• 한국동물위생학회지
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• 제25권3호
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• pp.295-297
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• 2002

This experiment was done to set up the immunohistochemical detection method for infectious hematopoietic necrosis virus(IHNV) antigens in the monolayers of CHSE-214 cell cultures inoculated with IHNV. Specific identification of IHNV antigens was detected in the cytoplasms of infected cells by the use of monoclonal antibodies to glycoproteins. The specific positive signal was observed as a distinct red color. The result showed that streptavidin alkaline phosphatase immunohistochemistry specifically identified IHNV antigens in infected cultured cells.

• 한국통신학회논문지
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• 제34권12A호
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• pp.962-970
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• 2009

본 논문에서는 Long Term Evolution (LTE) 시스템에서 새로 설치된 셀이 자율적으로 이웃 셀 정보를 수집하고 Physical Cell Identifier (PCI)를 결정하는 방안을 제안한다. PCI의 수는 한정되어 재사용이 필요하며, 도심 환경에서 Macro 셀 안에 Pico/Femto 셀과 같은 작은 크기의 셀이 다수 설치되면 PCI의 수는 더욱 제한될 것으로 예상된다. 따라서 제한된 수의 PCI를 효율적으로 할당하는 연구가 필요하다. 본 논문에서는 Self-Organization Network (SON) 환경에서 셀이 주변 셀들로부터 오는 수신신호세기를 수집하고, 이를 이용하여 PCI 재사용 효율을 높일 수 있도록 자율적으로 PCI를 할당하는 방안을 제안한다. 모의실험을 구성하여 제안한 방안이 적용된 경우의 성능을 분석하였고, 새로 설치되는 셀의 커버리지 타입에 따른 성능도 도출하고 분석하였다. 제안한 기법을 적용하면 시스템을 운용하는데 필요한 PCI의 수를 줄여 효율적으로 PCI를 재사용할 수 있음을 확인하였다

• 전자공학회논문지
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• 제50권8호
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• pp.39-44
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• 2013

LTE(Long Term Evolution)-Advanced에서는 저전력 피코셀(picocell)과 같은 소형셀을 중첩하여 배치해 시스템 성능을 향상시키기 위한 HetNet(Heterogeneous Network)에 대한 연구가 활발히 진행되고 있다. 또한 HetNet에서 데이터 오프로딩 효과를 증대시키기 위해 셀 영역 확장(CRE: Cell Range Expansion) 기술이 소개되었다. 본 논문에서는 최적의 오프로딩 효과를 위해 SINR(Signal to Interference plus Noise Ratio) 기반 셀 선택 기법을 제안한다. 셀 확장 영역에 존재하는 사용자의 간섭 관리를 위해 ABS를 사용하며, 스펙스럼 효율을 증가시키기 위하여 동적인 ABS 비율을 사용한다. 모의실험 결과, 제안한 기법에서 피코셀뿐만 아니라 매크로셀 사용자의 스펙트럼 효율이 향상되어 전체적인 사용자의 성능이 향상 된 것을 볼 수 있다.

• 한국항행학회논문지
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• 제16권1호
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• pp.96-102
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• 2012

모바일 인터넷 시스템의 목표는 고속 데이터 율, 낮은 지연 그리고 유연한 대역폭 진화를 제공할 수 있는 최적화된 패킷 무선접속기술을 제공하는 것이다. 따라서 연속적인 이동성과 서비스 품질 그리고 최소지연을 갖는 패킷 스위치 트래픽 목표를 제공하는 LTE 네트워크 구조가 설계되었다. LTE 시스템에서의 중요한 요구조건은 셀 경계에서의 BER 성능과 데이터 처리율을 개선하는 것이다. 이것은 통신 지역에서 지리적 영역과 데이터 처리율 측면에서 서비스의 일관성을 제공한다. 하지만 셀룰러 시스템에서 셀의 중앙과 경계지역 사용자 사이의 SINR 차이는 20 [dB] 정도가 된다. 이러한 차이는 통신 영역이 제한된 셀룰러 시스템에서 더욱 크다. 이 현상은 셀 중앙의 사용자에 비하여 셀 경계의 사용자에게 대단히 낮은 데이터 처리율 유발하고 큰 QoS 차이를 발생시킨다. 본 논문에서 인접 셀 간섭을 감소하기 위한 분석적인 방법을 제시하고 모바일 인터넷 환경에서 OFDM 시스템 파라미터에 따른 SIR 및 BER 성능을 보였다.

• Archives of Pharmacal Research
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• 제29권10호
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• pp.890-897
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• 2006

In inflammatory responses, induction of cytokines and other immune regulator genes in macrophages by pathogen-associated signal such as lipopolysaccharide (LPS) plays a crucial role. In this study, the gene expression profile changes by LPS treatment in the macrophage/monocyte lineage cell line RAW264.7 was investigated. A 60-mer oligonucleotide microarray of which probes target 32381 mouse genes was used. A reverse transcription-in vitro translation labeling protocol and a chemileuminescence detection system were employed. The mRNA expression levels in RAW264.7 cells treated for 6 h with LPS and the control vehicle were compared. 747 genes were up-regulated and 523 genes were down-regulated by more than 2 folds. 320 genes showing more than 4-fold change by LPS treatment were further classified for the biological process, molecular function, and signaling pathway. The biological process categories that showed high number of increased genes include the immunity and defense, the nucleic acid metabolism, the protein metabolism and modification, and the signal transduction process. The chemokine-cytokine signaling, interleukin signaling, Toll receptor signaling, and apoptosis signaling pathways involved high number of genes differentially expressed in response to LPS. These expression profile data provide more comprehensive information on LPS-target genes in RAW264.7 cells, which will be useful in comparing gene expression changes induced by extracts and compounds from anti-inflammatory medicinal herbs.

• Journal of Microbiology and Biotechnology
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• 제11권5호
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• pp.749-755
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• 2001

High Electromagnetic Field (EMF) with an intensity of 1 mT (Tesla) inhibited the growth of both human normal lung and immune T cell down to $20-30\%$, compared to that of an unexposed case. The human T-cells, Jurkat, were more severely affected by EMF than the human lung cells, which showed a relatively slow cell growth and substantial releas of $Ca^+2$ (3.5 times higher than the human T-cells). However, the growth of hepatoma carcinoma, Hep3B, was enhanced by twice that of an unexposed case. The EMF intensity and exposure time did not affect the growth of the cancer cells very much, while it significantly affected the growth of normal cells. Accordingly, it is possible that EMFs may play a role in the initiation of cancer. The EMFs disturbed the signal transduction and membrane systems, such that a five times higher amount of PKC-${\alpha}$ was released from the cell membrane than in the control. Extended exposure to EMFs, for more than 48 hours, also led to 1 $90\%$ necrotic death pattern from apoptotic cell death. Finally, EMF at an intensity of 1mT with a 24-T exposure promoted the differentiation of HL-60 cells to monocytes/macrophages, possibly causing potential acute leukemia.

• 대한한방내과학회지
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• 제26권1호
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• pp.74-92
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• 2005

Objectives/Methods : To analyze the effect of Injinchunggantang(IJCGT) to Interferon-${\alpha}/{\beta}$ signal transmission system in HepG2 cells, HepG2 Cell were treated with IJCGT. Also, revelation of MxA, 2'5'-OAS mRNA leaded by Interferon-${\alpha}/{\beta}$ and revelation and activation of Jak1, TYK1, and STAT 1, all main signal transmission factors, were analyzed. Results : The analysis resulted in the following 1. With interferon ${\alpha}/{\beta}$ there was no affect cell propagation of Hep G2 cells. With IJCGT alone, cell propagation of HepG2 was promoted, and cell propagation control function was recovered. 2. With interferon ${\alpha}/{\beta}$ cell death was unaffected. With IJCGT apoptosis of HepG2 cell was restrained, and the cell's reaction to interferon was unaffected. 3. With interferon ${\alpha}/{\beta}$ treatment mRNA revelation of MxA and 2'5'-OAS was induced. When HepG2 cells were injected with IJCGT without interferon ${\alpha}/{\beta}$ treatment, mRNA revelation of MxA and 2'5'-OAS increased in proportion to the treatment density. With pre-treatment of IJCGT, leaded with interferon ${\alpha}/{\beta}$, promoted revelation of MxA, 2'5' -OAS mRNA. 4. Though mRNA revelation of lakl, TYK1 and STAT1 was unaffected with IJCGT, activation of STAT1 was promoted with an increase of phosphorylation of STAT1 protein. With pre-treatment of IJCGT, Jak1, TYK2, STAT1 phosphorylation, leaded with interferon, strengthened. 5. TNF-a, IL-1b and LPS present, revelation of MxA and 2'5'-OAS mRNA leaded by interferon was restrained when HepG2 cells were treated with IJCGT, and the interferon signal transmission system restraint action leaded by inflammatory cytokines was moderated. Conclusion : These results support a role for IJGCT in promotion of anti-virus action through maintainance of the liver's sensibility toward interferon. A clinical study of an interferon treated patient treated also with IJGCT is needed to determine its efficacy.

• 한국통신학회논문지
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• 제34권9B호
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• pp.876-882
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• 2009

본 논문에서는 relay 기반 OFDMA 시스템에서 cell throughput 향상을 위한 Base Station (BS)과 Relay Station (RS)의 sub-cell 커버리지 조절 기법을 제안하였다. Relay 시스템에서는 BS-RS 링크에서 무선 자원을 추가로 소비하기 때문에, 이를 고려하지 않고 sub-cell 커버리지를 설정하면, 자원 사용량이 증가하여 throughput이 저하될 수 있기 때문에 자원 소모를 고려한 sub-cell 커버리지 설정이 필요하다. 이 때, 설정된 sub-cell 커버리지를 고정하여 운용할 수도 있지만, 트래픽 상황의 변화에 따라서 커버리지를 효과적으로 조절해주면, throughput 성능을 더욱 향상시킬 수 있다. 본 연구에서는 MS가 이동할 때에, 멀티홉 전송에 따른 relay link에서의 자원의 소모와 자원 재사용 정도를 함께 고려하여 sub-cell 커버리지를 조절하는 기법을 제안하고 분석하였다. 제안하는 커버리지 조절 기법에서는 BS와 RS로부터의 수신 SINR 값 비율로 threshold 값을 정하고 이를 이용하여 sub-cell 경계를 설정하였다. 그리고 트래픽의 변화에 따라 멀티홉에서의 자원의 소모와 자원 재사용을 고려한 effective transmitted bits per subchannel을 이용하여 sub-cell 경계를 적응적으로 조절하였다. 성능 분석을 위해 이 경우 cell throughput을 도출하였다. 제안하는 커버리지 조절 기법을 적용할 때, 고정하여 운용하는 경우에 비해, cell throughput이 향상되는 것을 확인하고, 정량적으로 분석하였다.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2008년도 추계학술대회A
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• pp.1458-1460
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• 2008

Tissue engineering is an interdisciplinary field that utilizes the principles of engineering and life sciences toward the creation of biological substitutes. Traditionally, major components of tissue engineering are cells, scaffolds, growth factors and recently biomechanical aspects have been given much attention. A large number of studies have reported that mechanical signals are of particular interest in either encouraging or inhibiting cellular responses. In tissue engineering, cell adhesion is a very important step, because quality of adhesion may determine a cell fate in the future. Elasticity of cell-adhesive substrate is found critical in regulating stem cell differentiation. Cells exert different contractile forces for cell migration, depending on substrate mechanics. Though tissue engineering is very interactive with diverse expertise, for a breakthrough, principles of biomechanics in tissue and cell level needs to be fully understood.

• Biomolecules & Therapeutics
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• 제16권1호
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• pp.1-8
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• 2008

Mitochondria are important sensor of apoptosis. $H_2O_2-induced$ cell death rate was enhanced by serum deprivation. In this study, we investigated whether serum deprivation using 0.5 or 3 % FBS induces apoptotic cell death through mitochondrial enzyme activation as compared to 10 % FBS. Apoptotic cell death was observed by chromosome condensation and the increase of sub-G0/G1 population. Serum deprivation reduced cell growth rate, which was confirmed by the decrease of S-phase population in cell cycle. Serum deprivation significantly increased caspase-9 activity and cytochrome c release from mitochondria into cytosol. Serum deprivation-induced mitochondrial changes were also indicated by the increase of ROS production and the activation of mitochondrial enzyme, succinate dehydrogenase. Mitochondrial enzyme activity increased by serum deprivation was reduced by the treatment with rotenone, mitochondrial electron transport inhibitor. In conclusion, serum deprivation induced mitochondrial apoptotic cell death through the elevation of mitochondrial changes such as ROS production, cytochrome c release and caspase-9 activation. It suggests that drug sensitivity could be enhanced by the increase of mitochondrial enzyme activity in serum-deprived condition.