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Jihyung Lee,Nahyun Lee,Jaechun Cho,Baekhee Lee,Kyunghyun Jin,Hyejee Kim,Younggyun Kim,Jaheon Kang,Heecheon You 대한인간공학회 2015 대한인간공학회 학술대회논문집 Vol.2015 No.10
Objective: The present study to evaluate an ergonomic gaze fixation induction method for gaze fixation during visual field testing developed and applied a gaze fixation identification algorithm to the gaze tracking data analysis. Background: Development of the gaze fixation identification algorithm is necessary to evaluate the degree of gaze fixation which is important for checking the reliabilities of visual field testing. Method: the present study investigated factors of gaze tracking data and developed an identification algorithm to identify gaze fixation. 32 men and women (29.0 ± 4.4 yr) participated in gaze fixation testing to evaluate three gaze fixation induction methods (black dot, flashing black dot, bulls eye and cross hair) in the aspects of correct fixation rate using gaze fixation identification algorithm. Results: It is necessary to analyze gaze location at 0.2 seconds intervals before and after target presenting for identify a gaze fixation in visual field testing. If one of two interval gaze trajectory is belong within visual angle 1° when the gaze tracking data analyzed in 0.2 seconds intervals before and after target presenting, the gaze fixation identification algorithm decide to fix the participant’s gaze to a fixation target when the target presents. Correct fixation rate of flashing black dot (91.5%) and bulls eye and cross hair (88.0%) are higher 5.5% and 1.5% than that of black dot (86.7%). Conclusion: The analysis using short interval gaze tracking data at before and after target presenting is more effective method in visual field testing for evaluating the degree of gaze fixation. Application: The gaze fixation identification algorithm is expected to be effectively used for monitor-based gaze tracking research.
Kwak, Eun-Young,Im, So Hee,Seo, Hyewon,Cho, Woon-Ki,Lee, Ye-Lim,Woo, Jaechun,Ahn, Sunjoo,Ahn, Sung-Hoon,Kwak, Hyun Jung,Ahn, Jin Hee,Bae, Myung Ae,Song, Jin Sook Informa UK Ltd. 2014 Xenobiotica Vol.44 No.5
<P>1. <?ri?>A novel diacylglyceride acyltransferase-1 (DGAT-1) inhibitor, 2-(4-(4-(5-(2-phenyl-5-(trifluoromethyl) oxazole-4-carboxamido)-1H-benzo[d]imidazol-2-yl)phenyl)cyclohexyl) acetic acid (KR-69232), was synthesized for a potential therapeutic use against several metabolic disorders, such as obesity, insulin resistance, and type II diabetes, characterized by excessive triglycerides (TGs) in the blood.</P><P>2. <?ri?>The half-lives against phase I metabolism were measured as 75.3 ± 20.9 min and over 120 min in rat and human liver microsomes, respectively. In Caco-2 cell monolayers, extremely low permeability (<0.13 × 10<SUP>−6 </SUP>cm/s) was seen in the absorptive direction, predicting limited intestinal absorption of KR-69232. This compound was highly bound to rat and human plasma proteins (>99.8%).</P><P>3. <?ri?>With the intravenous administration of KR-69232 in rats (1, 2, and 5 mg/kg), non-linear kinetics were observed at the highest dose, with significantly higher systemic clearance, higher volume of distribution, and lower dose-normalized AUC. Following oral administration, it exhibited low bioavailability (<10%) and was absorbed slowly (<I>T</I><SUB>max</SUB>, 3.8-5.2 h) over the dose range. We also confirmed that considerable KR-69232 remained in the intestine at <I>T</I><SUB>max</SUB>, demonstrating its limited absorption into the systemic circulation.</P>
IL-32γ attenuates airway fibrosis by modulating the integrin-FAK signaling pathway in fibroblasts
Hong, Gyong Hwa,Park, So-Young,Kwon, Hyouk-Soo,Bang, Bo-Ram,Lee, Jaechun,Kim, Sang-Yeob,Pack, Chan-Gi,Kim, Soohyun,Moon, Keun-Ai,Kim, Tae-Bum,Moon, Hee-Bom,Cho, You Sook BioMed Central 2018 Respiratory research Vol.19 No.-
<P><B>Background</B></P><P>Fibrosis in severe asthma often leads to irreversible organ dysfunction. However, the mechanism that regulates fibrosis remains poorly understood. Interleukin (IL)-32 plays a role in several chronic inflammatory diseases, including severe asthma. In this study, we investigated whether IL-32 is involved in fibrosis progression in the lungs.</P><P><B>Methods</B></P><P>Murine models of chronic airway inflammation induced by ovalbumin and <I>Aspergillus melleus</I> protease and bleomycin-induced pulmonary fibrosis were employed. We evaluated the degree of tissue fibrosis after treatment with recombinant IL-32γ (rIL-32γ). Expression of fibronectin and α-smooth muscle actin (α-SMA) was examined and the transforming growth factor (TGF)-β-related signaling pathways was evaluated in activated human lung fibroblasts (MRC-5 cells) treated with rIL-32γ.</P><P><B>Results</B></P><P>rIL-32γ significantly attenuated collagen deposition and α-SMA production in both mouse models. rIL-32γ inhibited the production of fibronectin and α-SMA in MRC-5 cells stimulated with TGF-β. Additionally, rIL-32γ suppressed activation of the integrin-FAK-paxillin signaling axis but had no effect on the Smad and non-Smad signaling pathways. rIL-32γ localized outside of MRC-5 cells and inhibited the interaction between integrins and the extracellular matrix without directly binding to intracellular FAK and paxillin.</P><P><B>Conclusions</B></P><P>These results demonstrate that IL-32γ has anti-fibrotic effects and is a novel target for preventing fibrosis.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (10.1186/s12931-018-0863-3) contains supplementary material, which is available to authorized users.</P>