398 research outputs found
ENU Mutagenesis Identifies Mice with Morbid Obesity and Severe Hyperinsulinemia Caused by a Novel Mutation in Leptin
- Author
- A Hinney
- A Strobel
- AD Strosberg
- B Dummler
- BC Moon
- C Jurinke
- Chen-Jee Hong
- Chia-Ning Yang
- Chih-Wei Hsu
- Chih-Ya Cheng
- Chuan-Kai Chou
- CT Montague
- D Chow
- ED Rosen
- EH Leiter
- F Peelman
- F Zhang
- F Zhang
- Gian Paolo Fadini
- H Knobelspies
- Huei-Fen Jheng
- I Mazen
- Irene H. Cheng
- IS Farooqi
- J Bravo
- J Folch
- JM Friedman
- JS Weber
- L Brunner
- L Holm
- L Niv-Spector
- L Niv-Spector
- L Zabeau
- L Zabeau
- M Di Girolamo
- M Haluzik
- MJ Boulanger
- MP Rutkowski
- Pei-Jane Tsai
- SA Verploegen
- Shih-Jen Tsai
- Shiow-Yi Chen
- SM Echwald
- TM Fong
- Y Sandowski
- Y Wang
- Y Zhang
- Ya-Tzu Lin
- Yau-Sheng Tsai
- Ying-Jay Liou
- You-Chung Chuang
- YS Tsai
- Publication venue
- Public Library of Science
- Publication date
- 09/12/2010
- Field of study
BACKGROUND: Obesity is a multifactorial disease that arises from complex interactions between genetic predisposition and environmental factors. Leptin is central to the regulation of energy metabolism and control of body weight in mammals. METHODOLOGY/PRINCIPAL FINDINGS: To better recapitulate the complexity of human obesity syndrome, we applied N-ethyl-N-nitrosourea (ENU) mutagenesis in combination with a set of metabolic assays in screening mice for obesity. Mapping revealed linkage to the chromosome 6 within a region containing mouse Leptin gene. Sequencing on the candidate genes identified a novel T-to-A mutation in the third exon of Leptin gene, which translates to a V145E amino acid exchange in the leptin propeptide. Homozygous Leptin(145E/145E) mutant mice exhibited morbid obesity, accompanied by adipose hypertrophy, energy imbalance, and liver steatosis. This was further associated with severe insulin resistance, hyperinsulinemia, dyslipidemia, and hyperleptinemia, characteristics of human obesity syndrome. Hypothalamic leptin actions in inhibition of orexigenic peptides NPY and AgRP and induction of SOCS1 and SOCS3 were attenuated in Leptin(145E/145E) mice. Administration of exogenous wild-type leptin attenuated hyperphagia and body weight increase in Leptin(145E/145E) mice. However, mutant V145E leptin coimmunoprecipitated with leptin receptor, suggesting that the V145E mutation does not affect the binding of leptin to its receptor. Molecular modeling predicted that the mutated residue would form hydrogen bond with the adjacent residues, potentially affecting the structure and formation of an active complex with leptin receptor within that region. CONCLUSIONS/SIGNIFICANCE: Thus, our evolutionary, structural, and in vivo metabolic information suggests the residue 145 as of special function significance. The mouse model harboring leptin V145E mutation will provide new information on the current understanding of leptin biology and novel mouse model for the study of human obesity syndrome
Comparative Analysis of Acid Sphingomyelinase Distribution in the CNS of Rats and Mice Following Intracerebroventricular Delivery
- Author
- A Amalfitano
- AM Cook
- AR Leventhal
- Christopher M. Treleaven
- DE Smith
- EA Obbens
- ED Kakkis
- EH Schuchman
- EJ Mufson
- HK Jin
- HK Jin
- James C. Dodge
- JC Dodge
- JC Dodge
- Jonathan A. Fidler
- K Slusarczyk
- KG Kapoor
- Lamya S. Shihabuddin
- LS Shihabuddin
- MA Passini
- MA Passini
- Mel Feany
- MR Del Bigio
- MS Luer
- NW Barton
- NW Barton
- P Harmatz
- R Hurwitz
- R Schiffmann
- R Tripathi
- Seng H. Cheng
- SJ Haines
- Tatyana V. Taksir
- Thomas Tamsett
- VC Anderson
- WW Yang
- YA Ioannou
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2010
- Field of study
Niemann-Pick A (NPA) disease is a lysosomal storage disorder (LSD) caused by a deficiency in acid sphingomyelinase (ASM) activity. Previously, we reported that biochemical and functional abnormalities observed in ASM knockout (ASMKO) mice could be partially alleviated by intracerebroventricular (ICV) infusion of hASM. We now show that this route of delivery also results in widespread enzyme distribution throughout the rat brain and spinal cord. However, enzyme diffusion into CNS parenchyma did not occur in a linear dose-dependent fashion. Moreover, although the levels of hASM detected in the rat CNS were determined to be within the range shown to be therapeutic in ASMKO mice, the absolute amounts represented less than 1% of the total dose administered. Finally, our results also showed that similar levels of enzyme distribution are achieved across rodent species when the dose is normalized to CNS weight as opposed to whole body weight. Collectively, these data suggest that the efficacy observed following ICV delivery of hASM in ASMKO mice could be scaled to CNS of the rat
Notch signaling contributes to the maintenance of both normal neural stem cells and patient-derived glioma stem cells
- Author
- A Aguirre
- A Louvi
- A Wu
- AH Shih
- AR Hallahan
- BW Purow
- CN Svendsen
- D Bonnet
- E Hulleman
- EH Schroeter
- F Gao
- Fang Gao
- G Struhl
- Gang Cheng
- GP Dotto
- HD Hemmati
- Hua Han
- JD Hoeck
- JS Nye
- K Mizutani
- K Tanigaki
- KE Hovinga
- Liang Li
- Liang Liang
- LS Campos
- Luo-An Fu
- M Al-Hajj
- Min-Hua Zheng
- MJ Go
- MS Jang
- R Chen
- R Galli
- S Hitoshi
- S Jarriault
- S Ma
- S Weijzen
- SK Singh
- SK Singh
- T Palomero
- T Reya
- TN Ignatova
- TO Alexson
- X Fan
- X Fan
- X Yuan
- XP Zhang
- Ya-Ning Wei
- Yi-Yang Hu
- Publication venue
- BioMed Central
- Publication date
- 01/01/2011
- Field of study
<p>Abstract</p> <p>Background</p> <p>Cancer stem cells (CSCs) play an important role in the development and recurrence of malignant tumors including glioma. Notch signaling, an evolutionarily conserved pathway mediating direct cell-cell interaction, has been shown to regulate neural stem cells (NSCs) and glioma stem cells (GSCs) in normal neurogenesis and pathological carcinogenesis, respectively. However, how Notch signaling regulates the proliferation and differentiation of GSCs has not been well elucidated.</p> <p>Methods</p> <p>We isolated and cultivate human GSCs from glioma patient specimens. Then on parallel comparison with NSCs, we inhibited Notch signaling using γ-secretase inhibitors (GSI) and assessed the potential functions of Notch signaling in human GSCs.</p> <p>Results</p> <p>Similar to the GSI-treated NSCs, the number of the primary and secondary tumor spheres from GSI-treated GSCs decreased significantly, suggesting that the proliferation and self-renewal ability of GSI-treated GSCs were attenuated. GSI-treated GSCs showed increased differentiation into mature neural cell types in differentiation medium, similar to GSI-treated NSCs. Next, we found that GSI-treated tumor spheres were composed of more intermediate progenitors instead of CSCs, compared with the controls. Interestingly, although inhibition of Notch signaling decreased the ratio of proliferating NSCs in long term culture, we found that the ratio of G2+M phase-GSCs were almost undisturbed on GSI treatment within 72 h.</p> <p>Conclusions</p> <p>These data indicate that like NSCs, Notch signaling maintains the patient-derived GSCs by promoting their self-renewal and inhibiting their differentiation, and support that Notch signal inhibitor GSI might be a prosperous candidate of the treatment targeting CSCs for gliomas, however, with GSI-resistance at the early stage of GSCs cell cycle.</p
Tumor-targeted delivery of biologically active TRAIL protein
- Author
- A Ashkenazi
- A Nesterov
- A-L Li
- B Liang
- B-F Jin
- C-H Wang
- CA Smith
- CH Contag
- CH Lee
- CM Cheng
- D Gericke
- D Lawrence
- DH Thamm
- EH Thiele
- EV Shashkova
- GH Pan
- H Walczak
- H Walczak
- H-Y Li
- H-Y Zhang
- J Nemunaitis
- J Zhao
- J-H Man
- JF Toso
- JM Wilson
- JR Mose
- JS Yoo
- K He
- KB Low
- KP Francis
- M Jo
- M Leverkus
- M Zhao
- M Zhao
- M Zhao
- ME Fox
- ME Wohlfahrt
- N Agrawal
- NK Green
- P-J Zhang
- RC Parker
- RJ Armitage
- RM Ryan
- RS Herbst
- S Armeanu
- SH Kim
- SK Kelley
- SR Wiley
- T Li
- T Sasaki
- T Zhou
- TS Griffith
- TY Lin
- W Fu
- W-H Li
- W-L Gong
- X Pan
- X-M Zhang
- Y Wang
- YA Yu
- YF Xu
- Publication venue
- Nature Publishing Group
- Publication date
- Field of study
The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a potent inducer of tumor cell apoptosis, but concerns of considerable liver toxicity limit its uses in human cancer therapy. Here, we show that i.v. injected Escherichia coli DH5α (E. coli DH5α) specifically replicates in solid tumors and metastases in live animals. E. coli DH5α does not enter tumor cells and suits for being the vector for soluble TRAIL (sTRAIL), which induces apoptosis by activating cell-surface death receptors. With the high ‘tumor-targeting' nature, we demonstrate that intratumoral (i.t.) and intravenous injection of sTRAIL-expressing E. coli DH5α results in the tumor-targeted release of biologically active molecules, which leads to a dramatic reduction in the tumor growth rate and the prolonged survival of tumor-bearing mice. TRAIL delivery by E. coli DH5α did not cause any detectable toxicity to any organs, suggesting that E. coli DH5α-delivered sTRAIL protein therapy may provide a feasible and effective form of treatment for solid tumors
Matrix Metalloproteinase-Induced Epithelial-Mesenchymal Transition in Breast Cancer
- Author
- A Ahmad
- A Boire
- A Gutierrez-Fernandez
- A Lochter
- A Lochter
- A Page-McCaw
- A Saghatelian
- A Schnelzer
- A Singh
- AM Martorana
- AS Ribeiro
- AY Strongin
- B Fingleton
- B Fingleton
- B Laffin
- BC Willis
- BG Rao
- BI Ratnikov
- BS Wiseman
- BS Wiseman
- C Gilles
- C Gilles
- C Gilles
- CJ Sympson
- CJ Sympson
- CM Overall
- CM Overall
- CM Overall
- CS Chen
- D Fiegen
- D Sarrio
- D Shook
- DC Radisky
- DC Radisky
- DC Radisky
- DC Radisky
- Derek C. Radisky
- DH Cai
- DH Cai
- E Janda
- E Morgunova
- E Roeb
- EH Lee
- EI Deryugina
- EM Tam
- ES Kim
- Evette S. Radisky
- F Moinfar
- FJ Moy
- FJ Vizoso
- G Finak
- G Rosenblum
- G Zheng
- GA McQuibban
- GA McQuibban
- GI Goldberg
- H Hugo
- H Kouros-Mehr
- H Matter
- H Mori
- H Mori
- H Nagase
- H Piccard
- HC Lien
- HY Ha
- I Bertini
- I Bertini
- I Ota
- IY Kim
- J Cao
- J Nightingale
- JA Allan
- JA Jacobsen
- JA Sparano
- JA West-Mays
- JB Buchanan
- JE Fata
- JF Fisher
- JH Li
- JL Duband
- JL Lauer-Fields
- JM Casar Del
- JP Thiery
- JP Witty
- K Almholt
- K Mori
- KD Cowden Dahl
- KD Miller
- KD Miller
- KJ Heppner
- KL Andarawewa
- L Chung
- L Devy
- L Ronnov-Jessen
- L Szabova
- LA Rudolph-Owen
- LE Kelemen
- LM Coussens
- LM Matrisian
- M Egeblad
- M Gioia
- M Ikejiri
- M Jechlinger
- M Kajita
- MD Martin
- MD Martin
- MD Sternlicht
- MD Sternlicht
- MD Sternlicht
- MH Lee
- MH Lee
- N Ramos-DeSimone
- NF Boyd
- NF Boyd
- OW Petersen
- P Jordan
- P Matos
- PA Rupp
- PE Steen Van den
- Q Meng
- Q Yu
- R Masson
- R Visse
- RA Bright
- RA Williamson
- S Cheng
- S Cheng
- S Faouzi
- S Monaco
- S Thiolloy
- S Urbanski
- S Wei
- SA Bartow
- SA Illman
- SM Alexander
- SR Wellings
- TD Duong
- TM Allington
- V Cantemir
- V Montel
- V Noe
- V Quesada
- W Song
- W Xian
- Y Hirai
- Y Hirai
- Y Ogata
- YA Wang
- Publication venue
- Springer US
- Publication date
- 01/01/2010
- Field of study
Matrix metalloproteinases (MMPs) degrade and modify the extracellular matrix (ECM) as well as cell-ECM and cell-cell contacts, facilitating detachment of epithelial cells from the surrounding tissue. MMPs play key functions in embryonic development and mammary gland branching morphogenesis, but they are also upregulated in breast cancer, where they stimulate tumorigenesis, cancer cell invasion and metastasis. MMPs have been investigated as potential targets for cancer therapy, but clinical trials using broad-spectrum MMP inhibitors yielded disappointing results, due in part to lack of specificity toward individual MMPs and specific stages of tumor development. Epithelial-mesenchymal transition (EMT) is a developmental process in which epithelial cells take on the characteristics of invasive mesenchymal cells, and activation of EMT has been implicated in tumor progression. Recent findings have implicated MMPs as promoters and mediators of developmental and pathogenic EMT processes in the breast. In this review, we will summarize recent studies showing how MMPs activate EMT in mammary gland development and in breast cancer, and how MMPs mediate breast cancer cell motility, invasion, and EMT-driven breast cancer progression. We also suggest approaches to inhibit these MMP-mediated malignant processes for therapeutic benefit
Measurement of the cross section for inclusive isolated-photon production in pp collisions at √s=13TeV using the ATLAS detector
- Author
- Aaboud M
- Aad G
- Abbott B
- Abdinov O
- Abeloos B
- Abidi SH
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abreu R
- Abulaiti Y
- Acharya BS
- Adachi S
- Adamczyk L
- Adelman J
- Adersberger M
- Adye T
- Affolder AA
- Afik Y
- Agatonovic-Jovin T
- Agheorghiesei C
- Aguilar-Saavedra JA
- Ahlen SP
- Ahmadov F
- Aielli G
- Akatsuka S
- Akerstedt H
- Akesson TPA
- Akilli E
- Akimov AV
- Alberghi GL
- Albert J
- Albicocco P
- Alconada Verzini MJ
- Alderweireldt SC
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexander G
- Alexopoulos T
- Alhroob M
- Ali B
- Aliev M
- Alimonti G
- Alison J
- Alkire SP
- Allbrooke BMM
- Allen BW
- Allport PP
- Aloisio A
- Alonso A
- Alonso F
- Alpigiani C
- Alshehri AA
- Alstaty MI
- Alvarez Piqueras D
- Alviggi MG
- Amadio BT
- Amelung C
- Amidei D
- Amor Dos Santos SP
- Amoroso S
- Amundsen G
- Anastopoulos C
- Ancu LS
- Andari N
- Andeen T
- Anders CF
- Anders JK
- Anderson KJ
- Andreazza A
- Andrei V
- Angelidakis S
- Angelozzi I
- Angerami A
- Anisenkov AV
- Anjos N
- Annovi A
- Antel C
- Antonelli M
- Antonov A
- Antrim DJ
- Anulli F
- Aoki M
- Arabidze G
- Arai Y
- Araque JP
- Araujo Ferraz V
- Araya ST
- Arce ATH
- Ardell RE
- Arduh FA
- Arguin J-F
- Argyropoulos S
- Arik M
- Armbruster AJ
- Armitage LJ
- Arnaez O
- Arnold H
- Arratia M
- Arslan O
- Artamonov A
- Artoni G
- Artz S
- Asai S
- Asbah N
- Ashkenazi A
- Asquith L
- Assamagan K
- Astalos R
- Astigarraga MEP
- Atkinson M
- Atlay NB
- Augsten K
- Avolio G
- Axen B
- Ayoub MK
- Azuelos G
- Baas AE
- Baca MJ
- Bachacou H
- Bachas K
- Backes M
- Bagnaia P
- Bahmani M
- Bahrasemani H
- Baines JT
- Bajic M
- Baker OK
- Bakker PJ
- Baldin EM
- Balek P
- Balli F
- Balunas WK
- Banas E
- Bandyopadhyay A
- Banerjee S
- Bannoura AAE
- Barajas CAC
- Barak L
- Barberio EL
- Barberis D
- Barbero M
- Barillari T
- Barisits M-S
- Barkeloo JT
- Barklow T
- Barlow N
- Barnes SL
- Barnett BM
- Barnett RM
- Barnovska-Blenessy Z
- Baroncelli A
- Barone G
- Barr AJ
- Barranco Navarro L
- Barreiro F
- Bartoldus R
- Barton AE
- Bartos P
- Basalaev A
- Bassalat A
- Bates RL
- Batista SJ
- Batley JR
- Battaglia M
- Bauce M
- Bauer F
- 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
- Behr JK
- Bell AS
- Bella G
- Bella LA
- Bellagamba L
- Bellerive A
- Bellomo M
- Belotskiy K
- Beltramello O
- Belyaev NL
- Benary O
- Benchekroun D
- Bender M
- Benekos N
- Benhammou Y
- Benitez J
- Benjamin DP
- Benoit M
- Bensinger JR
- Bentvelsen S
- Beresford L
- Beretta M
- Berge D
- Berger N
- Bergsten LJ
- Beringer J
- Berlendis S
- Berlingen JM
- Bernard NR
- Bernardi G
- Bernius C
- Bernlochner FU
- Berry T
- Berta P
- Bertella C
- Bertoli G
- Bertram IA
- Bertsche C
- Besjes GJ
- 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
- Bilokon H
- Bindi M
- Bingul A
- Bini C
- Biondi S
- Bisanz T
- 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
- Bock C
- Boehler M
- Boeriu OEV
- Boerner D
- Bogavac D
- Bogdanchikov AG
- Bohm C
- Boisvert V
- Bokan P
- Bold T
- Boldyrev AS
- Bolz AE
- Bomben M
- Bona M
- Boonekamp M
- Borisov A
- Borissov G
- Bortfeldt J
- Bortoletto D
- Bortolotto V
- Boscherini D
- Bosman M
- Boudreau J
- Bouhova-Thacker EV
- Boumediene D
- Bourdarios C
- Boutle SK
- Boveia A
- Boyd J
- Boyko IR
- Bozson AJ
- Bracinik J
- Brandt A
- Brandt G
- Brandt O
- Braren F
- Bratzler U
- Brau B
- Brau JE
- Bravo AG
- Brendlinger K
- Brennan AJ
- Brenner L
- Brenner R
- Bressler S
- Bret MC
- Briglin DL
- Bristow TM
- Britton D
- Britzger D
- Brochu FM
- Brock I
- Brock R
- Brooijmans G
- Brooks T
- Brooks WK
- Brosamer J
- Brost E
- Broughton JH
- Bruncko D
- Bruni A
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- Bruni LS
- Bruno S
- Brunt BH
- Bruschi M
- Bruscino N
- Bryant P
- Bryngemark L
- Buanes T
- Buat Q
- Buchholz P
- Buckley AG
- Budagov IA
- Buehrer F
- Bugge MK
- Bulekov O
- Bullock D
- Burch TJ
- Burdin S
- Burgard CD
- Burger AM
- Burghgrave B
- Burka K
- Burke S
- Burmeister I
- Burr JTP
- Buscher D
- Buscher V
- Bussey P
- Butler JM
- Buttar CM
- Butterworth JM
- Butti P
- Buttinger W
- Buzatu A
- Buzykaev AR
- Bylund OB
- Cabrera Urban S
- Caforio D
- Cai H
- Cairo VM
- Cakir IT
- 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
- Camarda S
- Camarri P
- Cameron D
- Caminal Armadans R
- Camincher C
- Campana S
- Campanelli M
- Camplani A
- Campoverde A
- Canale V
- Cantero J
- Cao T
- Caprini I
- Caprini M
- Capua M
- Carbone RM
- Cardarelli R
- Cardillo F
- Carli I
- Carli T
- Carlino G
- Carlson BT
- Carminati L
- Carney RMD
- Caron S
- Carquin E
- Carra S
- Carrillo-Montoya GD
- Casadei D
- Casado MP
- Casha AF
- Casolino M
- Casper DW
- Castelijn R
- Castillo Gimenez V
- Castillo IS
- Castillo LRF
- 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
- Chau CC
- Che S
- Cheatham S
- Chegwidden A
- Chekanov S
- Chekulaev SV
- Chelkov GA
- Chelstowska MA
- Chen C
- Chen C
- Chen H
- Chen J
- Chen S
- Chen S
- Chen X
- Chen Y
- Cheng HC
- Cheng HJ
- Cheplakov A
- Cheremushkina E
- Cheu E
- Cheung K
- Chevalier L
- Chiarella V
- Chiarelli G
- Chiodini G
- Chisholm AS
- Chitan A
- Chiu YH
- Chizhov MV
- Choi K
- Chomont AR
- Chouridou S
- Chow YS
- Christodoulou V
- Chu MC
- Chudoba J
- Chuinard AJ
- Chwastowski JJ
- Chytka L
- Ciftci AK
- Cinca D
- Cindro V
- Cioara IA
- Ciocio A
- Cirotto F
- Citron ZH
- Citterio M
- Ciubancan M
- Clark A
- Clark BL
- Clark MR
- Clark PJ
- Clarke RN
- Clement C
- Coadou Y
- Cobal M
- Coccaro A
- Cochran J
- Colasurdo L
- Cole B
- Colijn AP
- Collaboration ATLAS
- Collot J
- Colombo T
- Conde Muino P
- Coniavitis E
- Connell SH
- Connelly IA
- Constantinescu S
- Conti G
- Conventi F
- Cooke M
- Cooper-Sarkar AM
- Corga KDV
- Cormier F
- Cormier KJR
- Cornell SD
- Corradi M
- Correia AMH
- Corriveau F
- Cortes-Gonzalez A
- Costa G
- Costa MJ
- Costanzo D
- Cottin G
- Coutinho YA
- Cowan G
- Cox BE
- Cranmer K
- Crawley SJ
- Creager RA
- Cree G
- Crepe-Renaudin S
- Crescioli F
- Cribbs WA
- Cristinziani M
- Croft V
- Crosetti G
- Cueto A
- Cukierman AR
- Cummings J
- Curatolo M
- Cuth J
- Czekierda S
- Czodrowski P
- D'amen G
- D'Auria S
- D'eramo L
- D'Onofrio M
- Da Costa JGPF
- Da Via C
- Dabrowski W
- Dado T
- Dai T
- Dale O
- Dallaire F
- Dallapiccola C
- Dam M
- Damazio DO
- Dandoy JR
- Daneri MF
- Dang NP
- Daniells AC
- Dann NS
- Danninger M
- Dao V
- Darbo G
- Darmora S
- Dassoulas J
- Dattagupta A
- Daubney T
- Davey W
- David C
- Davidek T
- Davis DR
- Davison P
- Dawe E
- Dawson I
- de Asmundis R
- De Benedetti A
- De Bruin PHS
- De Castro S
- De Cecco S
- De Groot N
- de Jong P
- De la Torre H
- De Lorenzi F
- De Maria A
- De Pedis D
- De Regie JBDV
- de Renstrom PAB
- De Salvo A
- De Sanctis U
- De Santo A
- De K
- Debbe R
- Debenedetti C
- Dedovich DV
- Dehghanian N
- Deigaard I
- Del Gaudio M
- Del Peso J
- Delgove D
- Deliot F
- Delitzsch CM
- Dell'Acqua A
- Dell'Asta L
- Dell'Orso M
- Della Pietra M
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- Wingerter-Seez I
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- Winklmeier E
- Winston OJ
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- Wittgen M
- Wobisch M
- Wolf' TMH
- Wolf A
- Wolff R
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- Wong VWS
- Woods NL
- Worm SD
- Wosiek BK
- Wotschack J
- Wozniak KW
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- Yang Z
- Yao W-M
- Yap YC
- Yasu Y
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- Ye J
- Ye S
- Yeletskikh I
- Yigitbasi E
- Yildirim E
- Yildiz HD
- Yorita K
- Yoshihara K
- Young C
- Young CJS
- Yu J
- Yu J
- Yuen SPY
- Yusuff I
- Zabinski B
- Zacharis G
- Zaidan R
- Zaitsev AM
- Zakharchuk N
- Zalieckas J
- Zaman A
- Zambito S
- Zanzi D
- Zeitnitz C
- Zemaityte G
- Zemla A
- Zeng JC
- Zeng Q
- Zenin O
- Zenis T
- Zerwas D
- Zhang D
- Zhang D
- Zhang F
- Zhang G
- Zhang H
- Zhang J
- Zhang L
- Zhang L
- Zhang M
- Zhang P
- Zhang R
- Zhang R
- Zhang X
- Zhang Y
- Zhang Z
- Zhao X
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zhou B
- Zhou C
- Zhou L
- Zhou M
- Zhou M
- Zhou N
- Zhou Y
- Zhu CG
- Zhu H
- Zhu J
- Zhu Y
- Zhuang X
- Zhukov K
- Zibell A
- Zieminska D
- Zimine NI
- Zimmermann C
- Zimmermann S
- Zinonos Z
- Zinser M
- Ziolkowski M
- Zivkovic L
- Zobernig G
- Zoccoli A
- Zou R
- zur Nedden M
- Zwalinski L
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2017
- Field of study
Inclusive isolated-photon production in pp collisions at a centre-of-mass energy of 13TeVis studied with the ATLAS detector at the LHC using a data set with an integrated luminosity of 3.2fb−1. The cross section is measured as a function of the photon transverse energy above 125GeVin different regions of photon pseudorapidity. Next-to-leading-order perturbative QCD and Monte Carlo event-generator predictions are compared to the cross-section measurements and provide an adequate description of the data
Combined measurement of differential and total cross sections in the H → γγ and the H → ZZ* → 4ℓ decay channels at s=13 TeV with the ATLAS detector
- Author
- Aaboud M
- Aad G
- Abbott B
- Abdinov O
- Abeloos B
- Abhayasinghe DK
- Abidi SH
- 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
- Akilli E
- Akimov AV
- Alberghi GL
- Albert J
- Albicocco P
- Alconada Verzini MJ
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- 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 Gonzalez B
- Alviggi MG
- Amadio BT
- Amaral Coutinho Y
- Ambroz L
- Amelung C
- Amidei D
- Amor Dos Santos SP
- 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
- Araujo Pereira R
- Arce ATH
- Ardell RE
- Arduh FA
- Arguin J-F
- Argyropoulos S
- 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
- Atkin RJ
- Atkinson M
- Atlas Collaboration
- Atlay NB
- Augsten K
- Avolio G
- Avramidou R
- Axen B
- Ayoub MK
- Azuelos G
- Baas AE
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- Yusuff I
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- Zaidan R
- Zaitsev AM
- Zakharchuk N
- Zalieckas J
- Zambito S
- Zanzi D
- Zaripovas DR
- Zeitnitz C
- Zeißner SV
- Zemaityte G
- Zeng JC
- Zeng Q
- Zenin O
- Zerwas D
- Zgubič M
- Zhang D
- Zhang DF
- Zhang F
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- Zhang H
- Zhang J
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- Zhang L
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- Zhang P
- Zhang R
- Zhang R
- Zhang X
- Zhang Y
- Zhang Z
- Zhao P
- Zhao X
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zhou B
- Zhou C
- Zhou L
- Zhou M
- Zhou MS
- Zhou N
- Zhou Y
- 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 Nedden M
- Zwalinski L
- Álvarez Piqueras D
- Åkesson TPA
- Šfiligoj T
- Ženiš T
- Živković L
- Publication venue
- Elsevier
- Publication date
- 01/01/2018
- Field of study
A combined measurement of differential and inclusive total cross sections of Higgs boson production is performed using 36.1 fb−1 of 13 TeV proton–proton collision data produced by the LHC and recorded by the ATLAS detector in 2015 and 2016. Cross sections are obtained from measured H→γγ and H→ZZ*(→4ℓ event yields, which are combined taking into account detector efficiencies, resolution, acceptances and branching fractions. The total Higgs boson production cross section is measured to be 57.0−5.9 +6.0 (stat.) −3.3 +4.0 (syst.) pb, in agreement with the Standard Model prediction. Differential cross-section measurements are presented for the Higgs boson transverse momentum distribution, Higgs boson rapidity, number of jets produced together with the Higgs boson, and the transverse momentum of the leading jet. The results from the two decay channels are found to be compatible, and their combination agrees with the Standard Model predictions
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
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- Agheorghiesei C
- Aguilar-Saavedra JA
- Ahmadov F
- Aielli G
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- Akerstedt H
- Akilli E
- Akimov AV
- Alberghi GL
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- Alconada Verzini MJ
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- Aleksa M
- Aleksandrov IN
- Alexa C
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- Allen BW
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- Alshehri AA
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- Amaral Coutinho Y
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- Amelung C
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- Amor 
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- Amrouche CS
- Anastopoulos C
- Ancu LS
- Andari N
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- Anders CF
- Anders JK
- Anderson KJ
- Andreazza A
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- Angelozzi I
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- Aoki M
- Aperio Bella L
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- 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
Measurements of integrated and differential cross sections for isolated photon pair production in pp collisions at √s=8 TeV with the ATLAS detector
- Author
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- Aad G
- Abbott B
- Abdallah J
- Abdinov O
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- Abidi SH
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- Yildirim E
- Yildiz HD
- Yorita K
- Yoshihara K
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- Yuen SPY
- Yusuff I
- Zabinski B
- Zacharis G
- Zaidan R
- Zaitsev AM
- Zakharchuk N
- Zalieckas J
- Zaman A
- Zambito S
- Zanzi D
- Zeitnitz C
- Zemla A
- Zeng JC
- Zeng Q
- Zenin O
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- Zerwas D
- Zhang D
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- Zhang Z
- Zhao X
- Zhao Y
- Zhao Z
- Zhemchugov A
- Zhou B
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- Zhou M
- Zhou M
- Zhou N
- Zhu CG
- Zhu H
- Zhu J
- Zhu Y
- Zhuang X
- Zhukov K
- Zibell A
- Zieminska D
- Zimine NI
- Zimmermann C
- Zimmermann S
- Zinonos Z
- Zinser M
- Ziolkowski M
- Zivkovic L
- Zobernig G
- Zoccoli A
- Zou R
- Zwalinski L
- Publication venue
- 'American Physical Society (APS)'
- Publication date
- 01/01/2017
- Field of study
A measurement of the production cross section for two isolated photons in proton-proton collisions at a center-of-mass energy of √s=8 TeV is presented. The results are based on an integrated luminosity of 20.2 fb−1 recorded by the ATLAS detector at the Large Hadron Collider. The measurement considers photons with pseudorapidities satisfying |ηγ|40GeV and EγT,2>30 GeV for the two leading photons ordered in transverse energy produced in the interaction. The background due to hadronic jets and electrons is subtracted using data-driven techniques. The fiducial cross sections are corrected for detector effects and measured differentially as a function of six kinematic observables. The measured cross section integrated within the fiducial volume is 16.8 ± 0.8 pb . The data are compared to fixed-order QCD calculations at next-to-leading-order and next-to-next-to-leading-order accuracy as well as next-to-leading-order computations including resummation of initial-state gluon radiation at next-to-next-to-leading logarithm or matched to a parton shower, with relative uncertainties varying from 5% to 20%
Search for supersymmetry in events with four or more leptons in √s =13 TeV pp collisions with ATLAS
- Author
- Aaboud M
- Aad G
- Abbott B
- Abdinov O
- Abeloos B
- Abidi SH
- AbouZeid OS
- Abraham NL
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- Zobernig G
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- Álvarez Piqueras D
- Åkesson TPA
- Šfiligoj T
- Ženiš T
- Živković L
- Publication venue
- 'American Physical Society (APS)'
- Publication date
- 01/01/2018
- Field of study
Results from a search for supersymmetry in events with four or more charged leptons (electrons, muons and taus) are presented. The analysis uses a data sample corresponding to 36.1 fb −1 of proton-proton collisions delivered by the Large Hadron Collider at s √ =13 TeV and recorded by the ATLAS detector. Four-lepton signal regions with up to two hadronically decaying taus are designed to target a range of supersymmetric scenarios that can be either enriched in or depleted of events involving the production and decay of a Z boson. Data yields are consistent with Standard Model expectations and results are used to set upper limits on the event yields from processes beyond the Standard Model. Exclusion limits are set at the 95% confidence level in simplified models of General Gauge Mediated supersymmetry, where higgsino masses are excluded up to 295 GeV. In R -parity-violating simplified models with decays of the lightest supersymmetric particle to charged leptons, lower limits of 1.46 TeV, 1.06 TeV, and 2.25 TeV are placed on wino, slepton and gluino masses, respectively
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