65 research outputs found
Congenital Hypogonadotropic Hypogonadism Due to GNRH Receptor Mutations in Three Brothers Reveal Sites Affecting Conformation and Coupling
- Author
- A Antelli
- A Herbison
- A Leaños-Miranda
- A Meysing
- A Tabarin
- AK Topaloglu
- Anne Guiochon-Mantel
- B Francou
- B Karges
- C Bouvattier
- CE Elling
- Claire L. Newton
- D Soderlund
- E Costa
- F Brioude
- FP Pralong
- G Maya-Nunez
- GA Vagenakis
- GP Sykiotis
- GY Bédécarrats
- J Ballesteros
- J Bouligand
- J Sarfati
- J Young
- JA Ballesteros
- JA Janovick
- JA Janovick
- Jacques Young
- Javier A. Tello
- Jerome Bouligand
- K Morgan
- K Palczewski
- KK Arora
- L Chevrier
- L Oliveira
- LC Layman
- LC Layman
- LFG Silveira
- M Beranova
- M Chengalvala
- M Kottler
- ML Kottler
- MM Rosenkilde
- N de Roux
- N de Roux
- P Caron
- Robert P. Millar
- RP Millar
- S Bhattacharya
- S Hövelmann
- S Salenave
- S Trabado
- Stefan Strack
- Z-L Lu
- Z-L Lu
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Congenital hypogonadotropic hypogonadism (CHH) is characterized by low gonadotropins and failure to progress normally through puberty. Mutations in the gene encoding the GnRH receptor (GNRHR1) result in CHH when present as compound heterozygous or homozygous inactivating mutations. This study identifies and characterizes the properties of two novel GNRHR1 mutations in a family in which three brothers display normosmic CHH while their sister was unaffected. Molecular analysis in the proband and the affected brothers revealed two novel non-synonymous missense GNRHR1 mutations, present in a compound heterozygous state, whereas their unaffected parents possessed only one inactivating mutation, demonstrating the autosomal recessive transmission in this kindred and excluding X-linked inheritance equivocally suggested by the initial pedigree analysis. The first mutation at c.845 C>G introduces an Arg substitution for the conserved Pro 282 in transmembrane domain (TMD) 6. The Pro282Arg mutant is unable to bind radiolabeled GnRH analogue. As this conserved residue is important in receptor conformation, it is likely that the mutation perturbs the binding pocket and affects trafficking to the cell surface. The second mutation at c.968 A>G introduces a Cys substitution for Tyr 323 in the functionally crucial N/DPxxY motif in TMD 7. The Tyr323Cys mutant has an increased GnRH binding affinity but reduced receptor expression at the plasma membrane and impaired G protein-coupling. Inositol phosphate accumulation assays demonstrated absent and impaired Gαq/11 signal transduction by Pro282Arg and Tyr323Cys mutants, respectively. Pretreatment with the membrane permeant GnRHR antagonist NBI-42902, which rescues cell surface expression of many GNRHR1 mutants, significantly increased the levels of radioligand binding and intracellular signaling of the Tyr323Cys mutant but not Pro282Arg. Immunocytochemistry confirmed that both mutants are present on the cell membrane albeit at low levels. Together these molecular deficiencies of the two novel GNRHR1 mutations lead to the CHH phenotype when present as a compound heterozygote
Gas-phase fragmentation of the Ag+—phenylalanine complex: Cation—π interactions and radical cation formation
- Author
- A. D. Becke
- A. D. Becke
- A. D. Becke
- A. M. El-Nahas
- A. T. Blades
- A. T. Blades
- A. T. Blades
- B. A. Cerda
- B. A. Perera
- B. J. Smith
- C. L. Gatlin
- C. Lee
- C. Seto
- D. Wen
- E. R. Talaty
- F. Rogalewicz
- H. Lavant
- I. K. Chu
- J. B. Fenn
- M. J. Frisch
- N. Godbout
- N. N. Dookernan
- P. Hohenberg
- P. Hu
- P. Hu
- Q. P. Lei
- R. N. Grewal
- R. S. Brown
- S. Beranova
- S. Bouchonnet
- S. R. Wilson
- T. Shoeib
- T. Shoeib
- T. Shoeib
- T. Shoeib
- T. Yalcin
- V. W. M. Lee
- W. Kohn
- Y. Hoppilliard
- Y.-M. Chen
- Z. L. Cheng
- Z. L. Cheng
- Publication venue
- 'Elsevier BV'
- Publication date
- Field of study
Antiplatelet therapy with aspirin, clopidogrel, and dipyridamole versus clopidogrel alone or aspirin and dipyridamole in patients with acute cerebral ischaemia (TARDIS): a randomised, open-label, phase 3 superiority trial
- Author
- A Ahmed
- A Anthony
- A Asokanathan
- A Azim
- A Banerjee
- A Barkat
- A Barry
- A Benford
- A Blight
- A Bowring
- A Brigden
- A Buck
- A Butler
- A Dixit
- A Dodd
- A Hardwick
- A Hassan
- A Hedstrom
- A Hemsley
- A Joyson
- A Kenton
- A Lankester
- A Lehman
- A Manoj
- A McLoughlin
- A Misra
- A Mistri
- A Mohd Nor
- A Nair
- A Needle
- A Peacocke
- A Pusalkar
- A Ravindrane
- A Remegoso
- A Smith
- A Steele
- A Tevdoradze
- A Thomson
- A Tittle
- A Verrion
- A Warusevitane
- A Willberry
- A Wright
- Alan A Montgomery
- Amarenco
- Ankolekar
- Annemarei Ranta
- B Bhaskaran
- B Charles
- B Esisi
- B Gregary
- B Hairsine
- B Hazel
- B Hyams
- B Jupp
- B Kumar
- B Longland
- B Madigan
- B McClelland
- B Mokoena
- B Moynihan
- B Wadams
- Bamford
- Bath
- Bath
- Bath
- Benavente
- C Allcock
- C Ambulo
- C Athulathmudali
- C Bailey
- C Blank
- C Buckley
- C Clarke
- C Denniss
- C Dickson
- C Douglass
- C Doyle
- C Eglinton
- C Hays
- C Hewitt
- C Hilaire
- C Hubbuck
- C Jenkins
- C Kamara
- C Keaveney
- C Kelly
- C Khuoge
- C Krarup Hansen
- C Kruuse
- C Lawlor
- C McAlpine
- C McGhee
- C McInnes
- C Ovington
- C Padilla-Harris
- C Patel
- C Perkins
- C Price
- C Pringle
- C Rankin
- C Richardson
- C Roffe
- C Roughan
- C Schofield
- C Smith
- C Stevenson
- C Vernon
- C Vickers
- C Watchurst
- D Broughton
- D Bruce
- D Bruce
- D Butler
- D Button
- D Chadha
- D Dellafera
- D Esson
- D Eveson
- D Forrest
- D Hargroves
- D Hayward
- D Hilton
- D Hove
- D Howcroft
- D Kakabadze
- D Kelly
- D Manawadu
- D Mangion
- D Morgan
- D Morse
- D O'Kane
- D Sandler
- D Sims
- D Tomlin
- D Walstow
- D Waugh
- D Wilkinson
- D Wood
- Diane Havard
- Diener
- Diener
- E Amis
- E Barbon
- E Beranova
- E Brown
- E Campbell
- E Cattermole
- E Gamble
- E Giallombardo
- E Gibson
- E Horsley
- E Jinks
- E Keeling
- E Khoromana
- E Lawrence
- E Mckenzie
- E O'Brien
- E Osborne
- E Richards
- E Temlett
- E Veraque
- E Young
- F Barrett
- F Brodie
- F Faola
- F Hammonds
- F Harrington
- F K Chan
- F Kennedy
- F Leslie
- F Price
- F Shelton
- F Watson
- F Wright
- G Auld
- G Ayres
- G Bateman
- G Butt
- G Courtauld
- G Fletcher
- G Grimwood
- G Gunathilagan
- G Hann
- G Muddegowda
- G Rogers
- G Rose
- G Spurling
- G Storey
- G Thomas
- G Wilkes
- Geeganage
- Graham S Venables
- H Beadle
- H Bearne
- H Cochrane
- H Crowther
- H Eccleson
- H Emsley
- H Gow
- H Guy
- H H Jensen
- H Kingwell
- H Maguire
- H Rehman
- H Rudenko
- H Russell
- H Webb
- Hanne Christensen
- Hugh S Markus
- I Iniesta
- I J Watson
- I Jones
- I Martin
- I Memon
- I Natarajan
- I Shread
- I Toidze
- I Wynter
- J Aeron-Thomas
- J Bamford
- J Banns
- J Beavan
- J Bell
- J Buxton
- J Chambers
- J Chembala
- J Clarke
- J Corrigan
- J Cunningham
- J Davis
- J Dube
- J Duignan
- J Furnace
- J Gaylard
- J Good
- J Goodsell
- J Greig
- J Grocott
- J Hiden
- J Hindle
- J Howe
- J Hunt
- J Irvine
- J Kessell
- J Kok
- J Margalef
- J McIlmoyle
- J Mitchell
- J O'Callaghan
- J O'Connell
- J O'Reilly
- J Okwera
- J Paterson
- J Perez
- J Peters
- J Powell
- J Reddan
- J Roffe
- J Scott
- J Tomlinson
- J White
- J Wilson
- Jason P Appleton
- Johnston
- Johnston
- K A Kay
- K Ali
- K Anderson
- K Ayes
- K Castro
- K Chan
- K Chapman
- K Chatterjee
- K Deighton
- K Dizayee
- K Elfandi
- K Finney
- K Fotherby
- K Gill
- K Harkness
- K Harvey
- K Javaid
- K Jenkins
- K Knops
- K Marks
- K McCormick
- K Muhidden
- K Musarrat
- K Netherton
- K Preece
- K Rashed
- K Shaw
- K Smith
- K Storey
- K Whittamore
- K Whysall
- Kailash Krishnan
- Katie Flaherty
- L Bentsen
- L Boxall
- L Cowie
- L Dixon
- L Finlay
- L Glover
- L Guthrie
- L Holford
- L Howaniec
- L Hunt
- L Hyatt
- L Jackson
- L Johnson
- L Kerin
- L Lee-Carbon
- L M Christensen
- L Makawa
- L Manning
- L Matter
- L Mills
- L Mokoena
- L Montague
- L O'Shea
- L Ryan
- L Shaw
- L Sztriha
- Lees
- Lelia Duley
- Lisa J Woodhouse
- M Alao
- M Bajoriene
- M Ball
- M Barber
- M Bokhari
- M Burn
- M Chowdhury
- M Clarke
- M Cooper
- M Couser
- M Dent
- M Doherty
- M Fawcett
- M Funnell
- M G Metiu
- M Garside
- M Godfrey
- M Henry
- M Johnes
- M Kambafwile
- M Krasinska-Chavez
- M Macleod
- M Maddula
- M Niemierko
- M Osborn
- M Patel
- M Platton
- M Reader
- M Rodriguez
- M Sajid
- M Sein
- M Siddiqui
- M Smith
- M Srinivasan
- M Zaidi
- Maia Beridze
- Marc Randall
- Marilyn James
- MGG Soliman
- N Abano
- N Akiashvili
- N Beridze
- N Chopra
- N Dayal
- N Gilzeane
- N Jeyaraj
- N Kakabadze
- N Khanom
- N Khizanishvili
- N Lobjanidze
- N Motherwell
- N Persad
- N Rands
- N Sengupta
- N Sikondari
- N Temple
- Nikola Sprigg
- O Adegbaju
- O Balazikova
- O Geraghty
- O Orugun
- O Redjep
- O Speirs
- P Cariga
- P Christian
- P Cox
- P Daboo
- P Dangri
- P Datta
- P Farren
- P Findlay
- P Fitzell
- P Guyler
- P Harman
- P Howard
- P Jacob
- P Lai
- P Langhorne
- P Lingwood
- P Lopez
- P Murphy
- P Owusu-Agyei
- P Wanklyn
- P Webster
- P Wilding
- P Wilkinson
- Philip M Bath
- Polly Scutt
- R Bellfield
- R Brown
- R Carpio
- R Davies
- R Donnelly
- R Erande
- R Erande
- R Gascoyne
- R Ghatala
- R Graham
- R Icart Palau
- R Jarapa
- R Jolly
- R Keshvara
- R Kumar
- R Lakey
- R Namushi
- R Oliver
- R Rangasamay
- R Rowland-Axe
- R Sanyal
- R Shekhar
- R Sivakumar
- R Taylor
- R Williams
- Robert A Dineen
- Rothwell
- S Anand
- S Arif
- S Atkinson
- S Board
- S Booth
- S Brixey
- S Buddha
- S Butler
- S Clayton
- S Crawford
- S Dealing
- S Duty
- S Finlay
- S Ghosh
- S Gomm
- S Hassan
- S Hurdowar
- S Johnson-Holland
- S Jones
- S Keenan
- S Khan
- S Kunhunny
- S Leason
- S Lewis
- S Lucas
- S Lyjko
- S Maguire
- S Maheswaran
- S Mahmood
- S Mashate
- S McCann
- S Meenakshisundaram
- S Merotra
- S Munshi
- S Nelson
- S Norman
- S Nyabadza
- S Ragab
- S Raj
- S Ross
- S S Hansen
- S Stafford
- S Stevens
- S Stoddart
- S Sundayi
- S Szabo
- S Tennant
- S Tilby
- S Trippier
- S Tysoe
- S Windebank
- S Wong
- S Woodward
- Schulman
- Sprigg
- Stan Heptinstall
- Stuart J Pocock
- T Adedoyin
- T Ajao
- T Attygalle
- T Black
- T Cassidy
- T Fluskey
- T Fuller
- T Gordon
- T J Dobson
- T Kherkheulidze
- T Marsden
- T Nozedar
- T T Thomsen
- T Thompson
- T Tsanava
- Thompson G Robinson
- Timothy J England
- U Poultney
- V Cvoro
- V Hogg
- V Petrovic
- V Riddell
- V Sutton
- V Taylor
- W Sunman
- Wang
- Weir
- Willmot
- Wong
- Y Duodu
- Y Gruenbeck
- Z Mellor
- Z Naing
- Zhao
- Zhao
- Zhao
- Publication venue
- 'Elsevier BV'
- Publication date
- 20/12/2017
- Field of study
Background: Intensive antiplatelet therapy with three agents might be more effective than guideline treatment for preventing recurrent events in patients with acute cerebral ischaemia. We aimed to compare the safety and efficacy of intensive antiplatelet therapy (combined aspirin, clopidogrel, and dipyridamole) with that of guideline-based antiplatelet therapy.
Methods: We did an international, prospective, randomised, open-label, blinded-endpoint trial in adult participants with ischaemic stroke or transient ischaemic attack (TIA) within 48 h of onset. Participants were assigned in a 1:1 ratio using computer randomisation to receive loading doses and then 30 days of intensive antiplatelet therapy (combined aspirin 75 mg, clopidogrel 75 mg, and dipyridamole 200 mg twice daily) or guideline-based therapy (comprising either clopidogrel alone or combined aspirin and dipyridamole). Randomisation was stratified by country and index event, and minimised with prognostic baseline factors, medication use, time to randomisation, stroke-related factors, and thrombolysis. The ordinal primary outcome was the combined incidence and severity of any recurrent stroke (ischaemic or haemorrhagic; assessed using the modified Rankin Scale) or TIA within 90 days, as assessed by central telephone follow-up with masking to treatment assignment, and analysed by intention to treat. This trial is registered with the ISRCTN registry, number ISRCTN47823388.
Findings: 3096 participants (1556 in the intensive antiplatelet therapy group, 1540 in the guideline antiplatelet therapy group) were recruited from 106 hospitals in four countries between April 7, 2009, and March 18, 2016. The trial was stopped early on the recommendation of the data monitoring committee. The incidence and severity of recurrent stroke or TIA did not differ between intensive and guideline therapy (93 [6%] participants vs 105 [7%]; adjusted common odds ratio [cOR] 0·90, 95% CI 0·67–1·20, p=0·47). By contrast, intensive antiplatelet therapy was associated with more, and more severe, bleeding (adjusted cOR 2·54, 95% CI 2·05–3·16, p<0·0001).
Interpretation: Among patients with recent cerebral ischaemia, intensive antiplatelet therapy did not reduce the incidence and severity of recurrent stroke or TIA, but did significantly increase the risk of major bleeding. Triple antiplatelet therapy should not be used in routine clinical practice
Genetic mechanisms of critical illness in COVID-19.
- Author
- A A Roger Thompson
- A Abraheem
- A Agasou
- A Ahmed
- A Ali
- A Allan
- A Altabaibeh
- A Alvaro
- A Aspinwall
- A Ayers
- A Bamford
- A Barron
- A Bashyal
- A Bellini
- A Bociek
- A Botello
- A Bowes
- A Brady
- A Brayne
- A Brown
- A Brown
- A Butler
- A Campbell
- A Carter
- A Collins
- A Cowley
- A Cowton
- A Cowton
- A Cox
- A Crew
- A Dance
- A Daniel
- A Daniels
- A Dela Rosa
- A Drummond
- A Durie
- A E Heron
- A Easthope
- A Easthope
- A Evans
- A Fofano
- A Gales
- A Ganesan
- A Gardner
- A Garg
- A Gherman
- A Gordon
- A Gratrix
- A Gulati
- A Gupta
- A Haigh
- A Haldeos
- A Harrison
- A Harvey
- A Hayes
- A Higham
- A Higham
- A Hilldrith
- A Holden
- A Hormis
- A Hutcheon
- A Javaid
- A Joseph
- A Kaliappan
- A Katary
- A Kay
- A Kayani
- A Kent
- A Kirkby
- A Knight
- A Kubisz-Pudelko
- A Kuravi
- A Lewis
- A Loveridge
- A Lyle
- A Mayer
- A McAlpine
- A McCarthy
- A McGregor
- A McGregor
- A Meikle
- A Mitchell
- A Mitra
- A Morris
- A Morrison
- A Naranjo
- A Nicholson
- A Nicholson
- A Nilsson
- A Noakes
- A Patel
- A Pickard
- A Poole
- A Price
- A Puxty
- A Quinn
- A Quinn
- A Raithatha
- A Rattray
- A Reddy
- A Reed
- A Reyes
- A Rose
- A Rose
- A Rostron
- A Roy
- A Roynon-Reed
- A S Raj
- A Salberg
- A Sanderson
- A Serrano-Ruiz
- A Solesbury
- A Sukha
- A Swain
- A Tariq
- A Thomas
- A Thomas
- A Todd
- A Tomas
- A Tridente
- A Tucci
- A Turnbull
- A Uriel
- A Ustianowski
- A Vochin
- A Vuylsteke
- A Waite
- A Walden
- A Whileman
- A Wilkinson
- A Williams
- A Williams
- A Wilson
- A Zak
- A Zaki
- Achille Iolascon
- Adam Auton
- Adam Brown
- Agnese Verzuri
- Agostino Ognibene
- Agostino Riva
- Ailsa Golightly
- Alan Maclean
- Alessandra
- Alessandra Stella
- Alessandra Vergori
- Alessia Giorli
- Alexander J Mentzer
- Alice Donati
- Alison M Meynert
- Alistair Nichol
- Ana da Silva Filipe
- Andrea Antinori
- Andrea Cossarizza
- Andrea Ganna
- Andrea Tommasi
- Andrew Rambaut
- Andrew Stenhouse
- Andy Law
- Anjali J Shastri
- Anna Canaccini
- Anna Maria Pinto
- Annarita Giliberti
- Annemarie B Docherty
- Antonella D'Arminio Monforte
- Antonia Ying Wai Ho
- Antonio Di Biagio
- Antony Symons
- Arianna Emiliozzi
- Arianna Gabrieli
- Audrey Coutts
- B Anwar
- B Attwood
- B Baines
- B Blackledge
- B Borislavova
- B Chandler
- B Charles
- B Creagh-Brown
- B David
- B Deacon
- B Deacon
- B Digby
- B Faulkner
- B Fuller
- B Gumbrill
- B Gurung
- B Hadebe
- B Hairsine
- B Hopkins
- B Johnston
- B Lenagh
- B Masunda
- B Ogg
- B Patel
- B Player
- B Purewal
- B Scholefield
- B Shelley
- B Sloan
- B Thomas
- B Wadams
- B Welsh
- B Wilkinson
- B Winter-Goodwin
- B Yates
- Baillie J Kenneth
- Barbara Rossetti
- Beale Rupert
- Beatrice Alex
- Benjamin Bach
- Bretherick Andrew D
- Bruno Frediani
- C Adams
- C Ahmed
- C Almaden-Boyle
- C Ashbrook-Raby
- C Basikolo
- C Battle
- C Beazley
- C Beith
- C Borra
- C Brandwood
- C Brantwood
- C Burnett
- C Castro Delgado
- C Clark
- C Clulow
- C Collins
- C Cruz
- C Davis
- C Demetriou
- C Dennis
- C Dexter
- C Downes
- C Dunmore
- C Eastgate
- C Eckbad
- C Finch
- C Gibson
- C Gorman
- C Hays
- C Hewitt
- C Holl
- C Howcroft
- C Humphrey
- C Jackson
- C Jardine
- C Jennings
- C Jones
- C Kaye
- C Lynch
- C Lyons
- C McCulloch
- C McParland
- C McParland
- C Murphy
- C Parmar
- C Pawley
- C Phillips
- C Phillips
- C Pothecary
- C Pothecary
- C Prendergast
- C Price
- C Rishton
- C Sell
- C Shovelton
- C Sicat
- C Stuart
- C Summers
- C Swan
- C Thompson
- C Thorpe
- C Tibke
- C Tierney
- C Vigurs
- C Wells
- C Whitton
- C Whyte
- C Wrey Brown
- Cameron J Fairfield
- Carmelo Piscopo
- Carmen Marciano
- Caroline Abernathy
- Carrol Gamble
- Caterina Lo Rizzo
- Catherine A Shaw
- Catherine H Weldon
- Caulfield Mark
- Ceilia Boz
- Cesira Nencioni
- Chelsea Ye
- Chiara Fallerini
- Chiara Gabbi
- Chiara Spertilli
- Chloe Donohue
- Chris Ponting
- Christoper A Green
- Cinthia E Jannes
- Clare Jackson
- Clohisey Sara
- Cristina Mussini
- D Antcliffe
- D Bakthavatsalam
- D Banach
- D Baptista
- D Bell
- D Branney
- D Brealey
- D Brealey
- D Butcher
- D Butcher
- D Childs
- D Clarke
- D Collier
- D Collier
- D Cristiano
- D Dawson
- D Donaldson
- D Duffin
- D Fottrell-Gould
- D Golden
- D Griffin
- D Hamilton
- D Hawcutt
- D Hope
- D Horner
- D Kallon
- D Kaye
- D Kelly
- D Loader
- D Lomas
- D Martin
- D McGlynn
- D McLaughlanv
- D Melia
- D Menzies
- D Mullan
- D Pogson
- D Potla
- D Potoczna
- D Purohit
- D Raynard
- D Salutous
- D Salutous
- D Scaletta
- D Shaw
- D Skinner
- D Smyth
- D Strachan
- D Tetla
- D Thornton
- D Trodd
- D Vedage
- D Walker
- D Warren
- D Williams
- D Wood
- D Wright
- Daniela Francisci
- Daniella Coker
- Danilo Tacconi
- David A van Heel
- David Bennet
- David L Robertson
- David Stuart
- Dawn Law
- Debby Bogaert
- Derek Murphy
- Domenico A Coviello
- E Abaleke
- E Allan
- E Anastasescu
- E Andrews
- E Apetri
- E B Jude
- E Beech
- E Beranova
- E Bevan
- E Black
- E Brinkworth
- E Collins
- E Combes
- E Davies
- E Dobson
- E Dooks
- E Fisher
- E Gendall
- E Goff
- E Goodwin
- E Gordon
- E Heeney
- E Horsley
- E Hughes
- E Johnson
- E Knights
- E Lee
- E London
- E Maccacari
- E Massey
- E McKenna
- E Meadows
- E Moncur
- E Morino
- E Mwaura
- E Peasgood
- E Perkins
- E Radford
- E Raith
- E Raith
- E Salciute
- E Smith
- E Smithson
- E Stoddard
- E Stones
- E Thomas
- E Tilney
- E Timlick
- E Treus Gude
- E Virgilio
- E Watson
- E Wilby
- Edoardo Conticini
- Egle Saviciute
- Elena Bargagli
- Elena Desanctis
- Elisa Benetti
- Elisa Frullanti
- Elisabetta Menatti
- Elisabetta Schiaroli
- Ellie Mcmaster
- Emma C Thomson
- Emmanuelle Marques
- Enrico Martinelli
- Esther Duncan
- Esther Merlini
- Ewen M Harrison
- F Anderson
- F Auld
- F Bibi
- F Davies
- F Farquhar
- F Fisher
- F Hurford
- F Kibutu
- F McNeela
- F Moore
- F Nasir
- F Trim
- F Wakinshaw
- F Williams
- Fabio Lena
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- Stefania Mantovani
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- Stephanie Roberts
- Stephen R Knight
- Summers Charlotte
- Susanna Croci
- Susanna Guerrini
- T Anderson
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- Tammy Gilchrist
- Tenesa Albert
- Teresa Filshtein-Sonmez
- Thomas M Drake
- Thushan de Silva
- Tim Walsh
- Tom Fletcher
- Tom Solomon
- Tony Wackett
- Trevor Paterson
- Tullio Trotta
- Turtle Lance
- U Poultney
- V Amin
- V Anumakonda
- V Bastion
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- V Crickmore
- V Gopal
- V Irvine
- V Kasipandian
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- V Linnett
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- V Page
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- V Parris
- V Pristopan
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- V Sarathy
- V Thomas
- V Thwaites
- V Tuckey
- V Turner
- V Wagstaff
- V Waugh
- Valentina Anemoli
- Vanessa Sancho-Shimizu
- Victoria Shaw
- Vitart Veronique
- W Harrison
- W Khaliq
- W Khaliq
- W McCormick
- W Woodyatt
- Walker Susan
- Walsh Timothy
- Wang Bo
- Wei Shen Lim
- Wendy S Barclay
- William A Paxton
- William Greenhalf
- Wilson James F
- Wrobel Nicola
- Wu Yang
- X Qiu
- Y Baird
- Y Choudhury
- Y Hussain
- Y Jackson
- Y Thirlwall
- Yang Jian
- Yang Zhijian
- Z Alldis
- Z Belagodu
- Z Bradshaw
- Z Coton
- Z Daly
- Z Farzad
- Z Fernandez
- Z Garland
- Z Maqsood
- Z Omar
- Z Prime
- Z Scott
- Zechner Marie
- Zhai Ranran
- Zheng Chenqing
- Publication venue
- Nature
- Publication date
- 01/01/2020
- Field of study
Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
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.
- Archer K.
- Arden T.
- Arias S. S.
- Arif S.
- Armstrong J.
- Armstrong L.
- Armstrong R.
- Arning N.
- Arnold S.
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- 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
Determinants of recovery from post-COVID-19 dyspnoea: analysis of UK prospective cohorts of hospitalised COVID-19 patients and community-based controls
- Author
- Abel K
- Adamali H
- Adeloye D
- Adeyemi O
- Adrego R
- Aguilar Jimenez LA
- Ahmad Haider N
- Ahmad S
- Ahmed R
- Ahwireng N
- Ainsworth M
- Al-Sheklly B
- Alamoudi A
- Ali M
- Aljaroof M
- All AM
- Allan L
- Allen RJ
- Allerton L
- Allsop L
- Almeida P
- Altmann D
- Alvarez Corral M
- Amoils S
- Anderson D
- Antoniades C
- Arbane G
- Arias A
- Armour C
- Armstrong L
- Armstrong N
- Arnold D
- Arnold H
- Ashish A
- Ashworth A
- Ashworth M
- Aslani S
- Assefa-Kebede H
- Atkin C
- Atkin P
- Aul R
- Aung H
- Austin L
- Avram C
- Ayoub A
- Babores M
- Baggott R
- Bagshaw J
- Baguley D
- Bailey L
- Baillie JK
- Bain S
- Bakali M
- Bakau M
- Baldry E
- Baldwin D
- Baldwin M
- Ballard C
- Banerjee A
- Bang B
- Barker RE
- Barman L
- Barratt S
- Barrett F
- Basire D
- Basu N
- Bates A
- Bates M
- Batterham R
- Baxendale H
- Bayes H
- Beadsworth M
- Beckett P
- Beggs M
- Begum M
- Beirne P
- Bell D
- Bell R
- Bennett K
- Beranova E
- Bermperi A
- Berridge A
- Berry C
- Betts S
- Bevan E
- Bhui K
- Bingham M
- Birchall K
- Bishop L
- Bisnauthsing K
- Blaikely J
- Bloss A
- Bolger A
- Bolton CE
- Bonnington J
- Botkai A
- Bourne C
- Bourne M
- Bramham K
- Brear L
- Breen G
- Breeze J
- Briggs A
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- Brightling CE
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- Brown JS
- Brown JS
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- Burdett T
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- Chalder T
- Chalmers JD
- Chalmers JD
- Chambers RC
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- Chaudhuri N
- Checkley A
- Chen J
- Cheng Y
- Chetham L
- Childs C
- Chilvers ER
- Chinoy H
- Chiribiri A
- Chong-James K
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- Chrystal M
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- Zeidan L
- Zhao B
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- Zheng B
- Zongo O
- Publication venue
- 'Elsevier BV'
- Publication date
- 27/03/2023
- Field of study
Background The risk factors for recovery from COVID-19 dyspnoea are poorly understood. We investigated determinants of recovery from dyspnoea in adults with COVID-19 and compared these to determinants of recovery from non-COVID-19 dyspnoea. Methods We used data from two prospective cohort studies: PHOSP-COVID (patients hospitalised between March 2020 and April 2021 with COVID-19) and COVIDENCE UK (community cohort studied over the same time period). PHOSP-COVID data were collected during hospitalisation and at 5-month and 1-year follow-up visits. COVIDENCE UK data were obtained through baseline and monthly online questionnaires. Dyspnoea was measured in both cohorts with the Medical Research Council Dyspnoea Scale. We used multivariable logistic regression to identify determinants associated with a reduction in dyspnoea between 5-month and 1-year follow-up. Findings We included 990 PHOSP-COVID and 3309 COVIDENCE UK participants. We observed higher odds of improvement between 5-month and 1-year follow-up among PHOSP-COVID participants who were younger (odds ratio 1.02 per year, 95% CI 1.01–1.03), male (1.54, 1.16–2.04), neither obese nor severely obese (1.82, 1.06–3.13 and 4.19, 2.14–8.19, respectively), had no pre-existing anxiety or depression (1.56, 1.09–2.22) or cardiovascular disease (1.33, 1.00–1.79), and shorter hospital admission (1.01 per day, 1.00–1.02). Similar associations were found in those recovering from non-COVID-19 dyspnoea, excluding age (and length of hospital admission). Interpretation Factors associated with dyspnoea recovery at 1-year post-discharge among patients hospitalised with COVID-19 were similar to those among community controls without COVID-19. Funding PHOSP-COVID is supported by a grant from the MRC-UK Research and Innovation and the Department of Health and Social Care through the National Institute for Health Research (NIHR) rapid response panel to tackle COVID-19. The views expressed in the publication are those of the author(s) and not necessarily those of the National Health Service (NHS), the NIHR or the Department of Health and Social Care. COVIDENCE UK is supported by the UK Research and Innovation, the National Institute for Health Research, and Barts Charity. The views expressed are those of the authors and not necessarily those of the funders
Cohort Profile: Post-Hospitalisation COVID-19 (PHOSP-COVID) study
- Author
- Abel K
- Adamali H
- Adeloye D
- Adeyemi O
- Adrego R
- Ahmad S
- Ahmed R
- Ahwireng N
- Ainsworth M
- Al-Sheklly B
- Alamoudi A
- Ali M
- Aljaroof M
- All AM
- Allan L
- Allen RJ
- Allerton L
- Allsop L
- Almeida P
- Altmann D
- Amoils S
- Anderson D
- Anifowose S
- Antoniades C
- Arbane G
- Arias A
- Armour C
- Armour C
- Armstrong L
- Armstrong N
- Armstrong N
- Arnold D
- Arnold H
- Ashish A
- Ashworth A
- Ashworth M
- Aslani S
- Assefa-Kebede H
- Atkin C
- Atkin P
- Atkins H
- Aul R
- Aul R
- Aul R
- Aung H
- Austin L
- Avram C
- Ayoub A
- Babores M
- Baggott R
- Bagshaw J
- Baguley D
- Bailey L
- Baillie JK
- Baillie JK
- Baillie JK
- Baillie JK
- Baillie JK
- Baillie JK
- Bain S
- Bakali M
- Bakau M
- Bakerly ND
- Bakerly ND
- Baldry E
- Baldwin D
- Baldwin M
- Baldwin M
- Ballard C
- Banerjee A
- Bang B
- Barker RE
- Barman L
- Barratt S
- Barrett F
- Barrett S
- Basire D
- Basu N
- Basu N
- Bates A
- Bates M
- Batterham R
- Baxendale H
- Baxendale H
- Baxendale H
- Baxter G
- Bayes H
- Beadsworth M
- Beadsworth M
- Beckett P
- Beggs M
- Beggs M
- Begum M
- Beirne P
- Beirne P
- Beirne P
- Bell D
- Bennett K
- Beranova E
- Bermperi A
- Berridge A
- Berry C
- Berry C
- Berry C
- Berry C
- Betts S
- Bevan E
- Bhui K
- Bingham M
- Birchall K
- Bishop L
- Bishop N
- Bisnauthsing K
- Blaikely J
- Blaikley J
- Bloomfield C
- Bloss A
- Bolger A
- Bolton CE
- Bolton CE
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- Publication venue
- Oxford University Press (OUP)
- Publication date
- 18/12/2023
- Field of study
Nonergodicity in electron capture dissociation investigated using hydrated ion nanocalorimetry
- Author
- A. C. Harms
- A. Sawicka
- A. T. Iavarone
- B. M. Reinhard
- C. Berg
- C. E. Klots
- C. K. Siu
- C. Lin
- D. S. Belic
- E. A. Syrstad
- E. A. Syrstad
- E. A. Syrstad
- E. W. Robinson
- F. Kjeldsen
- F. Misaizu
- F. Misaizu
- F. Turecček
- F. Turecček
- F. Turecček
- F. W. McLafferty
- H. I. Kenttämaa
- H. J. Cooper
- H. Liu
- H. Liu
- H. Wang
- H. Watanabe
- I. Anusiewicz
- I. Dzidic
- I. W. Griffiths
- J. A. Taraszka
- J. C. Jurchen
- J. E. P. Syka
- J. Fedor
- J. H. Chen
- J. J. Coon
- J. L. Dye
- J. L. Dye
- J. V. Coe
- K. Breuker
- K. Breuker
- K. N. Marsh
- L. R. Anders
- M. F. Bush
- M. J. Dekrey
- M. J. Frisch
- M. Sanekata
- M. Sobczyk
- M. Sobczyk
- N. A. Kruger
- N. C. Polfer
- N. F. Dalleska
- N. Leymarie
- P. B. O’Connor
- P. D. Schnier
- P. Hvelplund
- P. Hvelplund
- P. Kebarle
- R. A. Zubarev
- R. A. Zubarev
- R. A. Zubarev
- R. A. Zubarev
- R. A. Zubarev
- R. B. Cody
- R. D. Leib
- R. Feistel
- R. L. Wong
- S. Beranova
- S. J. Valentine
- S. J. Valentine
- S. Matsuishi
- T. Baer
- T. Baer
- T. Chakraborty
- T. D. Märk
- V. Q. Nguyen
- W. D. Price
- X. H. Chen
- X. M. Han
- Y. Ge
- Y. Inokuchi
- Z. Shi
- Publication venue
- 'Elsevier BV'
- Publication date
- Field of study
Dimethyl fumarate in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial
- Author
- Abbas M.
- Abdul Rasheed A.
- Abdul A.
- Abdul-Kadir R.
- Abdusamad K.
- Abernethy K.
- Aboelela H.
- Abouzaid M.
- Abraham M.
- Abraham T.
- Abrams J.
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- Acton C.
- Adam F.
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- Al Balushi A.
- Al-Asadi A.
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- Al-Ramadhani B.
- Al-Saadi Z.
- Al-Shahi Salman R.
- Al-Sheklly B.
- Albert P.
- Alegria A.
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- Publication venue
- Springer Science and Business Media LLC
- Publication date
- 31/01/2024
- Field of study
Dimethyl fumarate (DMF) inhibits inflammasome-mediated inflammation and has been proposed as a treatment for patients hospitalised with COVID-19. This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing multiple treatments in patients hospitalised for COVID-19 (NCT04381936, ISRCTN50189673). In this assessment of DMF performed at 27 UK hospitals, adults were randomly allocated (1:1) to either usual standard of care alone or usual standard of care plus DMF. The primary outcome was clinical status on day 5 measured on a seven-point ordinal scale. Secondary outcomes were time to sustained improvement in clinical status, time to discharge, day 5 peripheral blood oxygenation, day 5 C-reactive protein, and improvement in day 10 clinical status. Between 2 March 2021 and 18 November 2021, 713 patients were enroled in the DMF evaluation, of whom 356 were randomly allocated to receive usual care plus DMF, and 357 to usual care alone. 95% of patients received corticosteroids as part of routine care. There was no evidence of a beneficial effect of DMF on clinical status at day 5 (common odds ratio of unfavourable outcome 1.12; 95% CI 0.86-1.47; p = 0.40). There was no significant effect of DMF on any secondary outcome
Tocilizumab in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial
- Author
- Abani O.
- Abbas A.
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- Abbasi S.
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- Abdallah N.
- Abdelaziz A.
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- Publication venue
- 'Elsevier BV'
- Publication date
- 01/05/2021
- Field of study
Background:
In this study, we aimed to evaluate the effects of tocilizumab in adult patients admitted to hospital with COVID-19 with both hypoxia and systemic inflammation.
Methods:
This randomised, controlled, open-label, platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing several possible treatments in patients hospitalised with COVID-19 in the UK. Those trial participants with hypoxia (oxygen saturation <92% on air or requiring oxygen therapy) and evidence of systemic inflammation (C-reactive protein ≥75 mg/L) were eligible for random assignment in a 1:1 ratio to usual standard of care alone versus usual standard of care plus tocilizumab at a dose of 400 mg–800 mg (depending on weight) given intravenously. A second dose could be given 12–24 h later if the patient's condition had not improved. The primary outcome was 28-day mortality, assessed in the intention-to-treat population. The trial is registered with ISRCTN (50189673) and ClinicalTrials.gov (NCT04381936).
Findings:
Between April 23, 2020, and Jan 24, 2021, 4116 adults of 21 550 patients enrolled into the RECOVERY trial were included in the assessment of tocilizumab, including 3385 (82%) patients receiving systemic corticosteroids. Overall, 621 (31%) of the 2022 patients allocated tocilizumab and 729 (35%) of the 2094 patients allocated to usual care died within 28 days (rate ratio 0·85; 95% CI 0·76–0·94; p=0·0028). Consistent results were seen in all prespecified subgroups of patients, including those receiving systemic corticosteroids. Patients allocated to tocilizumab were more likely to be discharged from hospital within 28 days (57% vs 50%; rate ratio 1·22; 1·12–1·33; p<0·0001). Among those not receiving invasive mechanical ventilation at baseline, patients allocated tocilizumab were less likely to reach the composite endpoint of invasive mechanical ventilation or death (35% vs 42%; risk ratio 0·84; 95% CI 0·77–0·92; p<0·0001).
Interpretation:
In hospitalised COVID-19 patients with hypoxia and systemic inflammation, tocilizumab improved survival and other clinical outcomes. These benefits were seen regardless of the amount of respiratory support and were additional to the benefits of systemic corticosteroids.
Funding:
UK Research and Innovation (Medical Research Council) and National Institute of Health Research
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