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Association of apolipoprotein E gene polymorphisms with blood lipids and their interaction with dietary factors
- Author
- A Ahmadzadeh
- A Munshi
- AA Mulligan
- AL Carvalho-Wells
- AM Bennet
- AM Fehily
- AM Gotto Jr
- AM McNeill
- Basma Ellahi
- BF Voight
- C Ehnholm
- C Zhang
- D El-Lebedy
- D Seripa
- E Komurcu-Bayrak
- E Mertens
- E Sarkkinen
- EN Smith
- F Cold
- G Ken-Dror
- GS Sagoo
- H Gylling
- H Wang
- HA Deshmukh
- Ian Givens
- IM Shatwan
- Israa M. Shatwan
- J Lopez-Miranda
- J Petkeviciene
- J Rip
- J Wang
- JA Nettleton
- JA Nettleton
- JE Eichner
- JM Ordovas
- JN Giger
- JN Hellwege
- JS Forrester
- Julie A. Lovegrove
- JW Yarnell
- JW Yarnell
- JY Hwang
- K Wu
- Karani S. Vimaleswaran
- KE Friday
- KG Jackson
- Kristian Hillert Winther
- KY Son
- L Zhou
- LE Viiri
- M Merkel
- Margaret P. Rayman
- MC Nierman
- MP Rayman
- MV Calabuig-Navarro
- NM McKeown
- O Ukkola
- P Barter
- P Couture
- P Mozas
- Peter Elwood
- PW Wilson
- RE Gregg
- RP Mensink
- S Kaser
- S Trompet
- SE Humphries
- SI Kring
- SU Shahid
- T Shah
- T Suwalak
- The Caerphilly and speedwell collaborative Group
- V Radha
- WT Friedewald
- Y Song
- Yoav Ben-Shlomo
- Z Zhang
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2018
- Field of study
Several candidate genes have been identified in relation to lipid metabolism, and among these, lipoprotein lipase (LPL) and apolipoprotein E (APOE) gene polymorphisms are major sources of genetically determined variation in lipid concentrations. This study investigated the association of two single nucleotide polymorphisms (SNPs) at LPL, seven tagging SNPs at the APOE gene, and a common APOE haplotype (two SNPs) with blood lipids, and examined the interaction of these SNPs with dietary factors.
METHODS:
The population studied for this investigation included 660 individuals from the Prevention of Cancer by Intervention with Selenium (PRECISE) study who supplied baseline data. The findings of the PRECISE study were further replicated using 1238 individuals from the Caerphilly Prospective cohort (CaPS). Dietary intake was assessed using a validated food-frequency questionnaire (FFQ) in PRECISE and a validated semi-quantitative FFQ in the CaPS. Interaction analyses were performed by including the interaction term in the linear regression model adjusted for age, body mass index, sex and country.
RESULTS:
There was no association between dietary factors and blood lipids after Bonferroni correction and adjustment for confounding factors in either cohort. In the PRECISE study, after correction for multiple testing, there was a statistically significant association of the APOE haplotype (rs7412 and rs429358; E2, E3, and E4) and APOE tagSNP rs445925 with total cholesterol (Pâ=â4âĂâ10-â4 and Pâ=â0.003, respectively). Carriers of the E2 allele had lower total cholesterol concentration (5.54â±â0.97 mmol/L) than those with the E3 (5.98â±â1.05 mmol/L) (Pâ=â0.001) and E4 (6.09â±â1.06 mmol/L) (Pâ=â2âĂâ10-â4) alleles. The association of APOE haplotype (E2, E3, and E4) and APOE SNP rs445925 with total cholesterol (Pâ=â2âĂâ10-â6 and Pâ=â3âĂâ10-â4, respectively) was further replicated in the CaPS. Additionally, significant association was found between APOE haplotype and APOE SNP rs445925 with low density lipoprotein cholesterol in CaPS (Pâ=â4âĂâ10-â4 and Pâ=â0.001, respectively). After Bonferroni correction, none of the cohorts showed a statistically significant SNP-diet interaction on lipid outcomes.
CONCLUSION:
In summary, our findings from the two cohorts confirm that genetic variations at the APOE locus influence plasma total cholesterol concentrations, however, the gene-diet interactions on lipids require further investigation in larger cohorts
Wnt signaling in triple-negative breast cancer
- Author
- A Ciupek
- A De
- A Esquela-Kerscher
- A Gucalp
- A Prat
- A Prat
- A Prat
- A Schech
- A Suzuki
- AI Khramtsov
- AL Stiegler
- AS Cleary
- B Cui
- B Howard
- B Kaufman
- B Samatanga
- BD Lehmann
- BT MacDonald
- BT MacDonald
- C Arce-Salinas
- C Gao
- C Henry
- C Laezza
- C Lindvall
- C Lindvall
- C Liu
- C Wang
- C Wang
- C-C Liu
- C-M Cruciat
- CA Hudis
- CC Huard
- CJ Creighton
- CM Perou
- CP Prasad
- CR Tate
- CY Janda
- D Castiglia
- D Wang
- DJ Sussman
- DV Tauriello
- E Bourhis
- E Gomez-Orte
- E Hilborn
- EF Byrne
- EM Shin
- F Chiacchiera
- FC Geyer
- FV Fuller-Pace
- G Corda
- G Wang
- G Wu
- G-B Jang
- GB Jang
- Group EBCTC.
- H Clevers
- H Farmer
- H Taipaleenmaki
- H Wang
- H Wang
- H Xu
- HC Moore
- HC Wong
- HE Bryant
- I Jarmoskaite
- J Cai
- J Dejmek
- J Roose
- J Schlessinger
- J Xu
- J-P Borg
- JA Sparano
- JD Kormish
- JN Goh
- JP Dijksterhuis
- JP Medema
- JP Solzak
- K Kast
- K Kikuchi
- K Pogoda
- K Tamai
- K Willert
- KA Avery-Kiejda
- KKN Guturi
- KM Cadigan
- KR Greenow
- L Azzolin
- L Azzolin
- L Cheng
- L Li
- L Li
- L Livraghi
- L Pusztai
- L Yang
- L Zhang
- M Botlagunta
- M Fiedler
- M Habu
- M Kai
- M Nishita
- M Peiris-Pages
- M Pistelli
- M Xie
- M Xu
- MC Rangel
- MD Burstein
- MK Mohammed
- MV Gammons
- N Dey
- N Takebe
- NM Badders
- O Tudoran
- P Eroles
- P Eroles
- P Linder
- P Polakis
- PS Weisman
- Q Jiang
- Q Yu
- R Bao
- R Chakrabarti
- R Habas
- R Takada
- R van Amerongen
- R Yasuhara
- RD Sicchieri
- RL Atkinson
- S Chen
- S Mohammadi Yeganeh
- S Mohammadi-Yeganeh
- S Rocak
- S Yin
- S Yin
- S Yin
- S Zhang
- S Zhang
- SA Ibrahim
- SM Huang
- SP Shah
- T Ishitani
- T Ishitani
- T Isobe
- T Ovcaricek
- T Phesse
- T Schwarz-Romond
- TC He
- TK Noah
- U Weierstall
- UD Kahlert
- V Lefebvre
- V Nikolova
- VC Jordan
- VE Ahn
- VF Merino
- VF Taelman
- VG Abramson
- VS Golubkov
- VS Li
- WD Foulkes
- WH Conrad
- X Gao
- X Jiang
- X Zeng
- Y Gong
- Y Liu
- Y Minami
- Y Shimono
- Y-R Liu
- YA Zeng
- YL Huang
- Z Cheng
- ZS Wu
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2017
- Field of study
Wnt signaling regulates a variety of cellular processes, including cell fate, differentiation, proliferation and stem cell pluripotency. Aberrant Wnt signaling is a hallmark of many cancers. An aggressive subtype of breast cancer, known as triple-negative breast cancer (TNBC), demonstrates dysregulation in canonical and non-canonical Wnt signaling. In this review, we summarize regulators of canonical and non-canonical Wnt signaling, as well as Wnt signaling dysfunction that mediates the progression of TNBC. We review the complex molecular nature of TNBC and the emerging therapies that are currently under investigation for the treatment of this disease
The disruption of proteostasis in neurodegenerative diseases
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- Publication venue
- 'American Institute of Mathematical Sciences (AIMS)'
- Publication date
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- Field of study
Cells count on surveillance systems to monitor and protect the cellular proteome which, besides being highly heterogeneous, is constantly being challenged by intrinsic and environmental factors. In this context, the proteostasis network (PN) is essential to achieve a stable and functional proteome. Disruption of the PN is associated with aging and can lead to and/or potentiate the occurrence of many neurodegenerative diseases (ND). This not only emphasizes the importance of the PN in health span and aging but also how its modulation can be a potential target for intervention and treatment of human diseases.info:eu-repo/semantics/publishedVersio
Pan-cancer analysis of whole genomes
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- The ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium View Correspondence (jump link)
- Thiessen
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- Thomas
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- Thompson
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- Waddell
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- Wintersinger
- Wiznerowicz
- Wolf
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- Woo
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- Wouters
- Wright
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- Wright A. J. k
- ws Ang
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- wv abg
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- x Eils
- x Yung
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- xc Lovat
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- xp Benz
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- xr Ghori
- xs Gundem
- Xue
- xv Luxton
- xw McDermott
- xy Visakorpi
- xz Whitaker
- Y. -E. ot
- Y. -J. k
- Y. -J. xn
- Y. abp
- Y. ae
- Y. ae
- Y. ae
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- Y. ai
- Y. aj
- Y. al
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- Y. ep
- Y. ez
- Y. ff
- Y. fr
- Y. fv
- Y. fv
- Y. gl
- Y. hl
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- Y. nh
- Y. nk
- Y. nz
- Y. rg
- Y. rj
- Y. rm
- Y. S. jf
- Y. uz
- Y. vr
- Y. wt
- Y. yc
- ya Al-Ahmadie
- Yachida
- Yamaguchi
- Yamaguchi T. N. k
- Yamamoto
- Yamaue
- Yang
- Yang
- Yang
- Yang
- Yang
- Yao
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- yb Ally
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- ye Auman
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- Yellapantula
- Yellapantula
- yh Bathe
- yj Baylin
- Yoon
- Yu
- Yu
- Yu
- Yuan
- Yugawa
- z ah
- Z. ej
- Z. ep
- Z. fr
- Z. hv
- Z. hy
- Z. jq
- Z. kt
- Z. oe
- Zaikova
- Zapatka
- zd Gershenwald
- Zenklusen
- Zeps
- zf Ghossein
- Zhang
- Zhang
- Zhang
- Zhang
- Zhang
- Zhang
- Zhang H. b
- Zhao
- Zheng
- Zhou
- Zhou
- Zhu
- Zhu
- zi zj
- zm Jayaseelan
- Zou
- Zou
- zt Kim
- zw Lewis
- Ă. A. th
- Ă. sk
- Publication venue
- Publication date
- 11/12/2019
- Field of study
Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe
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
- A Antolick
- A Arthur
- A Aslam
- Abaci F
- Abdullakutty J
- Abhaichand R
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- Aboufakher R
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- Abreu M
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- Acampora D
- Acampora M
- Accini Mendoza Jl
- Aceto L
- Acevedo B
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- Acheatel R
- Actis Mv
- Adams M
- Adjic Nc
- Affaki Gs
- Agarwal Dk
- Aggarwal Rk
- Agosta Gf
- Aguilar M
- Aguilar M
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- Ahmed Sh
- Ahn Y
- Aish B
- Aiub F
- Aiub J
- Ajax K
- Ajioka M
- Akai Y
- Akatova E
- Akrap B
- Al Joundi T
- Al-Khalili F
- Albisu J
- Alcalde Jm
- Alcide P
- Alfonso T
- Allen J
- Alllison Dc
- Almaliky T
- Amerena J
- Andersen K
- Andor M
- Angelova I
- Angiolillo D
- Anita S
- Anker Sd
- Antalik L
- Antonicelli R
- Aparicio Cv
- Apel T
- Apostolovic S
- Ara M
- Aragorn L
- Arango Jl
- Araujo Fonseca M
- Ardissino D
- Arenas Leon Jl
- Arevalo S
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- Arif I
- Armas E
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- Asim Oktay Ao
- Assarsson E
- Ata B
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- Atieh M
- Aull L
- Avalos V
- Avdonina N
- Awasthi Ak
- Axthelm C
- Ayala M
- Ayasse D
- Ayasse M
- Azizad M
- Azize Gm
- B Becker
- Baar M
- Babu R
- Backer T
- Badea C
- Baden M
- Baehl S
- Baek C
- Baeumer A
- Bagi Es
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- Bailey K
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- Baker A
- Baker C
- Bakhai A
- Bakker H
- Baksi A
- Baldin Mg
- Bali Hk
- Ballantyne C
- Ballmajo M
- Balode A
- Balukova E
- Bang Sa
- Banker D
- Banker K
- Baquero A
- Barbarash Ol
- Barbato E
- Barbosa E
- Barnett S
- Baron S
- Barreto M
- Barroso A
- Barroso W
- Bartkowiak A
- Bartosh L
- Bartuseviciene S
- Bashir K
- Baszak J
- Bata Ir
- Bayram E
- Beall K
- Beaudry M
- Beauregard La
- Beckett L
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- Belle Isle J
- Belohlavek J
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- Bender D
- Benedetti G
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- Berger V
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- Bergholtz T
- Bergler-Klein J
- Berk M
- Berli Ma
- Bernstein M
- Berra Fc
- Berti S
- Berulfsen A
- Bevilacqua Mt
- Bhadade S
- Bilazarian S
- Bilodeau N
- Binder A
- Binns Y
- Birdane A
- Bisne V
- Bitzer V
- Blagdon M
- Blahey M
- Blankenberg S
- Blazsek Z
- Bloch S
- Blom Kb
- Bluemel J
- Blumberg C
- Blumenthal R
- Bocanera M
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- Boivin Mc
- Bolduc H
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- Bolsmann C
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- Brady L
- Bramlet D
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- Briggs S
- Briké C
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- Budassi N
- Budkova J
- Bugan V
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- Burris H
- Burton C
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- Busak L
- Busic N
- Byars W
- BĂžen Rh
- C Clavier-Firmin
- C Conradie
- C Contzen
- C Cotes
- C Covert
- C Cuneo
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- Cabau Jr
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- Candusso R
- Cantor W
- CANTOS Trial Group. Krum H
- Capova L
- Carabajal T
- Carr K
- Carrillo J
- Caruso G
- Casala J
- Caso P
- Casoinic F
- Castillo J
- Castillo T
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- Cerda L
- Cermak O
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- Chambers J
- Chamblee T
- Chang K
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- Chang Wh
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- Chattin W
- Chauhan D
- Chauhan H
- Chaussé I
- Chavada J
- Chaverra I
- Chaware G
- Chee L
- Chella S
- Chen Cp
- Chen J
- Chen Mh
- Chen Y
- Chen Yc
- Chen Zc
- Cheng Jj
- Cheng S
- Cheng Sm
- Cherlin R
- Cheung D
- Chhabra A
- Chintala P
- Chiodi L
- Choi Aj
- Chou S
- Chouinard G
- Christensen L
- Christenson S
- Chung A
- Churina S
- Cifkova R
- Ciglenecki N
- Cioffi A
- Cislowski D
- Cleveland T
- Clocotan M
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- Colfer H
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- Collier D
- Collins R
- Coloma G
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- Coman S
- Commerford P
- Commerford P
- Conrado Y
- Cools F
- Cornel Jh
- Corona V
- Coronel J
- Cosgrove N
- Cosgrove S
- Cosmi F
- Costa Amorim R
- Coufalova Z
- Covell W
- Cox B
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- Crandall L
- Crawford G
- Crea F
- Crepps K
- Crocamo A
- Cromer M
- Cruz H
- Cruz H
- Cruz M
- Csala L
- Cucher F
- Cuentas I
- Cuervo A
- Curiac D
- Cymerman K
- Cyprian R
- Czerski T
- D'Amours Dg
- D Dash
- D Dattani
- D Denham
- D Desai
- D Desalle
- D Digangi
- D Dunn
- Da Costa F
- Da Silva A
- Da Silva D Jr
- Da Silva O Jr
- Dahlen G
- Dalseg Am
- Damron M
- Danik J
- Davalos C
- Dave B
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- Davis B
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- Dawood Sy
- Dayer M
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- De Caterina R
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- De Knijf K
- De Krumbach L
- De Los Milagros Had M
- De Los Rios M
- De Rosa S
- De Vos A
- De Wolf L
- Dean J
- Debnam S
- Decsi K
- Decsi Kl
- Dedek V
- Dedkova S
- Defosse C
- Degennaro N
- Dehning M
- Dela Llana A
- Delfonso F
- Delforge M
- Delgadillo T
- Dellasa M
- Dellborg M
- Dellorso M
- Demidova M
- Den Hartog F
- Denecke C
- Dengler T
- Dermitzakis A
- Deslongchamps F
- Dessalvi Cc
- Destro M
- Dettmer M
- Devasia T
- Deweerdt N
- Dhanak R
- Dhawan M
- Di Biase M
- Diago M
- Diaz M
- Dicken T
- Dickstein K
- Diederich C
- Diederich M
- Diehl R
- Diller P
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- Dimitrov G
- Diodati J
- Dobariya H
- Dobilas V
- Dodds G
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- Donahue K
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- Donaubauer T
- Dong X
- Dormidontova G
- Dorogova I
- Dos Santos A
- Dos Santos F
- Dos Santos P
- Doughty A
- Doughty L
- Dovgalevskiy Y
- Dovgolis S
- Dragutksy B
- Dreese M
- Drost I
- Drouin K
- Duchesne L
- Duckert A
- Duda N
- Dudarev M
- Dudhatra N
- Duff J
- Duhan S
- Dunhurst F
- Dussan Ma
- Dutka C
- Dwenger E
- Dzupina A
- DĂ©kĂĄny Jn
- E Eleuteri
- E Englmann
- Earl J
- East C
- Eaton C
- Eaves W
- Ebeling K
- Ebrahim I
- Eccleston D
- Echeverria L
- Eder F
- Edgerton L
- Edillo C
- Edwards J
- Edwards T
- Eichinger G
- Einhorn D
- Eki Y
- El Hachem M
- El Hafi S
- Ellenbroek D
- Ellis M
- Emil B
- Endo T
- Engelen W
- Erhard M
- Erickson B
- Ervin W
- Eskridge L
- Espinosa V
- Everett Bm
- F Fedele
- F Fonseca
- F Fucci
- Facello A
- Facello M
- Faghih M
- Fail P
- Falcon D
- Fang C
- Fang Cy
- Farias E
- Fattal P
- Fawson A
- Feitosa G
- Felario Junior Ga
- Felix L
- Feng Y
- Feng Z
- Ferdinand K
- Ferkl R
- Fernandez Aa
- Ferrari V
- Ferrario M
- Ferraz R
- Ferreira Dos Santos T
- Ferreira-Jardim A
- Fien E
- Filardi Pp
- Filho P
- Fintel D
- Firek C
- Fischer Sm
- Fisher J
- Fitilev S
- Fitz-Patrick D
- Fitzpatrick L
- Flaksa I
- Flather M
- Flezar M
- Fliesser-Goerzer E
- Flores E
- Flores E
- Flores Gs
- Flores H
- Floro T
- Foerster A
- Folkeringa Rj
- Fonseca A
- Fontaine S
- Forgon T
- Forgosh L
- Forker A
- Forster T
- Foster M
- Foucauld J
- Fowler V
- Fox B
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- Francoeur L
- Frandsen B
- Frandsen B
- Frankenstein L
- Fratczak M
- Freitas E
- French J
- Frivold G
- Fruchter G
- Fu G
- Fucak E
- Fuchs R
- Fucili A
- Fukuike C
- Fullerton D
- Fulop P
- Fulop T
- Fulwani M
- Furch G
- Furuseth B
- G Gacioch
- G Gosselin
- Gabito A
- Gabor M
- Gabriel J
- Gabrielli D
- Gaeb-Strasas B
- Gamba C
- Ganau A
- Gapon L
- Garas S
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- Garcia Pinna J
- Garcia Rinaldi R
- Garcia F
- Garcia N
- Garcia-Fragoso V
- Garcia-Portela M
- Garner K
- Gazizianova V
- Gelb R
- Genest J
- Genova D
- George F
- Germann H
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- Ghali J
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- Ghosh S
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- Godoy Sanchez M
- Goette A
- Goff R
- Goffinet C
- Gohel P
- Goldberg N
- Gomez Sanchez J
- Gonsorcik J
- Gonzales D
- Gonzales V
- Gonzalez E
- Gordeev I
- Gorges R
- Gospodinov K
- Gotcheva N
- Goudev A
- Gould R
- Govindaraj D
- Goyal B
- Goyal S
- Grabeau R
- Grable M
- Graham J
- Graham Ja
- Graif J
- Gralow J
- Gravellone M
- Gravenhorst-Muenter U
- Green E
- Greener R
- Greenway F
- Grieshaber V
- Griffin S
- Grigaraviciene I
- Grigorova V
- Gros C
- Grosse A
- Grover A
- Grundtvig M
- Gudipati Rvc
- Guerrero A
- Guillinta P
- Gundala Ak
- Gupta A
- Gupta A
- Gupta M
- Gupta V
- Gutmann J
- Guzman I
- Guzman P
- Gwyn M
- Gyorgyova E
- H Haldane
- H Hansen
- H Haught
- H Hill
- Haase F
- Haege R
- Haenel T
- Hage F
- Hageman T
- Hagemann D
- Hagenow A
- Hagiwara Y
- Haidar A
- Haider K
- Hakas J
- Haldis T
- Hall C
- Hall L
- Hall S
- Halliwell Tc
- Halpern S
- Hamer Bjb
- Hamud-Socoro A
- Han B
- Han S
- Hanak P
- Hanefeld M
- Hangyal T
- Hansson A
- Hanustiakova A
- Hao Y
- Hardas S
- Hardee L
- Harrell W
- Harrington A
- Harris B
- Hartleib M
- Hartwell J
- Hasan F
- Hasbani E
- Hasegawa K
- Hattler B
- Haughton G
- Haynes E
- Haywood A
- He Y
- He Z
- Heaney L
- Hecht J
- Heeren G
- Hegedus V
- Heider J
- Heisters J
- Henley L
- Hennig D
- Henriksson A
- Hermans K
- Hernandez E
- Hernandez I
- Hernandez M
- HernĂĄndez N
- Herrman Jp
- Herzog W
- Hess E
- Hettwer Magedanz E
- Hickey L
- Hiden C
- Hielscher S
- Higuchi T
- Higuchi Y
- Hilkert R
- Hilton T
- Himpel-Boenninghoff A
- Hinderaker P
- Hioki M
- Hirayama A
- Hiroma J
- Ho Cj
- Hodnett P
- Hoffman M
- Hofsoey K
- Hogan C
- Hollanders G
- Holmes Z
- Holoubek D
- Holscher A
- Hominal M
- Homza M
- Hong T
- Hong T
- Hoogslag Pam
- Horackova K
- Horak A
- Hornig M
- Horvat P
- Hosokawa S
- Hotchkiss D
- Houra M
- Hristova K
- Hsieh Ic
- Huang A
- Huang P
- Huang Ph
- Humbert J
- Hurtig U
- Hutchens E
- Huynh T
- Hwang Jj
- Hwang Jj
- Hyun K
- HĂ€rstedt N
- HĂživik Ho
- I Ilic
- I Ivanov
- Iachini K
- Iannopollo G
- Ibarra J
- Ibarra M
- Ibañez J
- Iby M
- Ichisawa M
- Igbokidi O
- Iijima T
- Ilahi T
- Ilic S
- Ilsley M
- Imbrognio M
- Imre Bs
- Inada T
- Inagaki M
- Indolfi C
- Infusino F
- Invitti C
- Ipp E
- Isaza D
- Istratoaie O
- Istvan Kp
- Iteld B
- Ito K
- Ivan P
- Iveta H
- Izmozherova N
- J Jiang
- J Johnson
- J Johnston
- J Jose
- Jacques G
- Jafri A
- Jafry B
- Jagtap P
- Jaguszewska G
- Jain A
- Jansen M
- Jardula M
- Jayasinghe R
- Jefferson D
- Jenkins R
- Jensen Ed
- Jeric M
- Jerzewski A
- Jeserich M
- Jia Z
- Jiang T
- Jiang X
- Jimenez D
- Jirvankar P
- Johansen Bb
- Johansen E
- Johansson K
- Johnson E
- Jones S
- Jonsson Je
- Joosten C
- Joshi U
- Julien Ve
- JuliĂŁo K
- Jure D
- Jure H
- Jutrisa N
- K Kaigawa
- K Katahira
- K Kiroglu
- K Kordic
- K Kostov
- Kabakchieva Vm
- Kaczmarek N
- Kafarakis P
- Kaiserova L
- Kajihara S
- Kala P
- Kaldara E
- Kalina A
- Kalkman C
- Kam J
- Kamensky G
- Kamiya H
- Kamiya J
- Kan G
- Kaneno Y
- Kanitz S
- Kapp I
- Kara Yd
- Karakai H
- Karel I
- Karpuram M
- Karsai Xz
- Kastelein Jjp
- Kataoka M
- Katona A
- Katova T
- Kaur H
- Kawahara M
- Kawai M
- Kawasaki T
- Kawka-Urbanek T
- Kazanskay E
- Ke Y
- Keba E
- Keenan S
- Kelehan S
- Kellnerova I
- Kelly R
- Kelt T
- Kendall T
- Kereiakes D
- Khan A
- Khan M
- Khan R
- Khan S
- Khariouzov A
- Khirmanov V
- Khromtsova O
- Kick J
- Kiefer R
- Kietselaer B
- Kim B
- Kim Ks
- Kim M
- Kimmel M
- King A
- King T
- Kirkland S
- Kiss Rg
- Kissel S
- Kitchens D
- Klamm M
- Klein C
- Klein P
- Klemsdal To
- Kleve R
- Klugherz B
- Knight J
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- Koba M
- Kobalava Z
- Kodem Dr
- Koeitti P
- Koenig W
- Kojima E
- Kok M
- Koldas N
- Koleckar P
- Kolikova V
- Kolleroy C
- Kolokathis F
- Komati S
- Komura Y
- Kondagunta V
- Konradi A
- Kooiman E
- Kopaczewski J
- KopczyĆska M
- Korban E
- Koren M
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- Korte M
- Korth-Wiemann B
- Kose V
- Kosmacheva E
- Kostakou P
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- Kotek L
- Kouz Sm
- Kovacic D
- Kovacs A
- Kozak M
- Kozlova S
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- Kreutter F
- Krupciakova B
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- Kuenzler J
- Kulibaba E
- Kulkarni L
- Kullal P
- Kultursay H
- Kumar Ks
- Kumbla M
- Kuntzsch A
- Kuo Jy
- Kuramochi T
- Kuruma T
- Kusnick B
- Kuzin A
- Kyo E
- L Levinson
- L Lim
- L Link
- L Liu
- Laane E
- Labovitz R
- Lachance P
- Lai Wt
- Lail J
- Lainscak M
- Lake J
- Lal S
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- Lappo M
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- Laszlo Z
- Latheef K
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- Lehman Kf
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- Lehmann D
- Leimbach W
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- Liberato Nl
- Libov I
- Lierse T
- Ligueros M
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- Lindner C
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- Lipchenko A
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- Liviu C
- Lock E
- Lohkare M
- Lok Dja
- Long C
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- Lorenzatti A
- Lousberg A
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- Lu Z
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- Lv Y
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- Lönnberg I
- M Malek
- M Mallagray
- M Mandati
- M Mandviwala
- M Marsters
- M Mays
- M Mcdonald
- M Medvegy
- M Meinrich
- M Mikus
- M Milanova
- M Moustafa
- Ma C
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- Macfadyen Jg
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- Majul C
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- Mbulaiteye A
- Mcalister R
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- Mccullough-O'Brien H
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- Mcintosh C
- Mckenzie A
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- Mckibbin A
- Mclaurin B
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- Mcpherson C
- Medina F
- Megalou A
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- Zineldine A.
- Zirlik A
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- 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-1ÎČ, 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-1ÎČ 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.
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
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- Abdel-Aziz AK
- Abdelfatah S
- Abdellatif M
- Abdoli A
- Abel S
- Abeliovich H
- Abildgaard MH
- Abudu YP
- Acevedo-Arozena A
- Adamopoulos IE
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- Aggarwal BB
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- Agrewala JN
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- Aguilar PV
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- Zhu B
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- Zhu H
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- Zhu W-G
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- Zhuang H
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- Zientara-Rytter K
- Zimmermann CM
- Ziviani E
- Zoladek T
- Zong W-X
- Zorov DB
- Zorzano A
- Zou W
- Zou Z
- Zou Z
- Zuryn S
- Zwerschke W
- 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
Multi-messenger observations of a binary neutron star merger
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- Zywucka N
- Publication venue
- 'American Astronomical Society'
- Publication date
- 01/01/2017
- Field of study
On 2017 August 17 a binary neutron star coalescence candidate (later designated GW170817) with merger time 12:41:04 UTC was observed through gravitational waves by the Advanced LIGO and Advanced Virgo detectors. The Fermi Gamma-ray Burst Monitor independently detected a gamma-ray burst (GRB 170817A) with a time delay of ~1.7 s with respect to the merger time. From the gravitational-wave signal, the source was initially localized to a sky region of 31 deg2 at a luminosity distance of 40+8-8 Mpc and with component masses consistent with neutron stars. The component masses were later measured to be in the range 0.86 to 2.26 Mo. An extensive observing campaign was launched across the electromagnetic spectrum leading to the discovery of a bright optical transient (SSS17a, now with the IAU identification of AT 2017gfo) in NGC 4993 (at ~40 Mpc) less than 11 hours after the merger by the One- Meter, Two Hemisphere (1M2H) team using the 1 m Swope Telescope. The optical transient was independently detected by multiple teams within an hour. Subsequent observations targeted the object and its environment. Early ultraviolet observations revealed a blue transient that faded within 48 hours. Optical and infrared observations showed a redward evolution over ~10 days. Following early non-detections, X-ray and radio emission were discovered at the transientâs position ~9 and ~16 days, respectively, after the merger. Both the X-ray and radio emission likely arise from a physical process that is distinct from the one that generates the UV/optical/near-infrared emission. No ultra-high-energy gamma-rays and no neutrino candidates consistent with the source were found in follow-up searches. These observations support the hypothesis that GW170817 was produced by the merger of two neutron stars in NGC4993 followed by a short gamma-ray burst (GRB 170817A) and a kilonova/macronova powered by the radioactive decay of r-process nuclei synthesized in the ejecta
Combination of searches for heavy spin-1 resonances using 139 fbâ1 of proton-proton collision data at s = 13 TeV with the ATLAS detector
- Author
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- Zwalinski L
- Ă kesson TPA
- Ăncel ĂO
- ĆœeniĆĄ T
- ĆœivkoviÄ 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 fbâ1 of proton-proton collisions at
= 13 TeV collected during 2015â2018 with the ATLAS detector at the CERN Large Hadron Collider. Analyses selecting quark pairs (qq, bb,
, and tb) or third-generation leptons (ÏÎœ and ÏÏ) 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
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
- Author
- A Abbott
- A Abou-Raya
- A Aljandali
- A Ambesi-Impiombato
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- Publication venue
- Publication date
- 09/08/2008
- Field of study
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
ICAR: endoscopic skullâbase surgery
- Author
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- London SD
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- Lund V
- Lund VJ
- Lund VJ
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- Luong A
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- Messerer M
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- Nuwer MR
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- O'Connell BP
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- Solares CA
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- Solari D
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- Stapleton AL
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- Sughrue ME
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- Thorp BD
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- Tomazic PV
- Tomita T
- Tosaka M
- Tosun F
- Trautmann JC
- Trifanescu R
- Tsang RK
- Tsirbas A
- Tu GY
- Tu M
- Turan N
- Turel MK
- Turel MK
- Turner JH
- TurriâZanoni M
- Tyrrell JB
- Tzortzidis F
- Ulfarsson E
- Unsal AA
- Upadhyay S
- Vaezeafshar R
- Valentine R
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- Varlotto JM
- VazâGuimaraes F
- VazâGuimaraes F
- Veeravagu A
- Vellutini Ede A
- Velthoven V
- Verrees M
- Verstegen MJT
- Vescan AD
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- Virgin F
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- Webb SM
- Weber AL
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- Weiland DA
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- Wilson PJ
- Wise SK
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- Wiseman SM
- Witte O
- Wong EHC
- Wood JW
- Woodworth BA
- Woodworth BA
- Wormald PJ
- Wu JS
- Wu W
- Xie L
- Xie T
- Xie T
- Xiong L
- Xu CC
- Xu F
- Xu R
- Xu Z
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- Yao WC
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- Yilmazlar S
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- Yunoue S
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- Zanation AM
- Zanation AM
- Zanation AM
- Zanation AM
- Zanation AM
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- Zwagerman NT
- Publication venue
- Publication date
- 01/07/2019
- Field of study
n/