• 정보처리학회논문지:소프트웨어 및 데이터공학
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• 제9권6호
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• pp.187-194
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• 2020

본 논문은 클라이언트의 익명성과 개인 정보를 보장하는 토르 네트워크에서 앙상블 학습을 이용한 웹사이트 핑거프린팅 방법을 제안한다. 토르네트워크에서 수집된 트래픽 패킷들로부터 웹사이트 핑거프린팅을 위한 훈련 문제를 구성하며, 트리 기반 앙상블 모델을 적용한 웹사이트 핑거프린팅 시스템의 성능을 비교한다. 훈련 특징 벡터는 트래픽 시퀀스에서 추출된 범용 정보, 버스트, 셀 시퀀스 길이, 그리고 셀 순서로부터 준비하며, 각 웹사이트의 특징은 고정 길이로 표현된다. 실험 평가를 위해 웹사이트 핑거프린팅의 사용에 따른 4가지 학습 문제(Wang14, BW, CW_T, CW_H)를 정의하고, CUMUL 특징 벡터를 사용한 지지 벡터 기계 모델과 성능을 비교한다. 실험 평가에서, BW 경우를 제외하고 제안하는 통계 기반 훈련 특징 표현이 CUMUL 특징 표현보다 우수하다.

• IMMUNE NETWORK
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• 제24권4호
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• pp.24.1-24.8
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• 2024

Complement C5a receptor (C5aR) signaling in immune cells has various functions, inducing inflammatory or anti-inflammatory responses based on the type of ligand present. The Co1 peptide (SFHQLPARSRPLP) has been reported to activate C5aR signaling in dendritic cells. We investigated the effect of C5aR signaling via the Co1 peptide on macrophages. In peritoneal macrophages, the interaction between C5aR and the Co1 peptide activated the mTOR pathway, resulting in the production of pro-inflammatory cytokines. Considering the close associations of mTOR signaling with IL-6 and TNF-α in macrophage training, our findings indicate that the Co1 peptide amplifies β-glucan-induced trained immunity. Overall, this research highlights a previously underappreciated aspect of C5aR signaling in trained immunity, and posits that the Co1 peptide is a potentially effective immunomodulator for enhancing trained immunity.

• Journal of Microbiology and Biotechnology
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• 제32권3호
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• pp.365-377
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• 2022

Mammalian target of rapamycin (mTOR) is a serine-threonine kinase member of the cellular phosphatidylinositol 3-kinase (PI3K) pathway, which is involved in multiple biological functions by transcriptional and translational control. mTOR is a downstream mediator in the PI3K/Akt signaling pathway and plays a critical role in cell survival. In cancer, this pathway can be activated by membrane receptors, including the HER (or ErbB) family of growth factor receptors, the insulin-like growth factor receptor, and the estrogen receptor. In the present work, we congregated an electronic network of mTORC1 built on an assembly of data using natural language processing, consisting of 470 edges (activations/interactions and/or inhibitions) and 206 nodes representing genes/proteins, using the Cytoscape 3.6.0 editor and its plugins for analysis. The experimental design included the extraction of gene expression data related to five distinct types of cancers, namely, pancreatic ductal adenocarcinoma, hepatic cirrhosis, cervical cancer, glioblastoma, and anaplastic thyroid cancer from Gene Expression Omnibus (NCBI GEO) followed by pre-processing and normalization of the data using R & Bioconductor. ExprEssence plugin was used for network condensation to identify differentially expressed genes across the gene expression samples. Gene Ontology (GO) analysis was performed to find out the over-represented GO terms in the network. In addition, pathway enrichment and functional module analysis of the protein-protein interaction (PPI) network were also conducted. Our results indicated NOTCH1, NOTCH3, FLCN, SOD1, SOD2, NF1, and TLR4 as upregulated proteins in different cancer types highlighting their role in cancer progression. The MCODE analysis identified gene clusters for each cancer type with MYC, PCNA, PARP1, IDH1, FGF10, PTEN, and CCND1 as hub genes with high connectivity. MYC for cervical cancer, IDH1 for hepatic cirrhosis, MGMT for glioblastoma and CCND1 for anaplastic thyroid cancer were identified as genes with prognostic importance using survival analysis.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2019년도 춘계학술대회
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• pp.33-33
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• 2019

The AKT signaling pathway is a highly regulated cell signaling system that forms a network with other cell signaling pathways. Hence, the AKT signaling pathway mediates several important cellular functions that include cell survival, proliferation, cell migration, and et cetera. Irregularities that led overactive AKT signaling have been linked to many diseases such as cancer and metabolic-associated diseases. Hence, modulating the overactive AKT signaling pathway via inhibitor is a tantalizing prospect for treatment of cancer and metabolic-associated diseases. Two inhibitors of the AKT signaling pathway will be presented in this symposium: 1) Bisleuconothine A (BisA), a bisindole alkaloid that inhibit autophagy and 2) Ceramicine B (CerB), a limonoid that inhibit adipogenesis. The first topic is on a bisindole alkaloid, BisA and its mechanism in inducing autophagosome formation in lung cancer cell line, A549.(1) Since most autophagy inducing agents generally induce apoptosis, we found that BisA does not induce apoptosis even in high dose. BisA up-regulation of LC3 lipidation is achieved through mTOR inactivation. The phosphorylation of PRAS40, a mTOR repressor was suppressed by BisA. This observation suggested that BisA inactivates mTOR via suppression of PRAS40 phosphorylation. Interestingly, the phosphorylation of AKT, an upstream regulator of PRAS40 phosphorylation was also down-regulated by BisA. These findings suggested that Bis-A induces autophagosomes formation by interfering with the AKT-mTOR signaling pathway. The second topic is on CerB and its mechanism in inhibiting adipogenesis in preadipocytes cell line, MC3T3-G2/PA6.(2,3) CerB inhibits the phosphorylation of protein kinase B (AKT) at the Thr308 position but not the Ser473. Consequently, the phosphorylation of FOXO3 which is located downstream of AKT is also inhibited. Considering that FOXO3 is an important regulator of PPARγ which is a key factor in adipogenesis, CerB may inhibit adipogenesis via the AKT-FOXO3 signaling pathway. Taken together, both BisA and CerB highlighted the potential of AKT signaling pathway modulation as an approach to induce autophagy and inhibit the formation of fat cells, respectively.

• 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.

• Transactions on Control, Automation and Systems Engineering
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• 제3권2호
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• pp.111-116
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• 2001

A neural network compensator for stick-slip friction phenomena in meashartonics servo systems is practically proposed to supplement the traditionally available position and velocity control loops for precise motion control. The neural network compensa-tor plays the role of canceling the effect of nonlinear slipping friction force. It works robustly and effectively in a real control system. This enables the mechatronics servo systems to provide more precise control in the digital computer. It was confirmed that the con-trol accuracy is improved near zero velocity and points of changing the moving direction through numerical simulation. However, asymptotic property on the steady state error of the normal operation points is guaranteed by the integral term of traditional velocity loop controller.

• 정보처리학회논문지:컴퓨터 및 통신 시스템
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• 제11권4호
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• pp.127-132
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• 2022

토르 (Tor, The Onion Router)와 같이 다수의 가상 컴퓨터 및 네트워크를 경유함으로써 이용자의 인터넷 접속에 대한 추적을 어렵게 하는 익명 암호통신 네트워크는 데이터 송수신 과정에서의 사용자 및 데이터 프라이버시 보호를 그 운영목적으로 하고 있다. 하지만 이러한 익명 암호통신 네트워크를 통한 불법 콘텐츠 공유 및 무기거래 등 부적절한 용도로의 악용 및 오용에 있어, 기존의 탐지 기법을 적용하거나 적절한 대응책을 마련하기에는 어려움이 따른다. 본 논문에서는 익명 암호통신에서도 특정 사이트에 대한 접근 정보를 높은 정확도로 유추할 수 있는 웹사이트 핑거프린팅 (website fingerprinting) 기법을 확장하여, 특정 사이트 뿐 아니라 알려지지 않은 사이트에 대해서도 서비스 유형을 특정하고 분류하는 방법을 강구함으로써 악의적 목적에 활용될 수 있는 은닉 사이트 또는 잠재적 불법 사이트에 대한 식별 방안을 제시한다.

• Food Science and Biotechnology
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• 제15권1호
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• pp.77-81
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• 2006

The dextransucrase activity of microorganisms which were identified as contributing to the fermentation of jeungpyeon made with yeast was measured. The dextran generated during fermentation was quantified and the viscosity changes were measured. The mechanism of network structure formation was clarified by observing the inside of the network structure over the fermentation periods ranging from 1 to 7 hr using scanning electron microscopy (SEM). The pH of jeungpyeon batter decreased significantly as the fermentation proceeded, whereas the viscosity increased. The identified lactic acid bacteria (LAB) were Leuconostoc mesenteroides subsp. mesenteroides, Pediococcus pentosaceus, Tetragenococcus halophilus, and Leuconostoc mesenteroides subsp. dextranicum. The yeast was identified as Saccharomyces cerevisiae A/Tor. Pretorien. The dextransucrase extracted from those microorganisms showed high activity. On the other hand, the amount of dextran generated from the batter increased significantly beyond 2 hr of fermentation, and the viscosity increment showed a similar trend. The SEM photos showed that the most homogeneous fine network structure was observed in the batter fermented for 2 hr. Therefore, we assumed that the dextran that was generated by microorganisms during fermentation interacted with the components of the batter to increase the stability of the network structure.

• 융합보안논문지
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• 제11권3호
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• pp.31-37
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• 2011

최근 네트워크상에 익명성을 보장하는 Mixed Network에 관한 연구가 활발히 진행되고 있다. 이는 노드간 암호화 통신을 이용하고 통신 경로도 수시로 변경되는 등 공격자에 대한 역추적 및 대응을 어렵게 만든다. 그럼에도 악의적인 형태의 인터넷 사용을 즐기는 사람들에 의해 지속적으로 진화되고 있으며, 새로운 형태의 기술이 지속적으로 개발되고 있는 상황이다. 이러한 상황에 익명네트워크를 이용하여 국가기관 및 기반시설에 대한 사이버공격이 대규모로 이루어진다면 국가차원에서 엄청난 재앙이 아닐 수 없다. 또한 향후에도 이러한 기술을 응용한 공격기법이 지속적으로 출현할 것으로 예상되고 있으나, 이에 대한 마땅한 대비책이 마련되어 있지 않다. 이에 본 논문에서는 다양한 익명네트워크 기술에 대한 분석 및 이를 이용한 사이버 공격에 효율적 대응을 위한 조기탐지 방안 연구를 진행하고자 한다.

• Molecules and Cells
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• 제41권10호
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• pp.881-888
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• 2018

During the cortical development, cells in the brain acquire somatic mutations that can be implicated in various neurodevelopmental disorders. There is increasing evidence that brain somatic mutations lead to sporadic form of epileptic disorders with previously unknown etiology. In particular, malformation of cortical developments (MCD), ganglioglioma (GG) associated with intractable epilepsy and non-lesional focal epilepsy (NLFE) are known to be attributable to brain somatic mutations in mTOR pathway genes and others. In order to identify such somatic mutations presenting as low-level in epileptic brain tissues, the mutated cells should be enriched and sequenced with high-depth coverage. Nevertheless, there are a lot of technical limitations to accurately detect low-level of somatic mutations. Also, it is important to validate whether identified somatic mutations are truly causative for epileptic seizures or not. Furthermore, it will be necessary to understand the molecular mechanism of how brain somatic mutations disturb neuronal circuitry since epilepsy is a typical example of neural network disorder. In this review, we overview current genetic techniques and experimental tools in neuroscience that can address the existence and significance of brain somatic mutations in epileptic disorders as well as their effect on neuronal circuitry.