Evidence map›Paper›PMID 26434682›Full record

ArticleScientific reports2015

Genetic variants in PLCB4/PLCB1 as susceptibility loci for coronary artery aneurysm formation in Kawasaki disease in Han Chinese in Taiwan.

Ying-Ju Lin, Jeng-Sheng Chang, Xiang Liu, Hsinyi Tsang, Wen-Kuei Chien, Jin-Hua Chen, Hsin-Yang Hsieh, Kai-Chung Hsueh, Yi-Tzone Shiao, Ju-Pi Li and 14 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  9. Comparative single-cell analysis of the adult heart and coronary vasculature.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
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  19. Review
  20. Whole-Genome Sequencing of Pharmacogenetic Drug Response in Racially Diverse Children with Asthma.American journal of respiratory and critical care medicine · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

24 authors at 7 institutions in 2 countries.

Ying-Ju LinGenetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
Jeng-Sheng ChangChildren's Hospital of China Medical University, Taichung, Taiwan.
Xiang LiuNational Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Hsinyi TsangNational Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Wen-Kuei ChienBiostatistics Center, College of Management, Taipei Medical University, Taipei, Taiwan.
Jin-Hua ChenBiostatistics Center, College of Management, Taipei Medical University, Taipei, Taiwan.
Hsin-Yang HsiehChildren's Hospital of China Medical University, Taichung, Taiwan.
Kai-Chung HsuehKai-Chung Hsueh Clinics, Taichung, Taiwan.
Yi-Tzone ShiaoHeart Center, China Medical University Hospital, Taichung, Taiwan.
Ju-Pi LiSchool of Chinese Medicine, China Medical University, Taichung, Taiwan.
Cheng-Wen LinDepartment of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan.
Chih-Ho LaiDepartment of Microbiology and Immunology, Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan, Taiwan.
Jer-Yuarn WuSchool of Chinese Medicine, China Medical University, Taichung, Taiwan.
Chien-Hsiun ChenSchool of Chinese Medicine, China Medical University, Taichung, Taiwan.
Jaung-Geng LinSchool of Chinese Medicine, China Medical University, Taichung, Taiwan.
Ting-Hsu LinGenetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
Chiu-Chu LiaoGenetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
Shao-Mei HuangGenetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
Yu-Ching LanDepartment of Health Risk Management, China Medical University, Taichung, Taiwan.
Tsung-Jung HoSchool of Chinese Medicine, China Medical University, Taichung, Taiwan.
Wen-Miin LiangGraduate Institute of Biostatistics, School of Public Health, China Medical University, Taichung, Taiwan.
Yi-Chun YehGraduate Institute of Biostatistics, School of Public Health, China Medical University, Taichung, Taiwan.
Jung-Chun LinSchool of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Fuu-Jen TsaiGenetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
China Medical University · TWTaipei Medical University · TWChina Medical University Hospital · TWInstitute of Biomedical Sciences, Academia Sinica · TWChang Gung University · TWNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kawasaki disease (KD) is an acute, inflammatory, and self-limited vasculitis affecting infants and young children. Coronary artery aneurysm (CAA) formation is the major complication of KD and the leading cause of acquired cardiovascular disease among children. To identify susceptible loci that might predispose patients with KD to CAA formation, a genome-wide association screen was performed in a Taiwanese KD cohort. Patients with both KD and CAA had longer fever duration and delayed intravenous immunoglobulin treatment time. After adjusting for these factors, 100 susceptibility loci were identified. Four genes were identified from a single cluster of 35 using the Ingenuity Pathway Analysis (IPA) Knowledge Base. Silencing KCNQ5, PLCB1, PLCB4, and PLCL1 inhibited the effect of lipopolysaccharide-induced endothelial cell inflammation with varying degrees of proinflammatory cytokine expression. PLCB1 showed the most significant inhibition. Endothelial cell inflammation was also inhibited by using a phospholipase C (PLC) inhibitor. The single nucleotide polymorphism rs6140791 was identified between PLCB4 and PLCB1. Plasma PLC levels were higher in patients with KD and CC+CG rs6140791genotypes, and these genotypes were more prevalent in patients with KD who also had CAA. Our results suggest that polymorphism of the PLCB4/B1 genes might be involved in the CAA pathogenesis of KD.

Indexed as

Child, PreschoolChinaCoronary AneurysmCoronary VesselsDown-RegulationFemaleGene ExpressionGenetic LociGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInfantInterleukinsKCNQ Potassium ChannelsMaleMucocutaneous Lymph Node SyndromeInterleukinsKCNQ5 protein, humanKCNQ Potassium ChannelsPhosphoinositide Phospholipase CPhospholipase C betaphospholipase C epsilonPLCB1 protein, humanPLCB4 protein, human

Identifiers

PMID26434682
PMCPMC4593004
OpenAlexW2412652201

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.