• 한국정보통신설비학회:학술대회논문집
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• 한국정보통신설비학회 2008년도 정보통신설비 학술대회
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• pp.486-490
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• 2008

본 논문에서는 Spurious NAK Suppression알고리즘을 통하여 RLP의 성능향상에 대한 기법을 제안한다. 일반적으로, Hybrid ARQ기법에서는 MAC과 Physical Layer에서의 Retransmission 및 Error Correction으로 무선환경에서의 Error를 줄이고 latency를 보장하고 있다. 그러나 Hybrid ARQ에서의 Multiple SAW나 Selective-ARQ에 의해서 인접한 Packet들 간의 out-of-sequence문제가 발생할 수 밖에 없으며, upper layer인 RLP(혹은 RLC)에서는 이를 re-sequencing하여야 하는 부담감이 생기게 된다. 본 논문에서는 RLP receiver에서의 re-sequencing방법에 있어서, 효율적으로 RLP-NAK의 전송시점을 결정하는 NAK suppression 방법을 제안하고 있으며, 실험을 통하여 높은 성능향상을 보임을 확인할 수 있다.

• 한국정보과학회논문지:정보통신
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• 제28권4호
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• pp.559-569
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• 2001

인터넷의 급속한 성장과 함께 멀티캐스트 프로토콜을 사용하는 어플리케이션들이 증가하고 있는 추세이다. 이러한 멀티캐스트 프로토콜에서 중요하게 요구되는 사항은 신뢰성과 확장성이다. 그 중 확장성을 향상시키기 위해서 여러 지역적 오류 복구 기법이 사용되고 있다. 본 논문에서는 기존의 지역적 오류 복구 기법에서 발생하는 제한점을 설명하고, 이 문제를 해결하기 위해서 보다 안정적이고 효과적인 프로토콜을 제안하였다. 제안된 프로토콜은 다음과 같은 세 가지 특성을 가진다. 첫 번째는 NAK 메시지를 기능에 따라 오류 복구 요청과 NAK-suppression으로 분리하여 각각 전송함으로써, 각 기능에 대해 최적화를 시키는 것이다. 두 번째는 점진적, 분산적으로 선정된 지역 대표가 오류 복구를 보다 결정적으로 수행하도록 하는 것이다. 세 번째는 제어 메시지의 TTL값을 동적으로 조정함으로써, 오류 복구 영역을 최소화시키는 것이다. 제안된 프로토콜은 시뮬레이션 상에서 다른 프로토콜과의 비교 실험을 통해 성능평가를 하였다. 실험 결과, 제안된 프로토콜은 오류 복구 시간과 네트워크 오버헤드를 감소시킴으로써 확장성을 향상시킨다는 것을 확인하였다.

• 정보처리학회논문지C
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• 제10C권3호
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• pp.311-316
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• 2003

본 논문은 멀티캐스트 혼잡제어방식 제안 중의 하나인 PGMCC의 공정성 향상 방법에 관한 것이다. 안정적인 멀티캐스트 전송과 혼잡제어를 위한 여러 가지 방법중에서 PGMCC는 유력한 방식으로 제안되었다. 하지만 PGMCC에도 고정된 타임 아웃 값의 사용과 불확실한 Acker 선출 등 공정성을 낮추는 요인들이 몇 가지 지적되고 있다. 본 논문에서는 타임 아웃 값을 네트워크 상황에 맞추어 적응적으로 가변시키고, 라우터에서의 쓰루풋 비교를 통한 선택적인 NAK 억압이라는 Acker 선출 방법을 도입하여 이와 같은 문제를 해결하여 공정성이 향상되는 것을 보인다.

• The Korean Journal of Physiology and Pharmacology
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• 제28권3호
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• pp.197-207
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• 2024

The potential of tivozanib as a treatment for oral squamous cell carcinoma (OSCC) was explored in this study. We investigated the effects of tivozanib on OSCC using the Ca9-22 and CAL27 cell lines. OSCC is a highly prevalent cancer type with a significant risk of lymphatic metastasis and recurrence, which necessitates the development of innovative treatment approaches. Tivozanib, a vascular endothelial growth factor receptor inhibitor, has shown efficacy in inhibiting neovascularization in various cancer types but has not been thoroughly studied in OSCC. Our comprehensive assessment revealed that tivozanib effectively inhibited OSCC cells. This was accompanied by the suppression of Bcl-2, a reduction in matrix metalloproteinase levels, and the induction of intrinsic pathway-mediated apoptosis. Furthermore, tivozanib contributed to epithelial-to-mesenchymal transition (EMT) inhibition by increasing E-cadherin levels while decreasing N-cadherin levels. These findings highlight the substantial anticancer potential of tivozanib in OSCC and thus its promise as a therapeutic option. Beyond reducing cell viability and inducing apoptosis, the capacity of tivozanib to inhibit EMT and modulate key proteins presents the possibility of a paradigm shift in OSCC treatment.

• Journal of Ginseng Research
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• 제39권1호
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• pp.61-68
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• 2015

Background: Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity. Methods: We investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models. Results: PPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-${\alpha}$, and prostaglandin $E_2$], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-${\alpha}$, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels. Conclusion: These results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).

• 대한본초학회지
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• 제27권1호
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• pp.59-64
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• 2012

Objective : This study was performed to evaluate the effect of Forsythiae Fructus (FF) ethanol extract on inflammatory cytokine production and its underlying mechanisms in mouse macrophages. Methods : Peritoneal macrophages from thioglycollate medium-injected mice were cultured and stimulated with lipopolysaccharide(LPS) or LPS/interferon(IFN)-${\gamma}$ for cytokine measurement and cellular signaling molecule analysis. Results : FF ethanol extract decreased the levels of secreted tumor necrosis factor(TNF)-${\alpha}$ and interleukin(IL)-6 in IFN-${\gamma}$/LPS-stimulated cells in a concentration-dependent manner. FF extract reduced IFN-${\gamma}$/LPS-induced STAT1 phosphorylation and LPS-induced p38 and JNK activation, but not ERK1/2 activity. The extract also inhibited LPS-induced $I{\kappa}B{\alpha}$ degradation through suppression of $I{\kappa}B{\alpha}$ kinase. Conclusions : These results suggest that FF ethanol extract affects the production of TNF-${\alpha}$ and IL-6 through inhibition of activation of STAT-1, $I{\kappa}B{\alpha}$, p38, and JNK.

• 동의생리병리학회지
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• 제25권5호
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• pp.799-806
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• 2011

This study was performed in order to evaluate the neuroprotective effect of Boyanghwano-tang (BYT) water extract on intracerebral hemorrhage (ICH). ICH was induced by the stereotaxic intrastriatal injection of bacterial collagenase type IV in Sprague-Dawley rats. BYT was orally given once a day for 3 days after ICH. Hematoma volume and percentage edema were examined. As imflammatory markers, myeloperoxidase (MPO)-positive neutrophils infiltration and iNOS expression in the peri-ICH regions were examined using immunohistochemistry. As cellular damage markers, c-Fos, Bax, and HSP72 positive cells in the peri-ICH regions were measured also. BYT significantly reduced the hematoma volume and percentage edema of the ICH-induced rat brain. In the peri-hematoma regions, BYT significantly reduced MPO-positive neutrophil infiltration and iNOS expression of the ICH-induced rat brain. Additionally, BYT significantly reduced c-Fos, Bax, and HSP72 positive cells in the peri-hematoma regions of the ICH-induced rat brain. These results suggest that BYT plays a neuroprotective role against ICH through suppression of inflammatory responses, apoptosis and cellular damage.

• Molecules and Cells
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• 제39권8호
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• pp.631-638
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• 2016

Glutathione peroxidase 3 (GPx3), an antioxidant enzyme, acts as a modulator of redox signaling, has immunomodulatory function, and catalyzes the detoxification of reactive oxygen species (ROS). GPx3 has been identified as a tumor suppressor in many cancers. Although hyper-methylation of the GPx3 promoter has been shown to down-regulate its expression, other mechanisms by which GPx3 expression is regulated have not been reported. The aim of this study was to further elucidate the mechanisms of GPx3 regulation. GPx3 gene analysis predicted the presence of ten glucocorticoid response elements (GREs) on the GPx3 gene. This result prompted us to investigate whether GPx3 expression is regulated by the glucocorticoid receptor (GR), which is implicated in tumor response to chemotherapy. The corticosteroid dexamethasone (Dex) was used to examine the possible relationship between GR and GPx3 expression. Dex significantly induced GPx3 expression in H1299, H1650, and H1975 cell lines, which exhibit low levels of GPx3 expression under normal conditions. The results of EMSA and ChIP-PCR suggest that GR binds directly to GRE 6 and 7, both of which are located near the GPx3 promoter. Assessment of GPx3 transcription efficiency using a luciferase reporter system showed that blocking formation of the GR-GRE complexes reduced luciferase activity by 7-8-fold. Suppression of GR expression by siRNA transfection also induced down-regulation of GPx3. These data indicate that GPx3 expression can be regulated independently via epigenetic or GR-mediated mechanisms in lung cancer cells, and suggest that GPx3 could potentiate glucocorticoid (GC)-mediated anti-infla-mmatory signaling in lung cancer cells.

• Journal of Ginseng Research
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• 제39권2호
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• pp.155-161
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• 2015

Background: Korean ginseng is an ethnopharmacologically valuable herbal plant with various biological properties including anticancer, antiatherosclerosis, antidiabetic, and anti-inflammatory activities. Since there is currently no drug or therapeutic remedy derived from Korean ginseng, we developed a ginsenoside-enriched fraction (AP-SF) for prevention of various inflammatory symptoms. Methods: The anti-inflammatory efficacy of AP-SF was tested under in vitro inflammatory conditions including nitric oxide (NO) production and inflammatory gene expression. The molecular events of inflammatory responses were explored by immunoblot analysis. Results: AP-SF led to a significant suppression of NO production compared with a conventional Korean ginseng saponin fraction, induced by both lipopolysaccharide and zymosan A. Interestingly, AP-SF strongly downregulated the mRNA levels of genes for inducible NO synthase, tumor necrosis factor-${\alpha}$, and cyclooxygenase) without affecting cell viability. In agreement with these observations, AP-SF blocked the nuclear translocation of c-Jun at 2 h and also reduced phosphorylation of p38, c-Jun N-terminal kinase, and TAK-1, all of which are important for c-Jun translocation. Conclusion: Our results suggest that AP-SF inhibits activation of c-Jun-dependent inflammatory events. Thus, AP-SF may be useful as a novel anti-inflammatory remedy.

• Archives of Pharmacal Research
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• 제22권2호
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• pp.99-107
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• 1999

A series of organosulfur compounds were synthesized with the aim of developing chemopreventive compounds active against hepatotoxicity and chemical carcinogesis. 2-(Allylthio) prazine (2-AP) was effective in inhibiting cytochrome P450 2E1-mediated catalytic activities and protein expression, and in inducing microsomal epoxide hydrolase and major glutathione S-transferases. 2-AP reduced the hepatotoxicity caused by toxicant sand elevated cellular GSH content. Development of skin tumors, pulmonary adenoma and aberrant crypt foci in colon by various chemical carcinogens was inhibited by 2-AP pretreatment. Anticarcinogenic effects of 2-AP at the stage of initiation of tumors were also observed in the aflatoxin B1 ($AFB_1$)-induced three-step medium-term hepatocarcinogenesis model. Reduction of $AFB_1$-DNA adduct by 2-AP appeared to result from the decreased formation of $AFB_1$-8,9-epoxide via suppression of cytochrome P450, while induction of GST 2-AP increases the excretion of glutathione-conjugated $AFB_1$ . 2-AP was a radioprotective agent effective against the lethal dose of total body irradiation and reduced radiation-induced injury in association with the elevation of detoxifying gene expression. 2-AP produces reactive oxygen species in vivo, which is not mediated with the thiol-dependent production of oxidants and that NF-KB activation is not involved in the induction of the detoxifying enzymes. the mechanism of chemoprotection by 2-AP may involve inhibition of the P450-mediated metabolic activation of chemical carcinogens and enhancement of electrophilic detoxification through induction of phase II detoxification enzymes which would facilitate the clearance of activated metabolites through conjugation reaction.