30 research outputs found
Measuring ultracool properties from the UKIDSS Large Area Survey
- Author
- Avril Day-Jones
- Ben Burningham
- Buragsser
- Burgasser
- Burgasser
- Burningham
- Chabrier
- Cruz
- David Pinfield
- Deacon
- Federico Marocco
- Hewett
- Hugh Jones
- James Clarke
- James Jenkins
- Joana Gomes
- Jose Gallardo
- Kirkpatrick
- Kirkpatrick
- Maria-Teresa Ruiz
- Marocco
- Maxted
- Metchev
- Nial Deacon
- Phil Lucas
- Pinfield
- Reylé
- Roberto Saglia
- Rocha-Pinto
- Schmidt
- Stephens
- Stuart Folkes
- Zenghua Zhang
- Publication venue
- 'EDP Sciences'
- Publication date
- 01/01/2013
- Field of study
This is an Open Access article distributed under the terms of the Creative Commons Attribution License 2.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly citedWe discuss the properties and of ultracool and brown dwarfs that can be measured from current large area surveys and how fundamental parameters, such as the mass function and formation history can be measured, describing our own first measurement of the formation history in the sub-stellar regime using data from the UKIDSS Large Area Survey
The 2dF Galaxy Redshift Survey: spectral types and luminosity functions
- Author
- Bland-Hawthorn Joss
- Cannon Russell
- Cole Shaun
- Colless Matthew
- Collins Chris
- Couch Warrick
- Dalton Gavin
- Deeley Kathryn
- Driver Simon P.
- Efstathiou George
- Ellis Richard S.
- Folkes Simon
- Frenk Carlos S.
- Glazebrook Karl
- Kaiser Nick
- Lahav Ofer
- Lewis Ian
- Lumsden Stuart
- Maddox Steve
- Peacock John
- Peterson Bruce A.
- Price Ian
- Ronen Shai
- Sutherland Will
- Taylor Keith
- Publication venue
- Royal Astronomical Society
- Publication date
- 19/09/1999
- Field of study
We describe the 2dF Galaxy Redshift Survey (2dFGRS) and the current status of the observations. In this exploratory paper, we apply a principal component analysis to a preliminary sample of 5869 galaxy spectra and use the two most significant components to split the sample into five spectral classes. These classes are defined by considering visual classifications of a subset of the 2dF spectra, and also by comparison with high-quality spectra of local galaxies. We calculate a luminosity function for each of the different classes and find that later-type galaxies have a fainter characteristic magnitude, and a steeper faint-end slope. For the whole sample we find M*=−19.7 (for Ω=1, H₀=100 km s⁻¹ Mpc⁻¹), α=−1.3, φ*=0.017. For class 1 (‘early-type’) we find M*=−19.6, α=−0.7, while for class 5 (‘late-type’) we find M*=−19.0, α=−1.7. The derived 2dF luminosity functions agree well with other recent luminosity function estimates
VISTA Variables in the <i>Vía Láctea</i> (VVV): Halfway Status and Results
- Author
- Ahumada Andrea Verónica
- Aigrain Suzanne
- Alonso García Javier
- Alonso María Victoria
- Amôres Eduardo B.
- Angeloni Rodolfo
- Arias Julia Inés
- Bandyopadhyay Reba
- Barbuy Beatriz
- Barbá Rodolfo Héctor
- Baume Gustavo Luis
- Beamin Juan Carlos
- Bedin Luigi
- Bica Eduardo
- Borissova Jordanka
- Bronfman Leonardo
- Carraro Giovanni
- Catelan Márcio
- Clariá Olmedo Juan José
- Contreras Carlos
- Cross Nicholas
- Davis Christopher
- Drew Janet E.
- Dékány István
- Emerson Jim P.
- Fariña Cecilia
- Feinstein Baigorri Carlos
- Fernández Lajús Eduardo Eusebio
- Folkes Stuart
- Gamen Roberto Claudio
- Geisler Douglas
- Gieren Wolfgang
- Goldman Bertrand
- González Oscar
- Gosling Andrew
- Grijs Richard de
- Gunthardt Guillermo Ivan
- Gurovich Sebastian
- Hambly Nigel C.
- Hanson Margaret
- Hempel Maren
- Hoare Melvin
- Irwin Mike J.
- Ivanov Valentin D.
- Jordán Andrés
- Kerins Eamonn
- Kinemuchi Karen
- Kurtev Radostin
- Longmore Andy
- Lucas Philip W.
- López Corredoira Martin
- Maccarone Tom
- Martínez Eduardo
- Masetti Nicola
- Mennickent Ronald E.
- Merlo David
- Messineo Maria
- Minniti Dante
- Mirabel Miquele Igor Félix
- Monaco Lorenzo
- Moni Bidin Christian
- Morelli Lorenzo
- Padilla Nelson
- Palma Tali
- Parisi María Celeste
- Parker Quentin
- Pavani Daniela
- Pietrukowicz Pawel
- Pietrzynski Grzegorz
- Pignata Giuliano
- Rejkuba Marina
- Rojas Alejandra
- Roman Lopes Alexandre
- Ruiz María Teresa
- Saito Roberto K.
- Sale Stuart E.
- Saviane Ivo
- Schreiber Matthias R.
- Schröder Anja C.
- Sharma Saurabh
- Smith Michael
- Sodré Jr. Laerte
- Soto Mario
- Stephens Andrew W.
- Tamura Motohide
- Tappert Claus
- Thompson Mark A.
- Toledo Ignacio
- Valenti Elena
- Vanzi Leonardo
- Weidmann Walter Alfredo
- Zoccali Manuela
- Publication venue
- Publication date
- 14/07/2020
- Field of study
The VISTA Variables in the Vía Láctea (VVV) survey is one of six near-infrared ESO public surveys, and is now in its fourth year of observing. Although far from being complete, the VVV survey has already delivered many results, some directly connected to the intended science goals (detection of variable stars, microlensing events, new star clusters), others concerning more exotic objects, e.g., novae. Now, at the end of the fourth observing period, and comprising roughly 50% of the proposed observations, the status of the survey, as well some of results based on the VVV data, are presented.Facultad de Ciencias Astronómicas y Geofísica
Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans
- Author
- Abbasi Z
- Abdul-Hamid M Akhlil
- Abel Paul D
- Abrams Paul H
- Adab Fawzi A
- Adamson Andrew
- Adeyoju A
- Adolfson Jan
- Afzal Naveed
- Ahiaku Ernest K N
- Ahmed Munir
- Al Sudani Mohammed L
- Al-Samarraie Amir S M
- Al-Samerraie [Unknown]
- Al-Singary Waleed
- Al-Sudani [Unknown]
- Alcock Christopher
- Alexander Kimberly
- Ali Zulfiqar
- Almond David J
- Alonzi Roberto
- Aly Markus
- Amin Al Olama Ali
- Anderson John
- Andrews Henry
- Andrews Steven
- Anjum Iqbal
- Anson Ken
- Anyamene Nicola A
- Apakama Ike
- Aparcia F
- Archbold J A A
- Arndt Volker
- Ash D
- Ashford Richard F U
- Auvinen Anssi
- Azzabi A
- Badenoch David
- Bahl Amit
- Bailey Karen
- Bailey M J
- Ball Andrew J
- Banerjee G
- Barber Jim
- Barber N
- Baria [Unknown]
- Barnes Douglas G
- Barros-Silva Joao
- Barwell Julian
- Bashir J
- Basu Pradip
- Bates Christopher A
- Batra Jyotsna
- Bax N A
- Baxter-Smith D
- Bdesha Amar
- Beacock Christopher J M
- Beaney Ronald P
- Beard Ralph
- Beatty John D
- Beck Rupert
- Beese Gail
- Beesley Sharon
- Bell C Richard W
- Bellringer James
- Benlloch Garcia Sara
- Benson Richard
- Beresford [Unknown]
- Bevis Christopher R A
- Bhana Rajanee
- Bhanot S
- Bhatnagar A
- Bhatt R I
- Birch Brian
- Birtle Alison
- Bishop M
- Biyani C Shekhar
- Blacklock A R E
- Blades Rosemary
- Bliss Peter
- Bloomfield David J
- Boddy S
- Bollina Prasad
- Bonnington Sue
- Booth C M
- Bose Pradeep
- Bott Michael C
- Bottomley David
- Boucher Nigel R
- Bowen J
- Bower Mark
- Bowsher W G
- Boyd P J R
- Bradshaw Lynne
- Bramble F James
- Brenner Hermann
- Brewster Simon F
- Briggs Tim
- Brock Cathryn
- Brock Sue
- Bromage Stephen
- Broms Michael
- Brough Richard
- Brown Andrew A
- Brown Paul
- Brown Paul M
- Brown Richard
- Brown Stephen
- Browning Tony J
- Bryan N
- Burgess Neil A
- Burns-Cox Nicholas
- Butterbach Katja
- Butterworth Paul C
- Cahill D
- Callaghan P S
- Calleary John
- Calleja M
- Calman Frances
- Camilleri Philip
- Campbell Alister
- Cannon Andrea
- Cannon-Albright Lisa
- Carnell Dawn M
- Carr T W
- Carter Adam C
- Carter Charles J M
- Carter Simon
- Castle Bruce M
- Catto James
- Cavalli-Bjoerkman Carin
- Chadwick David
- Chahal Rohit
- Chakraborti P
- Chappell [Unknown]
- Charig C
- Chetiyawardana Anula D
- Chilton Christopher
- Chinegwundoh F I
- Chong Irene
- Choudhury Ananya
- Chow Wai-Man
- Christmas Timothy J
- Christova Svetlana
- Churn Mark J
- Cieza-Borrella Clara
- Clarke Noel W
- Clavijo-Eisele Jorge
- Clements Judith A
- Coe M
- Coetzee Gerhard A
- Cohen N P
- Coker C
- Cole David J
- Cole O
- Cole Trevor
- Collins Angus
- Collins Gerald
- Collinson Matthew
- Conn I
- Connell C
- Conti David V
- Cook Audrey
- Cook Margaret
- Cooke Peter
- Cooksey Graeme
- Coombs L
- Cooper Debbie
- Copland Robert F
- Cornaby Andrew J
- Cornford P A
- Corolis [Unknown]
- Corr John
- Costello C B
- Coull Mrs N
- Cowan Richard
- Cox Angela
- Cox Robert
- Coyle C
- Crew Jeremy
- Crisp John C
- Cross W
- Cruger Dorthe
- Crundwell Malcolm
- Cummings [Unknown]
- Cybulski Cezary
- Dadaev Tokhir
- Dahar Nazeer
- Daniel Francis N
- Darrad J
- Daruwala Pallon
- Das Gautam
- Datta Shibendra
- Davidson S
- Davies Joseph
- Davis Michael
- Davison Owen W
- Dawkins Guy
- Dawson Chris
- De Bolla Alan R
- Dearnaley David
- Desai Ken M
- Deutsch George P
- Dick John
- Dickinson Andrew J
- Dickson Jeanette
- Dikov Tihomir
- Dinneen Michael
- Dixit Sanjay
- Dobbs H Jane
- Doble A
- Doble Andrew
- Dodds David
- Doherty Alan
- Donaldson P
- Donovan Jenny L
- Dooldeniya M
- Douglas S Fiona
- Down Liz
- Drake [Unknown]
- Duchesne Gill M
- Duffy Peter
- Dunn Michael
- Dunsmuir W D
- Durkan Garrett
- Durrani Sajid K
- Easton Douglas
- Eaton Alan C
- Eccles Diane
- Eckert Allison
- Eddy B
- Eden C D
- Edwards J
- Eeles Rosalind A
- El-Modir A
- Elkabir Jeremy
- Elliott Emma
- Elliott P Tony
- Ellis B W
- Ellis R
- Elves Andrew W S
- Elwell Christine
- Emberton Mark
- Emmerson Louise
- England Roland C D
- Errington R D
- Evans D Gareth
- Falconer Alison
- Fawcett Derek
- Featherston C
- Featherstone Carolyn J
- Feggetter Jeremy
- Ferguson C
- Fermont D
- Ferro Michael
- Fisher Cyril
- Fitzgerald Liesel
- Fitzgerlad Liesel M
- Fletcher Matthew
- Folkes A
- Ford Trevor F
- Foster Paul W
- Franks Kevin N
- Freedman Mathew
- Frim Olivera
- Gale Joanna
- Gallegos Christopher
- Gelister James S
- George Anne
- Ghana [Unknown]
- Gibbs Stephanie
- Gilbert Hugh
- Giles Graham G
- Gillatt David
- Glaholm John
- Glass Jonathan M
- Glenister James
- Goode Thomas D
- Gordon E M
- Govindasami Koveela
- Gower Richard L
- Graham John
- Green Damian
- Greenland Jonathan
- Grieve Robert
- Griffiths Thomas R L
- Gronberg Henrik
- Gujral Sandy
- Gupta Nishi
- Gurun Riza Murat
- Gustafsson Sven
- Guy Michelle
- Guy Peter J
- Haiman Christopher A
- Haldar Neil
- Halder N
- Haley James
- Hamdy F C
- Hamdy Freddie
- Hamilton C
- Hammonds John
- Hampson S J
- Hanbury Damien C
- Hardman P D John
- Harland Stephen J
- Harney John M
- Harper Peter
- Harris D
- Harris Sarah
- Harrison G S M
- Harriss D R
- Harvey-Hills N
- Hawkyard Simon
- Hazel Steve
- Hazelett Dennis J
- Heath Catherine M
- Heathcote Peter
- Hehir Michael
- Hellawell Giles O
- Henderson Brian E
- Hendry David
- Henley Mike
- Henrique Rui
- Henry Ann
- Herbert Pippa
- Herkommer Kathleen
- Hetherington John
- Hickish Tamas
- Hicks James A
- Hilman Serena
- Hindley Richard
- Hindmarsh John R
- Hines John
- Hingorani M
- Ho Edwin T S
- Hodgson Shirley
- Hoffman U
- Holden David
- Holding Peter
- Hollingdale A
- Hollins Graham W
- Holmes Simon A V
- Holt Sarah
- Hopper John L
- Horan Gail
- Horwich Alan
- Hoskin Peter
- Howell Graham P
- Howson Joanne
- Hrouda D
- Huddart Robert
- Hudson Liz
- Hughes Michael
- Hughes Owen
- Hughes Rob
- Humber Caroline
- Iacovou John W
- Ibrahim A
- Inglis John A
- Irving Stuart
- Irwin C
- Iversen Peter
- Izatt Louise
- Izegbu Victor
- Jameel Basharat
- James Michael J
- James N
- James R Lester
- Javle Pradip
- Jenkins P
- Jhavar Sameer
- Johansson Jan-Erik
- Jones Chris R
- Jones David A
- Jones Gareth
- Jones Mandy
- Joseph J
- Joss Shelagh
- Jugurnauth-Little Sara
- Kachakova Darina
- Kaisary Amir
- Kaliski Alexandre L
- Kaneva Radka
- Kapur G
- Karim O
- Karlsson Ami
- Karp Stephen J
- Kedda Mary-Anne
- Keeley F X
- Kelkar Anand R
- Kelleher J P
- Kelly John
- Kenwrick Sue
- Kerr Kris
- Key Tim J
- Khan F
- Khaw Kay-Tee
- Khoo Vincent
- Kibel Adam S
- Kierzek Andrzej
- Kimber Rachel M
- Kinder R
- Kirby Roger S
- Kirk David
- Kirkbride Peter
- Kirollos Magdi M
- Klarskov Peter
- Kluzniak Wojciech
- Kockelbergh Roger
- Koenig Philip C W C
- Kooiman Gordon G
- Koreich O
- Kote-Jarai Zsofia
- Koupparis Anthony
- Kourah Mohamed
- Kraus Sigurd
- Kujala Paula
- Kujawa Magda L
- Kulkarni Ravi
- Kumar M
- Kumar Rajeev
- Kunkler Ian H
- Kynaston H
- Kynaston Howard
- Lachlan Katherine L
- Laing Robert
- Lalloo Fiona
- Lancashire M
- Lane Athene
- Langley Stephen E M
- Laniado Marc
- Larner T R
- Lau Maurice W
- Lawrence W T
- Lawson Anne
- Le Roux Pieter J
- Leader Mary
- Lee A
- Lee J O
- Lee L
- Lemburger R John
- Lennon Teresa
- Leone Priscilla
- Leongamornlert Daniel
- Lester Jason
- Leung Hing
- Lewis D Christopher
- Lewis J
- Li Qiuyan
- Lim Hui-Yi
- Lin Hui-Yi
- Liston Thomas
- Livni Naomi
- Livsey Jacqueline
- Lloyd S
- Locke Imogen
- Lodge Richard
- Logue John
- Longmuir Mark
- Lophatananon Artitaya
- Lophatonanon Artitaya
- Lubinski Jan
- Lucas Malcolm G
- Luedeke Manuel
- Luscombe C J
- Lydon Anna
- Lynch Michael
- Lynn Naing N K
- Lyons Norma
- MacDermott James P A
- Macdonagh Ruaraidh P
- Macdonald [Unknown]
- Madaan Sanjeev
- Madhava Kudingila R
- Maeaettaenen Liisa
- Maguire Joseph
- Maher E R
- Mahmood Rana
- Maia Sofia
- Maier Christiane
- Mair Graeme H M
- Malone Greg
- Malone Peter R
- Mangar Stephen A
- Mantle Mark
- Mark I
- Marsden Gemma
- Mason M D
- Mason Malcolm
- Mason Robert
- Matanhelia [Unknown]
- Matenhelia Shyam
- Matthews Philip N
- McAleese J
- McBride Donna
- Mcdonnell Shannon K
- McDonnell Shannon K
- McFarlane Jonathan
- McGrath [Unknown]
- McIlhenny Craig
- McInerney Paul
- McIntosh Gregor
- McKinna F
- McLaren Duncan
- McLarty Esther
- McMenemin Rhona
- McNeill Alan
- McNicholas T A
- Meddings Robert N
- Mee A David
- Melcher Lucinda
- Memon [Unknown]
- Menzes Pravin
- Michael Agnieszka
- Miller Marek
- Mills Robert
- Mitchell S
- Mitev Vanio
- Mithal Natasha
- Mitkova Atanaska
- Mitra Anita
- Mobb Gillian E
- Moffat Leslie E F
- Mokete [Unknown]
- Money-Kyrle Julian
- Montgomery Bruce
- Moody Hilary
- Moody Martin P
- Morgan Angela
- Morley Roland
- Morris Sean B
- Morrison Patrick
- Mort Diana
- Mostafid Amir H
- Motiwala Hanif
- Mufti Gulzar
- Muir Gordon
- Muir Kenneth
- Mumtaz Faiz
- Murphy Michael
- Murray Alexandra
- Murray Keith W
- Murrell Shirley
- Murtola Teemu
- Muthukumar D
- Naerger Harry
- Namasivayam Siva
- Nargund Vinod
- Nawrocki [Unknown]
- Neal David E
- Neilson Donald
- Nethersell A
- Newby Jacqueline C
- Newman Hugh
- Newton R
- Nielsen Sune F
- Nordestgaard Børge G
- O'Boyle P J
- O'Brien J
- O'Brien Tim S
- O'Donnell H
- O'Donoghue E
- O'Donoghue Neil
- O'Reilly P
- O'Rourke J S
- O'Sullivan Joe
- O'Sullivan Patricia
- Oakley Neil
- Ogden Chris
- Ohja Hemant
- Oliver Tim
- Omara Tracy
- Ong Eng K
- Osborn David
- Ostler Peter
- Owen J
- Palfrey Edward
- Panades Miguel
- Panakis Niki
- Pancharatnam M
- Pandha Hardev
- Pantelides Michalakis L
- Panwar U
- Parikh Omi
- Park Hyun
- Park Jong Y
- Parker Chris
- Parker Christopher H
- Parys Bohdan T
- Pascoe Sarah
- Pashayan Nora
- Patel Anup
- Paterson Joan
- Pathack S
- Pati Jhumur
- Patterson Helen
- Pattu [Unknown]
- Paul A
- Paul Alan
- Paulo Paula
- Payne Heather
- Peake David
- Pedersen John
- Pedley I
- Pengelly A
- Peracha Amjad M
- Perry Matthew
- Persad Raj
- Peters John
- Pharoah Paul
- Philp N H
- Philp T
- Pickering Lisa M
- Pigott Katharine
- Pinto Pedro
- Plail R
- Plowman P Nicholas
- Pocock Richard D
- Pope A J
- Popert Rick
- Popov Elenko
- Porter Tim
- Potter John M
- Pow-Sang Julio
- Powell Christopher
- Powell Philip
- Powles Thomas B
- Prasad Krishna
- Prasad Seshadri Sri
- Prejbisz J W
- Prescott Stephen
- Protheroe Andrew
- Qureshi Khaver N
- Raby Nigel
- Radlein Selina
- Ragavan Narasimhan
- Raju Palaniappa G S
- Ramachandra Prakash B
- Raman R
- Rane Abhay
- Rankin Julia
- Rao Y
- Ratan Hari L
- Ravi Ramachandran
- Ravishankar K
- Read [Unknown]
- Reddy Paul J
- Rimington Peter R
- Rinckleb Antje
- Rincon Maria
- Riska Shaun
- Ritchie Peter A
- Roberts J Trevor
- Robertson Andrew
- Robinson Angus
- Robinson Anne C
- Robinson Lee Q
- Rochester Mark A
- Roder Andreas
- Rogers P B
- Rosario Derek
- Rosenbaum Tomas P
- Rothwell Neil
- Rowbotham Carl
- Rowe [Unknown]
- Rowley Kathryn
- Ruddy Deborah
- Rundle John
- Russell John M
- Ryan P G
- Sabharwal A
- Saggar Anand K
- Samanci Ali
- Sangar Vijay K
- Santos Joana
- Saunders Edward J
- Saunders Pamela
- Sawyer Emma J
- Saxby M F
- Schaid Daniel J
- Schleutker Johanna
- Schumacher Fredrick
- Schwaibold Hartwig
- Scoble John E
- Scrase Christopher
- Selim [Unknown]
- Sellers Thomas
- Sells Henry
- Sethia Krishna K
- Severi Gianluca
- Shackley David C
- Shaffer [Unknown]
- Shah Nihil
- Shakespeare D
- Shanley Sue
- Sharma Neerah K
- Sheehan Denise J
- Sherwin Elizabeth
- Shum Poh Lin
- Side Lucy
- Sidek Norma
- Signorello Lisa B
- Sikora Karol
- Simcock R
- Sinclair Andrew M
- Singh Pravin
- Siva M
- Slavov Chavdar
- Smith James
- Smith Michael F
- Sokal Michael
- Sole Graham M
- Southey Melissa C
- Speakman Mark J
- Spiers Alexander
- Spurdle Amanda
- Sreenivasan Thiagarajan
- Srihari Narayanan N
- Srinivasan [Unknown]
- Sriram Rajagopalan
- Staffurth John N
- Stanford Janet L
- Stattin Paer
- Stegmaier Christa
- Stephens Sarah
- Stewart D
- Stockdale Andrew
- Stott Mark A
- Stower M J
- Strachan John R
- Stuart Nicholas S A
- Sugden Elaine
- Summerton Duncan
- Sundar Santhanam
- Sundaram S K
- Suresh Gokarakonda
- Susnerwala Shabbir
- Swami Kuchibhotla S
- Symons Stephanie J
- Syndikus Isabel
- Taari Kimmo
- Tahir Saad
- Tammela Teuvo L
- Tammela Teuvo L J
- Tanquay J
- Taylor J W
- Taylor John W
- Teixeira Manuel R
- Terry T
- Thibodeau Stephen N
- Thomas Robert J
- Thomas Stephen A
- Thompson Alan
- Thompson Pauline
- Thomson Alastair H
- Thurston A
- Tidball Sarah
- Tillmans Lori
- Tilsley Owen
- Tindall Stuart F
- Tipples K
- Tong [Unknown]
- Toussi Hamid
- Toy Elizabeth W
- Travis Ruth C
- Trembath Richard C
- Tulloch David N
- Turner Kevin J
- Turner Megan
- Tweedle James
- Tymrakiewicz Malgorzata
- Tyrell C J
- Umez-Eronini N
- Urwin Graeme H
- Vale Justin A
- Van As [Unknown]
- Van As Nicholas
- Vasanthan Subramaniam
- Vesey Sean
- Vilarino-Varela Maria
- Violet John
- Virdi Jaspal
- Viñuela Ana
- Vlahova Aleksandrina
- Vogel Walther
- Wade Robert
- Wahlfors Tiina
- Waite Katherine
- Walker E M
- Walker Roger
- Wallace David M A
- Wallinder Hans
- Wang Liang
- Watkin Nicholas A
- Watson M E
- Waxman J H
- Waymont Brian
- Weaver Andrew
- Webb Ralph J
- Wedderburn Andrew
- Weischer Maren
- Wells Paula
- Wemyss-Holden G D
- Weston P M T
- Wheatley Duncan
- Whelan P
- Whillis D
- Whitmore Ian
- Wiklund Fredrik
- Wilde Adam D
- Wiles Vicki
- Wilkins Marie
- Wilkinson Rosemary
- Williams John H
- Williams Simon
- Willis Michael
- Wills Michael I
- Wilson J R
- Wilson Richard
- Winkler Mathias H
- Wise Marcus
- Wokozorczyk Dominika
- Wokołorczyk Dominika
- Wood Glenn
- Woodhams Simon
- Woodhouse C
- Woodward Cathryn
- Woolf [Unknown]
- Woolfenden K A
- Worlding Jane
- Wright Mark
- Wu Huihai
- WYLIE [Unknown]
- Wylie James P
- Wynne Chris
- Yeadon Trina
- Zachariah Babu
- Zang Angelika
- Zarkar A
- Zheng Wei
- Publication venue
- 'Oxford University Press (OUP)'
- Publication date
- 01/01/2015
- Field of study
Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have
fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in
25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16
regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of
correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP,
while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in
Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium
(LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region.
Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant
enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the
refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa,
an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of
PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent
signals within the same regio
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
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- Sabino Scolletta
- Samreen Ijaz
- Sandro Mancarella
- Sandro Panese
- Sara Amitrano
- Sara McDonald
- Sarah Law
- Sarah McCafferty
- Saverio Giuseppe Parisi
- Saye Khoo
- Scott Richard
- Semple Malcolm G
- Serafina Valente
- Serena Ludovisi
- Sergio Daga
- Seán Keating
- Shankar-Hari Manu
- Shen Xia
- Shih Barbara
- Shiranee Sriskandan
- Shona C Moore
- Silvia Cappelli
- Simona Marcantonio
- Simone Furini
- Sophie Halpin
- 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
- T Cosier
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- T Duncan
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- 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
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.
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- Abel L.
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- Abraheem A.
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
- Abd Elghafar M.S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
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- 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
Development and pre-clinical testing of a novel hypoxia-activated KDAC inhibitor
- Author
- Publication venue
- Publication date
- 23/03/2021
- Field of study
Tumor hypoxia is associated with therapy resistance and poor patient prognosis. Hypoxia-activated prodrugs, designed to selectively target hypoxic cells while sparing normal tissue, represent a promising treatment strategy. We report the pre-clinical efficacy of 1-methyl-2-nitroimidazole panobinostat (NI-Pano, CH-03), a novel bioreductive version of the clinically used lysine deacetylase inhibitor, panobinostat. NI-Pano was stable in normoxic (21% oxygen) conditions and underwent NADPH-CYP-mediated enzymatic bioreduction to release panobinostat in hypoxia (<0.1% oxygen). Treatment of cells grown in both 2D and 3D with NI-Pano increased acetylation of histone H3 at lysine 9, induced apoptosis and decreased clonogenic survival. Importantly, NI-Pano exhibited growth delay effects as a single agent in tumor xenografts. Pharmacokinetic analysis confirmed the presence of sub- micromolar concentrations of panobinostat in hypoxic mouse xenografts, but not in circulating plasma or kidneys. Together, our preclinical results provide a strong mechanistic rationale for the clinical development of NI-Pano for selective targeting of hypoxic tumors.<br /
Diffusion and solution of gases and vapors in styrene-butadiene block copolymers
- Author
- Publication venue
- 'Wiley'
- Publication date
- Field of study