357 research outputs found
Follow-up of atheroma burden with sequential whole body contrast enhanced MR angiography:a feasibility study
- Author
- A Benetos
- A Napoli
- A Roghi
- Allan D. Struthers
- C Lundberg
- D Gassull
- DG Kramer
- DH O’Leary
- DL Bhatt
- F Bamberg
- F Grothues
- Faisel Khan
- H-C Yoon
- J Wikström
- J. Graeme Houston
- Jill J. F. Belch
- JK Min
- Jonathan R. Weir-McCall
- JR Weir-McCall
- M Goyen
- M Goyen
- ML Bots
- N Diehm
- PG Steg
- Prasad G. Ramkumar
- RA Kronmal
- Richard D. White
- S Lehrke
- SA Waugh
- SC Ladd
- SJ Gandy
- SL Duce
- Stephen J. Gandy
- T Hansen
- YW Nielsen
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2016
- Field of study
Assess the feasibility of whole body magnetic resonance angiography (WB-MRA) for monitoring global atheroma burden in a population with peripheral arterial disease (PAD). 50 consecutive patients with symptomatic PAD referred for clinically indicated MRA were recruited. Whole body MRA (WB-MRA) was performed at baseline, 6 months and 3 years. The vasculature was split into 31 anatomical arterial segments. Each segment was scored according to degree of luminal narrowing: 0 = normal, 1 = <50 %, 2 = 50–70 %, 3 = 71–99 %, 4 = vessel occlusion. The score from all assessable segments was summed, and then normalised to the number of assessable vessels. This normalised score was divided by four (the maximum vessel score) and multiplied by 100 to give a final standardised atheroma score (SAS) with a score of 0–100. Progression was assessed with repeat measure ANOVA. 36 patients were scanned at 0 and 6 months, with 26 patients scanned at the 3 years follow up. Only those who completed all three visits were included in the final analysis. Baseline atherosclerotic burden was high with a mean SAS of 15.7 ± 10.3. No significant progression was present at 6 months (mean SAS 16.4 ± 10.5, p = 0.67), however there was significant disease progression at 3 years (mean SAS 17.7 ± 11.5, p = 0.01). Those with atheroma progression at follow-up were less likely to be on statin therapy (79 vs 100 %, p = 0.04), and had significantly higher baseline SAS (17.6 ± 11.2 vs 10.7 ± 5.1, p = 0.043). Follow up of atheroma burden is possible with WB-MRA, which can successfully quantify and monitor atherosclerosis progression at 3 years follow-up
Cohort comparison study of cardiac disease and atherosclerotic burden in type 2 diabetic adults using whole body cardiovascular magnetic resonance imaging
- Author
- A Langer
- A Lorenzo De
- AP Burke
- B Tuccillo
- C Lundberg
- DC Burgess
- Deirdre B. Cassidy
- DL Bhatt
- E Maffei
- F Bamberg
- G Danaei
- H Sakuma
- Helen Looker
- Helen M. Colhoun
- HM Findeisen
- J. Graeme Houston
- Jonathan R. Weir-McCall
- JR Weir-McCall
- KG Alberti
- LG Spagnoli
- Lynne McCormick
- M Syvänne
- N Mewton
- P Pajunen
- P Zimmet
- Petra Rauchhaus
- PR Moreno
- RQ Migrino
- RR Rubin
- S Ito
- S Lehrke
- S Natori
- S Weckbach
- SA Waugh
- SC Ladd
- Shona Z. Matthew
- SJ Gandy
- Stephen J. Gandy
- Suzanne L. Duce
- T Hansen
- T Hansen
- T Kawata
- T Kubo
- YW Nielsen
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2015
- Field of study
BACKGROUND: Whole body cardiovascular MR (WB CVMR) combines whole body angiography and cardiac MR assessment. It is accepted that there is a high disease burden in patients with diabetes, however the quantification of the whole body atheroma burden in both arterial and cardiac disease has not been previously reported. In this study we compare the quantified atheroma burden in those individuals with and without diabetes by clinical cardiovascular disease (CVD) status. METHODS: 158 participants underwent WB CVMR, and were categorised into one of four groups: (1) type 2 diabetes mellitus (T2DM) with CVD; (2) T2DM without CVD; (3) CVD without T2DM; (4) healthy controls. The arterial tree was subdivided into 31 segments and each scored according to the degree of stenosis. From this a standardised atheroma score (SAS) was calculated. Cardiac MR and late gadolinium enhancement images of the left ventricle were obtained for assessment of mass, volume and myocardial scar assessment. RESULTS: 148 participants completed the study protocol—61 % male, with mean age of 64 ± 8.2 years. SAS was highest in those with cardiovascular disease without diabetes [10.1 (0–39.5)], followed by those with T2DM and CVD [4 (0–41.1)], then those with T2DM only [3.23 (0–19.4)] with healthy controls having the lowest atheroma score [2.4 (0–19.4)]. Both groups with a prior history of CVD had a higher SAS and left ventricular mass than those without (p < 0.001 for both). However after accounting for known cardiovascular risk factors, only the SAS in the group with CVD without T2DM remained significantly elevated. 6 % of the T2DM group had evidence of silent myocardial infarct, with this subcohort having a higher SAS than the remainder of the T2DM group [7.7 (4–19) vs. 2.8 (0–17), p = 0.024]. CONCLUSIONS: Global atheroma burden was significantly higher in those with known cardiovascular disease and without diabetes but not in those with diabetes and cardiovascular disease suggesting that cardiovascular events may occur at a lower atheroma burden in diabetes. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12933-015-0284-2) contains supplementary material, which is available to authorized users
Generation of recombinant hyperimmune globulins from diverse B-cell repertoires
- Author
- Adams MS
- Adler AS
- Asensio MA
- Bartley CR
- Benzie E
- Büscher D
- Carrington CVF
- Carter KP
- Chamow SM
- Chiang Y
- Edgar RC
- Gautam BK
- Goldblatt D
- Gras A
- Jeanfreau R
- Johnson DS
- Keating SM
- Leong J
- Leong R
- Lim YW
- Lundberg CV
- Lynch H
- Manickam VA
- Medina-Cucurella AV
- Meyer EH
- Mizrahi RA
- Monroe B
- Mosher RA
- Muench MO
- Niedecken AR
- Oguin TH
- Olson C
- Pearce E
- Ramjag AT
- Richardson H
- Roalfe L
- Ross CA
- Saini J
- Simmons G
- Simons JF
- Spindler MJ
- Stadtmiller K
- Terencio JV
- Tinsley B
- Tracy L
- Wagner EK
- Walch MJ
- Wayham N
- Publication venue
- Publication date
- 01/08/2021
- Field of study
Plasma-derived polyclonal antibody therapeutics, such as intravenous immunoglobulin, have multiple drawbacks, including low potency, impurities, insufficient supply and batch-to-batch variation. Here we describe a microfluidics and molecular genomics strategy for capturing diverse mammalian antibody repertoires to create recombinant multivalent hyperimmune globulins. Our method generates of diverse mixtures of thousands of recombinant antibodies, enriched for specificity and activity against therapeutic targets. Each hyperimmune globulin product comprised thousands to tens of thousands of antibodies derived from convalescent or vaccinated human donors or from immunized mice. Using this approach, we generated hyperimmune globulins with potent neutralizing activity against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in under 3 months, Fc-engineered hyperimmune globulins specific for Zika virus that lacked antibody-dependent enhancement of disease, and hyperimmune globulins specific for lung pathogens present in patients with primary immune deficiency. To address the limitations of rabbit-derived anti-thymocyte globulin, we generated a recombinant human version and demonstrated its efficacy in mice against graft-versus-host disease
The oral microbiome – an update for oral healthcare professionals
- Author
- A Rinaldi
- A. M. L. Pedersen
- AM Pedersen
- AV Amerongen
- B Sampaio-Maia
- BT Rosier
- C Hannig
- C Hannig
- CJ Adler
- D Haubek
- DA Devine
- DA Relman
- DA Relman
- DR Donohoe
- E Theilade
- E Zaura
- E Zaura
- E. Zaura
- EA Franzosa
- EK Costello
- EL Gross
- FE Dewhirst
- G Hajishengallis
- G Hajishengallis
- H Marcotte
- HJ Busscher
- HP Lif
- I Cho
- I. L. C. Chapple
- IL Chapple
- IL Chapple
- J Kuczynski
- J Lederberg
- J Meyle
- J Ravel
- J van der Horst
- J Wu
- JA Gilbert
- JJ de Soet
- JJ Doel
- JO Lundberg
- JO Lundberg
- K Arimatsu
- K Schwarzberg
- L Forner
- M Costalonga
- M Govoni
- M Rylev
- M Slatkin
- M Woessner
- M Øilo
- M. Hannig
- M. Kilian
- M. S. Tonetti
- MF Zarco
- MG Dominguez-Bello
- MJ Blaser
- MM Grant
- MR Gillings
- N Takahashi
- OE Cornejo
- P de Pablo
- P. D. Marsh
- PD Marsh
- PD Marsh
- PD Marsh
- PD Marsh
- PD Marsh
- PD Marsh
- PI Diaz
- PJ Turnbaugh
- PJ Turnbaugh
- PL Holgerson
- R Krajmalnik-Brown
- R Sender
- RC Page
- RC Williams
- RM Donlan
- RP Darveau
- S Bikel
- S Bizzarro
- S Petti
- S Velmurugan
- SJ Salter
- SR Bordenstein
- SR Vartoukian
- TE Bramanti
- V Kapil
- V Kapil
- V. Meuric
- VM Barnes
- W Crielaard
- W van't Hof
- W. G. Wade
- WJ Loesche
- WL Siqueira
- X Xu
- Y Soga
- YH Li
- YL Liu
- YW Han
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2016
- Field of study
For millions of years, our resident microbes have coevolved and coexisted with us in a mostly harmonious symbiotic relationship. We are not distinct entities from our microbiome, but together we form a 'superorganism' or holobiont, with the microbiome playing a significant role in our physiology and health. The mouth houses the second most diverse microbial community in the body, harbouring over 700 species of bacteria that colonise the hard surfaces of teeth and the soft tissues of the oral mucosa. Through recent advances in technology, we have started to unravel the complexities of the oral microbiome and gained new insights into its role during both health and disease. Perturbations of the oral microbiome through modern-day lifestyles can have detrimental consequences for our general and oral health. In dysbiosis, the finely-tuned equilibrium of the oral ecosystem is disrupted, allowing disease-promoting bacteria to manifest and cause conditions such as caries, gingivitis and periodontitis. For practitioners and patients alike, promoting a balanced microbiome is therefore important to effectively maintain or restore oral health. This article aims to give an update on our current knowledge of the oral microbiome in health and disease and to discuss implications for modern-day oral healthcare
Mammalian Otolin: A Multimeric Glycoprotein Specific to the Inner Ear that Interacts with Otoconial Matrix Protein Otoconin-90 and Cerebellin-1
- Author
- A El-Amraoui
- A Rau
- AJ Hudspeth
- B Hurle
- C Sollner
- C Sollner
- D Bao
- David John Stuart Hulmes
- DJ Lim
- DM Ornitz
- DR Trune
- E Murayama
- E Murayama
- E Murayama
- E Verpy
- F Salvinelli
- G. William Wong
- GW Wong
- GW Wong
- GW Wong
- H Hirai
- H Shinkai
- H Tohse
- H Waki
- I Hughes
- I Thalmann
- I Zwaenepoel
- JA Petko
- JG Davis
- JM Gershoni
- Jonathan M. Peterson
- JS Oghalai
- K Julenius
- KG Pote
- KG Pote
- L Shapiro
- L Vitagliano
- LC Erway
- LJ Melton 3rd
- M Anniko
- M Cohen-Salmon
- M Mustapha
- M Torres
- M Yuzaki
- MA Moreno-Pelayo
- MC Simmler
- MC Simmler
- MD Ross
- Michael R. Deans
- PJ Kiss
- PJ Kozel
- PK Legan
- PK Legan
- PW Peake
- R Ghai
- R Paffenholz
- R Thalmann
- SM Jones
- SM Jones
- T Sreenath
- TM Squires
- TS Tsao
- TT Whitfield
- U Kishore
- UB Pajvani
- X Zhao
- X Zhao
- Y Wang
- Y Wang
- Y Wang
- YJ Kang
- YW Lundberg
- Publication venue
- Public Library of Science
- Publication date
- 01/09/2010
- Field of study
The mammalian otoconial membrane is a dense extracellular matrix containing bio-mineralized otoconia. This structure provides the mechanical stimulus necessary for hair cells of the vestibular maculae to respond to linear accelerations and gravity. In teleosts, Otolin is required for the proper anchoring of otolith crystals to the sensory maculae. Otoconia detachment and subsequent entrapment in the semicircular canals can result in benign paroxysmal positional vertigo (BPPV), a common form of vertigo for which the molecular basis is unknown. Several cDNAs encoding protein components of the mammalian otoconia and otoconial membrane have recently been identified, and mutations in these genes result in abnormal otoconia formation and balance deficits.Here we describe the cloning and characterization of mammalian Otolin, a protein constituent of otoconia and the otoconial membrane. Otolin is a secreted glycoprotein of ∼70 kDa, with a C-terminal globular domain that is homologous to the immune complement C1q, and contains extensive posttranslational modifications including hydroxylated prolines and glycosylated lysines. Like all C1q/TNF family members, Otolin multimerizes into higher order oligomeric complexes. The expression of otolin mRNA is restricted to the inner ear, and immunohistochemical analysis identified Otolin protein in support cells of the vestibular maculae and semi-circular canal cristae. Additionally, Otolin forms protein complexes with Cerebellin-1 and Otoconin-90, two protein constituents of the otoconia, when expressed in vitro. Otolin was also found in subsets of support cells and non-sensory cells of the cochlea, suggesting that Otolin is also a component of the tectorial membrane.Given the importance of Otolin in lower organisms, the molecular cloning and biochemical characterization of the mammalian Otolin protein may lead to a better understanding of otoconial development and vestibular dysfunction
Lineage-specific evolution of the vertebrate Otopetrin gene family revealed by comparative genomic analyses
- Author
- A Antonellis
- A Barski
- A Siepel
- AM Bronstein
- AW Higgins
- B Hurle
- B Hurle
- Belen Hurle
- BJ Keats
- C Larroux
- C Seiler
- C Sollner
- C Sollner
- D Weil
- David M Ornitz
- DS Williams
- E Darai-Ramqvist
- E Kim
- EE Eichler
- Eric D Green
- Evan E Eichler
- F Antonacci
- Francesca Antonacci
- H Kehrer-Sawatzki
- H Kremer
- I Hughes
- I Hughes
- I Hughes
- I Hughes
- Inna Hughes
- JA Bailey
- JA Bailey
- JC Jen
- JD Parsons
- JE Phillips
- JG Oas
- Joseph F Ryan
- JW Thomas
- JW Thomas
- K Essien
- KG Pote
- KG Pote
- KG Pote
- M Kurc
- MM Bever
- N Overlack
- NM Maas
- O Jaillon
- P Lichter
- PW Lane
- RH Waterston
- RW Blakesley
- S Cuddapah
- S Ernest
- S Giglio
- S Giglio
- S Schwartz
- SF Altschul
- SJ Wanner
- T Kido
- T Marques-Bonet
- T Newman
- TH Kim
- Tomas Marques-Bonet
- V Besson
- VV Novoselov
- WJ Kent
- X Chen
- Y Kikkawa
- YW Lundberg
- Z Cheng
- Z Jiang
- Publication venue
- BioMed Central
- Publication date
- 01/01/2011
- Field of study
Background: Mutations in the Otopetrin 1 gene (Otop1) in mice and fish produce an unusual bilateral vestibular pathology that involves the absence of otoconia without hearing impairment. The encoded protein, Otop1, is the only functionally characterized member of the Otopetrin Domain Protein (ODP) family; the extended sequence and structural preservation of ODP proteins in metazoans suggest a conserved functional role. Here, we use the tools of sequence-and cytogenetic-based comparative genomics to study the Otop1 and the Otop2-Otop3 genes and to establish their genomic context in 25 vertebrates. We extend our evolutionary study to include the gene mutated in Usher syndrome (USH) subtype 1G (Ush1g), both because of the head-to-tail clustering of Ush1g with Otop2 and because Otop1 and Ush1g mutations result in inner ear phenotypes. Results: We established that OTOP1 is the boundary gene of an inversion polymorphism on human chromosome 4p16 that originated in the common human-chimpanzee lineage more than 6 million years ago. Other lineage-specific evolutionary events included a three-fold expansion of the Otop genes in Xenopus tropicalis and of Ush1g in teleostei fish. The tight physical linkage between Otop2 and Ush1g is conserved in all vertebrates. To further understand the functional organization of the Ushg1-Otop2 locus, we deduced a putative map of binding sites for CCCTC-binding factor (CTCF), a mammalian insulator transcription factor, from genome-wide chromatin immunoprecipitation-sequencing (ChIP-seq) data in mouse and human embryonic stem (ES) cells combined with detection of CTCF-binding motifs. Conclusions: The results presented here clarify the evolutionary history of the vertebrate Otop and Ush1g families, and establish a framework for studying the possible interaction(s) of Ush1g and Otop in developmental pathways
Operation and performance of the ATLAS Tile Calorimeter in Run 1
- Author
- Aaboud M
- Aad G
- Abbott B
- Abdallah J
- Abdinov O
- Abeloos B
- Abhayasinghe DK
- Abidi SH
- Abouelfadl 
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abulaiti Y
- Acharya BS
- Adachi S
- Adamczyk L
- Adelman J
- Adersberger M
- Adiguzel A
- Adye T
- Affolder AA
- Afik Y
- Agheorghiesei C
- Aguilar-Saavedra JA
- Ahmadov F
- Aielli G
- Akatsuka S
- Akerstedt H
- Akilli E
- Akimov AV
- Alberghi GL
- Albert J
- Albicocco P
- Alconada Verzini MJ
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexander G
- Alexopoulos T
- Alhroob M
- Ali B
- Alimonti G
- Alison J
- Alkire SP
- Allaire C
- Allbrooke BMM
- Allen BW
- Allport PP
- Aloisio A
- Alonso A
- Alonso F
- Alpigiani C
- Alshehri AA
- Alstaty MI
- Alvarez 
- Alviggi MG
- Amadio BT
- Amaral Coutinho Y
- Ambroz L
- Amelung C
- Amidei D
- Amor 
- Amoroso S
- Amrouche CS
- Anastopoulos C
- Ancu LS
- Andari N
- Andeen T
- Anders CF
- Anders JK
- Anderson KJ
- Andreazza A
- Andrei V
- Anelli CR
- Angelidakis S
- Angelozzi I
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antonelli M
- Antrim DJA
- Anulli F
- Aoki M
- Aperio Bella L
- Arabidze G
- Arai Y
- Araque JP
- Araujo Ferraz V
- Arce ATH
- Ardell RE
- Arduh FA
- Argos FC
- Arguin J-
- Argyropoulos S
- Armadans R
- Armbruster AJ
- Armitage LJ
- Armstrong A
- Arnaez O
- Arnold H
- Arratia M
- Arslan O
- Artamonov A
- Artoni G
- Artz S
- Asai S
- Asbah N
- Ashkenazi A
- Asimakopoulou EM
- Asquith L
- Assamagan K
- Astalos R
- Astigarraga ME
- Atkin RJ
- Atkinson M
- Atlay NB
- Auerbach B
- Augsten K
- Avolio G
- Avramidou R
- Axen B
- Ayoub MK
- Azuelos G
- Álvarez Piqueras D
- Åkesson TPA
- Baas AE
- Baca MJ
- Bachacou H
- Bachas K
- Backes M
- Bagnaia P
- Bahilo JJL
- Bahmani M
- Bahrasemani H
- Bailey AJ
- Baines JT
- Bajic M
- Bakalis C
- Baker OK
- Bakker PJ
- Baldin EM
- Balek P
- Balli F
- Balunas WK
- Balz J
- Banas E
- Bandyopadhyay A
- Banerjee S
- Bannoura AAE
- Barak L
- Barbe WM
- Barberio EL
- Barberis D
- Barbero M
- Barillari T
- Barisits M
- Barkeloo J
- Barklow T
- Barlow N
- Barnea R
- Barnes SL
- Barnett BM
- Barnett RM
- Barnovska-Blenessy Z
- Baroncelli A
- Barone G
- Barr AJ
- Barranco Navarro L
- Barreiro Guimarães da Costa J
- Barreiro F
- Bartoldus R
- Barton AE
- Bartos P
- Basalaev A
- Bassalat A
- Bates RL
- Batista SJ
- Batlamous S
- Batley JR
- Battaglia M
- Bauce M
- Bauer F
- Bauer KT
- Bawa HS
- Beacham JB
- Beattie MD
- Beau T
- Beauchemin PH
- Bechtle P
- Beck HC
- Beck HP
- Becker K
- Becker M
- Becot C
- Beddall A
- Beddall AJ
- Bednyakov VA
- Bedognetti M
- Bee CP
- Beermann TA
- Begalli M
- Begel M
- Behera A
- Behr JK
- Bell AS
- Bella G
- Bellagamba L
- Bellerive A
- Bello FA
- Bellomo M
- Belotskiy K
- Belyaev NL
- Benary O
- Benchekroun D
- Bender M
- Benekos N
- Benhammou Y
- Benhar Noccioli E
- Benitez J
- Benjamin DP
- Benoit M
- Bensinger JR
- Bentvelsen S
- Beresford L
- Beretta M
- Berge D
- Bergeaas Kuutmann E
- Berger N
- Bergsten LJ
- Beringer J
- Berlendis S
- Bernard NR
- Bernardi G
- Bernius C
- Bernlochner FU
- Berry T
- Berta P
- Bertella C
- Bertoli G
- Bertram IA
- Besjes GJ
- Bessidskaia Bylund O
- Bessner M
- Besson N
- Bethani A
- Bethke S
- Betti A
- Bevan AJ
- Beyer J
- Bianchi RM
- Biebel O
- Biedermann D
- Bielski R
- Bierwagen K
- Biesuz NV
- Biglietti M
- Billoud TRV
- Bindi M
- Bingul A
- Bini C
- Biondi S
- Bisanz T
- Biswal JP
- Bittrich C
- Bjergaard DM
- Black JE
- Black KM
- Blair RE
- Blazek T
- Bloch I
- Blocker C
- Blue A
- Blumenschein U
- Blunier D
- Bobbink GJ
- Bobrovnikov VS
- Bocchetta SS
- Bocci A
- Boerner D
- Bogavac D
- Bogdanchikov AG
- Bohm C
- Boisvert V
- Bokan P
- Bold T
- Boldyrev AS
- Bolz AE
- Bomben M
- Bona M
- Bonilla JS
- Boonekamp M
- Borisov A
- Borissov G
- Bortfeldt J
- Bortoletto D
- Bortolotto V
- Boscherini D
- Bosman M
- Bossio Sola JD
- Bostanabad M
- Bouaouda K
- Boudreau J
- Bouhova-Thacker EV
- Boumediene D
- Bourdarios C
- Boutle SK
- Boveia A
- Boyd J
- Boyko IR
- Bozson AJ
- Bracinik J
- Brahimi N
- Brandt A
- Brandt G
- Brandt O
- Braren F
- Bratzler U
- Brau B
- Brau JE
- Breaden Madden WD
- Brendlinger K
- Brennan AJ
- Brenner L
- Brenner R
- Bressler S
- Brickwedde B
- Briglin DL
- Britton D
- Britzger D
- Brock I
- Brock R
- Brooijmans G
- Brooks T
- Brooks WK
- Brost E
- Broughton JH
- Brown H
- Bruckman de Renstrom PA
- Bruncko D
- Bruni A
- Bruni G
- Bruni LS
- Bruno S
- Brunt BH
- Bruschi M
- Bruscino N
- Bryant P
- Bryngemark L
- Buanes T
- Buat Q
- Buchholz P
- Buckley AG
- Budagov IA
- Bugge MK
- Bulekov O
- Bullock D
- Burch TJ
- Burdin S
- Burgard CD
- Burger AM
- Burghgrave B
- Burka K
- Burke S
- Burmeister I
- Burr JTP
- Busato E
- Buschmann E
- Bussey P
- Butler JM
- Buttar CM
- Butterworth JM
- Butti P
- Buttinger W
- Buzatu A
- Buzykaev AR
- Bührer F
- Büscher D
- Büscher V
- Cabras G
- Cabrera Urbán S
- Caforio D
- Cai H
- Cairo VMM
- Cakir I
- Cakir O
- Calace N
- Calafiura P
- Calandri A
- Calderini G
- Calfayan P
- Callea G
- Caloba LP
- Calvente Lopez S
- Calvet D
- Calvet S
- Calvet TP
- Calvetti M
- Camacho Toro R
- Camarda S
- Camarri P
- Cameron D
- Caminal 
- Camincher C
- Campana S
- Campanelli M
- Camplani A
- Campoverde A
- Canale V
- Cano Bret M
- Cantero J
- Cao T
- Cao Y
- Capeans Garrido MDM
- Caprini I
- Caprini M
- Capua M
- Carbone RM
- Cardarelli R
- Cardillo FC
- Carli I
- Carli T
- Carlino G
- Carlson BT
- Carminati L
- Carney RMD
- Caron S
- Carquin E
- Carrá S
- Carrillo-Montoya GD
- Casadei D
- Casado MP
- Casha AF
- Casolino M
- Casper DW
- Castelijn R
- Castillo Gimenez V
- Castillo FL
- Castro NF
- Catinaccio A
- Catmore JR
- Cattai A
- Caudron J
- Cavaliere V
- Cavallaro E
- Cavalli D
- Cavalli-Sforza M
- Cavasinni V
- Celebi E
- Ceradini F
- Cerda Alberich L
- Cerqueira AS
- Cerri A
- Cerrito L
- Cerutti F
- Cervelli A
- Cetin SA
- Chafaq A
- Chakraborty D
- Chan SK
- Chan WS
- Chan YL
- Chang P
- Chapman JD
- Charlton DG
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- Yao W
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- Yasu Y
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- Yigitbasi E
- Yildirim E
- Yildiz H
- Yorita K
- Yoshihara K
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- Yusuff I
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- Zalieckas J
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- Zemaityte G
- Zeng JC
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- Zerwas D
- Zgubič M
- Zhang D
- Zhang DF
- Zhang F
- Zhang G
- Zhang H
- Zhang J
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- Zhang L
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- Zhang Z
- Zhao P
- Zhao X
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zhou B
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- Zhu CG
- Zhu H
- Zhu HL
- Zhu J
- Zhu Y
- Zhuang X
- Zhukov K
- Zhulanov V
- Zibell A
- Zieminska D
- Zimine NI
- Zimmermann S
- Zinonos Z
- Zinser M
- Ziolkowski M
- Zobernig G
- Zoccoli A
- Zoch K
- Zorbas TG
- Zou R
- Zur 
- Zwalinski L
- Ženiš T
- Živković L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2018
- Field of study
The Tile Calorimeter is the hadron calorimeter covering the central region of the ATLAS experiment at the Large Hadron Collider. Approximately 10,000 photomultipliers collect light from scintillating tiles acting as the active material sandwiched between slabs of steel absorber. This paper gives an overview of the calorimeter’s performance during the years 2008–2012 using cosmic-ray muon events and proton–proton collision data at centre-of-mass energies of 7 and 8TeV with a total integrated luminosity of nearly 30 fb−1. The signal reconstruction methods, calibration systems as well as the detector operation status are presented. The energy and time calibration methods performed excellently, resulting in good stability of the calorimeter response under varying conditions during the LHC Run 1. Finally, the Tile Calorimeter response to isolated muons and hadrons as well as to jets from proton–proton collisions is presented. The results demonstrate excellent performance in accord with specifications mentioned in the Technical Design Report
Measurement and interpretation of same-sign W boson pair production in association with two jets in pp collisions at s = 13 TeV with the ATLAS detector
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- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 01/04/2024
- Field of study
This paper presents the measurement of fducial and diferential cross sections for both the inclusive and electroweak production of a same-sign W-boson pair in association with two jets (W±W±jj) using 139 fb−1 of proton-proton collision data recorded at a centre-of-mass energy of √s = 13 TeV by the ATLAS detector at the Large Hadron Collider. The analysis is performed by selecting two same-charge leptons, electron or muon, and at least two jets with large invariant mass and a large rapidity diference. The measured fducial cross sections for electroweak and inclusive W±W±jj production are 2.92 ± 0.22 (stat.) ± 0.19 (syst.)fb and 3.38±0.22 (stat.)±0.19 (syst.)fb, respectively, in agreement with Standard Model predictions. The measurements are used to constrain anomalous quartic gauge couplings by extracting 95% confdence level intervals on dimension-8 operators. A search for doubly charged Higgs bosons H±± that are produced in vector-boson fusion processes and decay into a same-sign W boson pair is performed. The largest deviation from the Standard Model occurs for an H±± mass near 450 GeV, with a global signifcance of 2.5 standard deviations
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
- Yin P
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- Zakareishvili T
- Zakharchuk N
- Zambito S
- Zanzi D
- Zaplatilek O
- Zeissner SV
- Zeitnitz C
- Zeng JC
- Zenger DT
- Zenin O
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- Zerradi S
- Zerwas D
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- Zhang G
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- Zhao P
- Zhao T
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zheng Z
- Zhong D
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- Zhu HL
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- Zhu Y
- Zhuang X
- Zhukov K
- Zhulanov V
- Zieminska D
- Zimine NI
- Zimmermann S
- Zinsser J
- Ziolkowski M
- 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
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.]
Combination of searches for heavy spin-1 resonances using 139 fb−1 of proton-proton collision data at s = 13 TeV with the ATLAS detector
- Author
- Aad G
- Aakvaag E
- Abbott B
- Abeling K
- Abicht NJ
- Abidi SH
- Aboelela M
- Aboulhorma A
- Abramowicz H
- Abreu H
- Abulaiti Y
- Acharya BS
- Ackermann A
- Adam Bourdarios C
- Adamczyk L
- Addepalli SV
- Addison MJ
- Adelman J
- Adiguzel A
- Adye T
- Affolder AA
- Afik Y
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahuja S
- Ai X
- Aielli G
- Aikot A
- Ait Tamlihat M
- Aitbenchikh B
- Aizenberg I
- Akbiyik M
- Akimov AV
- Akiyama D
- Akolkar NN
- Aktas S
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Albouy GL
- Alderweireldt S
- Alegria ZL
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi F
- Algren M
- Alhroob M
- Ali B
- Ali HMJ
- Ali S
- Alibocus SW
- Aliev M
- Alimonti G
- Alkakhi W
- Allaire C
- Allbrooke BMM
- Allen JF
- Allendes Flores CA
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alvarez Estevez M
- Alvarez Fernandez A
- Alves Cardoso M
- Alviggi MG
- Aly M
- Amaral Coutinho Y
- Ambler A
- Amelung C
- Amerl M
- Ames CG
- Amidei D
- Amirie KJ
- Amor Dos Santos SP
- Amos KR
- An S
- Ananiev V
- Anastopoulos C
- Andeen T
- Anders JK
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- Zhemchugov A
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- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 19/04/2024
- Field of study
A combination of searches for new heavy spin-1 resonances decaying into different pairings of W, Z, or Higgs bosons, as well as directly into leptons or quarks, is presented. The data sample used corresponds to 139 fb−1 of proton-proton collisions at
= 13 TeV collected during 2015–2018 with the ATLAS detector at the CERN Large Hadron Collider. Analyses selecting quark pairs (qq, bb,
, and tb) or third-generation leptons (τν and ττ) are included in this kind of combination for the first time. A simplified model predicting a spin-1 heavy vector-boson triplet is used. Cross-section limits are set at the 95% confidence level and are compared with predictions for the benchmark model. These limits are also expressed in terms of constraints on couplings of the heavy vector-boson triplet to quarks, leptons, and the Higgs boson. The complementarity of the various analyses increases the sensitivity to new physics, and the resulting constraints are stronger than those from any individual analysis considered. The data exclude a heavy vector-boson triplet with mass below 5.8 TeV in a weakly coupled scenario, below 4.4 TeV in a strongly coupled scenario, and up to 1.5 TeV in the case of production via vector-boson fusion
- …