Genome-Wide Association Study Identifies Novel Susceptibility Genes Associated with Coronary Artery Aneurysm Formation in Kawasaki Disease
Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as di...
Saved in:
Published in | PloS one Vol. 11; no. 5; p. e0154943 |
---|---|
Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Public Library of Science
12.05.2016
Public Library of Science (PLoS) |
Subjects | |
Online Access | Get full text |
ISSN | 1932-6203 1932-6203 |
DOI | 10.1371/journal.pone.0154943 |
Cover
Abstract | Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10(-9); OR = 32.22) and rs7922552 (P = 8.43 × 10(-9); OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10(-9); OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. |
---|---|
AbstractList | Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10
−9
; OR = 32.22) and rs7922552 (P = 8.43 × 10
−9
; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10
−9
; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 10-9; OR = 32.22) and rs7922552 (P = 8.43 10-9; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 10-9; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 x 10.sup.-9 ; OR = 32.22) and rs7922552 (P = 8.43 x 10.sup.-9 ; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 x 10.sup.-9 ; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10−9; OR = 32.22) and rs7922552 (P = 8.43 × 10−9; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10−9; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10(-9); OR = 32.22) and rs7922552 (P = 8.43 × 10(-9); OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10(-9); OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10 −9 ; OR = 32.22) and rs7922552 (P = 8.43 × 10 −9 ; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10 −9 ; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine. |
Audience | Academic |
Author | Jiao, Fuyong Kuo, Hsing-Chun Andrade, Jorge Kuo, Ho-Chang Chan, Wen-Ching Guo, Mindy Ming-Huey Yu, Hong-Ren Huang, Fu-Chen Huang, Ying-Hsien Li, Sung-Chou |
AuthorAffiliation | 1 Department of Pediatrics and Kawasaki Disease Center, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan 2 Genomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan Weill Medical College of Cornell University, UNITED STATES 4 Department of Nursing, Chang Gung University of Science and Technology, Chiayi, Taiwan 5 Center for Research Informatics, The University of Chicago, Chicago, Illinois, 60637, United States of America 3 Children's Hospital of Shaanxi Provincial People's Hospital and Jiaotong University, Xi'an, China |
AuthorAffiliation_xml | – name: 4 Department of Nursing, Chang Gung University of Science and Technology, Chiayi, Taiwan – name: 3 Children's Hospital of Shaanxi Provincial People's Hospital and Jiaotong University, Xi'an, China – name: 5 Center for Research Informatics, The University of Chicago, Chicago, Illinois, 60637, United States of America – name: Weill Medical College of Cornell University, UNITED STATES – name: 1 Department of Pediatrics and Kawasaki Disease Center, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan – name: 2 Genomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan |
Author_xml | – sequence: 1 givenname: Ho-Chang surname: Kuo fullname: Kuo, Ho-Chang – sequence: 2 givenname: Sung-Chou surname: Li fullname: Li, Sung-Chou – sequence: 3 givenname: Mindy Ming-Huey surname: Guo fullname: Guo, Mindy Ming-Huey – sequence: 4 givenname: Ying-Hsien surname: Huang fullname: Huang, Ying-Hsien – sequence: 5 givenname: Hong-Ren surname: Yu fullname: Yu, Hong-Ren – sequence: 6 givenname: Fu-Chen surname: Huang fullname: Huang, Fu-Chen – sequence: 7 givenname: Fuyong surname: Jiao fullname: Jiao, Fuyong – sequence: 8 givenname: Hsing-Chun surname: Kuo fullname: Kuo, Hsing-Chun – sequence: 9 givenname: Jorge surname: Andrade fullname: Andrade, Jorge – sequence: 10 givenname: Wen-Ching orcidid: 0000-0003-0034-7277 surname: Chan fullname: Chan, Wen-Ching |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27171184$$D View this record in MEDLINE/PubMed |
BookMark | eNqNk9tu0zAcxiM0xA7wBggiISG4aPExcbhAqgobFROTKIdLy7Gd1iOJi-1s9BV4atw1Rc00AcqFI_v3ffb_dJwctLbVSfIYgjHEOXx1aTvXinq8ittjACkpCL6XHMECo1GGAD7Y-z9Mjr2_BIBilmUPkkOUwxxCRo6SX2e6tY0efTNKpxPvrTQiGNum89CpdTpTug2mMtqnH-2VrtN556VeBVOa2oR1GtXxaKfTKr02YZlOrbOtcOt04oLeLK3u3No36al1zdbetOkHcS28-G7St8Zr4fXD5H4laq8f9etJ8uX03efp-9H5xdlsOjkfyRzRMIJYMlFRWhZ5pqWkGcwzwWgOWVYRpjBViCBWSoIzIktUlkRiqkGesSJXKJP4JHm69V3V1vM-jZ7DnDFKMAYkErMtoay45CtnmhgMt8Lwmw3rFly4YGStuSaqJAxIJVFFICriHWWBBZEIKVAQGr3e9Ld1ZaOVjPl0oh6YDk9as-QLe8UJyygoUDR40Rs4-6PTPvDGxBrUtWi17eK7GaAUwCLD_0ZzVpCCErR51rNb6N2J6KmFiLGatrLxiXJjyicxNpwDDGGkxndQ8VO6MTK2Z2Xi_kDwciCITNA_w0J03vPZ_NP_sxdfh-zzPXapRR2W3tbdpuP8EHyyX5Q_1djNRQRebwHprPdOV1yacNO5MTRTcwj4Zgh3SeObIeT9EEYxuSXe-f9V9ht4djYQ |
CitedBy_id | crossref_primary_10_1186_s12920_025_02121_8 crossref_primary_10_1016_j_cca_2017_05_019 crossref_primary_10_1016_j_jpeds_2019_05_024 crossref_primary_10_1186_s12864_018_5142_7 crossref_primary_10_3389_fmed_2019_00111 crossref_primary_10_1186_s12865_018_0282_8 crossref_primary_10_5808_gi_21046 crossref_primary_10_1155_2019_2849695 crossref_primary_10_3389_fped_2022_834306 crossref_primary_10_1007_s00246_018_1992_7 crossref_primary_10_3389_fimmu_2019_02813 crossref_primary_10_1016_j_oooo_2022_08_013 crossref_primary_10_1038_s41598_019_51137_5 crossref_primary_10_1007_s00431_017_2937_5 crossref_primary_10_1155_2018_8638096 crossref_primary_10_1002_jcla_23125 crossref_primary_10_12677_ACM_2024_142437 crossref_primary_10_3390_genes13010111 crossref_primary_10_4070_kcj_2023_0244 crossref_primary_10_1089_gtmb_2024_0035 crossref_primary_10_3389_fcvm_2020_00094 crossref_primary_10_1038_s41525_024_00419_7 crossref_primary_10_1186_s12969_021_00494_5 crossref_primary_10_4070_kcj_2018_0365 crossref_primary_10_1016_j_mvr_2021_104269 crossref_primary_10_1111_1756_185X_13218 crossref_primary_10_1155_2022_2114699 crossref_primary_10_2147_JIR_S331727 crossref_primary_10_1080_10903127_2020_1745339 crossref_primary_10_1038_s41598_020_60025_2 crossref_primary_10_1016_j_med_2021_05_007 crossref_primary_10_1016_j_clim_2020_108385 crossref_primary_10_1016_S2352_4642_24_00169_X crossref_primary_10_3389_fimmu_2018_01892 crossref_primary_10_1016_j_cyto_2018_08_029 crossref_primary_10_1038_s41584_022_00797_1 crossref_primary_10_1055_s_0044_1791196 crossref_primary_10_3389_fimmu_2022_802690 crossref_primary_10_3389_fped_2021_624798 crossref_primary_10_3389_fmed_2021_738850 crossref_primary_10_3390_brainsci12081022 crossref_primary_10_1038_s41431_021_00838_5 crossref_primary_10_1371_journal_pone_0184692 crossref_primary_10_1016_j_jfma_2017_07_001 crossref_primary_10_1016_j_drudis_2016_08_004 crossref_primary_10_1097_CRD_0000000000000786 |
Cites_doi | 10.1111/j.1365-2249.2009.03949.x 10.1016/j.jacc.2010.05.045 10.1161/CIRCRESAHA.116.305834 10.1007/s10875-012-9668-1 10.1097/00006454-199812000-00009 10.1371/journal.pone.0105195 10.1038/jhg.2013.43 10.1002/mgg3.79 10.1007/s00246-012-0223-x 10.1136/archdischild-2014-306427 10.1002/art.38976 10.1186/2045-3701-4-67 10.1371/journal.pone.0021800 10.1016/j.pedneo.2011.11.003 10.1016/j.imbio.2012.04.004 10.1038/srep04247 10.1111/j.1399-3038.2008.00779.x 10.1007/s00431-009-0925-0 10.1038/ng.2007.59 10.1007/s00246-011-0143-1 10.1371/journal.pone.0016853 10.1016/j.yjmcc.2013.04.021 10.1038/ng.981 10.1038/nprot.2010.182 10.1007/s11033-012-2022-0 10.1371/journal.pone.0081384 10.1007/s00439-010-0937-x 10.1371/journal.pone.0069685 10.1002/art.24261 10.1186/s12864-015-2323-5 10.1371/journal.pone.0017370 10.1038/tpj.2011.45 10.1111/all.12558 10.1038/jhg.2010.154 10.1007/s00431-006-0251-8 10.1586/eri.12.101 10.1038/ng.2227 10.1016/j.trsl.2013.02.002 10.1542/peds.2007-0815 10.7603/s40681-014-0010-5 10.1086/323155 10.1016/S0140-6736(04)16814-1 10.1097/INF.0000000000001039 10.1038/nrd2983 10.1161/01.ATV.0000065385.47152.FD 10.1038/gene.2014.47 10.1086/519795 10.3109/14397595.2013.854061 10.1007/s00439-013-1279-2 10.1038/srep05208 10.1007/s00431-009-1099-5 10.1097/BOR.0b013e32833cf051 10.1371/journal.pone.0103329 10.1371/journal.pgen.1000319 10.1111/j.1365-2249.2005.02821.x 10.1097/HCO.0b013e3283459893 10.1111/j.1744-313X.2010.00943.x 10.1371/journal.pone.0072037 10.1038/srep08194 10.1371/journal.pone.0091118 10.1111/j.1600-065X.2011.01055.x 10.3345/kjp.2012.55.1.18 10.1016/0735-1097(96)00099-X 10.1038/ng.2220 10.1002/jcla.21706 10.1371/journal.pone.0038635 |
ContentType | Journal Article |
Copyright | COPYRIGHT 2016 Public Library of Science 2016 Kuo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2016 Kuo et al 2016 Kuo et al |
Copyright_xml | – notice: COPYRIGHT 2016 Public Library of Science – notice: 2016 Kuo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2016 Kuo et al 2016 Kuo et al |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM IOV ISR 3V. 7QG 7QL 7QO 7RV 7SN 7SS 7T5 7TG 7TM 7U9 7X2 7X7 7XB 88E 8AO 8C1 8FD 8FE 8FG 8FH 8FI 8FJ 8FK ABJCF ABUWG AEUYN AFKRA ARAPS ATCPS AZQEC BBNVY BENPR BGLVJ BHPHI C1K CCPQU D1I DWQXO FR3 FYUFA GHDGH GNUQQ H94 HCIFZ K9. KB. KB0 KL. L6V LK8 M0K M0S M1P M7N M7P M7S NAPCQ P5Z P62 P64 PATMY PDBOC PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PTHSS PYCSY RC3 7X8 5PM DOA |
DOI | 10.1371/journal.pone.0154943 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Gale In Context: Opposing Viewpoints Gale In Context: Science ProQuest Central (Corporate) Animal Behavior Abstracts Bacteriology Abstracts (Microbiology B) Biotechnology Research Abstracts Nursing & Allied Health Database Ecology Abstracts Entomology Abstracts (Full archive) Immunology Abstracts Meteorological & Geoastrophysical Abstracts Nucleic Acids Abstracts Virology and AIDS Abstracts Agricultural Science Collection Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) ProQuest Pharma Collection Public Health Database Technology Research Database ProQuest SciTech Collection ProQuest Technology Collection ProQuest Natural Science Journals Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Materials Science & Engineering Collection ProQuest Central (Alumni) ProQuest One Sustainability ProQuest Central UK/Ireland Advanced Technologies & Aerospace Collection Agricultural & Environmental Science Collection ProQuest Central Essentials Biological Science Collection ProQuest Central Technology Collection Natural Science Collection Environmental Sciences and Pollution Management ProQuest One Community College ProQuest Materials Science Collection ProQuest Central Korea Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student AIDS and Cancer Research Abstracts SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Materials Science Database Nursing & Allied Health Database (Alumni Edition) Meteorological & Geoastrophysical Abstracts - Academic ProQuest Engineering Collection Biological Sciences Agriculture Science Database ProQuest Health & Medical Collection ProQuest Medical Database Algology Mycology and Protozoology Abstracts (Microbiology C) Biological Science Database Engineering Database Nursing & Allied Health Premium Advanced Technologies & Aerospace Database ProQuest Advanced Technologies & Aerospace Collection Biotechnology and BioEngineering Abstracts Environmental Science Database Materials Science Collection ProQuest Central Premium ProQuest One Academic (New) ProQuest Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition Engineering Collection Environmental Science Collection Genetics Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Agricultural Science Database Publicly Available Content Database ProQuest Central Student ProQuest Advanced Technologies & Aerospace Collection ProQuest Central Essentials Nucleic Acids Abstracts SciTech Premium Collection Environmental Sciences and Pollution Management ProQuest One Applied & Life Sciences ProQuest One Sustainability Health Research Premium Collection Meteorological & Geoastrophysical Abstracts Natural Science Collection Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) Engineering Collection Advanced Technologies & Aerospace Collection Engineering Database Virology and AIDS Abstracts ProQuest Biological Science Collection ProQuest One Academic Eastern Edition Agricultural Science Collection ProQuest Hospital Collection ProQuest Technology Collection Health Research Premium Collection (Alumni) Biological Science Database Ecology Abstracts ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts Environmental Science Collection Entomology Abstracts Nursing & Allied Health Premium ProQuest Health & Medical Complete ProQuest One Academic UKI Edition Environmental Science Database ProQuest Nursing & Allied Health Source (Alumni) Engineering Research Database ProQuest One Academic Meteorological & Geoastrophysical Abstracts - Academic ProQuest One Academic (New) Technology Collection Technology Research Database ProQuest One Academic Middle East (New) Materials Science Collection ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Central ProQuest Health & Medical Research Collection Genetics Abstracts ProQuest Engineering Collection Biotechnology Research Abstracts Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Bacteriology Abstracts (Microbiology B) Algology Mycology and Protozoology Abstracts (Microbiology C) Agricultural & Environmental Science Collection AIDS and Cancer Research Abstracts Materials Science Database ProQuest Materials Science Collection ProQuest Public Health ProQuest Nursing & Allied Health Source ProQuest SciTech Collection Advanced Technologies & Aerospace Database ProQuest Medical Library Animal Behavior Abstracts Materials Science & Engineering Collection Immunology Abstracts ProQuest Central (Alumni) MEDLINE - Academic |
DatabaseTitleList | Genetics Abstracts Agricultural Science Database MEDLINE - Academic MEDLINE |
Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 4 dbid: 8FG name: ProQuest Technology Collection url: https://search.proquest.com/technologycollection1 sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Sciences (General) Medicine |
DocumentTitleAlternate | CAA in Kawasaki Disease |
EISSN | 1932-6203 |
EndPage | e0154943 |
ExternalDocumentID | 1788543304 oai_doaj_org_article_e4db480cdc2f412997db93a4c22d0945 PMC4865092 4054542571 A453370311 27171184 10_1371_journal_pone_0154943 |
Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
GeographicLocations | Chicago Illinois United States--US Illinois China Taiwan |
GeographicLocations_xml | – name: China – name: Taiwan – name: United States--US – name: Illinois – name: Chicago Illinois |
GrantInformation_xml | – fundername: NCATS NIH HHS grantid: UL1 TR000430 – fundername: ; grantid: CMRPG8B0212 – fundername: ; grantid: CMRPG8D0521 – fundername: ; grantid: MOST 102-2314-B-182-053-MY3 – fundername: ; grantid: CMRPG8C1082 – fundername: ; grantid: CLRPG8D0112 – fundername: ; grantid: CMRPG8D0032 – fundername: ; grantid: UL1 TR000430 – fundername: ; grantid: CMRPG8D1561 |
GroupedDBID | --- 123 29O 2WC 53G 5VS 7RV 7X2 7X7 7XC 88E 8AO 8C1 8CJ 8FE 8FG 8FH 8FI 8FJ A8Z AAFWJ AAUCC AAWOE AAYXX ABDBF ABIVO ABJCF ABUWG ACGFO ACIHN ACIWK ACPRK ACUHS ADBBV ADRAZ AEAQA AENEX AEUYN AFKRA AFPKN AFRAH AHMBA ALIPV ALMA_UNASSIGNED_HOLDINGS AOIJS APEBS ARAPS ATCPS BAWUL BBNVY BCNDV BENPR BGLVJ BHPHI BKEYQ BPHCQ BVXVI BWKFM CCPQU CITATION CS3 D1I D1J D1K DIK DU5 E3Z EAP EAS EBD EMOBN ESX EX3 F5P FPL FYUFA GROUPED_DOAJ GX1 HCIFZ HH5 HMCUK HYE IAO IEA IGS IHR IHW INH INR IOV IPY ISE ISR ITC K6- KB. KQ8 L6V LK5 LK8 M0K M1P M48 M7P M7R M7S M~E NAPCQ O5R O5S OK1 OVT P2P P62 PATMY PDBOC PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO PTHSS PV9 PYCSY RNS RPM RZL SV3 TR2 UKHRP WOQ WOW ~02 ~KM 3V. BBORY CGR CUY CVF ECM EIF IPNFZ NPM RIG PMFND ESTFP PJZUB PPXIY PQGLB PUEGO 7QG 7QL 7QO 7SN 7SS 7T5 7TG 7TM 7U9 7XB 8FD 8FK AZQEC C1K DWQXO FR3 GNUQQ H94 K9. KL. M7N P64 PKEHL PQEST PQUKI RC3 7X8 5PM AAPBV ABPTK N95 |
ID | FETCH-LOGICAL-c725t-13c8af55b976ecc56176a857186f48d35d2428bc4364cb2bb4c35e076897d26c3 |
IEDL.DBID | M48 |
ISSN | 1932-6203 |
IngestDate | Sun Jul 02 11:04:14 EDT 2023 Wed Aug 27 01:26:38 EDT 2025 Thu Aug 21 14:23:29 EDT 2025 Fri Sep 05 12:38:55 EDT 2025 Fri Sep 05 13:00:13 EDT 2025 Fri Jul 25 11:45:46 EDT 2025 Thu Sep 25 01:20:07 EDT 2025 Tue Jun 10 20:46:50 EDT 2025 Fri Jun 27 04:22:37 EDT 2025 Fri Jun 27 04:42:00 EDT 2025 Thu May 22 21:32:07 EDT 2025 Wed Feb 19 02:41:45 EST 2025 Tue Jul 01 00:48:33 EDT 2025 Thu Apr 24 23:06:45 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 5 |
Language | English |
License | This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Creative Commons Attribution License |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c725t-13c8af55b976ecc56176a857186f48d35d2428bc4364cb2bb4c35e076897d26c3 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: Ho-Chang Kuo WCC. Performed the experiments: Ho-Chang Kuo MMG YHH Hsing-Chun Kuo. Analyzed the data: WCC. Contributed reagents/materials/analysis tools: Ho-Chang Kuo MMG YHH HRY FCH FJ. Wrote the paper: WCC YHH JA Ho-Chang Kuo. Organised and collected data: SCL. |
ORCID | 0000-0003-0034-7277 |
OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1371/journal.pone.0154943 |
PMID | 27171184 |
PQID | 1788543304 |
PQPubID | 1436336 |
ParticipantIDs | plos_journals_1788543304 doaj_primary_oai_doaj_org_article_e4db480cdc2f412997db93a4c22d0945 pubmedcentral_primary_oai_pubmedcentral_nih_gov_4865092 proquest_miscellaneous_1805501963 proquest_miscellaneous_1789495425 proquest_journals_1788543304 gale_infotracmisc_A453370311 gale_infotracacademiconefile_A453370311 gale_incontextgauss_ISR_A453370311 gale_incontextgauss_IOV_A453370311 gale_healthsolutions_A453370311 pubmed_primary_27171184 crossref_citationtrail_10_1371_journal_pone_0154943 crossref_primary_10_1371_journal_pone_0154943 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2016-05-12 |
PublicationDateYYYYMMDD | 2016-05-12 |
PublicationDate_xml | – month: 05 year: 2016 text: 2016-05-12 day: 12 |
PublicationDecade | 2010 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States – name: San Francisco – name: San Francisco, CA USA |
PublicationTitle | PloS one |
PublicationTitleAlternate | PLoS One |
PublicationYear | 2016 |
Publisher | Public Library of Science Public Library of Science (PLoS) |
Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
References | N Chopra (ref51) 2011; 26 NE Bowles (ref37) 2014; 2 A Shendre (ref46) 2014; 15 GM Clarke (ref48) 2011; 6 JC Burns (ref67) 1998; 17 K Maiellaro-Rafferty (ref52) 2013; 60 J Duan (ref29) 2014; 9 FJ Tsai (ref17) 2011; 6 CE Tacke (ref13) 2012; 10 Q Peng (ref23) 2012; 33 YJ Lin (ref43) 2009; 60 S Guiducci (ref64) 2011; 29 Y Onouchi (ref26) 2013; 13 Y Onouchi (ref19) 2012; 44 C Zhou (ref66) 2015; 8 D Burgner (ref14) 2009; 5 YC Huang (ref44) 2010; 37 T Oharaseki (ref71) 2014; 24 JJ Kim (ref34) 2012; 33 HC Kuo (ref38) 2014; 9 S Purcell (ref47) 2007; 81 YM Choi (ref56) 2012; 55 JJ Kim (ref35) 2013; 58 HC Kuo (ref8) 2012; 53 HC Kuo (ref33) 2015; 67 TM Ko (ref61) 2015; 116 RS Yeung (ref12) 2010; 22 HC Kuo (ref7) 2009; 20 WN Tseng (ref58) 2014; 9 RM Oates-Whitehead (ref3) 2003 T Matsubara (ref57) 2005; 141 W Wang (ref30) 2014; 4 IC Lin (ref59) 2012; 7 PJ Gavin (ref69) 2003; 23 H Igarashi (ref63) 2001; 19 MT Lin (ref36) 2013; 161 D Song (ref6) 2009; 168 HC Kuo (ref60) 2012; 32 JJ Kim (ref16) 2011; 129 J Lou (ref22) 2012; 39 CJ Chang (ref32) 2013; 8 KC Hsueh (ref39) 2010; 169 Y Youn (ref68) 2016; 35 YC Lee (ref18) 2012; 44 MT Lin (ref9) 2015; 100 YJ Lin (ref41) 2014; 4 H Wulff (ref55) 2009; 8 S Naoe (ref10) 1991; 41 LL Minich (ref4) 2007; 120 YJ Lin (ref45) 2013; 8 J Lou (ref31) 2015; 5 TJ Brown (ref11) 2001; 184 E Purevjav (ref53) 2010; 56 JC Burns (ref1) 2004; 364 JM Hildebrand (ref54) 2011; 244 CC Khor (ref15) 2011; 43 F Supek (ref49) 2011; 6 MM Guo (ref62) 2015; 70 HC Kuo (ref25) 2013; 8 HC Kuo (ref21) 2011; 6 AH Rowley (ref65) 2015; 16 Y Onouchi (ref20) 2008; 40 W Wang (ref27) 2014; 4 IC Lin (ref70) 2013; 218 AC Lau (ref72) 2009; 157 JC Burns (ref2) 1996; 28 Y Yan (ref28) 2013; 132 T Kim (ref5) 2007; 166 HC Kuo (ref24) 2011; 56 YT Chen (ref40) 2014; 28 YJ Lin (ref42) 2014; 4 G Mastrototaro (ref50) 2015 22081228 - Nat Genet. 2011 Dec;43(12):1241-6 25585854 - Allergy. 2015 Mar;70(3):310-8 25987543 - Cardiovasc Res. 2015 Jul 15;107(2):216-25 16045726 - Clin Exp Immunol. 2005 Sep;141(3):381-7 19604270 - Clin Exp Immunol. 2009 Aug;157(2):300-9 11528596 - J Infect Dis. 2001 Oct 1;184(7):940-3 23199405 - Expert Rev Anti Infect Ther. 2012 Oct;10(10):1203-15 1785339 - Acta Pathol Jpn. 1991 Nov;41(11):785-97 21430528 - Curr Opin Cardiol. 2011 May;26(3):196-203 22446962 - Nat Genet. 2012 May;44(5):517-21 22392047 - J Clin Immunol. 2012 Aug;32(4):746-52 17701901 - Am J Hum Genet. 2007 Sep;81(3):559-75 22105492 - Pediatr Cardiol. 2012 Apr;33(4):513-20 25122210 - PLoS One. 2014;9(8):e105195 21987091 - Pharmacogenomics J. 2013 Feb;13(1):52-9 23632046 - J Mol Cell Cardiol. 2013 Jul;60:151-60 21221998 - Hum Genet. 2011 May;129(5):487-95 25520923 - Biomedicine (Taipei). 2014;4:10 22359526 - Korean J Pediatr. 2012 Jan;55(1):18-23 25485088 - Cell Biosci. 2014 Nov 19;4(1):67 21789182 - PLoS One. 2011;6(7):e21800 20951326 - J Am Coll Cardiol. 2010 Oct 26;56(18):1493-502 25605650 - Circ Res. 2015 Feb 27;116(5):876-83 21533171 - PLoS One. 2011;6(4):e17370 26673981 - Pediatr Infect Dis J. 2016 Apr;35(4):457-9 24903211 - Sci Rep. 2014;4:5208 19159953 - Eur J Pediatr. 2009 Nov;168(11):1315-21 19438983 - Pediatr Allergy Immunol. 2009 May;20(3):266-72 18084290 - Nat Genet. 2008 Jan;40(1):35-42 24023612 - PLoS One. 2013;8(8):e72037 22737215 - PLoS One. 2012;7(6):e38635 8752822 - J Am Coll Cardiol. 1996 Jul;28(1):253-7 14584002 - Cochrane Database Syst Rev. 2003;(4):CD004000 26884859 - Int J Clin Exp Pathol. 2015;8(12):15879-86 24278430 - PLoS One. 2013;8(11):e81384 21385556 - Clin Exp Rheumatol. 2011 Jan-Feb;29(1 Suppl 64):S121-5 22633994 - Immunobiology. 2013 Feb;218(2):201-12 19180512 - Arthritis Rheum. 2009 Feb;60(2):604-10 25077179 - Mol Genet Genomic Med. 2014 Jul;2(4):356-61 24652666 - J Clin Lab Anal. 2014 Nov;28(6):435-9 22348488 - Pediatr Neonatol. 2012 Feb;53(1):4-11 25470559 - Arthritis Rheumatol. 2015 Mar;67(3):828-36 21160486 - J Hum Genet. 2011 Feb;56(2):161-5 19949402 - Nat Rev Drug Discov. 2009 Dec;8(12):982-1001 20618519 - Int J Immunogenet. 2010 Dec;37(6):439-43 26679344 - BMC Genomics. 2015;16:1076 23677057 - J Hum Genet. 2013 Aug;58(8):521-5 22017431 - Immunol Rev. 2011 Nov;244(1):55-74 15302199 - Lancet. 2004 Aug 7-13;364(9433):533-44 22361738 - Pediatr Cardiol. 2012 Oct;33(7):1046-53 25093412 - PLoS One. 2014;9(8):e103329 20616737 - Curr Opin Rheumatol. 2010 Sep;22(5):551-60 24621571 - PLoS One. 2014;9(3):e91118 24577620 - Sci Rep. 2014;4:4247 23454411 - Transl Res. 2013 Jun;161(6):513-5 25564534 - Arch Dis Child. 2015 Jun;100(6):542-7 23894522 - PLoS One. 2013;8(7):e69685 19882345 - Eur J Pediatr. 2010 Jun;169(6):713-9 11791654 - Clin Exp Rheumatol. 2001 Nov-Dec;19(6):751-6 21326860 - PLoS One. 2011;6(2):e16853 12692003 - Arterioscler Thromb Vasc Biol. 2003 Apr 1;23(4):576-81 23065250 - Mol Biol Rep. 2012 Dec;39(12):11137-44 23456091 - Hum Genet. 2013 Jun;132(6):669-80 19132087 - PLoS Genet. 2009 Jan;5(1):e1000319 25645453 - Sci Rep. 2015;5:8194 18025079 - Pediatrics. 2007 Dec;120(6):e1434-40 17033807 - Eur J Pediatr. 2007 May;166(5):421-5 24261768 - Mod Rheumatol. 2014 Jan;24(1):120-8 22446961 - Nat Genet. 2012 May;44(5):522-5 21293453 - Nat Protoc. 2011 Feb;6(2):121-33 25101798 - Genes Immun. 2014 Dec;15(8):534-42 9877364 - Pediatr Infect Dis J. 1998 Dec;17(12):1144-8 |
References_xml | – volume: 157 start-page: 300 issue: 2 year: 2009 ident: ref72 article-title: Inhibition of matrix metalloproteinase-9 activity improves coronary outcome in an animal model of Kawasaki disease publication-title: Clin Exp Immunol doi: 10.1111/j.1365-2249.2009.03949.x – volume: 56 start-page: 1493 issue: 18 year: 2010 ident: ref53 article-title: Nebulette mutations are associated with dilated cardiomyopathy and endocardial fibroelastosis publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2010.05.045 – volume: 116 start-page: 876 issue: 5 year: 2015 ident: ref61 article-title: CXCL10/IP-10 is a biomarker and mediator for Kawasaki disease publication-title: Circ Res doi: 10.1161/CIRCRESAHA.116.305834 – volume: 32 start-page: 746 issue: 4 year: 2012 ident: ref60 article-title: Inflammation-induced hepcidin is associated with the development of anemia and coronary artery lesions in Kawasaki disease publication-title: J Clin Immunol doi: 10.1007/s10875-012-9668-1 – volume: 17 start-page: 1144 issue: 12 year: 1998 ident: ref67 article-title: Intravenous gamma-globulin treatment and retreatment in Kawasaki disease. US/Canadian Kawasaki Syndrome Study Group publication-title: Pediatr Infect Dis J doi: 10.1097/00006454-199812000-00009 – volume: 29 start-page: S121 issue: 1 year: 2011 ident: ref64 article-title: Microparticles and Kawasaki disease: a marker of vascular damage? publication-title: Clin Exp Rheumatol – volume: 9 start-page: e105195 issue: 8 year: 2014 ident: ref58 article-title: IL-31 associated with coronary artery lesion formation in Kawasaki disease publication-title: PLoS One doi: 10.1371/journal.pone.0105195 – volume: 58 start-page: 521 issue: 8 year: 2013 ident: ref35 article-title: Identification of KCNN2 as a susceptibility locus for coronary artery aneurysms in Kawasaki disease using genome-wide association analysis publication-title: J Hum Genet doi: 10.1038/jhg.2013.43 – volume: 2 start-page: 356 issue: 4 year: 2014 ident: ref37 article-title: Kawasaki disease patients homozygous for the rs12252-C variant of interferon-induced transmembrane protein-3 are significantly more likely to develop coronary artery lesions publication-title: Mol Genet Genomic Med doi: 10.1002/mgg3.79 – volume: 33 start-page: 1046 issue: 7 year: 2012 ident: ref23 article-title: Single-nucleotide polymorphism rs2290692 in the 3'UTR of ITPKC associated with susceptibility to Kawasaki disease in a Han Chinese population publication-title: Pediatr Cardiol doi: 10.1007/s00246-012-0223-x – volume: 100 start-page: 542 issue: 6 year: 2015 ident: ref9 article-title: Acute and late coronary outcomes in 1073 patients with Kawasaki disease with and without intravenous gamma-immunoglobulin therapy publication-title: Arch Dis Child doi: 10.1136/archdischild-2014-306427 – volume: 67 start-page: 828 issue: 3 year: 2015 ident: ref33 article-title: Identification of an association between genomic hypomethylation of FCGR2A and susceptibility to Kawasaki disease and intravenous immunoglobulin resistance by DNA methylation array publication-title: Arthritis Rheumatol doi: 10.1002/art.38976 – volume: 4 start-page: 67 issue: 1 year: 2014 ident: ref41 article-title: Genetic variants of glutamate receptor gene family in Taiwanese Kawasaki disease children with coronary artery aneurysms publication-title: Cell Biosci doi: 10.1186/2045-3701-4-67 – volume: 6 start-page: e21800 issue: 7 year: 2011 ident: ref49 article-title: REVIGO summarizes and visualizes long lists of gene ontology terms publication-title: PLoS One doi: 10.1371/journal.pone.0021800 – volume: 53 start-page: 4 issue: 1 year: 2012 ident: ref8 article-title: Kawasaki disease: an update on diagnosis and treatment publication-title: Pediatr Neonatol doi: 10.1016/j.pedneo.2011.11.003 – volume: 218 start-page: 201 issue: 2 year: 2013 ident: ref70 article-title: Dectin-1/Syk signaling is involved in Lactobacillus casei cell wall extract-induced mouse model of Kawasaki disease publication-title: Immunobiology doi: 10.1016/j.imbio.2012.04.004 – volume: 4 start-page: 4247 year: 2014 ident: ref30 article-title: 8p22-23-rs2254546 as a susceptibility locus for Kawasaki disease: a case-control study and a meta-analysis publication-title: Sci Rep doi: 10.1038/srep04247 – volume: 20 start-page: 266 issue: 3 year: 2009 ident: ref7 article-title: Association of lower eosinophil-related T helper 2 (Th2) cytokines with coronary artery lesions in Kawasaki disease publication-title: Pediatr Allergy Immunol doi: 10.1111/j.1399-3038.2008.00779.x – volume: 168 start-page: 1315 issue: 11 year: 2009 ident: ref6 article-title: Risk factors for Kawasaki disease-associated coronary abnormalities differ depending on age publication-title: Eur J Pediatr doi: 10.1007/s00431-009-0925-0 – volume: 40 start-page: 35 issue: 1 year: 2008 ident: ref20 article-title: ITPKC functional polymorphism associated with Kawasaki disease susceptibility and formation of coronary artery aneurysms publication-title: Nat Genet doi: 10.1038/ng.2007.59 – volume: 33 start-page: 513 issue: 4 year: 2012 ident: ref34 article-title: Assessment of risk factors for Korean children with Kawasaki disease publication-title: Pediatr Cardiol doi: 10.1007/s00246-011-0143-1 – volume: 6 start-page: e16853 issue: 2 year: 2011 ident: ref17 article-title: Identification of novel susceptibility Loci for kawasaki disease in a Han chinese population by a genome-wide association study publication-title: PLoS One doi: 10.1371/journal.pone.0016853 – volume: 60 start-page: 151 year: 2013 ident: ref52 article-title: Altered regional cardiac wall mechanics are associated with differential cardiomyocyte calcium handling due to nebulette mutations in preclinical inherited dilated cardiomyopathy publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2013.04.021 – volume: 43 start-page: 1241 issue: 12 year: 2011 ident: ref15 article-title: Genome-wide association study identifies FCGR2A as a susceptibility locus for Kawasaki disease publication-title: Nat Genet doi: 10.1038/ng.981 – volume: 6 start-page: 121 issue: 2 year: 2011 ident: ref48 article-title: Basic statistical analysis in genetic case-control studies publication-title: Nat Protoc doi: 10.1038/nprot.2010.182 – volume: 39 start-page: 11137 issue: 12 year: 2012 ident: ref22 article-title: A functional polymorphism, rs28493229, in ITPKC and risk of Kawasaki disease: an integrated meta-analysis publication-title: Mol Biol Rep doi: 10.1007/s11033-012-2022-0 – volume: 8 start-page: e81384 issue: 11 year: 2013 ident: ref45 article-title: Association between GRIN3A gene polymorphism in Kawasaki disease and coronary artery aneurysms in Taiwanese children publication-title: PLoS One doi: 10.1371/journal.pone.0081384 – volume: 41 start-page: 785 issue: 11 year: 1991 ident: ref10 article-title: Kawasaki disease. With particular emphasis on arterial lesions publication-title: Acta Pathol Jpn – volume: 129 start-page: 487 issue: 5 year: 2011 ident: ref16 article-title: A genome-wide association analysis reveals 1p31 and 2p13.3 as susceptibility loci for Kawasaki disease publication-title: Hum Genet doi: 10.1007/s00439-010-0937-x – volume: 8 start-page: e69685 issue: 7 year: 2013 ident: ref25 article-title: A replication study for association of ITPKC and CASP3 two-locus analysis in IVIG unresponsiveness and coronary artery lesion in Kawasaki disease publication-title: PLoS One doi: 10.1371/journal.pone.0069685 – volume: 60 start-page: 604 issue: 2 year: 2009 ident: ref43 article-title: HLA-E gene polymorphism associated with susceptibility to Kawasaki disease and formation of coronary artery aneurysms publication-title: Arthritis Rheum doi: 10.1002/art.24261 – volume: 16 start-page: 1076 year: 2015 ident: ref65 article-title: The transcriptional profile of coronary arteritis in Kawasaki disease publication-title: BMC Genomics doi: 10.1186/s12864-015-2323-5 – volume: 6 start-page: e17370 issue: 4 year: 2011 ident: ref21 article-title: ITPKC single nucleotide polymorphism associated with the Kawasaki disease in a Taiwanese population publication-title: PLoS One doi: 10.1371/journal.pone.0017370 – volume: 13 start-page: 52 issue: 1 year: 2013 ident: ref26 article-title: ITPKC and CASP3 polymorphisms and risks for IVIG unresponsiveness and coronary artery lesion formation in Kawasaki disease publication-title: Pharmacogenomics J doi: 10.1038/tpj.2011.45 – volume: 70 start-page: 310 issue: 3 year: 2015 ident: ref62 article-title: Th17- and Treg-related cytokine and mRNA expression are associated with acute and resolving Kawasaki disease publication-title: Allergy doi: 10.1111/all.12558 – year: 2015 ident: ref50 article-title: Nebulette knockout mice have normal cardiac function but show Z-line widening and upregulation of cardiac stress markers publication-title: Cardiovasc Res – volume: 56 start-page: 161 issue: 2 year: 2011 ident: ref24 article-title: CASP3 gene single-nucleotide polymorphism (rs72689236) and Kawasaki disease in Taiwanese children publication-title: J Hum Genet doi: 10.1038/jhg.2010.154 – volume: 166 start-page: 421 issue: 5 year: 2007 ident: ref5 article-title: Predictive risk factors for coronary artery abnormalities in Kawasaki disease publication-title: Eur J Pediatr doi: 10.1007/s00431-006-0251-8 – volume: 10 start-page: 1203 issue: 10 year: 2012 ident: ref13 article-title: Management of acute and refractory Kawasaki disease publication-title: Expert Rev Anti Infect Ther doi: 10.1586/eri.12.101 – volume: 44 start-page: 522 issue: 5 year: 2012 ident: ref18 article-title: Two new susceptibility loci for Kawasaki disease identified through genome-wide association analysis publication-title: Nat Genet doi: 10.1038/ng.2227 – volume: 161 start-page: 513 issue: 6 year: 2013 ident: ref36 article-title: A genome-wide association analysis identifies novel susceptibility loci for coronary arterial lesions in patients with Kawasaki disease publication-title: Transl Res doi: 10.1016/j.trsl.2013.02.002 – volume: 120 start-page: e1434 issue: 6 year: 2007 ident: ref4 article-title: Delayed diagnosis of Kawasaki disease: what are the risk factors? publication-title: Pediatrics doi: 10.1542/peds.2007-0815 – volume: 4 start-page: 10 year: 2014 ident: ref42 article-title: Coronary artery aneurysms occurrence risk analysis between Kawasaki disease and LRP1B gene in Taiwanese children publication-title: Biomedicine (Taipei) doi: 10.7603/s40681-014-0010-5 – volume: 184 start-page: 940 issue: 7 year: 2001 ident: ref11 article-title: CD8 T lymphocytes and macrophages infiltrate coronary artery aneurysms in acute Kawasaki disease publication-title: J Infect Dis doi: 10.1086/323155 – volume: 364 start-page: 533 issue: 9433 year: 2004 ident: ref1 article-title: Kawasaki syndrome publication-title: Lancet doi: 10.1016/S0140-6736(04)16814-1 – volume: 35 start-page: 457 issue: 4 year: 2016 ident: ref68 article-title: Infliximab as the First Retreatment in Patients with Kawasaki Disease Resistant to Initial Intravenous Immunoglobulin publication-title: Pediatr Infect Dis J doi: 10.1097/INF.0000000000001039 – volume: 8 start-page: 982 issue: 12 year: 2009 ident: ref55 article-title: Voltage-gated potassium channels as therapeutic targets publication-title: Nat Rev Drug Discov doi: 10.1038/nrd2983 – volume: 23 start-page: 576 issue: 4 year: 2003 ident: ref69 article-title: Systemic arterial expression of matrix metalloproteinases 2 and 9 in acute Kawasaki disease publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/01.ATV.0000065385.47152.FD – volume: 15 start-page: 534 issue: 8 year: 2014 ident: ref46 article-title: High-density genotyping of immune loci in Kawasaki disease and IVIG treatment response in European-American case-parent trio study publication-title: Genes Immun doi: 10.1038/gene.2014.47 – volume: 81 start-page: 559 issue: 3 year: 2007 ident: ref47 article-title: PLINK: a tool set for whole-genome association and population-based linkage analyses publication-title: Am J Hum Genet doi: 10.1086/519795 – volume: 24 start-page: 120 issue: 1 year: 2014 ident: ref71 article-title: The role of TNF-alpha in a murine model of Kawasaki disease arteritis induced with a Candida albicans cell wall polysaccharide publication-title: Mod Rheumatol doi: 10.3109/14397595.2013.854061 – volume: 132 start-page: 669 issue: 6 year: 2013 ident: ref28 article-title: Combined analysis of genome-wide-linked susceptibility loci to Kawasaki disease in Han Chinese publication-title: Hum Genet doi: 10.1007/s00439-013-1279-2 – volume: 4 start-page: 5208 year: 2014 ident: ref27 article-title: The roles of Ca2+/NFAT signaling genes in Kawasaki disease: single- and multiple-risk genetic variants publication-title: Sci Rep doi: 10.1038/srep05208 – volume: 169 start-page: 713 issue: 6 year: 2010 ident: ref39 article-title: BTNL2 gene polymorphisms may be associated with susceptibility to Kawasaki disease and formation of coronary artery lesions in Taiwanese children publication-title: Eur J Pediatr doi: 10.1007/s00431-009-1099-5 – volume: 22 start-page: 551 issue: 5 year: 2010 ident: ref12 article-title: Kawasaki disease: update on pathogenesis publication-title: Curr Opin Rheumatol doi: 10.1097/BOR.0b013e32833cf051 – volume: 9 start-page: e103329 issue: 8 year: 2014 ident: ref29 article-title: A genetic variant rs1801274 in FCGR2A as a potential risk marker for Kawasaki disease: a case-control study and meta-analysis publication-title: PLoS One doi: 10.1371/journal.pone.0103329 – volume: 5 start-page: e1000319 issue: 1 year: 2009 ident: ref14 article-title: A genome-wide association study identifies novel and functionally related susceptibility Loci for Kawasaki disease publication-title: PLoS Genet doi: 10.1371/journal.pgen.1000319 – volume: 141 start-page: 381 issue: 3 year: 2005 ident: ref57 article-title: Immunological profile of peripheral blood lymphocytes and monocytes/macrophages in Kawasaki disease publication-title: Clin Exp Immunol doi: 10.1111/j.1365-2249.2005.02821.x – volume: 26 start-page: 196 issue: 3 year: 2011 ident: ref51 article-title: Genetics of sudden cardiac death syndromes publication-title: Curr Opin Cardiol doi: 10.1097/HCO.0b013e3283459893 – start-page: CD004000 issue: 4 year: 2003 ident: ref3 article-title: Intravenous immunoglobulin for the treatment of Kawasaki disease in children publication-title: Cochrane Database Syst Rev – volume: 37 start-page: 439 issue: 6 year: 2010 ident: ref44 article-title: Single nucleotide polymorphism rs2229634 in the ITPR3 gene is associated with the risk of developing coronary artery aneurysm in children with Kawasaki disease publication-title: Int J Immunogenet doi: 10.1111/j.1744-313X.2010.00943.x – volume: 8 start-page: e72037 issue: 8 year: 2013 ident: ref32 article-title: Replication and meta-analysis of GWAS identified susceptibility loci in Kawasaki disease confirm the importance of B lymphoid tyrosine kinase (BLK) in disease susceptibility publication-title: PLoS One doi: 10.1371/journal.pone.0072037 – volume: 8 start-page: 15879 issue: 12 year: 2015 ident: ref66 article-title: IVIG inhibits TNF-alpha-induced MMP9 expression and activity in monocytes by suppressing NF-kappaB and P38 MAPK activation publication-title: Int J Clin Exp Pathol – volume: 5 start-page: 8194 year: 2015 ident: ref31 article-title: Systematic confirmation study of GWAS-identified genetic variants for Kawasaki disease in a Chinese population publication-title: Sci Rep doi: 10.1038/srep08194 – volume: 19 start-page: 751 issue: 6 year: 2001 ident: ref63 article-title: Elevated serum levels of macrophage colony-stimulating factor in patients with Kawasaki disease complicated by cardiac lesions publication-title: Clin Exp Rheumatol – volume: 9 start-page: e91118 issue: 3 year: 2014 ident: ref38 article-title: Single-nucleotide polymorphism rs7251246 in ITPKC is associated with susceptibility and coronary artery lesions in Kawasaki disease publication-title: PLoS One doi: 10.1371/journal.pone.0091118 – volume: 244 start-page: 55 issue: 1 year: 2011 ident: ref54 article-title: Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions publication-title: Immunol Rev doi: 10.1111/j.1600-065X.2011.01055.x – volume: 55 start-page: 18 issue: 1 year: 2012 ident: ref56 article-title: Transforming growth factor beta receptor II polymorphisms are associated with Kawasaki disease publication-title: Korean J Pediatr doi: 10.3345/kjp.2012.55.1.18 – volume: 28 start-page: 253 issue: 1 year: 1996 ident: ref2 article-title: Sequelae of Kawasaki disease in adolescents and young adults publication-title: J Am Coll Cardiol doi: 10.1016/0735-1097(96)00099-X – volume: 44 start-page: 517 issue: 5 year: 2012 ident: ref19 article-title: A genome-wide association study identifies three new risk loci for Kawasaki disease publication-title: Nat Genet doi: 10.1038/ng.2220 – volume: 28 start-page: 435 issue: 6 year: 2014 ident: ref40 article-title: Association between SRC-1 gene polymorphisms and coronary artery aneurysms formation in Taiwanese children with Kawasaki disease publication-title: J Clin Lab Anal doi: 10.1002/jcla.21706 – volume: 7 start-page: e38635 issue: 6 year: 2012 ident: ref59 article-title: Augmented TLR2 expression on monocytes in both human Kawasaki disease and a mouse model of coronary arteritis publication-title: PLoS One doi: 10.1371/journal.pone.0038635 – reference: 23065250 - Mol Biol Rep. 2012 Dec;39(12):11137-44 – reference: 25485088 - Cell Biosci. 2014 Nov 19;4(1):67 – reference: 25101798 - Genes Immun. 2014 Dec;15(8):534-42 – reference: 18025079 - Pediatrics. 2007 Dec;120(6):e1434-40 – reference: 9877364 - Pediatr Infect Dis J. 1998 Dec;17(12):1144-8 – reference: 25520923 - Biomedicine (Taipei). 2014;4:10 – reference: 22633994 - Immunobiology. 2013 Feb;218(2):201-12 – reference: 17033807 - Eur J Pediatr. 2007 May;166(5):421-5 – reference: 23199405 - Expert Rev Anti Infect Ther. 2012 Oct;10(10):1203-15 – reference: 25093412 - PLoS One. 2014;9(8):e103329 – reference: 25470559 - Arthritis Rheumatol. 2015 Mar;67(3):828-36 – reference: 21987091 - Pharmacogenomics J. 2013 Feb;13(1):52-9 – reference: 21293453 - Nat Protoc. 2011 Feb;6(2):121-33 – reference: 24652666 - J Clin Lab Anal. 2014 Nov;28(6):435-9 – reference: 21789182 - PLoS One. 2011;6(7):e21800 – reference: 24903211 - Sci Rep. 2014;4:5208 – reference: 18084290 - Nat Genet. 2008 Jan;40(1):35-42 – reference: 21533171 - PLoS One. 2011;6(4):e17370 – reference: 22446962 - Nat Genet. 2012 May;44(5):517-21 – reference: 25564534 - Arch Dis Child. 2015 Jun;100(6):542-7 – reference: 25585854 - Allergy. 2015 Mar;70(3):310-8 – reference: 23456091 - Hum Genet. 2013 Jun;132(6):669-80 – reference: 25645453 - Sci Rep. 2015;5:8194 – reference: 24278430 - PLoS One. 2013;8(11):e81384 – reference: 22105492 - Pediatr Cardiol. 2012 Apr;33(4):513-20 – reference: 19180512 - Arthritis Rheum. 2009 Feb;60(2):604-10 – reference: 8752822 - J Am Coll Cardiol. 1996 Jul;28(1):253-7 – reference: 22737215 - PLoS One. 2012;7(6):e38635 – reference: 21326860 - PLoS One. 2011;6(2):e16853 – reference: 24023612 - PLoS One. 2013;8(8):e72037 – reference: 21430528 - Curr Opin Cardiol. 2011 May;26(3):196-203 – reference: 25987543 - Cardiovasc Res. 2015 Jul 15;107(2):216-25 – reference: 15302199 - Lancet. 2004 Aug 7-13;364(9433):533-44 – reference: 22446961 - Nat Genet. 2012 May;44(5):522-5 – reference: 17701901 - Am J Hum Genet. 2007 Sep;81(3):559-75 – reference: 11791654 - Clin Exp Rheumatol. 2001 Nov-Dec;19(6):751-6 – reference: 19949402 - Nat Rev Drug Discov. 2009 Dec;8(12):982-1001 – reference: 25122210 - PLoS One. 2014;9(8):e105195 – reference: 22392047 - J Clin Immunol. 2012 Aug;32(4):746-52 – reference: 20618519 - Int J Immunogenet. 2010 Dec;37(6):439-43 – reference: 20616737 - Curr Opin Rheumatol. 2010 Sep;22(5):551-60 – reference: 21160486 - J Hum Genet. 2011 Feb;56(2):161-5 – reference: 26679344 - BMC Genomics. 2015;16:1076 – reference: 25077179 - Mol Genet Genomic Med. 2014 Jul;2(4):356-61 – reference: 19438983 - Pediatr Allergy Immunol. 2009 May;20(3):266-72 – reference: 20951326 - J Am Coll Cardiol. 2010 Oct 26;56(18):1493-502 – reference: 24621571 - PLoS One. 2014;9(3):e91118 – reference: 23632046 - J Mol Cell Cardiol. 2013 Jul;60:151-60 – reference: 1785339 - Acta Pathol Jpn. 1991 Nov;41(11):785-97 – reference: 26673981 - Pediatr Infect Dis J. 2016 Apr;35(4):457-9 – reference: 21385556 - Clin Exp Rheumatol. 2011 Jan-Feb;29(1 Suppl 64):S121-5 – reference: 16045726 - Clin Exp Immunol. 2005 Sep;141(3):381-7 – reference: 22348488 - Pediatr Neonatol. 2012 Feb;53(1):4-11 – reference: 11528596 - J Infect Dis. 2001 Oct 1;184(7):940-3 – reference: 19604270 - Clin Exp Immunol. 2009 Aug;157(2):300-9 – reference: 23894522 - PLoS One. 2013;8(7):e69685 – reference: 22361738 - Pediatr Cardiol. 2012 Oct;33(7):1046-53 – reference: 22081228 - Nat Genet. 2011 Dec;43(12):1241-6 – reference: 24577620 - Sci Rep. 2014;4:4247 – reference: 12692003 - Arterioscler Thromb Vasc Biol. 2003 Apr 1;23(4):576-81 – reference: 26884859 - Int J Clin Exp Pathol. 2015;8(12):15879-86 – reference: 19159953 - Eur J Pediatr. 2009 Nov;168(11):1315-21 – reference: 22359526 - Korean J Pediatr. 2012 Jan;55(1):18-23 – reference: 19882345 - Eur J Pediatr. 2010 Jun;169(6):713-9 – reference: 23677057 - J Hum Genet. 2013 Aug;58(8):521-5 – reference: 23454411 - Transl Res. 2013 Jun;161(6):513-5 – reference: 24261768 - Mod Rheumatol. 2014 Jan;24(1):120-8 – reference: 21221998 - Hum Genet. 2011 May;129(5):487-95 – reference: 14584002 - Cochrane Database Syst Rev. 2003;(4):CD004000 – reference: 19132087 - PLoS Genet. 2009 Jan;5(1):e1000319 – reference: 22017431 - Immunol Rev. 2011 Nov;244(1):55-74 – reference: 25605650 - Circ Res. 2015 Feb 27;116(5):876-83 |
SSID | ssj0053866 |
Score | 2.415588 |
Snippet | Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in... |
SourceID | plos doaj pubmedcentral proquest gale pubmed crossref |
SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | e0154943 |
SubjectTerms | Aneurysm Aneurysms Arteries Biology and Life Sciences Blood vessels Cardiac muscle Cardiovascular disease Child Children Coding Coronary Aneurysm - complications Coronary Aneurysm - genetics Coronary arteries Coronary artery Coronary vessels Coronary Vessels - pathology Development and progression DNA methylation Drug dosages Gene expression Gene Ontology Genes Genetic aspects Genetic diversity Genetic Predisposition to Disease Genetic variance Genome-wide association studies Genome-Wide Association Study Genomes Genomics Genotyping Health risk assessment Heart diseases Heredity Hospitals Humans Immunoglobulins Informatics Intravenous administration Kawasaki disease Kawasaki syndrome Knowledge representation Laboratories Lesions Linkage Disequilibrium - genetics Matrix Metalloproteinase 9 - genetics Medical research Medicine Medicine and Health Sciences Models, Genetic Mucocutaneous lymph node syndrome Mucocutaneous Lymph Node Syndrome - complications Mucocutaneous Lymph Node Syndrome - genetics Muscles Mutation Neural coding Pathogenesis Patients Pediatrics Phosphorylation Physiological aspects Polymorphism, Single Nucleotide - genetics Precision medicine Proteomics Risk Factors Threonine Tubulin Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF Vasculitis |
SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3fb9MwELZQn3hBjF8LDDAICXjIlthO7DyOQTVADIkx2FvkOA5U6pJqWUH9F_irubPdqEET44GnVvU5Te6zz3fx3WdCnpkmTQqjWYy-OgQohYorbW2smFZFAzhLVyH34Sg_PBHvTrPTjaO-MCfM0wN7xe1ZUVdCJaY2rBGwOBWyrgquhWGshtDEsZcmRbIOprwNhlmc56FQjst0L-Cyu-hau-tYyQQfLUSOr3-wypPFvOsvczn_zJzcWIqmN8mN4EPSfX_vW-SabW-RrTBLe_oiUEm_vE1-wdfuzMZfZ7WlG0hQTB9cUV-l20CwTI-6H3ZOj5e9S3NxGbMrihfqh362pvjWlh4g6YE-X-ENWPxATsxVf0an60JIOmvpe_1T9-Ce0td-C-gOOZm--XxwGIfTF2IjWYZn1BulmyyrwGEBnMHPkrlWGaxleSNUzbMaVndVGcFzYSpWVcLwzOLGHkDEcsPvkkkL-t4mFIISznNAq8pyASZFG5nULNNW4y4pMxHhayhKE6jJ8YSMeen22ySEKF6zJQJYBgAjEg-9Fp6a4wr5V4jyIIvE2u4HGG5lGG7lVcMtIo9xjJS-SnUwD-W-gEfEswDSiDx1Ekiu0WL2zje97Pvy7ccv_yB0_Gkk9DwINR2ow-hQMQHPhKRdI8mdkSSYCDNq3sYRvdZKX6ZSqUzgqyzouR7llzc_GZrxopiR19pu6WQKCK7B5P9FRiUQAKONj8g9P3EG7TOZSghu4R_kaEqN4Bm3tLPvjv9cKKR9ZPf_B54PyHVwgXPMB0nZDplcnC_tQ3AzL6pHzqL8Bq_2e-w priority: 102 providerName: Directory of Open Access Journals – databaseName: ProQuest Central dbid: BENPR link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwELdGJyFe0DY-VjbAICTgIVvj2Pl4QGgbqwZoBW1s7C1ybGdU6pLSrKD-C_zV3DlOWNA0eGpVX9LY5zvf5e5-R8gLlfuDREnmoa0ODkoSe5k0xouZjJMc-BzZCrnDUXhwwj-cibMlMmpqYTCtstGJVlHrUuE78m0ffDXB0ft-O_3uYdcojK42LTSka62g31iIsVtkGVSyGPTI8u7-6PNRo5tBusPQFdAFkb_t-LU1LQuzZdHKeNA5oCyOf6ute9NJWV1niv6dUXnliBqukLvOtqQ79WZYJUumWCO3D130fI2sOkGu6CuHNv36HvkFX8sL430da0OvMItihuGC1oW8OfjTdFT-MBN6PK9sJoxNql1QvFHVXmc0xRe7dA9xEeRsgc9i8ANhMxfVBR02tZJ0XNCP8qeswIKl7-oo0X1yMtz_snfguQYNnoqYwDb2Kpa5EBnYNLAVwBSLQhkLOO7CnMc6EBoMgDhTPAi5yliWcRUIg7G_JNIsVMED0itg6dcJBb8lCELwNTMRctA6UkUDzYQ0EgOpTPVJ0HAlVQ69HJtoTFIbkovAi6kXOUVepo6XfeK1V01r9I5_0O8iw1taxN62P5Sz89SJcmq4zng8UFqxnIO5BHPJkkByxZiGCYg-eYrbJa0LWVsNku5wmCK2C_D75LmlQPyNAhN8zuW8qtL3n07_g-j4qEP00hHlJSyHkq6oAuaEuF4dys0OJWgR1Rlex83drEqV_pE3uLLZ8NcPP2uH8aaYtFeYcm5pEvC_4VS4gSYegI-Mx0CfPKxlqF19FvkR-L_wD1FHujrs6Y4U428WIp3HiAzJHt386BvkDti_ISaD-GyT9C5nc_MYbMzL7IlTHL8B3f19Hg priority: 102 providerName: ProQuest |
Title | Genome-Wide Association Study Identifies Novel Susceptibility Genes Associated with Coronary Artery Aneurysm Formation in Kawasaki Disease |
URI | https://www.ncbi.nlm.nih.gov/pubmed/27171184 https://www.proquest.com/docview/1788543304 https://www.proquest.com/docview/1789495425 https://www.proquest.com/docview/1805501963 https://pubmed.ncbi.nlm.nih.gov/PMC4865092 https://doaj.org/article/e4db480cdc2f412997db93a4c22d0945 http://dx.doi.org/10.1371/journal.pone.0154943 |
Volume | 11 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3db9MwELe27oUXxPhaYBSDkICHVI3jJM4DQltZGSAK2ij0LXIcZ1TqktKsQP4F_mrunA8tqHyIl7Sq76L6zmff2effEfJIpc4wVJLZ6KtDgBIKO5Za24JJEaag58DckHs78Y-n_PXMm22RpmZrLcBiY2iH9aSmq8Xg-5fyORj8M1O1IXAapsEyz_TAYI5xd5vsmBMjTObj7bkCWLfv1xfofseJ8MAQ44DjzTtrlYH0byfu3nKRF5u80l-TKy-tVuNr5GrtZtKDalzski2dXSe7tSEX9EmNNv30BvkBX_NzbX-aJ5peUhbFDMOSVhd5U4in6ST_qhf0dF2YTBiTVFtSfFHR8umE4sYuHSEuglyV-Ac0fiBsZlmc03FzV5LOM_pGfpMFeLD0RXVKdJNMx0cfRsd2XaDBVgHzsIy9EjL1vBh8GhgK4IoFvhQeLHd-ykXiegk4ACJW3PW5ilkcc-V6Gs_-wiBhvnJvkV4Got8jFOIW1_Uh1ow9n8OsI1UwTJgntcSDVKYs4jaqiFSNXo5FNBaROZILIIqpJBuhLqNalxaxW65lhd7xF_pD1HJLi9jb5od8dRbVphxpnsRcDFWiWMrBXYK-xKEruWIsgQ54FrmPYySqLrK2M0h0wKGLWC7AschDQ4H4Gxkm-JzJdVFEr959_Aei05MO0eOaKM1BHErWlyqgT4jr1aHc71DCLKI6zXs4ohupFJETCOFx3O0CzmaUb25-0DbjSzFpL9P52tCEEH_DqvAHGjGEGBmXAYvcrgynlX5jhhYJOibVUU-3JZt_NhDpXCAyJLvz35x3yRVwjX3ME3HYPuldrNb6HrifF3GfbAezAJ5i5OBz_LJPdg6PJu9P-mZDp29mnJ_O34ui |
linkProvider | Scholars Portal |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtR3bbtMw1BqdBLwgNi4rDGYQCHjI1jjOpQ8T2q1q6VrQLrC34DjOqNQlpVmZ-gt8FN_GOY4TFjQNXvbUqj5OY5_jc_G5EfJKJnarLQWzUFcHA6UdWJFQygqYCNoJ4NnXGXKDodc95h9O3JMF8qvMhcGwypInakYdZxLvyDdssNVcjtb3-8l3C7tGoXe1bKEhTGuFeFOXGDOJHX01vwATLt_s7QK-XzPW2Tva6Vqmy4AlfeZiL3YZiMR1IxDMsB7QJ3xPBC7wbC_hQey4MUixIJLc8biMWBRx6bgKHVhtP2aedOC5t8gixwuUBlnc3ht-OihlAXATzzMJe45vbxj6WJ9kqVrX1dG4UxOIum9AJR0ak3GWX6X6_h3BeUkkdu6Te0aXpVsF8S2RBZUuk9sD461fJkuGceT0ralu_e4B-QlfszNlfRnFil4iDooRjXNaJA4nYL_TYfZDjenhLNeRNzqId07xQXk1T8UUL5LpDtZhENM5vovCDyzTOc_PaKfMzaSjlPbFhchBY6a7hVfqITm-EVQ9Io0Utn6FULCTHMcD2zZyPQ5cTki_FTNXKIGOWyabxCmxEkpTLR2bdoxD7QL0wWoqNjlEXIYGl01iVbMmRbWQf8BvI8IrWKz1rX_IpqehYR2h4nHEg5aMJUs4qGewlqjtCC4Zi2EBbpOsIbmEReJsxbHCLQ5LxPYEdpO81BBY7yPFgKJTMcvzsPfx838AHR7UgN4YoCSD7ZDCJHHAmrCOWA1ytQYJXEvWhleQuMtdycM_5xtmlgR_9fCLahgfikGCqcpmGqYN9j5IoWtgghbY5Ch2muRxcYaq3We-7YO9Df_g105XDT31kXT0TZdk5wFWomRPrn_1NXKnezTYD_d7w_5Tchd0bw8DUWy2Shrn05l6BvrtefTcMBFKvt403_oN81W43Q |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtR1db9Mw0BpFmnhBbHysMJhBIOAha-M4cfKA0FipVsoKYhv0LTiOMyp1SWlWpv4FfhK_jrvECQuaBi97alWf3dh3vo_cFyFPVWJ3AyWZhbo6GCiBb0VSa8tn0g8SwLMoMuT2R97eEX83dscr5FeVC4NhlRVPLBh1nCl8R96xwVZzOVrfncSERXzs9V_PvlvYQQo9rVU7jZJEhnp5BuZb_mrQA1w_Y6z_9nB3zzIdBiwlmIt92JUvE9eNQCjDXkCXEJ70XeDXXsL92HFjkGB-pLjjcRWxKOLKcTU6rwIRM085sO41cl04nGPbCDGujT3gI55nUvUcYXcMZWzPslRvF3XRuNMQhUXHgFoutGbTLL9I6f07dvOcMOzfIjeNFkt3SrJbIys6XSer-8ZPv07WDMvI6QtT1_rlbfITvmYn2voyiTU9RxYUYxmXtEwZTsByp6Psh57Sg0VexNwU4btLigvl9TwdU3yFTHexAoOcL_FZNH5ggc5lfkL7VVYmnaR0KM9kDroy7ZX-qDvk6EoQdZe0Ujj6DULBQnIcD6zayPU48DepRDdmrtQSXbZMtYlTYSVUpk46tuuYhoXzT4C9VB5yiLgMDS7bxKpnzco6If-Af4MIr2GxynfxQzY_Dg3TCDWPI-53VaxYwkExg71EgSO5YiyGDbhtsoXkEpYpszWvCnc4bBEbE9ht8qSAwEofKd6ZY7nI83Dw4fN_AB18agA9N0BJBsehpEnfgD1hBbEG5GYDEviVagxvIHFXp5KHf242zKwI_uLhx_UwLorhganOFgVMAJY-yJ9LYPwuWOMocNrkXnmH6tNnwhZgacM_iMbtaqCnOZJOvhXF2LmPNSjZ_csffYusArcK3w9GwwfkBijdHkag2GyTtE7nC_0QFNvT6FHBQSj5etUs6zfthLZ5 |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Genome-Wide+Association+Study+Identifies+Novel+Susceptibility+Genes+Associated+with+Coronary+Artery+Aneurysm+Formation+in+Kawasaki+Disease&rft.jtitle=PloS+one&rft.au=Kuo%2C+Ho-Chang&rft.au=Li%2C+Sung-Chou&rft.au=Guo%2C+Mindy+Ming-Huey&rft.au=Huang%2C+Ying-Hsien&rft.date=2016-05-12&rft.pub=Public+Library+of+Science&rft.eissn=1932-6203&rft.volume=11&rft.issue=5&rft_id=info:doi/10.1371%2Fjournal.pone.0154943&rft_id=info%3Apmid%2F27171184&rft.externalDocID=PMC4865092 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1932-6203&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1932-6203&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1932-6203&client=summon |