613 research outputs found
University–industry collaboration: using meta-rules to overcome barriers to knowledge transfer
- Author
- A Davies
- A Dowling
- A Hall
- A Kane
- A Schoen
- A-C Pache
- A. Alexander
- AM Epp
- AS Miner
- AT Alexander
- AT Alexander
- AT Alexander
- AT Alexander
- AT Alexander
- B Bozeman
- C Argyris
- C Carter
- C O’Kane
- C Paradeise
- C Plewa
- C. Manolchev
- CN Bredillet
- CP Eveleens
- D Dubois
- D Martin
- D Sainsbury
- D Sull
- D Teece
- D. P. Martin
- DM Weckowska
- DN Sull
- DS Siegel
- DS Siegel
- E Albats
- E Bellini
- E Carayannis
- E Wit-de Vries
- F Rothaermel
- FN Brady
- G Kruss
- G Szulanski
- GS Halford
- J Bruneel
- J Christopher
- J Cranefield
- J Cunningham
- J Dowling
- J Howells
- J Howells
- JA Cunningham
- JA Cunningham
- JG Wacker
- JL Bradach
- K Debackere
- K Miller
- K Miller
- K Miller
- K. Miller
- KD Markman
- KG Hobbs
- KR Andrews
- L Argote
- L Xu
- M Alvesson
- M Easterby-Smith
- M Guerrero
- M McAdam
- M Perkmann
- M Perkmann
- M Perkmann
- M Perkmann
- M Schultz
- MA Chilton
- MC Suchman
- MJ Eppler
- N Lockett
- N Vargas
- OED
- P Bansal
- P Benneworth
- PACEC
- PH Thornton
- PM Swamidass
- R Davis
- R Ferguson
- R McAdam
- RE Litan
- RM Weischedel
- RP O’Shea
- RW Revans
- S Deetz
- S Robinson
- S Yusuf
- SH Liao
- SR Murray
- T-H Liu
- V Galán-Muros
- W Chapple
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 17/07/2018
- Field of study
This is the final version of the article. Available from Springer Verlag via the DOI in this record.University–industry knowledge transfer is an important source wealth of creation for all partners; however, the practical management of this activity within universities is often hampered by procedural rigidity either through the absence of decision-making protocols to reconcile conflicting priorities or through the inconsistent implementation of existing policies. This is problematic, since it can impede operational effectiveness, prevent inter-organisational knowledge-creation and hamper organisational learning. This paper addresses this issue by adopting a cross-discipline approach and presenting meta-rules as a solution to aid organisational decision making. It is proposed that meta-rules can help resolve tensions arising from conflicting priorities between academics, knowledge transfer offices and industry and help facilitate strategic alignment of processes and policies within and between organisations. This research contributes to the growing debate on the strategic challenges of managing knowledge transfer and presents meta-rules as a practical solution to facilitate strategic alignment of internal and external stakeholder tensions. Meta-rules has previously only been applied in a computer intelligence context however, this research proves the efficacy of meta rules in a university–industry knowledge transfer context. This research also has practical implications for knowledge transfer office managers who can use meta-rules to help overcome resource limitations, conflicting priorities and goals of diverse internal and external stakeholders
The EFF-1A Cytoplasmic Domain Influences Hypodermal Cell Fusions in C. elegans But Is Not Dependent on 14-3-3 Proteins.
- Author
- A Aitken
- A Ali
- A Berdichevsky
- A Fleissner
- A Ghosh-Roy
- A Sapir
- A Sapir
- AA Cuenca
- AM Blagborough
- B Bjerregaard
- B Podbilewicz
- B Podbilewicz
- B Podbilewicz
- C Barry
- Claude Prigent
- CQ Nguyen
- D Bridges
- D Duelli
- D Sanges
- DG Morton
- DI Cohen
- DM Duelli
- EH Chen
- EH Chen
- F Lluis
- G Shemer
- GE Parris
- H Fu
- H Sumer
- HC Aguilar
- J Li
- J Palma-Guerrero
- J Perez-Vargas
- J Plenefisch
- J Pomerantz
- J Yochem
- JA McKinnell
- Jacob J. del Campo
- JC Tilton
- JE Sulston
- JE Sulston
- Jessica H. Shinn-Thomas
- JH Shinn-Thomas
- Jianjun Wang
- JJ del Campo
- JM Pawelek
- JP Rasmussen
- JS Gilleard
- K Shilagardi
- L Timmons
- L Timmons
- M Chiorazzi
- M Koppen
- M Oren-Suissa
- M Oren-Suissa
- M Oren-Suissa
- MK Dougherty
- MR Roberts
- MR Schiller
- N Blom
- N Hatsugai
- ND Read
- O Avinoam
- O Avinoam
- PS Aguilar
- Q Yao
- R Benton
- R Benton
- RE Dutch
- S Balla
- S Brenner
- S Harrison
- S Keay
- S Martens
- S Rajasekaran
- S Shikano
- T Gattegno
- T Harkness
- T Melby
- T Mrowiec
- T Sergel
- T Zeev-Ben-Mordehai
- TW Hurd
- W Golinowski
- W Wang
- W Wang
- WA Mohler
- WA Mohler
- WA Mohler
- William A. Mohler
- WS Rasband
- Y Liu
- Y Shi
- YH Wong
- Publication venue
- Jefferson Digital Commons
- Publication date
- 01/01/2016
- Field of study
BACKGROUND: Regulatory and biophysical mechanisms of cell-cell fusion are largely unknown despite the fundamental requirement for fused cells in eukaryotic development. Only two cellular fusogens that are not of clear recent viral origin have been identified to date, both in nematodes. One of these, EFF-1, is necessary for most cell fusions in Caenorhabditis elegans. Unregulated EFF-1 expression causes lethality due to ectopic fusion between cells not developmentally programmed to fuse, highlighting the necessity of tight fusogen regulation for proper development. Identifying factors that regulate EFF-1 and its paralog AFF-1 could lead to discovery of molecular mechanisms that control cell fusion upstream of the action of a membrane fusogen. Bioinformatic analysis of the EFF-1A isoform\u27s predicted cytoplasmic domain (endodomain) previously revealed two motifs that have high probabilities of interacting with 14-3-3 proteins when phosphorylated. Mutation of predicted phosphorylation sites within these motifs caused measurable loss of eff-1 gene function in cell fusion in vivo. Moreover, a human 14-3-3 isoform bound to EFF-1::GFP in vitro. We hypothesized that the two 14-3-3 proteins in C. elegans, PAR-5 and FTT-2, may regulate either localization or fusion-inducing activity of EFF-1.
METHODOLOGY/PRINCIPAL FINDINGS: Timing of fusion events was slightly but significantly delayed in animals unable to produce full-length EFF-1A. Yet, mutagenesis and live imaging showed that phosphoserines in putative 14-3-3 binding sites are not essential for EFF-1::GFP accumulation at the membrane contact between fusion partner cells. Moreover, although the EFF-1A endodomain was required for normal rates of eff-1-dependent epidermal cell fusions, reduced levels of FTT-2 and PAR-5 did not visibly affect the function of wild-type EFF-1 in the hypodermis.
CONCLUSIONS/SIGNIFICANCE: Deletion of the EFF-1A endodomain noticeably affects the timing of hypodermal cell fusions in vivo. However, prohibiting phosphorylation of candidate 14-3-3-binding sites does not impact localization of the fusogen. Hypodermal membrane fusion activity persists when 14-3-3 expression levels are reduced
Whole-chromosome hitchhiking driven by a male-killing endosymbiont.
- Author
- A Bankevich
- A Duplouy
- A Mackintosh
- A Martin
- A Mazo-Vargas
- A Rambaut
- AE Wright
- AF Rives
- AJ Mongue
- B. Charlesworth
- CA Clarke
- CC Chang
- CR Lee
- D Bachtrog
- D Bryant
- D Charlesworth
- D. Charlesworth
- DAS Smith
- DAS Smith
- DAS Smith
- DAS Smith
- DAS Smith
- DAS Smith
- DAS Smith
- DAS Smith
- DAS Smith
- DF Owen
- DH Huson
- E Idris
- EA Hornett
- EL Westerman
- EM Leffler
- FA Simão
- FM Jiggins
- FM Jiggins
- FM Jiggins
- G Lunter
- G Lushai
- GA Van der Auwera
- GDD Hurst
- GDD Hurst
- Heliconius Genome Consortium T.
- I Pala
- IJ Gordon
- IJ Gordon
- J Kitano
- JA Balbuena
- JC Fay
- JK Herren
- JM Coughlan
- JW Davey
- JW Davey
- K Kunte
- KK Dasmahapatra
- L Wilfert
- L Zhang
- LP Pryszcz
- LZ Carabajal Paladino
- M a DePristo
- M Kirkpatrick
- M Steinemann
- MF Palopoli
- MF Richardson
- MJ Thompson
- N Dierckxsens
- NJ Nadeau
- O Delaneau
- O Delaneau
- P Nguyen
- PD Keightley
- PJ Wittkopp
- R Bouckaert
- R Bürger
- R Overbeek
- RD Reed
- RF Guerrero
- RK Aziz
- RR Bouckaert
- RR Bracewell
- S Guindon
- S Huang
- S Smith D a
- S Zhan
- SH Martin
- SM Van Belleghem
- V Ahola
- W Traut
- WR Rice
- Publication venue
- PLoS Biol
- Publication date
- 01/02/2020
- Field of study
Neo-sex chromosomes are found in many taxa, but the forces driving their emergence and spread are poorly understood. The female-specific neo-W chromosome of the African monarch (or queen) butterfly Danaus chrysippus presents an intriguing case study because it is restricted to a single 'contact zone' population, involves a putative colour patterning supergene, and co-occurs with infection by the male-killing endosymbiont Spiroplasma. We investigated the origin and evolution of this system using whole genome sequencing. We first identify the 'BC supergene', a broad region of suppressed recombination across nearly half a chromosome, which links two colour patterning loci. Association analysis suggests that the genes yellow and arrow in this region control the forewing colour pattern differences between D. chrysippus subspecies. We then show that the same chromosome has recently formed a neo-W that has spread through the contact zone within approximately 2,200 years. We also assembled the genome of the male-killing Spiroplasma, and find that it shows perfect genealogical congruence with the neo-W, suggesting that the neo-W has hitchhiked to high frequency as the male-killer has spread through the population. The complete absence of female crossing-over in the Lepidoptera causes whole-chromosome hitchhiking of a single neo-W haplotype, carrying a single allele of the BC supergene and dragging multiple non-synonymous mutations to high frequency. This has created a population of infected females that all carry the same recessive colour patterning allele, making the phenotypes of each successive generation highly dependent on uninfected male immigrants. Our findings show how hitchhiking can occur between the physically unlinked genomes of host and endosymbiont, with dramatic consequences
Current and prospective pharmacological targets in relation to antimigraine action
- Author
- A Bergerot
- A Buchwalder
- A Carlsson
- A Carlsson
- A Hughes
- A MaassenVanDenBrink
- A MaassenVanDenBrink
- A May
- A May
- A May
- A Pindon
- A Rouleau
- A Srikiatkhachorn
- A Sudilovsky
- A Tanoue
- A Wackenfors
- AC Honey
- AD Bennett
- AD Medhurst
- AD Michel
- AE Luebke
- AH Bom
- AH Calhoun
- AJ Kaumann
- AL Magos
- AM Aloisi
- AM Carruthers
- AM Lands
- AM Maagdenberg van den
- Antoinette MaassenVanDenBrink
- AP Ford
- AP Silva
- B Forssman
- B Gómez-Mancilla
- B Pouzet
- B Schaerlinger
- B Weiss
- BB Fredholm
- BB Hoffman
- BJ Francken
- BK Kobilka
- BK Rasmussen
- BW Somerville
- BW Somerville
- C Hofmann
- C Hohoff
- C Lampl
- C Tzourio
- CA Salvatore
- Carlos M. Villalón
- CG Dahlöf
- CM Villalón
- CM Villalón
- CM Villalón
- CM Villalón
- CN Sang
- CY Yu
- D Centurión
- D Hoyer
- D Hoyer
- D Sarsero
- DA Curran
- David Centurión
- DB Bylund
- DB Bylund
- DB Bylund
- DB Bylund
- DB Bylund
- DD Mitsikostas
- DD Mitsikostas
- DE Dluzen
- DJ Goldstein
- DJ Goldstein
- DJ Goldstein
- DL Jackson
- DM Pérez
- DR Poyner
- DR Thomas
- DR Thomas
- DS Millson
- DW Dodick
- E Del Bene
- E Enmark
- E Fabbretti
- E Fusayasu
- E Tronvik
- EA Barnard
- EA MacGregor
- EA MacGregor
- EA MacGregor
- EA MacGregor
- EM Cassidy
- EW Willems
- EW Willems
- EW Willems
- EW Willems
- F Facchinetti
- F Facchinetti
- F Marceau
- F Martínez
- FG Freitag
- FM Cutrer
- FM Cutrer
- FM Cutrer
- G Attali
- G Burnstock
- G D’Andrea
- G Trapani Di
- GA Lambert
- GA Michelotti
- GL Stiles
- GM Terwindt
- GW Price
- GW Smith
- H Doods
- H Heyck
- H Kaube
- H Kowa
- H Schrader
- HC Diener
- HM Vargas
- HO Kalkman
- HS Blaxall
- I Jansen-Olesen
- I Mody
- IH Page
- IT Forbes
- J Galitzky
- J Honkaniemi
- J Olesen
- J Olesen
- JA Charles
- JA Terrón
- JB Becker
- JC Jen
- JC Shih
- JD Carroll
- JD Classey
- JE Palmer
- JJ Fernández-Ruíz
- JL Brandes
- JM Brundege
- JM Cruickshank
- JM Orshal
- JP Dreier
- JP Hieble
- JP Hieble
- JR Arch
- JR Clements
- JR Docherty
- JR Fozard
- JW Lomasney
- JW Regan
- K Kapoor
- K Schmuck
- K Zimmermann
- KA Krobert
- KA Petersen
- KA Petersen
- Kayi Y. Chan
- KI Roon
- KJ Powell
- KL Hoskin
- KMA Welch
- KP Lesch
- KR Oliver
- KW Johnson
- L Edvinsson
- L Edvinsson
- L Hein
- LA Phebus
- LE Limbird
- LH Lassen
- LH Lassen
- LH Lassen
- LJ Smith
- LL Ven van de
- LM McLatchie
- M Anthony
- M Anthony
- M Boccuni
- M Cyr
- M Farkkila
- M Gasparo De
- M Hasselblatt
- M Iovino
- M Kallela
- M Mochi
- M Oshita
- M Peeters
- M Quartu
- M Spedding
- M Yanagisawa
- MA Moskowitz
- MA Moskowitz
- MD Ferrari
- MD Ferrari
- ME Bigal
- ME Erdal
- ME Moreau
- MG Garry
- MG Hanna
- MJ Kelly
- ML Hernández
- MM Rapport
- MT Piascik
- NG Bowery
- NJ Colson
- NJ Colson
- NJ Giffin
- NM Barnes
- NM Ramadan
- NM Ramadan
- NM Ramadan
- NT Mathew
- O Blin
- P Barbanti
- P Barbanti
- P Geppetti
- P Kastner
- P Roffey
- P Sarchielli
- P Sarchielli
- P Tfelt-Hansen
- P Tfelt-Hansen
- P Vries De
- P Vries De
- PD Drummond
- PD Drummond
- PJ Goadsby
- PJ Goadsby
- PJ Goadsby
- PJ Goadsby
- PJ Goadsby
- PJ Goadsby
- PJ Goadsby
- PJ Goadsby
- PL Durham
- PP Lakhlani
- PR Saxena
- PR Saxena
- PR Saxena
- PR Saxena
- Pramod R. Saxena
- PT Hurley
- QP Ma
- R Burstein
- R Cerbo
- R Hering-Hanit
- R Lodi
- R Quirion
- R Rabkin
- R Uddman
- R Würz
- RA Bond
- RA Ophoff
- RB Lipton
- RB McCall
- RE Widdop
- RJ Storer
- RJ Storer
- RJ Storer
- RL Weinshank
- RO Millán-Guerrero
- RO Millán-Guerrero
- RP Ahlquist
- RW Kimball
- RWM Broek van den
- S Akerman
- S Akerman
- S Akerman
- S Akerman
- S Akerman
- S Cotecchia
- S Ghelardoni
- S Gupta
- S Gupta
- S Gupta
- S Maude
- S Mehrotra
- S Mehrotra
- S Nag
- S Paterna
- S Shepheard
- S Stellar
- Saurabh Gupta
- SD Brain
- SD Silberstein
- SD Silberstein
- SD Silberstein
- SG Hamilton
- SJ Hill
- SJ Peroutka
- SJ Peroutka
- SJ Peroutka
- SJ Peroutka
- SJ Peroutka
- SJ Peroutka
- SJ Tallaksen-Greene
- SJ Tepper
- SM Lanier
- SP Alexander
- SP Cook
- SP Cook
- ST Lee
- Suneet Mehrotra
- T Attina
- T Ishida
- T Ishida
- T Matsubara
- T Takenaka
- TJ Murphy
- TM Buchanan
- TW Ho
- U Arulmani
- U Arulmani
- U Arulmani
- V Erspamer
- V Erspamer
- V Johannsson
- V Limmroth
- V Shaygannejad
- V Simonneaux
- VT Martin
- W Chai
- WF Stewart
- WI Bender
- WL Hasler
- WM Herrmann
- WS Lee
- Y Dumont
- Y Sahara
- Y Zhang
- YT Lau
- Z Cohen
- Z Zhang
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2008
- Field of study
Migraine is a recurrent incapacitating neurovascular disorder characterized by unilateral and throbbing headaches associated with photophobia, phonophobia, nausea, and vomiting. Current specific drugs used in the acute treatment of migraine interact with vascular receptors, a fact that has raised concerns about their cardiovascular safety. In the past, α-adrenoceptor agonists (ergotamine, dihydroergotamine, isometheptene) were used. The last two decades have witnessed the advent of 5-HT1B/1D receptor agonists (sumatriptan and second-generation triptans), which have a well-established efficacy in the acute treatment of migraine. Moreover, current prophylactic treatments of migraine include 5-HT2 receptor antagonists, Ca2+ channel blockers, and β-adrenoceptor antagonists. Despite the progress in migraine research and in view of its complex etiology, this disease still remains underdiagnosed, and available therapies are underused. In this review, we have discussed pharmacological targets in migraine, with special emphasis on compounds acting on 5-HT (5-HT1-7), adrenergic (α1, α2, and β), calcitonin gene-related peptide (CGRP 1 and CGRP2), adenosine (A1, A2, and A3), glutamate (NMDA, AMPA, kainate, and metabotropic), dopamine, endothelin, and female hormone (estrogen and progesterone) receptors. In addition, we have considered some other targets, including gamma-aminobutyric acid, angiotensin, bradykinin, histamine, and ionotropic receptors, in relation to antimigraine therapy. Finally, the cardiovascular safety of current and prospective antimigraine therapies is touched upon
Canagliflozin and Cardiovascular and Renal Outcomes in Type 2 Diabetes Mellitus and Chronic Kidney Disease in Primary and Secondary Cardiovascular Prevention Groups
- Author
- Abraham Oomman
- Accini Mendoza Jose Luis
- Agarwal R
- Aggarwal N
- Aizenberg D
- Akiyama Hitoshi
- Alamartine Eric
- Albisu Jp
- Alvarisqueta A
- Amodeo C
- Andreeva V
- Angelova A
- Aoki Hiromi
- Arcos Edgar
- Aronson R
- Asano Akimichi
- Avendano Jorge
- Bajaj H
- Bakris G
- Bartaskova Dagmar
- Bartolacci I
- Barton Petr
- Belobradkova Jana
- Berli Ma
- Bhushan Raju Sree
- Bompoint S
- Bonadonna Riccardo
- Bordonava A
- Borot Sophie
- Bregman R
- Brenner Bm
- Bull S
- Burst Volker
- Calella P
- Canani Lh
- Cannon Cp
- Cantero Mc
- Capuano G
- Cariou Bertrand
- Cartasegna Lr
- Casabella Ts
- Castellino Pietro
- Cercos E
- Ceriello Antonio
- Chacra Ar
- Charytan Dm
- Chen Nan
- Chen Qinkai
- Cherney D
- Cheung Nw
- Chiovato Luca
- Chouinard G
- Colaso Pdg
- Coloma Gc
- Colombo H
- Commendatore V
- Contieri Fld
- Conway J
- Cournoyer S
- Csecsei Gyongyi
- Csiky Botond
- Cuadrado J
- Cuneo Ca
- Cunha Borges Jl
- Cusumano Am
- D'Avila D
- da Costa Faa
- Danos Peter
- Daroza G
- de Almeida Rs
- de Brito Cm
- De Cosmo Salvatore
- de la Fuente Ral
- De Nicola Luca
- De Serres S
- de Souza P
- de Zeeuw D
- Deak Laszlo
- Deboni Lm
- Deepak Dewan
- Derosa Giuseppe
- Di Carlo Alberto
- Di Cianni Graziano
- Diaz Ruiz Jorge Ernesto Andres
- Diego Higuera Juan
- Dimitrov S
- Dohnalova Lenka
- Douthat Wg
- Dran Rd
- Drasnar Tomas
- Droste C
- Dube F
- Dudas Mihaly
- Dussol Bertrand
- Edwards R
- Edwin Fernando M.
- Faghih Markus
- Farias E
- Faulmann Grit
- Fauvel Jean-Pierre
- Felicio Js
- Ferkl Richard
- Fernandez Montenegro Maria Alicia
- Fernandez Mf
- Finkelstein H
- Fragale G
- Fraige F
- Franco Rjd
- Frasca Giovanni
- Fraser I
- Fretes Jo
- Fuiano Giorgio
- Gambaro Giovanni
- Gan Shenglian
- Garcia Ortiz Luis Hernando
- Garcia Nh
- Garibotto Giacomo
- Gastaldi A
- Gelersztein E
- Genadieva V
- Genova-Hristova G
- Giorda Carlo
- Glenny Ja
- Godoy Jorquera Juan Gonzalo
- Goldenberg R
- Gomes M
- Gonzalez Orellana Ronaldo Arturo
- Gonzalez Alexander
- Gonzalez Jp
- Gopalakrishnan Natarajan
- Gourdy Pierre
- Goycoa C
- Gracious Noble
- Greene T
- Greloni Gc
- Guerrero Raa
- Guinsburg A
- Gupta A
- Gupta M
- Hachmann Jct
- Halciakova Katarina
- Haller Hermann
- Hansraj Alva
- Harcsa Eleonora
- Hayashida Cy
- Heerspink Hjl
- Henein S
- Hermida S
- Hernandez Triana Eric
- Hissa Mn
- Hristozov K
- Iitsuka Tadashi
- Ines Molina de Salazar Dora
- Jain Dinesh
- Jardine Mj
- Jerwan-Keim Reinhold
- Johnson D
- Juncos Li
- Kajiyama Shizuo
- Kamenov Z
- Kashine Susumu
- Kawada Toshio
- Keitel E
- Keltai Katalin
- Keresztesi Sandor
- Keshavamurthy C. B.
- Khandwala H
- Khullar Dinesh
- Kiss
- Klein Alexandre
- Klokocnikova Vera
- Klyver Mi
- Kodera Takamoto
- Kohara Sk
- Kong Yaozhong
- Kono Hiroshi
- Konyves Laszlo
- Koundurdjiev A
- Kovar Richard
- Koyama Kazunori
- Kraft F
- Krynski F
- Kumeda Yasuro
- Lanchiotti Pv
- Lastuvka Jiri
- Le Meur Yannick
- Leiter L
- Levin A
- Levin A
- Li Detian
- Li Wenge
- Li Xuemei
- Lin Hongli
- Lisboa Hrk
- Liu Jian
- Lozanov L
- Lu Weiping
- Lukac Martin
- Madore F
- Mah Pm
- Mahaffey Kw
- Major Lajos
- Malaver Natalia
- Malberti Fabio
- Mandreoli Marcora
- Manisha Sahay
- Mannucci Edoardo
- Mao Hong
- Marchetta N
- Margaritov V
- Maxeiner Stephan
- Mcmahon A
- Medina Farina Marcelo
- Mele P
- Milagres R
- Mileder Margit
- Miyauchi Shozo
- Mizuyama Kazuyuki
- Molnar Marta
- Montenegro R
- Moreira Diaz Juan Pablo
- Mucsi Janos
- Muirhead N
- Neal B
- Neto Bg
- Nicholls K
- Nicolai S.
- Niiya Tetsuji
- Nonchev B
- Noronha I
- Novoa Pa
- Oishi Hiroko
- Orio Si
- Oroszlan Tamas
- Orsi Emanuela
- Ory Ivan
- Ota Satoshi
- Otreras F
- Oviedo A
- Packham D
- Panarotto D
- Papini Nr
- Paragh Gyorgy
- Paschen Bjoern
- Paul Haase Franklin
- Pecoits R
- Penfornis Alfred
- Pereira Ma
- Peringat Jayameena
- Perkovic V
- Pesickova Satu
- Peterfai Eva
- Peterka Karel
- Petro Gizella
- Petry Tbz
- Piatti Piermarco
- Pichette V
- Plassmann Georg
- Pollock C
- Portes Ed
- Prasad Narayan
- Proietto J
- Pumprla Jiri
- Rabasa-Lhoret R
- Raduan Ra
- Raffaele P
- Ramirez Roca Luis Alberto
- Ramos Cs
- Rangelov R
- Ren Yan
- Resk Jh
- Revesz Katalin
- Rista L
- Roberts A
- Roger S
- Rose Ludger
- Rosenthal N
- Rosero Ricardo
- Roussel Ronan
- Rychlik Ivan
- Saavedra Gajardo Victor
- Sabbag Arn
- Sakakibara Terue
- Sala J
- Sanches Fcc
- Sanchez Arenales Jose Antonio
- Sanchez Polo Jose Vicente
- Santoro Domenico
- Santos Jc
- Saporito W
- Saraiva Jfk
- Sasso Ferdinando Carlo
- Satyanarayana Rao K.
- Saudek Frantisek
- Saulnier Pierre-Jean
- Schiavi Lb
- Schuch T
- Scotton As
- Serviddio Gaetano
- Sessa H
- Shinkov A.
- Song Weihong
- Sreedhar Reddy
- Sreelatha Melemadathil
- Steele A
- Stella Andrea
- Sudhakar Bhimavarapu
- Sun Jiao
- Sun Lin
- Sun T
- Takacs Robert
- Takai Masahiko
- Tangri N
- Temelkova M
- Terront Lozano Monica Alexandra
- Tesar Vladimir
- Thervet Eric
- Thome F
- Tomonaga Osamu
- Torshizi A
- Trevisan Roberto
- Tsang V
- Tsujimoto Mitsuru
- Tu Ping
- Turatti Laa
- Turcios Juarez Erick
- Ulla Mr
- Valderrama Cometa Luis
- Valdez M
- Valenzuela Alex
- Valis Martin
- Vallejos A
- Vangel Sandor
- Vargas Alonso Ruben Dario
- Vasas Szilard
- Vejar Margarita
- Velichkova E
- Vencio Sac
- Veronelli Anna Maria
- Villarino A
- Villegas Ivan
- Visco Ve
- Vyasam Ramesh Chandra
- Wada Takashi
- Wakasugi Masakiyo
- Wakida Yasushi
- Wang Guixia
- Wassermann A
- Watanabe Takayuki
- Weiner Pavel
- Wheeler Dc
- Woo V
- Yakov A
- Yamada Masayo
- Yamada S
- Yanagida Kazuhiro
- Yanase Toshihiko
- Yang Jinkui
- Yavin Y
- Yin Aiping
- Yu Xueqing
- Yumita Wataru
- Yupanqui Hernan
- Zaidman Cj
- Zalunardo Nadia
- Zanella Mt
- Zanoli Luca
- Zaoui Philippe
- Zemek Stanislav
- Zhang H
- Zhao Minghui
- Zheng Hongguang
- Zinman B
- Zsom Marianna
- Publication venue
- 'Ovid Technologies (Wolters Kluwer Health)'
- Publication date
- 01/01/2019
- Field of study
Background: Canagliflozin reduces the risk of kidney failure in patients with type 2 diabetes mellitus and chronic kidney disease, but effects on specific cardiovascular outcomes are uncertain, as are effects in people without previous cardiovascular disease (primary prevention). Methods: In CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation), 4401 participants with type 2 diabetes mellitus and chronic kidney disease were randomly assigned to canagliflozin or placebo on a background of optimized standard of care. Results: Primary prevention participants (n=2181, 49.6%) were younger (61 versus 65 years), were more often female (37% versus 31%), and had shorter duration of diabetes mellitus (15 years versus 16 years) compared with secondary prevention participants (n=2220, 50.4%). Canagliflozin reduced the risk of major cardiovascular events overall (hazard ratio [HR], 0.80 [95% CI, 0.67-0.95]; P=0.01), with consistent reductions in both the primary (HR, 0.68 [95% CI, 0.49-0.94]) and secondary (HR, 0.85 [95% CI, 0.69-1.06]) prevention groups (P for interaction=0.25). Effects were also similar for the components of the composite including cardiovascular death (HR, 0.78 [95% CI, 0.61-1.00]), nonfatal myocardial infarction (HR, 0.81 [95% CI, 0.59-1.10]), and nonfatal stroke (HR, 0.80 [95% CI, 0.56-1.15]). The risk of the primary composite renal outcome and the composite of cardiovascular death or hospitalization for heart failure were also consistently reduced in both the primary and secondary prevention groups (P for interaction >0.5 for each outcome). Conclusions: Canagliflozin significantly reduced major cardiovascular events and kidney failure in patients with type 2 diabetes mellitus and chronic kidney disease, including in participants who did not have previous cardiovascular disease
Corrigendum to "Search for flavour-changing neutral-current couplings between the top quark and the photon with the ATLAS detector at √s=13 TeV" (Physics Letters B, 842 (2023), 137379)
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- Publication venue
- ELSEVIER
- Publication date
- 01/01/2023
- Field of study
Measurement and interpretation of same-sign W boson pair production in association with two jets in pp collisions at s = 13 TeV with the ATLAS detector
- Author
- Aad G
- Abbott B
- Abeling K
- Abicht NJ
- Abidi SH
- Aboulhorma A
- Abramowicz H
- Abreu H
- Abulaiti Y
- Abusleme Hoffman AC
- Acharya BS
- Adam Bourdarios C
- Adamczyk L
- Adamek L
- Addepalli SV
- Addison MJ
- Adelman J
- Adiguzel A
- Adye T
- Affolder AA
- Afik Y
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahuja S
- Ai X
- Aielli G
- Aikot A
- Ait Tamlihat M
- Aitbenchikh B
- Aizenberg I
- Akbiyik M
- Akimov AV
- Akiyama D
- Akolkar NN
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Albouy GL
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi F
- Algren M
- Alhroob M
- Ali B
- Ali HMJ
- Ali S
- Alibocus SW
- Aliev M
- Alimonti G
- Alkakhi W
- Allaire C
- Allbrooke BMM
- Allen JF
- Allendes Flores CA
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alvarez Estevez M
- Alvarez Fernandez A
- Alves Cardoso M
- Alviggi MG
- Aly M
- Amaral Coutinho Y
- Ambler A
- Amelung C
- Amerl M
- Ames CG
- Amidei D
- Amor Dos Santos SP
- Amos KR
- Ananiev V
- Anastopoulos C
- Andeen T
- Anders JK
- Andrean SY
- Andreazza A
- Angelidakis S
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antipov E
- Antonelli M
- Anulli F
- Aoki M
- Aoki T
- Aparisi Pozo JA
- Aparo MA
- Aperio Bella L
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- Chelkov GA
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- Zhemchugov A
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- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 01/04/2024
- Field of study
This paper presents the measurement of fducial and diferential cross sections for both the inclusive and electroweak production of a same-sign W-boson pair in association with two jets (W±W±jj) using 139 fb−1 of proton-proton collision data recorded at a centre-of-mass energy of √s = 13 TeV by the ATLAS detector at the Large Hadron Collider. The analysis is performed by selecting two same-charge leptons, electron or muon, and at least two jets with large invariant mass and a large rapidity diference. The measured fducial cross sections for electroweak and inclusive W±W±jj production are 2.92 ± 0.22 (stat.) ± 0.19 (syst.)fb and 3.38±0.22 (stat.)±0.19 (syst.)fb, respectively, in agreement with Standard Model predictions. The measurements are used to constrain anomalous quartic gauge couplings by extracting 95% confdence level intervals on dimension-8 operators. A search for doubly charged Higgs bosons H±± that are produced in vector-boson fusion processes and decay into a same-sign W boson pair is performed. The largest deviation from the Standard Model occurs for an H±± mass near 450 GeV, with a global signifcance of 2.5 standard deviations
Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy
- Author
- Abdallah J
- Abdul Ghani R
- Abdul Kadir K
- Abdullah R
- Abejuela Z
- Abouglila K
- Abraham O
- Abrahamsen I
- Abraira Munoz Ld
- Abramowitz M
- Abusnana S
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- Yupanqui H
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- Zanoli L
- Zaoui P
- Zateyshchikova A
- Zateyshshikov D
- Zaviriukha V
- Zemek S
- Zhang H
- Zhang Hong
- Zhao M
- Zheng H
- Zinman B
- Zinman Bernard
- Zlova T
- Zsom M
- Zub L
- Zykova T
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2019
- Field of study
BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to 300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m 2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years
Combination of searches for heavy spin-1 resonances using 139 fb−1 of proton-proton collision data at s = 13 TeV with the ATLAS detector
- Author
- Aad G
- Aakvaag E
- Abbott B
- Abeling K
- Abicht NJ
- Abidi SH
- Aboelela M
- Aboulhorma A
- Abramowicz H
- Abreu H
- Abulaiti Y
- Acharya BS
- Ackermann A
- Adam Bourdarios C
- Adamczyk L
- Addepalli SV
- Addison MJ
- Adelman J
- Adiguzel A
- Adye T
- Affolder AA
- Afik Y
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahuja S
- Ai X
- Aielli G
- Aikot A
- Ait Tamlihat M
- Aitbenchikh B
- Aizenberg I
- Akbiyik M
- Akimov AV
- Akiyama D
- Akolkar NN
- Aktas S
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Albouy GL
- Alderweireldt S
- Alegria ZL
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi F
- Algren M
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- Ali B
- Ali HMJ
- Ali S
- Alibocus SW
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- Alimonti G
- Alkakhi W
- Allaire C
- Allbrooke BMM
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- Allendes Flores CA
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- Alonso F
- Alpigiani C
- Alvarez Estevez M
- Alvarez Fernandez A
- Alves Cardoso M
- Alviggi MG
- Aly M
- Amaral Coutinho Y
- Ambler A
- Amelung C
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- Ames CG
- Amidei D
- Amirie KJ
- Amor Dos Santos SP
- Amos KR
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- Ananiev V
- Anastopoulos C
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- Zhemchugov A
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- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Springer Nature
- Publication date
- 19/04/2024
- Field of study
A combination of searches for new heavy spin-1 resonances decaying into different pairings of W, Z, or Higgs bosons, as well as directly into leptons or quarks, is presented. The data sample used corresponds to 139 fb−1 of proton-proton collisions at
= 13 TeV collected during 2015–2018 with the ATLAS detector at the CERN Large Hadron Collider. Analyses selecting quark pairs (qq, bb,
, and tb) or third-generation leptons (τν and ττ) are included in this kind of combination for the first time. A simplified model predicting a spin-1 heavy vector-boson triplet is used. Cross-section limits are set at the 95% confidence level and are compared with predictions for the benchmark model. These limits are also expressed in terms of constraints on couplings of the heavy vector-boson triplet to quarks, leptons, and the Higgs boson. The complementarity of the various analyses increases the sensitivity to new physics, and the resulting constraints are stronger than those from any individual analysis considered. The data exclude a heavy vector-boson triplet with mass below 5.8 TeV in a weakly coupled scenario, below 4.4 TeV in a strongly coupled scenario, and up to 1.5 TeV in the case of production via vector-boson fusion
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
- Author
- A Abbate
- A Abhyankar
- A Adams
- A Agafina
- A Akyea-Djamson
- A Alan
- A Alfieri
- A Alfrey
- A Alvarisqueta
- A Amos
- A Anadiotis
- A Anneveldt
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- Z Zilahi
- Zadionchenko V
- Zadra R
- Zagozen P
- Zaidman C
- Zalazar L
- Zaman A
- Zangroniz P
- Zarate J
- Zareczky P
- Zarifis I
- Zdrenghea D
- Zebrack J
- Zena N
- Zhang J
- Zhang W
- Zhang Y
- Zhao R
- Zhou H
- Zidova M
- Zielinski M
- Zieve F
- Zineldine A.
- Zirlik A
- Zucchetti C
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
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