• Journal of Information Science Theory and Practice
• /
• v.10 no.spc
• /
• pp.1-11
• /
• 2022

As data-based research activities and outcomes increase and ontact or non-face-to-face activities become common, the demand for easy utilization of resources, tools, functions, and easily accessible information required for research in the R&D sector has increased accordingly. With the rapid increase in the demand for collaborative research based on online platforms, research support institutions strive to provide venues for research activities that merge various information and functions. ScienceON, an integrated science & technology (S&T) knowledge infrastructure service developed and operated by the Korea Institute of S&T Information (KISTI), supports open collaboration by connecting and merging all the information, functions, and infrastructure required for research activities. This paper describes the online research activity support tool provided by ScienceON and the remarkable results achieved through this activity. Specifically, the excellent creation of the following flow of meta-material research activities in the ontact space is elucidated. First, the papers required for a meta-material analysis are retrieved, virtual simulation is conducted with the experimental data extracted from the papers, and research data are accumulated. ScienceON's tools for supporting ontact research activity will play a role as an important service in the era of digital transformation and open science.

• Proceedings of the Korean Society for Emotion and Sensibility Conference
• /
• 2009.11a
• /
• pp.183-185
• /
• 2009

As imaging technology develops, magnetic resonance imaging (MRI) techniques have contributed to the understanding of brain function by providing anatomical structure of the brain and functional imaging related to information processing. Manganese-enhanced MRI (MEMRI) techniques can provide useful information about functions of the nervous system. However, systematic studies regarding information processing of pain have not been conducted. The purpose of this study was to detect brain activation during painful electrical stimulation using MEMRI with high spatial resolution. Male Sprague-Dawley rats (250-300 g) were divided into 3 groups: normal control, sham stimulation, and electric stimulation. Rats were anesthetized with 2.5% isoflurane for surgery. Polyethylene catheter (PE-10) was placed in the external carotid artery to administrate mannitol and MnCl2. The blood brain barrier (BBB) was broken by 20% D-mannitol under anesthesia mixed with urethane and a-chloralose. The hind limb was electrically stimulated with a 2Hz (10V) frequency while MnCl2 was infused. Brain activation induced by electrical stimulation was detected using a 4.7 T MRI. Remarkable signal enhancement was observed in the primary sensory that corresponds to sensory tactile stimulation at the hind limb region. These results suggest that signal enhancement is related to functional activation following electrical stimulation of the peripheral receptive field.

• The Korean Journal of Physiology and Pharmacology
• /
• v.13 no.3
• /
• pp.161-168
• /
• 2009

In the peripheral nerves, injury-induced cytokines and growth factors perform critical functions in the activation of both the MEK/ERK and JAK/STAT3 pathways. In this study, we determined that nerve injury-induced ERK activation was temporally correlated with STAT3 phosphorylation at the serine 727 residue. In cultured Schwann cells, we noted that ERK activation is required for the serine phosphorylation of STAT3 by neuropoietic cytokine interleukin-6 (IL-6). Serine phosphorylated STAT3 by IL-6 was transported into Schwann cell nuclei, thereby indicating that ERK may regulate the transcriptional activity of STAT3 via the induction of serine phosphorylation of STAT3. Neuregulin-1 (NRG) also induced the serine phosphorylation of STAT3 in an ERK-dependent fashion. In contrast with the IL-6 response, serine phosphorylated STAT3 induced by NRG was not detected in the nucleus, thus indicating the non-nuclear function of serine phosphorylated STAT3 in response to NRG. Finally, we determined that the inhibition of ERK prevented injury-induced serine phosphorylation of STAT3 in an ex-vivo explants culture of the sciatic nerves. Collectively, the results of this study show that ERK may be an upstream kinase for the serine phosphorylation of STAT3 induced by multiple stimuli in Schwann cells after peripheral nerve injury.

• Proceedings of the KOSOMBE Conference
• /
• v.1997 no.05
• /
• pp.150-155
• /
• 1997

Modelling and Simulation of the activation process for the myocardium is meaningful to understand special excitation conduction system in the heart and to study cardiac functions. In this paper, we propose two dimensional cellular automata model for the activation process of the myocardium and simulated by means of discrete time and discrete event algorithm. In the model, cells are classified into anatomically similar characteristic parts of heart; SA node, internodal tracks, AV node, His bundle, bundle branch and four layers of the ventricular muscle, each of which has a set of cells with preassigned properties, that is, activation time, refractory duration and conduction time between neighbor cell. Each cell in this model has state variables to represent the state of the cell and has some simple state transition rules to change values of state variables executed by state transition function. Simulation results are as follows. First, simulation of the normal and abnormal activation process for the myocardium has been done with discrete time and discrete event formalism. Next, we show that the simulation results of discrete time and discrete event cell space model is the same. Finally, we compare the simulation time of discrete event myocardium model with discrete time myocardium models and show that the discrete event myocardium model spends much less simulation time than discrete time myocardium model and conclude the discrete event simulation method Is excellent in the simulation time aspect if the interval deviation of event time is large.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 2003.11a
• /
• pp.78-78
• /
• 2003

Inulin, an active component of Chicorium intybus root, has been shown to stimulate the growth of bifidobacteria, and inhibit colon carcinogenesis. NO mediates a number of the host-defense functions of activated macrophages, including antimicrobial and tumoricidal activity. We examined the effect of inulin on the synthesis of NO in RAW 264.7 cells. Inulin alone had no effect, whereas inulin with IFN-ν synergistically increased the NO production and inducible NO synthase (iNOS) expression in RAW 264.7 cells. Synergy between IFN-ν and inulin was mainly dependent on inulin-induced TNF-${\alpha}$ secretion. Also, protein kinase C (PKC)-${\alpha}$ was involved in the inulin-induced NO production. Inulin-mediated NO production was inhibited by the protein tyrosine kinase (PTK) inhibitor, tyrphostin AG126. Since iNOS gene transcriptions have been shown to be under the control of the NF -$\kappa$B/Rel family of transcription factors, we assessed the effect of inulin on NF -$\kappa$B/Rel using an EMSA. Inulin produced strong induction of NF-$\kappa$B/Rel binding, whereas AP-l binding was slightly induced in RAW 264.7 cells. Inulin stimulated phosphorylation and degradation of I$\kappa$B-${\alpha}$. These results suggest that in IFN-ν-primed RAW 264.7 cells inulin might stimulate NO synthesis via activation of PKC-${\alpha}$ and PTK, resulting in the activation of NF-$\kappa$B.

• BMB Reports
• /
• v.50 no.1
• /
• pp.25-30
• /
• 2017

In the central nervous system, viral infection can induce inflammation by up-regulating pro-inflammatory mediators that contribute to enhanced infiltration of immune cells into the central nervous areas. Celastrol is known to exert various regulatory functions, including anti-microbial activities. In this study, we investigated the regulatory effects and the mechanisms of action of celastrol against astrocytes activated with polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, as a model of pro-inflammatory mediated responses. Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. In addition, celastrol significantly suppressed poly(I:C)-induced activation of JNK MAPK and STAT1 signaling pathways. Furthermore, celastrol significantly suppressed poly(I:C)-induced activation of the $NF-{\kappa}B$ signaling pathway. These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/$NF-{\kappa}B$ in astrocytes.

• Molecules and Cells
• /
• v.20 no.2
• /
• pp.241-246
• /
• 2005

PDK-1 activates PI3-kinase/Akt signaling and regulates fundamental cellular functions, such as growth and survival. NF-${\kappa}B$ is involved in the induction of a variety of cellular genes affecting immunity, inflammation and the resistance to apoptosis induced by some anti-cancer drugs. Even though the crucial involvement of the PI3-kinase/Akt pathway in the anti-apoptotic activation of NF-${\kappa}B$ is well known, the exact role of PDK-1 as well as PI3-kinase/Akt in NF-vactivation is not understood. Here we demonstrate that PDK-1 plays a pivotal role in transcriptional activation of NF-${\kappa}B$ by dissociating the transcriptional co-repressor HDAC1 from the p65 subunit of NF-${\kappa}B$. The association of CBP with p65 was not directly modulated by PDK-1 or by PI3-kinase. Etoposide activated NF-${\kappa}B$ through PI3-kinase/Akt, and the transcription activation domain (TAD) of p65 was further activated by wild-type PDK-1. Overexpression of a dominant negative PDK-1 mutant decreased etoposide-induced NF-${\kappa}B$ transcription and further down-regulated the ectopic HDAC1-mediated decrease in NF-${\kappa}B$ transcriptional activity. Thus activation of PDK-1 relieves the HDAC1-mediated repression of NF-${\kappa}B$ that may be related to basal as well as activated transcription by NF-${\kappa}B$. This effect may also explain the role of the PI3-kinase/PDK-1 pathway in the anti-apoptotic function of NF-${\kappa}B$ associated with the chemoresistance of cancer cells.

• YAKHAK HOEJI
• /
• v.51 no.6
• /
• pp.482-489
• /
• 2007

Kaempferitrin, isolated from Kenaf (Hibiscus cannabinus), was examined to evaluate its modulatory effects on antigen-presenting cell functions of macrophages/monocytes such as phagocytosis of foreign materials, up-regulation of costimulatory molecules (CD40, CD80 and CD86), adhesion molecule activation, and antigen processing and presentation. Kaempferitrin strongly blocked up-regulation of CD40, CD80 and CD86, but not pattern recognition receptor (PRR) (e.g., TLR2). It also suppressed functional activation of CD29 (${\beta}1$-integrins), as assessed by cell-cell adhesion assay, required for T cell-antigen-presenting cell (APC) interaction. Furthermore, this compound did not block a simple activation of CD29, as assessed by cell-fibronectin adhesion assay. However, the compound did not diminish phagocytic uptake, an initial step for antigen processing, and ROS generation in RAW264.7 cells. In particular, to understand molecular mechanism of kaempferitrin-mediated inhibition, the regulatory role of LPS-induced signaling events was examined using immunoblotting analysis. Interestingly, this compound dose dependently suppressed the phosphorylation of $I{\kappa}B{\alpha}$, Src, Akt and Syk, demonstrating that it can negatively modulate the activation of these signaling enzymes. Therefore, our data suggested that kaempferitrin may be involved in regulating APC function-relevant immune responses of macrophages and monocytes by regulating intracellular signaling.

• Molecules and Cells
• /
• v.43 no.1
• /
• pp.58-65
• /
• 2020

Fat mass and obesity-associated (FTO) gene helps to regulate energy homeostasis in mammals by controlling energy expenditure. In addition, FTO functions in the regulation of obesity and adipogenic differentiation; however, a role in osteogenic differentiation is unknown. This study investigated the effects of FTO on osteogenic differentiation of C3H10T1/2 cells and the underlying mechanism. Expression of osteogenic and endoplasmic reticulum (ER) stress markers were characterized by reverse-transcriptase polymerase chain reaction and western blotting. Alkaline phosphatase (ALP) staining was performed to assess ALP activity. BMP2 treatment increased mRNA expression of osteogenic genes and FTO. Overexpression of FTO increased expression of the osteogenic genes distal-less homeobox5 (Dlx5) and runt-related transcription factor 2 (Runx2). Activation of adenosine monophosphate-activated protein kinase (AMPK) increased FTO expression, and there was a positive feedback loop between FTO and p-AMPK. p-AMPK and FTO induced mild ER stress; however, tunicamycin-induced severe ER stress suppressed FTO expression and AMPK activation. In summary, FTO induces osteogenic differentiation of C3H10T1/2 cells upon BMP2 treatment by inducing mild ER stress via a positive feedback loop with p-AMPK. FTO expression and AMPK activation induce mild ER stress. By contrast, severe ER stress inhibits osteogenic differentiation by suppressing FTO expression and AMPK activation.

• Journal of Practical Engineering Education
• /
• v.13 no.2
• /
• pp.233-242
• /
• 2021

In this paper, as a liberal arts course for non-majors, we proposed a supervised learning artificial neural network parameter optimization method and a basic education method for activation function to design a basic artificial neural network subject curriculum. For this, a method of finding a parameter optimization solution in a spreadsheet without programming was applied. Through this training method, you can focus on the basic principles of artificial neural network operation and implementation. And, it is possible to increase the interest and educational effect of non-majors through the visualized data of the spreadsheet. The proposed contents consisted of artificial neurons with sigmoid and ReLU activation functions, supervised learning data generation, supervised learning artificial neural network configuration and parameter optimization, supervised learning artificial neural network implementation and performance analysis using spreadsheets, and education satisfaction analysis. In this paper, considering the optimization of negative parameters for the sigmoid neural network and the ReLU neuron artificial neural network, we propose a training method for the four performance analysis results on the parameter optimization of the artificial neural network, and conduct a training satisfaction analysis.