• 정보과학회 논문지
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• 제43권9호
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• pp.974-982
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• 2016

프로그램 변이 분석은 분석대상 프로그램의 코드를 변형한 다양한 프로그램 변이를 활용해 분석대상 프로그램의 특성을 분석하는 기법이다. 효과적인 변이 분석을 위해서는 분석대상 프로그램의 동작을 다양하게 변화시키는 유용한 변형 연산자의 사용이 필수적이다. 현재까지 Java 프로그램을 대상으로 제안된 변이 생성 도구들은 변형 연산자의 종류가 제한적이거나, 최근 Java 언어 요소로 작성된 분석대상 프로그램의 경우 올바른 변이 생성을 지원하지 못하는 한계가 있다. 본 논문은 Java 프로그램을 위한 새로운 변이 생성 도구 Mutagen4J를 소개한다. Mutagen4J는 기존 연구를 통해 유용한 것으로 알려진 프로그램 변형 연산자를 추가로 지원하며, 최근 Java 언어요소를 처리함으로써, Java 프로그램에 대한 효과적인 변이 분석을 지원한다. 기존 Java 프로그램 변이 생성 도구와 비교 실험을 수행한 결과, Mutagen4J이 기존 도구보다 유용한 변이를 평균 2.3배 생성하였다.

• Clinical and Experimental Reproductive Medicine
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• 제27권2호
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• pp.179-182
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• 2000

This study was performed to determine whether the $LH{\beta}$-subunit gene missense mutation is present in Korean infertile patients with 46,XX POF women. The variants of $LH{\beta}$ exon 2 (Trp 8Arg; TGG to CGG and Ile15Thr; ATC to ACC) were studied in forty-four 46,XX idiopathic POF and 54 nonpregnant women. The $LH{\beta}$ exon 2 variants were more frequent in POF patients (20.5%) than nonpregnant (16.7%) women (p>0.05). POF patients with the variant was slightly higher than nonpregnant women with the variant.

• 한국통신학회논문지
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• 제34권2B호
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• pp.130-142
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• 2009

본 논문에서는 기존의 TCP 변종들을 바탕으로 종단 간의 경로 상에서 나타나는 네트워크 특성에 가장 적응이 잘 이루어진 변종의 알고리즘을 선택하는 TCP의 자동 적응 프레임워크를 제안한다. 프로토콜 선택의 문제가 중요한 이유는 모든 네트워크 환경에 적합한 단일 버전의 프로토콜이 존재하지 않기 때문이며, 이것은 각 네트워크 마다 TCP의 성능 저하 원인이 서로 다르기 때문이다. 이러한 판단 및 프로토콜의 적응이 가능하게 하기 위해 본 논문에서는 기존에 연구되어 왔던 여러 가지 네트워크 측정 기법들과 TCP 변종들을 하나로 합치는 과정을 거쳤으며, 여기에 각 TCP들의 성능 정보들을 제공하여 세션 중간에 적절한 전송 알고리즘을 선택하여 사용할 수 있도록 하였다. 시뮬레이션 실험을 통해 우리는 종단 간으로 여러 환경 하에서 높은 성능을 이끌어낼 수 있다는 것을 보였으며, 제안한 방법이 지금까지 연구되어온 여러 TCP 변종들이 실제로 적절하게 활용될 수 있도록 하는데 중요한 역할을 할 것으로 판단한다.

• 융합보안논문지
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• 제20권1호
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• pp.9-14
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• 2020

암호학에서 최소화에 관한 많은 연구가 이루어지고 있다. 안전한 최소의 블록암호는 이러한 연구주제 중의 하나이며, 이븐(Even)과 맨서(Mansour)는 간단한 블록암호를 제안하였다. 이븐-맨서 스킴은 하나의 치환(permutation)과 두 개의 표백화키(whitening key)를 갖는 일종의 블록암호이다. 이븐-맨서 스킴에 관련된 연구는 블록암호의 안전성과 설계에 대한 이해에 큰 도움을 준다. 이븐-맨서 스킴과 이의 변형된 스킴의 안전성을 분석하기 위한 많은 시도들이 제안되어 왔다. 우리는 이븐-맨서 스킴의 새로운 변형된 스킴을 제시하고 기존의 변형된 스킴을 소개한다. 우리는 이븐-맨서 스킴의 변형된 스킴의 안전성에 초점을 맞추고 키의 크기에 따르는 안전성의 변화를 제시한다. 우리는 이븐-맨서 스킴의 변형된 스킴의 안전성을 증명하고 일반화된 이븐-맨서 스킴이 최소의 블록암호로 적합하지 않음을 보인다.

• Genomics & Informatics
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• 제12권4호
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• pp.187-194
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• 2014

Metabolic syndrome (METS) is a disorder of energy utilization and storage and increases the risk of developing cardiovascular disease and diabetes. To identify the genetic risk factors of METS, we carried out a genome-wide association study (GWAS) for 2,657 cases and 5,917 controls in Korean populations. As a result, we could identify 2 single nucleotide polymorphisms (SNPs) with genome-wide significance level p-values (< $5{\times}10^{-8}$), 8 SNPs with genome-wide suggestive p-values ($5{\times}10^{-8}{\leq}$ p < $1{\times}10^{-5}$), and 2 SNPs of more functional variants with borderline p-values ($5{\times}10^{-5}{\leq}$ p < $1{\times}10^{-4}$). On the other hand, the multiple correction criteria of conventional GWASs exclude false-positive loci, but simultaneously, they discard many true-positive loci. To reconsider the discarded true-positive loci, we attempted to include the functional variants (nonsynonymous SNPs [nsSNPs] and expression quantitative trait loci [eQTL]) among the top 5,000 SNPs based on the proportion of phenotypic variance explained by genotypic variance. In total, 159 eQTLs and 18 nsSNPs were presented in the top 5,000 SNPs. Although they should be replicated in other independent populations, 6 eQTLs and 2 nsSNP loci were located in the molecular pathways of LPL, APOA5, and CHRM2, which were the significant or suggestive loci in the METS GWAS. Conclusively, our approach using the conventional GWAS, reconsidering functional variants and pathway-based interpretation, suggests a useful method to understand the GWAS results of complex traits and can be expanded in other genomewide association studies.

• BMB Reports
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• 제40권1호
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• pp.15-21
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• 2007

Breast cancer is the most common malignancy among women, and mutations in the BRCA1 gene produce increased susceptibility to these malignancies in certain families. In this study, the forward 1-13 exons of breast cancer associated gene BRCA1 were cloned from breast cancer cell line ZR-75-30 by RT-PCR method. Sequence analysis showed that nine BRCA1 splice forms were isolated and characterized, compared with wild-type BRCA1 gene, five splice forms of which were novel. These splice isoforms were produced from the molecular mechanism of 5' and 3' alternative splicing. All these splice forms deleting exon 11b and the locations of alternative splicing were focused on two parts:one was exons 2 and 3, and the other was exons 9 and 10. These splice forms accorded with GT-AG rule. Most these BRCA1 splice variants still kept the original reading frame. Western blot analysis indicated that some BRCA1 splice variants were expressed in ZR-75-30 cell line at the protein level. In addition, we confirmed the presence of these new transcripts of BRCA1 gene in MDA-MB-435S, K562, Hela, HLA, HIC, H9, Jurkat and human fetus samples by RT-PCR analysis. These results suggested that breast cancer associated gene BRCA1 may have unexpectedly a large number of splice variants. We hypothesized that alternative splicing of BRCA1 possibly plays a major role in the tumorigenesis of breast and/or ovarian cancer. Thus, the identification of cancer-specific splice forms will provide a novel source for the discovery of diagnostic or prognostic biomarkers and tumor antigens suitable as targets for therapeutic intervention.

• Molecules and Cells
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• 제23권3호
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• pp.391-397
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• 2007

FAM92A1 (named FAM92A1-271) belongs to the family of proteins with conserved DUF1208 domains. Its function remains elusive. We identified two novel transcript variants (FAM92A1-251, FAM92A1-289) of FAM92A1. The presence of these transcripts in cancerous and normal cells, as well as their influence on cell prolifera-tion and apoptosis, were investigated. The subcellular location of FAM92A1 was determined by fluorescence microscopy. We found that FAM92A1-271 and FAM92A1-289 were highly expressed in both normal and cancerous cells, but FAM92A1-251 was only expressed at a mo-derate level in both types of cell. Overexpression of FAM92A1-271, FAM92A1-251 and FAM92A1-289 inhibited cell proliferation, caused S-phase arrest and induced apoptosis. Subcellular localization showed that FAM92A1 localizes to the nucleus. Our results show that FAM92A1 has different splicing variants, and that it may take part in regulating cell proliferation and apoptosis.

• KSII Transactions on Internet and Information Systems (TIIS)
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• 제5권1호
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• pp.24-51
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• 2011

When supporting both voice and TCP in a wireless multihop network, there are two conflicting goals: to protect the VoIP traffic, and to completely utilize the remaining capacity for TCP. We investigate the interaction between these two popular categories of traffic and find that conventional solution approaches, such as enhanced TCP variants, priority queues, bandwidth limitation, and traffic shaping do not always achieve the goals. TCP and VoIP traffic do not easily coexist because of TCP aggressiveness and data burstiness, and the (self-) interference nature of multihop traffic. We found that enhanced TCP variants fail to coexist with VoIP in the wireless multihop scenarios. Surprisingly, even priority schemes, including those built into the MAC such as RTS/CTS or 802.11e generally cannot protect voice, as they do not account for the interference outside communication range. We present VAGP (Voice Adaptive Gateway Pacer) - an adaptive bandwidth control algorithm at the access gateway that dynamically paces wired-to-wireless TCP data flows based on VoIP traffic status. VAGP continuously monitors the quality of VoIP flows at the gateway and controls the bandwidth used by TCP flows before entering the wireless multihop. To also maintain utilization and TCP performance, VAGP employs TCP specific mechanisms that suppress certain retransmissions across the wireless multihop. Compared to previous proposals for improving TCP over wireless multihop, we show that VAGP retains the end-to-end semantics of TCP, does not require modifications of endpoints, and works in a variety of conditions: different TCP variants, multiple flows, and internet delays, different patterns of interference, different multihop topologies, and different traffic patterns.

• Parasites, Hosts and Diseases
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• 제59권5호
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• pp.447-455
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• 2021

Vivax malaria incidence in Korea is now decreased and showing a low plateau. Nowadays, vivax malaria in Korea is expected to be successfully eliminated with anti-malaria chemotherapy, primaquine, and vector control. The glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with potential hemolytic anemia after primaquine administration. This inborn disorder has a pivotal polymorphism with genetic variants and is the most prevalent X-chromosome-linked disorder. The prevalence of G6PD deficiency was previously reported negligible in Korea. As the population of multicultural families pertaining marriage immigrants and their adolescents increases, it is necessary to check G6PD deficiency for them prior to primaquine treatment for vivax malaria. The prevalence of G6PD variants and G6PD deficiency in multicultural families was performed in 7 counties and 2 cities of Jeollanam-do (Province), Gyeonggi-do, and Gangwon-do. A total of 733 blood samples of multicultural family participants were subjected to test the phenotypic and genetic G6PD deficiency status using G6PD enzyme activity quantitation kit and PCR-based G6PD genotyping kit. The G6PD phenotypic deficiency was observed in 7.8% of male adolescent participants and 3.2% of materfamilias population. Based on the PCR-based genotyping, we observed total 35 participants carrying the mutated alleles. It is proposed that primaquine prescription should seriously be considered prior to malaria treatment.

• Journal of Interdisciplinary Genomics
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• 제3권1호
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• pp.21-24
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• 2021

Purpose: Activating mutations of the calcium-sensing receptor (CASR) are a rare genetic disorder, and result in autosomal dominant hypocalcemia with hypercalciuria (ADHH). ADHH exhibited varying degrees of hypocalcemia. In this study, we report the clinical and molecular characteristics of activating variants in CASR patients diagnosed in Korea. Methods: This study included three patients with activating variants of CASR confirmed by biochemical and molecular analysis of CASR. Clinical and biochemical findings were reviewed chart retrospectively. Mutation analysis of CASR was performed by Sanger sequencing. Results: Subject 1 showed severe symptoms from the neonatal period and had difficulty in controlling the medications that were administered. Subject 2 was identified as having a novel variant of CASR with hypocalcemia and a low parathyroid hormone that were found in the neonatal period. During a course without medication, hypocalcemia occurred suddenly around 2 years of age. Subject 3 was diagnosed with hypoparathyroidism with hypocalcemic seizures starting from the neonatal period. About 4 years without taking medication with any symptom. However, at 10 years old revisited by repetitive hypocalcemic seizure events. Subject 1 and 3, were heterozygous for c.2474A>T (p.Y825F), c.2395G>A (p.E799K) located in the transmembrane domain (TMD) of CASR. Subject 2 was heterozygous for c.403A>C (S430L) located in the extracellular domain (ECD) of CASR. Conclusion: We reported 3 patients who have activating CASR variant with different onset and severity of symptoms. In the future, further study is needed to determine how the protein level according to the location of the mutation of CASR affects the degree of symptoms.