392 research outputs found
Effects of Imatinib Mesylate (Gleevec) on Human Islet NF-kappaB Activation and Chemokine Production In Vitro
- Author
- A Templeton
- A Tsapas
- A Wullaert
- AB Rabson
- AE Karlsen
- BC Chen
- Bernhard Ryffel
- C Louvet
- C Xiao
- CY Ito
- D Dingli
- D Eizirik
- D Mokhtari
- D Mokhtari
- D Veneri
- Dariush Mokhtari
- DB Costa
- DL Eizirik
- G Nelson
- IM Ghobrial
- J Couzin
- J Saldeen
- J Saldeen
- JA Bluestone
- JE Hutti
- K Nihira
- L Larsen
- L Reber
- M Breccia
- M Breccia
- M Breccia
- M Cnop
- M Igoillo-Esteve
- M Karin
- MS Han
- MY Donath
- N Agostino
- Nils Welsh
- P Arun
- PJ Little
- R HĂ€gerkvist
- R HĂ€gerkvist
- R HĂ€gerkvist
- RA Liberatore
- RN Saha
- S Fitter
- S Gur
- S Mariani
- T Goto
- T Lu
- T Maekawa
- Tao Lu
- Tingting Li
- W Zhang
- Z Chodorowski
- Publication venue
- Public Library of Science
- Publication date
- 14/09/2011
- Field of study
Imatinib Mesylate (Gleevec) is a drug that potently counteracts diabetes both in humans and in animal models for human diabetes. We have previously reported that this compound in human pancreatic islets stimulates NF-ÎșB signaling and islet cell survival. The aim of this study was to investigate control of NF-ÎșB post-translational modifications exerted by Imatinib and whether any such effects are associated with altered islet gene expression and chemokine production in vitro.Human islets were either left untreated or treated with Imatinib for different timepoints. IÎșB-α and NF-ÎșB p65 phosphorylation and methylation were assessed by immunoblot analysis. Islet gene expression was assessed using a commercial Pathway Finder microarray kit and RT-PCR. Islet chemokine production was determined by flow cytometric bead array analysis.Human islet IÎșB-α and Ser276-p65 phosphorylation were increased by a 20 minute Imatinib exposure. Methylation of p65 at position Lys221 was increased after 60 min of Imatinib exposure and persisted for 3 hours. Microarray analysis of islets exposed to Imatinib for 4 hours revealed increased expression of the inflammatory genes IL-4R, TCF5, DR5, I-TRAF, I-CAM, HSP27 and IL-8. The islet release of IL-8 was augmented in islets cultured over night in the presence of Imatinib. Following 30 hours of Imatinib exposure, the cytokine-induced IÎșB-α and STAT1 phosphorylation was abolished and diminished, respectively. The cytokine-induced release of the chemokines MIG and IP10 was lower in islets exposed to Imatinib for 30 hours.Imatinib by itself promotes a modest activation of NF-ÎșB. However, a prolonged exposure of human islets to Imatinib is associated with a dampened response to cytokines. It is possible that Imatinib induces NF-ÎșB preconditioning of islet cells leading to lowered cytokine sensitivity and a mitigated islet inflammation
eXtraembryonic ENdoderm (XEN) Stem Cells Produce Factors that Activate Heart Formation
- Author
- A Arai
- A Foley
- A Goldbeter
- A Holtzinger
- A Nagy
- AC Foley
- AC Foley
- AC Foley
- AC Foley
- AG Jacobson
- AG Jacobson
- AK Sater
- AK Sater
- AM Wobus
- AM Wobus
- Ann C. Foley
- Anna-Katerina Hadjantonakis
- Bernadette Breant
- BG Bruneau
- BR Keegan
- C Biben
- C Gissel
- C Mummery
- C Mummery
- CL Cai
- CL Mummery
- CL Mummery
- CM Liberatore
- CY Lim
- D Franco
- DG Wilkinson
- EJ Park
- G Dennis Jr
- GS Kwon
- H Matsui
- H Wei
- IO Sirbu
- IO Sirbu
- J Artus
- JA White
- JM Lehman
- JĂ©rĂŽme Artus
- K Brown
- Kemar Brown
- KR Boheler
- L Liu
- L Yang
- M Abu-Abed
- M Ashburner
- M Gannon
- M Honda
- M Stary
- M Yasunaga
- Michael Xavier Doss
- N Nascone
- P Gadue
- PJ Tesar
- PP Tam
- R Diez del Corral
- R Diez del Corral
- R Edgar
- R Ilagan
- R Pal
- R Passier
- RA Espinoza-Lewis
- RG Gourdie
- RM Nijmeijer
- S Abu-Abed
- SL Fullilove
- SS Abu-Abed
- Stephanie Legros
- T Kunath
- T Takahashi
- T Thomas
- T Yatskievych
- TA Drysdale
- VA Schneider
- VM Christoffels
- W Huang da
- Y Saga
- Publication venue
- Public Library of Science
- Publication date
- 01/10/2010
- Field of study
Initial specification of cardiomyocytes in the mouse results from interactions between the extraembryonic anterior visceral endoderm (AVE) and the nascent mesoderm. However the mechanism by which AVE activates cardiogenesis is not well understood, and the identity of specific cardiogenic factors in the endoderm remains elusive. Most mammalian studies of the cardiogenic potential of the endoderm have relied on the use of cell lines that are similar to the heart-inducing AVE. These include the embryonal-carcinoma-derived cell lines, END2 and PYS2. The recent development of protocols to isolate eXtraembryonic ENdoderm (XEN) stem cells, representing the extraembryonic endoderm lineage, from blastocyst stage mouse embryos offers new tools for the genetic dissection of cardiogenesis.Here, we demonstrate that XEN cell-conditioned media (CM) enhances cardiogenesis during Embryoid Body (EB) differentiation of mouse embryonic stem (ES) cells in a manner comparable to PYS2-CM and END2-CM. Addition of CM from each of these three cell lines enhanced the percentage of EBs that formed beating areas, but ultimately, only XEN-CM and PYS2-CM increased the total number of cardiomyocytes that formed. Furthermore, our observations revealed that both contact-independent and contact-dependent factors are required to mediate the full cardiogenic potential of the endoderm. Finally, we used gene array comparison to identify factors in these cell lines that could mediate their cardiogenic potential.These studies represent the first step in the use of XEN cells as a molecular genetic tool to study cardiomyocyte differentiation. Not only are XEN cells functionally similar to the heart-inducing AVE, but also can be used for the genetic dissection of the cardiogenic potential of AVE, since they can be isolated from both wild type and mutant blastocysts. These studies further demonstrate the importance of both contact-dependent and contact-independent factors in cardiogenesis and identify potential heart-inducing proteins in the endoderm
A Role for the Non-Receptor Tyrosine Kinase Abl2/Arg in Experimental Neuroinflammation
- Author
- AJ Koleske
- AL Miller
- Alexander N. Scherer
- Anthony J. Koleske
- ANZgene
- B Nagar
- B. Thomas BÀckström
- C Bianchi
- D Bixby
- DA Hafler
- Dan Holmberg
- E Wakeland
- E Weisberg
- F Terabe
- Freja Aksel Jacobsen
- G Azizi
- GD Kruh
- H Dai
- Hera BragadĂłttir
- HF Harbo
- International Multiple Sclerosis Genetics C
- J Aman
- J Colicelli
- J Karlsson
- JA Spudich
- JD Rioux
- Jeppe Mouritsen
- JJ Gu
- JK Burkhardt
- JM Golas
- L Jansson
- M Hasegawa
- M Sundvall
- MM Miller
- MV Adzemovic
- N Yazawa
- NA Patsopoulos
- O Crespo
- P Coutre le
- P Markel
- PA Zipfel
- PA Zipfel
- Q Wang
- RA Liberatore
- RT Paniagua
- Samra Sardar
- SE Baranzini
- SE Hernandez
- T Lindvall
- T Matsushita
- UC Rogner
- WD Bradley
- WS Huang
- Y Huang
- Y Wang
- Y Zhan
- YL Lin
- Z Lu
- Ă Andersson
- Ă sa Andersson
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
The magnetic RayleighâTaylor instability in solar prominences
- Author
- A Asai
- A Berlicki
- A Hillier
- A Hillier
- A Hillier
- A Hillier
- A Hillier
- A Hillier
- A Hillier
- A LĂłpez Ariste
- A LĂłpez Ariste
- A Miura
- AA Ballegooijen van
- AJ DĂaz
- AJ DĂaz
- AK Kulkarni
- AL Moser
- AS Hillier
- AZ Dolginov
- B Schmieder
- B Schmieder
- B-I Jun
- B-I Jun
- B-I Jun
- BJ Daly
- C Xia
- C Xia
- D Orozco SuĂĄrez
- D Orozco SuĂĄrez
- DE Innes
- DE Innes
- DE Innes
- DE McKenzie
- DH Mackay
- DL Youngs
- DR Williams
- DS Brown
- E Khomenko
- E Khomenko
- E Leonardis
- E Tandberg-Hanssen
- F Cattaneo
- F Reale
- FT Gratton
- G Aulanier
- G Aulanier
- G Dimonte
- G Stellmacher
- G Taylor
- G Toma de
- GJD Petrie
- H Isobe
- H Isobe
- H Takahashi
- HC Spruit
- HC Spruit
- HR Gilbert
- I Hachisu
- I Moortel De
- J Carlyle
- J Carlyle
- J Chae
- J Chae
- J DudĂk
- J Matsumoto
- J Terradas
- J Terradas
- J Terradas
- J Terradas
- J-J Aly
- JJ Hester
- JL Culhane
- JL Leroy
- JM Stone
- JM Stone
- JR Lemen
- JT Karpen
- JWS Blokland
- JWS Blokland
- K Ahn
- K Shibata
- K Shibata
- K Shibata
- KAP Singh
- L Driel-Gesztelyi van
- L-J Guo
- Lord Rayleigh
- M Dyke van
- M Kruskal
- M Kuperus
- M Liggett
- M Luna
- M Luna
- M Ryutova
- MC Kelley
- MS Freed
- MS Ruderman
- MS Ruderman
- N Labrosse
- N Labrosse
- O Engvold
- O Porth
- P Antolin
- P Heinzel
- P Heinzel
- PJ Levens
- R Casini
- R Keppens
- R Kippenhahn
- R Oliver
- RA Chevalier
- RA Chevalier
- RF Allen
- S Chandrasekhar
- S Gosain
- S GunĂĄr
- S Liberatore
- S Liberatore
- S Takasao
- S Toriumi
- S Tsuneta
- SL Savage
- SN Borovikov
- T Berger
- T Berger
- T Kaneko
- T Kaneko
- T Kaneko
- T Kosugi
- T Takahashi
- T Yokoyama
- T-J Cao
- TC Mouschovias
- TD Arber
- TE Berger
- TE Berger
- TE Berger
- TJ Okamoto
- TJ Okamoto
- TJ Okamoto
- TJ Okamoto
- U Anzer
- VM Nakariakov
- VS Titov
- X Zhai
- Y Lin
- Y Shen
- Y Su
- Y Su
- Z Sturrock
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Redox regulation of mitochondrial fission, protein misfolding, synaptic damage, and neuronal cell death: potential implications for Alzheimerâs and Parkinsonâs diseases
- Author
- A Nikolaev
- AB Knott
- AC Poole
- AK Lutz
- AM Isaacs
- AV Panov
- B Westermann
- BR Hu
- C Delettre
- C Haass
- C Hetz
- C Iadecola
- C Wang
- CR Chang
- D Trotti
- D Yao
- DG Breckenridge
- DH Cho
- DS Bredt
- DS Bredt
- DT Hess
- E Bonfoco
- E Bossy-Wetzel
- E Bossy-Wetzel
- E Bossy-Wetzel
- E Clementi
- EM Schuman
- ER Kandel
- ES Wong
- G Liot
- G Melino
- G Wang
- GE Hardingham
- GM Shankar
- GT Liberatore
- H Chen
- H Li
- H Shimura
- H Wang
- H Yuan
- HH Low
- HM Abu-Soud
- HR Waterham
- HS Chen
- HS Ko
- I Sliskovic
- J Emerit
- J Garthwaite
- J Haendeler
- JA White
- JB Mannick
- JC Greene
- JD Atkin
- JS Beckman
- JS Stamler
- JS Stamler
- JS Stamler
- JS Stamler
- JS Stamler
- JS Stamler
- JT Cribbs
- JW Olney
- JW Olney
- K Hirai
- K Kijima
- KJ Barnham
- KJ Conn
- KK Chung
- KK Chung
- KL Lim
- KN Houk
- KR Pitts
- L Nowak
- L Tenneti
- M Ankarcrona
- M Gu
- M Karbowski
- M Lafon-Cazal
- M Matos
- MF Beal
- MJ Barsoum
- MJ LaVoie
- ML Mayer
- MM Lyles
- MR Cookson
- MR Hara
- MT Lin
- MW Cleeter
- N Exner
- N Kang-Decker
- N Nakamura
- N Taguchi
- P Hantraye
- PE Chabrier
- PH Reddy
- PJ Muchowski
- PP Zhu
- Q Wang
- R Medeiros
- R Ramachandran
- R Yonashiro
- RA Quintanilla
- RJ Youle
- RK Dagda
- RL Frederick
- RV Rao
- S Dimmeler
- S Li
- S Papadia
- S Papadia
- S Przedborski
- S Tanaka
- S Wasiak
- S Zuchner
- SA Lipton
- SA Lipton
- SA Lipton
- SA Lipton
- SJ Baloyannis
- SL Budd
- SR Jaffrey
- Stuart A. Lipton
- SZ Lei
- T Kitada
- T Uehara
- TJ OâDell
- Tomohiro Nakamura
- VL Dawson
- VS Laar Van
- WD Parker Jr
- WK Kim
- WS Liang
- X Wang
- X Wang
- X Wang
- YB Choi
- Z Gu
- Z Huang
- Z Li
- Publication venue
- Springer US
- Publication date
- 01/01/2010
- Field of study
Normal mitochondrial dynamics consist of fission and fusion events giving rise to new mitochondria, a process termed mitochondrial biogenesis. However, several neurodegenerative disorders manifest aberrant mitochondrial dynamics, resulting in morphological abnormalities often associated with deficits in mitochondrial mobility and cell bioenergetics. Rarely, dysfunctional mitochondrial occur in a familial pattern due to genetic mutations, but much more commonly patients manifest sporadic forms of mitochondrial disability presumably related to a complex set of interactions of multiple genes (or their products) with environmental factors (GÂ ĂÂ E). Recent studies have shown that generation of excessive nitric oxide (NO), in part due to generation of oligomers of amyloid-ÎČ (AÎČ) protein or overactivity of the NMDA-subtype of glutamate receptor, can augment mitochondrial fission, leading to frank fragmentation of the mitochondria. S-Nitrosylation, a covalent redox reaction of NO with specific protein thiol groups, represents one mechanism contributing to NO-induced mitochondrial fragmentation, bioenergetic failure, synaptic damage, and eventually neuronal apoptosis. Here, we summarize our evidence in Alzheimerâs disease (AD) patients and animal models showing that NO contributes to mitochondrial fragmentation via S-nitrosylation of dynamin-related protein 1 (Drp1), a protein involved in mitochondrial fission. These findings may provide a new target for drug development in AD. Additionally, we review emerging evidence that redox reactions triggered by excessive levels of NO can contribute to protein misfolding, the hallmark of a number of neurodegenerative disorders, including AD and Parkinsonâs disease. For example, S-nitrosylation of parkin disrupts its E3 ubiquitin ligase activity, and thereby affects Lewy body formation and neuronal cell death
Microglial activation and chronic neurodegeneration
- Author
- A Czlonkowska
- A Flugel
- A Mildner
- A Nimmerjahn
- A Roy
- A Sasaki
- AC Murphy
- AJ Nimmo
- B Ajami
- B Liu
- B Liu
- B Liu
- BA Yankner
- BA Yankner
- BD Trapp
- BM Babior
- C Barcia
- C Cunningham
- C Knott
- C Speth
- CA Colton
- CA Jordan
- CC Chao
- CJ Henry
- CL Mack
- CM Long-Smith
- D Blum-Degen
- D Davalos
- D Soulet
- DA Gayle
- DC Wu
- DC Wu
- DW Moss
- E Polazzi
- EA Ling
- EC Hirsch
- ED Hall
- EE Olson
- EG McGeer
- F Alliot
- F Alliot
- F Aloisi
- F Cicchetti
- F Geissmann
- GL Finch
- GT Liberatore
- GW Kreutzberg
- H Konishi
- H Liao
- H Mao
- H Mao
- H Takeuchi
- HJ Forman
- HJ Nam
- HK Gao
- HM Gao
- HM Gao
- HM Gao
- HM Gao
- HM Gao
- HN Sun
- I Dalmau
- I Kurkowska-Jastrzebska
- J Rodriguez-Pallares
- J Rogers
- J Turchan-Cholewo
- J Turchan-Cholewo
- J Yamada
- JE Bell
- JK Harrison
- JK Lee
- JK Lee
- JP Godbout
- JW Langsten
- JW Langsten
- JW Peterson
- K Blinzinger
- K Sriram
- K Sriram
- K Sriram
- KJ Min
- KM Boje
- KR Miller
- KZ Guyton
- L Meda
- L Morris
- L Qian
- L Qin
- L Qin
- L Qin
- L Qin
- L Qin
- L Zecca
- LJ Lawson
- LJ Lawson
- M Mogi
- M Sawada
- M Tsuda
- MA Lynch
- MB Graeber
- MB Graeber
- ME Bamberger
- Melinda E. Lull
- Michelle L. Block
- MK McCoy
- ML Block
- ML Block
- ML Block
- ML Block
- ML Block
- ML Block
- ML Block
- MO Ziehn
- NA Brabers
- P Rezaie
- P Rio-Hortega del
- P Teismann
- PE Batchelor
- PE Batchelor
- PL McGeer
- PL McGeer
- PL McGeer
- PM Carvey
- PM Carvey
- Q Si
- R Schreck
- R Shechter
- RA Adams
- RB Banati
- RB Banati
- RM Hoek
- RM Ransohoff
- S Elkabes
- S Hunot
- S Lehnardt
- S Levesque
- S Pawate
- S Przedborski
- SC Lee
- SC Morgan
- SD Hurley
- SD Hurley
- SP Green
- SY Won
- T Morioka
- T Muller
- T Nagatsu
- T Nagatsu
- T Wang
- T Wang
- T Wang
- TC Frank-Cannon
- V Jackson-Lewis
- W Zhang
- W Zhang
- WF Hickey
- WJ Streit
- WJ Streit
- WJ Streit
- X Wu
- XF Wu
- Y Huh
- Y Li
- Y Liu
- Y Ouchi
- Y Ouchi
- Y Zhong
- YS Kim
- Z Ling
- Z Pei
- Z Siskova
- ZD Ling
- ZH Feng
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/10/2010
- Field of study
Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurode-generative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1ÎČ, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinsonâs disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype
Measurements of Higgs bosons decaying to bottom quarks from vector boson fusion production with the ATLAS experiment at â=13TeV
- Author
- Aad G
- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abud AA
- Abulaiti Y
- Acharya BS
- Achkar B
- Adam L
- Adamczyk L
- Adamek L
- Adelman J
- Adiguzel A
- Adorni S
- Adye T
- Affolder AA
- Afik Y
- Agapopoulou C
- Agaras MN
- Aggarwal A
- Agheorghiesei C
- Aguilar-Saavedra JA
- Agullo PM
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahnen JV
- Ai X
- Aielli G
- Akatsuka S
- Akbiyik M
- Akilli E
- Akimov AV
- Al Khoury K
- Alberghi GL
- Albert J
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi A
- Alfonsi F
- Alhroob M
- Ali B
- Ali S
- Aliev M
- Alimonti G
- Allaire C
- Allbrooke BMM
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alves FLL
- Alviggi MG
- Ambler A
- Ambroz L
- Amelung C
- Amidei D
- Amoroso S
- Amrouche CS
- Anastopoulos C
- Andari N
- Andeen T
- Anders JK
- Andrean SY
- Andreazza A
- Andrei V
- Anelli CR
- Angelidakis S
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antipov E
- Antonelli M
- Antrim DJA
- Anulli F
- Aoki M
- Aparo MA
- Aranda CP
- Aranzabal N
- Araya ST
- Arcangeletti C
- Arce ATH
- Arguin J-F
- Argyropoulos S
- Arling J-H
- Armbruster AJ
- Armstrong A
- Arnaez O
- Arnold H
- Artoni G
- Asada H
- Asai K
- Asai S
- Asawatavonvanich T
- Asbah NA
- Asimakopoulou EM
- Asquith L
- Assahsah J
- Assamagan K
- Astalos R
- Astigarraga MEP
- Atkin RJ
- Atkinson M
- Atlay NB
- Atmasiddha PA
- Augsten K
- Austrup VA
- Avolio G
- Ayoub MK
- Azuelos G
- Babal D
- Bachacou H
- Bachas K
- Backman F
- Bagnaia P
- Bahilo JJL
- Bahrasemani H
- Bailey AJ
- Bailey VR
- Baines JT
- Bakalis C
- Baker OK
- Bakker PJ
- Bakos E
- Balaji S
- Balasubramanian R
- Baldin EM
- Balek P
- Balli F
- Balunas WK
- Balz J
- Banas E
- Bandieramonte M
- Bandyopadhyay A
- Barak L
- Barbe WM
- Barberio EL
- Barberis D
- Barbero M
- Barbour G
- Barillari T
- Barisits M-S
- Barkeloo J
- Barklow T
- Barnett BM
- Barnett RM
- Barnovska-Blenessy Z
- Baroncelli A
- Barone G
- Barr AJ
- Barreiro F
- Barron U
- Barsov S
- Bartels F
- Bartoldus R
- Bartolini G
- Barton AE
- Bartos P
- Basalaev A
- Basan A
- Bassalat A
- Basso MJ
- Basson CR
- Bates RL
- Batlamous S
- Batley JR
- Batool B
- Battaglia M
- Bauce M
- Bauer F
- Bauer P
- Bawa HS
- Bayirli A
- Beacham JB
- Beau T
- Beauchemin PH
- Becherer F
- Bechtle P
- Beck HP
- Becker K
- Becot C
- Beddall AJ
- Bednyakov VA
- Bee CP
- Beermann TA
- Begalli M
- Begel M
- Behera A
- Behr JK
- Beisiegel F
- Belfkir M
- Bella G
- Bella LA
- Bellagamba L
- Bellerive A
- Bello FAD
- Bellos P
- Beloborodov K
- Belotskiy K
- Belyaev NL
- Benchekroun D
- Benekos N
- Benhammou Y
- Benjamin DP
- Benoit M
- Bensinger JR
- Bentvelsen S
- Beresford L
- Beretta M
- Berge D
- Berger N
- Bergmann B
- Bergsten LJ
- Beringer J
- Berlendis S
- Berlingen JM
- Bernardi G
- Bernius C
- Bernlochner FU
- Berry T
- Berta P
- Berthold A
- Bertram IA
- Bethke S
- Betti A
- Bevan AJ
- Bhatta S
- Bhattacharya DS
- Bhattarai P
- Bhopatkar VS
- Bi R
- Bianchi RM
- Biebel O
- Biedermann D
- Bielski R
- Bierwagen K
- Biesuz NV
- Biglietti M
- Billoud TRV
- Bindi M
- Bingul A
- Bini C
- Biondi S
- Birch-sykes CJ
- Birman M
- Bisanz T
- Biswal JP
- Biswas D
- Bitadze A
- Bittrich C
- BjĂžrke K
- Blazek T
- Bloch I
- Blocker C
- Blue A
- Blumenschein U
- Bobbink GJ
- Bobrovnikov VS
- Boeriu OEV
- Bogavac D
- Bogdanchikov AG
- Bohm C
- Boisvert V
- Bokan P
- Bolanos GR
- Bold T
- Bomben M
- Bona M
- Bonilla JS
- Boonekamp M
- Booth CD
- Borbély AG
- Borecka-Bielska HM
- Borgna LS
- Borisov A
- Borissov G
- Bortoletto D
- Bosca SR
- Boscherini D
- Bosman M
- Bostanabad MG
- Bouaouda K
- Boudreau J
- Bouhova-Thacker EV
- Boumediene D
- Bouquet R
- Bourdarios CA
- Boveia A
- Boyd J
- Boye D
- Boyko IR
- Bozson AJ
- Bracinik J
- Brahimi N
- Brandt G
- Brandt O
- Braren F
- Brau B
- Brau JE
- Brendlinger K
- Brener R
- Brenner L
- Brenner R
- Bressler S
- Bret MC
- Brickwedde B
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- Buschmann E
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- Butterworth JM
- Buttinger W
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- Calace N
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- Calvet D
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- Cheremushkina E
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- Chevalérias TJA
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- Chitan A
- Chiu I
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- Cieri D
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- Ciocio A
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- da Costa JBG
- Da Cunha Sargedas De Sousa MJ
- Da Fonseca Pinto JV
- Da Via C
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- Yexley MR
- Yildiz HD
- Yin P
- Yorita K
- Yoshihara K
- Young C
- Young CJS
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- Zaazoua M
- Zabinski B
- Zacharis G
- Zaffaroni E
- Zagazeta LFG
- Zahreddine J
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- Zakharchuk N
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- Zeitnitz C
- ZeiĂner SV
- Zemaityte G
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- Zhang X
- Zhang Y
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- Zhao Y
- Zhao Z
- Zhemchugov A
- Zheng Z
- Zhong D
- Zhou B
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- Zhou H
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- Zhu C
- Zhu CG
- Zhu H
- Zhu HL
- Zhu J
- Zhu Y
- Zhuang X
- Zhukov K
- Zhulanov V
- Zieminska D
- Zimine NI
- Zimmermann S
- Zinonos Z
- Ziolkowski M
- Zoccoli A
- Zoch K
- Zorbas TG
- Zou R
- Zwalinski L
- Ă kesson TPA
- Ăncel ĂO
- ĆœeniĆĄ T
- ĆœivkoviÄ L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 23/06/2021
- Field of study
The paper presents a measurement of the Standard Model Higgs Boson decaying to b-quark pairs in the vector boson fusion (VBF) production mode. A sample corresponding to 126 fbâ1 of sâ=13TeV protonâproton collision data, collected with the ATLAS experiment at the Large Hadron Collider, is analyzed utilizing an adversarial neural network for event classification. The signal strength, defined as the ratio of the measured signal yield to that predicted by the Standard Model for VBF Higgs production, is measured to be 0.95+0.38â0.36 , corresponding to an observed (expected) significance of 2.6 (2.8) standard deviations from the background only hypothesis. The results are additionally combined with an analysis of Higgs bosons decaying to b-quarks, produced via VBF in association with a photon
Muon reconstruction and identification efficiency in ATLAS using the full Run 2 pp collision data set at \sqrt{s}=13 TeV
- Author
- Aad G
- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abud AA
- Abulaiti Y
- Acharya BS
- Achkar B
- Adam L
- Adamczyk L
- Adamek L
- Adelman J
- Adiguzel A
- Adorni S
- Adye T
- Affolder AA
- Afik Y
- Agapopoulou C
- Agaras MN
- Aggarwal A
- Agheorghiesei C
- Aguilar-Saavedra JA
- Agullo PM
- Ahmad A
- Ahmadov F
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- Ahnen JV
- Ai X
- Aielli G
- Akatsuka S
- Akbiyik M
- Akesson TPA
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- Alberghi GL
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- Aleksa M
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- Zhemchugov A
- Zheng Z
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- Zorbas TG
- Zou R
- Zwalinski L
- Publication venue
- 'Springer Fachmedien Wiesbaden GmbH'
- Publication date
- 01/01/2021
- Field of study
This article documents the muon reconstruction and identification efficiency obtained by the ATLAS experiment for 139 \hbox {fb}^{-1} of pp collision data at \sqrt{s}=13 TeV collected between 2015 and 2018 during Run 2 of the LHC. The increased instantaneous luminosity delivered by the LHC over this period required a reoptimisation of the criteria for the identification of prompt muons. Improved and newly developed algorithms were deployed to preserve high muon identification efficiency with a low misidentification rate and good momentum resolution. The availability of large samples of Z\rightarrow \mu \mu and J/\psi \rightarrow \mu \mu decays, and the minimisation of systematic uncertainties, allows the efficiencies of criteria for muon identification, primary vertex association, and isolation to be measured with an accuracy at the per-mille level in the bulk of the phase space, and up to the percent level in complex kinematic configurations. Excellent performance is achieved over a range of transverse momenta from 3 GeV to several hundred GeV, and across the full muon detector acceptance of |\eta |<2.7
Dijet Resonance Search with Weak Supervision Using root S=13 TeV pp Collisions in the ATLAS Detector
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- Zhemchugov A
- Zheng Z
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- Zimmermann S
- Zinonos Z
- Ziolkowski M
- Zivkovic L
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- Zorbas TG
- Zou R
- Zu Theenhausen HM
- Zwalinski L
- Publication venue
- AMER PHYSICAL SOC
- Publication date
- 25/09/2020
- Field of study
This Letter describes a search for narrowly resonant new physics using a machine-learning anomaly
detection procedure that does not rely on signal simulations for developing the analysis selection. Weakly
supervised learning is used to train classifiers directly on data to enhance potential signals. The targeted
topology is dijet events and the features used for machine learning are the masses of the two jets. The
resulting analysis is essentially a three-dimensional search A â BC, for mA ⌠OĂ°TeVĂ, mB; mC âŒ
OĂ°100 GeVĂ and B, C are reconstructed as large-radius jets, without paying a penalty associated with
a large trials factor in the scan of the masses of the two jets. The full run 2 ffiffi
s p Œ 13 TeV pp collision
dataset of 139 fbâ1 recorded by the ATLAS detector at the Large Hadron Collider is used for the search.
There is no significant evidence of a localized excess in the dijet invariant mass spectrum between 1.8 and
8.2 TeV. Cross-section limits for narrow-width A, B, and C particles vary with mA, mB, and mC. For
example, when mA ÂŒ 3 TeV and mB âł 200 GeV, a production cross section between 1 and 5 fb is
excluded at 95% confidence level, depending on mC. For certain masses, these limits are up to 10 times
more sensitive than those obtained by the inclusive dijet search. These results are complementary to the
dedicated searches for the case that B and C are standard model boson
Measurement of the ttÂŻttÂŻ production cross section in pp collisions at âs=13 TeV with the ATLAS detector
- Author
- Aad G
- Abbott B
- Abbott DC
- Abed Abud A
- Abeling K
- Abhayasinghe DK
- Abidi SH
- Abramowicz H
- Abreu H
- Abulaiti Y
- Abusleme Hoffman AC
- Acharya BS
- Achkar B
- Adam Bourdarios C
- Adam L
- Adamczyk L
- Adamek L
- Adelman J
- Adiguzel A
- Adorni S
- Adye T
- Affolder AA
- Afik Y
- Agapopoulou C
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Aguilar-Saavedra JA
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ai X
- Aielli G
- Akatsuka S
- Akbiyik M
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- Ă kesson TPA
- Ăncel ĂO
- ĆœeniĆĄ T
- ĆœivkoviÄ L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 16/11/2021
- Field of study
A measurement of four-top-quark production using proton-proton collision data at a centre-of-mass energy of 13 TeV collected by the ATLAS detector at the Large Hadron Collider corresponding to an integrated luminosity of 139 fbâ1 is presented. Events are selected if they contain a single lepton (electron or muon) or an opposite-sign lepton pair, in association with multiple jets. The events are categorised according to the number of jets and how likely these are to contain b-hadrons. A multivariate technique is then used to discriminate between signal and background events. The measured four-top-quark production cross section is found to be 26+17â15 fb, with a corresponding observed (expected) significance of 1.9 (1.0) standard deviations over the background-only hypothesis. The result is combined with the previous measurement performed by the ATLAS Collaboration in the multilepton final state. The combined four-top-quark production cross section is measured to be 24+7â6 fb, with a corresponding observed (expected) signal significance of 4.7 (2.6) standard deviations over the background-only predictions. It is consistent within 2.0 standard deviations with the Standard Model expectation of 12.0 ± 2.4 fb
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