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13 research outputs found

Whole-genome sequencing reveals host factors underlying critical COVID-19

Author: Abd Elghafar M. S.
Abdel-Aziz M.
Abdelrazik M.
Abdollahi H.
Abdullah T.
Abecasis G. R.
Abedalthagafi M.
Abel L.
Abernathy C.
Abraheem A.
Abul-Husn N. S.
Acquilini D.
Adams C.
Adams E. L.
Adams K.
Adamsara A.
Adanini O.
Adeleye O.
Adra D.
Afilalo J.
Afilalo M.
Afolabi D.
Afrasiabi Z.
Agasou A.
Agrawal S.
Aguero D.
Ahmad N.
Ahmadi S.
Ahmed A.
Ahmed C.
Akeroyd L.
Akhtar M. N.
Akinkugbe O.
Aksentijevich A.
Al-Afghani H.
Al-Awdah L.
Alaamery M.
Alahmadey Z. Z.
Alaverdian D.
Alavere H.
Albader A.
Albaiceta G. M.
Albakri J. K.
AlBardis H.
Albeladi M.
Albesher N.
Albrich W.
AlDhawi N.
Aldridge J.
Aleagha A. E.
Alexander P.
Alfonso J.
Alghamdi B.
Alghamdi J.
Ali A.
Ali A.
Ali I. A. M.
Ali S.
Aliannejad R.
Aljawini N.
AlJohani S.
Alkwai S.
Allan A.
Allan E.
Allan J.
Alldis Z.
Allen L.
Allen M.
Allen S.
Allibone S.
Allison K. S.
Allos R.
Ally S. M.
AlMalik A.
Almalki F.
Almohammed I.
Almutairi M.
Alotaibi S.
Alowayn A. M.
Alqahtani S.
Alqubaishi F.
Alrashed M.
Alshareef A.
Alsolm E.
Alswailm M.
Altabaibeh A.
Alvaro A.
AlZahrani D.
Amin V.
Amirsavadkouhi A.
Amitrano S.
Anastasescu E.
Anderson F.
Anderson J.
Anderson M.
Anderson P.
Anderson S.
Anderson S.
Anderson T.
Andolfo I.
Andretta F.
Andreucci E.
Andrew A.
Andrew B.
Andrew G.
Andrews E.
Andrews S. J.
Anedda F.
Anemoli V.
Annis A.
Antcliffe D.
Antinori A.
Antoni M. D.
Anumakonda V.
Apetri E.
Aquino M.
Arabi Y. M.
Aravindan L.
Arbane G.
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Zyndorf M.
Publication venue: 'Springer Science and Business Media LLC'
Publication date: 01/01/2022
Field of study

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

PubliCatt

Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia

Case Reports1. A Late Presentation of Loeys-Dietz Syndrome: Beware of TGFβ Receptor Mutations in Benign Joint Hypermobility

Author: Adu Aderonke
Ahmad Yasmeen
Ahmad Yasmeen
Akil Mohammed
Alavi A.
Alten Rieke
Alten Rieke
Alten Rieke
Ang Andrea
Arendt C.
Arthanari S.
Arthanari S.
Askari Ayman
Atchia Ismael
Axford J.
Aynsley Sarah
Aynsley Sarah
Baker Daniel
Bakshi Jyoti
Bakshi Jyoti
Balint Peter
Baskar Sangeetha
Batra Rajbir
Becerra Elena
Bell Aubrey
Bennett B.
Bensen William
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Zimmermann Birgit
Publication venue
Publication date: 02/08/2017
Field of study

Background: Thoracic aortic aneurysms (TAA) and dissections are not uncommon causes of sudden death in young adults. Loeys-Dietz syndrome (LDS) is a rare, recently described, autosomal dominant, connective tissue disease characterized by aggressive arterial aneurysms, resulting from mutations in the transforming growth factor beta (TGFβ) receptor genes TGFBR1 and TGFBR2. Mean age at death is 26.1 years, most often due to aortic dissection. We report an unusually late presentation of LDS, diagnosed following elective surgery in a female with a long history of joint hypermobility. Methods: A 51-year-old Caucasian lady complained of chest pain and headache following a dural leak from spinal anaesthesia for an elective ankle arthroscopy. CT scan and echocardiography demonstrated a dilated aortic root and significant aortic regurgitation. MRA demonstrated aortic tortuosity, an infrarenal aortic aneurysm and aneurysms in the left renal and right internal mammary arteries. She underwent aortic root repair and aortic valve replacement. She had a background of long-standing joint pains secondary to hypermobility, easy bruising, unusual fracture susceptibility and mild bronchiectasis. She had one healthy child age 32, after which she suffered a uterine prolapse. Examination revealed mild Marfanoid features. Uvula, skin and ophthalmological examination was normal. Results: Fibrillin-1 testing for Marfan syndrome (MFS) was negative. Detection of a c.1270G > C (p.Gly424Arg) TGFBR2 mutation confirmed the diagnosis of LDS. Losartan was started for vascular protection. Conclusions: LDS is a severe inherited vasculopathy that usually presents in childhood. It is characterized by aortic root dilatation and ascending aneurysms. There is a higher risk of aortic dissection compared with MFS. Clinical features overlap with MFS and Ehlers Danlos syndrome Type IV, but differentiating dysmorphogenic features include ocular hypertelorism, bifid uvula and cleft palate. Echocardiography and MRA or CT scanning from head to pelvis is recommended to establish the extent of vascular involvement. Management involves early surgical intervention, including early valve-sparing aortic root replacement, genetic counselling and close monitoring in pregnancy. Despite being caused by loss of function mutations in either TGFβ receptor, paradoxical activation of TGFβ signalling is seen, suggesting that TGFβ antagonism may confer disease modifying effects similar to those observed in MFS. TGFβ antagonism can be achieved with angiotensin antagonists, such as Losartan, which is able to delay aortic aneurysm development in preclinical models and in patients with MFS. Our case emphasizes the importance of timely recognition of vasculopathy syndromes in patients with hypermobility and the need for early surgical intervention. It also highlights their heterogeneity and the potential for late presentation. Disclosures: The authors have declared no conflicts of interes

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Whole-genome sequencing reveals host factors underlying critical COVID-19

Author: Abd Elghafar M.S.
Abdel-Aziz M.
Abdelrazik M.
Abdollahi H.
Abdullah T.
Abecasis G.R.
Abecasis G.R.
Abedalthagafi M.
Abel L.
Abernathy C.
Abraheem A.
Abul-Husn N.S.
Acquilini D.
Adams C.
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Adeleye O.
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Afilalo J.
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Zhou W.
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Zlatopolsky M.
Zongo O.
Zucchi P.
Zyndorf M.
Zöllner S.
Åsvold B.O.
Publication venue: Springer Science and Business Media LLC
Publication date: 07/07/2022
Field of study

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

White Rose Research Online

Voltammetric Response of Zeolite‐Modified Electrodes

Author: Brenda R. Shaw
Christopher J. Lanczycki
Jeffrey A. Sargeant
Kenneth E. Creasy
Marta Tirhado
Publication venue: 'The Electrochemical Society'
Publication date
Field of study

Crossref

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

Archivio istituzionale della ricerca - Politecnico di Milano

Archivio della ricerca - Università degli studi di Napoli Federico II

Archivio della Ricerca - Università degli Studi di Siena

Archivio istituzionale della ricerca - Alma Mater Studiorum Università di Bologna

Archivio istituzionale della ricerca - Università di Genova

UTUPub

Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia

Archivio istituzionale della ricerca - Università di Padova

Wild Ungulates as Disseminators of Shiga Toxin-Producing Escherichia coli in Urban Areas

Author: A Donohue-Rolfe
A García-Sánchez
A Mora
Alan B. Franklin
Amber Powell
BC Lubow
CL Gyles
CL Meays
CM Hurvich
CR Hale
DW Walter
E Scallan
Elaine Scallan
F Hibert
H Henderson
Hugh Maguire
J. Jeffrey Root
JC Paton
JJ Gilbreath
JM Sargeant
JR Fischer
JT Brooks
Justin W. Fischer
Kurt C. VerCauteren
LA Branham
LC Chase
M Bardiau
MA Karmali
Markus M. Heimesaat
Mary K. Cichon
MD Grund
Michael J. Lavelle
S Hoffmann
S Sánchez
SJ Olsen
T de Sablet
U Reischl
Publication venue: 'Public Library of Science (PLoS)'
Publication date
Field of study

Crossref

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Abedalthagafi M
Abel L
Abel L
Abellan J
Abernathy C
Abraheem A
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Adanini O
Afolabi D
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Agravante K
Agravante K
Agrawal S
Aguado JM
Aguilar C
Aguilar PM
Aguilera-Albesa S
Ahmad N
Ahmadhaider N
Ahmed A
Ahmed C
Aitkin E
Akeroyd L
Akhtar MN
Akinkugbe O
Al-Moasseb H
Alasdair F
Alba J
Albu S
Alcalá-Gallardo KAM
Alcoba-Florez J
Aldridge J
Alex B
Alexander P
Alfonso J
Algarin-Lara HR
Ali A
Ali HH
Ali IAM
Ali S
Allan A
Allan E
Allan J
Alldis Z
Allen L
Allen M
Allen S
Allibone S
Allison KS
Ally SM
Almadana V
Almaden-Boyle C
Almeida J
Almoguera B
Alonso MR
Altabaibeh A
Alvarez N
Alvaro A
Alves MDM
Amamio M
Amamio M
Amin V
Anastasescu E
Anderson J
Anderson M
Anderson P
Anderson S
Anderson S
Anderson T
Andreou P
Andreu-Bernabeu Á
Andrew A
Andrew B
Andrew G
Andrews J
Andrikopoulos P
Antcliffe D
Antoine P
Antonijoan MR
Antony S
Anumakonda V
Anwer M
Apetri E
Aquino M
Arana-Arri E
Aranda C
Arango C
Araque C
Araujo IMT
Araujo NK
Aravindan L
Arbane G
Arcanjo AC
Archer K
Arden T
Arias SS
Arif S
Armistead J
Armstrong D
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Armstrong R
Arnaiz A
Arnott A
Arora M
Arranz MJ
Artiga M-J
Ashby K
Ashok SR
Ashraf S
Ashton L
Aslibekyan S
Astin-Chamberlain R
Atayeva N
Attwood B
Atwal I
Auld F
Austin K
Austin P
Auton A
Avello-Malaver Y
Ayers A
Ayuso C
Bach B
Badal B
Baddeley A
Bafitis V
Baikady RR
Bailey L
Baillie JK
Baillie JK
Baillie K
Baines D
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Baker M
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Baldión-Elorza AM
Bamford A
Bamford A
Bamford P
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Bandla N
Bano S
Baptista D
Baptista-Rosas RC
Barber R
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Barclay C
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Barclay WS
Barker J
Barker M
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Barranco-Díaz A
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Barrera-Penagos V
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Bevan E
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Bezerra JF
Bezerra MAC
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Blakemore H
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Cordero-Lorenzana ML
Corella D
Corin C
Cornell S
Cornell T
Corner A
Corral MA
Corrales A
Cortes-Sanchez JL
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Costa TX
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Coton Z
Cottam L-J
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Cuerda VM
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Dantas-Komatsu RCS
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Darnaude MT
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de Araújo JNG
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de Gordoa LO-R
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de Juan C
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de la Horra C
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De Queiroz JG
de Quirós FGB
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de Sousa Alves Neri JL
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Dexter C
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Diaz-Caneja CM
Dickson H
Dietl B
Digby B
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Ding L
Diz-de Almeida S
Djeugam B
Doble P
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Docherty AB
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Domínguez-Garrido E
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Elliott K
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Eltayeb A
Emblem J
Enciso-Olivera CO
English K
Eros A
Escudero G
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España PP
Estévez JV
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Farquhar F
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Ferguson S
Fernandes F
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Fernandez Z
Fernandez-Caballero L
Fernandez-Nestosa MJ
Fernandez-Roman J
Fernández AM
Fernández FA
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Fernández-Cruz A
Fernández-Robelo U
Fernández-Rodríguez A
Fernández-Sampedro M
Fernández-Sánchez R
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Ferrero SF
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Fumadó V
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Gago-Domínguez M
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Gallego N
Gallo JPV
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Garcia-Cerrada C
Garcia-García J
García FR
García I
García L
García M
García MG
García PM
García-de-Vicuña A
García-García I
García-Ibarbia C
García-Montero AC
García-Soidán A
García-Vázquez E
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Gascoyne R
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Gnanapragasam P
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Gonzalez-Sagrado M
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Oteo JA
Owen S
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O’Connell S
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O’Connor D
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Pinho SMT
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Pinsach-Abuin ML
Pinzuti I
Pinzón LA
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Pirie S
Pita G
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Player B
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Pogreban T
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Polgar O
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Pollakis G
Pompa-Mera EN
Ponting CP
Poole A
Poole M
Pope R
Popescu M
Porras MS
Porras-Hurtado GL
Postovalova E
Pothecary C
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Potla D
Potoczna D
Potts K
Poulaka M
Poultney U
Prados MCS
Prady H
Prager K
Pratley A
Prendergast C
Prentice L
Preston S
Price A
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Priestley V
Prime Z
Pristopan V
Pritchard K
Pritchard L
Proudfoot N
Prout R
Pryce J
Prysyazhna O
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Pujol A
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Shastri AJ
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Shelton JF
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Shepherd A
Shepperson A
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Woolcock M
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Wreybrown C
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Yáñez Z
Zak A
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Zambon M
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Zapatamartinez M
Zapatero-Gaviria A
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Zborowski AC
Zechner M
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Álvarez BG
Álvarez-Benítez Y
Álvarez-Navia F
Íñiguez M
Publication venue: Springer Nature
Publication date: 17/05/2023
Field of study

Data availability: Downloadable summary data are available through the GenOMICC data site (https://genomicc.org/data). Summary statistics are available, but without the 23andMe summary statistics, except for the 10,000 most significant hits, for which full summary statistics are available. The full GWAS summary statistics for the 23andMe discovery dataset will be made available through 23andMe to qualified researchers under an agreement with 23andMe that protects the privacy of the 23andMe participants. For further information and to apply for access to the data, see the 23andMe website (https://research.23andMe.com/dataset-access/). All individual-level genotype and whole-genome sequencing data (for both academic and commercial uses) can be accessed through the UKRI/HDR UK Outbreak Data Analysis Platform (https://odap.ac.uk). A restricted dataset for a subset of GenOMICC participants is also available through the Genomics England data service. Monocyte RNA-seq data are available under the title ‘Monocyte gene expression data’ within the Oxford University Research Archives (https://doi.org/10.5287/ora-ko7q2nq66). Sequencing data will be made freely available to organizations and researchers to conduct research in accordance with the UK Policy Framework for Health and Social Care Research through a data access agreement. Sequencing data have been deposited at the European Genome–Phenome Archive (EGA), which is hosted by the EBI and the CRG, under accession number EGAS00001007111.Extended data figures and tables are available online at https://www.nature.com/articles/s41586-023-06034-3#Sec21 .Supplementary information is available online at https://www.nature.com/articles/s41586-023-06034-3#Sec22 .Code availability: Code to calculate the imputation of P values on the basis of SNPs in linkage disequilibrium is available at GitHub (https://github.com/baillielab/GenOMICC_GWAS).Acknowledgements: We thank the members of the Banco Nacional de ADN and the GRA@CE cohort group; and the research participants and employees of 23andMe for making this work possible. A full list of contributors who have provided data that were collated in the HGI project, including previous iterations, is available online (https://www.covid19hg.org/acknowledgements).Change history: 11 July 2023: A Correction to this paper has been published at: https://doi.org/10.1038/s41586-023-06383-z. -- In the version of this article initially published, the name of Ana Margarita Baldión-Elorza, of the SCOURGE Consortium, appeared incorrectly (as Ana María Baldion) and has now been amended in the HTML and PDF versions of the article.Copyright © The Author(s) 2023, Critical illness in COVID-19 is an extreme and clinically homogeneous disease phenotype that we have previously shown1 to be highly efficient for discovery of genetic associations2. Despite the advanced stage of illness at presentation, we have shown that host genetics in patients who are critically ill with COVID-19 can identify immunomodulatory therapies with strong beneficial effects in this group3. Here we analyse 24,202 cases of COVID-19 with critical illness comprising a combination of microarray genotype and whole-genome sequencing data from cases of critical illness in the international GenOMICC (11,440 cases) study, combined with other studies recruiting hospitalized patients with a strong focus on severe and critical disease: ISARIC4C (676 cases) and the SCOURGE consortium (5,934 cases). To put these results in the context of existing work, we conduct a meta-analysis of the new GenOMICC genome-wide association study (GWAS) results with previously published data. We find 49 genome-wide significant associations, of which 16 have not been reported previously. To investigate the therapeutic implications of these findings, we infer the structural consequences of protein-coding variants, and combine our GWAS results with gene expression data using a monocyte transcriptome-wide association study (TWAS) model, as well as gene and protein expression using Mendelian randomization. We identify potentially druggable targets in multiple systems, including inflammatory signalling (JAK1), monocyte–macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A).GenOMICC was funded by Sepsis Research (the Fiona Elizabeth Agnew Trust), the Intensive Care Society, a Wellcome Trust Senior Research Fellowship (to J.K.B., 223164/Z/21/Z), the Department of Health and Social Care (DHSC), Illumina, LifeArc, the Medical Research Council, UKRI, a BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070 and BBS/E/D/30002275) and UKRI grants MC_PC_20004, MC_PC_19025, MC_PC_1905 and MRNO2995X/1. A.D.B. acknowledges funding from the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z), the Edinburgh Clinical Academic Track (ECAT) programme. This research is supported in part by the Data and Connectivity National Core Study, led by Health Data Research UK in partnership with the Office for National Statistics and funded by UK Research and Innovation (grant MC_PC_20029). Laboratory work was funded by a Wellcome Intermediate Clinical Fellowship to B.F. (201488/Z/16/Z). We acknowledge the staff at NHS Digital, Public Health England and the Intensive Care National Audit and Research Centre who provided clinical data on the participants; and the National Institute for Healthcare Research Clinical Research Network (NIHR CRN) and the Chief Scientist’s Office (Scotland), who facilitate recruitment into research studies in NHS hospitals, and to the global ISARIC and InFACT consortia. GenOMICC genotype controls were obtained using UK Biobank Resource under project 788 funded by Roslin Institute Strategic Programme Grants from the BBSRC (BBS/E/D/10002070 and BBS/E/D/30002275) and Health Data Research UK (HDR-9004 and HDR-9003). UK Biobank data were used in the GSMR analyses presented here under project 66982. The UK Biobank was established by the Wellcome Trust medical charity, Medical Research Council, Department of Health, Scottish Government and the Northwest Regional Development Agency. It has also had funding from the Welsh Assembly Government, British Heart Foundation and Diabetes UK. The work of L.K. was supported by an RCUK Innovation Fellowship from the National Productivity Investment Fund (MR/R026408/1). J.Y. is supported by the Westlake Education Foundation. SCOURGE is funded by the Instituto de Salud Carlos III (COV20_00622 to A.C., PI20/00876 to C.F.), European Union (ERDF) ‘A way of making Europe’, Fundación Amancio Ortega, Banco de Santander (to A.C.), Cabildo Insular de Tenerife (CGIEU0000219140 ‘Apuestas científicas del ITER para colaborar en la lucha contra la COVID-19’ to C.F.) and Fundación Canaria Instituto de Investigación Sanitaria de Canarias (PIFIISC20/57 to C.F.). We also acknowledge the contribution of the Centro National de Genotipado (CEGEN) and Centro de Supercomputación de Galicia (CESGA) for funding this project by providing supercomputing infrastructures. A.D.L. is a recipient of fellowships from the National Council for Scientific and Technological Development (CNPq)-Brazil (309173/2019-1 and 201527/2020-0)

Brunel University Research Archive

A second update on mapping the human genetic architecture of COVID-19

Author: Abd Elghafar MS
Abdel-Aziz M
Abdelrazik M
Abdullah MS
Abe R
Abe S
Abel L
Abel L
Abernathy C
Abraham R
Abraheem A
Abu Alragheb BO
Abulail JA
Acklery A
Acosta-Herrera M
Adachi T
Adachi Y
Adam R
Adams C
Adams K
Adams N
Adanini O
Afifi N
Afilalo J
Afilalo M
Afolabi D
Afrasiabi Z
Afset JE
Agasou A
Aghemo A
Agravante K
Agrawal A
Agrawal S
Aguado JM
Aguilar C
Aguilar SEV
Aguilar-Salinas CA
Aguilera-Albesa S
Agüero D
Ahmad HF
Ahmad N
Ahmadhaider N
Ahmed A
Ahmed C
Ahram M
Ai M
Ain Q
Aitkin E
Akeroyd L
Akhtar MN
Akinkugbe O
Al-Ani A
Al-Ja’afreh MM
Al-Kadash A
Al-Kasasbeh MM
Al-Moasseb H
Al-Muftah W
Al-Sarraj Y
Alamer LM
Alasdair F
Alawneh FM
Alawneh LM
Albaiceta GM
Albano G
Albillos A
Albrecht W
Aldridge J
Alexander P
Alfonso J
Alhousani TN
Ali A
Ali HH
Ali IAM
Ali S
Aliberti S
ALjalamdeh M
Allan A
Allan E
Allan J
Alldis Z
Allen L
Allen M
Allen S
Allen U
Allibone S
Allison KS
Allouzy SK
Ally SM
Almadana V
Almaden-Boyle C
Almoguera B
Alpuche-Aranda C
AlRawashdeh TJ
Alsafadi DB
Alshaer W
Alsoub FS
Altabaibeh A
Alvarez N
Alvaro A
Alzuraiqi MR
Amamio M
Aman NF
Amin V
Amiya S
Ampuero J
Anan R
Anastasescu E
Andersen S
Anderson J
Anderson M
Anderson P
Anderson S
Anderson S
Anderson T
Ando A
Andrade V
Andreou P
Andreu-Bernabeu Á
Andrew A
Andrew B
Andrew G
Andrews J
Andrews S
Andrews SJ
Angelini C
Ansari AI
Antcliffe D
Antoine P
Antony S
Anumakonda V
Anwer M
Anzai T
Apetri E
Aquino M
Aquino-Gálvez A
Arai D
Arakelyan A
Arana-Arri E
Arana-Arri E
Arango C
Aravindan L
Arbane G
Archer K
Arden T
Arias SS
Arif S
Arimura K
Armistead J
Armstrong D
Armstrong J
Armstrong L
Armstrong R
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Arnoldo S
Arnott A
Arora J
Arora M
Arranz MJ
Arranz MJ
Arribas-Rodriguez E
Artiga M-J
Arumugam P
Asakura T
Asano K
Aschard H
Ashby K
Ashok SR
Ashraf S
Ashton L
Asimakopoulos A
Aslibekyan S
Asselta R
Astin-Chamberlain R
Atayeva N
Athanasiou L
Atkinson EG
Attwood B
Atwal I
Augustin M
Auld D
Auld F
Austin K
Austin P
Auton A
Avetyan D
Awano N
Awasthi S
Ayers A
Ayo NI
Ayuso C
Aziz F
Aziz N
Azuma M
Azuure C
Azzolini E
Baba R
Baba T
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Badal B
Badalamenti S
Baddeley A
Badia JR
Badji RM
Bafitis V
Bahmer T
Baikady RR
Bailey L
Baillie JK
Baines D
Baines K
Baird T
Baird Y
Baker M
Bakthavatsalam D
Balaconis MK
Baldini M
Balla D
Bals R
Bamford A
Bamford A
Bamford P
Banach D
Banales JM
Banasik K
Banasik K
Bancroft H
Band G
Bandera A
Bandla N
Bani younis FM
Bano S
Baptista D
Baptista-Rosas RC
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Barberena-Jonas C
Barberis L
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Barclay L
Barker J
Barker M
Barnes KC
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Barnetche JM
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Barreda-Sánchez M
Barreira A
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Barrett F
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Basikolo C
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Below JE
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Benkenstein S
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Butler-Laporte G
Butler-Laporte G
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Butterworth-Cowin N
Button H
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Caballero-Garralda A
Cabral-Ortega L
Cabrelli L
Cabrero DG
Cadenas IF
Cadilla CL
Cagova L
Cal-Sabater P
Calderón EJ
Calderón EJ
Cale E
Callaghan M
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Campbell A
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Campbell R
Campbell S
Campigotto A
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Cantú-Brito C
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Cappadona C
Cappelli C
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Carbonell C
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Cardwell A
Carmody M
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Carnahan M
Carpani R
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Carter A
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Castelao JE
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Castoldi M
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Caulfield MJ
Cavallero A
Cavazza A
Cave A
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Cawthron K
Cazzaniga M
Cea C
Ceballos FC
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Cejudo TG
Ceriotti F
Cerpa LC
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Chadwick R
Chaliasos K
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Chandler B
Chandna H
Chang D
Chang TS
Chao G
Chapman S
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Cheatley PL
Cheema Y
Chen H-H
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Chercoles AG
Cherian S
Chernitsov A
Chertkow H
Cherubini A
Chesters K
Chetam L
Cheung AM
Cheyne C
Chiba S
Chihara Y
Chikowore P
Childs D
Chiquete E
Chirino-Pérez A
Chirouze C
Chisholm C
Chiu A
Choe K-W
Choudhr O
Choudhury Y
Chowdhary S
Christaki E
Christian MA
Chubachi S
Chueca N
Chuhan NT
Chukkambotla S
Chung M
Churchhouse C
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Chávez-Manzanera E
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Cirulli ET
Citerio G
Claire D-R
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Clarey E
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Clark M
Clark M
Clark R
Clark R
Clark S
Clark V
Clarke N
Clarkson M
Clausen M
Clayton S
Clement I
Clements S
Coates C
Cobat A
Cochrane P
Cockerill H
Cockrell M
Coe R
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Coghlan P
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Colbert SMC
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Collins V
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Colombo A
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Conde-Vicente R
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Cookson R
Cooper J
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Corbetta A
Corcoran E
Corcoran K
Cordero-Lorenzana ML
Cordioli M
Cordioli M
Corin C
Cornberg M
Cornell S
Cornell T
Cornely OA
Corner A
Corral MA
Cortes B
Cortes-Sanchez JL
Corton M
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Cosgrove D
Cosier T
Costantino G
Cother N
Coto E
Coton Z
Cottam L-J
Cottle J
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Coventry T
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Cowan J
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Cowton A
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Coyle J
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Crawley R
Creagh-Brown B
Crew A
Crickmore V
Cristiano D
Croft M
Crook DW
Crooks K
Crowe R
Crowley M
Cruz C
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Cruz-Bautista I
Cruz-Cruz AD
Csabi P
Cuerda VM
Cullell N
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Cunningham A
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Cáceres M
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Dalmau D
Dalton C
Daly M
Daly MJ
Daly Z
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DAmato F
Damås JK
Dance A
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Daniel E
Daniel P
Daniels A
Darcis G
Dark P
Darlington K
Darnaude MT
Darnell S
Das M
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Dasgin J
Daubney E
Davey M
David B
Davidson N
Davidyants M
Davies A
Davies C
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Davies E
Davies F
Davies G
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Davies J
Davies K
Davies L
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Davies R
Davies S
Davis A
Davis C
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Davis LK
Davison C
Dawson A
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Day A
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Daya M
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De Cid R
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De Felipe Mimbrera A
De Gordoa LO-R
De Heredia ML
De Jesús Carrera García K
De Jesús Suárez López J
De la Horra C
De León-Garduño AP
De los Ángeles Vargas-Martínez M
De Martino-Rodríguez A
De Neef M
De Pablo R
De Quirós FGB
De Rojas I
De Salazar A
Deacon B
Dean C
Dearden J
DeAth Y
Debette S
Debreceni G
DeDiego ML
Deery J
Degenhardt F
Del Campo-Pérez V
Del Consuelo Rodríguez Mancilla M
Delaney J
Deleuze J-F
Delgado CC
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Dell A
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Denmade C
Dennis C
Dent K
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Depante M
Desai KJ
Devine L
Dexter C
Diaba C
Dickson H
Didriksen M
Dietl B
Digby B
Digby S
Ding L
Ding Y
Dinh KM
Dixit RD
Diz-de Almeida S
Djeugam B
Dobaño C
Doble P
Dobosz P
Dobson E
Dodd A
Dodds S
Dolan H
Domingo C
Domingos P
Domínguez-Garrido E
Domínguez-Mayoral A
Donaldson A
Donaldson D
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Donne B
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Donner K
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Donovan S
Dooks E
Doonan R
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Douillard V
Doverman K
Downes C
Dreher M
Drummond A
Dube J
Duberley S
Ducharme FM
Dudman S
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Duffield J
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Duffy D
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Duga S
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Duncan T
Dunhill J
Dunmore C
Dunn J
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Durie A
Durrans LJ
Durrant G
Durán RG
Durán-Gómez M
Duskova M
Dutta AK
Dykes J
Dyrhol-Riise AM
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Décary S
Díaz-Olavarrieta C
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El-Shanshory MR
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Elías-López D
Emblem J
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España PP
Espinosa-Parrilla Y
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Evitts J
Ezeobu O
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Falcone EL
Fan CC
Fariñas MC
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Farquhar F
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Fave M-J
Faverio P
Fawkes A
Fazaal J
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Feldt-Rasmussen U
Felton T
Feng Y-CA
Ferguson S
Fernandes F
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Fernandes MR
Fernandez R
Fernandez Z
Fernandez-Cadenas I
Fernandez-Roman J
Fernandez-Ruiz J
Fernández J
Fernández-Robelo U
Fernández-Rodríguez A
Fernández-Villa T
Ferrando C
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Figuera Basso ME
Filipe H
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Francis S
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Frankham J
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Fritzler M
Frost V
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Fuentes M
Fuentes-Guajardo M
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Fujiwara A
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Fukuyama S
Funatsu Y
Fung CYJ
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Galván-Femenia I
Galván-Femenía I
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Garant J-M
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Garcia-Aymerich J
Garcia-Etxebarria K
Garcia-Fernandez A-E
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García-Clemente M
García-García L
García-Grimshaw M
García-Madrona S
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Georgiou I
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Glasgow S
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Gloria EFD
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Herbrick J-A
Herdman-Grant R
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Hernández Cordero AI
Hernández I
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Hirano T
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Holter JC
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Horby P
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Huang Y-WJ
Hubbard K
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Huerta-Chagoya A
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Huffenberger A
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Irvine V
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Ishikura H
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Isogai S
Isono T
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Ito A
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Jaime-Capetillo ME
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Jamieson A
Jang HY
Jang YR
Jansen P
Jaramillo MAMD
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Jemec GB
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Jennings C
Jensen B-EO
Jeong H
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Jermy B
Jerome E
Jerry D
Jetha C
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Jhanji S
Jimenez-Sousa MA
Jiménez D
Jiménez-Xarrié E
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Jobes L
Joefield T
Johansson PI
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Joseph A
Joseph R
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Joshi CG
Joshi MN
Joshy A
Jouanguy E
Joubert P
Joy R
Jude E
Julienne H
Julià A
Junaid A
Jung KJ
Juzenas S
Kabata H
Kadiri S
Kagaya T
Kaja E
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Kajtor I
Kaliappan A
Kallon D
Kalman JL
Kamal L
Kamangu B
Kamata H
Kamath P
Kamundi C
Kanai M
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Kanai T
Kanaoka K
Kanda H
Kanehiro A
Kanellopoulou A
Kaneyama Y
Kang YM
Kannan T
Kanu R
Kapoor R
Karadeniz Z
Karczewski KJ
Karjalainen J
Karlsen TH
Karlson EW
Karthik K
Kasipandian V
Kassam J
Kassymbek K
Katary A
Katayama K
Kato K
Kaufmann DE
Kaul S
Kaunisto M
Kausar R
Kaushik D
Kavanagh L
Kawai Y
Kawamura K
Kawana A
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Kawashima H
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Kennedy-Hay S
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Khade R
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Khalifeh Z
Khaliq W
Khamitov S
Khan EA
Khan H
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Khan MI
Khan Z
Khera J
Khodamoradi Y
Kibutu F
Kikuchi T
Kildal AB
Kilroy S
Kim A
Kim B-J
Kim HA
Kim JY
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Kim Y-S
Kim YJ
Kimizuka Y
Kimura A
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Kinch A
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Kitamura H
Kitching A
Kitson R
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Knighton A
Knights E
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Kousathanas A
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Kraft J
Krasnenko A
Krieger JE
Krishnamurthy V
Kristiansson K
Król Z
Kubisz-Pudelko A
Kumanogoh A
Kumar R
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Kupiec K
Kuravi A
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Kwon KT
Kwong ASF
Kym S
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Lake V
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Lamond Z
Lamorte G
Lancaster N
Lancoma-Malcolm I
Landeg B
Landmesser U
Lange C
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Langridge E
Langton H
Laouénan C
Lapadula E
Lapunzina P
Larman G
Larsen MAH
Latham S
Lathrop GM
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Latiano A
Latif M
Lattig MC
Latz E
Lauder C
Laurent L
Law A
Law D
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Law S
Lawless JF
Lawton T
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Lean R
Leaver S
Ledgard C
Lee E
Lee H
Lee HS
Lee JE
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Lee JY
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Lee SHT
Lees R
Lefloch E
Leggett S
Lehmann C
Leigh M
Lejman A
Lemaçon A
Lenagh B
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Lenning OB
Lennon L
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Lenz TL
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Lerner-Ellis J
Lewis A
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León SR
Liderth S
Lidstone-Scott R
Liew J
Liggett S
Lim L
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Lin S-K
Lind A
Lindergard G
Linfield-Brown G
Ling L
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Linnett V
Liontos A
Lipcsey M
Lippert LJ
Lisboa A
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Llucià-Carol L
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London E
Long K
Loosley R
Lopez-Rodriguez R
Lorah S
Lorenti M
Lorenzo-Salazar JM
Lorusso R
Love N
Loveridge A
Low E
Lozano F
Lu JT
Lu W
Lubimbi G
Lucas R
Luchessi AD
Ludwig KU
Ludwig N
Luna MTT
Luna-Moreno D
Luna-Ramírez SA
Lye A
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Lynch C
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MacCallum N
MacDonald G
Macgillivray L
MacGoey P
Macharia I
Mackay C
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Mackintosh K
Maclean A
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Macías EM
Maeda S
Maeda Y
Maeno T
Mahajan A
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Maizcordoba M
Maj C
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Maleady-Crowe F
Malik A
Malinauskas T
Mallinson J
Mallon L
Malvestiti F
Manabe T
Mancebo E
Mandla R
Manley R
Manna S
Manso K
Mansour TA
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Mantovani A
Manunta M
Mapfunde I
Maqsood Z
Marani M
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Maricic T
Markozannes G
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Marshall J
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Martagón-Rosado A
Martin AR
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Martin HC
Martin J
Martin T
Martin-Nalda A
Martindale T
Martinelli-Boneschi F
Martinez ML
Martinez-Lopez I
Martinez-Nieto O
Martinez-Perez A
Martinez-Resendez MF
Martins L
Martinson V
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Marttila MM
Martí-Fàbregas J
Martín J
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Martín-López C
Martínez AIR
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Masjuan J
Maslove D
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Masunda B
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Maswadeh AB
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Matheson J
Mathew B
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Matsuda F
Matt R
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Matthews J
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Matveev V
May P
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Maya-Miles D
Mayangao I
Mayer A
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Maynard V
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Mcintyre L
McIvor S
McKechnie S
McKenley I
McKenna E
McKie H
McLaughlan D
McLeod SL
McLoughlin L
Mcmaster E
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McParland C
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Medina-Gomez C
Medina-Gómez C
Medrano FJ
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Melville J
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Menéndez-Valladares P
Mepham S
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Mercer O
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Meredith M
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Mesonero F
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Metryka A
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Mitchell AM
Mitchelmore O
Mitra A
Miyano S
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Miyazaki Y
Miyazawa N
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Mochimaru T
Modi B
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Mohamed AAS
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Moncur E
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Monnery S
Montano N
Montaser R
Montgomery H
Montpetit A
Monzani V
Moore F
Moore L
Moore LSP
Moore SC
Mooser V
Morales-Sosa PA
Morano EMH
Moreno V
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Moreno-Cuesta J
Moreno-Estrada A
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Morrison DR
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Murdoch E
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Muñóz-Hernández LL
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Nakamura A
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Nakamura Y
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Nicholson A
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Niemi MEK
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Nikitas N
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Openshaw PJM
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Orlikowska I
Ortega-Paino E
Ortiz AB
Osbourne W
Ostadreza M
Ostermann M
Ostrowski M
Ostrowski SR
Ostrowski SR
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Oxspring S
Oyamada Y
Ozaki S
Oziegb M
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O’Connell AM
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O’Connell S
O’Connor D
O’Connor G
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Page V
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Pajak S
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Palmieri O
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Papathanasiou A
Papenburg J
Papiol S
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Paraboschi EM
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Pargana E
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Park H-Y
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Parris V
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Patch C
Patel A
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Patel M
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Patel SK
Patel T
Patel ZZ
Paterson AD
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Pathak GA
Pathan N
Patience D
Patil A
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Pawley C
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Pellegrin I
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Peschuck A
Pesenti A
Pestaña D
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Peterkin Z
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Petty LE
Peyrassol X
Peyvandi F
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Pink I
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Pinzuti I
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Pirie S
Pirinen M
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Place M
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Player B
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Plotnikov N
Pogreban T
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Polgar O
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Polikowsky HG
Poller W
Pompa-Mera EN
Pontali E
Ponting CP
Poole A
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Pope R
Popescu M
Popov I
Porras MS
Porras-Hurtado GL
Postovalova E
Pothecary C
Potla D
Potoczna D
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Poulaka M
Poultney U
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Pratley A
Preatoni P
Prendergast C
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Puxty A
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Qiu X
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Quaid S
Queiroz JGD
Quereda C
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Quintela I
Quinto-Cortés CD
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Revill A
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Rodriguez-Frias F
Rodriguez-Garcia JA
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Romero-Gómez M
Romero-Molina ÁO
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Rybniker J
Ryu J
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Sagara H
Sageshima H
Saha R
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Sailybayeva A
Sainsbury H
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Sakagami S
Sakuntabhai A
Salada S
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Salciute E
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Salmi S
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Samakomva T
Samir A
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Sanabria GME
Sanchez - Rodriguez A
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Segura-Kato Y
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Serra-Llovich A
Serrano-Heras G
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Shamah-Levy T
Shankar-Hari M
Shanmugasundaram P
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Shiel R
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Shimizu T
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Shiomi T
Ship L
Shirai Y
Shiroyama T
Shivanathan I
Shokkar R
Shoko T
Shoma A
Shoremekun A
Short A
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Shorter S
Shortt J
Shovelton C
Shuey MM
Shuker K
Sibbett L
Sicat C
Sidall E
Siddiq A
Sierra-Vargas MP
Sifuentes-Osornio J
Silbiger VN
Silva AX
Silva P
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Sims T
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Sinclair S
Sinfield E
Singh I
Singh J
Singler K
Singleton J
Sipeky C
Sirui Z
Sitonik M
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Skogen V
Skurk C
Skyes D
Slack L
Slater V
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Slawson N
Slevin K
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Smagulova Z
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Smeaton J
Smedley C
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Smoller JW
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Sonehara K
Sonobe K
Soria JM
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Spencer CCA
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Spinner CD
Spivey M
Springle P
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Sri-Chandana C
Srikaran S
St-Cyr J
Stacey A
Stagg C
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Stapleton L
Stark KJ
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Stern S
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Stoddard E
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Sugiyama M
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Sukhatme MG
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Sutherland S-B
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Szabo D
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Szentpéteri JL
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Takaku Y
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Takata T
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Takeda Y
Takeuchi M
Taki R
Tamayo E
Tamayo-Velasco A
Tampsett R
Tanaka A
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Tanate A
Tanck A
Taneski F
Tani M
Tanigawa Y
Tanino Y
Taniyama D
Tanudjaja F
Taracido-Fernandez JC
Tardif N
Tariq A
Tateishi T
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Thirumaran M
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Thomas A
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Torky MS
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Torres-Espíndola LM
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Trembath RC
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Treus E
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Zamudio IPM
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Zawadzki P
Zawati MH
Zborowski AC
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Zhlawi MWJ
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Zhou W
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Zongo O
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Álvarez BG
Ávila-Arcos MA
Ávila-Arcos MC
Özer O
Überla K
Þorsteinsdóttir U
Publication venue: Nature Research
Publication date: 21/06/2023
Field of study

Spiral - Imperial College Digital Repository