76 research outputs found
Biobehavioral Indices of Emotion Regulation Relate to School Attitudes, Motivation, and Behavior Problems in a Low-Income Preschool Sample
- Publication venue
- 'Wiley'
- Publication date
- 01/12/2006
- Field of study
Effective emotion regulation may promote resilience and preschool classroom adjustment by supporting adaptive peer interactions and engagement in learning activities. We investigated how hypothalamus-pituitary-adrenal axis (HPA) regulation, cardiac reactivity, and classroom emotion displays related to adjustment among low-income preschoolers attending Head Start. A total of 62 four-year-olds completed a laboratory session including a baseline soothing video; emotion-eliciting slides/video clips, and recovery. Salivary cortisol, heart rate, and vagal tone were measured throughout. Independent coders used handheld computers to observe classroom emotion expression/regulation. Teachers rated child motivation, persistence/attention, learning attitudes, and internalizing/externalizing symptoms. Results reveal associations between biobehavioral markers of regulatory capacity and early school adjustment.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73847/1/annals.1376.043.pd
Equal opportunities and diversity changing employment patterns in the European electricity industry: A Report for EPSU, EMCEF and EURELECTRIC
- Publication venue
- European Commission
- Publication date
- 01/01/2004
- Field of study
Observed and predicted effects of climate change on species abundance in protected areas
- Author
- Alison Johnston
- Andrew Douse
- Andy Brown
- Bernard Cadiou
- Bernard Deceuninck
- Bradbury Richard B.
- Chamberlain Daniel Edward
- Cook Aonghais S. C. P.
- Crick Humphrey Q. P.
- Dodd Andrew M.
- Fré
- Helen Pontier
- Malcolm Ausden
- McCall Rob A.
- Menno Hornman
- Nancy Ockendon
- Newson Stuart E.
- Olivia Crowe
- Pearce Higgins James W.
- Rehfisch Mark M.
- Staffan Roos
- Stroud David A.
- Thaxter Chris B.
- Thomas Chris D.
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2013
- Field of study
Biallelic Mutations in MRPS34 Lead to Instability of the Small Mitoribosomal Subunit and Leigh Syndrome
- Author
- Assouline Zahra
- Bai Renkui
- Bodaert Nathalie
- Byrnes James
- Calvo Sarah E.
- Christodoulou John
- Compton Alison G.
- Cristian Ingrid
- Falk Marni J.
- Filipovska Aleksandra
- Haude Katrina
- Houten Sander M.
- Lake Nicole J.
- McCormick Elizabeth M.
- Metodiev Metodi D.
- Mootha Vamsi K.
- Mountford Hayley S.
- Pulman Juliette
- Retterer Kyle
- Richman Tara R.
- Rio Marelene
- Ruzzenente Benedetta
- Rötig Agnes
- Schadt Eric E.
- Sherpa Mingma D.
- Stroud David A.
- Thorburn David R.
- Webb Bryn D.
- Zangarelli Coralie
- Zhang Zhancheng
- Zolkipli-Cunningham Zarazuela
- Publication venue
- Publication date
- 01/01/2017
- Field of study
The synthesis of all 13 mitochondrial DNA (mtDNA)-encoded protein subunits of the human oxidative phosphorylation (OXPHOS) system is carried out by mitochondrial ribosomes (mitoribosomes). Defects in the stability of mitoribosomal proteins or mitoribosome assembly impair mitochondrial protein translation, causing combined OXPHOS enzyme deficiency and clinical disease. Here we report four autosomal-recessive pathogenic mutations in the gene encoding the small mitoribosomal subunit protein, MRPS34, in six subjects from four unrelated families with Leigh syndrome and combined OXPHOS defects. Whole-exome sequencing was used to independently identify all variants. Two splice-site mutations were identified, including homozygous c.321+1G>T in a subject of Italian ancestry and homozygous c.322−10G>A in affected sibling pairs from two unrelated families of Puerto Rican descent. In addition, compound heterozygous MRPS34 mutations were identified in a proband of French ancestry; a missense (c.37G>A [p.Glu13Lys]) and a nonsense (c.94C>T [p.Gln32∗]) variant. We demonstrated that these mutations reduce MRPS34 protein levels and the synthesis of OXPHOS subunits encoded by mtDNA. Examination of the mitoribosome profile and quantitative proteomics showed that the mitochondrial translation defect was caused by destabilization of the small mitoribosomal subunit and impaired monosome assembly. Lentiviral-mediated expression of wild-type MRPS34 rescued the defect in mitochondrial translation observed in skin fibroblasts from affected subjects, confirming the pathogenicity of MRPS34 mutations. Our data establish that MRPS34 is required for normal function of the mitoribosome in humans and furthermore demonstrate the power of quantitative proteomic analysis to identify signatures of defects in specific cellular pathways in fibroblasts from subjects with inherited 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
- 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
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- C Gorman
- C Hays
- C Hewitt
- C Holl
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- C Humphrey
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- 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
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- D Butcher
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- D Golden
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- D Hamilton
- D Hawcutt
- D Hope
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- D Kallon
- D Kaye
- D Kelly
- D Loader
- D Lomas
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- D McGlynn
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- D Tetla
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- 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
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- E Raith
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- E Smith
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- 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
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- G Hobden
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- G Lubimbi
- G Maloney
- G Martir
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- G Randell
- G Sadera
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- 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
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- H Curgenven
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- H Rangarajan
- H Rehman
- H Reschreiter
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- H T-Michael
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- 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
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- I D Clement
- I Edmond
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- I Hussain
- I Lancoma-Malcolm
- I Leadbitter
- I Nagra
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- I Otahal
- I Turner-Bone
- I Welters
- I White
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- 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
- J Hornsby
- J Hulme
- J Hunt
- 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
- J Mallinson
- J Martin
- J Matthews
- J McCormick
- J Medhora
- J Melville
- J Moreno Cuesta
- J Morgan
- J Naisbitt
- J Norris
- J North
- J Parkin
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- J Perez
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- J Pheby
- J Philbin
- J Pinnell
- J Queiroz
- J Radhakrishnan
- J Reid
- J Rhodes
- J Riches
- J Ritzema
- J Ruddy
- J Ryan-Smith
- J Scriven
- J Scriven
- J Scriven
- J Shiel
- J Singh
- J Singleton
- J Smith
- J Sowter
- J Strickley
- J Summers
- J Taylor
- J Tebbutt
- J Texeira
- J Thomas
- J Thrush
- J Tomlinson
- J Valentine
- J Whiteside
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- J Willson
- J Zamikula
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- Jane Weaver
- Janet Harrison
- Janet T Scott
- Janie F Shelton
- Jen Meikle
- Jo Dalton
- Johnny Millar
- Jorge Esparza-Gordillo
- Jose E Krieger
- Julian A Hiscox
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- K Xavier
- Katarzyna Hafezi
- Keating Sean
- Kenneth A Mclean
- Kirstie Morrice
- Klaric Lucija
- Klenerman Paul
- Knight Julian
- Kousathanas Athanasios
- L Abel
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- L Kittridge
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- M Abdelrazik
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- M Newton
- M Oblak
- M Odam
- M Ostermann
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- M Robinson
- M Sangombe
- M Shankar-Hari
- M Sim
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- M Smith
- M Smith
- M Spivey
- M T Hijazi
- M Taylor
- M Taylor
- M Taylor
- M Taylor
- M Taylor
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- M Thirumaran
- M Thomas
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- M Verlander
- M Vertue
- M Watters
- M White
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- M Williams
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- M Woodruff
- M Young
- Maaike Swets
- Mahdad Noursadeghi
- Manu Shankar-Hari
- Marco Castori
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- Margherita Baldassarri
- Mari E K Niemi
- Mari Ward
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- Maria Bandini
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- Maria Palmieri
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- Marta Corridi
- Maslove David
- Massimiliano Fabbiani
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- McAuley Danny
- Meera Chand
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- Michelle Girvan
- Millar Jonathan
- Mirella Bruttini
- Miriana D'Alessandro
- Montgomery Hugh
- Moore Shona C
- Moutsianas Loukas
- Murphy Lee
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- N Ahmad
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- Turtle Lance
- U Poultney
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- 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
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- Y Thirlwall
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- Yang Zhijian
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- Z Bradshaw
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- Z Fernandez
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- Z Maqsood
- Z Omar
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- 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
Canagliflozin and renal outcomes in type 2 diabetes and nephropathy
- Author
- A Kaldun Nossuli
- Aamir Jamal
- Adalbert Schiller
- Adam Cheifetz
- Adarsh Daswani
- Adeera Levin
- Adline Ghazi
- Adrian Guinsburg
- Adriana Cif
- Adriana Gabriela Onaca
- Adriana Ilavska
- Adriana Villarino
- Agarwal R.
- Agnieszka Starzec
- Ahmed Arif
- Ahmed Awad
- Aiping Yin
- Akimichi Asano
- Alan Jackson
- Alan McMahon
- Alan Perlman
- Alberto Di Carlo
- Alberto Esquenazi
- Alejandra Oviedo
- Alejandro Valdes Depeda
- Aleksandra Kendereski
- Alex Valenzuela
- Alexander Dreval
- Alexander Gonzalez
- Alexander Shinkov
- Alexander Turchin
- Alexandre Klein
- Alfonso Soto Gonzalez
- Alfred Penfornis
- Alfredo Chew Wong
- Alfredo Wassermann
- Ali Torshizi
- Alicia Chilito
- Alina Agafyina
- Alison Dawson
- Alva Hansraj
- Amer Al-Karadsheh
- Amorin Remus Popa
- Amrendra Kumar
- Amy Sprague
- Ana Limos
- Ana Maria Cusumano
- Ana Maria Elosegui
- Anabella Amigo
- Anatoliy Kazmirchuk
- Andrea Phillips
- Andrea Stella
- Andreas Maddux
- Andrej Dzupina
- Andres Alvarisqueta
- Andrew Johnson
- Andrew O'Shaughnessy
- Andrew Steele
- Andrian Yakov
- Andrzej Januszewicz
- Andrzej Madej
- Angelina Angelova
- Anibal Gastaldi
- Anil Gupta
- Anita Bhajan Manocha
- Anjanette Tan
- Anna Kaminska
- Anna Maria Veronelli
- Anna Strzelecka
- Anna Zateyshchikova
- Anselmo Bordonava
- Antanas Navickas
- Anthony Gunstone
- Anthony Roberts
- Antonio Ceriello
- Antonio Galan Serrano
- Antonio Scafuto Scotton
- Antonio Terrelonge
- Antônio Roberto Chacra
- Anupama Gowda
- Arjun D Sinha
- Armando Perez
- Ashot Mkrtumyan
- Atanas Koundurdjiev
- Augusto Vallejos
- Aurelian-Emil Ranetti
- Ayim Akyea-Djamson
- Aysha Badat
- Bakris G.
- Baldev Singh
- Barbara Greco
- Barbara Kaczmarek
- Barbara Rewerska
- Barry M Brenner
- Belia Martin Del Camp Blanco
- Bernard Zinman
- Bertrand Cariou
- Bertrand Dussol
- Bhasker Mehta
- Bhimavarapu Sudhakar
- Björn Paschen
- Bompoint S.
- Borys Mankovskyy
- Botond Csiky
- Boyan Nonchev
- Brenner B. M.
- Brett Kissela
- Brian Nichol
- Bruce Neal
- Bruce Trippe
- Bruno Geloneze Neto
- Bull S.
- Byung-Wan Lee
- C B Keshavamurthy
- Cannon C. P.
- Capuano G.
- Carlo Giorda
- Carlos Alberto Cuneo
- Carlos Arauz-Pacheco
- Carlos Barrera
- Carlos Perez
- Carmel Hawley
- Carmen Crisan
- Carol Pollock
- Carolyn Droste
- Caroucel Chuateco
- Caryl David
- Cecilia Garcia Ballesteros
- Cecilia Jimeno
- Celso Amodeo
- Cesar Javier Zaidman
- Cesar Yoiti Hayashida
- Chamberlain Obialo
- Chang-Hsun Hsieh
- Charles Cook
- Charles Kaupke
- Charytan D. M.
- Chek Loong Loh
- Chen Leia
- Cheol-Young Park
- Chih-Ching Lin
- Christopher P Cannon
- Christy Yao
- Chu P. -L.
- Chwen-Tzuei Chang
- Chye Lee Gan
- Clara Barrios
- Claude Galphin
- Claudia Goycoa
- Claudia Moreira de Brito
- Clodoaido Caringal
- Cristian Serafinceanu
- Cristina Toarba
- Cristobal Morales Portillo
- Csaba Kovesdy
- Cynthia Bowman-Stroud
- Cynthia Christiano
- Cynthia Mustieles Rocha
- Cyrus Desouza
- Cássio Slompo Ramos
- Dagmar Bartaskova
- Dale Crawford Allison
- Dalia Kozloviene
- Dan Scharfstein
- Dana Cosma
- Daniel Coyne
- Daniel Hiser
- Daniel Kolansky
- Daniel Panarotto
- Daniel Pella
- Daniel Weiner
- Daniil Chizhov
- Dariusz Sowinski
- Darren K McGuire
- Davesh Sennik
- David C Wheeler
- David Cherney 3rd
- David Gorson
- David Johnson
- David M Charytan
- David Packham
- David Scott
- David Wheeler
- De Zeeuw D.
- Debbie Cohen-Stein
- Debbie Mascaro
- Deepak Koppolu
- Dennis Levinson
- Derek Lewis
- Detian Li
- Devasmita Dev
- Devesh Patel
- Dewan Deepak
- Dick de Zeeuw
- Diego Aizenberg
- Dinesh Jain
- Dinesh Khullar
- Diogo Belo
- Dmitry Zateyshshikov
- Domenico Santoro
- Domingos d'Avila
- Donald Brandon
- Donald Fraser
- Dong-Wan Chae
- Dora Inés Molina de Salazar
- Dorota Mlodawska-Choluj
- Doru Negru
- Edgar Arcos
- Edoardo Mannucci
- Eduardo Farias
- Edward Watson
- Edwards R.
- Egle Gaupsiene
- Egle Urbanaviciene
- Ekaterina Velichkova
- Elena Christofides
- Elena Grineva
- Elena Kolmakova
- Elena Shutemova
- Eleonora Harcsa
- Elizabeth Barranco
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- Elizete Keitel
- Eloisa Tellez Chavez
- Emanuela Orsi
- Emil Martinka
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- Grazyna Orlowska-Kowalik
- Grazyna Popenda
- Greene T.
- Greg Fulcher
- Gregorio Obrador
- Gregorio Obrador Vera
- Grit Faulmann
- Guadalupe Morales Franco
- Guillermo Fragale
- Guixia Wang
- Gulam Latiff
- Gustavo Cristian Greloni
- Guy Chouinard
- Gyongyi Csecsei
- Gyorgy Paragh
- Halyna Tomashkevych
- Hans Prozesky
- Harpreet Bajaj
- Hasnain Khandwala
- Hector Rodriguez
- Heerspink H. J. L.
- Helena Oosthuizen
- Hendrik Nortje
- Henry Watson
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- Hernan Yupanqui
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- Hiralal Maheshwari
- Hiroko Oishi
- Hiromi Aoki
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- Hiroshi Kono
- Hitoshi Akiyama
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- Hong Mao
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- Hongli Lin
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- Weihong Song
- Weiping Lu
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- Wenge Li
- Wheeler D. C.
- Wladmir Saporito
- Xuemei Li
- Xueqing Yu
- Yamil Canaan
- Yan Ren
- Yannick Le Meur
- Yaozhong Kong
- Yasuro Kumeda
- Yasushi Wakida
- Yavin Y.
- Yeong Hoon Kim
- Yevgeniya Svyshchenko
- Young Min Cho
- Yulia Samoylova
- Yung-Chuan Lu
- Yuriy Mostovoy
- Yuriy Shwartz
- Yvette Ethel Yap
- Zaynab Abejuela
- Zdravko Kamenov
- Zeid Khitan
- Zhang H.
- Zinman B.
- Zishan Ali
- Zuzana Ochodnicka
- Ângela Regina Nazario Sabbag
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2019
- Field of study
BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years
Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity
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- 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
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- 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)
The ATLAS fast tracKer system
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- Abbott B.
- Abbott D. C.
- Abed Abud A.
- Abeling K.
- Abhayasinghe D. K.
- Abidi S. H.
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- Åkesson T. P. A.
- Öncel Ö. O.
- Ženiš T.
- Živković L.
- Publication venue
- 'IOP Publishing'
- Publication date
- 01/01/2021
- Field of study
The ATLAS Fast TracKer (FTK) was designed to provide full tracking for the ATLAS high-level trigger by using pattern recognition based on Associative Memory (AM) chips and fitting in high-speed field programmable gate arrays. The tracks found by the FTK are based on inputs from all modules of the pixel and silicon microstrip trackers. The as-built FTK system and components are described, as is the online software used to control them while running in the ATLAS data acquisition system. Also described is the simulation of the FTK hardware and the optimization of the AM pattern banks. An optimization for long-lived particles with large impact parameter values is included. A test of the FTK system with the data playback facility that allowed the FTK to be commissioned during the shutdown between Run 2 and Run 3 of the LHC is reported. The resulting tracks from part of the FTK system covering a limited η-ϕ region of the detector are compared with the output from the FTK simulation. It is shown that FTK performance is in good agreement with the simulation. © The ATLAS collaboratio
Configuration and performance of the ATLAS b-jet triggers in Run 2
- Author
- Aad G
- Abbott B
- Abbott DC
- Abed Abud A
- Abeling K
- Abhayasinghe DK
- Abidi SH
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abulaiti Y
- Acharya BS
- Achkar B
- Adam Bourdarios C
- Adam L
- Adamczyk L
- Adamek L
- Adelman J
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- Alberghi GL
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- Alconada Verzini MJ
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- Aleksa M
- Aleksandrov IN
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- Zhemchugov A
- Zheng Z
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- Zorbas TG
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- Publication venue
- 'Springer Fachmedien Wiesbaden GmbH'
- Publication date
- 01/12/2021
- Field of study
Several improvements to the ATLAS triggers used to identify jets containing b-hadrons (b-jets) were implemented for data-taking during Run 2 of the Large Hadron Collider from 2016 to 2018. These changes include reconfiguring the b-jet trigger software to improve primary-vertex finding and allow more stable running in conditions with high pile-up, and the implementation of the functionality needed to run sophisticated taggers used by the offline reconstruction in an online environment. These improvements yielded an order of magnitude better light-flavour jet rejection for the same b-jet identification efficiency compared to the performance in Run 1 (2011–2012). The efficiency to identify b-jets in the trigger, and the conditional efficiency for b-jets that satisfy offline b-tagging requirements to pass the trigger are also measured. Correction factors are derived to calibrate the b-tagging efficiency in simulation to match that observed in data. The associated systematic uncertainties are substantially smaller than in previous measurements. In addition, b-jet triggers were operated for the first time during heavy-ion data-taking, using dedicated triggers that were developed to identify semileptonic b-hadron decays by selecting events with geometrically overlapping muons and jets
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.
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- Baggott R
- Bagshaw J
- Baguley D
- Bailey L
- Baillie J.K.
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- Bakali M
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- Ballard C
- Bandula Steven
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- Thomas-Woods T.
- Thompson A A Roger
- Thompson T
- Thornton T
- Thorpe M
- Thwaites Ryan S.
- Tilley Jo
- Tinker N
- Tiongson Gerlynn F
- Tobin Martin
- Tomlinson Johanne
- Tong C
- Toshner Mark
- Touyz R.
- Treibel Thomas A
- Tripp K.A.
- Tunnicliffe Elizabeth M.
- Turnbull A
- Turner E
- Turner Kim
- Turner Sarah
- Turner Victoria
- Turney Sharon
- Turtle Lance
- Turton Helena
- Ugoji Jacinta
- Ugwuoke R
- Upthegrove R
- Valabhji J.
- Ventura M
- Vere Joanne
- Vickers Carinna
- Vinson B
- Wade Elaine
- Wade Phillip
- Wain Louise V
- Wainwright Tania
- Wajero Lilian O.
- Walder S
- Walker S
- Walker S.
- Wall E
- Wallis T
- Walmsley S
- Walsh J.A.
- Walsh S.
- Warburton Louise
- Ward T J C
- Warwick Katie
- Wassall Helen
- Waterson Samuel
- Watson Ekaterina
- Watson James
- Watson L.
- Webster M
- Weir-McCall Jonathan R
- Welch C
- Welch H.
- Welsh B.
- Wessely S.
- West Sophie
- Weston Heather
- Wheeler H
- White Sonia
- Whitehead Victoria
- Whitney J.
- Whittaker S
- Whittam Beverley
- Whitworth V
- Wight A
- Wild James M
- Wilkins M.
- Wilkinson D
- Williams B
- Williams Jenny
- Williams N
- Williams Nick
- Williams-Howard S.A.
- Willicombe M.
- Willis Gemma
- Willoughby J
- Wilson Ann
- Wilson D
- Wilson Imogen
- Window Nicola
- Witham M.
- Wolf-Roberts Rebecca
- Wood Chloe
- Woodhead F
- Woods Janet
- Wootton Daniel G.
- Wormleighton J
- Worsley J.
- Wraith D
- Wrey Brown Caroline
- Wright C.
- Wright L
- Wright S.
- Wyles J.
- Wynter Inez
- Xie Cheng
- Xu M
- Yasmin Najira
- Yasmin S
- Yates Tom
- Yip K P
- Young A.
- Young B.
- Young Susan
- Yousuf A J
- 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
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