220 research outputs found
GWAS for discovery and replication of genetic loci associated with sudden cardiac arrest in patients with coronary artery disease
- Author
- A Bayes de Luna
- A Rakhit
- AB Lehtinen
- AL Price
- AM Shearman
- B Devlin
- Bradley E Aouizerat
- CS Carlson
- CT January
- DE Arking
- DP Zipes
- Eric Vittinghoff
- HV Huikuri
- I Splawski
- J Hallmayer
- Jeffrey E Olgin
- KC Chang
- L Conde
- L Excoffier
- LR Dekker
- Ludmila Pawlikowska
- M Eijgelsheim
- MD Tobin
- MG Kibriya
- N Sotoodehnia
- N Sotoodehnia
- PD Thomas
- Pui-Yan Kwok
- RC Balijepalli
- RJ Klein
- SC Schuit
- SE Lehnart
- Stacy L Musone
- WH Kao
- X Jouven
- Y Friedlander
- Y Liu
- ZH Tseng
- ZH Tseng
- ZH Tseng
- Zian H Tseng
- ZJ Zheng
- Publication venue
- BioMed Central
- Publication date
- 01/01/2011
- Field of study
<p>Abstract</p> <p>Background</p> <p>Epidemiologic evidence suggests a heritable component to risk for sudden cardiac arrest independent of risk for myocardial infarction. Recent candidate gene association studies for community sudden cardiac arrests have focused on a limited number of biological pathways and yielded conflicting results. We sought to identify novel gene associations for sudden cardiac arrest in patients with coronary artery disease by performing a genome-wide association study.</p> <p>Methods</p> <p>Tagging SNPs (n = 338,328) spanning the genome were typed in a case-control study comparing 89 patients with coronary artery disease and sudden cardiac arrest due to ventricular tachycardia or ventricular fibrillation to 520 healthy controls.</p> <p>Results</p> <p>Fourteen SNPs including 7 SNPs among 7 genes (ACYP2, AP1G2, ESR1, DGES2, GRIA1, KCTD1, ZNF385B) were associated with sudden cardiac arrest (all p < 1.30 × 10<sup>-7</sup>), following Bonferroni correction and adjustment for population substructure, age, and sex; genetic variation in ESR1 (p = 2.62 × 10<sup>-8</sup>; Odds Ratio [OR] = 1.43, 95% confidence interval [CI]:1.277, 1.596) has previously been established as a risk factor for cardiovascular disease. In tandem, the role of 9 genes for monogenic long QT syndrome (LQT1-9) was assessed, yielding evidence of association with CACNA1C (LQT8; p = 3.09 × 10<sup>-4</sup>; OR = 1.18, 95% CI:1.079, 1.290). We also assessed 4 recently published gene associations for sudden cardiac arrest, validating NOS1AP (p = 4.50 × 10<sup>-2</sup>, OR = 1.15, 95% CI:1.003, 1.326), CSMD2 (p = 6.6 × 10<sup>-3</sup>, OR = 2.27, 95% CI:1.681, 2.859), and AGTR1 (p = 3.00 × 10<sup>-3</sup>, OR = 1.13, 95% CI:1.042, 1.215).</p> <p>Conclusion</p> <p>We demonstrate 11 gene associations for sudden cardiac arrest due to ventricular tachycardia/ventricular fibrillation in patients with coronary artery disease. Validation studies in independent cohorts and functional studies are required to confirm these associations.</p
β-defensin 1 expression in HCV infected liver/liver cancer: an important role in protecting HCV progression and liver cancer development
- Author
- A Aceti
- A Krishnan
- AL Rasmussen
- AM Gressner
- AO Kaseb
- AS Hamid
- AX Zhu
- B Daniele
- CD Donald
- CJ Liu
- CQ Sun
- D Yang
- DG McArt
- E Fransvea
- E Lawitz
- E Ricci
- EG Davis
- F Canal
- G Kaltsa
- G Lehne
- G Zhang
- H Ikezaki
- HF Kwok
- HY Lim
- J Chen
- J Inayoshi
- J Jarczak
- J Lamb
- J Lamb
- J Raschig
- JZ Dong
- K Baghy
- K Endo
- K Harada
- L Braida
- LK Ryan
- M Frye
- M Wenghoefer
- MP Manns
- MR Schneider
- MW Taylor
- Q Han
- R Diao
- RS Bullard
- S Alp
- S Buraschi
- S Joly
- S Pol
- S Roessler
- SA Johnstone
- SD Zhang
- T Osada
- TM Shafee
- WK Sung
- X Bai
- Y Wei
- Y Yang
- Y Zhang
- Y Zhang
- Z Horvath
- ZH Gao
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/10/2017
- Field of study
Abstract β-defensin family plays a role in host defense against viral infection, however its role in HCV infection is still unknown. In this study, we demonstrated that β-defensin 1 was significantly reduced in HCV-infected liver specimens. Treatment with interferon and ribavirin upregulated β-defensin-1, but not other β-defensin tested, with the extent and duration of upregulation associated with treatment response. We investigated β-defensin family expression in liver cancer in publicly available datasets and found that among all the β-defensins tested, only β-defensin 1 was significantly downregulated, suggesting β-defensin 1 plays a crucial role in liver cancer development. Further analysis identified E-cadherin as the top positive correlated gene, while hepatocyte growth factor-regulated tyrosine kinase substrate as the top negative correlated gene. Expression of two proteoglycans were also positively correlated with that of β-defensin 1. We have also identified small molecules as potential therapeutic agents to reverse β-defensin 1-associated gene signature. Furthermore, the downregulation of β-defensin 1 and E-cadherin, and upregulation of hepatocyte growth factor-regulated tyrosine kinase substrate, were further confirmed in liver cancer and adjacent normal tissue collected from in-house Chinese liver cancer patients. Together, our results suggest β-defensin 1 plays an important role in protecting HCV progression and liver cancer development
Feedforward Inhibition and Synaptic Scaling – Two Sides of the Same Coin?
- Author
- A Bacci
- AJ Watt
- AL Yuille
- AL Yuille
- AP Dempster
- C Assisi
- Christian Keck
- Cristina Savin
- D Marr
- DJ Heeger
- DL Ringach
- F Pouille
- F Pouille
- FS Chance
- G Hinton
- G Sclar
- GG Turrigiano
- GG Turrigiano
- GG Turrigiano
- HA Swadlow
- I Klinkenberg
- IM Elfadel
- IM Finn
- J Bruna
- J Echegoyen
- J Fellous
- J Fiser
- J Lücke
- JH Reynolds
- JS Isaacson
- Jörg Lücke
- KR Leslie
- LF Abbott
- M Carandini
- M Ranzato
- M Sahani
- M Stopfer
- M Wehr
- N Ueda
- NC Rabinowitz
- NC Rust
- O Schwartz
- O Schwartz
- Olaf Sporns
- P Berkes
- P Dayan
- R Neal
- RJ Douglas
- RO Duda
- S Deneve
- SA Baccus
- SB Hofer
- SC Liu
- SP Kuo
- SR Olsen
- SR Olsen
- T Fukai
- T Kwok
- T Lochmann
- T Ohshiro
- V Mante
- W Gerstner
- W Mittmann
- Y LeCun
- Y Shu
- ZH Mao
- Publication venue
- Public Library of Science
- Publication date
- 22/03/2012
- Field of study
Feedforward inhibition and synaptic scaling are important adaptive processes that control the total input a neuron can receive from its afferents. While often studied in isolation, the two have been reported to co-occur in various brain regions. The functional implications of their interactions remain unclear, however. Based on a probabilistic modeling approach, we show here that fast feedforward inhibition and synaptic scaling interact synergistically during unsupervised learning. In technical terms, we model the input to a neural circuit using a normalized mixture model with Poisson noise. We demonstrate analytically and numerically that, in the presence of lateral inhibition introducing competition between different neurons, Hebbian plasticity and synaptic scaling approximate the optimal maximum likelihood solutions for this model. Our results suggest that, beyond its conventional use as a mechanism to remove undesired pattern variations, input normalization can make typical neural interaction and learning rules optimal on the stimulus subspace defined through feedforward inhibition. Furthermore, learning within this subspace is more efficient in practice, as it helps avoid locally optimal solutions. Our results suggest a close connection between feedforward inhibition and synaptic scaling which may have important functional implications for general cortical processing
An immune dysfunction score for stratification of patients with acute infection based on whole-blood gene expression
- Author
- Addison J
- Allcock A
- Andreou P
- Antclife D
- Arawwawala D
- Armitage K
- Atkinson J
- Baldwin J
- Baudouin S
- Bion J
- Bland M
- Bowrey S
- Brett S
- Brown A
- Bullock L
- Burnham KL
- Cano-Gamez E
- Carrera R
- Cuesta JM
- Davenport EE
- de Gordoa LOR
- Doherty N
- Drage S
- Durcan J
- Errington E
- Faras-Arraya R
- Fletcher S
- Galley H
- Garrard C
- Glister G
- Goh C
- Gordon AC
- Gordon T
- Grier S
- Guleri A
- Hales D
- Hall E
- Hall P
- Hall S
- Harrison D
- Hewlett J
- Higham C
- Hinds CJ
- Humphreys J
- Hutton P
- Jacques N
- Kapila A
- Kazembe S
- Kitson D
- Knight JC
- Krige A
- Kwok A
- Laha S
- Lees S
- Lowes S
- Malick ZH
- McCauley M
- McKechnie S
- Millar J
- Millo J
- Mills G
- Mitchell N
- Mitchell-Inwang C
- Moreno J
- Mountford L
- Nilson A
- Overend L
- Parsons P
- Perry EJ
- Peters-Sengers H
- Prowse H
- Raymode P
- Rich N
- Roberts E
- Rosbergen M
- Roughton S
- Ruel S
- Scicluna BP
- Short A
- Smith DA
- Smiths A
- Smolen S
- Soar J
- Swan K
- Taylor J
- Templeton M
- Tennant H
- Thompson J
- van der Poll T
- Venatesh P
- Waddington N
- Walsh A
- Walsh H
- Ward G
- Webster N
- Wilde J
- Williams S
- Willis H
- Wilson R
- Young D
- Publication venue
- 'American Association for the Advancement of Science (AAAS)'
- Publication date
- 01/01/2022
- Field of study
Dysregulated host responses to infection can lead to organ dysfunction and sepsis, causing millions of global deaths each year. To alleviate this burden, improved prognostication and biomarkers of response are urgently needed. We investigated the use of whole-blood transcriptomics for stratification of patients with severe infection by integrating data from 3149 samples from patients with sepsis due to community-acquired pneumonia or fecal peritonitis admitted to intensive care and healthy individuals into a gene expression reference map. We used this map to derive a quantitative sepsis response signature (SRSq) score reflective of immune dysfunction and predictive of clinical outcomes, which can be estimated using a 7- or 12-gene signature. Last, we built a machine learning framework, SepstratifieR, to deploy SRSq in adult and pediatric bacterial and viral sepsis, H1N1 influenza, and COVID-19, demonstrating clinically relevant stratification across diseases and revealing some of the physiological alterations linking immune dysregulation to mortality. Our method enables early identification of individuals with dysfunctional immune profiles, bringing us closer to precision medicine in infection
An immune dysfunction score for stratification of patients with acute infection based on whole-blood gene expression.
- Author
- Addison J
- Allcock A
- Allcock A
- Andreou P
- Andrews S
- Antcliffe D
- Arawwawala D
- Armitage K
- Atkinson J
- Baldwin J
- Baudouin S
- Bellingan G
- Bentley A
- Bercades G
- Bion J
- Bland M
- Boluda S
- Bonner S
- Bowrey S
- Brett S
- Brown A
- Bullock L
- Burnham K
- Burnham KL
- Calder V
- Cano-Gamez E
- Carrera R
- Cawthor L
- Cuesta JM
- Davenport E
- Davenport EE
- Doherty N
- Drage S
- Durcan J
- Errington E
- Faras-Arraya R
- Fletcher S
- GAinS Investigators
- Galley H
- Garrard C
- Garrard C
- Glister G
- Goh C
- Goh C
- Goodridge V
- Gordon AC
- Gordon T
- Grier S
- Guleri A
- Hales D
- Hall E
- Hall P
- Hall S
- Harrison D
- Hewlett J
- Higgins D
- Higham C
- Higham C
- Hind C
- Hinds CJ
- Hugil K
- Humphreys J
- Hutton P
- Jacques N
- Jefferies F
- Kapila A
- Kazembe S
- Kitson D
- Knight J
- Knight JC
- Krige A
- Kuper M
- Kwok A
- Laha S
- Lees S
- Lowes S
- Malick ZH
- Mappleback S
- Marshall R
- Maugeri N
- Mccalman K
- McCauley M
- McKechnie S
- McKechnie S
- McLees E
- Mi Y
- Millar J
- Millo J
- Mills G
- Mitchell N
- Mitchell-Inwang C
- Montgomery H
- Moreno J
- Mountford L
- Nilson A
- Ochelli-Okpue A
- Ortiz-Ruiz de Gordoa L
- Overend L
- Pahary S
- Parsons P
- Payne H
- Perry EJ
- Peters-Sengers H
- Prowse H
- Purdy A
- Radhakrishnan J
- Raymode P
- Rich N
- Roberts E
- Rosbergen M
- Roughton S
- Ruel S
- Ryu JH
- Scicluna BP
- Short A
- Smith DA
- Smiths A
- Smolen S
- Soar J
- Soar J
- Stotz M
- Swan C
- Swan K
- Taylor J
- Templeton M
- Tennant H
- Thompson J
- Van der Poll T
- Venatesh P
- Waddington N
- Walsh A
- Walsh H
- Ward G
- Watson D
- Webster N
- Whitehead I
- Wilde J
- Williams S
- Willis H
- Wilson R
- Young D
- Publication venue
- 'American Association for the Advancement of Science (AAAS)'
- Publication date
- 16/09/2022
- Field of study
Dysregulated host responses to infection can lead to organ dysfunction and sepsis, causing millions of global deaths each year. To alleviate this burden, improved prognostication and biomarkers of response are urgently needed. We investigated the use of whole-blood transcriptomics for stratification of patients with severe infection by integrating data from 3149 samples from patients with sepsis due to community-acquired pneumonia or fecal peritonitis admitted to intensive care and healthy individuals into a gene expression reference map. We used this map to derive a quantitative sepsis response signature (SRSq) score reflective of immune dysfunction and predictive of clinical outcomes, which can be estimated using a 7- or 12-gene signature. Last, we built a machine learning framework, SepstratifieR, to deploy SRSq in adult and pediatric bacterial and viral sepsis, H1N1 influenza, and COVID-19, demonstrating clinically relevant stratification across diseases and revealing some of the physiological alterations linking immune dysregulation to mortality. Our method enables early identification of individuals with dysfunctional immune profiles, bringing us closer to precision medicine in infection
Pooled analysis of WHO Surgical Safety Checklist use and mortality after emergency laparotomy
- Author
- Aahlin EK
- Aamer A
- Aaniana K
- Ababneh A
- Abaliksta T
- Abantanga F
- Abantanga F
- Abbas A
- Abbas M
- Abbasy J
- Abbo O
- Abbo O
- Abbott T
- Abbouch M
- Abd El Galeel A
- Abd El Hameed OS
- Abd El Hamid N
- Abd El Salam Y
- Abd El Slam M
- Abd El-Salam F
- Abd Elrasoul Y
- Abd-Elmawla M
- Abd-Elrasoul Y
- Abdallah E
- Abdallah E
- Abdel-Aty A
- Abdel-Hameed N
- Abdel-Kader SM
- Abdel-Wahab NYE
- Abdelaal A
- Abdelaty M
- Abdelazeam AR
- Abdelazim G
- Abdelaziz MA
- Abdelbadeai K
- Abdelfatah A
- AbdelFattah I
- Abdelgelil A
- Abdelghany S
- Abdelhady S
- Abdelhamed R
- Abdelhamid A
- Abdelhaq A
- Abdelkader M
- Abdelkader M
- Abdelkader O
- Abdelkareem A
- Abdelkhalek M
- Abdelmageed E
- Abdelmotaleb I
- Abdelraheim M
- Abdelraouf AM
- Abdelrouf DM
- Abdelshafy M
- Abdelshakour M
- Abdrabou AK
- Abdul-Latif S
- Abdulaziz H
- Abdulaziz M
- Abdulbagi O
- Abdulgawad M
- Abdulhakeem EM
- Abdullah AAN
- Abdullah MA
- Abdullah N
- Abdullah NAN
- Abdullah NAN
- Abdullahi L
- Abdurrazzaaq A
- Abebe NS
- Abebe NS
- Abem OE
- Aber A
- Abington E
- Abiola O
- Aboarab A
- Aboelella M
- Aboelmagd O
- Aboelsoud MR
- Aboraya M
- Aboraya M
- Abouelnasr A
- Aboul-Naga MS
- Abouzahra A
- Abouzaid A
- Abozaid M
- Abozeid K
- Abozyed MAF
- Abu Qumbos A
- Abu-toyour M
- Abubakr M
- Abudeeb H
- Abuowda Y
- Abuqwaider E
- Abusalem L
- Abuseif M
- Abushamleh S
- Acharya P
- Ackom E
- Acquah E
- Adam A
- Adam N
- Adams R
- Adamu A
- Adawi I
- Adawi M
- Adebanjo A
- Adebanjo A
- Adebola O
- Adedeji A
- Adekoya A
- Adel A
- Adel A
- Adel BE
- Adel I
- Adella FJ
- Adelshone A
- Ademuyiwa A
- Ademuyiwa A
- Ademuyiwa AO
- Ademuyiwa AO
- Ademuyiwa AO
- Ademuyiwa AO
- Adenekan B
- Adeniran J
- Adeniran J
- Adeniyi A
- Adeniyi A
- Adesanya O
- Adesanya O
- Adesina A
- Adesina A
- Adesuyi A
- Adeyeye A
- Adeyeye A
- Adeyeye A
- Adham W
- Adhitama N
- Adil M
- Adisa AO
- Adisa AO
- Adu-Aryee N
- Afana S
- Afandy A
- Afifi AM
- Afzal M
- Agalianos C
- Agalianos C
- Agarwal A
- Agarwal A
- Agarwal A
- Agbedinu K
- Agius M
- Aglan A
- Aguado Suarez N
- Aguilar-Jimenez J
- Aguilera M
- Aguilera ML
- Aguilera ML
- Aguilera ML
- Aguilera O
- Aguilera-Arevalo M-L
- Ahlonsou G
- Ahlqvist S
- Ahlqvist S
- Ahlqvist S
- Ahmed A
- Ahmed A
- Ahmed A
- Ahmed EA
- Ahmed H
- Ahmed H
- Ahmed H
- Ahmed LAM
- Ahmed S
- Ahmed S
- Ahmed SM
- Ahounou EYS
- Aigrain Y
- Aiyaman C
- Ajah J
- Ajai O
- Ajao A
- Ajao AE
- Ajiboye A
- Akatibo E
- Akeel N
- Akhtar M
- Akoto E
- Akpenyi O
- Al Amin S
- Al Attar SM
- Al Awwad S
- Al Barrawi FE
- Al Bastawis F
- Al Meligy A
- Al Rafati AAR
- Al Raouf EA
- Al Saied G
- Al Subaie N
- Al-Aarag AA-R
- Al-Azraqi IAA
- Al-Bahrani A
- Al-Buhaisi A
- Al-Dakka E
- Al-Faifi JJ
- Al-faqawi M
- Al-farram H
- Al-Hameedi HII
- Al-Hasani RKMJ
- Al-khatib A
- Al-Mallah A
- Al-Marakby D
- Al-Mousa M
- Al-Nahrawi S
- Al-Obaedi O
- Al-saqqa S
- Al-Saqqa SW
- Al-Saqqa SW
- Al-shammari A
- Al-Slaibi I
- Al-taher T
- Alaael-Dein S
- Alada M
- Alahmady O
- Alakaloko F
- Alakaloko F
- Alaloul E
- Alamin S
- Alamoudi M
- Alamoudi U
- Albeladi B
- Albiety A
- Alcca Ticona W
- Aldalaq A
- Aldhafeeri S
- Aledrisy M
- Alejos Bermudez YE
- Alexander P
- Alexander P
- Alexander P
- Alexandre C
- Alfarsi MA
- Alghamdi A
- Alghamdi B
- Alghamdi M
- Alghamdi MSA
- Algohary O
- Alhabli I
- Alhady K
- Alhammali T
- Alhassan B
- Alhazmi W
- Alhendy M
- Alherz M
- Ali A
- Ali A
- Ali A
- Ali CDM
- Ali E
- Ali FM
- Ali H
- Ali S
- Ali SAWEW
- Ali SS
- Ali THA
- Ali W
- Alihonou T
- Alimi Q
- Alis H
- Aliyu H
- Aliyu M
- Aliyu S
- Aljboor K
- Aljiffry M
- Aljiffry M
- Aljohani E
- Aljohani E
- Aljohani S
- Alkaaki A
- Alkammash A
- Alkelani M
- Alkhabbaz D
- Alkhouri M
- Allam M
- Allam M
- Allam Y
- Allegri A
- Allegri A
- Allen JLY
- Allott R
- Almallah A
- Almoflihi A
- Almuallem S
- Almy J
- Alnaby MH
- Alnawam E
- Alnuqaydan SA
- Alnusairat A
- Alomar IN
- Alqahtani E
- Alqahtani S
- Alrahawy M
- Alrajraji M
- Alrifaie A
- AlRowais M
- Alsaggaf M
- Alsaggaf MU
- Alsaggaf MU
- Alser OH
- Alshareef R
- Altaf A
- Altaf A
- Altamimi A
- Altamimi A
- Altamimi A
- Altamimi A
- Altamini A
- Altarayra M
- Althwainy A
- Altibi A
- Altinel Y
- Altinel Y
- Altoe F
- Altwigry AM
- Altwijri A
- Alvarado Jaramillo R
- Alvarez Barreda LM
- Alvi AR
- Alwafai MG
- Aly AK
- Aly MYM
- Alyacoubi S
- Alyahya R
- Alyami R
- Alyami R
- AlYoussef I
- Alzahrani A
- Alzahrani M
- Alzahrani M
- Alzayat T
- Aman NF
- Amandito R
- Amandito R
- Amandito R
- Amandito R
- Ambrona-Zafra D
- Ambrozeviciute V
- Ameen M
- Amer MA
- Amin HAA
- Amin J
- Amin J
- Amjad M
- Ammar M
- Ammar MS
- Amoah M
- Amoako J
- Amoako PT
- Amoako-Boateng M
- Amole I
- Amreia M
- Amreia M
- Anandkumar D
- Anderson D
- Anderson F
- Anderson R
- Anderson-Knight H
- Andersson L
- Andika FFA
- Andreotti D
- Andres Garcia-Marin J
- Andress C
- Andriola V
- Ang YL
- Angelieri D
- Anis E
- Ansaloni L
- Ansaloni L
- Ansaloni L
- Ansaloni L
- Ansaloni L
- Antar S
- Antezana D
- Anthoulakis C
- Anthoulakis C
- Antoniozzi A
- Anwar AW
- Anwar N
- Anwer W
- Anyanwu L-J
- Anyanwu L-J
- Aonzo P
- Appeadu-Mensah W
- Appiah EK
- Aql S
- Aquilino F
- Arachchi PP
- Arachchige LAJJ
- Arafa O
- Arafa S
- Arango MCM
- Arango MCM
- Aranzabal Durand SY
- Araujo R
- Arcudi C
- Ardley R
- Arenas A
- Arevalo Azmitia JR
- Arias Pacheco RD
- Arman S
- Arman S
- Armando ChunguiBravo J
- Armellini A
- Arnaud A
- Arnaud AP
- Arnaud AP
- Arnaud AP
- Arroyo Basto CA
- Arshad MM
- Arslan E
- Arsyad HM
- Arthur T
- Arulampalam T
- Aruldas N
- Asal M
- Asar YH
- Asare-Bediako K
- Asele FA
- Ashour A
- Ashour A
- Ashour K
- Ashraf SF
- Ashtari M
- Ashton A
- Asi F
- Asilah SMD
- Assal A
- Assouto PA
- Asturia S
- Asumah H
- Ata A
- Ata AAA
- Ata AY
- Atiyeh A
- Atkins ET
- Atkinson K
- Atobatele K
- Attallah NA
- Attard M
- Attia A
- Attia AM
- Augestad KM
- Aung KP
- Austraite A
- Aviles S
- Avoka A
- Awad I
- Awad SA
- Awadallah S
- Awuku-Asabre J
- Ayad S
- Ayandipo O
- Ayandipo OO
- Aydin MC
- Ayyar S
- Aziz DNA
- Aziz MRA
- Aziz NA
- Azizeldine MG
- Azmitia Mendizabal CA
- Azodo IA
- Azzie G
- Azzie G
- Azzis O
- Baba S
- Bachri H
- Badawy M
- Badenjki MA
- Badicel M
- Badr A
- Badr MFM
- Badwi NM
- Badwi NM
- Badwy A
- Bahar S
- Baheeg M
- Bailey K
- Baillie K
- Baillie K
- Baird A
- Bakhaidar M
- Baki BE
- Bakr A
- Bakry HM
- Bala M
- Balalis D
- Baldacchino M
- Balducci G
- Balila RMH
- Balkan AZA
- Ballouhey Q
- Balmaceda R
- Balmaceda R
- Balmaceda R
- Balogun F
- Baltrunas R
- Baluch F
- Bamford R
- Bamicha A
- Bamicha A
- Banaitis VJ
- Bandi A
- Bandoh D
- Bani-Sadar A
- Banipal GS
- Baraka H
- Barakat SAE
- Barendegere V
- Barker T
- Barkolias C
- Barmayehvar B
- Barnabas GN
- Barnacle J
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- Komolafe O
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- Kong C
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- Kordorwu HEK
- Korkolis D
- Kosai NR
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- Kostov E
- Kotb AHE-B
- Kotecha D
- Koto MZ
- Kotobi H
- Koumpa F
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- Madrid Barrientos LA
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- Mohamed M
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- Mohamed MM
- Mohamed O
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- Mohammad A
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- Montrimaite M
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- Sahel S
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- Samaraweera DI
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- Semeda N
- Semiz A
- Sena-Ruiz F
- Senanayake KJ
- Senanayake WSMKJ
- Setiawan J
- Seto DM
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- Sfougaris D
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- Shahbaz AR
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- Shahine A
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- Publication venue
- Publication date
- 15/10/2018
- Field of study
Background The World Health Organization (WHO) Surgical Safety Checklist has fostered safe practice for 10 years, yet its place in emergency surgery has not been assessed on a global scale. The aim of this study was to evaluate reported checklist use in emergency settings and examine the relationship with perioperative mortality in patients who had emergency laparotomy. Methods In two multinational cohort studies, adults undergoing emergency laparotomy were compared with those having elective gastrointestinal surgery. Relationships between reported checklist use and mortality were determined using multivariable logistic regression and bootstrapped simulation. Results Of 12 296 patients included from 76 countries, 4843 underwent emergency laparotomy. After adjusting for patient and disease factors, checklist use before emergency laparotomy was more common in countries with a high Human Development Index (HDI) (2455 of 2741, 89.6 per cent) compared with that in countries with a middle (753 of 1242, 60.6 per cent; odds ratio (OR) 0.17, 95 per cent c.i. 0.14 to 0.21, P <0001) or low (363 of 860, 422 per cent; OR 008, 007 to 010, P <0.001) HDI. Checklist use was less common in elective surgery than for emergency laparotomy in high-HDI countries (risk difference -94 (95 per cent c.i. -11.9 to -6.9) per cent; P <0001), but the relationship was reversed in low-HDI countries (+121 (+7.0 to +173) per cent; P <0001). In multivariable models, checklist use was associated with a lower 30-day perioperative mortality (OR 0.60, 0.50 to 073; P <0.001). The greatest absolute benefit was seen for emergency surgery in low- and middle-HDI countries. Conclusion Checklist use in emergency laparotomy was associated with a significantly lower perioperative mortality rate. Checklist use in low-HDI countries was half that in high-HDI countries.Peer reviewe
Measurements of differential cross-sections in top-quark pair events with a high transverse momentum top quark and limits on beyond the Standard Model contributions to top-quark pair production with the ATLAS detector at √s = 13 TeV
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- Yildiz HD
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- Zeissner SV
- Zeitnitz C
- Zeng JC
- Zenger DT
- Zenin O
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- Zerwas D
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- Zhao P
- Zhao T
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- Zhao Z
- Zhemchugov A
- Zheng Z
- Zhong D
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- Zhu Y
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- Zhukov K
- Zhulanov V
- Zieminska D
- Zimine NI
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- Zorbas TG
- Zormpa O
- Zou W
- Zwalinski L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Cross-section measurements of top-quark pair production where the hadronically decaying top quark has transverse momentum greater than 355 GeV and the other top quark decays into ℓνb are presented using 139 fb−1 of data collected by the ATLAS experiment during proton-proton collisions at the LHC. The fiducial cross-section at s = 13 TeV is measured to be σ = 1.267 ± 0.005 ± 0.053 pb, where the uncertainties reflect the limited number of data events and the systematic uncertainties, giving a total uncertainty of 4.2%. The cross-section is measured differentially as a function of variables characterising the tt¯ system and additional radiation in the events. The results are compared with various Monte Carlo generators, including comparisons where the generators are reweighted to match a parton-level calculation at next-to-next-to-leading order. The reweighting improves the agreement between data and theory. The measured distribution of the top-quark transverse momentum is used to search for new physics in the context of the effective field theory framework. No significant deviation from the Standard Model is observed and limits are set on the Wilson coefficients of the dimension-six operators OtG and Otq(8), where the limits on the latter are the most stringent to date. [Figure not available: see fulltext.]
Measurement of the energy asymmetry in t(t)over-barj production at 13 TeV with the ATLAS experiment and interpretation in the SMEFT framework
- Author
- Aad G
- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
- Aboulhorma A
- Abramowicz H
- Abreu H
- Abud A Abed
- Abulaiti Y
- Abusleme Hoffman AC
- Acharya BS
- Achkar B
- Adam L
- Adamczyk L
- Adamek L
- Addepalli S
- Adelman J
- Adiguzel A
- Adorni S
- Adye T
- Affolder AA
- Afik Y
- Agapopoulou C
- Agaras MN
- Agarwala J
- Aggarwal A
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- Ahmad A
- Ahmadov F
- Ahmed WS
- Ai X
- Aielli G
- Aizenberg I
- Akatsuka S
- Akbiyik M
- Akesson TPA
- Akimov A
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Alconada Verzini MJ
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- Aleksa M
- Aleksandrov IN
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- Zhemchugov A
- Zheng Z
- Zhong D
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- Publication venue
- 'Springer Fachmedien Wiesbaden GmbH'
- Publication date
- 28/04/2022
- Field of study
A measurement of the energy asymmetry in jet-associated top-quark pair production is presented using 139fb−1
139
fb
-
1
of data collected by the ATLAS detector at the Large Hadron Collider during pp collisions at s=13TeV
s
=
13
TeV
. The observable measures the different probability of top and antitop quarks to have the higher energy as a function of the jet scattering angle with respect to the beam axis. The energy asymmetry is measured in the semileptonic ttˉ
t
t
¯
decay channel, and the hadronically decaying top quark must have transverse momentum above 350GeV
350
GeV
. The results are corrected for detector effects to particle level in three bins of the scattering angle of the associated jet. The measurement agrees with the SM prediction at next-to-leading-order accuracy in quantum chromodynamics in all three bins. In the bin with the largest expected asymmetry, where the jet is emitted perpendicular to the beam, the energy asymmetry is measured to be −0.043±0.020
-
0.043
±
0.020
, in agreement with the SM prediction of −0.037±0.003
-
0.037
±
0.003
. Interpreting this result in the framework of the Standard Model effective field theory (SMEFT), it is shown that the energy asymmetry is sensitive to the top-quark chirality in four-quark operators and is therefore a valuable new observable in global SMEFT fits
Determination of the parton distribution functions of the proton using diverse ATLAS data from pp collisions at √s = 7, 8 and 13 TeV
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- Zhemchugov A
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- Zhulanov V
- Zieminska D
- Zimine NI
- Zimmermann S
- Zinsser J
- Ziolkowski M
- Zoccoli A
- Zoch K
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- Zou W
- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
This paper presents an analysis at next-to-next-to-leading order in the theory of quantum chromodynamics for the determination of a new set of proton parton distribution functions using diverse measurements in pp collisions at \sqrt{s} = 7, 8 and 13 TeV, performed by the ATLAS experiment at the Large Hadron Collider, together with deep inelastic scattering data from ep collisions at the HERA collider. The ATLAS data sets considered are differential cross-section measurements of inclusive W^{±} and Z/gamma^{*} boson production, W^{±} and Z boson production in association with jets, t\bar{t} production, inclusive jet production and direct photon production. In the analysis, particular attention is paid to the correlation of systematic uncertainties within and between the various ATLAS data sets and to the impact of model, theoretical and parameterisation uncertainties. The resulting set of parton distribution functions is called ATLASpdf21
Modelling and computational improvements to the simulation of single vector-boson plus jet processes for the ATLAS experiment
- Author
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- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
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- Zakharchuk N
- Zambito S
- Zanzi D
- Zaplatilek O
- Zeissner SV
- Zeitnitz C
- Zeng JC
- Zenin O
- Zenis T
- Zenz S
- Zerradi S
- Zerwas D
- Zhang B
- Zhang DF
- Zhang G
- Zhang J
- Zhang K
- Zhang L
- Zhang M
- Zhang R
- Zhang S
- Zhang X
- Zhang X
- Zhang Z
- Zhao H
- Zhao P
- Zhao T
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zheng Z
- Zhong D
- Zhou B
- Zhou C
- Zhou H
- Zhou N
- Zhou Y
- Zhu C
- Zhu CG
- Zhu H
- Zhu HL
- Zhu J
- Zhu Y
- Zhuang X
- Zhukov K
- Zhulanov V
- Zieminska D
- Zimine NI
- Zimmermann S
- Zinsser J
- Ziolkowski M
- Zivkovic L
- Zoccoli A
- Zoch K
- Zorbas TG
- Zormpa O
- Zou W
- Zwalinski L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
This paper presents updated Monte Carlo configurations used to model the production of single electroweak vector bosons (W, Z/gamma*) in association with jets in proton-proton collisions for the ATLAS experiment at the Large Hadron Collider. Improvements pertaining to the electroweak input scheme, parton-shower splitting kernels and scale-setting scheme are shown for multi-jet merged configurations accurate to next-to-leading order in the strong and electroweak couplings. The computational resources required for these set-ups are assessed, and approximations are introduced resulting in a factor three reduction of the per-event CPU time without affecting the physics modelling performance. Continuous statistical enhancement techniques are introduced by ATLAS in order to populate low cross-section regions of phase space and are shown to match or exceed the generated effective luminosity. This, together with the lower per-event CPU time, results in a 50% reduction in the required computing resources compared to a legacy set-up previously used by the ATLAS collaboration. The set-ups described in this paper will be used for future ATLAS analyses and lay the foundation for the next generation of Monte Carlo predictions for single vector-boson plus jets production
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