture of the robot is briefly illustrated with emphasis on the three parallelogram arrangements of the cables and composition of elastic telescopic rod structure. This robot has larger workspace and greater tension than previous under-constrained CDPRs. Secondly, the kinematic and dynamic models of the robot are established. On this basis, the parameters of the spring installed in the telescopic rod are optimized and determined considering both the acceleration and cable force through using the differential evolution (DE) algorithm. Thirdly, dynamic stability analysis of the robot under impulsive disturbances is performed according to the Gauss principle of least constraint (GPLC). The results of a simulation case show that this robot has better dynamic stability in comparison with conventional under-constraint CDPR because of the presence of the elastic telescopic rod. The measurement results in the workspace are obtained through dynamic simulation. Finally, the experiments are performed based on numerical simulation. The feasibility of the CDPR is verified via the experiments and simulations.
RhoGDI2 induced malignant phenotypes of pancreatic cancer cells via regulating Snail expression
Yi Bin,Hu You,Zhu Dongming,Yao Jun,Zhou Jian,Zhang Yi,He Zhilong,Zhang Lifeng,Zhang Zixiang,Yang Jian,Tang Yuchen,Huang Yujie,Li Dechun,Liu Qiuhua 한국유전학회 2022 Genes & Genomics Vol.44 No.5
Background: Rho GDP dissociation inhibitor 2 (RhoGDI2) has been shown to contribute to the aggressive phenotypes of human cancers, such as tumor metastasis and chemoresistance. Objective: This study aimed to assess the effects of RhoGDI2 on tumor progression and chemoresistance in pancreatic cancer cells. Methods: The expression of RhoGDI2 in pancreatic cancer cells was detected by Western blot analysis. Gain-of-function and loss-of-function approaches were done to examine the malignant phenotypes of the RhoGDI2-expressing or RhoGDI2-depleting cells. The correlation between RhoGDI2 and Snail was also analyzed. Results: Differential expression of RhoGDI2 protein in pancreatic cancer cell lines was identified. Gain-of-function and loss-of-function experiments showed that RhoGDI2 induced the malignant phenotypes of pancreatic cancer cells, including proliferation, migration, invasion, and gemcitabine (GEM) chemoresistance. The upregulation of RhoGDI2 stimulated the expression of Snail, resulting in the altered expression of epithelial marker E-cadherin and mesenchymal marker Vimentin, which were characteristics of the tumorigenic activity of epithelial-mesenchymal transition. The expression of RhoGDI2 and Snail was upregulated in clinical tumor samples, and higher expression of RhoGDI2 or Snail was significantly associated with poor patient survival in pancreatic ductal adenocarcinoma (PDAC). Conclusion: The findings indicated that RhoGDI2 promoted GEM resistance and tumor progression in pancreatic cancer and that RhoGDI2 might be a potential therapeutic target in patients with PDAC.
Melatonin Attenuates Mitochondrial Damage in Aristolochic Acid-Induced Acute Kidney Injury
Sun Jian,Pan Jinjin,Liu Qinlong,Cheng Jizhong,Tang Qing,Ji Yuke,Cheng Ke,wang Rui,Liu Liang,Wang Dingyou,Wu Na,Zheng Xu,Li Junxia,Zhang Xueyan,Zhu Zhilong,Ding Yanchun,Zheng Feng,Li Jia,Zhang Ying,Yua 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.1
Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN). AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.