43 research outputs found
Early peroral feeding after pancreaticoduodenecomy
- Publication venue
- 'Liga-Inform, Ltd.'
- Publication date
- 01/12/2019
- Field of study
Objective. To analyze the various ways for enteral feeding after pancreaticoduodenectomy.
Materials and methods. There were investigated the results of pancreaticoduodenectomy, performed in 78 patients, suffering tumors of pancreatic head and periampullary zone, in whom various methods of nutritive support, in 2003 - 2017 yrs were applied. For comparative analysis the patients were divided into two groups: the first - 39 patients, perioperative treatment of whom was conducted in accordance to the ERAS program, and the second - 39 patients, who were treated using a standard method. In patients of the first group the effects of a peroral way of nutrition were compared, as well as combined peroral and enteral nutrition via microjejunostomy. There were studied the terms of restoration of peroral feeding, the gastrostasis rate, the nutrition calorage during 7 postoperative days, levels of general protein and albumin on the first, third and seventh postoperative day.
Results. In 33 (84.6%) patients of the first group the peroral nutrition restoration have occurred in complete order to the protocol. The gastrostasis rate in patients of the first group was essentially lesser, than in patients of the second group. In the first group this complication have occurred in 6 (15.4%) patients, in the second group - in 14 (35.9%) patients (p = 0.009). Dynamics of level of general protein and albumin of the blood in postoperative period did not depend on method and energetic estimate of the nutrition.
Conclusion. Application of peroral feeding, in accordance to the concept of the program for accelerated restoration of the patients, survived after pancreaticododenectomy, constitutes an optimal way for the nutrient support of an organism and permits to reduce the gastrostasis rate trustworthily
Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response.
- Author
- Publication venue
- Publication date
- 26/10/2016
- Field of study
The Frank-Starling mechanism allows the amount of blood entering the heart from the veins to be precisely matched with the amount pumped out to the arterial circulation. As the heart fills with blood during diastole, the myocardium is stretched and oxidants are produced. Here we show that protein kinase G Iα (PKGIα) is oxidant-activated during stretch and this form of the kinase selectively phosphorylates cardiac phospholamban Ser16-a site important for diastolic relaxation. We find that hearts of Cys42Ser PKGIα knock-in (KI) mice, which are resistant to PKGIα oxidation, have diastolic dysfunction and a diminished ability to couple ventricular filling with cardiac output on a beat-to-beat basis. Intracellular calcium dynamics of ventricular myocytes isolated from KI hearts are altered in a manner consistent with impaired relaxation and contractile function. We conclude that oxidation of PKGIα during myocardial stretch is crucial for diastolic relaxation and fine-tunes the Frank-Starling response
Long-lasting blood pressure lowering effects of nitrite are NO-independent and mediated by hydrogen peroxide, persulfides, and oxidation of protein kinase G1α redox signalling
- Author
- Akaike
- Akashi
- Alessandra Borgognone
- Bailey
- Bernadette O Fernandez
- Bianco
- Bogdandi
- Bondonno
- Browner
- Bryan
- Burgoyne
- Cortese-Krott
- Cuello
- Dejam
- DeMartino
- Donzelli
- Feelisch
- Forouzanfar
- Fukuto
- Guimarães
- Ida
- Joanna J Goodwin
- Kalyanaraman
- Kayleigh Griffiths
- Krych-Madej
- Madhani
- Magdalena Minnion
- Maher
- Martin Feelisch
- Melanie Madhani
- Michael P Frenneaux
- Miriam M Cortese-Krott
- Montenegro
- Nicholas D Gollop
- Oleksandra Prysyazhna
- Oliveira-Paula
- Ono
- Perlman
- Philip Eaton
- Pick
- Pinder
- Prysyazhna
- Rosie M Hayes
- Sheehe
- Shimokawa
- Siddiqi
- Singh
- Stubbert
- Takaaki Akaike
- Titov
- Titov
- Tomoaki Ida
- Publication venue
- 'Oxford University Press (OUP)'
- Publication date
- 01/01/2020
- Field of study
Aims Under hypoxic conditions, nitrite (NO2-) can be reduced to nitric oxide (NO) eliciting vasorelaxation. However, nitrite also exerts vasorelaxant effects of potential therapeutic relevance under normal physiological conditions via undetermined mechanisms. We, therefore, sought to investigate the mechanism(s) by which nitrite regulates the vascular system in normoxia and, specifically, whether the biological effects are a result of NO generation (as in hypoxia) or mediated via alternative mechanisms involving classical downstream targets of NO [e.g. effects on protein kinase G1 alpha (PKG1 alpha)]. Methods and results Ex vivo myography revealed that, unlike in thoracic aorta (conduit vessels), the vasorelaxant effects of nitrite in mesenteric resistance vessels from wild-type (WT) mice were NO-independent. Oxidants such as H2O2 promote disulfide formation of PKG1 alpha, resulting in NO- cyclic guanosine monophosphate (cGMP) independent kinase activation. To explore whether the microvascular effects of nitrite were associated with PKG1 alpha oxidation, we used a Cys42Ser PKG1 alpha knock-in (C42S PKG1 alpha KI; 'redox-dead') mouse that cannot transduce oxidant signals. Resistance vessels from these C42S PKG1 alpha KI mice were markedly less responsive to nitrite-induced vasodilation. Intraperitoneal (i.p.) bolus application of nitrite in conscious WT mice induced a rapid yet transient increase in plasma nitrite and cGMP concentrations followed by prolonged hypotensive effects, as assessed using in vivo telemetry. In the C42S PKG1 alpha KI mice, the blood pressure lowering effects of nitrite were lower compared to WT. Increased H2O2 concentrations were detected in WT resistance vessel tissue challenged with nitrite. Consistent with this, increased cysteine and glutathione persulfide levels were detected in these vessels by mass spectrometry, matching the temporal profile of nitrite's effects on H2O2 and blood pressure. Conclusion Under physiological conditions, nitrite induces a delayed and long-lasting blood pressure lowering effect, which is NO-independent and occurs via a new redox mechanism involving H2O2, persulfides, and PKG1 alpha oxidation/activation. Targeting this novel pathway may provide new prospects for anti-hypertensive therapy
Disulfide-activated protein kinase G I alpha regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response
- Author
- BL Prosser
- BR Nelson
- D Maestrini
- DA Eisner
- DD Browning
- DG Allen
- DH MacLennan
- DH MacLennan
- DJ Greensmith
- DM Bers
- DM Bers
- E Lee
- EH Wilkes
- F Garofalo
- FP Knowlton
- GC Fan
- HA Shiels
- J Markwalder
- JJ Allen
- JK Oh
- JP Glaves
- JP Huggins
- JR Burgoyne
- JR Burgoyne
- K Haghighi
- KL Koss
- L Qin
- L Raeymaekers
- M Kato
- M Kumar
- N Dephoure
- O Frank
- O Prysyazhna
- O Rudyk
- O Rudyk
- P Casado
- P Casado
- PM Muller
- R Jacob
- R Tom
- S Schauble
- SH Francis
- T Oki
- V Alverdi
- V Rajeeve
- V Sivakumaran
- W Fuller
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 26/10/2016
- Field of study
British Heart Foundation, European Research Council (ERC Advanced award), Medical Research Council and the Department of Health via the NIHR cBRC award to Guy’s & St Thomas’ NHS Foundation Trust.
Part supported by the NIHR University College London Hospitals Biomedical Research Centre
Redox Control of Protein Kinase G I alpha Fine-Tunes the Frank-Starling Law of the Heart in Vivo by Regulating Diastolic Relaxation
- Author
- Publication venue
- Publication date
- 01/11/2016
- Field of study
Whole-genome sequencing reveals host factors underlying critical COVID-19
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- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G. R.
- Abedalthagafi M.
- Abel L.
- Abernathy C.
- Abraheem A.
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- Acquilini D.
- Adams C.
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- Adams K.
- Adamsara A.
- Adanini O.
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- Adra D.
- Afilalo J.
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- Wyllie D. H.
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- Xue X.
- Yadav A.
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- Yun N.
- Zainy T.
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- Zaki A.
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- Zanella I.
- Zborowski A. C.
- Zeberg H.
- Zechner M.
- Zguro K.
- Zhang M.
- Zhao J. H.
- Zheng C.
- Zhou W.
- Zitter L.
- Zlatopolsky M.
- Zollner S.
- Zongo O.
- Zucchi P.
- 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
Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity
- Author
- 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. 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. Easthorpe
- 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. Noakes
- A. Patel
- A. Pickard
- 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 Brown
- Adam Krętowski
- Adriana Roży
- Agnese Verzuri
- Agnieszka Adamek
- Agnieszka Bielska
- Agostino Ognibene
- Agostino Riva
- Ailsa Golightly
- Alan Maclean
- Albert Tenesa
- Aleksandra Berkan-Kawinska
- Aleksandra Jezela-Stanek
- Aleksandra Starosz
- Alessandra Guarnaccia
- Alessandra Renieri &
- Alessandra Stella
- Alessandra Vergori
- Alessandro Pancrazzi
- Alessia Giorli
- Alice Donati
- Alison Meynert
- Alistair Nichol
- Anders Larsson
- Andrea Antinori
- Andrea Cossarizza
- Andrea Gabbuti
- Andrea Tommasi
- Andrew D. Bretherick
- Andrew Law
- Andrew Stenhouse
- Andrzej Eljaszewicz
- Andrzej Horban
- Andy Law
- Angelica Pagliazzi
- Angie Fawkes
- Anke Hinney
- Anna Canaccini
- Anna Kruk
- Anna Maria Pinto
- Anna Moniuszko-Malinowska
- Anna Parfieniuk-Kowerda
- Anna Piekarska
- Anna Szałkowska
- Annarita Giliberti
- Anne Richmond
- Antonella D. ’Arminio Monforte
- Antonella Vincenti
- Antonia Ho
- Antonio Di Biagio
- Antonio Perrella
- Arianna Emiliozzi
- Arianna Gabrieli
- Arsalin Azzadin
- Asma Al Thani &
- Athanasios Kousathanas
- Audrey Coutts
- Axel Schmidt
- Axel Schmidt
- 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. Johnson
- 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
- Barbara Rossetti
- Barbara Shih
- Barbara Sobala-Szczygiel
- Beata Puzanowska
- Benedetta Romanin
- Björn Jensen
- Bo Wang
- Brent Richards
- 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. Eastgate
- 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. 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
- Carlo Maj
- Carmelo Piscopo
- Caroline Abernathy
- Caterina Lo Rizzo
- Ce Dunmore
- Cecilia Costa
- Ceilia Boz
- Cesira Nencioni
- Chadi Saad
- Charles Hinds
- Charlotte Summers
- Chenqing Zheng
- Chiara Barbieri
- Chiara Fallerini
- Chiara Gabbi
- Chiara Spertilli Raffaelli
- Chris P. Ponting
- Chris Ponting
- Christian Herr
- Christof Winter
- Christoph D. Spinner
- Clark D. Russell
- Claudia Suardi
- Claudio Ferri
- Clemens M. Wendtner
- 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. Golden
- D. Griffin
- 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
- Danilo Tacconi
- Danny McAuley
- David Bennett
- David Harrison
- David Maslove
- Davide Grassi
- Davide Romani
- Dawn Law
- Diana Alaverdian
- Diana Martonik
- Diego Ripamonti
- Domenico A. Coviello
- Dorota Pasko
- Dorota Zarębska-Michaluk
- E. Abaleke
- E. Allan
- E. Anastasescu
- E. Andrews
- E. Apetri
- 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. Jude
- 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. Salciute L. Grauslyte
- E. Smith
- E. Smithson
- E. Stoddard
- E. Stones
- E. Thomas
- E. Tilney
- E. Timlick
- E. Treus Gude
- E. Virgilio
- E. Watson
- E. Wilby
- E. Wraith
- Edoardo Conticini
- Elena Andreucci
- Elena Bargagli
- Elena Desanctis
- Elisa Benetti
- Elisa Frullanti
- Elisabetta Menatti
- Elisabetta Schiaroli
- Ellie Mcmaster
- Elvina Gountouna
- Emanuele Catena
- Enrico Cabri
- Enrico Martinelli
- Erika Fiorentini
- Erola Pairo-Castineira
- Erola Pairo-Castineira
- Esther Duncan
- Eugenia Quiros-Roldan
- Eva C. Schulte
- Eva C. Schulte
- 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
- Fabian Brand
- Fabio Lena
- Faisal Almalki
- Federica Gaia Miraglia
- Federico Anedda
- Federico Franchi
- Ferdinando Giannattasio
- Filip Taneski
- Filippo Aucella
- Filippo Biscarini
- Fiona Griffiths
- Floriana Valentino
- Francesca Andretta
- Francesca Ariani
- Francesca Colombo
- Francesca Fava
- Francesca Gatti
- Francesca Mari
- Francesca Minnai
- Francesca Montagnani
- Francesca Vichi
- Francesco Bianchi
- Francesco Brancati
- Francesco Castelli
- Francesco Menichetti
- Francesco Paciosi
- Francesco Raimondi
- Francesco Vladimiro Segala
- Francis P. Crawley
- Franco Maggiolo
- Franco Marinangeli
- 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. Randell
- G. Sadera
- G. Seddon
- G. Sera Howe
- G. Sloane
- G. Subramanian
- G. Tsinaslanidis
- G. Turner
- G. Watson
- G. Wray
- Gabriela Sokołowska
- Gabriella Coiro
- Gabriella Doddato
- Gabriella Maria Squeo
- GEN-COVID Multicenter Study
- Genni Spargi
- GenOMICC Consortium
- Giada Beligni
- Gian Piero Caldarelli
- Gianfranco Parati
- Giovanna Morelli
- Giulia Gori
- Giuseppe Fiorentino
- Giuseppe Merla
- Giusy Tiseo
- Graeme Grimes
- Guillaume Butler-Laporte
- Guillaume Butler-Laporte
- 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. 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
- Hadeel AlBardis
- Hamdi Mbarek
- Hanning Mal
- Helen Szoor-McElhinney
- Hugh Montgomery
- Hugo Zeberg
- Hugo Zeberg
- 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. Otaha
- I. Otahal
- I. Turner-Bone
- I. Welters
- I. White
- I. Wynter
- Ilaria Meloni
- Ilaria Rancan
- Immacolata Andolfo
- Isabella Zanella
- Iwona Mozer-Lisewska
- J. Allan
- J. Barker
- J. Bewley
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- Tammy Gilchrist
- Thorsten Brenner
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- Umberto Zuccon
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- Urszula Polowianiuk
- V. Amin
- V. Anumakonda
- V. Bastion
- V. Cannons
- V. Crickmore
- V. Gopal
- V. Irvine
- V. Kasipandian
- V. Krishnamurthy
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- V. Sarathy
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- V. Tuckey
- V. Turner
- V. Wagstaff
- V. Waugh
- Valentina Anemoli
- Valentina Borgo
- Valentina Perticaroli
- Verena Keitel
- Veronique Vitart
- W. Harrison
- W. Khaliq
- W. Khaliq
- W. McCormick
- W. Woodyatt
- Wadha Al-Muftah
- WES/WGS Working Group Within the HGI
- Wiktoria Izdebska
- Wilna Oosthuyzen
- X. Qiu
- Xia Shen
- Y. Baird
- Y. Choudhury
- Y. Hussain
- Y. Jackson
- Y. Thirlwall
- Yanara Marincevic-Zuniga
- Yang Wu
- Yaser Al-Sarraj
- Z. Alldis
- Z. Belagodu
- Z. Bradshaw
- Z. Coton
- Z. Daly
- Z. Farzad
- Z. Fernandez
- Z. Garland
- Z. Maqsood
- Z. Omar
- Z. Prime
- Z. Scott
- Zhijian Yang
- Publication venue
- Publication date
- 01/01/2022
- Field of study
The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)
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
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- 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
Abstracts from the 8th International Conference on cGMP Generators, Effectors and Therapeutic Implications
- Author
- Adam Snook
- Adrian J. Hobbs
- Aikaterini I. Argyriou
- Albert Smolenski
- Albert T. Profy
- Alessandro Cataliotti
- Alexander Froese
- Alexander Kollau
- Alexander Kollau
- Alexander Vincent
- Alexandre Dumoulin
- Ali Banijamali
- Alisa Kamynina
- Amie J. Moyes
- Amrita Ahluwalia
- Andrea Gerling
- Andrea Hembre Ulsund
- Andrea Neubauer
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Friebe
- Andreas Güldner
- Andreas Papapetropoulos
- Andrew Tobin
- Andriana Stamopoulou
- Andrzej Weichsel
- Angela McLaughlin
- Angelos Vachaviolos
- Annemarie Aue
- Annemarie Aue
- Annemarie Aue
- Antonius C. F. Gorren
- Arnab Ghosh
- Arno Fritsch
- Astrid Schrammel
- Astrid Schrammel
- Astrid Schrammel
- Astrid Weiss
- Athanassios Giannis
- Atsuko Okamoto
- Attila Oláh
- Axel Gödecke
- B. Selin Kenet
- Balázs Tamás Németh
- Banumathi Sankaran
- Barbara Voussen
- Barbara Voussen
- Barbara Wilhelm
- Bernd J. Pichler
- Bernd Mayer
- Bernd Mayer
- Bernd Mayer
- Bernd Wissinger
- Boris Tchernychev
- Béla Merkely
- Camila B. Almeida
- Carine M. Boustany
- Carla F. F. Penteado
- Catherine Mansfield
- Cheng-Yu Chen
- Chieri Takeuchi
- Choel Kim
- Choel Kim
- Choel Kim
- Choel Kim
- Chris Sarko
- Christian Dees
- Christian Meier
- Christian Schön
- Christine E. Gee
- Christopher Newton-Cheh
- Claire Poulet
- Clara D. Ledsky
- Cor de Wit
- Cor de Witt
- Corina Russwurm
- Cornelia Virus
- Courtney Shea
- Csaba Mátyás
- César Ibarra-Alvarado
- Damian Brockschnieder
- Daniel P. Zimmer
- Daniel Richards
- Daniela Bertinetti
- Dante Merlino
- Darren Casteel
- Darren E. Casteel
- David A. Kass
- David Kilpatrick
- David Langleben
- David Langleben
- Deborah M. Dickey
- Dennis Busse
- Dennis J. Stuehr
- Diane Wong
- Dianna M. Milewicz
- Dieter Groneberg
- Dieter Groneberg
- Dieter Groneberg
- Ditta Zobor
- Dominik M. Fischer
- Donald B. Bloch
- Dong I. Lee
- Dongjian Hu
- Donté A. Stevens
- Doris Koesling
- Doris Koesling
- Doris Koesling
- Doris Koesling
- Doris Koesling
- Dorit Möhrle
- Eberhart Zrenner
- Edward Seto
- Ekkehard Grünig
- Elena Walter
- Elke Butt
- Emmanuel S. Buys
- Emrah Eroglu
- Erik S. Blomain
- Ernst-Martin Füchtbauer
- Eugen Franz
- Eugen Franz
- Evanthia Mergia
- Fabian Schwiering
- Fabian Schwiering
- Fabian Schwiering
- Fabiola Zakia Mónica
- Ferid Murad
- Fernando F. Costa
- Finn Olav Levy
- Finn Olav Levy
- Finn Olav Levy
- Finn Olav Levy
- Flavia Menezes
- Francheska Colon-Gonzalez
- Frank Eitner
- Friederike Cuello
- Friedrich Grimminger
- Friedrich W. Herberg
- Friedrich W. Herberg
- Fritz G. Rathjen
- Fritz G. Rathjen
- Frode Berven
- G-Yoon Jamie Im
- G. Todd Milne
- G. Todd Milne
- G. Todd Milne
- Gaia Calamera
- Gaia Calamera
- Garyfalia Makrynitsa
- Georgios A. Spyroulias
- Gerald Wölkart
- Gerburg K. Schwaerzer
- Gerhard Hannig
- Gilbert W. Kim
- Glenn A. Reinhart
- Gordon L. Warren
- Guang Liu
- Guang Liu
- Guang-Rong Wang
- Gzona Bajraktari
- Gábor Szabó
- Gérald Simonneau
- Hanan Chweih
- Hannes Schmidt
- Hannes Schmidt
- Hans-Ulrich Häring
- Harald H. H. W. Schmidt
- Harald Langer
- Hariharan Subramanian
- Heinz G. Körschen
- Henriette Andresen
- Heribert Schunkert
- Hirofumi Tachibana
- Hiroshi Hosoda
- Hiroshi Hosoda
- Holly Clifford
- Hong Wang
- Hongxing Chen
- Hossein-Ardeschir Ghofrani
- Hu Sheng Qian
- Huaqun Zhang
- Hyazinth Dobrowinski
- Hyun-Soon Geisler
- Ibrahim J. Domian
- Inmaculada Silos-Santiago
- Ioannis I. Alexandropoulos
- Isabelle Lamarre
- Jaime L. Masferrer
- Jaime L. Masferrer
- James C. Campbell
- James E. Sheppeck
- James E. Sheppeck
- James R. Klinger
- James Wakefield
- Jan D. Huizinga
- Jan Giesen
- Jana Wobst
- Jeanette Erdmann
- Jenna Scotcher
- Jennifer E. Van Eyk
- Jenny Tobin
- Jens Schlossmann
- Jeong Joo Kim
- Jeong Joo Kim
- Jeremy R. Egbert
- Jeremy Richman
- Jerid W. Robinson
- Jerid W. Robinson
- Jessica A. Wales
- Jieru E. Lin
- Joerg Reinders
- Johanna Weiss
- Johannes-Peter Stasch
- John T. Fassett
- Jonas Keppler
- Jonathan C. Schisler
- Joon Jung
- Joon Jung
- Jordi Villà-Freixa
- Joseph R. Burgoyne
- Julia Davydova
- Julia Gorelik
- Jun Hino
- Jun Hino
- Jürgen Burhenne
- Ka Bian
- Kanako Takamatsu
- Karl Ulrich Bartz-Schmidt
- Karoline Dröbner
- Katharina Beck
- Katharina Beck
- Katharina Frank
- Katherine Hall
- Kathleen A. Lincoln
- Katja Stehfest
- Katrin Reimann
- Kenji Kangawa
- Kenji Kangawa
- Kenji Kangawa
- Kerstin Jurk
- Kim C. Mansky
- Kim Tang
- Kimberly Long
- Kirk L. Peterson
- Kjestine Schmidt
- Kjestine Schmidt
- Kjetil W. Andressen
- Kjetil Wessel Andressen
- Kjetil Wessel Andressen
- Koichi Miura
- Koichi Miura
- Konstantina Stathopoulou
- Kristen M. Kokkonen
- Kristin Hartmann
- Kálmán Benke
- Lai Wen
- Lai Wen
- Lan Zhao
- Lars I. Leichert
- Laurinda A. Jaffe
- Laurinda A. Jaffe
- Laurinda Jaffe
- Leia C. Shuhaibar
- Lincoln R. Potter
- Lincoln R. Potter
- Lincoln R. Potter
- Linda Breci
- Lise Román Moltzau
- Lise Román Moltzau
- Liying Qin
- Luis Agulló
- Lukas Rüttiger
- M. Wittwer
- Mahmood Alam
- Mai Kadomatsu
- Manuela Harloff
- Manuela Zaccolo
- Manuela Zaccolo
- Mara Goetz
- Marc Humbert
- Marcel A. Krüger
- Marcus Olbrich
- Maria Hernandez-Valladares
- Marianne Bjørnerem
- Marina Bantzi
- Marissa Opelt
- Marissa Opelt
- Marius M. Hoeper
- Marius Ueffing
- Mark Aronovitz
- Mark Currie
- Mark G. Currie
- Mark J. Ranek
- Markus Waldeck-Weiermair
- Markus Wolters
- Markus Wolters
- Markus Wolters
- Marlies Knipper
- Martin Biel
- Martin Deile
- Martin Floor
- Martin Thunemann
- Martin Thunemann
- Masayuki Sasaki
- Mathew M. Mannion
- Mathias Seeliger
- Matthias Broser
- Matthias Karck
- Meinoshin Okumura
- Meinrad Gawaz
- Mi Kyung Chang
- Michael J. Shipston
- Michael Paolillo Hannes Schmidt
- Michael Russwurm
- Michael Russwurm
- Michael Russwurm
- Michael Russwurm
- Michel Négrerie
- Mihály Ruppert
- Mika Takai
- Miki Arai
- Mikiya Miyazato
- Mikiya Miyazato
- Min Zhang
- Monte S. Willis
- Moritz Lehners
- Motofumi Kumazoe
- Motofumi Kumazoe
- Motofumi Kumazoe
- Nadine Mauro
- Nadja I. Bork
- Nancy D. Dalton
- Navin Kapur
- Nazareno Paolocci
- Nicholas Blixt
- Nicola Conran
- Nicole Eichert
- Nicoletta C. Surdo
- Obiajulu Agha
- Oleksandra Prysyazhna
- Oleksandra Prysyazhna
- Oleksandra Prysyazhna
- Olena Rudyk
- Olga N. Petrova
- Oliver Pagel
- on behalf of the Ironwood team
- Ornella Manfra
- Pablo Colorado
- Pamela L. Brito
- Paul A. Corris
- Paul A. Renhowe
- Paul C. Harrison
- Paul S. Frenette
- Pavel I. Nedvetsky
- Pavel Jansa
- Peter Germano
- Peter Hegemann
- Peter P. Rainer
- Peter Ruth
- Peter Sandner
- Peter Sandner
- Peter Wright
- Philip Eaton
- Philip Eaton
- Philip Eaton
- Philip Eaton
- Philipp Henning
- Ping Zhang
- Péter Hegedűs
- Q. Luo
- Ralf Kühn
- Ralph Schermuly
- Raymond L. Benza
- RD-CURE consortium
- Regine Mühlfriedel
- Reiner Frey
- Renate Pilz
- Rene Zahedi
- Renee Sarno
- Renee Sarno
- Reshma S. Baliga
- Richard C. Page
- Richard Karas
- Robert Baumgartner
- Robert Blanton
- Robert Feil
- Robert Feil
- Robert Feil
- Robert Feil
- Robert Feil
- Robert Feil
- Robert Lukowski
- Robert Naeije
- Robert Solinga
- Roger Flores-Costa
- Roland Malli
- Ronald J. Holewinski
- Ryan Fryer
- S. A. Dames
- S. Bruce King
- Sandra Frankenreiter
- Sandy M. Chu
- Sara S. O. Saad
- Sara Vandenwijngaert
- Sarah Helena Nies
- Sarah Jacobson
- Sarah Jacobson
- Saurav Misra
- Scott A. Waldman
- Sean P. Parsons
- Selene J. Sollie
- Sevil Korkmaz-Icöz
- Shatanik Mukherjee
- Shiliang Li
- Shinpei Kawaoka
- Shun Hiroi
- Shunhui Zhuang
- Sian E. Harding
- Silja Meier
- Simone Romoli
- Sivakanan Loganathan
- Sonia Donzelli
- Sophie Schobesberger
- Stavros Topouzis
- Stefan Hell
- Stefan Z. Lutz
- Stefanie Peters
- Steffen Wolter
- Stepan Gambaryan
- Stephan Rosenkranz
- Steven S. Pullen
- Stylianos Michalakis
- Susanne Feil
- Susanne Feil
- Susanne Kohl
- Susanne Krasemann
- Sylvia Nikkho
- Sylvie Bernier
- Sylvie G. Bernier
- Takashi Nojiri
- Takashi Nojiri
- Takashi Nojiri
- Takeshi Tokudome
- Takeshi Tokudome
- Tamás Radovits
- Thomas G. Oertner
- Thorsten Kessler
- Timothy Calamaras
- Tobias Bauch
- Tobias Peters
- Ulrich Walter
- Ulrike Scheib
- Ulrike Zimmermann
- V. Kaila
- Viacheslav O. Nikolaev
- Viacheslav O. Nikolaev
- Viacheslav O. Nikolaev
- Viacheslav O. Nikolaev
- Vikas Kapil
- Vineet Agrawal
- Vu Thao-Vi Dao
- Walter E. Haefeli
- Wendy Baur
- William R. Montfort
- Wilson A. Ferreira
- Wolfgang F. Graier
- Yasutake Tanaka
- Yigao Huang
- Ying-Ju Sung
- Yue Dai
- Yusu Gu
- Yutaka Suzuki
- Zhi Cheng Jing
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2017
- Field of study
This work was supported by a restricted research grant of Bayer AG
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.
- 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.
- Agüero D.
- Ahmad N.
- Ahmadi S.
- Ahmed A.
- Ahmed C.
- 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.
- 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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- 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