• 인터넷정보학회논문지
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• 제12권2호
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• pp.1-8
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• 2011

본 논문에서는 무선인지시스템에서 스펙트럼 센싱을 효율적으로 수행하기 위한 선택적 협력 스펙트럼 검출 기법을 제안한다. 제안된 알고리즘에서는 각 무선인지 사용자가 자신의 유도비(likelihood ratio)를 기반으로 자신의 센싱 신뢰도를 평가하고, 센싱 신뢰도에 따른 타이머를 활용하는 경쟁기반의 센싱 결과 보고 메커니즘을 활용한다. 이를 통해, 제안된 선택적 협력 스펙트럼 기법에서는 가장 높은 센싱 신뢰도를 갖는 무선인지 사용자만이 국부 스펙트럼 센싱값을 융합센터로 전송함으로써, 스펙트럼 센싱의 성능을 일정한 레벨로 유지하고, 협력 스펙트럼 센싱의 단점인 제어 트래픽 및 협력 센싱 시간을 줄이는 이점을 갖는다.

• 한국전자통신학회논문지
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• 제13권5호
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• pp.1043-1050
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• 2018

본 논문은 인지 무선(CR, Cognitive Radio) 네트워크에서 우선 사용자(Primary User)의 존재 유무를 2차 사용자(Secondary User)가 결정하기 위하여 협력 센싱을 사용하는 환경에서 스펙트럼 센싱의 감지 성능을 높이기 위해 강화 학습(Reinforce learning) 기반으로 최적의 인지 무선 사용자 선택하는 협력 센싱 방안을 제안한다. 협력 센싱을 통해 파악한 전역 센싱 결과와 인지 무선 사용자의 센싱 결과 간의 유사도에 따라 정확도가 높은 사용자를 파악한다. 이 정확도를 강화학습의 보상으로 사용하여 협력 센싱을 수행할수록 전역 결정과 일치하는 센싱 정보를 전송하는 사용자를 선택할 수 있다. 실험 결과 제안한 기법이 기존 협력 센싱 대비 향상된 스펙트럼 감지 성능을 보임을 확인할 수 있다.

• 한국작물학회:학술대회논문집
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• 한국작물학회 2017년도 9th Asian Crop Science Association conference
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• pp.90-90
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• 2017

Regulation of seed dormancy is important in many grains to prevent pre-harvest sprouting. To identify and understand the gene related to seed dormancy regulation, we have screened for viviparous phenotypes of rice mutant lines generated by insertion of Ds transposon in a Korean Japonica cultivar (Dongjin) background. One of the mutants, which represented viviparous phenotype, was selected for further seed dormancy regulation studies and designated dor1. The dor1 mutant has single Ds insertion in the second exon of OsDor1 gene encoding glycine-rich protein. The seeds of dor1 mutant showed a higher germination potential and reduced abscisic acid (ABA) sensitivity compared to wild type Dongjin. Over-expression of Dor1 complements the viviparous phenotype of dor1 mutant, indicating that Dor1 function in seed dormancy regulation. Subcellular localization assay of Dor1-GFP fusion protein revealed that the OsDor1 protein mainly localized to membrane and the localization of OsDOR1 was influenced by presence of a giberelin (GA) receptor OsGID1. Further bimolecular fluorescence complementation (BiFC) analysis indicated that OsDOR1 interact with OsGID1. The combined results suggested that OsDOR1 regulates seed dormancy by interacting with OsGID1 in GA response. Additionally, expression of OsDOR1 partially complemented the cold sensitivity of Escherichia coli BX04 mutant lacking four cold shock proteins, indicating that OsDOR1 possessed RNA chaperone activity.

• 한국환경보건학회지
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• 제37권4호
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• pp.289-297
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• 2011

Objectives: To estimate the microbial contaminant load discharged from livestock farms, we randomly selected livestock farmers of cattle, swine, and fowl and collected bacterial strains from domestic animals' feces and compost samples. Recently, as multi-antibiotic-resistant bacteria and super bacteria showing resistance to a variety of antibiotics have been reported one after another, the ecological and health hazard of antibiotic-resistant bacteria is emerging as an important issue. Methods: Monitored indicator microorganism constituents were totak coliform (TC), fecal coliform (FC), and aerobic bacteria. The multi-antibiotic-resistant bacteria were identified from investigated indicator microorganisms by 16S rRNA sequencing. Results: By microbiological analysis, the largest population of aerobic bacteria ($1.5{\times}10^5$ CFU/g) was found in cattle fecal compost, and total coliforms ($1.1{\times}10^7$ CFU/g) and fecal coliforms ($1.0{\times}10^5$ CFU/g) were found primarily in swine fecal compost, while the lowest population was found in fowl fecal compost. Among the 67 strains separated from aerobic bacteria, five strains expressing high antibiotic resistance were selected in each sample. We found the multi-antibiotic resistant strains to be Shigella boydii, Staphylococcus lentus, Acinetobacter sp. and Brevibacterium luteolum. Conclusions: These results suggest that increasing numbers of multi-antibiotic-resistant bacteria in the environment have a close relation to the reckless use of antibiotics with livestock.

• IMMUNE NETWORK
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• 제24권1호
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• pp.1.1-1.6
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• 2024

IL-18 binding protein (IL-18BP) was originally discovered in 1999 while attempting to identify an IL-18 receptor ligand binding chain (also known as IL-18Rα) by subjecting concentrated human urine to an IL-18 ligand affinity column. The IL-18 ligand chromatography purified molecule was analyzed by protein microsequencing. The result revealed a novel 40 amino acid polypeptide. To isolate the complete open reading frame (ORF), various human and mouse cDNA libraries were screened using cDNA probe derived from the novel IL-18 affinity column bound molecule. The identified entire ORF gene was thought to be an IL-18Rα gene. However, IL-18BP has been proven to be a unique soluble antagonist that shares homology with a variety of viral proteins that are distinct from the IL-18Rα and IL-18Rβ chains. The IL-18BP cDNA was used to generate recombinant IL-18BP (rIL-18BP), which was indispensable for characterizing the role of IL-18BP in vitro and in vivo. Mammalian cell lines were used to produce rIL-18BP due to its glycosylation-dependent activity of IL-18BP (approximately 20 kDa). Various forms of rIL-18BP, intact, C-terminal his-tag, and Fc fusion proteins were produced for in vitro and in vivo experiments. Data showed potent neutralization of IL-18 activity, which seems promising for clinical application in immune diseases involving IL-18. However, it was a long journey from discovery to clinical use although there have been various clinical trials since IL-18BP was discovered in 1999. This review primarily covers the discovery of IL-18BP along with how basic research influences the clinical development of IL-18BP.

• Molecules and Cells
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• 제39권7호
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• pp.557-565
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• 2016

The paired immunoglobulin-like type 2 receptor (PILR) family consists of two functionally opposite members, inhibitory $PILR{\alpha}$ and activating $PILR{\beta}$ receptors. PILRs are widely expressed in various immune cells and interact with their ligands, especially CD99 expressed on activated T cells, to participate in immune responses. Here we investigated whether PILR-derived agonists inhibit ${\beta}1$ integrin activity as ligands for CD99. PILR-derived peptides as well as PILR-Fc fusion proteins prevented cell adhesion to fibronectin through the regulation of ${\beta}1$ integrin activity. Especially, PILRpep3, a representative 3-mer peptide covering the conserved motifs of the PILR extracellular domain, prevented the clustering and activation of ${\beta}1$ integrin by dephosphorylating FAK and vinculin, which are major components of focal adhesion. In addition, PILRpep3 inhibited transendothelial migration of monocytes as well as endothelial cell tube formation. Furthermore, upon intraperitoneal injection of PILRpep3 into mice with collagen-induced arthritis, the inflammatory response of rheumatoid arthritis was strongly suppressed. Taken together, these results suggest that PILR-derived agonist ligands may prevent the inflammatory reactions of rheumatoid arthritis by activating CD99.