7 research outputs found
Effects of alirocumab on types of myocardial infarction: insights from the ODYSSEY OUTCOMES trial
- Author
- Abbas J
- Abbate A
- Abdullakutty J
- Abhyanakar AD
- Aboyans V
- Abrantes JAM
- Abu-Fadel M
- Acevedo M
- Adamkova V
- Adhyapak S
- Agarwal H
- Aggarwal R
- Aggarwal RK
- Aguirre A
- Ahmed H
- Ahremark U
- Ahuad Guerrero RA
- Aidar Ayoub JC
- Airaksinen JK
- Aitken D
- Akatova E
- Akhter F
- Ako J
- Akright L
- Akyea-Djamson A
- Al Joundi T
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- Alcocer Gamba MA
- Alexander JH
- Alexander K
- Alexandru TM
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- Alonso Martin JJ
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- Amarasekera S
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- Yin W-H
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- Yoon JH
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- Zahger D
- Zaidman CJ
- Zainea M
- Zaman A
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- Zhang W
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- Zong W
- Zrazhevsky K
- Zuniga JDH
- Zurakowski A
- Zuran I
- Zweiker R
- Publication venue
- 'Oxford University Press (OUP)'
- Publication date
- 01/01/2019
- Field of study
Aims The third Universal Definition of Myocardial Infarction (MI) Task Force classified MIs into five types: Type 1, spontaneous; Type 2, related to oxygen supply/demand imbalance; Type 3, fatal without ascertainment of cardiac biomarkers; Type 4, related to percutaneous coronary intervention; and Type 5, related to coronary artery bypass surgery. Low-density lipoprotein cholesterol (LDL-C) reduction with statins and proprotein convertase subtilisin–kexin Type 9 (PCSK9) inhibitors reduces risk of MI, but less is known about effects on types of MI. ODYSSEY OUTCOMES compared the PCSK9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome (ACS) and elevated LDL-C (≥1.8 mmol/L) despite intensive statin therapy. In a pre-specified analysis, we assessed the effects of alirocumab on types of MI. Methods and results Median follow-up was 2.8 years. Myocardial infarction types were prospectively adjudicated and classified. Of 1860 total MIs, 1223 (65.8%) were adjudicated as Type 1, 386 (20.8%) as Type 2, and 244 (13.1%) as Type 4. Few events were Type 3 (n = 2) or Type 5 (n = 5). Alirocumab reduced first MIs [hazard ratio (HR) 0.85, 95% confidence interval (CI) 0.77–0.95; P = 0.003], with reductions in both Type 1 (HR 0.87, 95% CI 0.77–0.99; P = 0.032) and Type 2 (0.77, 0.61–0.97; P = 0.025), but not Type 4 MI. Conclusion After ACS, alirocumab added to intensive statin therapy favourably impacted on Type 1 and 2 MIs. The data indicate for the first time that a lipid-lowering therapy can attenuate the risk of Type 2 MI. Low-density lipoprotein cholesterol reduction below levels achievable with statins is an effective preventive strategy for both MI types.For complete list of authors see http://dx.doi.org/10.1093/eurheartj/ehz299</p
Effect of alirocumab on mortality after acute coronary syndromes. An analysis of the ODYSSEY OUTCOMES randomized clinical trial
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- Zeiher AM
- Zhang R
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- Zheleznyy V
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- Zrazhevsky K
- Zurakowski A
- Zuran I
- Zweiker R
- Publication venue
- 'Ovid Technologies (Wolters Kluwer Health)'
- Publication date
- 04/01/2019
- Field of study
Background: Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstrated reductions in major adverse cardiovascular events, but not death. We assessed the effects of alirocumab on death after index acute coronary syndrome. Methods: ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) was a double-blind, randomized comparison of alirocumab or placebo in 18 924 patients who had an ACS 1 to 12 months previously and elevated atherogenic lipoproteins despite intensive statin therapy. Alirocumab dose was blindly titrated to target achieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL. We examined the effects of treatment on all-cause death and its components, cardiovascular and noncardiovascular death, with log-rank testing. Joint semiparametric models tested associations between nonfatal cardiovascular events and cardiovascular or noncardiovascular death. Results: Median follow-up was 2.8 years. Death occurred in 334 (3.5%) and 392 (4.1%) patients, respectively, in the alirocumab and placebo groups (hazard ratio [HR], 0.85; 95% CI, 0.73 to 0.98; P=0.03, nominal P value). This resulted from nonsignificantly fewer cardiovascular (240 [2.5%] vs 271 [2.9%]; HR, 0.88; 95% CI, 0.74 to 1.05; P=0.15) and noncardiovascular (94 [1.0%] vs 121 [1.3%]; HR, 0.77; 95% CI, 0.59 to 1.01; P=0.06) deaths with alirocumab. In a prespecified analysis of 8242 patients eligible for ≥3 years follow-up, alirocumab reduced death (HR, 0.78; 95% CI, 0.65 to 0.94; P=0.01). Patients with nonfatal cardiovascular events were at increased risk for cardiovascular and noncardiovascular deaths (P<0.0001 for the associations). Alirocumab reduced total nonfatal cardiovascular events (P<0.001) and thereby may have attenuated the number of cardiovascular and noncardiovascular deaths. A post hoc analysis found that, compared to patients with lower LDL-C, patients with baseline LDL-C ≥100 mg/dL (2.59 mmol/L) had a greater absolute risk of death and a larger mortality benefit from alirocumab (HR, 0.71; 95% CI, 0.56 to 0.90; Pinteraction=0.007). In the alirocumab group, all-cause death declined wit h achieved LDL-C at 4 months of treatment, to a level of approximately 30 mg/dL (adjusted P=0.017 for linear trend). Conclusions: Alirocumab added to intensive statin therapy has the potential to reduce death after acute coronary syndrome, particularly if treatment is maintained for ≥3 years, if baseline LDL-C is ≥100 mg/dL, or if achieved LDL-C is low. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402
Non-targeted detection of food adulteration using an ensemble machine-learning model
- Publication venue
- Nature Publishing Group
- Publication date
- 03/05/2024
- Field of study
202405 bcrcVersion of RecordRGCOthersHKSAR ITF project grant titled Big-data-enabled Collaborative Database for Non-targeted Contaminants DetectionLogistics and Supply Chain MultiTech R&D Centre Limited (LSCM)Hong Kong Polytechnic University Strategic FundPublishedC
A common mechanism of proteasome impairment by neurodegenerative disease-associated oligomers
- Author
- A Ciechanover
- A Ciechanover
- A Ciechanover
- A Jan
- A Köhler
- A Sandberg
- AF Kisselev
- AF Kisselev
- AY Feuvre Le
- B Calamini
- B Luan
- BP Tseng
- C Haass
- C McKinnon
- D Finley
- D Voges
- DC Rubinsztein
- DJ Selkoe
- DL Castillo-Carranza
- DM Smith
- DM Smith
- DM Walsh
- E Emmanouilidou
- E Lindersson
- FG Whitby
- GM Adams
- GN DeMartino
- GN DeMartino
- GP Lotz
- HC Besche
- HC Tai
- IH Cheng
- J Brettschneider
- J Labbadia
- J Rabl
- JN Keller
- K Martinez-Fonts
- KS McNaught
- KSP McNaught
- KSP McNaught
- KV Ramachandran
- L Bedford
- L Gregori
- L Stefanis
- M Ahmed
- M Arrasate
- M Díaz-Hernández
- M Díaz-Hernández
- M Groll
- M Groll
- M Hashimoto
- M Kristiansen
- M Lopez-Salon
- M Unno
- M Wehmer
- ME Matyskiela
- MH Glickman
- NF Bence
- NYY Zhang
- P Deriziotis
- P Unverdorben
- P Śled
- PM Chu
- R Fonseca
- R Kayed
- R Kayed
- R Kayed
- S Asano
- S Barghorn
- S Lesné
- S Oh
- SE Lesné
- SJ Russell
- SL Bernstein
- SN Djakovic
- SN Djakovic
- T Yang
- TG Gillette
- V Cecarini
- W Xie
- WH Choi
- Y Tanaka
- Y Yu
- Z Li
- Z Ortega
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2018
- Field of study
Disruption of the ubiquitin proteasome system (UPS) is often associated with neurodegenerative diseases. Here the authors demonstrate the existence of a general mechanism of proteasomal impairment triggered by a specific protein oligomer structure, irrespective of its protein constituent
The ATLAS experiment at the CERN Large Hadron Collider: a description of the detector configuration for Run 3
- Author
- Aad G
- Abbott B
- Abbott DC
- Abdallah J
- Abeling K
- Abidi SH
- Aboulhorma A
- Abovyan S
- Abramowicz H
- Abreu H
- Abulaiti Y
- Abusleme Hoffman AC
- Acharya BS
- Adam Bourdarios C
- Adamczyk L
- Adamek L
- Addepalli SV
- Adelman J
- Adersberger M
- Adiguzel A
- Adorni S
- Adye T
- Affolder AA
- Afik Y
- Agaras MN
- Agarwala J
- Aggarwal A
- Agheorghiesei C
- Aguilar-Saavedra JA
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahuja S
- Ai X
- Aielli G
- Ait Tamlihat M
- Aitbenchikh B
- Aizenberg I
- Akbiyik M
- Akhperjanyan G
- Akimov AV
- Al Khoury K
- Alberghi GL
- Albert J
- Albicocco P
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi A
- Alfonsi F
- Alhroob M
- Ali B
- Ali S
- Aliev M
- Alimonti G
- Alkakhi W
- Allaire C
- Allard J
- Allbrooke BMM
- Allendes Flores CA
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alvarez Estevez M
- Alvarez Gonzalez B
- 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
- Andari N
- Andeen T
- Anders JK
- Andrean SY
- Andreazza A
- Anelli CR
- Angelidakis S
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antipov E
- Antonelli M
- Antonescu M
- Antrim DJA
- Anulli F
- Aoki M
- Aoki T
- Aparisi Pozo JA
- Aparo MA
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- Argyris A
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- Bird GA
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- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- IOP Publishing
- Publication date
- 01/05/2024
- Field of study
Abstract
The ATLAS detector is installed in its experimental cavern
at Point 1 of the CERN Large Hadron Collider. During Run 2 of the
LHC, a luminosity of
ℒ = 2 × 1034 cm-2 s-1 was
routinely achieved at the start of fills, twice the design
luminosity. For Run 3, accelerator improvements, notably luminosity
levelling, allow sustained running at an instantaneous luminosity of
ℒ = 2 × 1034 cm-2 s-1,
with an average of up to 60 interactions per bunch crossing. The
ATLAS detector has been upgraded to recover Run 1 single-lepton
trigger thresholds while operating comfortably under Run 3 sustained
pileup conditions. A fourth pixel layer 3.3 cm from the beam axis
was added before Run 2 to improve vertex reconstruction and
b-tagging performance. New Liquid Argon Calorimeter digital
trigger electronics, with corresponding upgrades to the Trigger and
Data Acquisition system, take advantage of a factor of 10 finer
granularity to improve triggering on electrons, photons, taus, and
hadronic signatures through increased pileup rejection. The inner
muon endcap wheels were replaced by New Small Wheels with Micromegas
and small-strip Thin Gap Chamber detectors, providing both precision
tracking and Level-1 Muon trigger functionality. Trigger coverage of
the inner barrel muon layer near one endcap region was augmented
with modules integrating new thin-gap resistive plate chambers and
smaller-diameter drift-tube chambers. Tile Calorimeter scintillation
counters were added to improve electron energy resolution and
background rejection. Upgrades to Minimum Bias Trigger Scintillators
and Forward Detectors improve luminosity monitoring and enable total
proton-proton cross section, diffractive physics, and heavy ion
measurements. These upgrades are all compatible with operation in
the much harsher environment anticipated after the High-Luminosity
upgrade of the LHC and are the first steps towards preparing ATLAS
for the High-Luminosity upgrade of the LHC. This paper describes
the Run 3 configuration of the ATLAS detector.</jats:p
Recommended from our members
The ATLAS experiment at the CERN Large Hadron Collider: a description of the detector configuration for Run 3
- Author
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- Abbott B
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- Abdallah J
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- Burr JTP
- Burton CD
- Burzynski JC
- Busch EL
- Bussey PJ
- Butler JM
- Buttar CM
- Butterworth JM
- Buttinger W
- Buxo Vazquez CJ
- Buzykaev AR
- Büscher V
- Cabras G
- Cabrera Urbán S
- Cadoux F
- Caforio D
- Cai H
- Cai Y
- Cairo VMM
- Cakir O
- Calabro D
- Calace N
- Calafiura P
- Calderini G
- Calfayan P
- Callea G
- Caloba LP
- Calvet D
- Calvet S
- Calvet TP
- Calvetti M
- Camacho Toro R
- Camarda S
- Camarero Munoz D
- Camarri P
- Camerlingo MT
- Cameron D
- Camincher C
- Campanelli M
- Camplani A
- Canale V
- Canesse A
- Cano Bret M
- Cantero J
- Cao NYY
- Cao Y
- Cap S
- Capitolo E
- Capocasa F
- Capradossi G
- Capua M
- Cara GB
- Carbone A
- Cardarelli R
- Cardenas JCJ
- Cardillo F
- Cardot CA
- Carli T
- Carlino G
- Carlotta MD
- Carlotto JI
- Carlson BT
- Carlson EM
- Carlson KJ
- Carminati L
- Carnesale M
- Caron S
- Carquin E
- Carratta G
- Carrio Argos F
- Carrá S
- Carter JWS
- Carter TM
- Casado MP
- Caserio A
- Casha AF
- Cassese C
- Castiglia EG
- Castillo Garcia L
- Castillo Gimenez V
- Castillo FL
- Castro NF
- Catinaccio A
- Catmore JR
- Cavaliere V
- Cavalli N
- Cavasinni V
- Celebi E
- Celli F
- Centonze MS
- Ceradini F
- Cerny K
- Cerqueira AS
- Cerri A
- Cerrito L
- Cerutti F
- Cervelli A
- Cetin SA
- Chadi Z
- Chakraborty D
- Chala M
- Chaleil Th
- Chan J
- Chan SK
- Chan WY
- Chapman JD
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- Chargeishvili B
- Charlton DG
- Charman TP
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- Chau CC
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- Chekulaev SV
- Chelkov GA
- Chen A
- Chen B
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- Chen H
- Chen H
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- Chen S
- Chen SJ
- Chen X
- Chen X
- Chen Y
- Cheng CL
- Cheng HC
- Cheong S
- Cheplakov A
- Cheremushkina E
- Cherepanova E
- Cherkaoui El Moursli R
- Cheu E
- Cheung K
- Chevalier L
- Chevillot N
- Chiarella V
- Chiarelli G
- Chiedde N
- Chiodini G
- Chisholm AS
- Chitan A
- Chitishvili M
- Chiu YH
- Chizhov MV
- Choi K
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- Chou Y
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- Chowdhury T
- Christopher LD
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- Chu KL
- Chu MC
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- Chudoba J
- Chwastowski JJ
- Ciapetti G
- Ciapetti M
- Ciecko RP
- Cieri D
- Ciesla KM
- Cindro V
- Ciocio A
- Cirotto F
- Citron ZH
- Citterio M
- Ciubotaru DA
- Ciungu BM
- Clark A
- Clark BL
- Clark PJ
- Clavijo Columbie JM
- Clawson SE
- Cleland W
- Clemens JC
- Clement C
- Clercx J
- Clissa L
- Coadou Y
- Cobal M
- Coccaro A
- Coelho Barrue RF
- Coelho Lopes De Sa R
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- Constable M
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- Cooke HG
- Cooper-Sarkar AM
- Corbaz F
- Cormier F
- Corpe LD
- Corradi M
- Corrigan EE
- Corriveau F
- Corsetti S
- Cortes-Gonzalez A
- Costa De Paiva TCP
- Costa MJ
- Costanza F
- Costanzo D
- Cote BM
- Cowan G
- Cowley JW
- Cranmer K
- Crescioli F
- Crespo-Lopez O
- Cristinziani M
- Cristoforetti M
- Croft V
- Crosetti G
- Crépé-Renaudin S
- Cueto A
- Cuhadar Donszelmann T
- Cui H
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- Curcio F
- Czodrowski P
- Czurylo MM
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- D'Amico V
- D'Auria S
- D'Eramo L
- D'Onofrio A
- D'Onofrio M
- D'Uffizi D
- D'uffizi M
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- Da Fonseca Pinto JV
- Da Via C
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- Dawson I
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- De Fazio B
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- de Jong P
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- De Vivie De Regie JB
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- Del Peso J
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- Demichev M
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- Denisov SP
- Derendarz D
- Derue F
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- Deschamps H
- Desforge D
- Dette K
- Deutsch C
- Di Bello FA
- Di Ciaccio A
- Di Ciaccio L
- Di Domenico A
- Di Donato C
- Di Girolamo A
- Di Gregorio G
- Di Luca A
- Di Micco B
- Di Nardo R
- Di Petrillo KF
- Di Stante L
- Diaconu C
- Dias Do Vale T
- Dias FA
- Diaz Capriles FG
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- Dreyer E
- Drivas-koulouris I
- Drobac AS
- Drozdova M
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- Durglishvili A
- Dury B
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- Dyckes GI
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- Dziurdzia P
- Díez Cornell S
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- Eggleston MG
- Egidio Purcino De Souza E
- Ehrke LF
- Eigen G
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- Ekelof T
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- El Ghazali Y
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- Fausten C
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- Filthaut F
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- Fleck I
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- Flierl BM
- Flores Castillo LR
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- Fomichev I
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- Formica A
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- Gasiorowski SJ
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- Zonca E
- Zorbas TG
- Zormpa O
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- Zullo A
- Zwalinski L
- Åkesson TPA
- Öncel ÖO
- Ženiš T
- Živković L
- Publication venue
- Journal of Instrumentation
- Publication date
- 23/05/2024
- Field of study
Abstract
The ATLAS detector is installed in its experimental cavern
at Point 1 of the CERN Large Hadron Collider. During Run 2 of the
LHC, a luminosity of
ℒ = 2 × 1034 cm-2 s-1 was
routinely achieved at the start of fills, twice the design
luminosity. For Run 3, accelerator improvements, notably luminosity
levelling, allow sustained running at an instantaneous luminosity of
ℒ = 2 × 1034 cm-2 s-1,
with an average of up to 60 interactions per bunch crossing. The
ATLAS detector has been upgraded to recover Run 1 single-lepton
trigger thresholds while operating comfortably under Run 3 sustained
pileup conditions. A fourth pixel layer 3.3 cm from the beam axis
was added before Run 2 to improve vertex reconstruction and
b-tagging performance. New Liquid Argon Calorimeter digital
trigger electronics, with corresponding upgrades to the Trigger and
Data Acquisition system, take advantage of a factor of 10 finer
granularity to improve triggering on electrons, photons, taus, and
hadronic signatures through increased pileup rejection. The inner
muon endcap wheels were replaced by New Small Wheels with Micromegas
and small-strip Thin Gap Chamber detectors, providing both precision
tracking and Level-1 Muon trigger functionality. Trigger coverage of
the inner barrel muon layer near one endcap region was augmented
with modules integrating new thin-gap resistive plate chambers and
smaller-diameter drift-tube chambers. Tile Calorimeter scintillation
counters were added to improve electron energy resolution and
background rejection. Upgrades to Minimum Bias Trigger Scintillators
and Forward Detectors improve luminosity monitoring and enable total
proton-proton cross section, diffractive physics, and heavy ion
measurements. These upgrades are all compatible with operation in
the much harsher environment anticipated after the High-Luminosity
upgrade of the LHC and are the first steps towards preparing ATLAS
for the High-Luminosity upgrade of the LHC. This paper describes
the Run 3 configuration of the ATLAS detector.</jats:p
Risk categorization using New American College of Cardiology/American Heart Association guidelines for cholesterol management and its relation to alirocumab treatment following acute coronary syndromes
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- Publication venue
- 'Ovid Technologies (Wolters Kluwer Health)'
- Publication date
- 01/08/2019
- Field of study
Background: The 2018 US cholesterol management guidelines recommend additional lipid-lowering therapies for secondary prevention in patients with low-density lipoprotein cholesterol ≥70 mg/dL or non−high-density lipoprotein cholesterol ≥100 mg/dL despite maximum tolerated statin therapy. Such patients are considered at very high risk (VHR) based on a history of >1 major atherosclerotic cardiovascular disease (ASCVD) event or a single ASCVD event and multiple high-risk conditions. We investigated the association of US guideline-defined risk categories with the occurrence of ischemic events after acute coronary syndrome and reduction of those events by alirocumab, a PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor. Methods: In the ODYSSEY OUTCOMES trial (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab), patients with recent acute coronary syndrome and residual dyslipidemia despite optimal statin therapy were randomly assigned to alirocumab or placebo. The primary trial outcome (major adverse cardiovascular events, ie, coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or hospitalization for unstable angina) was examined according to American College of Cardiology/American Heart Association risk category. Results: Of 18 924 participants followed for a median of 2.8 years, 11 935 (63.1%) were classified as VHR: 4450 (37.3%) had multiple prior ASCVD events and 7485 (62.7%) had 1 major ASCVD event and multiple high-risk conditions. Major adverse cardiovascular events occurred in 14.4% of placebo-treated patients at VHR versus 5.6% of those not at VHR. In the VHR category, major adverse cardiovascular events occurred in 20.4% with multiple prior ASCVD events versus 10.7% with 1 ASCVD event and multiple high-risk conditions. Alirocumab was associated with consistent relative risk reductions in both risk categories (hazard ratio=0.84 for VHR; hazard ratio=0.86 for not VHR; Pinteraction=0.820) and by stratification within the VHR group (hazard ratio=0.86 for multiple prior ASCVD events; hazard ratio=0.82 for 1 major ASCVD event and multiple high-risk conditions; Pinteraction=0.672). The absolute risk reduction for major adverse cardiovascular events with alirocumab was numerically greater (but not statistically different) in the VHR group versus those not at VHR (2.1% versus 0.8%; Pinteraction=0.095) and among patients at VHR with multiple prior ASCVD events versus a single prior ASCVD event (2.4% versus 1.8%; Pinteraction=0.661). Conclusions: The US guideline criteria identify patients with recent acute coronary syndrome and dyslipidemia who are at VHR for recurrent ischemic events and who may derive a larger absolute benefit from treatment with alirocumab. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402