• IMMUNE NETWORK
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• 제13권5호
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• pp.184-193
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• 2013

Co-signaling molecules are surface glycoproteins that positively or negatively regulate the T cell response to antigen. Co-signaling ligands and receptors crosstalk between the surfaces of antigen-presenting cells (APCs) and T cells, and modulate the ultimate magnitude and quality of T cell receptor (TCR) signaling. In the past 10 years, the field of co-signaling research has been advanced by the understanding of underlying mechanisms of the immune modulation led by newly identified co-signaling molecules and the successful preclinical and clinical trials targeting co-inhibitory molecules called immune checkpoints in the treatment of autoimmune diseases and cancers. In this review, we briefly describe the characteristics of well-known B7 co-signaling family members regarding the expression, functions and therapeutic implications and to introduce newly identified B7 members such as B7-H5, B7-H6, and B7-H7.

• 한국전기전자재료학회:학술대회논문집
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• 한국전기전자재료학회 2001년도 하계학술대회 논문집
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• pp.855-858
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• 2001

The stress induced leakage currents of thin silicon oxides is investigated in the VLSI implementation of a self learning neural network integrated circuits using a linearity synapse transistor. The channel current for the thickness dependence of stress current, transient current, and stress induced leakage currents has been measured in oxides with thicknesses between 41 ${\AA}$, 86${\AA}$, which have the channel width ${\times}$ length 10 ${\times}$1${\mu}$m, 10 ${\times}$0.3${\mu}$m respectively. The stress induced leakage currents will affect data retention in synapse transistors and the stress current, transient current is used to estimate to fundamental limitations on oxide thicknesses. The synapse transistor made by thin silicon oxides has represented the neural states and the manipulation which gaves unipolar weights. The weight value of synapse transistor was caused by the bias conditions. Excitatory state and inhitory state according to weighted values affected the channel current. The stress induced leakage currents affected excitatory state and inhitory state.

• IMMUNE NETWORK
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• 제14권6호
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• pp.328-332
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• 2014

Dexamethasone (Dex) was shown to inhibit the differentiation, maturation, and antigen-presenting function of dendritic cells (DC) when added during DC generation or maturation stages. Here, we examined the direct effects of Dex on MHC-restricted antigen processing. Macrophages were incubated with microencapsulated ovalbumin (OVA) in the presence of different concentrations of Dex for 2 h, and the efficacy of OVA peptide presentation was evaluated using OVA-specific CD8 and CD4 T cells. Dex inhibited both class I- and class II-restricted presentation of OVA to T cells; this inhibitory effect on antigen presentation was much more potent in immature macrophages than in mature macrophages. The presentation of the exogenously added OVA peptide SIINFEKL was not blocked by Dex. In addition, short-term treatment of macrophages with Dex had no discernible effects on the phagocytic activity, total expression levels of MHC molecules or co-stimulatory molecules. These results demonstrate that Dex inhibits intracellular processing events of phagocytosed antigens in macrophages.

• 대한전기학회논문지:전력기술부문A
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• 제48권4호
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• pp.419-427
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• 1999

We propose an algorithm for obtaining the optimal node number of hidden units in dynamic neural networks. The dynamic nerual networks comprise of dynamic neural units and neural processor consisting of two dynamic neural units; one functioning as an excitatory neuron and the other as an inhibitory neuron. Starting out with basic network structure to solve the problem of control, we find optimal neural structure by multiplication and combining dynamic neural unit. Numerical examples are presented for nonlinear systems. Those case studies showed that the proposed is useful is practical sense.

• 지능정보연구
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• 제11권2호
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• pp.81-103
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• 2005

신경계의 뉴런 구조는 흥분 뉴런과 억제 뉴런으로 구성되며 각각의 흥분 뉴런과 억제 뉴런은 주동근 뉴런(agonistic neuron)에 의해 활성화되며 길항근 뉴런(antagonist neuron)에 의해 비활성화 된다. 본 논문에서는 인간 신경계의 생리학적 뉴런 구조를 분석하여 퍼지 논리를 이용한 생리학적 퍼지 신경망을 제안한다. 제안된 구조는 주동근 뉴런에 의해 흥분 뉴런이 될 수 있는 뉴런들을 선택하여 흥분시켜 출력층으로 전달하고 나머지 뉴런들을 억제시켜 출력층에 전달시키지 않는다. 신경계를 기반으로 한 제안된 생리학적 퍼지 신경망의 학습구조는 입력층, 학습 데이터의 특징을 분류하는 중간층, 그리고 출력 층으로 구성된다. 제안된 퍼지 신경망의 학습 및 인식 성능을 평가하기 위해 정확성이 요구되는 의학의 한 분야인 기관지 편평암 영상 인식과 영상 인식의 주요 응용 분야인 차량번호판 인식에 적용하여 기존의 신경망과 성능을 비교 분석하였다. 실험 결과에서는 제안된 생리학적 퍼지 신경망이 기존의 신경망보다 학습 시간과 수렴성이 개선되었을 뿐만 아니라, 인식에 있어서도 우수한 성능이 있음을 확인하였다.

• IMMUNE NETWORK
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• 제8권1호
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• pp.13-20
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• 2008

Background: Coptis chinensis rhizome has been used as a medicinal herb in traditional Oriental medicine. We investigated the effects of Coptis chinensis extract on inflammatory mediators and delayed type hypersensitivity in mice. Methods: The inhibitory effect of ethanolic extract of Coptis chinensis (CCE) on cell proliferation was evaluated using MTS assay. The lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and the Con A-activated mouse splenocytes were cultured with various concentrations of CCE. Total nitric oxide (NO) production was determined by Griess reaction. The amounts of secreted prostaglandine E2 ($PGE_2$), interleukin (IL)-2 and IFN-${\gamma}$ were measured by ELISA. To investigate the in vivo anti-inflammatory effect of CCE, oxazolone-induced delayed type hypersensitivity (DTH) model was used. Results: The CCE at $100{\mu}g/ml$ significantly blocked the LPS-induced production of pro-inflammatory mediators (NO and PGE) in RAW264.7 macrophages. Also, it significantly inhibited cell proliferation and cytokine (IL-2 and IFN-${\gamma}$) production in splenocytes. Furthermore, when splenocytes from CCE fed mice (200 mg/kg for 2 weeks) were activated with Con A, cell proliferation and cytokine production were significantly inhibited. In addition, CCE decreased in vivo inflammation in oxazolone-induced DTH model mice. Conclusion: We suggest that Coptis chinensis can be used as an anti-inflammatory drug by exerting an inhibitory effect in inflammatory mediator- and cell-mediated inflammation.

• 한방안이비인후피부과학회지
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• 제23권2호
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• pp.81-108
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• 2010

Objective : Thujae Orientalis Folium (TOF) can cool the blood and stop bleeding, eliminate phlegm and relieve cough in Oriental medicine. In addition, the fresh is used alone externally. Recently, TOF is known to have anti-tumor component. And also known to have tyrosinase inhibitory effect. Method : For these reasons, this study was designed to investigate anti-cancer and whitening activities of TOF. In this experiment, effects of TOF on proliferation rates of melanoma cells and on changes in genetic profiles were investigated. The genetic profile for the effect on human derived melanoma cell, SK-MEL-2, was measured using microarray technique, and the functional analysis on these genes was conducted. Results : Total 541 genes were up-regulated and 1,079 genes down-regulated in cells treated with TOF. Genes induced by TOF were mainly concerned with anti-cancer effects and apoptosis. Genes suppresed by TOF were related in extracellular signalling pathway. The network of total protein interactions was measured using cytoscape program, and some key molecules, such as THAP1, MAX1, STAM2, SMAD6, CYCS, PEX5, PSEN1, NONO, MAP2K7 and CREB1 that can be used for elucidation of therapeutical mechanism of medicine in future were identified. Conculusion : These results suggest possibility of TOF as anti-cancer drug for human melanoma. In addition, the present author also suggest that related mechanisms are involved in inhibition of several cancer pathway, activation of apoptosis pathway and suppression of general metabolic pathway.

• 대한인간공학회지
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• 제33권5호
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• pp.377-386
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• 2014

Objective: In this study, we used resting-state fMRI data to map differences in functional connectivity between a comprehensive set of 8 distinct cortical and subcortical brain regions in healthy controls and Internet addicts. We also investigated the relationship between resting state connectivity strength and the level of psychopathology (ex. score of internet addiction scale and score of Barratt impulsiveness scale). Background: There is a lot of evidence of relationship between Internet addiction and impaired inhibitory control. Clinical evidence suggests that Internet addicts have a high level of impulsivity as measured by behavioral task of response inhibition and a self report questionnaire. Method: 15 Internet addicts and 15 demographically similar non-addicts participated in the current resting-state fMRI experiment. For the connectivity analysis, regions of interests (ROIs) were defined based on the previous studies of addictions. Functional connectivity assessment for each subject was obtained by correlating time-series across the ROIs, resulting in $8{\times}8$ matrixs for each subject. Within-group, functional connectivity patterns were observed by entering the z maps of the ROIs of each subject into second-level one sample t test. Two sample t test was also performed to examine between group differences. Results: Between group, the analysis revealed that the connectivity in between the orbito frontal cortex and inferior parietal cortex, between orbito frontal cortex and putamen, between the orbito frontal cortex and anterior cingulate cortex, between the insula and anterior cingulate cortex, and between amydgala and insula was significantly stronger in control group than in the Internet addicts, while the connectivity in between the orbito frontal cortex and insula showed stronger negative correlation in the Internet addicts relative to control group (p < 0.001, uncorrected). No significant relationship between functional connectivity strength and current degree of Internet addiction and degree of impulsitivy was seen. Conclusion: This study found that Internet addicts had declined connectivity strength in the orbitofrontal cortex (OFC) and other regions (e.g., ACC, IPC, and insula) during resting-state. It may reflect deficits in the OFC function to process information from different area in the corticostriatal reward network. Application: The results might help to develop theoretical modeling of Internet addiction for Internet addiction discrimination.

• IMMUNE NETWORK
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• 제2권1호
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• pp.19-24
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• 2002

Background: Salvia miltiorrhiza (SM), a traditional oriental medicine, has been reported to have anti-tumor properties, but its exact mechanism remains to be elucidated. In this study, we investigated several of the molecular events that occur in human breast carcinoma MCF-7 cells and human pulmonary adenocarcinoma A549 cells. Methods: For this purpose, we evaluated the growth-inhibitory effect of SM in association with the expressions of p53, p21, cyclin D1, and pRb, which are known to be involved in cell cycle arrest. The extent of thymidine incorporation was also examined to assess G1/S phase cell cycle arrest in both cells by $^3H$-thymidine incorporation. Results: Our results show that SM inhibits the growth and the proliferation of MCF-7 and A549 cells. Furthermore, we also observed increased expression of p21 via a p53-dependent pathway in both cell lines after treating with SM. In addition, treatment with SM for 24 hours caused the suppression of hyperphosphorylated retinoblastoma protein (pRb) expression and the dephosphorylation of pRb. Conclusion: These findings suggest that the growth inhibitory and the anti-proliferation effects of SM on MCF-7 cells and A549 cells are mediated via the decreased expression and dephosphorylation of pRB by p21 up-regulation in a p53-dependent manner. To the best of our knowledge, this study is the first to report upon the molecular mechanisms involved in SM-induced tumor cell growth inhibition.

• Journal of Microbiology and Biotechnology
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• 제33권4호
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• pp.449-462
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• 2023

Previously, we confirmed that Mychonastes sp. 246 methanolic extract (ME) markedly reduced the viability of BxPC-3 human pancreatic cancer cells. However, the underlying mechanism ME remained unclear. Hence, we attempted to elucidate the anticancer effect of ME on BxPC-3 human pancreatic cancer cells. First, we investigated the components of ME and their cytotoxicity in normal cells. Then, we confirmed the G1 phase arrest mediated growth inhibitory effect of ME using a cell counting assay and cell cycle analysis. Moreover, we found that the migration-inhibitory effect of ME using a Transwell migration assay. Through RNA sequencing, Gene Ontology-based network analysis, and western blotting, we explored the intracellular mechanisms of ME in BxPC-3 cells. ME modulated the intracellular energy metabolism-related pathway by altering the mRNA levels of IGFBP3 and PPARGC1A in BxPC-3 cells and reduced PI3K and mTOR phosphorylation by upregulating IGFBP3 and 4E-BP1 expression. Finally, we verified that ME reduced the growth of three-dimensional (3D) pancreatic cancer spheroids. Our study demonstrates that ME suppresses pancreatic cancer proliferation through the IGFBP3-PI3K-mTOR signaling pathway. This is the first study on the anticancer effect of the ME against pancreatic cancer, suggesting therapeutic possibilities and the underlying mechanism of ME action.