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Institution

Yonsei University

EducationSeoul, South Korea
About: Yonsei University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Population & Cancer. The organization has 50162 authors who have published 106172 publications receiving 2279044 citations. The organization is also known as: Yonsei.
Topics: Population, Cancer, Medicine, Thin film, Breast cancer


Papers
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Journal ArticleDOI
TL;DR: In this paper, a first-principles density-functional method and tight-binding calculation of graphyne was used to find Dirac cones with reversed chirality and momentum shift of the Dirac point in graphyne.
Abstract: We study \ensuremath{\alpha}, \ensuremath{\beta}, and \ensuremath{\gamma} graphyne, a class of graphene allotropes with carbon triple bonds, using a first-principles density-functional method and tight-binding calculation. We find that graphyne has versatile Dirac cones and it is due to remarkable roles of the carbon triple bonds in electronic and atomic structures. The carbon triple bonds modulate effective hopping matrix elements and reverse their signs, resulting in Dirac cones with reversed chirality in \ensuremath{\alpha} graphyne, momentum shift of the Dirac point in \ensuremath{\beta} graphyne, and switch of the energy gap in \ensuremath{\gamma} graphyne. Furthermore, the triple bonds provide chemisorption sites of adatoms which can break sublattice symmetry while preserving planar $s{p}^{2}$-bonding networks. These features of graphyne open new possibilities for electronic applications of carbon-based two-dimensional materials and derived nanostructures.

296 citations

Journal ArticleDOI
TL;DR: This review provides a concise overview of NLRs and their role in infection, immunity, and disease, particularly from clinical perspectives.
Abstract: Nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are pattern-recognition receptors similar to toll-like receptors (TLRs). While TLRs are transmembrane receptors, NLRs are cytoplasmic receptors that play a crucial role in the innate immune response by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Based on their N-terminal domain, NLRs are divided into four subfamilies: NLRA, NLRB, NLRC, and NLRP. NLRs can also be divided into four broad functional categories: inflammasome assembly, signaling transduction, transcription activation, and autophagy. In addition to recognizing PAMPs and DAMPs, NLRs act as a key regulator of apoptosis and early development. Therefore, there are significant associations between NLRs and various diseases related to infection and immunity. NLR studies have recently begun to unveil the roles of NLRs in diseases such as gout, cryopyrin-associated periodic fever syndromes, and Crohn's disease. As these new associations between NRLs and diseases may improve our understanding of disease pathogenesis and lead to new approaches for the prevention and treatment of such diseases, NLRs are becoming increasingly relevant to clinicians. In this review, we provide a concise overview of NLRs and their role in infection, immunity, and disease, particularly from clinical perspectives.

296 citations

Journal ArticleDOI
Chiea Chuen Khor1, Chiea Chuen Khor2, Sonia Davila2, Sonia Davila1, Willemijn B. Breunis3, Yi-Ching Lee4, Chisato Shimizu5, Chisato Shimizu6, Victoria J. Wright7, Rae S. M. Yeung8, Dennis E.K. Tan1, Kar Seng Sim1, Jie Jin Wang9, Jie Jin Wang10, Tien Yin Wong11, Tien Yin Wong9, Tien Yin Wong2, Junxiong Pang1, Junxiong Pang2, Paul Mitchell9, Rolando Cimaz12, Nagib Dahdah13, Yiu-fai Cheung14, Guo Ying Huang15, Wanling Yang14, In Sook Park16, Jong-Keuk Lee16, Jer-Yuarn Wu4, Michael Levin7, Jane C. Burns6, Jane C. Burns5, David Burgner17, David Burgner18, Taco W. Kuijpers3, Martin L. Hibberd2, Martin L. Hibberd1, Yu-Lung Lau14, Jing Zhang14, Xiao Jing Ma15, Fang Liu15, Lin Wu15, Jeong Jin Yoo16, Soo-Jong Hong16, Kwi Joo Kim16, Jae-Jung Kim16, Young-Mi Park16, Young Mi Hong19, Sejung Sohn19, Gi Young Jang20, Kee Soo Ha20, Hyo Kyoung Nam20, Jung Hye Byeon20, Sin Weon Yun21, Myung Ki Han16, Kyung-Yil Lee22, Ja Young Hwang22, Jung Woo Rhim22, Min Seob Song23, Hyoung Doo Lee24, Dong Soo Kim25, Jae Moo Lee25, Jeng Sheng Chang, Fuu Jen Tsai26, Chi Di Liang27, Ming-Ren Chen28, Hsin Chi28, Nan Chang Chiu28, Fu Yuan Huang28, Luan-Yin Chang29, Li-Min Huang29, Ho-Chang Kuo27, Kao Pin Huang27, Meng Luen Lee, Betau Hwang30, Yhu Chering Huang27, Pi Chang Lee, Miranda Odam16, Miranda Odam18, Frank T. Christiansen18, Campbell S. Witt31, Paul N. Goldwater5, Paul N. Goldwater32, Nigel Curtis17, Nigel Curtis16, Pamela Palasanthiran5, John B. Ziegler5, Michael D. Nissen33, Clare Nourse33, Irene M. Kuipers3, J Ottenkamp3, Judy Geissler3, Maarten H Biezeveld3, Carline E. Tacke3, Luc Filippini5, Paul A. Brogan34, Nigel Klein34, Vanita Shah34, M J Dillon34, Robert Booy35, Delane Shingadia35, Anu Bose35, Thomas Mukasa35, Robert Tulloh36, Colin Michie37, Jane W. Newburger38, Annette L. Baker38, Anne H. Rowley39, Stanford T. Shulman39, Wilbert H. Mason40, Masato Takahashi40, Marian E. Melish5, Adriana H. Tremoulet6, Ananth C. Viswanathan41, Elena Rochtchina41, John Attia10, Rodney J. Scott, Elizabeth G. Holliday, Stephen B. Harrap9 
TL;DR: The involvement of the FCGR2A locus may have implications for understanding immune activation in Kawasaki disease pathogenesis and the mechanism of response to intravenous immunoglobulin, the only proven therapy for this disease.
Abstract: Kawasaki disease is a systemic vasculitis of unknown etiology, with clinical observations suggesting a substantial genetic contribution to disease susceptibility. We conducted a genome-wide association study and replication analysis in 2,173 individuals with Kawasaki disease and 9,383 controls from five independent sample collections. Two loci exceeded the formal threshold for genome-wide significance. The first locus is a functional polymorphism in the IgG receptor gene FCGR2A (encoding an H131R substitution) (rs1801274; P = 7.35 × 10(-11), odds ratio (OR) = 1.32), with the A allele (coding for histadine) conferring elevated disease risk. The second locus is at 19q13, (P = 2.51 × 10(-9), OR = 1.42 for the rs2233152 SNP near MIA and RAB4B; P = 1.68 × 10(-12), OR = 1.52 for rs28493229 in ITPKC), which confirms previous findings(1). The involvement of the FCGR2A locus may have implications for understanding immune activation in Kawasaki disease pathogenesis and the mechanism of response to intravenous immunoglobulin, the only proven therapy for this disease.

295 citations

Journal ArticleDOI
TL;DR: The results of this study provide useful guidelines for reliable variant identification from deep sequencing of personal genomes by observing different biases toward specific types of SNP genotyping errors by the different variant callers.
Abstract: The success of clinical genomics using next generation sequencing (NGS) requires the accurate and consistent identification of personal genome variants. Assorted variant calling methods have been developed, which show low concordance between their calls. Hence, a systematic comparison of the variant callers could give important guidance to NGS-based clinical genomics. Recently, a set of high-confident variant calls for one individual (NA12878) has been published by the Genome in a Bottle (GIAB) consortium, enabling performance benchmarking of different variant calling pipelines. Based on the gold standard reference variant calls from GIAB, we compared the performance of thirteen variant calling pipelines, testing combinations of three read aligners—BWA-MEM, Bowtie2 and Novoalign—and four variant callers—Genome Analysis Tool Kit HaplotypeCaller (GATK-HC), Samtools mpileup, Freebayes and Ion Proton Variant Caller (TVC), for twelve data sets for the NA12878 genome sequenced by different platforms including Illumina2000, Illumina2500 and Ion Proton, with various exome capture systems and exome coverage. We observed different biases toward specific types of SNP genotyping errors by the different variant callers. The results of our study provide useful guidelines for reliable variant identification from deep sequencing of personal genomes.

295 citations

Proceedings ArticleDOI
01 Jun 2019
TL;DR: Zhang et al. as discussed by the authors proposed an Attention-based Dropout Layer (ADL) which utilizes the self-attention mechanism to process the feature maps of the model, which is composed of two key components: hiding the most discriminative part from the model for capturing the integral extent of object, and highlighting the informative region for improving the recognition power.
Abstract: Weakly Supervised Object Localization (WSOL) techniques learn the object location only using image-level labels, without location annotations. A common limitation for these techniques is that they cover only the most discriminative part of the object, not the entire object. To address this problem, we propose an Attention-based Dropout Layer (ADL), which utilizes the self-attention mechanism to process the feature maps of the model. The proposed method is composed of two key components: 1) hiding the most discriminative part from the model for capturing the integral extent of object, and 2) highlighting the informative region for improving the recognition power of the model. Based on extensive experiments, we demonstrate that the proposed method is effective to improve the accuracy of WSOL, achieving a new state-of-the-art localization accuracy in CUB-200-2011 dataset. We also show that the proposed method is much more efficient in terms of both parameter and computation overheads than existing techniques.

295 citations


Authors

Showing all 50632 results

NameH-indexPapersCitations
Younan Xia216943175757
Peer Bork206697245427
Ralph Weissleder1841160142508
Hyun-Chul Kim1764076183227
Gregory Y.H. Lip1693159171742
Yongsun Kim1562588145619
Jongmin Lee1502257134772
James M. Tiedje150688102287
Guanrong Chen141165292218
Kazunori Kataoka13890870412
Herbert Y. Meltzer137114881371
Peter M. Rothwell13477967382
Tae Jeong Kim132142093959
Shih-Chang Lee12878761350
Ming-Hsuan Yang12763575091
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023203
2022753
20217,800
20207,310
20196,827
20186,298