• 한국전자파학회논문지
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• 제19권6호
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• pp.677-687
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• 2008

본 논문에서 제안한 무선 인지 기반 초광대역(UWB) 시스템은 주파수 자원 이용 효율성을 높이기 위한 주파수 공유 기술인 UWB와 무선 인지 기술이 결합된 기술로, 본 논문에서는 무선 인지 기술을 이용하여 타 시스템과의 간섭을 회피하여 성능 향상을 보임을 확인하고자 한다. 본 논문에서는 타 통신 시스템과의 간섭 문제를 해결하기 위하여 무선 인지 기술을 MB-OFDM UWB 시스템에 적용하였으며, 간섭 신호 측정을 위한 방안으로는 FCC에서 제안한 간섭 온도 모델을 사용하였다. 간섭 온도 측정을 통해 시스템의 채널 용량을 계산한 후 간섭 상황을 해결하는 방안을 제안한다. 계산 과정의 인지 엔진의 연산 알고리즘으로는 유전 알고리즘을 사용하였다. 시뮬레이션 결과, 제안된 방식은 현재 문제시될 수 있는 UWB 통신 시스템에서의 간섭 문제를 해결하는데 좋은 효과가 있음을 확인하였다.

• 인터넷정보학회논문지
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• 제1권2호
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• pp.69-88
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• 2000

요약 분산 시스템의 전체적인 성능에 가장 큰 영향을 미치는 요인 중의 하나는, 소프트웨어 컴포넌트를 어떻게 효율적으로 분산시키는가 하는 것이다. 현재 태스크 기반의 시스템을 분할하여 분산 환경에 할당하는 문제는 연구가 많이 진행되었으나, 객체 지향 프로그램을 구성하는 각 객체들을 분산 객체 환경에 할당하는 기법에 대한 연구는 상대적으로 미약하다. 본 논문에서는 이미 개발되어 있는 C++ 응용 프로그램을 분할하여 C++ 객체들을 CORBA 기반의 분산 객체 환경에 할당하기 위한 그래프 모델을 정의하고, 이를 바탕으로 한 분산 객체 할당 알고리즘을 제안한다. 분산 시스템의 성능은, 주로 객체간의 병렬성, 각 프로세서에 드는 부하의 균등성, 네트워크 상의 통신 량에 의해 결정된다. 이 세 가지 요인을 동시에 최적화하는 해를 찾기 위하여. 본 논문의 분산 객체 할당 기법은 Niched Pareto 유전자 알고리즘(NPGA)에 바탕을 두고 있다. 전형적인 C++ 응용 프로그램에 대한 CORBA 시스템에서의 실험을 통하여 본 논문의 그래프 모델과 객체 할당 알고리즘의 유효성을 검증한다.

• 한국정보통신학회논문지
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• 제14권11호
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• pp.2514-2520
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• 2010

본 논문은 진화기법을 이용하여 최적의 보안 대응전략을 자동생성 하는 방법의 제안을 목적으로 한다. 정보통신 환경에 대한 침해에 의한 피해가 급증함에 따라 다양한 보안 기술에 대한 연구가 활발히 이루어지고 있다. 그러나 다양한 네트워크 환경에 대한 보안 기술들의 연통 상황을 고려한 최적의 대응 전략을 생성하는데 어려움이었다. 따라서 본 논문에서는 대응방법을 유전자로 표현하여 유전 알고리즘을 적용함으로써 대응방법들에 대한 최적의 조합으로서 최적 대응 전략을 생성하였다. 또한 시뮬레이션을 이용하여 다양한 상황에 대한 대용방법의 적용에 따른 취약성을 정량적으로 평가함으로써 적합도를 평가하였다. 끝으로 제안한 방법을 구현한 시스템에 대한 실험을 통하여 타당성을 검토하였다.

• 한국정보통신학회논문지
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• 제20권3호
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• pp.491-498
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• 2016

소프트웨어 정의 네트워크는 네트워크 제어 기능을 데이터 전송 기능으로부터 물리적으로 분리하여 소프트웨어적으로 구현한다. 광범위한 지역으로 소프트웨어 정의 네트워크를 설치하기 위해서는 다중의 제어기가 요구되며, 제어기의 배치는 소프트웨어 정의 네트워크 성능에 중요한 영향을 미친다. 본 논문에서는 소프트웨어 정의 네트워크에서 효율적인 제어기 배치를 위한 메타 휴리스틱 알고리즘인 타부 서치 알고리즘을 제안한다. 보다 좋은 결과를 효과적으로 얻기 위해 새로운 타부 서치의 이웃해 생성 방식을 제안한다. 제안된 알고리즘은 소프트웨어 정의 네트워크에서 최소 전송지연과 실행속도 관점에서 성능을 평가하며, 유전 알고리즘 및 랜덤방법과 비교하여 제안된 알고리즘의 성능이 우수함을 보인다.

• 한국시뮬레이션학회논문지
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• 제21권4호
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• pp.65-73
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• 2012

함정 전투체계는 무기체계, 정보통신 등의 기술 발전으로 인한 복잡한 전장 환경에 따라 인간이 개입하여 다양한 전술을 운용해야 한다. 따라서 에이전트 기반의 국방 M&S 시스템의 연구가 최근 들어 활발히 진행되고 있다. 그러나 현존하는 에이전트 기반 M&S 시스템은 고정된 전술을 적용하여 분석하는데 그치고 있다. 본 논문에서는 함정 교전에서 보다 적합한 대응을 찾기 위해 환경변화에 능동적으로 대처할 수 있도록 강화 학습 기능을 갖으며, 또한 유전 알고리즘을 이용하여 세대별 진화 학습 기능을 갖는 에이전트 모델링 방법론을 제안하였다. 타당성 검증을 위해 서해상에서 벌어지는 가상의 1:1 함정교전 시뮬레이션을 수행하였고, 이를 통해 함정 교전에 있어 강화 및 진화 학습이 가능함을 검증하였다.

• Preventive Nutrition and Food Science
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• 제16권4호
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• pp.394-407
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• 2011

Better understanding of the complex factors leading to human diseases will be necessary for both long term prevention and for managing short and long-term health problems. The underlying causes, leading to a global health crisis in both acute and chronic diseases, include finite global health care resources for sustained healthy human survival, the population explosion, increased environmental pollution, decreased clean air, water, food distribution, diminishing opportunities for human self-esteem, increased median life span, and the interconnection of infectious and chronic diseases. The transition of our pre-human nutritional requirements for survival to our current culturally-shaped diet has created a biologically-mismatched human dietary experience. While individual genetic, gender, and developmental stage factors contribute to human diseases, various environmental and culturally-determined factors are now contributing to both acute and chronic diseases. The transition from the hunter-gatherer to an agricultural-dependent human being has brought about a global crisis in human health. Initially, early humans ate seasonally-dependent and calorically-restricted foods, during the day, in a "feast or famine" manner. Today, modern humans eat diets of caloric abundance, at all times of the day, with foods of all seasons and from all parts of the world, that have been processed and which have been contaminated by all kinds of factors. No longer can one view, as distinct, infectious agent-related human acute diseases from chronic diseases. Moreover, while dietary and environmental chemicals could, in principle, cause disease pathogenesis by mutagenic and cytotoxic mechanisms, the primary cause is via "epigenetic", or altered gene expression, modifications in the three types of cells (e.g., adult stem; progenitor and terminally-differentiated cells of each organ) during all stages of human development. Even more significantly, alteration in the quantity of adult stem cells during early development by epigenetic chemicals could either increase or decrease the risk to various stem cell-based diseases, such as cancer, later in life. A new concept, the Barker hypothesis, has emerged that indicates pre-natal maternal dietary exposures can now affect diseases later in life. Examples from the studies of the atomic bomb survivors should illustrate this insight.

• 수산해양교육연구
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• 제28권1호
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• pp.59-68
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• 2016

For comparison of tetracycline-resistant ($Tc^R$) genes, we obtained 21 and 14 $Tc^R$ Staphylococcus spp. from marine environment and human patient, respectively. Although all isolates from human were identified as Staphylococcus aureus, higher proportion of $Tc^R$ isolates (12 out of 14) from human were utilizing tet(M) gene compared to that of $Tc^R$ isolates (6 out of 21) from marine environment. Additionally, collaborated utilization of tet(M) and erm(A) in $Tc^R-Em^R$ S. aureus in human patient, but not in $Tc^R$ Staphylococcus spp. isolates from marine environment was also characterized. Based on the nucleotide sequence of transposon related to $Tc^R$ gene, we confirmed the origin of tet(M) gene in $Tc^R$ Staphylococci isolated from marine environments and human are derived from Tn916/1545-like and Tn5801 transposon, respectively. It is the first report showing the presence of Tn5801 in all $Tc^R$ S. aureus carrying tet(M) in human patient. Alignment of the fully sequenced tet(M) from marine environmental isolates was also agreed with the determined transposons by showing the genomic mosaic structure composed with three genomic parts from Tn916/1545 and unknown transposons. Genetic characteristics of these tet(M) in environmental isolates were similar to each other but different from those in isolates from human showing only tet(M) from Tn916/5801 type. It may imply the presence of less dramatic communication of antibiotic resistant genes between Staphylococci isolated from marine environment and human.

• Journal of mucopolysaccharidosis and rare diseases
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• 제1권1호
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• pp.2-4
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• 2015

Though the rate of incidence of each rare disease, including mucopolysaccharidosis (MPS), is low, this is not the case if they are taken as a whole. Rare diseases often have genetic causes and vary in type. However, the signs and symptoms vary greatly by disease, making it difficult to make accurate diagnoses and conduct necessary research, which is why we believe it is a field that deserves more attention and research. It is important to establish an infrastructure of experts in each country and promote cooperation within the Asia-Pacific region in order to improve specialist training and communication. Given the need for a system of cooperation, the Asia Pacific MPS Network (APMN) was established by several MPS experts in South Korea, Japan, and Taiwan in January 2013. Thereafter, the Asia Pacific MPS Registry (APMR), an electronic remote data system, was established by the APMN. Then, the Association for Research of MPS & Rare Diseases (ARMRD), an academic society that supports research on MPS and other rare diseases, was established by President Dong-Kyu Jin in April in 2015. The main task of the ARMRD is to support APMN-related work. The ARMRD published a uniform guideline that reflects the characteristics and circumstances of local patients through the Korean MPS Expert Council. Now, the APMN, APMR, and the annual Korean MPS Symposium are supported by ARMRD. Organizations like the APMN and APMR are necessary because international cooperation and collaboration are needed to conduct clinical trials on those diseases. ARMRD members hope to encourage the interest of experts and researchers of MPS & rare diseases as well as active participation in the research and treatment of patients suffering from rare diseases, including MPS, to ultimately improve the quality of life of the patients as well as their families.

• 대한미생물학회지
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• 제21권2호
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• pp.171-179
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• 1986

The HLA class II region encodes a series of polymorphic glycoproteins that form cell surface heterodimers each consisting of one $\alpha$ and one $\beta$ chain. Thess class II molecules are encoded by genes clustered within three loci. DP, DQ, and DR are functfonally implicated as regulatory signals in intercellular communication during the immune resposes. The phenotypic hallmark of the HLA complex is a high degree of structural and functional polymorphism. Detailed analysis. of such polymorphisms should aid in understanding the molecular basis for associations between HLA and diseases. We have used techniques of restriction enzyme fragment analysis by Southern blotting to investigate polymorphisms associated with DQ $\beta$ class II genes on haplotypes expressing the HLA-DR4 and -DQw3 specificities. The endonucleases Hind III and Bam HI were used to identify a specific DQ $\beta$ genomic polymorphism that precisely corrresponds with the reactivity of a monoclonal antibody A-10-83, previously shown to define a serologic split of DQw3. This study identifies two allelic DQ va. riants. DQw3.1 and DQw3.2. We used these specific genotypic markers to investigate the genomic basis of the association of DR4 with insulin-dependent diabetes mellitus(IDDM) and seropositive juvenile rheumatoid arthritis(JRA). The DR4 positive IDDM demonstrate the predominant expression of DQw3.2 and the very rare expression of DQw3.l. However, in haplotype matched siblings from two IDDM families, all of the DR4 positive siblings display a IDDM-associated DQw3.2 allele. Thus, both affected and healthy individuals can carry the same haplotypes and genomic markers, demonstrating that thess specific allelic variants are genetic elements that indicate a increased risk of IDDM but are not in fact disease specific. We contrasted this result with a similar analysis of patients with another DR4-associated disease, JRA. In contrast to the preponderance of the DQw3.2 allele in IDDM, the JRA patients expressed either the DQw3.1 or the DQw3.2 allele and sometimes both, without apparent association with disease expession. The different genomic markers reported here within HLA-DQ region potentially an analysis of HLA-associated function and disease susceptibility.

• 생물정신의학
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• 제21권4호
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• pp.118-127
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• 2014

Along with language, socialization is a unique feature of the human being. There is a continuous debate regarding whether the development of socialization is innate, and conducted by the environment in the growing process, or the result of the interaction of both aspects. If socialization is the result of the interaction with the environment or is an acquired developmental process, the following question rises. "Is there a 'critical period' for the development of socialization?" Although there are a huge number of studies seeking for treatment and solutions for developmental delay or deficits of socialization, it is very complicated question to answer. Historical figures such as 'Hugh Blair' of Borgue in England, and 'the wild boy of Aveyron' in France, seem to have innate socialization deficits. Nowadays patients with non-verbal learning disorder, social communication disorder, or autism spectrum disorder seem to have genetic defects. On the other hand, Harry Harlow's monkey experiments, hikikomori of Japan, Romanian orphans and patients with reactive attachment disorder seem to display social deficits due to environmental factors. However, it is not easy to clearly draw a line between innate or acquired factors. Therefore, rather than subdividing the diseases for etiological and pathophysiological approach to heterogenous groups with the common denominator of social deficit, and for the research of pathophysiology and treatment development, the authors suggest a comprehensive concept of "social dysfunction spectrum."