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Zhong-Yi Chu,Shao-Bo Yan,Jian Hu,Shan Lu 제어·로봇·시스템학회 2018 International Journal of Control, Automation, and Vol.16 No.2
Underactuated gripper has a broad application in the field of space robot and industrial robot because of its better shape-adaptation. However, because of the underactuated characteristics, it is a great challenge to accurately obtain the displacement of the contact point between the finger and grasped object, which makes it difficult to control the gripper grasp stably, especially the environmental parameters are unknown. This paper develops the identification of the unknown environmental parameters using a tactile array sensor based on the recursive leastsquares (RLS) method. The unknown environments are described as linear systems with unknown dynamics, and the environmental parameters are identified using the measured contact force and the derived displacement of the contact point which is obtained through the underactuated gripper dynamics. Meanwhile, an impedance adaptive control is presented to match the variability of the environment parameters, and the desired impedance model is imposed to the underactuated gripper to achieve stable grasp. A cost function that measures the contact force, velocity and displacement error is defined, and the critical impedance parameters are found to minimize it. At last, a co-simulation of ADAMS and MATLAB for an underactuated gripper grasp is implemented to show the feasibility of environmental parameters identification and its adaptive method.
( Yan Wu ),( Jian Mei Guo ),( Nan Sun ),( Shao Min Zhong ),( Rong Tao ) 한국피부장벽학회 2013 한국피부장벽학회지 Vol.15 No.2
The atopic dermatitis is characterized by disruption of skin barrier and colonization of S.aureus. However, the mutual impact of damaged skin barrier and increased S.aureus has not been fully elucidated. Here we used the SKH-1 hairless mice to establish acute barrier dysfunction model and evaluated the mutual impact of damaged skin barrier function and colonization of S.aureus. Skin barrier was destroyed by repeat tape-stripping. Then 36 SKH-1 mice were divided into 6 groups, namely the control group, barrier impaired group, S. aureus inoculated group, barrier impaired +S. aureus inoculated group, “wrapping group” (referred to barrier impaired +wrapping+S. aureus inoculation) and “moisturizing group” (referred to barrier impaired + moisturizer + S. aureus). S. aureus on the skin were collected after 24 hours for verification and quantify. The physiological parameters related to skin barrier were detected before and immediately after impairing of barrier function, after wrapping/moisturizing, 4 hours and 24 hours after inoculation of S. aureus. In this study, we found that There was a little S. aureus grown on intact skin in only inoculation group, while the number of S. aureus in impaired barrier group increased dramatically (P<0.05); the colonization of S. aureus in both wrapping and moisturizing group decreased obviously compared with the barrier impaired group (P <0.05), Fig1, which mean that restoring the barrier function could greatly reduced the colonization of S. aureus. On the other hand the colonization of S. aureus on impaired barrier could inhibit the recovery of skin barrier function, with higher pH and TEWL compared with other groups in similar time points(P<0.05). The wrapping and moisturizing may eliminate the suppression of barrier function recovery caused by inoculation of S. aureus, Fig 2.
Wang, Hui-Ju,Shao, Jian-Zhong,Xiang, Li-Xin,Shen, Jia Korean Society for Biochemistry and Molecular Biol 2006 Journal of biochemistry and molecular biology Vol.39 No.6
Interleukin-2 enhancer binding factor 2 (ILF2) was reported to regulate transcription of interleukin-2 (IL-2), a central cytokine in the regulation of T-cell responses. This property of ILF2 was well characterized in human and mammals, but little is known in bony fish. In this paper, an ILF2 homologue was cloned and well characterized from Tetraodon nigrovirid is for the further investigation of the function of ILF2 in bony fish. The full-length Tetraodon ILF2 cDNA was 1380 bp in size and contained an open reading frame (ORF) of 1164 bp that translates into a 387 amino-acid peptide with a molecular weight of 42.9 kDa, a 5' untranslated region (UTR) of 57 bp, and a 3' UTR of 159 bp containing a poly A tail. The deduced peptide of Tetraodon ILF2 shared an overall identity of 58%~93% with other known ILF2 sequences, and contained two N-glycosylation sites, two N-myristoylation sites, one RGD cell attachment sequence, six protein kinase C phosphorylation sites, one amino-terminal RGG-rich single-stranded RNA-binding domain, and a DZF zinc-finger nucleic acid binding domain, most of which were highly conserved through species compared. Constitutive expression of Tetraodon ILF2 was observed in all tissues examined, including gill, gut, head kidney, spleen, liver, brain and heart. The highest expression was detected in heart, followed by liver, head kidney and brain. Stimulation with LPS did not significantly alter the expression of Tetraodon ILF2. Gene organization analysis showed that the Tetraodon ILF2 gene have fifteen exons, one more than other known ILF2 genes in human and mouse. Genes up- and down-stream from the Tetraodon ILF2 were Rpa12, Peroxin-11b, Smad4, Snapap and Txnip homologue, which were different from that in human and mouse.
Yang Hui-Hui,Jiang Hui-Ling,Tao Jia-Hao,Zhang Chen-Yu,Xiong Jian-Bing,Yang Jin-Tong,Liu Yu-Biao,Zhong Wen-Jing,Guan Xin-Xin,Duan Jia-Xi,Zhang Yan-Feng,Liu Shao-Kun,Jiang Jian-Xin,Zhou Yong,Guan Cha-Xi 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citratemt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor–mediated inhibition of Idh3α and Slc25a1 induced citratemt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citratemt levels and rescued AECs from necroptosis. Mechanistically, citratemt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citratemt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citratemt accumulation was inhibited in FUNDC1-knockout AECs. We show that citratemt accumulation is a novel target for protection against ALI involving necroptosis.