415 research outputs found
miRpower: a web-tool to validate survival-associated miRNAs utilizing expression data from 2178 breast cancer patients
- Author
- A Goldhirsch
- AK Pandey
- András Lánczky
- András Szabó
- AV Antonov
- B Chen
- B Gyorffy
- B Gyorffy
- B Györffy
- B Győrffy
- Balázs Győrffy
- C Blenkiron
- Cancer Genome Atlas Network
- CP Goswami
- E Enerly
- E Rinaldis de
- E Schooneveld van
- F Meng
- FM Buffa
- G Bertoli
- Giulia Bottai
- Gyöngyi Munkácsy
- H Dvinge
- HE Gee
- J Ferlay
- K Kleivi Sahlberg
- L Mattos-Arruda De
- L Santarpia
- Libero Santarpia
- M Dowsett
- MV Iorio
- MV Iorio
- P Parrella
- R Aguirre-Gamboa
- S Volinia
- SJ Song
- X Chen
- Y Okada
- Ádám Nagy
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2016
- Field of study
PURPOSE: The proper validation of prognostic biomarkers is an important clinical issue in breast cancer research. MicroRNAs (miRNAs) have emerged as a new class of promising breast cancer biomarkers. In the present work, we developed an integrated online bioinformatic tool to validate the prognostic relevance of miRNAs in breast cancer. METHODS: A database was set up by searching the GEO, EGA, TCGA, and PubMed repositories to identify datasets with published miRNA expression and clinical data. Kaplan-Meier survival analysis was performed to validate the prognostic value of a set of 41 previously published survival-associated miRNAs. RESULTS: All together 2178 samples from four independent datasets were integrated into the system including the expression of 1052 distinct human miRNAs. In addition, the web-tool allows for the selection of patients, which can be filtered by receptors status, lymph node involvement, histological grade, and treatments. The complete analysis tool can be accessed online at: www.kmplot.com/mirpower . We used this tool to analyze a large number of deregulated miRNAs associated with breast cancer features and outcome, and confirmed the prognostic value of 26 miRNAs. A significant correlation in three out of four datasets was validated only for miR-29c and miR-101. CONCLUSIONS: In summary, we established an integrated platform capable to mine all available miRNA data to perform a survival analysis for the identification and validation of prognostic miRNA markers in breast cancer
Expanding the allelic spectrum of ELOVL4‐related autosomal recessive neuro‐ichthyosis
- Author
- Publication venue
- Wiley
- Publication date
- 14/07/2023
- Field of study
Background Very long-chain fatty acids (VLCFAs) composed of more than 20 carbon atoms are essential in the biosynthesis of cell membranes in the brain, skin, and retina. VLCFAs are elongated beyond 28 carbon atoms by ELOVL4 enzyme. Variants in ELOVL4 are associated with three Mendelian disorders: autosomal dominant (AD) Stargardt-like macular dystrophy type 3, AD spinocerebellar ataxia, and autosomal recessive disorder congenital ichthyosis, spastic quadriplegia and impaired intellectual development (ISQMR). Only seven subjects from five unrelated families with ISQMR have been described, all of which have biallelic single-nucleotide variants. Methods We performed clinical exome sequencing on probands from four unrelated families with neuro-ichthyosis. Results We identified three novel homozygous ELOVL4 variants. Two of the families originated from the same Saudi tribe and had the exact homozygous exonic deletion in ELOVL4, while the third and fourth probands had two different novel homozygous missense variants. Seven out of the eight affected subjects had profound developmental delay, epilepsy, axial hypotonia, peripheral hypertonia, and ichthyosis. Delayed myelination and corpus callosum hypoplasia were seen in two of five subjects with brain magnetic rosonance imaging and cerebral atrophy in three. Conclusion Our study expands the allelic spectrum of ELOVL4-related ISQMR. The detection of the same exonic deletion in two unrelated Saudi family from same tribe suggests a tribal founder mutation
Search for direct pair production of the top squark in all-hadronic final states in proton-proton collisions at s√=8 TeV with the ATLAS detector
- Author
- Aad G
- Abbott B
- Abdallah J
- Abdinov O
- Aben R
- Abi B
- Abolins M
- AbouZeid OS
- Abramowicz H
- Abreu H
- Abreu R
- Abulaiti Y
- Acharya BS
- Adamczyk L
- Adams DL
- Adelman J
- Adomeit S
- Adye T
- Agatonovic-Jovin T
- Aguilar-Saavedra JA
- Agustoni M
- Ahlen SP
- Ahmadov F
- Aielli G
- Akerstedt H
- Akesson TPA
- Akimoto G
- Akimov AV
- Alberghi GL
- Albert J
- Albrand S
- Alconada Verzini MJ
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexander G
- Alexandre G
- Alexopoulos T
- Alhroob M
- Alimonti G
- Alio L
- Alison J
- Allbrooke BMM
- Allison LJ
- Allport PP
- Almond J
- Aloisio A
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- Alpigiani C
- Altheimer A
- Alviggi MG
- Amako K
- Amaral Coutinho Y
- Amelung C
- Amidei D
- Amor Dos Santos SP
- Amorim A
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- Amram N
- Amundsen G
- Anastopoulos C
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- Zurzolo G
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2014
- Field of study
The results of a search for direct pair production of the scalar partner to the top quark using an integrated luminosity of 20.1fb−1 of proton–proton collision data at √s = 8 TeV recorded with the ATLAS detector at the LHC are reported. The top squark is assumed to decay via t˜→tχ˜01 or t˜→ bχ˜±1 →bW(∗)χ˜01 , where χ˜01 (χ˜±1 ) denotes the lightest neutralino (chargino) in supersymmetric models. The search targets a fully-hadronic final state in events with four or more jets and large missing transverse momentum. No significant excess over the Standard Model background prediction is observed, and exclusion limits are reported in terms of the top squark and neutralino masses and as a function of the branching fraction of t˜ → tχ˜01 . For a branching fraction of 100%, top squark masses in the range 270–645 GeV are excluded for χ˜01 masses below 30 GeV. For a branching fraction of 50% to either t˜ → tχ˜01 or t˜ → bχ˜±1 , and assuming the χ˜±1 mass to be twice the χ˜01 mass, top squark masses in the range 250–550 GeV are excluded for χ˜01 masses below 60 GeV
Search for pair-produced long-lived neutral particles decaying to jets in the ATLAS hadronic calorimeter in ppcollisions at √s=8TeV
- Author
- Aad G
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- Yen AL
- Yildirim E
- Yildiz HD
- Yilmaz M
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- Youssef S
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- Yusuff I
- Zabinski B
- Zaidan R
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- Zanello L
- Zanzi D
- Zeitnitz C
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- Zemla A
- Zengel K
- Zenin O
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- Zhao Z
- Zhemchugov A
- Zhong J
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- Zhuang X
- Zhukov K
- Zibell A
- Zieminska D
- Zimine NI
- Zimmermann C
- Zimmermann R
- Zimmermann S
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- Zinonos Z
- Ziolkowski M
- Zobernig G
- Zoccoli A
- zur Nedden M
- Zurzolo G
- Zutshi V
- Zwalinski L
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2014
- Field of study
The ATLAS detector at the Large Hadron Collider at CERN is used to search for the decay of a scalar boson to a pair of long-lived particles, neutral under the Standard Model gauge group, in 20.3fb−1of data collected in proton–proton collisions at √s=8TeV. This search is sensitive to long-lived particles that decay to Standard Model particles producing jets at the outer edge of the ATLAS electromagnetic calorimeter or inside the hadronic calorimeter. No significant excess of events is observed. Limits are reported on the product of the scalar boson production cross section times branching ratio into long-lived neutral particles as a function of the proper lifetime of the particles. Limits are reported for boson masses from 100 GeVto 900 GeV, and a long-lived neutral particle mass from 10 GeVto 150 GeV
Temporomandibular disorder is more prevalent among patients with primary headaches in a tertiary outpatient clinic
- Author
- Ana Karine Farias da Trindade Coelho Pereira
- Anderson GC
- Ballegaard V
- Bertoli FM
- Bezov D
- Branco LP
- Brunna Thaís Luckwu de Lucena
- Campos JADB
- Ciancaglini R
- Dando WE
- Fonseca DM
- Fragoso YD
- Franco AL
- Franco AL
- Giorvan Ânderson dos Santos Alves
- Glaros AG
- Gonçalves DA
- Gonçalves DA
- Gonçalves MC
- Graff-Radford SB
- Isabella Araújo Mota
- James Felipe Tomaz-Morais
- Leeuw R
- Look JO
- Luciana Barbosa de Sousa Lucena
- Nomura K
- Okeson JP
- Rasmussen BK
- Rd Leeuw
- Ricardo Dias de Castro
- Roe CM
- Schiffman E
- Stuginski-Barbosa J
- Publication venue
- 'FapUNIFESP (SciELO)'
- Publication date
- Field of study
Loss of UGP2 in brain leads to a severe epileptic encephalopathy, emphasizing that bi-allelic isoform-specific start-loss mutations of essential genes can cause genetic diseases.
- Author
- Al Azri F
- Al Futaisi A
- Al Murshedi F
- Al-Quait L
- Alahmadi KO
- Aldosary M
- Almass R
- Almohanna F
- AlMuhaizea MA
- Alsagob M
- Alwadaee S
- Aronica E
- Awartani K
- Barakat TS
- Bauer P
- Begtrup A
- Berdowski WM
- Bernstein JA
- Bertoli-Avella AM
- Brick L
- Brooks AS
- Capo I
- Cheema HA
- Colak D
- Coskun S
- Dababo AM
- Darmiyan FM
- de Valk WG
- Dehghani M
- Doosti M
- Efthymiou S
- Ercan-Sencicek AG
- Eslahi A
- Ghazvini M
- Gunel M
- Hamad MHA
- Hertecant J
- Houlden H
- Jacobs EH
- Kamsteeg E-J
- Kandaswamy KK
- Karimiani EG
- Kaya N
- Khazaei Z
- Kohler JN
- Kozenko M
- Mani R
- Maroofian R
- Medici-van den Herik E
- Mehrjardi MYV
- Mojarrad M
- Monaghan KG
- Nikoncuk A
- Passi GR
- Perenthaler E
- Putar D
- Qubbaj W
- Rana N
- Retterer K
- Salih MA
- Torene R
- van den Berg P
- van der Linde HC
- van Ham TJ
- van IJcken WFJ
- van Slegtenhorst M
- Vandrovcova J
- Yousefi S
- Zafar F
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 09/12/2019
- Field of study
Developmental and/or epileptic encephalopathies (DEEs) are a group of devastating genetic disorders, resulting in early-onset, therapy-resistant seizures and developmental delay. Here we report on 22 individuals from 15 families presenting with a severe form of intractable epilepsy, severe developmental delay, progressive microcephaly, visual disturbance and similar minor dysmorphisms. Whole exome sequencing identified a recurrent, homozygous variant (chr2:64083454A > G) in the essential UDP-glucose pyrophosphorylase (UGP2) gene in all probands. This rare variant results in a tolerable Met12Val missense change of the longer UGP2 protein isoform but causes a disruption of the start codon of the shorter isoform, which is predominant in brain. We show that the absence of the shorter isoform leads to a reduction of functional UGP2 enzyme in neural stem cells, leading to altered glycogen metabolism, upregulated unfolded protein response and premature neuronal differentiation, as modeled during pluripotent stem cell differentiation in vitro. In contrast, the complete lack of all UGP2 isoforms leads to differentiation defects in multiple lineages in human cells. Reduced expression of Ugp2a/Ugp2b in vivo in zebrafish mimics visual disturbance and mutant animals show a behavioral phenotype. Our study identifies a recurrent start codon mutation in UGP2 as a cause of a novel autosomal recessive DEE syndrome. Importantly, it also shows that isoform-specific start-loss mutations causing expression loss of a tissue-relevant isoform of an essential protein can cause a genetic disease, even when an organism-wide protein absence is incompatible with life. We provide additional examples where a similar disease mechanism applies
Loss of C2orf69 defines a fatal autoinflammatory syndrome in humans and zebrafish that evokes a glycogen-storage-associated mitochondriopathy
- Author
- Akarsu NA
- Ali NA
- Alsubhi A
- Arman-Bilir O
- Bard FA
- Bascom CC
- Bauer P
- Bertoli-Avella A
- Boisson B
- Casanova J-L
- Cepni E
- Cetinkaya A
- Ceylaner S
- Chaabouni M
- Chai G
- Chia CY
- Choo SC
- Cimen DU
- Coon JJ
- Efthymiou S
- Eyaid W
- Georgiadou D
- Gilani N
- Gleeson JG
- Gumruk F
- Gurel A
- Hasbini D
- Ho L
- Houlden H
- Isfort RJ
- Isikay S
- Kayserili H
- Keng SS
- Khotaei GT
- Laine C
- Lee C
- Liang C
- Loh AYT
- Lupski JR
- Ly TTN
- Maier M
- Maroofian R
- Mathuru AS
- Maurer-Stroh S
- Mbarek H
- Mitani T
- Nathan FM
- Ordonez N
- Pagliarini DJ
- Paul F
- Pehlivan D
- Rensvold J
- Reversade B
- Rezaei N
- Seet SH
- Seyedpour S
- Shishkova E
- Simsek-Kiper PO
- Sirota FL
- Sng D
- Sotiropoulou K
- Talim B
- Teoh TS
- Traspas RM
- Tripolszki K
- Unal S
- Wong HH
- Xue S
- Yarali N
- Yilmaz E
- Zaki MS
- Zhang S
- Publication venue
- CELL PRESS
- Publication date
- 01/07/2021
- Field of study
Summary
Human C2orf69 is an evolutionarily conserved gene whose function is unknown. Here, we report eight unrelated families from which 20 children presented with a fatal syndrome consisting of severe autoinflammation and progredient leukoencephalopathy with recurrent seizures; 12 of these subjects, whose DNA was available, segregated homozygous loss-of-function C2orf69 variants. C2ORF69 bears homology to esterase enzymes, and orthologs can be found in most eukaryotic genomes, including that of unicellular phytoplankton. We found that endogenous C2ORF69 (1) is loosely bound to mitochondria, (2) affects mitochondrial membrane potential and oxidative respiration in cultured neurons, and (3) controls the levels of the glycogen branching enzyme 1 (GBE1) consistent with a glycogen-storage-associated mitochondriopathy. We show that CRISPR-Cas9-mediated inactivation of zebrafish C2orf69 results in lethality by 8 months of age due to spontaneous epileptic seizures, which is preceded by persistent brain inflammation. Collectively, our results delineate an autoinflammatory Mendelian disorder of C2orf69 deficiency that disrupts the development/homeostasis of the immune and central nervous systems
Pin1 and neurodegeneration: a new player for prion disorders?
- Author
- Anderson JP Walker DE, Goldstein JM, et al.
- Bae B-I Xu H, Igarashi S, et al.
- Bayer E Goettsch S, Mueller JW, et al.
- Bertoni A Giuliano P, Galgani M, et al.
- Binder LI Guillozet-Bongaarts AL, Garcia-Sierra
- Brettschneider J Del Tredici K, Lee VM, et al.
- Cancino GI Miller FD, Kaplan DR
- Chen C-H Li W, Sultana R, et al.
- Cisbani G Cicchetti F
- Dauer W Przedborski S
- Frankenfield KN Powers ET, Kelly JW
- Gendron TF Petrucelli L
- Ghosh A Saminathan H, Kanthasamy A, et al.
- Giannopoulos PN Robertson C, Jodoin J, et al.
- Grison A Mantovani F, Comel A, et al.
- Hardy J Selkoe DJ
- Huang Y Mucke L
- Innes BT Sowole MA, Gyenis L, et al.
- Iqbal K Grundke-Iqbal I
- Kardos J Kiss B, Micsonai A, et al.
- Kim S Nollen EA, Kitagawa K, et al.
- Kimura T Tsutsumi K, Taoka M, et al.
- LaFerla FM
- Lee M-S Kao S-C, Lemere CA, et al.
- Lee S-J Kim D-C, Choi B-H, et al.
- Liou Y-C Sun A, Ryo A, et al.
- Liou Y-C Zhou XZ, Lu KP
- Lu KP Hanes SD, Hunter T
- Lu KP Zhou XZ
- Ma SL Pastorino L, Zhou XZ, et al.
- Martin LJ Pan Y, Price AC, et al.
- Matena A Sinnen C, van den Boom J, et al.
- Mogi M Kondo T, Mizuno Y, et al.
- Nakamura K Greenwood A, Binder L, et al.
- Negro A Meggio F, Bertoli A, et al.
- Nixon RA Shea TB
- Pastorino L Sun A, Lu P-J, et al.
- Prusiner SB
- Prusiner SB
- Prusiner SB
- Prusiner SB
- Ross CA Aylward EH, Wild EJ, et al.
- Rouget R Sharma G, LeBlanc AC
- Rudrabhatla P Jaffe H, Pant HC
- Ryo A Togo T, Nakai T, et al.
- Schmitz M Lüllmann K, Zafar S, et al.
- Smet C Sambo A-V, Wieruszeski J-M, et al.
- Sorrentino G Mioni M, Giorgi C, et al.
- Sultana R Boyd-Kimball D, Poon HF, et al.
- Supattapone S Muramoto T, Legname G, et al.
- Taylor JP Hardy J, Fischbeck KH
- Trevitt CR Hosszu LLP, Batchelor M, et al.
- Uchida T Takamiya M, Takahashi M, et al.
- Vöhringer-Martinez E Verstraelen T, Ayers PW
- Wang G-R Shi S, Gao C, et al.
- Wang J-Z Zhang Y
- Yotsumoto K Saito T, Asada A, et al.
- Yuan A Sasaki T, Rao MV, et al.
- Zhou Z Xiao G
- Zita MM Marchionni I, Bottos E, et al.
- Publication venue
- 'American Institute of Mathematical Sciences (AIMS)'
- Publication date
- 01/01/2015
- Field of study
Pin1 is a peptidyl-prolyl isomerase that catalyzes the cis/trans conversion of phosphorylated proteins at serine or threonine residues which precede a proline. The peptidyl-prolyl isomerization induces a conformational change of the proteins involved in cell signaling process. Pin1 dysregulation has been associated with some neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Huntington's disease. Proline-directed phosphorylation is a common regulator of these pathologies and a recent work showed that it is also involved in prion disorders. In fact, prion protein phosphorylation at the Ser-43-Pro motif induces prion protein conversion into a disease-associated form. Furthermore, phosphorylation at Ser-43-Pro has been observed to increase in the cerebral spinal fluid of sporadic Creutzfeldt-Jakob Disease patients. These findings provide new insights into the pathogenesis of prion disorders, suggesting Pin1 as a potential new player in the disease. In this paper, we review the mechanisms underlying Pin1 involvement in the aforementioned neurodegenerative pathologies focusing on the potential role of Pin1 in prion disorders
Reproductive health of women with and without disabilities in South India, the SIDE study (South India Disability Evidence) study: a case control study
- Author
- A Dixon-Ibarra
- A Reichard
- BA Ferri
- C Morton
- C Thomas
- D Walsh-Gallagher
- DL Smith
- FM Chevarley
- Gudlavalleti Venkata S Murthy
- Jayanthi Sagar
- JF Trani
- JG Lipson
- JP Niemeier
- K Blackford
- K Bremer
- K Piotrowski
- L Taggart
- LI Iezzoni
- LI Iezzoni
- LI Iezzoni
- LN Choudhary
- M Redshaw
- MA Nosek
- MV Gudlavalleti
- N Groce
- Neena John
- O Prilleltensky
- R Lang
- S Bertoli
- S Mitra
- S Mudge
- SM Nicolau
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Anatomy of the sign-problem in heavy-dense QCD
- Author
- Adam E Romero
- Aranda C Padilla
- Arjanovic MM
- Armadans R Caminal
- Astigarraga ME Pozo
- Barajas CA Chavez
- Bechtle P
- Beck HP
- Becker K
- Becker M
- Beckingham M
- Becot C
- Beddall A
- Beddall AJ
- Bednyakov VA
- Bedognetti M
- Bee CP
- Beemster LJ
- Beermann TA
- Begel M
- Behr JK
- Belanger-Champagne C
- Bell AS
- Bella G
- Bellagamba L
- Bellerive A
- Bellomo M
- Belotskiy K
- Beltramello O
- Belyaev NL
- Benary O
- Benchekroun D
- Bender M
- Bendtz K
- Benekos N
- Benhammou Y
- Benitez J
- Benjamin DP
- Bensinger JR
- Bentvelsen S
- Beresford L
- Beretta M
- Berge D
- Berger N
- Berghaus F
- Beringer J
- Berlendis S
- Berlingen J Montejo
- Bernard NR
- Bernius C
- Bernlochner FU
- Berry T
- Berta P
- Bertella C
- Bertoli G
- Bertolucci F
- Bertram IA
- Bertsche C
- Bertsche D
- Besjes GJ
- Bessner M
- Besson N
- Betancourt C
- Bethke S
- Bevan AJ
- Bhimji W
- Bianchi RM
- Bianchini L
- Bianco M
- Biebel O
- Biedermann D
- Bielski R
- Biesuz NV
- Biglietti M
- Bilokon H
- Bindi M
- Binet S
- Bingul A
- Bini C
- Biondi S
- Bjergaard DM
- Black CW
- Black JE
- Black KM
- Blackburn D
- Blair RE
- Blanchard J-B
- Blanco JE
- Blazek T
- Bloch I
- Blocker C
- Blum W
- Blumenschein U
- Blunier S
- Bobbink GJ
- Bobrovnikov VS
- Bocchetta SS
- Bocci A
- Bock C
- Boehler M
- Boeriu OE Vickey
- Boerner D
- Bogaerts JA
- Bogavac D
- Bogdanchikov AG
- Bohm C
- Boisvert V
- Bold T
- Boldea V
- Boldyrev AS
- Bomben M
- Bona M
- Boonekamp M
- Borisov A
- Borissov G
- Bortfeldt J
- Bortoletto D
- Bortolotto V
- Bos K
- Boscherini D
- Bosman M
- Bossio Sola JD
- Boudreau J
- Bouffard J
- Bouhova-Thacker EV
- Boumediene D
- Bourdarios C
- Bousson N
- Boutle SK
- Boveia A
- Boyd J
- Boyko IR
- Bracinik J
- Brandt A
- Brandt G
- Brandt O
- Bratzler U
- Brau B
- Brau JE
- Braun HM
- Bravo A Gascon
- Brendlinger K
- Brennan AJ
- Brenner L
- Brenner R
- Bressler S
- Bret M Cano
- 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
- Bruneliere R
- Bruni A
- Bruni G
- Brunt BH
- Bruschi M
- Bruscino N
- Bryant P
- Bryngemark L
- Buanes T
- Buat Q
- Buchholz P
- Buckley AG
- Budagov IA
- Buehrer F
- Buescher D
- Buesher V
- Bugge MK
- Bulekov O
- Bullock D
- Burckhart H
- Burdin S
- Burgard CD
- Burghgrave B
- Burka K
- Burke S
- Burmeister I
- Busato E
- Bussey P
- Butler JM
- Butt AI
- Buttar CM
- Butterworth JM
- Butti P
- Buttinger W
- Buzatu A
- Buzykaev AR
- Bylund O Bessidskaia
- Cabrera Urban S
- Caforio D
- Cairo VM
- Cakir O
- Calace N
- Calafiura P
- Calandri A
- Calderini G
- Calfayan P
- Caloba LP
- Calvet D
- Calvet S
- Calvet TP
- Camarda S
- Camarri P
- Cameron D
- Camincher C
- Campana S
- Campanelli M
- Campoverde A
- Canale V
- Canepa A
- Cantero J
- Cantrill R
- Cao T
- Caprini I
- Caprini M
- Capua M
- Caputo R
- Carbone RM
- Cardarelli R
- Cardillo F
- Carli I
- Carli T
- Carlino G
- Carminati L
- Caron S
- Carquin E
- Carrillo-Montoya GD
- Carter JR
- Carvalho J
- Casadei D
- Casado MP
- Casolino M
- Casper DW
- Castaneda-Miranda E
- Castelli A
- Castillo Gimenez V
- Castillo I Santoyo
- Castilloa LR Flores
- Castro NF
- Catinaccio A
- Catmore JR
- Cattai A
- Caudron J
- Cavaliere V
- Cavalli D
- Cavalli-Sforza M
- Cavasinni V
- Ceradini F
- Cerda Alberich L
- Cerio BC
- Cerqueira AS
- Cerri A
- Cerrito L
- Cerutti F
- Cerv M
- Cervelli A
- Cetin SA
- Chafaq A
- Chakraborty D
- Chan SK
- Chan YL
- Chang P
- Chapman JD
- Charlton DG
- Chatterjee A
- Chau CC
- Che S
- Cheatham S
- Chegwidden A
- Chekanov S
- Chekulaev SV
- Chelkov GA
- Chelstowska MA
- Chen C
- Chen H
- Chen K
- Chen S
- Chen S
- Chen X
- Chen Y
- Cheng HC
- Cheng HJ
- Cheng Y
- Cheplakov A
- Cheremushkina E
- Cherkaoui El Moursli R
- Chernyatin V
- Cheu E
- Chevalier L
- Chiarella V
- Chiarelli G
- Chiodini G
- Chisholm AS
- Chitan A
- Chizhov MV
- Choi K
- Chomont AR
- Chouridou S
- Chow BKB
- Christodoulou V
- Chromek-Burckhart D
- Chudoba J
- Chuinard AJ
- Chwastowski JJ
- Chytka L
- Ciapetti G
- Ciftci AK
- Cinca D
- Cindro V
- Cioara IA
- Ciocio A
- Cirotto F
- Citron ZH
- Ciubancan M
- Clark A
- Clark BL
- Clark PJ
- Clarke RN
- Clement C
- Coadou Y
- Cobal M
- Coccaro A
- Cochran J
- Codina E Perez
- Coffey L
- Colasurdo L
- Cole B
- Cole S
- Colijn AP
- Collot J
- Colombo T
- Compostella G
- Conde Muino P
- Coniavitis E
- Connell SH
- Connelly IA
- Consorti V
- Constantinescu S
- Conta C
- Conti G
- Conventi F
- Cooke M
- Cooper BD
- Cooper-Sarkar AM
- Cornelissen T
- Corradi M
- Correia AM Henriques
- Corriveau F
- Corso-Radu A
- Cortes-Gonzalez A
- Cortiana G
- Costa G
- Costa MJ
- Costanzo D
- Cottin G
- Cowan G
- Cox BE
- Cranmer K
- Crawley SJ
- Cree G
- Crepe-Renaudin S
- Crescioli F
- Cribbs WA
- Cristinziani M
- Croft V
- Crosetti G
- Cummings J
- Curatolo M
- Cuth J
- Cuthbert C
- Czirr H
- Czodrowski P
- D'Auria S
- D'Onofrio M
- Da Costa J Goncalves Pinto Firmino
- Da Cunha Sargedas De Sousa MJ
- Da Via C
- Dabrowski W
- Dai T
- Dale O
- Dallaire F
- Dallapiccola C
- Dam M
- Damazio D Oliveira
- Dandoy JR
- Dang NP
- Daniells AC
- Dann NS
- Danninger M
- Dao V
- Darbo G
- Darmora S
- Dassoulas J
- Dattagupta A
- Davey W
- David C
- Davidek T
- Davies M
- Davison P
- Davygora Y
- Dawe E
- Dawson I
- Daya-Ishmukhametova RK
- de Andrade Filho L Manhaes
- De Asmundisa R
- De Benedetti A
- De Bruin PH Sales
- De Castro S
- De Cecco S
- De Groot N
- de Jong P
- De la Torre H
- de Lima DE Ferreira
- De Lorenzi F
- De Mendizabal J Bilbao
- De Pedis D
- De Regie JB De Vivie
- de Renstrom PA Bruckman
- De Salvo A
- De Sanctis U
- De Santo A
- De K
- Dearnaley WJ
- Debbe R
- Debenedetti C
- Dedovich DV
- Deigaard I
- Del Peso J
- Del Prete T
- Delgove D
- Deliot F
- Delitzsch CM
- Deliyergiyev M
- Dell'Acqua A
- Dell'Asta L
- Dell'Orso M
- Della Pietra M
- della Volpe D
- Delmastro M
- Delsart PA
- Deluca C
- DeMarco DA
- Demers S
- Demichev M
- Demilly A
- Denisov SP
- Denysiuk D
- Derendarz D
- Derkaoui JE
- Derue F
- Dervan P
- Desch K
- Deterre C
- Dette K
- Deviveiros PO
- Dewhurst A
- Dhaliwal S
- Di Ciaccio A
- Di Ciaccio L
- Di Clemente WK
- Di Donato C
- Di Girolamo A
- Di Girolamo B
- Di Micco B
- Di Nardo R
- Di Simone A
- Di Sipio R
- Di Valentino D
- Diaconu C
- Diamond M
- Dias FA
- Diaz MA
- Diehl EB
- Dietrich J
- Diglio S
- Dimitrievska A
- Dingfelder J
- Dita P
- Dita S
- Dittus F
- Djama F
- Djobava T
- Djuvsland JI
- do Vale MAB
- Dobos D
- Dobre M
- Doglioni C
- Dohmae T
- Dolejsi J
- Dolezal Z
- Dolgoshein BA
- Donadelli M
- Donati S
- Dondero P
- Donini J
- Donszelmann T Cuhadar
- Dopke J
- Doria A
- Dova MT
- Doyle AT
- Drechsler E
- Dris M
- Du Y
- Duarte-Campderros J
- Duchovni E
- Duckeck G
- Ducu OA
- Duda D
- Dudarev A
- Duflot L
- Duguid L
- Duhrssen M
- Dunford M
- Duren M
- Durglishvili A
- Duschinger D
- Dutta B
- Dyndal M
- Eckardt C
- Ecker KM
- Edgar RC
- Edson W
- Edwards NC
- Eifert T
- Eigen G
- Einsweiler K
- Ekelof T
- El Kacimi M
- Ellajosyula V
- Ellert M
- Elles S
- Ellinghaus F
- Elliot AA
- Ellis N
- Elmsheuser J
- Elsing M
- Emeliyanov D
- Enari Y
- Endner OC
- Endo M
- Ennis JS
- Erdmann J
- Ereditato A
- Ernis G
- Ernst J
- Ernst M
- Errede S
- Ertel E
- Escalier M
- Esch H
- Escobar C
- Esposito B
- Etienvre AI
- Etzion E
- Evans H
- Ezhilov A
- Fabbri F
- Fabbri L
- Facini G
- Fakhrutdinov RM
- Falciano S
- Falla RJ
- Faltova J
- Fang Y
- Fanti M
- Farbin A
- Farilla A
- Farina C
- Farooque T
- Farrell S
- Farrington SM
- Farthouat P
- Fassi F
- Fassnacht P
- Fassouliotis D
- Favareto A
- Fawcett WJ
- Fayard L
- Fedin OL
- Fedorko W
- Feigl S
- Feligioni L
- Feng C
- Feng EJ
- Feng H
- Fenyuk AB
- Feremenga L
- Fernandez Martinez P
- Ferrando J
- Ferrari A
- Ferrari P
- Ferrari R
- Ferrer A
- Ferrere D
- Ferretti C
- Fiedler F
- Filipcic A
- Filipuzzi M
- Filthaut F
- Fincke-Keeler M
- Finelli KD
- Fiolhaisa MCN
- Fiorini L
- Firan A
- Fischer A
- Fischer C
- Fischer J
- Fisher WC
- Flaschel N
- Fleck I
- Fleischmann P
- Fletcher G
- Fletcher GT
- Fletcher RRM
- Flick T
- Floderus A
- Flowerdew MJ
- Forcolin GT
- Formica A
- Forti A
- Foster AG
- Fournier D
- Fox H
- Fracchia S
- Francavilla P
- Franchini M
- Francis D
- Franconi L
- Franklin M
- Frate M
- Fraternalia M
- Freeborn D
- Fressard-Batraneanu SM
- Friedrich F
- Froidevaux D
- Frost JA
- Fukunaga C
- Fusayasu T
- Fuster J
- Gabaldon C
- Gabizon O
- Gabrielli A
- Gabrielli A
- Gach GP
- Gadatsch S
- Gadomski S
- Gagliardi G
- Gagnon LG
- Gagnon P
- Galea C
- Galhardo B
- Gallas EJ
- Gallop BJ
- Gallus P
- Galster G
- Gan KK
- Gao J
- Gao Y
- Gao YS
- Garcia Navarro JE
- Garcia BR Mellado
- Garcia C
- Garcia JA Benitez
- Garcia RF Naranjo
- Garcia-Sciveres M
- Gardner RW
- Garelli N
- Garonne V
- Garrido MDM Capeans
- Garron Nicolas
- Gatti C
- Gaudiello A
- Gaudio G
- Gaur B
- Gauthier L
- Gavrilenko IL
- Gay C
- Gaycken G
- Gazis EN
- Gecse Z
- Gee CNP
- Geich-Gimbel Ch
- Geisler MP
- Gemme C
- Genest MH
- Geng C
- Gentile S
- George S
- Gerbaudo D
- Gershon A
- Ghasemi S
- Ghazlane H
- Giacobbe B
- Giagu S
- Giannelli M Faucci
- Giannetti P
- Gibbard B
- Gibson SM
- Gignac M
- Gilchriese M
- Gillam TPS
- Gillberg D
- Gilles G
- Gingrich DM
- Giokaris N
- Giordani MP
- Giorgi FM
- Giorgi FM
- Giraud PF
- Giromini P
- Giugni D
- Giuliani C
- Giulini M
- Gjelsten BK
- Gkaitatzis S
- Gkialas I
- Gkougkousis EL
- Gladilin LK
- Glasman C
- Glatzer J
- Glaysher PCF
- Glazov A
- Goblirsch-Kolb M
- Godlewski J
- Goldfarb S
- Golling T
- Golubkov D
- Gomes A
- Goncalo R
- Gonella L
- Gongadze A
- Gonzalez de la Hoz S
- Gonzalez-Sevilla S
- Goossens L
- Gorbounov PA
- Gordon HA
- Gorelov I
- Gorini B
- Gorini E
- Gorisek A
- Gornicki E
- Goshaw AT
- Gossling C
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- Zwalinski L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2016
- Field of study
QCD at finite densities of heavy quarks is investigated
using the density-of-states method. The phase factor
expectation value of the quark determinant is calculated to
unprecedented precision as a function of the chemical potential.
Results are validated using those from a reweighting
approach where the latter can produce a significant signalto-noise
ratio. We confirm the particle–hole symmetry at low
temperatures, find a strong sign problem at intermediate values
of the chemical potential, and an inverse Silver Blaze
feature for chemical potentials close to the onset value: here,
the phase-quenched theory underestimates the density of the
full theory
- …