• 한국정보통신학회논문지
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• 제19권8호
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• pp.1785-1796
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• 2015

본 논문에서는 각 단말에 2개 이상의 안테나의 간섭 정렬을 이용한 X채널에서 직교 및 준직교 시공간 블록 부호를 통하여 더 높은 다이버시티와 전력 이득을 달성하고자 했다. 제안한 방법으로 다이버시티 차수는 직교 시공간 블록 부호에서 최대에 도달한 반면, 준직교 시공간 블록 부호에서는 유효 채널 행렬의 비 직교성에 의해 약간의 성능 저하가 나타났다. 수신기의 유효 채널 행렬에서의 유리한 구조에 의해 단순 제로 포싱 수신기는 최대 다이버시티 차수를 달성하는 반면, 간섭 제거 수신기는 성능이 저하되었다. 기존의 방법과 비교했을 때, 시뮬레이션 결과는 제안된 방법이 같은 스펙트럼 효율을 얻으면서, 3-4개의 안테나의 각 단의 직교 시공간 블록 부호의 경우 각각 목표 비트 에러율 10^-4에서 14dB와 16.5bB의 이득을 얻는 것을 증명하였다. 또한 4개의 안테나의 각 단의 준직교 시공간 블록 부호의 경우 같은 목표 비트 에러율에서 10dB의 이득을 얻었다.

• 정보과학회 논문지
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• 제42권4호
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• pp.475-482
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• 2015

높은 성능의 의미역 인식 시스템의 개발을 위해서는 대상 도메인에 대한 대량의 수동 태깅 학습 데이터가 필요하다. 그러나 충분한 크기의 의미역 인식용 학습 데이터는 오직 소수의 도메인에서만 존재한다. 소스 도메인의 시스템을 상대적으로 매우 작은 학습 데이터를 가진 다른 도메인에 적용할 경우 한국어 의미역 인식 기술은 15% 정도 성능 하락이 발생한다. 이러한 도메인 변경에서의 성능 하락 현상을 최소화하기 위해 본 논문에서는 2 가지 기법을 제시한다. 첫째, 도메인 적응 방법론의 하나인 Prior 모델에 기반하여 개발된 한국어 의미역 인식 시스템을 위한 도메인 적응 알고리즘을 제안한다. 둘째, 크기가 작은 타겟 도메인 데이터를 이용할 때 데이터 희귀 문제의 감소를 위해 소스 도메인 데이터 이용시 보다 단순화된 형태소 태그와 구문 태그 자질을 사용할 것을 제안한다. 뉴스 도메인에서 개발된 시스템의 위키피디아 도메인에의 적용과 관련하여 다른 연구의 도메인 적응 기술과 우리가 제안한 방법을 비교 실험하였다. 우리의 두 가지 방법을 같이 사용할 때 더 높은 성능을 달성하는 것을 관찰하였다. 우리 시스템은 F1-score 64.3% 성능으로서 기존의 다른 도메인 적응 기술들과 비교하여 2.4~3.1% 더 높은 성능을 가지는 것으로 관찰되었다.

• Animal cells and systems
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• 제6권3호
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• pp.263-269
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• 2002

The p53 tumor suppressor gene is among the most frequently mutated and studied genes in human cancer, but the mechanisms by which it sur presses tumor formation remain unclear. DNA damage regulates both the protein levels of p53 and its affinity for specific DNA sequences. Stabilization of p53 in response to DNA damage is caused by its dissociation from Mdm2, a downstream target gene of p53 and a protein that targets p53 for degradation in the proteosome. Recent studies have suggested that phosphorylation of human p53 at Ser20 is important for stabilizing p53 in response to DNA damage through disruption of the interaction between Mdm2 and p53. We generated mice with an allele encoding changes at Ser20, known to be essential for p53 accumulation following DNA damage, to enable analyses of p53 stabilization in vivo. Our data showed that the mutant p53 was clearly defective for full stabilization of p53 in response to DNA damage. We concluded that Ser20 phosphorylation is critical for modulating the negative regulation of p53 by Mdm2, probably through phosphorylation-dependent inhibition of p53-Mdm2 interaction in the physiological context.

• 한국통신학회논문지
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• 제32권6B호
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• pp.325-333
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• 2007

설계된 HW IP를 응용수준에서 제어하기 위해 OS상에서의 디바이스 드라이버가 요구된다. 디바이스 드라이버의 개발은 하드웨어와 OS에 대해 시스템 개발자의 정확한 이해가 필요하며 하드웨어 개발 기간과 비용의 많은 부분을 차지한다. 본 논문에서는 OS정보, 하드웨어 특징정보를 이용하여 OS에 따른 디바이스 드라이버를 인터페이스 회로와 함께 자동 생성하는 시스템의 구축에 대해 제시한다. 제안한 시스템에서는 효율적인 디바이스 드라이버 자동생성을 위해 디바이스 드라이버의 기본골격과 함수 모듈 코드, 헤더파일 테이블 등을 라이브러리로 구축하여 입력 데이터에 따라 선택되어 디바이스 드라이버가 자동생성 되도록 하였다. 제안된 방법으로 ARM922T 코어에 삼성 3.5인치 TFT-LCD를 장착하여 커널버전 ARM-Linux 2.4.19를 탑재한 후 디바이스 드라이버를 자동 생성하여 커널에 등록한 뒤 하드웨어에 write 연산을 실행하는데 걸린 시간을 비교한 결과 매뉴얼로 설계한 디바이스 드라이버에 비해 1.12%의 감소를 보였다. 커널 컴파일 후의 코드 사이즈는 0.17%의 증가를 보였다. 생성된 디바이스 드라이버는 응용프로그램 레벨에서 하드웨어를 제어할 때 발생하는 지연시간을 고려하면 실제 성능의 차이가 없음을 보인다. 본 논문에서 제안한 시스템을 사용하여 시스템 개발기간을 단축할 수 있다.

• 동의생리병리학회지
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• 제18권3호
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• pp.759-766
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• 2004

In the present study, we investigated the effects of aqueous extract of the healthful decoction utilizing Phellinus linteus (HDPL) on the cell growth of human lung carcinoma tumor cell line A549. Exposure of A549 cells to HDPL resulted in growth inhibition and induction of apoptosis in a dose-dependent manner as measured by hemocytometer counts, fluorescence microscopy and flow cytometric analysis. This increase in apoptosis was associated with inhibition and/or degradation of apoptotic target proteins such as poly(ADP-ribose) polymerase (PARP), b-catenin and phospholipase C- 1 (PLC- 1) protein. HDPL treatment induced the down-regulation of anti-apoptotic Bcl-2 expression, an anti-apoptotic gene, however, the level of Bax. a pro-apoptotic gene, was increased by HDPL treatment. In addition, HDPL-induced apoptotis of A549 cells was connected with activation of caspase-3 and caspase-9 protease in a dose-dependent manner, however, the levels of inhibitor of apoptosis proteins family were remained unchanged. Taken together, these results indicated that the anti-proliferative effects of HDPL were associated with the induction of apoptotic cell death through regulation of several major growth regulatory gene products such as Bcl-2 family expression and caspase protease activity, and HDPL may have therapeutic potential in human lung cancer.

• 상하수도학회지
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• 제12권1호
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• pp.52-61
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• 1998

Nitrification and denitrification are important processes in the landfill site as they are deeply related with degradation and stabilization of refuse. Also nitrous oxide ($N_2O$) which is released from both nitrification and denitrification is known as greenhouse gas (GHG). The purpose of this study was to clarify the process by which $N_2O$ produced using $^{15}N$ isotope. Nitrate which was labeled to 10.08% with $^{15}KNO_3$ was used and $N_2O$ was analyzed with GC mass. Results was that even also when $O_2$ of bulk was 15%, $N_2O$ was released from denitrification. And as concentrations of $O_2$ increase, sum of $N_2O$ was released from denitrification. And as concentrations of $O_2$ increase, sum of $N_2O$ and $N_2$ was decreased and ratios of $N_2O$ in the reduced gases were increased. FISH technics also adaped to confirm whether which of nitrifiers existed in the substrates. When NEU was used of which the target was ammonia oxidizing bacteria, nitrifier was not detected at all. So it was confirmed that during the reaction denitrification was dominant process. Total bacteria distributions which were detected by EUB probe explained that as $O_2$ increase the number of bacteria also increase, but between the 10-15% of $O_2$ there was no any differences.

• IMMUNE NETWORK
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• 제11권3호
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• pp.135-154
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• 2011

The great discovery of microRNAs (miRNAs) has revolutionized current cell biology and medical science. miRNAs are small conserved non-coding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region of specific messenger RNAs for degradation or translational repression. New members of the miRNA family are being discovered on a daily basis and emerging evidence has demonstrated that miRNAs play a major role in a wide range of developmental process including cell proliferation, cell cycle, cell differentiation, metabolism, apoptosis, developmental timing, neuronal cell fate, neuronal gene expression, brain morphogenesis, muscle differentiation and stem cell division. Moreover, a large number of studies have reported links between alterations of miRNA homeostasis and pathological conditions such as cancer, psychiatric and neurological diseases, cardiovascular disease, and autoimmune disease. Interestingly, in addition, miRNA deficiencies or excesses have been correlated with a number of clinically important diseases ranging from cancer to myocardial infarction. miRNAs can repress the gene translation of hundreds of their targets and are therefore well-positioned to target a multitude of cellular mechanisms. As a consequence of extensive participation in normal functions, it is quite logical to ask the question if abnormalities in miRNAs should have importance in human diseases. Great discoveries and rapid progress in the past few years on miRNAs provide the hope that miRNAs will in the near future have a great potential in the diagnosis and treatment of many diseases. Currently, an explosive literature has focussed on the role of miRNA in human cancer and cardiovascular disease. In this review, I briefly summarize the explosive current studies about involvement of miRNA in various human cancers and cardiovascular disease.

• Journal of Acupuncture Research
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• 제20권5호
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• pp.93-106
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• 2003

Objective : To investigate the possible molecular mechanism(s) of melittin as a candidate of anti-cancer drug, we examined the effects of the compound on the growth of human lung carcinoma cell line A549. Methods: MTT, morphological changes, DAPI staining, Western blot, RT-PCR and in vitro prostaglandin E2 (PGE2) accumulation assays were performed. Results: The anti-proliferative effect by melittin treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. Melittin induced apoptotic cell death in a concentration-dependent manner, which was associated with inhibition or degradation of apoptotic target proteins such as ${\beta}$-catenin, poly(ADP-ribose) polymerase(PARP) and phospholipase $C-{\gamma}1(PLC-{\gamma}1)$. Melittin treatment inhibited the expression of cyclooxygenase-2(COX-2) and accumulation of PGE2 in aconcentration-dependent fashion. In addition, Melittin treatment induced the down-regulation of telomerase reverse transcriptase(hTERT) and proto-oncogene c-myc expression of A549 cells. Conclusions: Taken together, these findings suggest that melittin-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products, and melittin may have therapeutic potential in human lung cancer.

• 항공우주시스템공학회지
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• 제12권3호
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• pp.9-17
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• 2018

지구 관측용 소형 위성카메라의 경우, 중대형 위성에 비해 상대적으로 약한 구조 안정성으로 인해 열악한 발사환경 및 우주환경에서 광부품의 정렬오차가 발생하기 쉽다. 발생한 정렬오차는 위성카메라의 광학 성능 저하를 유발시킨다. 본 연구에서는 소형 위성 카메라의 정렬오차를 보상하기 위하여 3축 포커스 메커니즘을 제안하였다. 이 메커니즘은 3개의 압전 작동기로 구성되어 x-축, y-축 틸트 및 디스페이스(De-space) 보정을 수행할 수 있다. 포커스 메커니즘의 설계 요구조건은 슈미트-카세그레인(Schmidt-Cassegrain) 타입의 목표 광학계 설계에서 도출되었다. 부경 정렬오차 보상을 위하여 부 반사경의 뒤에 포커스 메커니즘을 부착하여 부경의 3축 운동을 제어하였다. 이 때 파면오차로 인한 광학 성능 저하를 최소화하기 위한 플렉셔를 Box-Behnken 실험계획법을 통하여 설계하였으며, ANSYS를 이용하여 파면오차 해석을 수행하였다. 제작된 포커스 메커니즘은 작동기의 수학적 모델링, PID 제어기 설계, 서보 제어실험을 통해 서보성능을 검증하였다.

• The Korean Journal of Physiology and Pharmacology
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• 제14권2호
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• pp.91-97
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• 2010

Epidermal keratinocytes overgrow in response to ultraviolet-B (UVB), which may be associated with skin photoaging and cancer development. Recently, we found that HIF-$1{\alpha}$ controls the keratinocyte cell cycle and thereby contributes to epidermal homeostasis. A further study demonstrated that HIF-$1{\alpha}$ is down-regulated by UVB and that this process is involved in UVB-induce skin hyperplasia. Therefore, we hypothesized that the forced expression of HIF-$1{\alpha}$ in keratinocytes would prevent UVB-induced keratinocyte overgrowth. Among several agents known to induce HIF-$1{\alpha}$, pyrithione-zinc (Py-Zn) overcame the UVB suppression of HIF-$1{\alpha}$ in cultured keratinocytes. Mechanistically, Py-Zn blocked the degradation of HIF-$1{\alpha}$ protein in keratinocytes, while it did not affect the synthesis of HIF-$1{\alpha}$. Moreover, the p21 cell cycle inhibitor was down-regulated after UVB exposure, but was robustly induced by Py-Zn. In mice repeatedly irradiated with UVB, the epidermis became hyperplastic and HIF-$1{\alpha}$ disappeared from nuclei of epidermal keratinocytes. However, a cream containing Py-Zn effectively prevented the skin thickening and up-regulated HIF-$1{\alpha}$ to the normal level. These results suggest that Py-Zn is a potential agent to prevent UVB-induced photoaging and skin cancer development. This work also provides insight into a molecular target for treatment of UVB-induced skin diseases.