183 research outputs found
Characterization of the Row Geometric Mean Ranking with a Group Consensus Axiom
- Author
- C Genest
- CR Johnson
- EU Choo
- G Crawford
- G Rabinowitz
- HP Young
- J Aczél
- J Barzilai
- J Barzilai
- J Fichtner
- J GonzĂĄlez-DĂaz
- J PĂ©rez
- KJ Arrow
- L CsatĂł
- L CsatĂł
- L CsatĂł
- L CsatĂł
- LĂĄszlĂł CsatĂł
- M Brunelli
- M Brunelli
- M Lundy
- MG Kendall
- N Bryson
- P Chebotarev
- R Brink van den
- R Janicki
- S BozĂłki
- S Nitzan
- TK Dijkstra
- TL Saaty
- TL Saaty
- TL Saaty
- WD Cook
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2018
- Field of study
An axiomatic approach is applied to the problem of extracting a ranking of
the alternatives from a pairwise comparison ratio matrix. The ordering induced
by row geometric mean method is proved to be uniquely determined by three
independent axioms, anonymity (independence of the labelling of alternatives),
responsiveness (a kind of monotonicity property) and aggregation invariance,
which requires the preservation of group consensus, that is, the pairwise
ranking between two alternatives should remain unchanged if unanimous
individual preferences are combined by geometric mean.Comment: 17 pages, 2 figure
Exploring Predictors of Outcome in the Psychosis Prodrome: Implications for Early Identification and Intervention
- Author
- A Fornito
- A Malla
- AD Eastvold
- AE Pinkham
- AE Pinkham
- AE Simon
- AF Mirsky
- AJ Russell
- AJ Saykin
- AR Yung
- AR Yung
- AR Yung
- BA Cornblatt
- BA Cornblatt
- BA Cornblatt
- BC Ho
- BD Peters
- BJ Casey
- BL Schwartz
- C Pantelis
- C Pantelis
- C Ranganath
- Carrie E. Bearden
- CD Frith
- CD Frith
- CL McKibbin
- CS Carter
- CS Carter
- CW Smith
- D Nieman
- D Sun
- D Tamlyn
- DC Glahn
- DC Javitt
- DE Job
- DL Penn
- DL Penn
- DL Penn
- DM Barch
- DN Allen
- DO Perkins
- DR Combs
- E Bartok
- E Bora
- EA Holthausen
- FG Happe
- G Bryson
- GD Honey
- GH Ihnen
- GJ Pickup
- GK Wood
- GP Amminger
- H Wimmer
- H Witthaus
- I Feinberg
- J Addington
- J Addington
- J Klosterkotter
- J Lieberman
- J Perner
- JA Martin
- JD Mayer
- JH Yoon
- JM Gold
- JM Gold
- JM Lappin
- JN Giedd
- JS Brekke
- KA Hawkins
- KH Karlsgodt
- KH Nuechterlein
- KJ Friston
- KL Davis
- KM Prasad
- KS Kee
- KS Kee
- L Clare
- L Erlenmeyer-Kimling
- LD Selemon
- LJ Phillips
- LS Schenkel
- M Brune
- M Brune
- M Hambrecht
- M Liang
- M Marshall
- M Walterfang
- M Walterfang
- Maria Jalbrzikowski
- MF Green
- MF Green
- MF Green
- MJ Jafri
- MJ Sergi
- MJ Sergi
- N Docherty
- N Docherty
- N Frommann
- N Gogtay
- NE Haren van
- P Bebbington
- P Jones
- P Kinderman
- P Milev
- PD Harvey
- PD McGorry
- PW Corrigan
- R Adolphs
- R Condray
- R Cosway
- R Fuller
- R Hurlemann
- R Mizrahi
- R Morice
- R Pukrop
- R Pukrop
- R Roncone
- R Rosenthal
- R Schlosser
- R Toomey
- R Vauth
- RM Bilder
- RS Keefe
- RS Keefe
- S Park
- S Silverstein
- SE Meyer
- SJ Blakemore
- SJ Borgwardt
- SJ Borgwardt
- SJ Borgwardt
- SJ Wood
- SJ Wood
- SJ Wood
- SL Kerr
- SM Couture
- SM Francey
- SR McGurk
- T Lencz
- T Paus
- T. Takahashi
- TA Niendam
- TA Niendam
- TA Niendam
- Tara A. Niendam
- TD Cannon
- TD Cannon
- TD Cannon
- TH McGlashan
- TH McGlashan
- TH McGlashan
- TH McGlashan
- TJ Miller
- TJ Miller
- TK Larsen
- U Gschwandtner
- U Gschwandtner
- W Wolwer
- WJ Brewer
- WJ Brewer
- WJ Brewer
- WP Horan
- Y Liu
- YS Chung
- Publication venue
- Springer US
- Publication date
- 01/01/2009
- Field of study
Functional disability is a key component of many psychiatric illnesses, particularly schizophrenia. Impairments in social and role functioning are linked to cognitive deficits, a core feature of psychosis. Retrospective analyses demonstrate that substantial functional decline precedes the onset of psychosis. Recent investigations reveal that individuals at clinical-high-risk (CHR) for psychosis show impairments in social relationships, work/school functioning and daily living skills. CHR youth also demonstrate a pattern of impairment across a range of cognitive domains, including social cognition, which is qualitatively similar to that of individuals with schizophrenia. While many studies have sought to elucidate predictors of clinical deterioration, specifically the development of schizophrenia, in such CHR samples, few have investigated factors relevant to psychosocial outcome. This review integrates recent findings regarding cognitive and social-cognitive predictors of outcome in CHR individuals, and proposes potential directions for future research that will contribute to targeted interventions and improved outcome for at-risk youth
Following the genes: a framework for animal modeling of psychiatric disorders
- Author
- A Bertolino
- A Guilmatre
- A Hayashi-Takagi
- A Meyer-Lindenberg
- A Morozov
- A Piton
- A Sirota
- AA Chubykin
- AA Grace
- AC Lionel
- AC Need
- AE RĂŒnker
- Akira Sawa
- AM Geurts
- AS Bassett
- B Moghaddam
- B Xu
- B Xu
- Bita Moghaddam
- BJ O'Roak
- BR Arenkiel
- C Betancur
- C Betancur
- C Holden
- CA Walsh
- CM Powell
- Consortium ISR
- CP Schaaf
- CR Marshall
- CS Carter
- D Carroll
- D Ehninger
- D Pinto
- D Tropea
- DE Reich
- DF Levinson
- DH O'Connor
- DJ Blake
- DT Miller
- DT Miller
- EM Morrow
- ET Cirulli
- FH Lee
- FJ Samaha
- G Buzsaki
- G Dolen
- G Gonzalez-Burgos
- G Horev
- G Huang
- GM Cooper
- GM Cooper
- H Moore
- H Najmabadi
- H Stefansson
- H Stefansson
- H Taniguchi
- HC Mefford
- HC Mefford
- HC Steinhausen
- HJ Williams
- II Gottesman
- II Gottesman
- J Blundell
- J De Fruyt
- J Elia
- J McClellan
- J Nakatani
- J Peca
- J Sebat
- J Sebat
- J Shi
- JA Cardin
- JA Kearney
- JE Belforte
- JE Chubb
- JE Lisman
- JI Friedman
- JK Millar
- JK Millar
- JL Daniels
- JM McClellan
- JN Betley
- JR Gibson
- JR Lupski
- JS Isaacson
- JT Glessner
- JT Glessner
- JW Bohland
- K Hartwich
- K Tabuchi
- K Wang
- Kevin J Mitchell
- KJ Mitchell
- KJ Mitchell
- KJ Mitchell
- KM Spencer
- KM Tye
- KP Lesch
- L Luo
- L van der Weyden
- LA Weiss
- LE Vissers
- LL Colgin
- M Baker
- M Etherton
- M Feyder
- M Karayiorgou
- M Karayiorgou
- M Kvajo
- MA Bangash
- MA Williams
- MC Keller
- MC O'Donovan
- MP van den Heuvel
- MR Etherton
- MS Ching
- N Osbun
- N Risch
- N Risch
- NM Williams
- NR Wray
- O Bozdagi
- O Peñagarikano
- O Yizhar
- O Yizhar
- OD Howes
- P Bob
- P Fazzari
- P Fries
- P Fries
- P Fuentealba
- P Jedlicka
- P Lichtenstein
- P Lichtenstein
- P Seeman
- P Sklar
- PF Sullivan
- PJ Uhlhaas
- PJ Uhlhaas
- PJ Uhlhaas
- Psychiatric Genetics Consortium
- R Anney
- R Kariminejad
- R Tandon
- R Tandon
- R Willi
- RA Myers
- RE Amir
- S Girirajan
- S Gong
- S Jamain
- S Mah
- S Raychaudhuri
- S Ripke
- SA Hays
- SE Bryson
- SE Schipul
- SE Smith
- SJ Sanders
- SK Sundaram
- SL Girard
- SM Purcell
- SP Dickson
- SR Gilman
- SV Shmelkov
- T Hakami
- T Klassen
- T Klausberger
- T Korotkova
- T Nagai
- T Sigurdsson
- T Walsh
- TK Berdyyeva
- TR Insel
- V Vacic
- VS Sohal
- W Singer
- WC Skarnes
- World Health Organisation
- WT Brown
- X Cui
- X Han
- Y-T Chang
- YY Shi
- Z Josh Huang
- Publication venue
- BioMed Central
- Publication date
- 01/01/2011
- Field of study
The number of individual cases of psychiatric disorders that can be ascribed to identified, rare, single mutations is increasing with great rapidity. Such mutations can be recapitulated in mice to generate animal models with direct etiological validity. Defining the underlying pathogenic mechanisms will require an experimental and theoretical framework to make the links from mutation to altered behavior in an animal or psychopathology in a human. Here, we discuss key elements of such a framework, including cell type-based phenotyping, developmental trajectories, linking circuit properties at micro and macro scales and definition of neurobiological phenotypes that are directly translatable to humans
What Do We Know About Neuropsychological Aspects Of Schizophrenia?
- Author
- A Aleman
- A Bandura
- A Martinez-Aran
- A Martinez-Aran
- A Reichenberg
- AB Hollingshead
- AE Schwartzman
- AE Schwartzman
- AI Tröster
- AL Mishara
- AS Bellack
- B Wexler
- Barton W. Palmer
- BE Seaton
- BE Seaton
- BK Lebowitz
- BR Rund
- BS Strauss
- BW Palmer
- BW Palmer
- BW Palmer
- BW Palmer
- C Boake
- C Boake
- C Torrent
- CA Depp
- CE Bearden
- CE Hartwell
- CG Watson
- CI Cohen
- CM MacLeod
- CM Wilk
- CR Bowie
- CS Carter
- D Dickinson
- D Dickinson
- D Wechsler
- DH Barlow
- DI Velligan
- DI Velligan
- DJ Schretlen
- DL Braff
- DM Wright
- DN Allen
- DN Allen
- DN Allen
- DV Jeste
- E Aylward
- E Bleuler
- E Bora
- E Kraepelin
- E Rawlings
- E Walker
- EA Berg
- EA Holthausen
- EF Torrey
- EP Bleuler
- ET Fey
- EW Twamley
- EW Twamley
- EW Twamley
- FT Leonberger
- G Cassens
- G Goldstein
- G Goldstein
- G Goldstein
- G Goldstein
- G Price
- G Winterer
- GH Pijnenborg
- GJ Bryson
- GJ McLachlan
- GV Nayak
- H Babcock
- H Hippius
- H Meltzer
- HE Spohn
- I Vahia
- J Cohen
- J Crilly
- J Paris
- J Zubin
- JA Gladsjo
- JB Rotter
- JD Evans
- JD Ragland
- JE Partington
- JH Ward
- JI Friedman
- JK Zubieta
- JL Rapoport
- JS Paulsen
- JT Cavanagh
- JV May
- K Goldstein
- K Goldstein
- K Goldstein
- K Goldstein
- K Marwick
- KA Woodberry
- KD Denicoff
- KJ Friston
- Kremen W. S., Lyons, M. J., Boake, C., Xian, H., Jacobson, K. C., Waterman, B., et al
- KS Kee
- L DeLisi
- L White
- LA Flashman
- LJ Chapman
- LJ Seidman
- LJ Seidman
- LR Squire
- LS Vigotsky
- LT Eyler
- LT Eyler
- M Albus
- M Bolles
- M Davidson
- M Fioravanti
- M Gracia Dominguez de
- M Greicius
- M Kubicki
- M Shenton
- M Walterfang
- MF Green
- MF Green
- MF Green
- MF Green
- MF Green
- ML Silverstein
- MM Kurtz
- MM Kurtz
- MP Wittman
- MS Keshavan
- MU Shad
- N Cameron
- N Cameron
- ND Woodward
- ND Woodward
- P McGuire
- P Satz
- PD Harvey
- PJ Harrison
- PJ Harrison
- PS Goldman-Rakic
- R Vauth
- RF Zec
- RI Mesholam-Gately
- RK Heaton
- RK Heaton
- RK Heaton
- RK Heaton
- RK Heaton
- RK Heaton
- RK Heaton
- RM Bilder
- Robert K. Heaton
- RSE Keefe
- RSE Keefe
- RSE Keefe
- RT Lange
- RW Buchanan
- RW Heinrichs
- RW Heinrichs
- RW Heinrichs
- RW Heinrichs
- RW Payne
- S Klingberg
- S Lawrie
- S Levin
- Sharron E. Dawes
- SK Hill
- SK Hill
- SK Liu
- SM Couture
- SM El-Badri
- SM Weinberg
- SR Marder
- T Ilonen
- TE Goldberg
- The Psychological Corporation
- TK Rajji
- TR Insel
- TW Weickert
- W Mischel
- W Spielmeyer
- WP Horan
- WS Kremen
- WT Carpenter
- WW Leung
- WW Lothrop
- Y Assaf
- Y Stern
- Publication venue
- Springer US
- Publication date
- 01/01/2009
- Field of study
Application of a neuropsychological perspective to the study of schizophrenia has established a number of important facts about this disorder. Some of the key findings from the existing literature are that, while neurocognitive impairment is present in most, if not all, persons with schizophrenia, there is both substantial interpatient heterogeneity and remarkable within-patient stability of cognitive function over the long-term course of the illness. Such findings have contributed to the firm establishment of neurobiologic models of schizophrenia, and thereby help to reduce the social stigma that was sometimes associated with purely psychogenic models popular during parts of the 20th century. Neuropsychological studies in recent decades have established the primacy of cognitive functions over psychopathologic symptoms as determinants of functional capacity and independence in everyday functioning. Although the cognitive benefits of both conventional and even second generation antipsychotic medications appear marginal at best, recognition of the primacy of cognitive deficits as determinants of functional disability in schizophrenia has catalyzed recent efforts to develop targeted treatments for the cognitive deficits of this disorder. Despite these accomplishments, however, some issues remain to be resolved. Efforts to firmly establish the specific neurocognitive/neuropathologic systems responsible for schizophrenia remain elusive, as do efforts to definitively demonstrate the specific cognitive deficits underlying specific forms of functional impairment. Further progress may be fostered by recent initiatives to integrate neuropsychological studies with experimental neuroscience, perhaps leading to measures of deficits in cognitive processes more clearly associated with specific, identifiable brain systems
De Novo Truncating Mutations in WASF1 Cause Intellectual Disability with Seizures.
- Author
- Afzal M
- Aitman T
- Alachkar H
- Alavijeh OS
- Ali S
- Ali S
- Allen L
- Allsup D
- Ambegaonkar G
- Ancliff P
- Anderson J
- Antrobus R
- Armstrong R
- Arno G
- Arumugakani G
- Ashford S
- Astle W
- Attwood A
- Austin S
- Babbs C
- Bacchelli C
- Bakchoul T
- Bariana TK
- Baxendale H
- Bennett D
- Bethune C
- Bibi S
- Bitner-Glindzicz M
- Bleda M
- Boggard HJ
- Bolton-Maggs P
- Booth C
- Boycott KM
- Boycott KM
- Bradley JR
- Brady A
- Brown M
- Browning M
- Brudno M
- Bryson C
- Bulman D
- Burns S
- Calleja P
- Canham N
- Carmichael J
- Carss KJ
- Carss KJ
- Caulfield M
- Chalmers E
- Chambers J
- Chandra A
- Charles P
- Chinnery P
- Chitre M
- Chong S
- Church C
- Clement E
- Clements-Brod N
- Clowes V
- Coghlan G
- Colby E
- Collins J
- Collins P
- Cook HT
- Cookson V
- Cooper N
- Corris PA
- Creaser-Myers A
- Dacosta R
- Daugherty L
- Davies S
- Davis J
- De Vries M
- Deegan P
- Deevi SVV
- Deshpande C
- Devlin L
- Dewhurst E
- Dixon P
- Doffinger R
- Dolling H
- Dormand N
- Drewe E
- Duarte ST
- Dyack S
- Dyment D
- Edgar D
- Egner W
- Emmerson I
- Erber WN
- Erwood M
- Estiu C
- Everington T
- Eyries M
- Favier R
- Firth H
- Fletcher D
- Flinter F
- Frary A
- French C
- Freson K
- Furie B
- Furnell A
- Gale D
- Gall H
- Gardham A
- Gattens M
- Gebhart J
- Ghali N
- Ghataorhe PK
- Ghio S
- Ghofrani A
- Ghurye R
- Gibbs JSR
- Gilmour K
- Ginsberg L
- Girerd B
- Gissen P
- Goddard S
- Gomez K
- Gordins P
- Gosal D
- Greene D
- Greenhalgh A
- Greinacher A
- Gresele P
- Grigoriadou S
- Grozeva D
- GrÀf S
- Hackett S
- Hadden R
- Hadinnapola C
- Hague B
- Hague R
- Haimel M
- Halmagyi C
- Hammerton T
- Harper L
- Hart D
- Hartley T
- Hayman G
- Heemskerk JWM
- Henderson R
- Hensiek A
- Henskens Y
- Herwadkar A
- Holden S
- Holder M
- Holder S
- Horvath R
- Houweling AC
- Hu F
- Hudson G
- Huissoon A
- Humbert M
- Hurst J
- InâT Veld AH
- Ito Y
- James R
- Johnson S
- Jolles S
- Josifova D
- Kazmi R
- Keeling D
- Kelleher P
- Kelly AM
- Kennedy F
- Keren B
- Kernohan KD
- Kiely DG
- Kingston N
- Kovacs G
- Koziell A
- Krishnakumar D
- Kuijpers TW
- Kumararatne D
- Kurian MA
- Kurian MA
- Laffan MA
- Lambert MP
- Lango-Allen H
- Lawrie A
- Layton M
- Lear S
- Lees M
- Lentaigne C
- Levine AP
- Liesner R
- Linger R
- Longhurst H
- Lorenzo L
- Louka E
- Machado R
- Mackenzie A
- Maclaren R
- Mahdi-Rogers M
- Maher E
- Maimaris J
- Majewski J
- Makris M
- Mangles S
- Manson A
- Manzur A
- Mapeta R
- Marey I
- Markus HS
- Marschall H-U
- Marshall A
- Martin JM
- Masati L
- Mathias M
- Matser V
- Matthews E
- Maw A
- McCarthy M
- McDermott E
- McGowan S
- McJannet C
- Meacham S
- Mead A
- Meehan S
- Megy K
- Mehta S
- Mendonça C
- Michaelides M
- Millar CM
- Moledina S
- Montani D
- Moore A
- Morrell NW
- Mumford A
- Murng S
- Murphy E
- Nava C
- Nejentsev S
- Noorani S
- Noordegraaf AV
- Nurden P
- Oksenhendler E
- Ormondroyd L
- Othman S
- Ouwehand WH
- Papadia S
- Park S-M
- Parker A
- Pasi J
- Patch C
- Paterson J
- Payne J
- Peacock AJ
- Peerlinck K
- Penkett CJ
- Pepke-Zaba J
- Perry DJ
- Pfundt R
- Pollock V
- Polwarth G
- Ponsford M
- Qasim W
- Quinti I
- Ranganathan L
- Rankin J
- Rankin S
- Raymond FL
- Raymond FL
- Rayner-Matthews P
- Rehnstrom K
- Reid E
- Reilly M
- Renton T
- Revel-Vilk S
- Rhodes CJ
- Rice A
- Richards M
- Richardson S
- Richter A
- Roberts I
- Rondina M
- Ross RVM
- Rosser E
- Roughley C
- Roy N
- Rue-Albrecht K
- Saleem M
- Samarghitean C
- Sanchis-Juan A
- Sanchis-Juan A
- Sandford R
- Santra S
- Sargur R
- Savic S
- Scelsi L
- Schotte G
- Schulman S
- Schulze H
- Scott R
- Scully M
- Seneviratne S
- Sewell C
- Shamardina O
- Shipley D
- Simeoni I
- Simpson M
- Sivapalaratnam S
- Smith KGC
- Sohal A
- Soubrier F
- Southgate L
- Staines S
- Staples E
- Stark H
- Stauss H
- Stein P
- Stephens J
- Stirrups K
- Stock S
- Stubbs M
- Suntharalingam J
- Tait RC
- Talks K
- Tan R
- Tan Y
- Thachil J
- Thaventhiran J
- Themistocleous A
- Thomas E
- Thomas M
- Thompson D
- Thrasher A
- Tischkowitz M
- Titterton C
- Toh C-H
- Toshner M
- Treacy CM
- Trembath R
- Tuna S
- Turek W
- Turro E
- Vale T
- Van Bokhoven H
- Van Essen A
- Van Geet C
- Van Ravenswaaij-Arts C
- Van Zuydam N
- Veltman M
- Vogt J
- Von Ziegenweldt J
- Wakeling E
- Walker S
- Walker S
- Wanjiku I
- Warner TQ
- Wassmer E
- Watkins H
- Watson H
- Watt C
- Webster A
- Wei W
- Welch S
- Westbury S
- Wharton J
- Whitehorn D
- Whitworth J
- Wilkins M
- Willcocks L
- Williamson C
- Wong EKS
- Woods G
- Wort SJ
- Yates K
- Yeatman N
- Yong P
- Young T
- Yu Wai Man P
- Yu P
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2018
- Field of study
Next-generation sequencing has been invaluable in the elucidation of the genetic etiology of many subtypes of intellectual disability in recent years. Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WAS protein family member 1 (WASF1) in five unrelated individuals with moderate to profound intellectual disability with autistic features and seizures. WASF1, also known as WAVE1, is part of the WAVE complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three variants are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using fibroblast cells from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 cause a rare form of intellectual disability
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
- Author
- Abdel-Aziz AK
- Abdelfatah S
- Abdellatif M
- Abdoli A
- Abel S
- Abeliovich H
- Abildgaard MH
- Abudu YP
- Acevedo-Arozena A
- Adamopoulos IE
- Adeli K
- Adolph TE
- Adornetto A
- Aflaki E
- Agam G
- Agarwal A
- Aggarwal BB
- Agnello M
- Agostinis P
- Agrewala JN
- Agrotis A
- Aguilar PV
- Ahmad ST
- Ahmed ZM
- Ahumada-Castro U
- Aits S
- Aizawa S
- Akkoc Y
- Akoumianaki T
- Akpinar HA
- Al-Abd AM
- Al-Akra L
- Al-Gharaibeh A
- Alaoui-Jamali MA
- Alberti S
- Alcocer-GĂłmez E
- Alessandri C
- Ali M
- Alim Al-Bari MA
- Aliwaini S
- Alizadeh J
- Almacellas E
- Almasan A
- Alonso A
- Alonso GD
- Altan-Bonnet N
- Altieri DC
- Alves da Costa C
- Alves S
- Alzaharna MM
- Amadio M
- Amantini C
- Amaral C
- Ambrosio S
- Amer AO
- Ammanathan V
- An Z
- Andersen SU
- Andrabi SA
- Andrade-Silva M
- Andres AM
- Angelini S
- Ann D
- Anozie UC
- Ansari MY
- Antas P
- Antebi A
- AntĂłn Z
- Anwar T
- Apetoh L
- Apostolova N
- Araki T
- Araki Y
- Arasaki K
- Araya J
- AraĂșjo WL
- Arden C
- Arguelles S
- Arias E
- Arikkath J
- Arimoto H
- Ariosa AR
- Armstrong-James D
- Arnauné-Pelloquin L
- Aroca A
- Arroyo DS
- Arsov I
- Artero R
- Arévalo M-A
- Asaro DML
- Aschner M
- Ashrafizadeh M
- Ashur-Fabian O
- Atanasov AG
- Au AK
- Auberger P
- Auner HW
- Aurelian L
- Autelli R
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- Ălvarez ĂMC
- Ăvalos Y
- Ănal G
- ĂstĂŒn S
- ÄoliÄ M
- ÄokiÄ J
- Ćœerovnik E
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
Observation of a New Excited Beauty Strange Baryon Decaying to Îb- Ï+Ï-
- Author
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- Publication venue
- American Physical Society
- Publication date
- 01/01/2021
- Field of study
The Îb-Ï+Ï- invariant mass spectrum is investigated with an event sample of proton-proton collisions at s=13 TeV, collected by the CMS experiment at the LHC in 2016-2018 and corresponding to an integrated luminosity of 140 fb-1. The ground state Îb- is reconstructed via its decays to J/ÏÎ- and J/ÏÎK-. A narrow resonance, labeled Îb(6100)-, is observed at a Îb-Ï+Ï- invariant mass of 6100.3±0.2(stat)±0.1(syst)±0.6(Îb-) MeV, where the last uncertainty reflects the precision of the Îb- baryon mass. The upper limit on the Îb(6100)- natural width is determined to be 1.9 MeV at 95% confidence level. The low Îb(6100)- signal yield observed in data does not allow a measurement of the quantum numbers of the new state. However, following analogies with the established excited Îc baryon states, the new Îb(6100)- resonance and its decay sequence are consistent with the orbitally excited Îb- baryon, with spin and parity quantum numbers JP=3/2-
Measurement of the inclusive and differential Higgs boson production cross sections in the decay mode to a pair of Ï Leptons in pp collisions at sqrt[s]=13ââTeV
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- Watson IJ
- Wayne M
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- Weber HA
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- Wen Y
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- Whitbeck A
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- Wickramage N
- Wickramarathna DDC
- Wiedenbeck S
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- Yan F
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- Yang S
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- Yao Y
- Yarar H
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- Yohay R
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- Yuldashev BS
- Yumiceva F
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- Zacharopoulou A
- Zahid S
- Zaleski S
- Zalewski P
- Zanetti M
- Zarubin A
- Zarucki M
- Zecchinelli AG
- Zeinali M
- Zeuner WD
- Zghiche A
- Zhang F
- Zhang H
- Zhang J
- Zhang L
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- Zhizhin I
- Zhokin A
- Zhu DH
- Zhu RY
- Ziemons T
- Zoi I
- Zolkapli Z
- Zorbakir IS
- Zorbilmez C
- Zotto P
- Zotz A
- Zou D
- Zou R
- Zucchetta A
- Zumerle G
- Zuo X
- Zuolo D
- Zygala L
- Ălvarez FernĂĄndez A
- Ăzçelik Ă
- Publication venue
- 'American Physical Society (APS)'
- Publication date
- 01/01/2022
- Field of study
Measurements of the inclusive and differential fiducial cross sections of the Higgs boson are presented, using the Ï lepton decay channel. The differential cross sections are measured as functions of the Higgs boson transverse momentum, jet multiplicity, and transverse momentum of the leading jet in the event, if any. The analysis is performed using proton-proton collision data collected with the CMS detector at the LHC at a center-of-mass energy of 13ââTeV and corresponding to an integrated luminosity of 138ââfb^{-1}. These are the first differential measurements of the Higgs boson cross section in the final state of two Ï leptons. In final states with a large jet multiplicity or with a Lorentz-boosted Higgs boson, these measurements constitute a significant improvement over measurements performed in other final states
Look before you leap - individual variation in social vigilance shapes socio-spatial group properties in an agent-based model
- Author
- A Treves
- AX Lopez-Lujan
- B Thierry
- Berry M. Spruijt
- BMA Goossens
- BT Hirsch
- C Blois-Heulin
- C Blois-Heulin
- C Busse
- C Sueur
- C Teufel
- C Torres de Assumpção
- CH Janson
- CH Southwick
- CK Hemelrijk
- CK Hemelrijk
- CL Hall
- CP Schaik van
- D Maestripieri
- D Post van der
- D Rasmussen
- D Watts
- E Evers
- EB Keverne
- Elisabeth H. M. Sterck
- Ellen Evers
- EM Barrows
- G Cowlishaw
- G Roberts
- GC Keys
- GD Jensen
- GR Emory
- GVN Powell
- H Vries de
- H Vries de
- Han de Vries
- HB Virgo
- HR Pulliam
- IR Inglis
- J Altmann
- J Itani
- JG Robinson
- JH Kaufmann
- JJ Bryson
- JM Black
- K Imanishi
- K Immelmann
- K Wada
- KE Bonnie
- KRL Hall
- LA Isbell
- M Yamada
- MA Elgar
- MRA Chance
- MRA Chance
- MRA Chance
- N Kutsukake
- NG Caine
- NL McNelis
- P Freniere La
- P Hogeweg
- PL Pannozzo
- R Steenbeek
- RA Hinde
- RH Haude
- RO Deaner
- S Coussi-Korbel
- SA Rands
- SC Alberts
- SL Washburn
- T Caraco
- TE Rowell
- TK Pitcairn
- TM Caro
- W Sellers
- WD Hamilton
- Y Sugiyama
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Biallelic Mutation of ARHGEF18, Involved in the Determination of Epithelial Apicobasal Polarity, Causes Adult-Onset Retinal Degeneration
- Author
- Aitman T
- Alachkar H
- Ali M
- Ali S
- Allen HL
- Allen L
- Allsup D
- Ambegaonkar G
- Anderson J
- Antrobus R
- Armstrong R
- Arno G
- Arno G
- Arno G
- Arumugakani G
- Ashford S
- Astle W
- Attwood A
- Austin S
- Bacchelli C
- Bakchoul T
- Balda MS
- Bariana TK
- Baxendale H
- Bennett D
- Bethune C
- Bibi S
- Bitner-Glindzicz M
- Black G
- Bleda M
- Boggard H
- Bolton-Maggs P
- Booth C
- Bradley JR
- Brady A
- Brown M
- Browning M
- Bryson C
- Burns S
- Calleja P
- Canham N
- Carmichael J
- Carss K
- Carss KJ
- Caulfield M
- Chalmers E
- Chandra A
- Cheetham ME
- Cheetham ME
- Chinnery P
- Chitre M
- Church C
- Clement E
- Clements-Brod N
- Clowes V
- Coghlan G
- Collins P
- Cooper N
- Creaser-Myers A
- DaCosta R
- Daugherty L
- Davies S
- Davis J
- De Vries M
- Deegan P
- Deevi SVV
- Deshpande C
- Devlin L
- Dewhurst E
- Doffinger R
- Dormand N
- Downes S
- Drewe E
- Edgar D
- Egner W
- Erber WN
- Erwood M
- Everington T
- Favier R
- Fiorentino A
- Fiorentino A
- Firth H
- Fletcher D
- Flinter F
- Fox JC
- Frary A
- Freson K
- Furie B
- Furnell A
- Gale D
- Gardham A
- Gattens M
- Ghali N
- Ghataorhe PK
- Ghurye R
- Gibbs S
- Gillespie R
- Gilmour K
- Gissen P
- Goddard S
- Gomez K
- Gordins P
- Greene D
- Greenhalgh A
- Greinacher A
- Grigoriadou S
- Grozeva D
- GrÀf S
- Hackett S
- Hadinnapola C
- Hague R
- Haimel M
- Halford S
- Hall G
- Halmagyi C
- Hammerton T
- Hardcastle AJ
- Hardcastle AJ
- Hart D
- Hayman G
- Heemskerk JWM
- Henderson R
- Hensiek A
- Henskens Y
- Herwadkar A
- Holden S
- Holder GE
- Holder M
- Holder S
- Hu F
- Huissoon A
- Hull S
- Humbert M
- Hurst J
- Inglehearn C
- Ingram S
- James R
- Jolles S
- Josifova D
- Kazmi R
- Keeling D
- Kelleher P
- Kelly AM
- Kennedy F
- Khan K
- Kiely D
- Kingston N
- Koziell A
- Krishnakumar D
- Kuijpers TW
- Kumararatne D
- Kurian M
- Laffan MA
- Lambert MP
- Lawrie A
- Lear S
- Lees M
- Lentaigne C
- Liesner R
- Linger R
- Lise S
- Longhurst H
- Lord E
- Lorenzo L
- Machado R
- Mackenzie R
- MacLaren R
- Maher E
- Maimaris J
- Mangles S
- Manson A
- Manson F
- Mapeta R
- Markus HS
- Martin J
- Masati L
- Mathias M
- Matser V
- Matter K
- Maw A
- McDermott E
- McJannet C
- McKibbin M
- Meacham S
- Meehan S
- Megy K
- Mehta S
- Michaelides M
- Michaelides M
- Millar CM
- Moledina S
- Moore A
- Moore AT
- Morrell N
- Mumford A
- Murng S
- Murphy E
- Nejentsev S
- Nemeth A
- Noorani S
- Noordegraaf AV
- Nurden P
- Oksenhendler E
- Ouwehand WH
- Papadia S
- Park S-M
- Parker A
- Pasi J
- Patch C
- Paterson J
- Payne J
- Peacock A
- Peerlinck K
- Penkett CJ
- Pepke-Zaba J
- Perry DJ
- Plagnol V
- Plagnol V
- Pollock V
- Polwarth G
- Ponitkos N
- Ponsford M
- Poulter J
- Qasim W
- Quinti I
- Rankin J
- Rankin S
- Raymond FL
- Raymond FL
- Rehnstrom K
- Reid E
- Rhodes CJ
- Richards M
- Richardson S
- Richter A
- Roberts I
- Robson AG
- Rondina M
- Rosser E
- Roughley C
- Rue-Albrecht K
- Samarghitean C
- Sanchis-Juan A
- Sandford R
- Santra S
- Sargur R
- Savic S
- Schulman S
- Schulze H
- Scott R
- Scully M
- Seneviratne S
- Sergouniotis P
- Sewell C
- Shamardina O
- Shipley D
- Simeoni I
- Sivapalaratnam S
- Smith K
- Sohal A
- Southgate L
- Staines S
- Staples E
- Stauss H
- Stein P
- Stephens J
- Stirrups K
- Stock S
- Suntharalingam J
- Tait RC
- Talks K
- Tan Y
- Thachil J
- Thaventhiran J
- Thomas E
- Thomas M
- Thompson D
- Thrasher A
- Tischkowitz M
- Titterton C
- Toh C-H
- Toomes C
- Toshner M
- Treacy C
- Trembath R
- Tuna S
- Turek W
- Turro E
- Van Geet C
- van Heyningen V
- Veltman M
- Vogt J
- von Ziegenweldt J
- Wakeling E
- Wanjiku I
- Warner TQ
- Wassmer E
- Watkins H
- Webster A
- Webster AR
- Webster AR
- Welch S
- Westbury S
- Wharton J
- Whitehorn D
- Wilkins M
- Willcocks L
- Williamson C
- Woods G
- Wort J
- Yeatman N
- Yong P
- Young T
- Yu J
- Yu P
- Zihni C
- Publication venue
- Publication date
- 02/02/2017
- Field of study
Mutations in more than 250 genes are implicated in inherited retinal dystrophy; the encoded proteins are involved in a broad spectrum of pathways. The presence of unsolved families after highly parallel sequencing strategies suggests that further genes remain to be identified. Whole-exome and -genome sequencing studies employed here in large cohorts of affected individuals revealed biallelic mutations in ARHGEF18 in three such individuals. ARHGEF18 encodes ARHGEF18, a guanine nucleotide exchange factor that activates RHOA, a small GTPase protein that is a key component of tight junctions and adherens junctions. This biological pathway is known to be important for retinal development and function, as mutation of CRB1, encoding another component, causes retinal dystrophy. The retinal structure in individuals with ARHGEF18 mutations resembled that seen in subjects with CRB1 mutations. Five mutations were found on six alleles in the three individuals: c.808A>G (p.Thr270Ala), c.1617+5G>A (p.Asp540Glyfsâ63), c.1996C>T (p.Arg666â), c.2632G>T (p.Glu878â), and c.2738_2761del (p.Arg913_Glu920del). Functional tests suggest that each disease genotype might retain some ARHGEF18 activity, such that the phenotype described here is not the consequence of nullizygosity. In particular, the p.Thr270Ala missense variant affects a highly conserved residue in the DBL homology domain, which is required for the interaction and activation of RHOA. Previously, knock-out of Arhgef18 in the medaka fish has been shown to cause larval lethality which is preceded by retinal defects that resemble those seen in zebrafish Crumbs complex knock-outs. The findings described here emphasize the peculiar sensitivity of the retina to perturbations of this pathway, which is highlighted as a target for potential therapeutic strategies
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