21 research outputs found
Influenza Virus A Infection of Human Monocyte and Macrophage Subpopulations Reveals Increased Susceptibility Associated with Cell Differentiation
- Author
- A Bender
- A Hayman
- A Mantovani
- A McColl
- Anthony A. Nash
- B Passlick
- BG Hale
- BG Hale
- C Pauligk
- CY Cheung
- D Jackson
- David Jackson
- DB Ettensohn
- DM Mosser
- E Turpin
- F Geissmann
- F Hayden
- FA Verreck
- FO Martinez
- GK Geiss
- H Fesq
- HP Jersmann
- HP Jersmann
- HW Ziegler-Heitbrock
- HW Ziegler-Heitbrock
- I Fujimoto
- I Mori
- Ian Dransfield
- J Cros
- J McGill
- J Savill
- J Skrzeczynska-Moncznik
- JK Taubenberger
- K Sun
- KL Lin
- KM Giles
- L Ziegler-Heitbrock
- L Ziegler-Heitbrock
- LA Perrone
- Lionel G. Filion
- M Nain
- MA Hoeve
- Marieke A. Hoeve
- MB Torchinsky
- MC Chan
- ME Nemeroff
- MJ Kim
- N Shibuya
- NC Di Paolo
- NM Stamatos
- NV Serbina
- P Palese
- R Le Goffic
- Richard E. Randall
- RJ Snelgrove
- S Franz
- S Goerdt
- S Gordon
- S Haskill
- S Herold
- S Matikainen
- SP Hart
- ST Jennings
- T Horimoto
- T Takizawa
- T Takizawa
- TC Dawson
- V Turchiarelli
- W Wu
- WJ Wurzer
- WW Thompson
- Y Hashimoto
- Y Leverrier
- Y Li
- Y Watanabe
- Y Watanabe
- YJ Chang
- Z Chen
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Influenza virus infection accounts for significant morbidity and mortality world-wide. Interactions of the virus with host cells, particularly those of the macrophage lineage, are thought to contribute to various pathological changes associated with poor patient outcome. Development of new strategies to treat disease therefore requires a detailed understanding of the impact of virus infection upon cellular responses. Here we report that human blood-derived monocytes could be readily infected with the H3N2 influenza virus A/Udorn/72 (Udorn), irrespective of their phenotype (CD14++/CD16−, CD14++/CD16+ or CD14dimCD16++), as determined by multi-colour flow cytometry for viral haemagglutinin (HA) expression and cell surface markers 8–16 hours post infection. Monocytes are relatively resistant to influenza-induced cell death early in infection, as approximately 20% of cells showed influenza-induced caspase-dependent apoptosis. Infection of monocytes with Udorn also induced the release of IL-6, IL-8, TNFα and IP-10, suggesting that NS1 protein of Udorn does not (effectively) inhibit this host defence response in human monocytes. Comparative analysis of human monocyte-derived macrophages (Mph) demonstrated greater susceptibility to human influenza virus than monocytes, with the majority of both pro-inflammatory Mph1 and anti-inflammatory/regulatory Mph2 cells expressing viral HA after infection with Udorn. Influenza infection of macrophages also induced cytokine and chemokine production. However, both Mph1 and Mph2 phenotypes released comparable amounts of TNFα, IL-12p40 and IP-10 after infection with H3N2, in marked contrast to differential responses to LPS-stimulation. In addition, we found that influenza virus infection augmented the capacity of poorly phagocytic Mph1 cells to phagocytose apoptotic cells by a mechanism that was independent of either IL-10 or the Mer receptor tyrosine kinase/Protein S pathway. In summary, our data reveal that influenza virus infection of human macrophages causes functional alterations that may impact on the process of resolution of inflammation, with implications for viral clearance and lung pathology
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.
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- Wulandari R.
- Wyllie D. H.
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- Xue X.
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- Zongo O.
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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
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
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- C Almaden-Boyle
- C Ashbrook-Raby
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- C Beazley
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- C Brandwood
- C Brantwood
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- C Castro Delgado
- C Clark
- C Clulow
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- C Demetriou
- C Dennis
- C Dexter
- C Downes
- C Dunmore
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- C Gorman
- C Hays
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- C Holl
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- C Jardine
- C Jennings
- C Jones
- C Kaye
- C Lynch
- C Lyons
- C McCulloch
- C McParland
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- C Murphy
- C Parmar
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- C Phillips
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- C Pothecary
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- C Prendergast
- C Price
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- C Sell
- C Shovelton
- C Sicat
- C Stuart
- C Summers
- C Swan
- C Thompson
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- C Vigurs
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- C Whitton
- C Whyte
- C Wrey Brown
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- 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
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- D Baptista
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- D Brealey
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- D Butcher
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- D Cristiano
- D Dawson
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- 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
- Fawkes Angie
- Federico Anedda
- Federico Franchi
- Ferdinando Giannattasio
- Filip Taneski
- Filippo Aucella
- Filippo Biscarini
- Floriana Valentino
- Fourman Max Head
- Francesca Andretta
- Francesca Fava
- Francesca Gatti
- Francesca Mari
- Francesca Montagnani
- Francesco Castelli
- Francesco Raimondi
- Furniss James
- G Andrew
- G Arbane
- G Bell
- G Bercades
- G Croston
- G Debreceni
- G Durrant
- G Hambrook
- G Hobden
- G Houston
- G Hughes
- G Jones
- G Lubimbi
- G Maloney
- G Martir
- G Millen
- G Mills
- G O'Connor
- G Padden
- G Randell
- G Sadera
- G Seddon
- G Sera Howe
- G Sloane
- G Subramanian
- G Tsinaslanidis
- G Turner
- G Watson
- G Wray
- Gabriella Coiro
- Gabriella Doddato
- Gail Carson
- Gardar Sveinbjornsson
- Gary Leeming
- Genni Spargi
- Georgios Pollakis
- Giacomo Zanelli
- Gian Piero Caldarelli
- Giancarlo Bosio
- Giuseppe Fiorentino
- Giuseppe Merla
- Gountouna Elvina
- Graham S Cooke
- Griffiths Fiona
- Grimes Graeme
- H Bancroft
- H Bates
- H Belfield
- H Blackman
- H Blakemore
- H Brooke
- H Button
- H Coles
- H Curgenven
- H Filipe
- H Fox
- H Golding
- H Hill
- H Holcombe
- H Houlden
- H Jeffrey
- H Kent
- H Langton
- H McGuinness
- H Meghari
- H Millward
- H Moore
- H Parker
- H Pearson
- H Prady
- H Quinn
- H Rangarajan
- H Rehman
- H Reschreiter
- H Riley
- H Sainsbury
- H Savill
- H Sturgeon
- H T-Michael
- H Tench
- H Tiveran
- H Turner
- H Whittle
- H Willis
- H Wood
- Haley Chris
- Hanning Mal
- Harrison David
- Hayley Hardwick
- Hayward Caroline
- Helen Szoor-McElhinney
- Hinds Charles
- Ho Antonia
- Horby Peter
- I Ali Mohamed Ali
- I Balagosa
- I Birkinshaw
- I Burn
- I Chadbourn
- I D Clement
- I Edmond
- I Frost
- I Hass
- I Hussain
- I Lancoma-Malcolm
- I Leadbitter
- I Nagra
- I Otahal
- I Otahal
- I Turner-Bone
- I Welters
- I White
- I Wynter
- Ilaria Meloni
- Immacolata Andolfo
- Isabella Zanella
- J Allan
- J Barker
- J Bewley
- J Biddle
- J Birch
- J Birch
- J Bradley-Potts
- J Brown
- J Bryant
- J Butler
- J Camsooksai
- J Carter
- J Caterson
- J Cebrian Suarez
- J Cockerill-Taylor
- J Cole
- J Colley
- J Cooper
- J Cupitt
- J Cuttler
- J Daglish
- J Dasgin
- J Dawson
- J Dearden
- J Deery
- J Donnachie
- J Dykes
- J Easton
- J Egan
- J Fernandez Roman
- J Finn
- J Fletcher
- J Frankham
- J Gaylard
- J Gill
- J Godden
- J Goodsell
- J Gregory
- J Greig
- J Gurasashvili
- J Hardy
- J Harris
- J Hatton
- J Hawes
- J Highgate
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- J Hulme
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- J Hutter
- J Ingham
- J Jones
- J Jones
- J K Baillie
- J Kassam
- J Kenneth Baillie
- J Kenneth Baillie
- J Keshet-Price
- J Liew
- J Little
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- Janet T Scott
- Janie F Shelton
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- Johnny Millar
- Jorge Esparza-Gordillo
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- K Dent
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- Katarzyna Hafezi
- Keating Sean
- Kenneth A Mclean
- Kirstie Morrice
- Klaric Lucija
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- Knight Julian
- Kousathanas Athanasios
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- L Allen
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- L McMorrow
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- Louise Cullum
- Louise Macgillivray
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- Luca Cantarini
- Luca Guidelli
- Luca Masucci
- Luisa Tavecchia
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- S Turney
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- Samreen Ijaz
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- Sandro Panese
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- Sophie Venturelli
- Stefania Mantovani
- Stefano Baratti
- Stefano Ceri
- Stefano Rusconi
- Stella Aslibekyan
- Stephanie Roberts
- Stephen R Knight
- Summers Charlotte
- Susanna Croci
- Susanna Guerrini
- T Anderson
- T Arden
- T Baird
- T Behan
- T Bemand
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- T Coventry
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- T Kannan
- T Lawton
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- T Martin
- T McHugh
- T Newman
- T Nortcliffe
- T O Jones
- T Pogreban
- T Rees
- T Samakomva
- T Smith
- T Smith
- T Szakmany
- T Varghes
- T Williams
- T Wood
- 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
- V Cannons
- V Crickmore
- V Gopal
- V Irvine
- V Kasipandian
- V Krishnamurthy
- V Lake
- V Linnett
- V Martinson
- V Nagarajan
- V Page
- V Parris
- V Parris
- V Pristopan
- V Ratnam
- V Rivers
- 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
Intraperitoneal drain placement and outcomes after elective colorectal surgery: international matched, prospective, cohort study
- Author
- Aba M
- Abdellatif M
- Abdelmahmoud S
- Abu Hassan F
- Acil C
- Adarkwah P
- Adarraga J
- Adderley O
- Adefolaju A
- Afzal A
- Afzal Z
- Agarwal H
- Agnes A
- Agostinelli L
- Ahari D
- Ahmad H
- Ahmad R
- Ahmad S
- Ahmed N
- Ahmed N
- Ahmed WUR
- Ahmed WUR
- Akhbari M
- Akintunde A
- Akkaya YM
- Akram J
- Aktas MK
- Aktas MK
- Aktas MK
- Aktaş A
- Akula Y
- Al Nassrallah M
- Al-Habsi R
- Alam F
- Albino V
- Alfadhel S
- Ali T
- Alicata F
- Aljić A
- Allison W
- Almeida T
- Alonso Batanero E
- Alonso Batanero E
- Alsaif A
- Alsusa H
- Altaf R
- Altay L
- Altinel Y
- Altiner S
- Altomare DF
- Altomare DF
- Altunsu S
- Alvarez-Gallego M
- Amendola A
- Amjad T
- Amjad T
- Anabitarte Bautista O
- Anastasi A
- Anderson K
- Andolfi E
- Andolfi E
- Andrejevic P
- Andrejevic P
- Angarano E
- Angelini E
- Angelini M
- Angrisani M
- Anoldo P
- Anthony A
- Antropoli C
- Antypas A
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- Appleton B
- Argyriou A
- Arnold A
- Arnold A
- Arslan ER
- Asero S
- Ashaye A
- Ashdown T
- Asim K
- Aslam A
- Atar C
- Ates J
- Atıcı N
- Atiyah Z
- Attaallah W
- Atzeni J
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- Yap SHK
- Yasin I
- Yates C
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- Yeo JY
- Yick C
- Yick C
- Yıldırım A
- Yogarajah T
- Yoldas T
- Yotsov T
- Yousaf H
- Yousuff M
- Yánez C
- Yüksel E
- Zabiyaka M
- Zafer F
- Zafer F
- Zaffaroni G
- Zagibová D
- Zagorac Z
- Zaheer M
- Zahid A
- Zahid M
- Zaidi M
- Zambon M
- Zammit-Maempel M
- Zanframundo C
- Zanni M
- Zayed M
- Zazza S
- Zeidan Z
- Zhang Y
- Zhu L
- Zhu X
- Ziolkowska K
- Ziolkowska K
- Zografos G
- Zonta S
- Çetin B
- Ölmez M
- Özbalcı GS
- Özen D
- Özen D
- Öztürk OU
- Čustović S
- Štefanová H
- Ευσταθίου Η
- Publication venue
- 'Oxford University Press (OUP)'
- Publication date
- 01/01/2022
- Field of study
Despite current guidelines, intraperitoneal drain placement after elective colorectal surgery remains widespread. Drains were not associated with earlier detection of intraperitoneal collections, but were associated with prolonged hospital stay and increased risk of surgical-site infections.Background Many surgeons routinely place intraperitoneal drains after elective colorectal surgery. However, enhanced recovery after surgery guidelines recommend against their routine use owing to a lack of clear clinical benefit. This study aimed to describe international variation in intraperitoneal drain placement and the safety of this practice. Methods COMPASS (COMPlicAted intra-abdominal collectionS after colorectal Surgery) was a prospective, international, cohort study which enrolled consecutive adults undergoing elective colorectal surgery (February to March 2020). The primary outcome was the rate of intraperitoneal drain placement. Secondary outcomes included: rate and time to diagnosis of postoperative intraperitoneal collections; rate of surgical site infections (SSIs); time to discharge; and 30-day major postoperative complications (Clavien-Dindo grade at least III). After propensity score matching, multivariable logistic regression and Cox proportional hazards regression were used to estimate the independent association of the secondary outcomes with drain placement. Results Overall, 1805 patients from 22 countries were included (798 women, 44.2 per cent; median age 67.0 years). The drain insertion rate was 51.9 per cent (937 patients). After matching, drains were not associated with reduced rates (odds ratio (OR) 1.33, 95 per cent c.i. 0.79 to 2.23; P = 0.287) or earlier detection (hazard ratio (HR) 0.87, 0.33 to 2.31; P = 0.780) of collections. Although not associated with worse major postoperative complications (OR 1.09, 0.68 to 1.75; P = 0.709), drains were associated with delayed hospital discharge (HR 0.58, 0.52 to 0.66; P < 0.001) and an increased risk of SSIs (OR 2.47, 1.50 to 4.05; P < 0.001). Conclusion Intraperitoneal drain placement after elective colorectal surgery is not associated with earlier detection of postoperative collections, but prolongs hospital stay and increases SSI risk
Time-dependent LXR/RXR pathway modulation characterizes capillary remodeling in inflammatory corneal neovascularization
- Author
- A Amanzada
- A Castrillo
- A Mukwaya
- A Mukwaya
- A Noelia
- A Pozzi
- A Stahl
- A Yoshimura
- AE Myhre
- AM Mostafa
- Anthony Mukwaya
- Anton Lennikov
- AU Ahmed
- AV Nguyen
- BA Laffitte
- BB Peebo
- BB Peebo
- Beatrice Peebo
- C Cursiefen
- C Lei
- C Tang
- C Tang
- D Baitsch
- D Jo
- D Walcher
- E Liu
- EC Carlson
- EC Carlson
- F Storti
- GD Barish
- H Mechoulam
- H Xiong
- H Yang
- H Yasukawa
- J Amaral
- J Savill
- JY Oh
- KR Steffensen
- L Yue
- Lasse Jensen
- M Gimbrone Jr
- M Kubo
- M Massaro
- M Simons
- MA Gillespie
- MA Sarayba
- Maria Xeroudaki
- Mieszko Lachota
- MR Dana
- N Ebihara
- N Tamehiro
- N Zelcer
- NA Said
- Neil Lagali
- P Ballerini
- P Lu
- P Mirabelli
- P Romagnani
- Pierfrancesco Mirabelli
- PS Bhattacharjee
- Q Wang
- R Geyeregger
- R Skerrett
- R Strieter
- RK Lim
- S Nakao
- S Sangaletti
- S Sangaletti
- S Shinriki
- S Yoshida
- SA Kliewer
- SB Joseph
- SD Hanlon
- SE Goldblum
- SR Pickens
- SS-M Zhang
- T Couffinhal
- T Hayashi
- T Kimura
- T Yoshimura
- TF Lane
- Y Fan
- Y Liu
- Y Xing
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Whole-genome sequencing reveals host factors underlying critical COVID-19
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- Abd Elghafar M.S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G.R.
- Abecasis G.R.
- Abedalthagafi M.
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- Abernathy C.
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- Abul-Husn N.S.
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- Ahmed A.
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- Akeroyd L.
- Akhtar M.N.
- Akinkugbe O.
- Aksentijevich A.
- Al Harthi F.
- Al Mutairi A.
- Al-Afghani H.
- Al-Awdah L.
- Alaamery M.
- Alahmadey Z.Z.
- Alaverdian D.
- Alavere H.
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- Albaiceta G.M.
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- Ali A.
- Ali I.A.M.
- Ali S.
- Aliannejad R.
- Aljawini N.
- AlJohani S.
- Alkwai S.
- Allan A.
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- Alldis Z.
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- Allen S.
- Allibone S.
- Allison K.S.
- Allos R.
- Almaden-Boyle C.
- AlMalik A.
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- Almohammed I.
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- Alotaibi S.
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- Alrashed M.
- Alshareef A.
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- 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.
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- Whitton C.
- Whyte C.
- Wicks S.J.
- Wilby E.
- Wilcox L.
- Wilcox R.
- Wild H.
- Wild L.
- Wild L.
- Wilding L.
- Wiles M.
- Wilkins J.
- Wilkinson A.
- Wilkinson B.
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- Williams A.T.
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- Williams M.
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- Wilson D.J.
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- Wright J.
- Wright M.
- Wrobel N.
- Wu Y.
- Wulandari R.
- Wyllie D.H.
- Wynter I.
- Xavier K.
- Xue X.
- Yadav A.
- Yang J.
- Yassen A.M.
- Yates B.
- Ye C.
- Yun N.
- Zainy T.
- Zak A.
- Zaki A.
- Zamikula J.
- Zanella I.
- Zborowski A.C.
- Zeberg H.
- Zechner M.
- Zechner M.
- Zguro K.
- Zhang M.
- Zhao J.H.
- Zheng C.
- Zhou W.
- Zitter L.
- 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
Multiorgan MRI findings after hospitalisation with COVID-19 in the UK (C-MORE): a prospective, multicentre, observational cohort study
- Author
- Abel K
- Adamali H.
- Adeloye D
- Adeyemi Oluwaseun
- Adrego Rita
- Aguilar Jimenez Laura A.
- Ahmad Haider N
- Ahmad Shanaz
- Ahmed R
- Ahwireng Nyarko
- Ainsworth Mark
- Al-Sheklly B.
- Alamoudi Asma
- Alfaro-Almagro Fidel
- Ali Mariam
- Aljaroof M
- Allan L
- Allen R J
- Allerton Lisa
- Allsop Lynne
- Allt Ann Marie
- Almeida Paula
- Altmann Danny
- Alvarez Corral Maria
- Amoils S.
- Anderson David
- Antoniades C
- Arbane Gill
- Arias Ava Maria
- Armour C.
- Armstrong Lisa
- Armstrong Natalie
- Arnold David
- Arnold H
- Ashish A
- Ashworth Andrew
- Ashworth M
- Aslani S
- Assefa-Kebede Hosanna
- Atkin C
- Atkin Paul
- Aul Raminder
- Aung H
- Austin Liam
- Avram Cristina
- Ayoub A.
- Babores M.
- Baggott R
- Bagshaw J
- Baguley D
- Bailey L
- Baillie J.K.
- Bain S
- Bakali M
- Bakau M
- Baldry E
- Baldwin D
- Baldwin M
- Ballard C
- Bandula Steven
- Banerjee A
- Bang Dongchun
- Barker R E
- Barman L
- Barratt Shaney
- Barrett Fiona
- Basire Donna
- Basu N.
- Bates A
- Bates M
- Batterham R
- Baxendale H
- Bayes Hannah
- Beadsworth M.
- Beckett P
- Beggs Mark
- Begum M
- Beirne Paul
- Bell Murdina
- Bell R
- Bennett Kaytie
- Beranova Eva
- Bermperi Areti
- Berridge Anthony
- Berry C.
- Betts Sarah
- Bevan Emily
- Bhui K
- Bingham Michelle
- Birchall K
- Bishop L.
- Bisnauthsing Karen
- Blaikely J.
- Bloss Angela
- Bolger A.
- Bolton Charlotte E.
- Bonnington J.
- Botkai A
- Bourne Charlotte
- Bourne Michelle
- Bramham K.
- Brear Lucy
- Breen G
- Breeze Jonathon
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- Brightling Christopher E
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- Chablani Manish
- Chalder Trudie
- Chalmers James D.
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- Charalambou A
- Chaudhuri N
- Checkley A
- Chen Jin
- Cheng Yutung
- Chetham Luke
- Childs C
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- Jayaraman Bhagy
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- Jezzard Peter
- Jiwa Kasim
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- Lawrie Allan
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- Layton Alison
- Lea A
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- Lovegrove Wayne
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- Lukaschuk Elena
- Lye Alison
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- Mukaetova-Ladinska Elizabeta
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- Novotny Petr
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- Nwafor Lorenza
- Nwanguma Uchechi
- Nyaboko J
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- O'Brien Linda
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- Odell Natasha
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- Olaosebikan Olaoluwa
- Oliver Catherine
- Omar Zohra
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- Ostermann Marlies
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- Strong-Sheldrake Sophia
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- Walsh S.
- Warburton Louise
- Ward T J C
- Warwick Katie
- Wassall Helen
- Waterson Samuel
- Watson Ekaterina
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- Webster M
- Weir-McCall Jonathan R
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- Wessely S.
- West Sophie
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- White Sonia
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- Whittaker S
- Whittam Beverley
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- Wilkinson D
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- Wilson Ann
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- Wood Chloe
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- Wyles J.
- Wynter Inez
- Xie Cheng
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- Yasmin Najira
- Yasmin S
- Yates Tom
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- Zawia Amira
- Zeidan Lisa
- Zhao Bang
- Zheng Bang
- Zongo O.
- Publication venue
- Elsevier
- Publication date
- 22/09/2023
- Field of study
Introduction:
The multiorgan impact of moderate to severe coronavirus infections in the post-acute phase is still poorly understood. We aimed to evaluate the excess burden of multiorgan abnormalities after hospitalisation with COVID-19, evaluate their determinants, and explore associations with patient-related outcome measures.
Methods:
In a prospective, UK-wide, multicentre MRI follow-up study (C-MORE), adults (aged ≥18 years) discharged from hospital following COVID-19 who were included in Tier 2 of the Post-hospitalisation COVID-19 study (PHOSP-COVID) and contemporary controls with no evidence of previous COVID-19 (SARS-CoV-2 nucleocapsid antibody negative) underwent multiorgan MRI (lungs, heart, brain, liver, and kidneys) with quantitative and qualitative assessment of images and clinical adjudication when relevant. Individuals with end-stage renal failure or contraindications to MRI were excluded. Participants also underwent detailed recording of symptoms, and physiological and biochemical tests. The primary outcome was the excess burden of multiorgan abnormalities (two or more organs) relative to controls, with further adjustments for potential confounders. The C-MORE study is ongoing and is registered with ClinicalTrials.gov, NCT04510025.
Findings:
Of 2710 participants in Tier 2 of PHOSP-COVID, 531 were recruited across 13 UK-wide C-MORE sites. After exclusions, 259 C-MORE patients (mean age 57 years [SD 12]; 158 [61%] male and 101 [39%] female) who were discharged from hospital with PCR-confirmed or clinically diagnosed COVID-19 between March 1, 2020, and Nov 1, 2021, and 52 non-COVID-19 controls from the community (mean age 49 years [SD 14]; 30 [58%] male and 22 [42%] female) were included in the analysis. Patients were assessed at a median of 5·0 months (IQR 4·2–6·3) after hospital discharge. Compared with non-COVID-19 controls, patients were older, living with more obesity, and had more comorbidities. Multiorgan abnormalities on MRI were more frequent in patients than in controls (157 [61%] of 259 vs 14 [27%] of 52; p<0·0001) and independently associated with COVID-19 status (odds ratio [OR] 2·9 [95% CI 1·5–5·8]; padjusted=0·0023) after adjusting for relevant confounders. Compared with controls, patients were more likely to have MRI evidence of lung abnormalities (p=0·0001; parenchymal abnormalities), brain abnormalities (p<0·0001; more white matter hyperintensities and regional brain volume reduction), and kidney abnormalities (p=0·014; lower medullary T1 and loss of corticomedullary differentiation), whereas cardiac and liver MRI abnormalities were similar between patients and controls. Patients with multiorgan abnormalities were older (difference in mean age 7 years [95% CI 4–10]; mean age of 59·8 years [SD 11·7] with multiorgan abnormalities vs mean age of 52·8 years [11·9] without multiorgan abnormalities; p<0·0001), more likely to have three or more comorbidities (OR 2·47 [1·32–4·82]; padjusted=0·0059), and more likely to have a more severe acute infection (acute CRP >5mg/L, OR 3·55 [1·23–11·88]; padjusted=0·025) than those without multiorgan abnormalities. Presence of lung MRI abnormalities was associated with a two-fold higher risk of chest tightness, and multiorgan MRI abnormalities were associated with severe and very severe persistent physical and mental health impairment (PHOSP-COVID symptom clusters) after hospitalisation.
Interpretation:
After hospitalisation for COVID-19, people are at risk of multiorgan abnormalities in the medium term. Our findings emphasise the need for proactive multidisciplinary care pathways, with the potential for imaging to guide surveillance frequency and therapeutic stratification
Deep mtDNA subdivision within Linnean species in an endemic radiation of tiger beetles from New Zealand (genus Neocicindela)
- Publication venue
- 'Elsevier BV'
- Publication date
- 16/10/2012
- Field of study
The invertebrate fauna of New Zealand is of great interest as a geologically tractable model for the study of species diversification, but direct comparisons with closely related lineages elsewhere are lacking. Integrating population-level analyses with studies of taxonomy and clade diversification, we performed mtDNA analysis on Neocicindela (Cicindelidae, tiger beetles) for a broad sample of populations from 11 of 12 known species and 161 specimens (three loci, 1883 nucleotides), revealing 123 distinct haplotypes. Phylogenetic reconstruction recovered two main lineages, each composed of 5-6 Linnean species whose origin was dated to 6.66 and 7.26. Mya, while the Neocicindela stem group was placed at 10.82. ±. 0.48. Mya. Species delimitation implementing a character-based (diagnostic) species concept recognized 19 species-level groups that were in general agreement with Linnean species but split some of these into mostly allopatric subgroups. Tree-based methods of species delimitation using a mixed Yule-coalescence model were inconclusive, and recognized 32-51 entities (including singletons), splitting existing species into up to 8 partially sympatric groups. These findings were different from patterns in the Australian sister genus Rivacindela, where character-based and tree-based methods were previously shown to produce highly congruent groupings. In Neocicindela, the pattern of mtDNA variation was characterized by high intra-population and intra-species haplotype divergence, the coexistence of divergent haplotypes in sympatry, and a poor correlation of genetic and geographic distance. These observations combined suggest a scenario of phylogeographic divergence and secondary contact driven by orogenetic and climatic changes of the Pleistocene/Pliocene. The complex evolutionary history of most species of Neocicindela due to the relative instability of the New Zealand biota resulted in populations of mixed ancestry but not in a general loss of genetic variation. © 2011 Elsevier Inc.This work was funded in part by Grant NER/A/S/2000/00489 of the Natural Environment Research Council (NERC).Peer Reviewe
Reinterpreting western use of coercion in Bosnia‐Herzegovina: Assurances and carrots were crucial
- Author
- Anthony Lake W.
- Art Robert J.
- Atkinson Rick
- Atkinson Rick
- Barber Lionel
- Bellamy Christopher
- Bertram Christoph
- Bryant Lee
- Cook Robin
- Cowell Alan
- Daly Emma
- Dodd Tom
- Drozdiak William
- Fletcher Martin
- Freedman Lawrence
- Friedman Thomas L.
- Gellman Barton
- George Alexander L.
- Gordon Michael R.
- Gow James
- Harvey Frank
- Horvitz Paul F.
- Jakobsen Peter Viggo
- Jeffrey Smith R.
- Kinzer Stephen
- Leng Russell J.
- Lewis Anthony
- Lippman Thomas W.
- Lloyd John
- Lucarelli Sonia
- Marr Andrew
- Moore Patrick
- Nelan Bruce W.
- Nelson Mark M.
- Pape Robert A.
- Peter Viggo Jakobsen
- Posen Barry R.
- Post Tom
- Ricks Thomas E.
- Rieff David
- Rose Lt.‐Gen. Michael
- Savill Annika
- Silber Laura
- Sudetic Chuck
- Tetts Gillian
- Thurow Roger
- Whitney Craig R.
- Zimmermann Warren
- Publication venue
- 'Informa UK Limited'
- Publication date
- Field of study
Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity
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- Publication venue
- country:DEU
- Publication date
- 01/01/2021
- Field of study