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Event-triggered H∞ Control for Switched Systems Under Multiple Attacks
Ying Xu,Xiaowu Mu,Guifang Cheng 제어·로봇·시스템학회 2023 International Journal of Control, Automation, and Vol.21 No.4
This article investigates the event-triggered H∞ control for networked switched systems under multiple attacks and transmission delay. A novel model of multiple attacks is constructed by considering stochastic false data injection attack and periodic denial-of-service (DoS) attack. The event-triggered strategy is proposed by using the mode information of switched system and periodicity of DoS attack. Then, sufficient conditions are obtained to ensure mean-square exponential stability and H∞ performance of the closed-loop switched system. Furthermore, the controller gains and event-triggered parameters of subsystems are derived. Finally, a numerical example is given to verify the effectiveness and feasibility of the results.
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Jun Ma,Xiao Song,Xiaowu Xu,Yiping Mou 대한암학회 2019 Cancer Research and Treatment Vol.51 No.1
Purpose Our aim was to detect the potential role of interleukin 11 (IL-11) in the development of chemo-resistance in gastric cancer and to reveal the mechanism involved in the process. Materials and Methods Here, we used flow cytometry to examine the percentage of cancer-associated-fibroblasts in tumor samples from chemo-resistant and -sensitive gastric cancer patients. Using MTT assay, we detected the cell viability under different conditions. Using quantitative real-time polymerase chain reaction and Western blotting, we determined the target expressions in mRNA and protein levels. We also performed immunohistochemistry and immunofluorescence to detect the target proteins under different conditions. Animal models were constructed to verify the potential role of IL-11 in chemo-resistant develop in vivo. Results Herein, we observed enriched cancer associated fibroblasts in drug resistant tumor tissues from gastric patients. Those fibroblasts facilitate the chemotherapeutic drugs resistance development through the secretion of IL-11, which activates the IL-11/IL-11R/gp130/ JAK/STAT3 anti-apoptosis signaling pathway in gastric cancer cells. We found that the combination of chemotherapeutic drugs and JAK inhibitor overcomes the resistance and increases the survival of mice with gastric cancer xenografts. Conclusion Our results demonstrated that IL-11 contributed to the obtain of resistance to chemotherapy drugs through gp130/JAK/STAT3/Bcl2 pathway, and targeting the IL-11 signaling pathway induced by fibroblasts might be a promising strategy to overcome the multi-drugs resistant cancer in clinic.
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Lianmin Ji,Licheng Zhang,Dong Shi,Xiaowu Peng,Jinfeng Li,Yuze zhang,Taoshan Xu,Lijuan Liao 한국공업화학회 2022 Journal of Industrial and Engineering Chemistry Vol.113 No.-
The degradation of TBP has become a stumbling block to the industrial continuous production of lithiumchloride extraction from brines with high Mg/Li ratio by solvent extraction. To develop a more stable andmore efficient extraction system, a novel amide system, containing newly synthesized extractant N,N-bis(2-ethylhexyl)-2-methoxyacetamide (NBEHMOA), FeCl3 6H2O and sulfonated kerosene, was proposed inthis work. Compared with TBP and N523, NBEHMOA extracted Li+ and H+ in the sequence of TBP ˃NBEHMOA ˃ N523 and N523 ˃ TBP ˃ NBEHMOA respectively. The solution containing 5.5 mol/L LiCland 0.5 mol/L HCl was used as the eluent in the scrubbing process. A Li+ extraction efficiency of 96.7%and 22.31 g/L Li+ in the stripping solution were achieved by the whole process with counter-currenttwelve stages. The extraction mechanism investigated via FT-IR spectroscopy illustrated that the metalions Fe3+ and Li+ were mainly coordinated by the carbonyl C = O in NBEHMOA. This novel amide systemcan successfully achieve the cascade extraction effect for lithium, Li/Mg separation and avoid the generationof phase interface objects through counter-current extraction of lithium from brine at a lower acidity. This work provided a novel extraction system to recover lithium from the higher magnesium/lithiumratio brines.
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Dihydroartemisinin inhibits HepG2.2.15 proliferation by inducing cellular senescence and autophagy
( Jiang Zou ),( Qiang Ma ),( Ru Sun ),( Jiajing Cai ),( Hebin Liao ),( Lei Xu ),( Jingruo Xia ),( Guangcheng Huang ),( Lihua Yao ),( Yan Cai ),( Xiaowu Zhong ),( Xiaolan Guo ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.8
Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro. DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, γ-H<sub>2</sub>AX, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy. [BMB Reports 2019; 52(8): 520-525]
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