34 research outputs found
Modeling of Non-WSSUS Double-Rayleigh Fading Channels for Vehicular Communications
- Author
- Publication venue
- 'Hindawi Limited'
- Publication date
- 01/01/2017
- Field of study
Descomposición de datos multi-espectrales: interfaz gráfica para Matlab
- Publication venue
- Tecnológico Nacional de México / Instituto Tecnológico de Celaya
- Publication date
- 09/04/2018
- Field of study
Avances recientes han permitido el desarrollo de dispositivos capaces de capturar información en múltiples longitudes de onda. Estos datos tienen diversas aplicaciones con el problema en común de cómo interpretarlos. Una de las técnicas utilizadas con este fin es la descomposición espectral, que separa los datos de una muestra en sus componentes básicos y concentraciones proporcionales. Nuestro trabajo previo ha estado enfocado en la descomposición espectral de datos de fluorescencia multiespectral, donde se han desarrollado métodos que proporcionan una solución cuantitativa, robusta y rápida, la cual no está limitada por el número de componentes que se pueden caracterizar. En este trabajo, presentamos una interface desarrollada en Matlab que puede estimar los perfiles característicos de los componentes constituyentes de una muestra y sus abundancias. En caso de que no se tenga información alguna sobre la muestra, nos permite obtener además el número de componentes en ella. El artículo hace una descripción del software y sus herramientas.Además, se ejemplifica su uso en la caracterización de muestras ex-vivo de arterias coronarias. El programa se encuentra disponible de manera gratuita y provee al usuario de una herramienta fácil de usar para el análisis de datos multi o hiper-espectrales.Palabra(s) Clave(s): descomposición ciega, fluorescencia endógena, interfaz gráfica, optimización cuadrática, quimiometría
Global patient outcomes after elective surgery: prospective cohort study in 27 low-, middle- and high-income countries.
- Author
- Ab Majid MA
- Ab Rahman AS
- Ab Rahman R
- Abayasinghe C
- Abbott T
- Abdullah NH
- Abdur-Rahman L
- Abeloos J
- Abernethy C
- Abidin UN
- Abrunhosa A
- Absar M
- Adam S
- Adams D
- Adams G
- Adamson M
- Adekola O
- Adelaja Y
- Ademola A
- Adenekan A
- Adenike O
- Adeolu AA
- Adetoye A
- Adewale B
- Adigun T
- Adolfsson A
- Aflori L
- Africander C
- Afshari A
- Agarwal V
- Agodirin O
- Aguero Vera M
- Aguzzoli C
- Ahmad A
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- Ahmad T
- Ahmad T
- Ahmad Y
- Ahmed A
- Ahmed J
- Ai Y
- Aignatoaie M
- Aimoniotou-Georgiou E
- Akanmu O
- Akerman N
- Akinwale M
- Akring I
- Al 'Amri K
- Al Anizi M
- Al hussaini S
- Al-Soudaine Y
- Aladin H
- Alagbe-Briggs O
- Alaman Laguarda G
- Albaj S
- Alcock D
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- Aldecoa C
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- Zamudio D
- Zangrillo A
- Zapata DDM
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- Zonneveldt H
- Zou X
- Zoulamoglou M
- Zsisku L
- Publication venue
- 'Oxford University Press (OUP)'
- Publication date
- 01/01/2016
- Field of study
BACKGROUND: As global initiatives increase patient access to surgical treatments, there remains a need to understand the adverse effects of surgery and define appropriate levels of perioperative care. METHODS: We designed a prospective international 7-day cohort study of outcomes following elective adult inpatient surgery in 27 countries. The primary outcome was in-hospital complications. Secondary outcomes were death following a complication (failure to rescue) and death in hospital. Process measures were admission to critical care immediately after surgery or to treat a complication and duration of hospital stay. A single definition of critical care was used for all countries. RESULTS: A total of 474 hospitals in 19 high-, 7 middle- and 1 low-income country were included in the primary analysis. Data included 44 814 patients with a median hospital stay of 4 (range 2-7) days. A total of 7508 patients (16.8%) developed one or more postoperative complication and 207 died (0.5%). The overall mortality among patients who developed complications was 2.8%. Mortality following complications ranged from 2.4% for pulmonary embolism to 43.9% for cardiac arrest. A total of 4360 (9.7%) patients were admitted to a critical care unit as routine immediately after surgery, of whom 2198 (50.4%) developed a complication, with 105 (2.4%) deaths. A total of 1233 patients (16.4%) were admitted to a critical care unit to treat complications, with 119 (9.7%) deaths. Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries. CONCLUSIONS: Poor patient outcomes are common after inpatient surgery. Global initiatives to increase access to surgical treatments should also address the need for safe perioperative care. STUDY REGISTRATION: ISRCTN5181700
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
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- 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
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- B Blackledge
- B Borislavova
- B Chandler
- B Charles
- B Creagh-Brown
- B David
- B Deacon
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- B Digby
- B Faulkner
- B Fuller
- B Gumbrill
- B Gurung
- B Hadebe
- B Hairsine
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- B Ogg
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- E Treus Gude
- E Virgilio
- E Watson
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- Egle Saviciute
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- Enrico Martinelli
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- F Anderson
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- H Tiveran
- H Turner
- H Whittle
- H Willis
- H Wood
- Haley Chris
- Hanning Mal
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- Helen Szoor-McElhinney
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- Ho Antonia
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- I Ali Mohamed Ali
- I Balagosa
- I Birkinshaw
- I Burn
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- I Edmond
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- Stephanie Roberts
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- Summers Charlotte
- Susanna Croci
- Susanna Guerrini
- T Anderson
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- Tammy Gilchrist
- Tenesa Albert
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- Tony Wackett
- Trevor Paterson
- Tullio Trotta
- Turtle Lance
- U Poultney
- V Amin
- V Anumakonda
- V Bastion
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- V Crickmore
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- 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
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- 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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- Adanini O.
- Adeleye O.
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- Afilalo J.
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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
Stroke genetics informs drug discovery and risk prediction across ancestries
- Author
- Aamodt AH
- Abedi Vida
- Adams Hieab
- Adebajo OJ
- Adeoye AM
- Afzal S
- Ago Tetsuro
- Agunloye A
- Akinyemi J
- Akinyemi Rufus
- Akpa O
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- Almgren P
- Alvarez-Sabin J
- Amin N
- Amouyel Philippe
- Anderson CD
- Anderson Christopher D.
- Aparicio HJ
- Arenillas JF
- Armasu SM
- Armstrong Nicole D.
- Arnett DK
- Arulogun O
- Attia J
- Ay H
- Bae Hee-Joon
- Bakker Mark K.
- Bammler TK
- Bartz Traci M.
- Bastarache Lisa
- Beiser AS
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- Benavente OR
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- Blay N
- Boerwinkle E
- Boncoraglio GB
- Bordes Constance
- Braekkan SK
- Brody JA
- Brouwers PJAM
- Brown RD
- Brumpton BM
- Buring JE
- Bustamante M
- Butterworth AS
- Børte Sigrid
- Cain Anael
- Campos F
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- Caro Ilana
- Carrera C
- Carty CL
- Caso V
- Castillo J
- Chasman Daniel I.
- Chauhan Ganesh
- Chen JS
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- Chen Pei-Hsin
- Chen WM
- Chen YP
- Chen Zhengming
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- Cho Kelly
- Choi SH
- Chong Michael R.
- Chowhan A
- Christensen Kaare
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- Cotlarciuc I
- Cruchaga Carlos
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- Strauch K
- Strbian Daniel
- Suchon P
- Sudlow CLM
- Sumoy L
- Sun Yan V.
- Sung YJ
- Sutoh Yoichi
- Takai T
- Tanaka H
- Tang WH
- Tanislav C
- Tanno Kozo
- Tatlisumak Turgut
- Taylor KD
- Teumer A
- Thijs VNS
- Thomas LF
- Thomassen Jesper Qvist
- Thorleifsson G
- Thorsteinsdottir U
- Tiainen M
- Tiedt Steffen
- Tiwari Hemant K.
- Tomppo Liisa
- Torres-Aguila Nuria P.
- Touze E
- Traylor M
- Trompet Stella
- Trégouët David-Alexandre
- Tsugane S
- Tuladhar Anil Man
- Turman C
- Turnbull I
- Tybjærg-Hansen Anne
- Tzourio C
- Uitterlinden AG
- Ungethum K
- Uvere E
- Valdimarsson EM
- van der Laan SW
- van der Lee SJ
- van Dijk EJ
- van Dijk GW
- van Duijn CM
- van Norden AGW
- van Oostenbrugge RJ
- van Rooij FGW
- van Setten J
- van Vugt M
- van Vugt Marion
- Vaura Felix C.
- Verma SS
- Verma Stefali S.
- Vermeer SE
- Vibo Riina
- Visser MC
- Vives-Bauza C
- Vlieg AV
- Volker U
- Volzke H
- Vonk JMJ
- Wahab K
- Wakai K
- Walters M
- Walters Robin G.
- Wang C
- Wang L
- Wang RQ
- Wareham NJ
- Wassertheil-Smoller Sylvia
- Weir D
- Wennberg Patrik
- Wermer MJH
- Wiggins Kerri L.
- Willer CJ
- Williams SR
- Wilson JG
- Wilson Peter W. F.
- Winsvold Bendik Slagsvold
- Wolfe CDA
- Wong QN
- Woo Daniel
- Worrall Bradford B.
- Xu Huichun
- Yaffe K
- Yamaji T
- Yang Chaojie
- Yang CR
- Yang Qiong
- Yonova-Doing Ekaterina
- Yoon Kyungheon
- Yu CQ
- Yusuf S
- Zand Ramin
- Zhou W
- Zonderman AB
- Zwart John-Anker
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 22/12/2022
- Field of study
Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.</p
Global burden and strength of evidence for 88 risk factors in 204 countries and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021
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- Abate K.H.
- Abate Y.H.
- Abbafati C.
- Abbasgholizadeh R.
- Abbasi M.A.
- Abbasi-Kangevari M.
- Abbasian M.
- Abbasifard M.
- Abd ElHafeez S.
- Abd-Elsalam S.
- Abdi P.
- Abdollahi M.
- Abdoun M.
- Abdulah D.M.
- Abdullahi A.
- Abebe M.
- Abedi A.
- Abedi A.
- Abegaz T.M.
- Abeldaño Zuñiga R.A.
- Abiodun O.
- Abiso T.L.
- Aboagye R.G.
- Abolhassani H.
- Abouzid M.
- Aboye G.B.
- Abreu L.G.
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- Abu-Zaid A.
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- Abubakar B.
- Abukhadijah H.J.J.
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- Adane M.M.
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- Wongsin U.
- Wozniak S.
- Wu C.
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- Xia J.
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- Zamagni G.
- Zaman S.B.
- Zandieh G.G.Z.
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- Zare I.
- Zarimeidani F.
- Zastrozhin M.S.
- Zeng Y.
- Zhai C.
- Zhang A.L.
- Zhang H.
- Zhang L.
- Zhang M.
- Zhang Y.
- Zhang Z.
- Zhang Z.-J.
- Zhao H.
- Zhao J.T.
- Zhao X.-J.G.
- Zhao Y.
- Zhao Y.
- Zheng P.
- Zhong C.
- Zhou J.
- Zhou J.
- Zhou S.
- Zhu B.
- Zhu L.
- Zhu Z.
- Ziaeian B.
- Ziafati M.
- Zielińska M.
- Zimsen S.R.M.
- Zoghi G.
- Zoller T.
- Zumla A.
- Zyoud S.H.
- Zyoud S.H.
- Ärnlöv J.
- Publication venue
- Elsevier BV
- Publication date
- 16/05/2024
- Field of study
Background: Understanding the health consequences associated with exposure to risk factors is necessary to inform public health policy and practice. To systematically quantify the contributions of risk factor exposures to specific health outcomes, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 aims to provide comprehensive estimates of exposure levels, relative health risks, and attributable burden of disease for 88 risk factors in 204 countries and territories and 811 subnational locations, from 1990 to 2021. Methods: The GBD 2021 risk factor analysis used data from 54 561 total distinct sources to produce epidemiological estimates for 88 risk factors and their associated health outcomes for a total of 631 risk–outcome pairs. Pairs were included on the basis of data-driven determination of a risk–outcome association. Age-sex-location-year-specific estimates were generated at global, regional, and national levels. Our approach followed the comparative risk assessment framework predicated on a causal web of hierarchically organised, potentially combinative, modifiable risks. Relative risks (RRs) of a given outcome occurring as a function of risk factor exposure were estimated separately for each risk–outcome pair, and summary exposure values (SEVs), representing risk-weighted exposure prevalence, and theoretical minimum risk exposure levels (TMRELs) were estimated for each risk factor. These estimates were used to calculate the population attributable fraction (PAF; ie, the proportional change in health risk that would occur if exposure to a risk factor were reduced to the TMREL). The product of PAFs and disease burden associated with a given outcome, measured in disability-adjusted life-years (DALYs), yielded measures of attributable burden (ie, the proportion of total disease burden attributable to a particular risk factor or combination of risk factors). Adjustments for mediation were applied to account for relationships involving risk factors that act indirectly on outcomes via intermediate risks. Attributable burden estimates were stratified by Socio-demographic Index (SDI) quintile and presented as counts, age-standardised rates, and rankings. To complement estimates of RR and attributable burden, newly developed burden of proof risk function (BPRF) methods were applied to yield supplementary, conservative interpretations of risk–outcome associations based on the consistency of underlying evidence, accounting for unexplained heterogeneity between input data from different studies. Estimates reported represent the mean value across 500 draws from the estimate's distribution, with 95% uncertainty intervals (UIs) calculated as the 2·5th and 97·5th percentile values across the draws. Findings: Among the specific risk factors analysed for this study, particulate matter air pollution was the leading contributor to the global disease burden in 2021, contributing 8·0% (95% UI 6·7–9·4) of total DALYs, followed by high systolic blood pressure (SBP; 7·8% [6·4–9·2]), smoking (5·7% [4·7–6·8]), low birthweight and short gestation (5·6% [4·8–6·3]), and high fasting plasma glucose (FPG; 5·4% [4·8–6·0]). For younger demographics (ie, those aged 0–4 years and 5–14 years), risks such as low birthweight and short gestation and unsafe water, sanitation, and handwashing (WaSH) were among the leading risk factors, while for older age groups, metabolic risks such as high SBP, high body-mass index (BMI), high FPG, and high LDL cholesterol had a greater impact. From 2000 to 2021, there was an observable shift in global health challenges, marked by a decline in the number of all-age DALYs broadly attributable to behavioural risks (decrease of 20·7% [13·9–27·7]) and environmental and occupational risks (decrease of 22·0% [15·5–28·8]), coupled with a 49·4% (42·3–56·9) increase in DALYs attributable to metabolic risks, all reflecting ageing populations and changing lifestyles on a global scale. Age-standardised global DALY rates attributable to high BMI and high FPG rose considerably (15·7% [9·9–21·7] for high BMI and 7·9% [3·3–12·9] for high FPG) over this period, with exposure to these risks increasing annually at rates of 1·8% (1·6–1·9) for high BMI and 1·3% (1·1–1·5) for high FPG. By contrast, the global risk-attributable burden and exposure to many other risk factors declined, notably for risks such as child growth failure and unsafe water source, with age-standardised attributable DALYs decreasing by 71·5% (64·4–78·8) for child growth failure and 66·3% (60·2–72·0) for unsafe water source. We separated risk factors into three groups according to trajectory over time: those with a decreasing attributable burden, due largely to declining risk exposure (eg, diet high in trans-fat and household air pollution) but also to proportionally smaller child and youth populations (eg, child and maternal malnutrition); those for which the burden increased moderately in spite of declining risk exposure, due largely to population ageing (eg, smoking); and those for which the burden increased considerably due to both increasing risk exposure and population ageing (eg, ambient particulate matter air pollution, high BMI, high FPG, and high SBP). Interpretation: Substantial progress has been made in reducing the global disease burden attributable to a range of risk factors, particularly those related to maternal and child health, WaSH, and household air pollution. Maintaining efforts to minimise the impact of these risk factors, especially in low SDI locations, is necessary to sustain progress. Successes in moderating the smoking-related burden by reducing risk exposure highlight the need to advance policies that reduce exposure to other leading risk factors such as ambient particulate matter air pollution and high SBP. Troubling increases in high FPG, high BMI, and other risk factors related to obesity and metabolic syndrome indicate an urgent need to identify and implement interventions. Funding: Bill & Melinda Gates Foundation
Evaluation of appendicitis risk prediction models in adults with suspected appendicitis
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- Hunter I
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- Hussain A
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- Orizu M
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- Padilla-Valverde D
- Paget C
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- Pala M
- Palani-Velu Lk
- Palani-Velu Lk
- Pan Y
- Panagiotopoulos Sp
- Panda N
- Panda N
- Panda N
- Pandey V
- Pandya D
- Pandya R
- Paniagua M
- Pankin Gp
- Papandrea M
- Parajó Ae
- Paramasevon Kr
- Pareja-Ciuró F
- Parisi A
- Park Jh
- Park Jh
- Parkola Mj
- Parra Jm
- Parwaiz I
- Pascua-Sole M
- Pascual-Miguelañez I
- Pasquali S
- Pata F
- Pata F
- Pata F
- Pata F
- Pata F
- Pata F.
- Pata G
- Pata G
- Pata G
- Patel As
- Patel By
- Patel By
- Patel C
- Patel H
- Patel Mm
- Patel N
- Patel Pk
- Patel Rt
- Patil Sd
- Patti S
- Pau R
- Payne Cj
- Payne Re
- Payá-Llorente C
- Payá-Llorente C
- Peacock M
- Pearce J
- Pearce J
- Pearce L
- Pearce L
- Pearson R
- Pedder A
- Peirce Cb
- Peiris Gb
- Peixoto R
- Peleki A
- Peleki A
- Pellegrino L
- Pellicanò Ga
- Pellicer-Franco E
- Pellino G
- Pento V
- Pento V
- Peponis C
- Peprah D
- Pereira A
- Pereira Am
- Pereira J
- Pereira-Mosquera E
- Perera Mi
- Perez-Calvo J
- Perin A
- Pertile D
- Pertile D
- Peña-Barturen C
- Phelan L
- Photiou D
- Pierre R
- Pietrabissa A
- Pigem A
- Pila U
- Pilkington Jp
- Pineño-Flores C
- Pinillos-Somalo A
- Pinkney Td
- Pinkney Td
- Pinkney Td
- Pinna E
- Pino-Perez O
- Pirari Pf
- Pisanu A
- Piu F
- Planellas P
- Plua-Muniz Kt
- Poacher A
- Podda F
- Podda M
- Podda M
- Podda M
- Poillucci G
- Pollard H
- Ponchietti L
- Popova D
- Poudevigne M
- Prats Ma
- Prideaux A
- Prieto-Nieto Mi
- Primo Jc
- Pronin S
- Provenza G
- Puerta E
- Pulighe F
- Pullabatla-Venkata Up
- Punj S
- Pérez-Sanchez Le
- Quddus A
- Quill S
- Quinn Em
- Quinn Hc
- Rabie M
- Rabie Ma
- Rabie Mr
- Radwan Rw
- Radwan Rw
- Rahim A
- Rahman M
- Rahmani Ls
- Rajagopal S
- Rajaram R
- Rajaretnam N
- Rajjoub Y
- Rallage H
- Ramcharan S
- Ramirez L
- Ramirez-Redondo Aa
- Ramos Xh
- Ramos-Bernado Mi
- Ramírez-Faraco M
- Ranathunga S
- Rangarajan K
- Rao M
- Rao V
- Raofi A
- Rashid M
- Rate A
- Ravindran R
- Raymond M
- Raza Ss
- Recreo Ac
- Reddy A
- Reddy A
- Redmond Ae
- Redondo E
- Redondo E
- Redondo-Calvo Fj
- Reese G
- Regina G
- Rehman S
- Rehman S
- Rekhraj S
- Ren Kz
- Renshaw S
- Renshaw S
- Renzi Cr
- Resende Fm
- Rezacova M
- Rezvani S
- Riaz W
- Riba-Combatti L
- Ribaudo M
- Ribeiro B
- Rich Je
- Richardson Td
- Ridaura N
- Riera E
- Rigby S
- Rigney B
- Rinkoff S
- Ripoli Mc
- Robb Hd
- Robertson C
- Robinson A
- Robinson A
- Robinson D
- Robinson D
- Rocha R
- Rodger V
- Rodicio-Miravalles Jl
- Rodriguez L
- Rodriguez-Lopez M
- Rodriguez-Lopez M
- Rodriguez-Lopez M
- Rodríguez Ec
- Rojo Ja
- Roldán-Ortiz S
- Rolph R
- Romano J
- Romano R
- Romario Uf
- Romoli L
- Roncero Ls
- Ronda Rn
- Roomi S
- Rosa Mj
- Rosat A
- Roscio F
- Roscio F
- Roscio F
- Rossi C
- Rossi D
- Rossi Gm
- Roth N
- Rothnie K
- Roxburgh C
- Roy C
- Ruano A
- Rubbini M
- Rudland I
- Ruffolo C
- Rufo E
- Ruggiu Gv
- Ruiz-Marín M
- Ruiz-Marín M
- Rupani S
- Rupasinghe Sn
- Rupasinghe Sn
- Rutherford Dg
- Ruzvidzo F
- Ruzzenente A
- Saad M
- Saad M
- Saavedra-Chacón M
- Saba A
- Sabia D
- Sacco R
- Sacks R
- Sadek S
- Saghir N
- Sagnotta A
- Sagnotta A
- Saha A
- Sahay Sj
- Sahnan K
- Sahnan K
- Sainz B
- Sainz B
- Sajid Ms
- Salama Y
- Salamone G
- Salamone G
- Salamone G
- Salamone G
- Salandini Mc
- Salem A
- Salim S
- Salva Ab
- Salvador H
- Samartin C
- Sammarco G
- Sammarco G
- Samuel M
- Sana S
- Sanchez Er
- Sanchez Er
- Sanchez L
- Sanchez-Garcia S
- Sanchez-Guillen L
- Sanchez-Guillen L
- Sanchez-Martinez A
- Sancho-Muriel J
- Sandu L
- Sanna S
- Santamaria C
- Santamaría Pc
- Santarrufina-Martínez S
- Santos Sc
- Santurro L
- Sanz-Navarro S
- Sarmah P
- Sarmah P
- Sarmah P
- Sarveswaran J
- Sasia D
- Sasia D
- Saunders S
- Savill A
- Savino G
- Savino G
- Savioli F
- Scabini S
- Scabini S
- Scabini S
- Scandroglio Is
- Scanlon K
- Scatizzi M
- Scialandrone G
- Scricciolo M
- Sebastian Jf
- Sebastián-Tomás Jc
- Seddon Tc
- Segalini E
- Segura-Sampedro Jj
- Sena G
- Sena-Ruiz F
- Seneviratne N
- Sepe C
- Serventi F
- Serventi F
- Seth M
- Setshwaelo T
- Sezen E
- Sgardelis P
- Sgrò A
- Sgrò A
- Sgrò A
- Shah J
- Shah K
- Shah Sm
- Shah Sm
- Shaikh Ia
- Shakoor Z
- Shanmuganathan V
- Shanmugarajah K
- Sharma A
- Sharma A
- Sharma P
- Sharp Ol
- Sharp Ol
- Shaw Av
- Shepherd Ja
- Sherif Ma
- Shet S
- Shetty Vd
- Shingler G
- Shiwani Mh
- Shrestha D
- Shurlock J
- Sian T
- Siaw O
- Siddique K
- Siddiqui Mn
- Siddiqui Za
- Sierra-Grañón Je
- Siggens Kl
- Sihra N
- Silva A
- Silva I
- Silvestri V
- Simioni A
- Simmonds L
- Simmonds L
- Simo V
- Simoes J
- Simpson Dj
- Singh A
- Singh J
- Singh P
- Singh S
- Singhal T
- Singhal T
- Sivaloganathan P
- Skalamera I
- Skerritt C
- Slezak I
- Smallcombe N
- Smart Cj
- Smart Cj
- Smart Nj
- Smart Nj
- Smoker H
- Soares A. S.
- Soares As
- Soares As
- Soares As
- Soares As
- Soares As
- Soh B
- Solaini L
- Solar-García L
- Soliani P
- Solinas L
- Sooriyamoorthy T
- Soria-Aledo V
- Soria-Aledo V
- Soriano Jt
- Sorrentino L
- Sousa Hs
- Souter J
- Sparta C
- Spaziani A
- Speake D
- Speake D
- Springate El
- Sreedharan L
- Sreedharan L
- Staderini F
- Stecca T
- Stella M
- Stephens Gf
- Stephens Gf
- Stevenson R
- Stewart Dj
- Stoica I
- Storey R
- Stoyanov Ti
- Strachan E
- Strange Ja
- Stubbs Bm
- Stupalkowska W
- Stupalkowska W
- Suarez-Cabrera A
- Suero Ca
- Sultana A
- Summerfield L
- Sunter H
- Surg Pt
- Suriyakumar S
- Suárez-Sánchez A
- Swords C
- Symons N
- Szentpali K
- Szucs A
- Szucs A
- Sánchez-Cifuentes A
- Sánchez-Fuentes Mn
- Sánchez-Rubio M
- Tabain V
- Taglietti L
- Tague Le
- Tahir W
- Tailor K
- Tallon-Aguilar L
- Tallon-Aguilar L
- Tamayo-López Mj
- Tamborska A
- Tamini N
- Tamini N
- Tamini N
- Tan Cy
- Tan Cy
- Tan E
- Tan Hl
- Tan S
- Tang Am
- Tapiolas I
- Tarazi M
- Tatulli F
- Tay Yh
- Tayeh S
- Taylor M
- Taylor Ns
- Taylor Ns
- Taze D
- Tee A
- Tejero-Pintor Fj
- Tenconi Sm
- Tezas S
- Thaha Ma
- Thakral N
- Thakur D
- Thava B
- Thavanesan N
- Thavanesan N
- Thaventhiran Aj
- Theodoropoulou K
- Thomas At
- Thomas L
- Thompson C
- Thompson Db
- Thompson Db
- Thompson R
- Thompson R
- Thoukididou Sn
- Tiedt La
- Tiedt La
- Ting N
- Tinoco-González J
- Tinsley Bj
- Tognarelli Jm
- Tojal A
- Tokidis E
- Tomasoni M
- Tonini V
- Toomey D
- Toomey Db
- Torkington J
- Torkington J
- Torrado Aa
- Torrance A
- Torrance A
- Townsend Dc
- Townsend Dc
- Tozer Pj
- Trail M
- Trail M
- Trastulli S
- Trew F
- Trostchansky I
- Trujillo-Diaz Jj
- Tsang B
- Tudyka V
- Tudyka V
- Turnbull A
- Turner Ej
- Tutino R
- Twum-Barima Cs
- Twum-Barima Cs
- Tyler R
- Tyler R
- Ugarte-Sierra B
- Vacca A
- Vaccari S
- Vakis S
- Valente Pm
- Valiani Sv
- Vallejo-Bernad C
- Vallve-Bernal M
- Van Boxel Gi
- Vance-Daniel J
- Vannucchi A
- Varcada M
- Vargas-Pierola Hj
- Vaughan Em
- Vaughan Em
- Vazquez-Fernandez Ap
- Vega L
- Velchuru Vr
- Velho R
- Venkata Up
- Venkatasubramaniam Ak
- Venn Ml
- Venn Ml
- Venugopal R
- Verea S
- Veres T
- Veres T
- Verroiotou M
- Vescio G
- Vettoretto N
- Vigorita V
- Vijay V
- Vila-Zarate C
- Villarejo-Campos P
- Vinnicombe Z
- Viscosi F
- Vitish-Sharma P
- Viviani E
- Viñas Nl
- Vohra R
- Vohra R
- Vulcano I
- Waite K
- Walji Hd
- Walsh E
- Walsh Tn
- Walters Kj
- Walters U
- Wardle Bg
- Wardle Bg
- Wardle Sd
- Warren O
- Warren Oj
- Warusavitarne J
- Watfah J
- Watson N
- Wauchope J
- Weatherburn Lw
- Weaver J
- Weegenaar Cr
- Weegenaar Cr
- Welsh S
- Wensley F
- West H
- West H
- Wheatstone S
- Wheeler C
- Whewell He
- White F
- Whitehorn Se
- Whitehorn Se
- Whitehouse P
- Whiteman E
- Whittaker L
- Wiggill S
- Wijesundera K
- Wilcox G
- Wilkin R
- Wilkin R
- Wilkin R
- Wilkin R
- Wilkin R. J. W.
- Williams Gl
- Williams M
- Williams R
- Williams S
- Wilson Ej
- Wilson M
- Winter Dc
- Winter Dc
- Wolff J
- Wong A
- Wong C
- Wong J
- Wong J
- Wong Ml
- Wong Sy
- Woo R
- Wood Cs
- Woodrow C
- Woodward A
- Woodward B
- Woodward B
- Worku D
- Worku D
- Wright E
- Wright Hl
- Wu F
- Xidas A
- Yalamarthi S
- Yang P
- Yanni F
- Yardimci E
- Yasin T
- Yen Sk
- Yeung K
- Yeung K
- Yoganathan S
- Yoong S
- Youssef H
- Yow L
- Yow L
- Zaborowski A
- Zadi Az
- Zalla T
- Zarka Za
- Zarka Za
- Zarog Ma
- Zelazek M
- Zerpa C
- Zhang Ay
- Zhou S
- Zorrilla L
- Zuin M
- Zurleni Tz
- Publication venue
- 'Wiley'
- Publication date
- 01/01/2019
- Field of study
Background
Appendicitis is the most common general surgical emergency worldwide, but its diagnosis remains challenging. The aim of this study was to determine whether existing risk prediction models can reliably identify patients presenting to hospital in the UK with acute right iliac fossa (RIF) pain who are at low risk of appendicitis.
Methods
A systematic search was completed to identify all existing appendicitis risk prediction models. Models were validated using UK data from an international prospective cohort study that captured consecutive patients aged 16–45 years presenting to hospital with acute RIF in March to June 2017. The main outcome was best achievable model specificity (proportion of patients who did not have appendicitis correctly classified as low risk) whilst maintaining a failure rate below 5 per cent (proportion of patients identified as low risk who actually had appendicitis).
Results
Some 5345 patients across 154 UK hospitals were identified, of which two‐thirds (3613 of 5345, 67·6 per cent) were women. Women were more than twice as likely to undergo surgery with removal of a histologically normal appendix (272 of 964, 28·2 per cent) than men (120 of 993, 12·1 per cent) (relative risk 2·33, 95 per cent c.i. 1·92 to 2·84; P < 0·001). Of 15 validated risk prediction models, the Adult Appendicitis Score performed best (cut‐off score 8 or less, specificity 63·1 per cent, failure rate 3·7 per cent). The Appendicitis Inflammatory Response Score performed best for men (cut‐off score 2 or less, specificity 24·7 per cent, failure rate 2·4 per cent).
Conclusion
Women in the UK had a disproportionate risk of admission without surgical intervention and had high rates of normal appendicectomy. Risk prediction models to support shared decision‐making by identifying adults in the UK at low risk of appendicitis were identified
Whole-genome sequencing reveals host factors underlying critical COVID-19
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- 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
Voltage-oriented input-output linearization controller as maximum power point tracking technique for photovoltaic systems
- Author
- Publication venue
- 'Institute of Electrical and Electronics Engineers (IEEE)'
- Publication date
- 01/06/2015
- Field of study
This paper presents a robust input-output linearization controller as maximum power point tracking (MPPT) technique in a photovoltaic (PV) buck dc-dc converter with applications to dc microgrids, solar vehicles, or stand-alone systems. Due to the control structure proposed in this paper, the MPPT control system is able to track very fast irradiance changes. Meanwhile, the internal stability of the overall closed-loop system is guaranteed for different load scenarios. A sector condition is only required for the load current, which is satisfied for most of the current PV applications. In turn, this condition implies the robustness against oscillations in the dc bus voltage. Finally, the MPPT control system is validated through experimental results, where the closed-loop performance is evaluated under abrupt irradiance and set-point changes, parametric uncertainty, and dc bus load variations.Fil: Espinoza Trejo, Diego R.. Universidad Autónoma de San Luis Potosí; MéxicoFil: Bárcenas Bárcenas, Ernesto. Universidad Autónoma de San Luis Potosí; MéxicoFil: Campos Delgado, Daniel U.. Universidad Autónoma de San Luis Potosí; MéxicoFil: de Angelo, Cristian Hernan. Universidad Nacional de Río Cuarto. Facultad de Ingeniería. Departamento de Electricidad y Electrónica; Argentin