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An LMI Approach to Consensus in Second-Order Multi-Agent Systems
Huanyu Zhao,Shengyuan Xu,Deming Yuan 제어·로봇·시스템학회 2011 International Journal of Control, Automation, and Vol.9 No.6
This paper deals with the consensus problem of the second-order multi-agent systems based on linear system theory. By a system transformation, the consensus problem is converted to the stability problem of a linear system. The second-order systems considered include the systems with both the fixed topology and the Markov switching topology. Necessary and sufficient conditions of consensus or mean square consensus are obtained. The results are extended to the cases of the uncertain transition probability rates and time-delay, respectively. Finally, a simulation example is given to show the effectiveness of the presented results.
Zongye Cai,Jian Li,Qi Zhuang,Xueming Zhang,Ancai Yuan,Lan Shen,Kang Kang,Bo Qu,Yuanjia Tang,Jun Pu,Deming Gou,Jieyan Shen 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Pulmonary vascular remodeling due to excessive proliferation and resistance to apoptosis of pulmonary artery smooth muscle cells (PASMCs) is the hallmark feature of pulmonary arterial hypertension (PAH). Recent evidence suggests that miR-125a-5p plays a role in a rat model of monocrotaline-induced PAH (MCT-PAH); however, the underlying mechanism is currently unknown. Here, we examined the expression profile of miR-125a-5p in MCT-PAH rats and investigated the putative therapeutic effect of miR-125a-5p using the miR-125a-5p agomir. In addition, the miR-125a- 5p agomir or antagomir was transfected into rat PASMCs, and proliferation and apoptosis were measured. Activity of the miR-125a-5p target STAT3 was measured using a luciferase reporter assay, and the expression of downstream molecules was measured using RT–qPCR and/or western blot analysis. Importantly, inducing miR-125a-5p expression in vivo slowed the progression of MCT-PAH by reducing systolic pulmonary arterial pressure, the Fulton index, and pulmonary vascular remodeling. Moreover, overexpressing miR-125a-5p inhibited the proliferation and promoted the apoptosis of PASMCs. In addition, stimulating PASMCs with TGF-β1 or IL-6 upregulated miR-125a-5p expression, whereas overexpressing miR-125a-5p reduced TGF-β1 and IL-6 production, as well as the expression of their downstream targets STAT3 and Smad2/3; in contrast, downregulating miR-125a-5p increased TGF-β1 and IL-6 production. Finally, a dual-luciferase reporter assay revealed that miR-125a-5p targets the 3′-UTR of STAT3, suppressing the downstream molecules PCNA, Bcl-2, and Survivin. Taken together, these findings suggest that miR-125a-5p ameliorates MCT-PAH in rats, has a negative feedback regulation with TGF-β1 and IL-6, and regulates the proliferation and apoptosis of PASMCs by directly targeting STAT3.