Distal End Force Estimation of Tendon-sheath Mechanism Using a Spring Sheath

Jeonghan Kim,Kyungnam Kim,Yechan Seo,Junyoung Park,Byung Gon Kim,Sooyong Choi,Chanwoo Kim,Daehie Hong 한국정밀공학회 2023 International Journal of Precision Engineering and Vol.24 No.12

Tendon-sheath mechanism (TSM) is often used as a power transmission system in many applications, such as rehabilitation, wearables, and endoscopic surgery robots. It comprises a tendon for transmitting the power and a sheath to guide the tendon. The tendon passes through a narrow and harsh pathway to actuate an end-effector. Consequently, TSM exhibits highly nonlinear force transmission characteristics, resulting in poor control performance. Additionally, attaching and using a force feedback sensor at its distal end is virtually impossible in most applications owing to space constraints and safety concerns. To address these drawbacks, this study proposes a novel sensing spring wire to estimate the distal end force in TSM. Unlike existing methods, the proposed technique does not require complex hyperparameters or modeling and uses only a mechanical part to predict the force. The sensing wire is composed of the sheath. The biocompatibility, simple structure, and small size of the spring sheath facilitate convenient interaction with the existing TSM. Additionally, the spring sheath exhibits the characteristics of a spring, which ensures a linear relationship between the displacement and force. The results indicate that after calibrating the spring sensor, the distal end force can be easily determined using the proximal force despite the absence of an electrical sensor. In situations where the friction is different for each shape, when the force at the distal end was estimated using only the force at the proximal end measured by the sensor, the average RMSE was 75.91mN and the maximum error was 176.52mN. The proposed method verifies that the proximal tension and displacement data are sufficient to estimate the force.

Controlled Fabrication of Graphene Oxide Thin Film with Uniformly-Distributed Wrinkled Structures

Jeonghan Kim,Seokjun Kim,Songkil Kim 대한기계학회 2021 대한기계학회 춘추학술대회 Vol.2021 No.11

VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease

Kim, Jeonghan,Gupta, Rajeev,Blanco, Luz P.,Yang, Shutong,Shteinfer-Kuzmine, Anna,Wang, Kening,Zhu, Jun,Yoon, Hee Eun,Wang, Xinghao,Kerkhofs, Martijn,Kang, Hyeog,Brown, Alexandra L.,Park, Sung-Jun,Xu, American Association for the Advancement of Scienc 2019 Science Vol.366 No.6472

<P><B>VDACs are MOM's ruin</B></P><P>Mitochondrial DNA (mtDNA) is normally kept within the mitochondria. It can be released into the cytosol in response to stress and thus encounter cytosolic DNA sensors, triggering type I interferon responses. During apoptosis, mtDNA release is mediated by macropores in the mitochondrial outer membrane (MOM) created by oligomerization of the proteins BAX and BAK. Kim <I>et al.</I> found that during oxidative stress, mtDNA escapes instead through macropores formed by oligomerization of voltage-dependent anion channels (VDACs) (see the Perspective by Crow). In a mouse model of lupus, an inhibitor of VDAC oligomerization diminished mtDNA release and downstream signaling events. This treatment reduced lupus-like symptoms in the model, suggesting a potential therapeutic route for conditions mediated by mtDNA release.</P><P><I>Science</I>, this issue p. 1531; see also p. 1445</P><P>Mitochondrial stress releases mitochondrial DNA (mtDNA) into the cytosol, thereby triggering the type Ι interferon (IFN) response. Mitochondrial outer membrane permeabilization, which is required for mtDNA release, has been extensively studied in apoptotic cells, but little is known about its role in live cells. We found that oxidatively stressed mitochondria release short mtDNA fragments via pores formed by the voltage-dependent anion channel (VDAC) oligomers in the mitochondrial outer membrane. Furthermore, the positively charged residues in the N-terminal domain of VDAC1 interact with mtDNA, promoting VDAC1 oligomerization. The VDAC oligomerization inhibitor VBIT-4 decreases mtDNA release, IFN signaling, neutrophil extracellular traps, and disease severity in a mouse model of systemic lupus erythematosus. Thus, inhibiting VDAC oligomerization is a potential therapeutic approach for diseases associated with mtDNA release.</P>

Effects of protein kinase Cdelta and phospholipase C-gamma1 on monocyte chemoattractant protein-1 expression in taxol-induced breast cancer cell death.

Kim, Yoon Suk,An, Hyoung Tae,Kim, Jeonghan,Ko, Jesang D.A. Spandidos 2009 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.24 No.6

<P>Monocyte chemoattractant protein-1 (MCP-1) is a CC chemokine that plays an important role in immune cell migration. It has been reported that chemokines, including MCP-1, are involved in angiogenesis and metastasis. However, the exact role of chemokines in cancer development is still obscure. We investigated the involvement of MCP-1 in taxol-induced breast cancer cell death. The anti-cancer drug taxol induced MCF-7 breast cancer cell death. Treatment with taxol increased the mRNA expression level of MCP-1 in a dose- and time-dependent manner. Up-regulation of MCP-1 by taxol was augmented in cells treated with rottlerin, a specific inhibitor of protein kinase Cdelta (PKCdelta). In addition, taxol-induced MCP-1 expression was reduced by the ectopic expression of PKCdelta in a dose-dependent manner, indicating that PKCdelta plays a negative role in taxol-induced MCP-1 expression in MCF-7 cells. On the other hand, taxol-induced up-regulation of MCP-1 was reduced in cells treated with U73122, an inhibitor of phospholipase C (PLC), and ectopic expression of PLC-gamma1 increased the expression of MCP-1 in taxol-treated MCF-7 cells, indicating that PLC-gamma1 functions as a positive regulator in taxol-induced MCP-1 expression. These results indicate that MCP-1 is involved in taxol-induced breast cancer cell death and we propose that taxol induces up-regulation of MCP-1 by affecting both positive and negative regulatory signaling pathways.</P>

Effects of Substrate Morphology and Postelectrodeposition on Structure of Cu Foam and Their Application for Li-Ion Batteries

Kim, RyoungHee,Han, DongWook,Nam, DoHwan,Kim, JeongHan,Kwon, HyukSang The Electrochemical Society 2010 Journal of the Electrochemical Society Vol.157 No.5

Human sLZIP promotes atherosclerosis <i>via</i> MMP-9 transcription and vascular smooth muscle cell migration

Kim, Jeonghan,Ko, Jesang The Federation of American Societies for Experimen 2014 The FASEB Journal Vol.28 No.11

<P>Atherosclerosis is a chronic inflammatory response of the vascular wall, and immune responses are involved in every phase of atherosclerosis, from initiation, to progression, and finally to plaque rupture. Cytokines are the major atherogenic mediators that promote plaque formation and progression by activation of inflammatory cells. They induce expressions of matrix metalloproteinases (MMPs), leading to vascular smooth muscle cell (VSMC) migration in atherosclerotic lesions. Although chronic inflammatory mediators, including tumor necrosis factor α (TNF-α) and MMPs, exacerbate atherosclerosis, the molecular mechanism of atherogenesis remains unclear. In this study we investigated the role of a novel transcription factor the human small leucine zipper protein (sLZIP) in TNF-α-induced MMP expression, VSMC migration, and atherosclerosis progression. The proinflammatory cytokine TNF-α enhanced sLZIP expression by 3-fold <I>via</I> activation of NF-κB signaling. sLZIP induced MMP-9 transcription and the proteolytic activity of MMP-9 by 2.8- and 3.2-fold (<I>P</I>< 0.05), respectively, in macrophages, leading to enhancement of VSMC migration by 2.7-fold (<I>P</I><0.005). <I>sLZIP</I><SUP><I>OE</I>/+</SUP> (sLZIP transgenic); <I>LDLR</I><SUP>−/−</SUP> mice fed a high-cholesterol diet exhibited enhanced arterial plaque formation and increased VSMC migration from the media into the intima by 2.8- and 2.6-fold (<I>P</I><0.01), respectively, compared with atherosclerosis-prone <I>LDLR</I><SUP>−/−</SUP> mice. These results indicate that human sLZIP plays a critical role in development of atherosclerosis and can be used as a therapeutic target molecule for treatment of atherosclerosis.—Kim, J., Ko, J. Human sLZIP promotes atherosclerosis <I>via</I> MMP-9 transcription and vascular smooth muscle cell migration.</P>

Effect of neoadjuvant chemotherapy on effect-site concentration of propofol for sedation in patients with breast cancer

Kim Myounghun,Lee Jeonghan,Jinhyeok Kim,Choi Beomseok,기승희 대한마취통증의학회 2023 Anesthesia and pain medicine Vol.18 No.1

Background: Some studies have demonstrated that chemotherapy drugs enhance sensitivity to anesthetics owing to its systemic toxicity, while others have demonstrated that chemotherapy drugs have no effect. This study aimed to determine whether neoadjuvant chemotherapy influences the effect-site concentration (Ce) of propofol for sedation in patients with breast cancer. Methods: This study included patients aged 19–75 years who were scheduled to undergo breast cancer surgery under general anesthesia. Patients who received neoadjuvant chemotherapy were assigned to group C, whereas those who never received chemotherapy were assigned to group N. Propofol was administered through an effect-site target-controlled infusion, and the (MOAA/S) score and Bispectral Index (BIS) were recorded. When the plasma concentration and Ce were equal to the target Ce, and if the MOAA/S score did not change, the target Ce was increased by 0.2 μg/ml; otherwise, the Ce was maintained for 2 min and then increased. This process was repeated until the MOAA/S score became 0. Results: No significant differences were observed in Ce values at each sedation level between both groups. Ce values for loss of consciousness (LOC) of groups C and N were 2.76 ± 0.29 and 2.67 ± 0.27 μg/ml (P = 0.285), respectively. However, the BIS value at LOC of group C (63.87 ± 7.04) was lower than that (68.44 ± 6.01) of group N (P = 0.018).Conclusions: Neoadjuvant chemotherapy for breast cancer has no effect on the Ce of propofol for sedation.

Molecular mechanisms of mitochondrial DNA release and activation of the cGAS-STING pathway

Kim Jeonghan,Kim Ho-Shik,Chung Jay H. 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis.

비즈니스 프로세스와 서비스 관리를 위한 온톨로지 표현 방법

김정한(Jeonghan Kim),윤상현(Sanghyun Yun),염근혁(Keunhyuk Yeom) 한국정보과학회 2010 한국정보과학회 학술발표논문집 Vol.37 No.1A

Analysis on Degradation of Ferroelectric Memory

Sangwoo Kim,Jeonghan Kim,Soi Jeong,Kiryun Kwon,Changhyeon Han,Eunchan Park,Jiyong Yim,Been Kwak,Jiwon You,Daewoong Kwon 한국차세대컴퓨팅학회 2022 한국차세대컴퓨팅학회 학술대회 Vol.2022 No.10

Subthreshold swing degradation of ferroelectric-gate field effect transistor (FeFET) memory are analyzed through DC and fast drain current (ID)-gate voltage (VG) measurements. From the fast ID-VGs before endurance cycling, it is revealed that acceptor-like traps with millisecond-order response time mainly exist in the gate oxide of FeFETs and the traps cause the different subthreshold swing (SS) between erase and program states.