44 research outputs found
Early detection of dry bubble disease in Agaricus bisporus using volatile compounds
- Publication venue
- Elsevier
- Publication date
- 01/03/2024
- Field of study
Lecanicillium fungicola is a pathogen of the commercial white button mushroom (Agaricus bisporus) and is the causal agent of dry bubble disease, which can cause severe economic losses to mushroom growers. Volatile compounds were measured by GC/MS techniques over pure cultures of mycelia on agars, over microcosms of growing mushrooms, and over harvested mushrooms to identify compounds that might give an early warning of the disease. The mushroom strain tested was Agaricus bisporus, strain Sylvan A15; either deliberately infected with L. fungicola or water as a control. Over microcosms, the appearance of β-copaene, β-cubebene, and α-cedrene coincided with, but did not precede, the earliest visual signs of the disease. Mushrooms with dry bubble symptoms also had high levels of β barbatene and an unknown diterpene (UK 1821). Over some harvested mushroom sets, high levels of cis-α-bisabolene developed as a defence reaction to infection
Implicit Bias Mask 2023: Predicting Implicit Biases Fosters Growth Mindset
- Author
- Publication venue
- DigitalCommons@WayneState
- Publication date
- 06/11/2023
- Field of study
Creating advice-taking reinforcement learners
- Author
- A. Barto
- A. Barto
- A. Ginsberg
- A. Weigend
- C. Crangle
- C. Watkins
- D. Chapman
- D. Gordon
- D. J. Mostow
- D. Noelle
- D. Ourston
- F. Hayes-Roth
- G. Monahan
- G. Tesauro
- G. Towell
- G. Towell
- H. Berenji
- J. Elman
- J. Levine
- J. McCarthy
- J. Shavlik
- Jude W. Shavlik
- L. Kaelbling
- L. Lin
- L. M. Fu
- L. Zadeh
- M. Pazzani
- N. Nilsson
- P. Frasconi
- R. Maclin
- R. Sutton
- R. Sutton
- Richard Maclin
- S. Mahadevan
- S. Suddarth
- T. Dietterich
- Y. Abu-Mostafa
- Y. Cun Le
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/1996
- Field of study
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Effect of Hydrocortisone on Mortality and Organ Support in Patients With Severe COVID-19: The REMAP-CAP COVID-19 Corticosteroid Domain Randomized Clinical Trial.
- Author
- Abbass Hakam
- Adhikari Neill
- Affleck Julia
- Agno Sathianathan Ronan
- Ahmad Norfaizan
- Ahmed Iram
- Ainscough Kate
- Al Qasim Eman
- Al Swaidan Lolowa
- Al-Bassam Wisam
- Al-Beidh Farah
- Al-Beidh Farah
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- Alegria Ana
- Alexander Brian
- Alexander Peter
- Allan Angela
- Allan Elizabeth
- Allen Louise
- Allibone Suzanne
- Amaro dos Santos Catorze Teodoro
- Anderson Tom
- Andric Zdravko
- Angus Derek
- Angus Derek C
- Anjum Aisha
- Ankert Juliane
- Annane Djillali
- Annane Djillali
- Anstey Matthew
- Antcliffe David
- Aparicio Christelle
- Appelt Peter
- Arabi Yaseen
- Arabi Yaseen
- Arbane Gill
- Archer Simon
- Aref Noah
- Arias Ana-Marie
- Arishi Hatim
- Arnold Donald
- Asghar Adeeba
- Ashelford Angela
- Attwood Ben
- Austin Karen
- Aysel Florescu Simin
- Azaiz Amine
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- Badie Julio
- Bagshaw Sean
- Baillie Kenneth
- Baker Evelyn
- Bakthavatsalam Dhanalakshmi
- Bamford Peter
- Banach Dorota
- Bannard-Smith Jonathan
- Barbazza Leanne
- Barber Russell
- Barge Deborah
- Barnes Nicky
- Baršić Bruno
- Bashyal Archana
- Basile Kim
- Bass Frances
- Bates Michelle
- Bauchmuller Kris
- Bean Sarah
- Beane Abigail
- Beane Abigail
- Beasley Richard
- Begin Phillipe
- Bellemare David
- Benettaib Fatna
- Benzekri Dalila
- Berdaguer Fernando Daniel
- Bergin Colin
- Berry Lindsay
- Berry Lindsay
- Berry Scott
- Berry Scott
- Bhimani Zahra
- Bhimani Zahra
- Bihari Shailesh
- Bihari Shilesh
- Binnie Alexandra
- Bion Julian
- Biradar Vishwanath
- Birch Janine
- Birch Jenny
- Birchall Katie
- Birkinshaw Isobel
- Black Ethel
- Bloos Frank
- Board Jasmin
- Bone Allsion
- Bonner Stephen
- Bonten Marc
- Bonten Marc
- Borgatta Barbara
- Borrill Zoe
- Bosch Ziekenhuis Jeroen
- Boschert Catherine
- Bossard Isabelle
- Boumahni Dounia
- Bourgoin Charlotte
- Bourne Michelle
- Bourne Richard
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- Boyd Craig
- Bracke Stephanie
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- Bradbury Charlotte
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- Brailsford Jane
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- Brunkhorst Frank
- Budd Joanna
- Buehner Ulrike
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- Burns Karen
- Burt Karen
- Buscher Hergen
- Butler Amelia
- Butler M
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- Chen Yan
- Cheng Allen
- Cheng Allen C
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- Cirstea Emanuel
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- Zhao Xiao Bei
- Zinzoni Vanessa
- Zitter Letizia
- Đimoti Renata
- Publication venue
- JAMA: Journal of the American Medical Association
- Publication date
- 06/10/2020
- Field of study
Importance: Evidence regarding corticosteroid use for severe coronavirus disease 2019 (COVID-19) is limited. Objective: To determine whether hydrocortisone improves outcome for patients with severe COVID-19. Design, Setting, and Participants: An ongoing adaptive platform trial testing multiple interventions within multiple therapeutic domains, for example, antiviral agents, corticosteroids, or immunoglobulin. Between March 9 and June 17, 2020, 614 adult patients with suspected or confirmed COVID-19 were enrolled and randomized within at least 1 domain following admission to an intensive care unit (ICU) for respiratory or cardiovascular organ support at 121 sites in 8 countries. Of these, 403 were randomized to open-label interventions within the corticosteroid domain. The domain was halted after results from another trial were released. Follow-up ended August 12, 2020. Interventions: The corticosteroid domain randomized participants to a fixed 7-day course of intravenous hydrocortisone (50 mg or 100 mg every 6 hours) (n = 143), a shock-dependent course (50 mg every 6 hours when shock was clinically evident) (n = 152), or no hydrocortisone (n = 108). Main Outcomes and Measures: The primary end point was organ support-free days (days alive and free of ICU-based respiratory or cardiovascular support) within 21 days, where patients who died were assigned -1 day. The primary analysis was a bayesian cumulative logistic model that included all patients enrolled with severe COVID-19, adjusting for age, sex, site, region, time, assignment to interventions within other domains, and domain and intervention eligibility. Superiority was defined as the posterior probability of an odds ratio greater than 1 (threshold for trial conclusion of superiority >99%). Results: After excluding 19 participants who withdrew consent, there were 384 patients (mean age, 60 years; 29% female) randomized to the fixed-dose (n = 137), shock-dependent (n = 146), and no (n = 101) hydrocortisone groups; 379 (99%) completed the study and were included in the analysis. The mean age for the 3 groups ranged between 59.5 and 60.4 years; most patients were male (range, 70.6%-71.5%); mean body mass index ranged between 29.7 and 30.9; and patients receiving mechanical ventilation ranged between 50.0% and 63.5%. For the fixed-dose, shock-dependent, and no hydrocortisone groups, respectively, the median organ support-free days were 0 (IQR, -1 to 15), 0 (IQR, -1 to 13), and 0 (-1 to 11) days (composed of 30%, 26%, and 33% mortality rates and 11.5, 9.5, and 6 median organ support-free days among survivors). The median adjusted odds ratio and bayesian probability of superiority were 1.43 (95% credible interval, 0.91-2.27) and 93% for fixed-dose hydrocortisone, respectively, and were 1.22 (95% credible interval, 0.76-1.94) and 80% for shock-dependent hydrocortisone compared with no hydrocortisone. Serious adverse events were reported in 4 (3%), 5 (3%), and 1 (1%) patients in the fixed-dose, shock-dependent, and no hydrocortisone groups, respectively. Conclusions and Relevance: Among patients with severe COVID-19, treatment with a 7-day fixed-dose course of hydrocortisone or shock-dependent dosing of hydrocortisone, compared with no hydrocortisone, resulted in 93% and 80% probabilities of superiority with regard to the odds of improvement in organ support-free days within 21 days. However, the trial was stopped early and no treatment strategy met prespecified criteria for statistical superiority, precluding definitive conclusions. Trial Registration: ClinicalTrials.gov Identifier: NCT02735707
Genetic mechanisms of critical illness in COVID-19.
- Author
- A A Roger Thompson
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- S Whiteley
- S Williams
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- S Yussuf
- 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
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- 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
- T Coventry
- T Duncan
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- T O Jones
- T Pogreban
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- T Smith
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- 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
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- V Pristopan
- V Ratnam
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- V Sarathy
- V Thomas
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- V Tuckey
- V Turner
- V Wagstaff
- V Waugh
- Valentina Anemoli
- Vanessa Sancho-Shimizu
- Victoria Shaw
- Vitart Veronique
- W Harrison
- W Khaliq
- W Khaliq
- W McCormick
- W Woodyatt
- Walker Susan
- Walsh Timothy
- Wang Bo
- Wei Shen Lim
- Wendy S Barclay
- William A Paxton
- William Greenhalf
- Wilson James F
- Wrobel Nicola
- Wu Yang
- X Qiu
- Y Baird
- Y Choudhury
- Y Hussain
- Y Jackson
- Y Thirlwall
- Yang Jian
- Yang Zhijian
- Z Alldis
- Z Belagodu
- Z Bradshaw
- Z Coton
- Z Daly
- Z Farzad
- Z Fernandez
- Z Garland
- Z Maqsood
- Z Omar
- Z Prime
- Z Scott
- Zechner Marie
- Zhai Ranran
- Zheng Chenqing
- Publication venue
- Nature
- Publication date
- 01/01/2020
- Field of study
Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
- Abd Elghafar M. S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G. R.
- Abedalthagafi M.
- Abel L.
- Abernathy C.
- Abraheem A.
- Abul-Husn N. S.
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- Walker S.
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- Wanying Z.
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- White K.
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- Wilkinson B.
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- Williams F.
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- Williams M.
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- Williams T.
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- Willis H.
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- Wood H. -L.
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- Wrobel N.
- Wu Y.
- Wulandari R.
- Wyllie D. H.
- Wynter I.
- Xavier K.
- Xue X.
- Yadav A.
- Yang J.
- Yassen A. M.
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- Ye C.
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- Zainy T.
- Zak A.
- 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
Design of a study to determine the impact of insecticide resistance on malaria vector control: a multi-country investigation
- Author
- Abraham Peter Mnzava
- Achile Massougbodji
- Adam Ismail Bashir
- Alioun Adechoubou
- Aurore Hounto
- BL Sharp
- BL Sharp
- C Lengeler
- C Sismanidis
- C Strode
- Celestin Kouambeng
- Charles Mbogo
- CVA Edi
- Dipak K Swain
- E Chanda
- Elfatih M Malik
- Eric Ochomo
- Etienne Fondjo
- Evan Mathenge
- G Davey Smith
- H Ranson
- HD Mawejje
- Herman Parfait Awono-Ambene
- Hmooda Toto Kafy
- I Kleinschmidt
- Immo Kleinschmidt
- J Bagi
- J Etang
- J Hemingway
- JNK Rao
- John Bradley
- Josiane Etang
- Jude Bigoga
- K Hargreaves
- Kamaraju Raghavendra
- KH Toe
- Khalid Elmardi
- KI Barnes
- Kiambo Njagi
- Krishanthi Subramaniam
- L McCarroll
- Lawrence Muthami
- Luna Kamau
- Mariam Okê-Sopoh
- Martin Akogbeto
- Martin James Donnelly
- Nabie Bayoh
- Neena Valecha
- P Muller
- P Nwane
- P Nwane
- Philippa West
- PS Walsh
- PW Gething
- R Doll
- R Maharaj
- Rajendra Bhatt
- RJ Hayes
- S Mitchell
- S Schwartz
- SN Mitchell
- Stata Corporation
- Teresa Kinyari
- Tessa Bellamy Knox
- WA Hawley
- WHO
- WHO
- WHO
- WHO
- WHO
- Zinga José Nkuni
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Safety and efficacy of fluoxetine on functional outcome after acute stroke (AFFINITY): a randomised, double-blind, placebo-controlled trial
- Author
- -Thi Binh Nguyen
- Abul Mamun
- Ai Ling Tan
- Aicuratiya Withanage
- Aileen Wu
- Alan J. McDougall
- Alanah Bailey
- Alejandra Malavera
- Alessandro Zagami
- Alexis Brown
- Altman
- Amanda Boudville
- Amanda Masterson
- Amy Kunchok
- Amy McDonald
- An-Gia Pham
- Andrew Evans
- Andrew Granger
- Andrew H. Ford
- Andrew Lee
- Andrew Moey
- Andrew Murray
- Angela Abraham
- Anh-Hai Dam
- Anh-Ngoc Nguyen
- Anne Claxton
- Annie Winker
- Benjamin Nham
- Benjamin Trewin
- Beverley Macdonald
- Bhavesh Lallu
- Bich-Thi Doan
- Binh-Nguyen Pham
- Binh-Thanh Nguyen
- Binh-Thanh Nguyen
- Binh-Thi Thanh Nguyen
- Binh-Van Le
- Boon L. Tan
- Brett Jones
- Bronwen Pepperell
- Bruno
- Brännström
- Camelia Burdusel
- Cameron Redpath
- Candice Delcourt
- Caroline Roberts
- Casey Hair
- Cassandra McLennan
- Cecilia Cappelen-Smith
- Chantal Baldwin
- Chermaine Chua
- Cheryl Carcel
- Chi-Minh Do
- Chi-Van Nguyen
- Chinh-Dinh Duong
- Chollet
- Christie Drummond
- Christopher Etherton-Beer
- Christopher Taylor
- Chun Phua
- Chung-Quang Do
- Cipriani
- Clare Williams
- Colette Sanctuary
- Colette Sanctuary
- Colette Sanctuary
- Colette Sanctuary
- Counsell
- Coupland
- Craig Davenport
- Craig S. Anderson
- Cuong-Van Pham
- Cynthia Chen
- Dai-Quoc Khuong
- Danielle Wheelwright
- Darshan Ghia
- David Blacker
- David Jackson
- David Shivlal
- de Jager
- Deborah Field
- Dennis
- Dennis Cordato
- Dev Nathani
- Diana Ramirez
- Diana Schmid
- Duncan
- Dung Do Nguyen
- Dung-Tien Nguyen
- Duong-Huu Luong
- Duong-Van Kieu
- Ehsan E. Shandiz
- Elizabeth Pepper
- Elizabeth Ray
- Emily Duckett
- Emma Siracusa
- Erik Lundström
- Essie Low
- Fintan O'Rourke
- Fix Sangvatanakul
- Gab Silver
- Gary Cheuk
- Geoffrey A. Donnan
- Giang-Truong Nguyen
- Giau-Thi Kim Tran
- Gillian E. Mead
- Gillian Edmonds
- Graeme J. Hankey
- Graham
- Gregory Carter
- Ha-Thi Hai Dinh
- Ha-Thi Thu Nguyen
- Ha-Van Mai
- Hai-Thanh Ngo
- Hanh-Cao Dang
- Hanh-Hong Dang
- Hanh-Thi Truc Phan
- Hankey
- Hannah Coyle
- Hannah Coyle
- Harry McNaughton
- Heike Burnet
- Helen Baines
- Hien-Thi Bich Nguyen
- Hillary Hayes
- Ho Choong
- Hoa-Ngoc Nguyen
- Hoa-Van Hoang
- Hoai-Thi Le
- Hong-Thi Tran
- Hop-Quang Huynh
- Howard
- Huong-Huynh To Dinh
- Huong-Thi Bich Nguyen
- Huong-Thi Nguyen
- Huy Thai
- Huy-Quoc Huynh
- Huy-Thang Nguyen
- Huyen-Ngoc Lu
- Huyen-Thanh Han
- Jenni White
- Jenni White
- Jenni White
- Jennifer Bergqvist
- Jennifer Massey
- Jeremy Christley
- Jeremy Lanford
- Jess Tsoleridis
- John Chalissery
- John Gommans
- Judith Dunne
- Julia O'Dea
- Kapila Abeysuriya
- Karen Knight
- Karen Ruddell
- Karim Mahawish
- Kate Hickey
- Katherine Mohr
- Kerri-Ann Whittaker
- Kerry Boyle
- Kerry Boyle
- Khanh-Kim Le
- Khanh-Thi Ngoc Thach
- Khoa-Duy Dao
- Kim Oakley
- Kimberley Veitch
- Kimberley Veitch
- Kimberley Veitch
- Kimberley Veitch
- Kirsty Page
- Koushik Nagesh
- Kraglund
- Lai-Kin Wong
- Lan-Tuong Vu
- Lap-Van Dinh
- Latitia Kernaghan
- Lauren Tarrant
- Laurent Billot
- Lay Kho
- Legg
- Leon Flicker
- Lim
- Lina Lee
- Lindsey Bunce
- Linh-Hai Nguyen
- Linh-Thi Cam Dam
- Linh-Thi Cam Le
- Linh-Thi My Le
- Loan-Thi Ngoc Vo
- Loan-Thi Nguyen
- Loan-Tran Truc Mai Le
- Long-Thanh Nguyen
- Long-Van Nguyen
- Lorralee Deane
- Louise Rigney
- Luisa Hewitt
- Luisa Hewitt
- Luisa Hewitt
- Luyen-Van Truong
- Ly-Thi Khanh Tran
- Lynda Southwell
- Mai-Hue Nguyen
- Maree Duroux
- Maree L. Hackett
- Maria Lopez
- Marjan Tabesh
- Mark Rollason
- Martin Jude
- Martin Krause
- Martin S. Dennis
- Mead
- Mead
- Mead
- Mead
- Megan Ewing
- Megan O'Neill
- Megan O'Neill
- Megan Ratcliffe
- Melissa Daines
- Melissa Spooner
- Merridie Rees
- Michael Pollack
- Michael Pollack
- Michelle Carr
- Michelle Tang
- Minh-Thao Nguyen
- Miriam Priglinger
- Monique Hourn
- Monique Hourn
- Monique Hourn
- Monique Hourn
- Mudassar Latif
- Na Le
- Nga-Thuy Lam
- Ngan-Thi Le
- Ngoc-Duc Ngo
- Ngoc-Hoang Nguyen
- Ngoc-Thuy Nhu Dinh
- Ngoc-Xuan Huynh
- Nha-Thi Thanh Dao
- Nhu-Quynh Truong
- Nicole O'Loughlin
- Ninh-Hong Le
- Noreen Mughal
- Norman
- Oanh-Thi Kieu Ha
- Oanh-Thi Le
- Osvaldo P. Almeida
- Patricia Morgan
- Paul Stockle
- Paula Broughton
- Pesi Katrak
- Peter New
- Phuong-Doan Nguyen
- Phuong-Hoai Tran
- Phuong-Hong Tran
- Phuong-Thai Truong
- Phuong-Thanh Trinh
- Phuong-Thi Do
- Phuong-Viet Dao
- Qi Cheng
- Qi Cheng
- Qiang Li
- Qilong Yi
- Queenie Leung
- Quoc-Nguyen Bao Pham
- Quyen-Thi Ngoc Pham
- Quynh-Nhu Le
- Rachael McCoy
- Rachael McQueen
- Ramesh Sahathevan
- Raymond Kumar
- Richard Geraghty
- Richard I. Lindley
- Robert Herbert
- Romesh Markus
- Rosanna Robertson
- Sally Ormond
- Sam Akbari
- Sam Akbari
- Sam Bolitho
- Sam-Hoanh Nguyen
- Samantha Shone
- Sandercock
- Sang-Van Nguyen
- Sara Laubscher
- Sarah Barrett
- Sarah Mccormack
- Severine Bompoint
- Shabeel Askar
- Shenae Peterson
- Sherisse Celestino
- Si-Tri Le
- Stanley Levy
- Steel
- Stephen Davis
- Stephen Jan
- Steven Faux
- Sumana Gopinath
- Sung-Phuoc Pham
- Susan Day
- Susan DeCaigney
- Susan Walker
- Tabitha Hartwell
- Tai-Anh Nguyen
- Tai-Ngoc Tran
- Tam-Nhat Dang
- Tan-Van Vo
- Thai-Nguyen Thanh Pham
- Tham-Hong Pham
- Thang-Ba Nguyen
- Thanh-Trung Tran
- Thao-Thi Thu Nguyen
- Thomas Lung
- Thuc-Van Tran
- Thuong-Thi Huyen Dang
- Thuy-Anh Diem Nguyen
- Thuy-Le Vu Kieu
- Thuy-Thi Vu
- Timothy Kleinig
- Timothy R. Bates
- Tissa Wijeratne
- Toan-Dinh Le
- Ton-Duy Mai
- Toni Withiel
- Tram-Ngoc Bui
- Tram-Thi Bich Ngo
- Trang-Le Huyen Nguyen
- Trang-Mai Tong
- Trang-Thi Huyen Le
- Trinh-Thi Kim Ngo
- Trung-Xuan Vuong
- Tuan-Quoc Dinh
- Tuan-Van Le
- Tue-Chau Bui
- Tuyen-Van Nguyen
- Uyen-Ha Hong
- Uyen-Thi To Hoang
- van der Vliet
- Vanessa Maxwell
- Vathani Surendran
- Veronica Duque
- Veronica Murray
- Vien-Chi Le
- Vinh-Phuong Do
- Vishal Patel
- Vivian Fu
- Vy-Tuong Nguyen
- Wang
- Ware
- Williams
- Wilson Vallat
- Yash Gawarikar
- Ye Min Kuang
- Yen-Bao Mai
- Yen-Hai Nguyen
- Yvonne Liu
- Zeljka Calic
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2020
- Field of study
Background
Trials of fluoxetine for recovery after stroke report conflicting results. The Assessment oF FluoxetINe In sTroke recoverY (AFFINITY) trial aimed to show if daily oral fluoxetine for 6 months after stroke improves functional outcome in an ethnically diverse population.
Methods
AFFINITY was a randomised, parallel-group, double-blind, placebo-controlled trial done in 43 hospital stroke units in Australia (n=29), New Zealand (four), and Vietnam (ten). Eligible patients were adults (aged ≥18 years) with a clinical diagnosis of acute stroke in the previous 2–15 days, brain imaging consistent with ischaemic or haemorrhagic stroke, and a persisting neurological deficit that produced a modified Rankin Scale (mRS) score of 1 or more. Patients were randomly assigned 1:1 via a web-based system using a minimisation algorithm to once daily, oral fluoxetine 20 mg capsules or matching placebo for 6 months. Patients, carers, investigators, and outcome assessors were masked to the treatment allocation. The primary outcome was functional status, measured by the mRS, at 6 months. The primary analysis was an ordinal logistic regression of the mRS at 6 months, adjusted for minimisation variables. Primary and safety analyses were done according to the patient's treatment allocation. The trial is registered with the Australian New Zealand Clinical Trials Registry, ACTRN12611000774921.
Findings
Between Jan 11, 2013, and June 30, 2019, 1280 patients were recruited in Australia (n=532), New Zealand (n=42), and Vietnam (n=706), of whom 642 were randomly assigned to fluoxetine and 638 were randomly assigned to placebo. Mean duration of trial treatment was 167 days (SD 48·1). At 6 months, mRS data were available in 624 (97%) patients in the fluoxetine group and 632 (99%) in the placebo group. The distribution of mRS categories was similar in the fluoxetine and placebo groups (adjusted common odds ratio 0·94, 95% CI 0·76–1·15; p=0·53). Compared with patients in the placebo group, patients in the fluoxetine group had more falls (20 [3%] vs seven [1%]; p=0·018), bone fractures (19 [3%] vs six [1%]; p=0·014), and epileptic seizures (ten [2%] vs two [<1%]; p=0·038) at 6 months.
Interpretation
Oral fluoxetine 20 mg daily for 6 months after acute stroke did not improve functional outcome and increased the risk of falls, bone fractures, and epileptic seizures. These results do not support the use of fluoxetine to improve functional outcome after stroke
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.
- Abecasis G.R.
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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