Discovery of novel eGFR-associated multiple independent signals using a quasi-adaptive method

A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To i...

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Vydáno v:Frontiers in genetics Ročník 13; s. 997302
Hlavní autoři: Ghasemi, Sahar, Becker, Tim, Grabe, Hans J., Teumer, Alexander
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland Frontiers Media S.A 31.10.2022
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ISSN:1664-8021, 1664-8021
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Abstract A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To increase statistical power for detecting independent associations in GWAS loci, we improved our recently developed quasi-adaptive method estimating SNP-specific alpha levels for the conditional analysis, and applied it to the GWAS meta-analysis results of eGFR among 783,978 European-ancestry individuals. Among known eGFR loci, we revealed 19 new independent association signals that were subsequently replicated in the United Kingdom Biobank (n = 408,608). These associations have remained undetected by conditional analysis using the established conservative genome-wide significance level of 5 × 10 –8 . Functional characterization of known index SNPs and novel independent signals using colocalization of conditional eGFR association results and gene expression in cis across 51 human tissues identified two potentially causal genes across kidney tissues: TSPAN33 and TFDP2 , and three candidate genes across other tissues: SLC22A2, LRP2 , and CDKN1C . These colocalizations were not identified in the original GWAS. By applying our improved quasi-adaptive method, we successfully identified additional genetic variants associated with eGFR. Considering these signals in colocalization analyses can increase the precision of revealing potentially functional genes of GWAS loci.
AbstractList A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To increase statistical power for detecting independent associations in GWAS loci, we improved our recently developed quasi-adaptive method estimating SNP-specific alpha levels for the conditional analysis, and applied it to the GWAS meta-analysis results of eGFR among 783,978 European-ancestry individuals. Among known eGFR loci, we revealed 19 new independent association signals that were subsequently replicated in the United Kingdom Biobank (n = 408,608). These associations have remained undetected by conditional analysis using the established conservative genome-wide significance level of 5 × 10 . Functional characterization of known index SNPs and novel independent signals using colocalization of conditional eGFR association results and gene expression in across 51 human tissues identified two potentially causal genes across kidney tissues: and , and three candidate genes across other tissues: , and . These colocalizations were not identified in the original GWAS. By applying our improved quasi-adaptive method, we successfully identified additional genetic variants associated with eGFR. Considering these signals in colocalization analyses can increase the precision of revealing potentially functional genes of GWAS loci.
A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To increase statistical power for detecting independent associations in GWAS loci, we improved our recently developed quasi-adaptive method estimating SNP-specific alpha levels for the conditional analysis, and applied it to the GWAS meta-analysis results of eGFR among 783,978 European-ancestry individuals. Among known eGFR loci, we revealed 19 new independent association signals that were subsequently replicated in the United Kingdom Biobank (n = 408,608). These associations have remained undetected by conditional analysis using the established conservative genome-wide significance level of 5 × 10–8. Functional characterization of known index SNPs and novel independent signals using colocalization of conditional eGFR association results and gene expression in cis across 51 human tissues identified two potentially causal genes across kidney tissues: TSPAN33 and TFDP2, and three candidate genes across other tissues: SLC22A2, LRP2, and CDKN1C. These colocalizations were not identified in the original GWAS. By applying our improved quasi-adaptive method, we successfully identified additional genetic variants associated with eGFR. Considering these signals in colocalization analyses can increase the precision of revealing potentially functional genes of GWAS loci.
A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To increase statistical power for detecting independent associations in GWAS loci, we improved our recently developed quasi-adaptive method estimating SNP-specific alpha levels for the conditional analysis, and applied it to the GWAS meta-analysis results of eGFR among 783,978 European-ancestry individuals. Among known eGFR loci, we revealed 19 new independent association signals that were subsequently replicated in the United Kingdom Biobank (n = 408,608). These associations have remained undetected by conditional analysis using the established conservative genome-wide significance level of 5 × 10 –8 . Functional characterization of known index SNPs and novel independent signals using colocalization of conditional eGFR association results and gene expression in cis across 51 human tissues identified two potentially causal genes across kidney tissues: TSPAN33 and TFDP2 , and three candidate genes across other tissues: SLC22A2, LRP2 , and CDKN1C . These colocalizations were not identified in the original GWAS. By applying our improved quasi-adaptive method, we successfully identified additional genetic variants associated with eGFR. Considering these signals in colocalization analyses can increase the precision of revealing potentially functional genes of GWAS loci.
A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To increase statistical power for detecting independent associations in GWAS loci, we improved our recently developed quasi-adaptive method estimating SNP-specific alpha levels for the conditional analysis, and applied it to the GWAS meta-analysis results of eGFR among 783,978 European-ancestry individuals. Among known eGFR loci, we revealed 19 new independent association signals that were subsequently replicated in the United Kingdom Biobank (n = 408,608). These associations have remained undetected by conditional analysis using the established conservative genome-wide significance level of 5 × 10-8. Functional characterization of known index SNPs and novel independent signals using colocalization of conditional eGFR association results and gene expression in cis across 51 human tissues identified two potentially causal genes across kidney tissues: TSPAN33 and TFDP2, and three candidate genes across other tissues: SLC22A2, LRP2, and CDKN1C. These colocalizations were not identified in the original GWAS. By applying our improved quasi-adaptive method, we successfully identified additional genetic variants associated with eGFR. Considering these signals in colocalization analyses can increase the precision of revealing potentially functional genes of GWAS loci.A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a heritable trait, and recent application of genome-wide association studies (GWAS) successfully identified multiple eGFR-associated genetic loci. To increase statistical power for detecting independent associations in GWAS loci, we improved our recently developed quasi-adaptive method estimating SNP-specific alpha levels for the conditional analysis, and applied it to the GWAS meta-analysis results of eGFR among 783,978 European-ancestry individuals. Among known eGFR loci, we revealed 19 new independent association signals that were subsequently replicated in the United Kingdom Biobank (n = 408,608). These associations have remained undetected by conditional analysis using the established conservative genome-wide significance level of 5 × 10-8. Functional characterization of known index SNPs and novel independent signals using colocalization of conditional eGFR association results and gene expression in cis across 51 human tissues identified two potentially causal genes across kidney tissues: TSPAN33 and TFDP2, and three candidate genes across other tissues: SLC22A2, LRP2, and CDKN1C. These colocalizations were not identified in the original GWAS. By applying our improved quasi-adaptive method, we successfully identified additional genetic variants associated with eGFR. Considering these signals in colocalization analyses can increase the precision of revealing potentially functional genes of GWAS loci.
Author Becker, Tim
Teumer, Alexander
Grabe, Hans J.
Ghasemi, Sahar
AuthorAffiliation 3 DZHK (German Center for Cardiovascular Research), Partner Site Greifswald , Greifswald , Germany
2 Department of Psychiatry and Psychotherapy , University Medicine Greifswald , Greifswald , Germany
4 German Center for Neurodegenerative Diseases DZNE, Site Rostock/Greifswald , Greifswald , Germany
1 Institute for Community Medicine , University Medicine Greifswald , Greifswald , Germany
AuthorAffiliation_xml – name: 1 Institute for Community Medicine , University Medicine Greifswald , Greifswald , Germany
– name: 4 German Center for Neurodegenerative Diseases DZNE, Site Rostock/Greifswald , Greifswald , Germany
– name: 2 Department of Psychiatry and Psychotherapy , University Medicine Greifswald , Greifswald , Germany
– name: 3 DZHK (German Center for Cardiovascular Research), Partner Site Greifswald , Greifswald , Germany
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Cites_doi 10.1001/jama.2010.39
10.1038/ki.2010.550
10.1016/j.clim.2013.08.005
10.1016/S2213-8587(15)00040-6
10.1097/01.asn.0000123691.46138.e2
10.2215/CJN.09741110
10.1038/s41588-018-0047-6
10.1159/000488946
10.1152/ajprenal.90257.2008
10.1371/journal.pgen.1004383
10.1016/j.ajhg.2010.11.011
10.2202/1544-6115.1437
10.1038/s41467-019-11576-0
10.1093/hmg/dds369
10.1038/ng.3190
10.1371/journal.pgen.1002584
10.1038/srep46835
10.1056/NEJMoa041031
10.1038/s41586-018-0579-z
10.1023/b:pham.0000029286.45788.ad
10.1172/JCI141801
10.1016/j.ajhg.2018.07.004
10.1038/ng.2352
10.1016/S0140-6736(13)60595-4
10.1038/ki.2009.85
10.1038/s41467-019-09861-z
10.1371/journal.pone.0194044
10.1038/s41467-019-11704-w
10.1007/s00467-009-1381-9
10.1038/ki.2010.531
10.1093/bioinformatics/btp596
10.1038/ng.568
10.12659/MSM.892141
10.1038/ncomms10023
10.1093/bioinformatics/btab332
10.1093/hmg/ddz263
10.1016/j.ajhg.2016.07.012
10.1038/s41467-018-07867-7
10.1038/s41588-019-0407-x
10.1016/j.ajhg.2017.05.004
10.1016/S0140-6736(10)60674-5
10.1098/rstb.2012.0362
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Keywords expression quantitative trait loci (eQTL)
SNP-specific alpha-level
genome-wide association studies (GWAS)
colocalization
conditional association analysis
estimated glomerular filtration rate (eGFR)
Language English
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Weiqiu Cheng, University of Oslo, Norway
Edited by: Yaowu Liu, Southwestern University of Finance and Economics, China
This article was submitted to Statistical Genetics and Methodology, a section of the journal Frontiers in Genetics
Ryan Sun, University of Texas MD Anderson Cancer Center, United States
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References Gorski (B15) 2017; 7
Kottgen (B25) 2010; 42
Giambartolomei (B12) 2014; 10
Wuttke (B42) 2019; 51
Lee (B26) 2018; 13
Bycroft (B5) 2018; 562
Pattaro (B35) 2012; 8
Mahajan (B29) 2016; 99
Okada (B34) 2012; 44
Aguet (B1) 2019
Loh (B27) 2005; 47
Graham (B16) 2019; 10
Chasman (B6) 2012; 21
Ko (B24) 2017; 100
Aoki (B2) 2008; 295
Kang (B23) 2009; 8
Morris (B31) 2019; 10
Kanai (B22) 2018; 50
Hishida (B20) 2018; 47
Doke (B8) 2021; 131
Hellwege (B17) 2019; 10
Matsushita (B30) 2015; 3
Gansevoort (B9) 2013; 382
Hemmelgarn (B18) 2010; 303
Yang (B43) 2011; 88
Nielsen (B33) 2010; 25
Weiner (B40) 2014; 15
Gansevoort (B10) 2011; 80
Gillies (B13) 2018; 103
Wu (B41) 2019; 28
Ghasemi (B11) 2021; 37
Go (B14) 2004; 351
Astor (B3) 2011; 79
Luu (B28) 2013; 149
Teumer (B38) 2019; 10
Hosaka (B21) 2009; 75
Sun (B37) 2015; 21
Bello (B4) 2011; 6
Urakami (B39) 2004; 21
Nica (B32) 2013; 368
van der Velde (B7) 2010; 375
Herold (B19) 2009; 25
Pattaro (B36) 2016; 7
References_xml – volume: 303
  start-page: 423
  year: 2010
  ident: B18
  article-title: Relation between kidney function, proteinuria, and adverse outcomes
  publication-title: JAMA
  doi: 10.1001/jama.2010.39
– volume: 79
  start-page: 1331
  year: 2011
  ident: B3
  article-title: Lower estimated glomerular filtration rate and higher albuminuria are associated with mortality and end-stage renal disease. A collaborative meta-analysis of kidney disease population cohorts
  publication-title: Kidney Int.
  doi: 10.1038/ki.2010.550
– volume: 149
  start-page: 388
  year: 2013
  ident: B28
  article-title: TSPAN33 is a novel marker of activated and malignant B cells
  publication-title: Clin. Immunol.
  doi: 10.1016/j.clim.2013.08.005
– volume: 3
  start-page: 514
  year: 2015
  ident: B30
  article-title: Estimated glomerular filtration rate and albuminuria for prediction of cardiovascular outcomes: A collaborative meta-analysis of individual participant data
  publication-title: Lancet. Diabetes Endocrinol.
  doi: 10.1016/S2213-8587(15)00040-6
– volume: 15
  start-page: 1307
  year: 2014
  ident: B40
  article-title: Chronic kidney disease as a risk factor for cardiovascular disease and all-cause mortality: A pooled analysis of community-based studies
  publication-title: J. Am. Soc. Nephrol.
  doi: 10.1097/01.asn.0000123691.46138.e2
– volume: 6
  start-page: 1418
  year: 2011
  ident: B4
  article-title: Associations among estimated glomerular filtration rate, proteinuria, and adverse cardiovascular outcomes
  publication-title: Clin. J. Am. Soc. Nephrol.
  doi: 10.2215/CJN.09741110
– volume: 50
  start-page: 390
  year: 2018
  ident: B22
  article-title: Genetic analysis of quantitative traits in the Japanese population links cell types to complex human diseases
  publication-title: Nat. Genet.
  doi: 10.1038/s41588-018-0047-6
– volume: 47
  start-page: 304
  year: 2018
  ident: B20
  article-title: Genome-wide association study of renal function traits: Results from the Japan multi-institutional collaborative cohort study
  publication-title: Am. J. Nephrol.
  doi: 10.1159/000488946
– volume: 295
  start-page: F165
  year: 2008
  ident: B2
  article-title: Kidney-specific expression of human organic cation transporter 2 (OCT2/SLC22A2) is regulated by DNA methylation
  publication-title: Am. J. Physiol. Ren. Physiol.
  doi: 10.1152/ajprenal.90257.2008
– volume: 10
  start-page: e1004383
  year: 2014
  ident: B12
  article-title: Bayesian test for colocalisation between pairs of genetic association studies using summary statistics
  publication-title: PLoS Genet.
  doi: 10.1371/journal.pgen.1004383
– volume: 88
  start-page: 76
  year: 2011
  ident: B43
  article-title: Gcta: A tool for genome-wide complex trait analysis
  publication-title: Am. J. Hum. Genet.
  doi: 10.1016/j.ajhg.2010.11.011
– volume: 8
  start-page: Article23
  year: 2009
  ident: B23
  article-title: Weighted multiple hypothesis testing procedures
  publication-title: Stat. Appl. Genet. Mol. Biol.
  doi: 10.2202/1544-6115.1437
– volume: 10
  start-page: 4130
  year: 2019
  ident: B38
  article-title: Genome-wide association meta-analyses and fine-mapping elucidate pathways influencing albuminuria
  publication-title: Nat. Commun.
  doi: 10.1038/s41467-019-11576-0
– volume: 21
  start-page: 5329
  year: 2012
  ident: B6
  article-title: Integration of genome-wide association studies with biological knowledge identifies six novel genes related to kidney function
  publication-title: Hum. Mol. Genet.
  doi: 10.1093/hmg/dds369
– volume: 47
  start-page: 284
  year: 2005
  ident: B27
  article-title: Efficient Bayesian mixed model analysis increases association power in large cohorts
  publication-title: Nat. Genet.
  doi: 10.1038/ng.3190
– start-page: 787903
  volume-title: The GTEx Consortium atlas of genetic regulatory effects across human tissues
  year: 2019
  ident: B1
– volume: 8
  start-page: e1002584
  year: 2012
  ident: B35
  article-title: Genome-wide association and functional follow-up reveals new loci for kidney function
  publication-title: PLoS Genet.
  doi: 10.1371/journal.pgen.1002584
– volume: 7
  start-page: 46835
  year: 2017
  ident: B15
  article-title: Corrigendum: 1000 genomes-based meta-analysis identifies 10 novel loci for kidney function
  publication-title: Sci. Rep.
  doi: 10.1038/srep46835
– volume: 351
  start-page: 1296
  year: 2004
  ident: B14
  article-title: Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization
  publication-title: N. Engl. J. Med.
  doi: 10.1056/NEJMoa041031
– volume: 562
  start-page: 203
  year: 2018
  ident: B5
  article-title: The UK biobank resource with deep phenotyping and genomic data
  publication-title: Nature
  doi: 10.1038/s41586-018-0579-z
– volume: 21
  start-page: 976
  year: 2004
  ident: B39
  article-title: Creatinine transport by basolateral organic cation transporter hOCT2 in the human kidney
  publication-title: Pharm. Res.
  doi: 10.1023/b:pham.0000029286.45788.ad
– volume: 131
  start-page: e141801
  year: 2021
  ident: B8
  article-title: Transcriptome-wide association analysis identifies DACH1 as a kidney disease risk gene that contributes to fibrosis
  publication-title: J. Clin. Investig.
  doi: 10.1172/JCI141801
– volume: 103
  start-page: 232
  year: 2018
  ident: B13
  article-title: An eQTL landscape of kidney tissue in human nephrotic syndrome
  publication-title: Am. J. Hum. Genet.
  doi: 10.1016/j.ajhg.2018.07.004
– volume: 44
  start-page: 904
  year: 2012
  ident: B34
  article-title: Meta-analysis identifies multiple loci associated with kidney function-related traits in east Asian populations
  publication-title: Nat. Genet.
  doi: 10.1038/ng.2352
– volume: 382
  start-page: 339
  year: 2013
  ident: B9
  article-title: Chronic kidney disease and cardiovascular risk: Epidemiology, mechanisms, and prevention
  publication-title: Lancet
  doi: 10.1016/S0140-6736(13)60595-4
– volume: 75
  start-page: 1308
  year: 2009
  ident: B21
  article-title: Megalin and nonmuscle myosin heavy chain IIA interact with the adaptor protein disabled-2 in proximal tubule cells
  publication-title: Kidney Int.
  doi: 10.1038/ki.2009.85
– volume: 10
  start-page: 1847
  year: 2019
  ident: B16
  article-title: Sex-specific and pleiotropic effects underlying kidney function identified from GWAS meta-analysis
  publication-title: Nat. Commun.
  doi: 10.1038/s41467-019-09861-z
– volume: 13
  start-page: e0194044
  year: 2018
  ident: B26
  article-title: Genome-wide association analysis identifies multiple loci associated with kidney disease-related traits in Korean populations
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0194044
– volume: 10
  start-page: 3842
  year: 2019
  ident: B17
  article-title: Mapping eGFR loci to the renal transcriptome and phenome in the VA Million Veteran Program
  publication-title: Nat. Commun.
  doi: 10.1038/s41467-019-11704-w
– volume: 25
  start-page: 813
  year: 2010
  ident: B33
  article-title: Proteinuria and events beyond the slit
  publication-title: Pediatr. Nephrol.
  doi: 10.1007/s00467-009-1381-9
– volume: 80
  start-page: 93
  year: 2011
  ident: B10
  article-title: Lower estimated GFR and higher albuminuria are associated with adverse kidney outcomes. A collaborative meta-analysis of general and high-risk population cohorts
  publication-title: Kidney Int.
  doi: 10.1038/ki.2010.531
– volume: 25
  start-page: 3275
  year: 2009
  ident: B19
  article-title: Intersnp: Genome-wide interaction analysis guided by a priori information
  publication-title: Bioinformatics
  doi: 10.1093/bioinformatics/btp596
– volume: 42
  start-page: 376
  year: 2010
  ident: B25
  article-title: New loci associated with kidney function and chronic kidney disease
  publication-title: Nat. Genet.
  doi: 10.1038/ng.568
– volume: 21
  start-page: 195
  year: 2015
  ident: B37
  article-title: Inhibition of MiR-199a-5p reduced cell proliferation in autosomal dominant polycystic kidney disease through targeting CDKN1C
  publication-title: Med. Sci. Monit.
  doi: 10.12659/MSM.892141
– volume: 7
  start-page: 10023
  year: 2016
  ident: B36
  article-title: Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms10023
– volume: 37
  start-page: 3521
  year: 2021
  ident: B11
  article-title: Assessment of significance of conditionally independent GWAS signals
  publication-title: Bioinformatics
  doi: 10.1093/bioinformatics/btab332
– volume: 28
  start-page: 4161
  year: 2019
  ident: B41
  article-title: Colocalization of GWAS and eQTL signals at loci with multiple signals identifies additional candidate genes for body fat distribution
  publication-title: Hum. Mol. Genet.
  doi: 10.1093/hmg/ddz263
– volume: 99
  start-page: 636
  year: 2016
  ident: B29
  article-title: Trans-ethnic fine mapping highlights kidney-function genes linked to salt sensitivity
  publication-title: Am. J. Hum. Genet.
  doi: 10.1016/j.ajhg.2016.07.012
– volume: 10
  start-page: 29
  year: 2019
  ident: B31
  article-title: Trans-ethnic kidney function association study reveals putative causal genes and effects on kidney-specific disease aetiologies
  publication-title: Nat. Commun.
  doi: 10.1038/s41467-018-07867-7
– volume: 51
  start-page: 957
  year: 2019
  ident: B42
  article-title: A catalog of genetic loci associated with kidney function from analyses of a million individuals
  publication-title: Nat. Genet.
  doi: 10.1038/s41588-019-0407-x
– volume: 100
  start-page: 940
  year: 2017
  ident: B24
  article-title: Genetic-variation-driven gene-expression changes highlight genes with important functions for kidney disease
  publication-title: Am. J. Hum. Genet.
  doi: 10.1016/j.ajhg.2017.05.004
– volume: 375
  start-page: 2073
  year: 2010
  ident: B7
  article-title: Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: A collaborative meta-analysis
  publication-title: Lancet
  doi: 10.1016/S0140-6736(10)60674-5
– volume: 368
  start-page: 20120362
  year: 2013
  ident: B32
  article-title: Expression quantitative trait loci: Present and future
  publication-title: Philos. Trans. R. Soc. Lond. B Biol. Sci.
  doi: 10.1098/rstb.2012.0362
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Snippet A decreased estimated glomerular filtration rate (eGFR) leading to chronic kidney disease is a significant public health problem. Kidney function is a...
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SubjectTerms colocalization
conditional association analysis
estimated glomerular filtration rate (eGFR)
expression quantitative trait loci (eQTL)
Genetics
genome-wide association studies (GWAS)
SNP-specific alpha-level
Title Discovery of novel eGFR-associated multiple independent signals using a quasi-adaptive method
URI https://www.ncbi.nlm.nih.gov/pubmed/36386835
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