69 research outputs found
Altered Antioxidant-Oxidant Status in the Aqueous Humor and Peripheral Blood of Patients with Retinitis Pigmentosa
- Author
- A Bagnis
- A Behndig
- A Catala
- A Dong
- A Friebe
- Alfred Lewin
- AM Stanzial
- B Falsini
- C Ayuso
- C Hamel
- C Punzo
- C Romero
- CA Curcio
- CP Verdon
- Cristina Martínez-Fernández de la Cámara
- Cristina Marín-Lambíes
- D Salom
- David Hervás
- David Salom
- DY Yu
- DY Yu
- EL Berson
- EL Berson
- Elena Aller
- EM Vingolo
- H Ohguro
- I Minagawa
- IY Haddad
- J Shen
- JC Rivera
- JE Grunwald
- JG Flanagan
- José María Millán
- K Akeo
- K Komeima
- K Komeima
- K Komeima
- KG Schmidt
- L Guo
- LB Mamo
- LI Lau
- LM Rapp
- M Cellini
- M Cellini
- M Kalloniatis
- M Schaumberger
- Ma Dolores Sequedo
- Manuel Díaz-LLopis
- ME Langham
- MH Sun
- MM Sanz
- N Yoshida
- N Yoshida
- NG Bazan
- O Jung
- P Ahuja-Jensen
- R Mancino
- Regina Rodrigo
- RM Peters
- RN Frank
- RW Massof
- S Arai-Gaun
- S Kimura
- S Usui
- S Usui
- S Usui
- SC Beutelspacher
- SM Ferreira
- SY Lee
- T Cronin
- T Léveillard
- Teresa Jaijo
- TJ Break
- X Liu
- X Qi
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- 01/01/2013
- Field of study
Retinitis Pigmentosa is a common form of hereditary retinal degeneration constituting the largest Mendelian genetic cause of blindness in the developed world. It has been widely suggested that oxidative stress possibly contributes to its pathogenesis. We measured the levels of total antioxidant capacity, free nitrotyrosine, thiobarbituric acid reactive substances (TBARS) formation, extracellular superoxide dismutase (SOD3) activity, protein, metabolites of the nitric oxide/cyclic GMP pathway, heme oxygenase-I and inducible nitric oxide synthase expression in aqueous humor or/and peripheral blood from fifty-six patients with retinitis pigmentosa and sixty subjects without systemic or ocular oxidative stress-related disease. Multivariate analysis of covariance revealed that retinitis pigmentosa alters ocular antioxidant defence machinery and the redox status in blood. Patients with retinitis pigmentosa present low total antioxidant capacity including reduced SOD3 activity and protein concentration in aqueous humor. Patients also show reduced SOD3 activity, increased TBARS formation and upregulation of the nitric oxide/cyclic GMP pathway in peripheral blood. Together these findings confirmed the hypothesis that patients with retinitis pigmentosa present reduced ocular antioxidant status. Moreover, these patients show changes in some oxidative-nitrosative markers in the peripheral blood. Further studies are needed to clarify the relationship between these peripheral markers and retinitis pigmentosa
The collateral circulation determines cortical infarct volume in anterior circulation ischemic stroke
- Author
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
The importance of imprinting in the human placenta.
- Author
- A Lewis
- A Plagge
- A Thurston
- AC Enders
- AC Ferguson-Smith
- AC Ferguson-Smith
- AI Diplas
- AL Fowden
- AM Carter
- AM Carter
- Anne C. Ferguson-Smith
- BM Cattanach
- BV Skryabin
- C Gicquel
- CB Oudejans
- CP Sibley
- D Frank
- D Haig
- D Haig
- D Haig
- D Mancini-DiNardo
- D Monk
- D Monk
- D Monk
- D Monk
- D Takai
- D Umlauf
- DP Barlow
- DR Arnold
- E Li
- F Ding
- F Guillemot
- F Guillemot
- F Ubeda
- FM Smith
- G Pardi
- Gudrun E. Moore
- GV Fitzpatrick
- H Cui
- H Munier-Lehmann
- I Hatada
- I Iglesias-Platas
- IM Buntinx
- IY Yotova
- J Liu
- J McGrath
- J McMinn
- JA Graves
- Jennifer M. Frost
- JL Thorvaldsen
- JM Bowen
- JR Engel
- JY Shin
- K Green
- K Hannula
- K Knox
- K Mitsuya
- K Takahashi
- KD Tremblay
- KG Pringle
- L Lefebvre
- L Lunghi
- L Redrup
- M Charalambous
- M Charalambous
- M Constancia
- M Constancia
- M Kaneda
- MA Frevel
- MA Surani
- MD Dean
- MM Lau
- MP Hitchins
- MP Lee
- MS Bartolomei
- N Blagitko
- N Kanayama
- NM Gude
- P Arnaud
- P Georgiades
- PA Leighton
- PM Coan
- PM Coan
- Q Wang
- R Terranova
- RD Nicholls
- RJ Baker
- S Abu-Amero
- S Apostolidou
- SJ Tunster
- SM Davies
- ST da Rocha
- T Ludwig
- T Miyamoto
- T Moore
- T Sahoo
- TJ Cole
- TM DeChiara
- TM DeChiara
- U von Rango
- V Romanelli
- W Mayer
- W Reik
- WN Cooper
- Y Yan
- YS Moon
- ZQ Wang
- Publication venue
- Publication date
- 01/07/2010
- Field of study
As a field of study, genomic imprinting has grown rapidly in the last 20 years, with a growing figure of around 100 imprinted genes known in the mouse and approximately 50 in the human. The imprinted expression of genes may be transient and highly tissue-specific, and there are potentially hundreds of other, as yet undiscovered, imprinted transcripts. The placenta is notable amongst mammalian organs for its high and prolific expression of imprinted genes. This review discusses the development of the human placenta and focuses on the function of imprinting in this organ. Imprinting is potentially a mechanism to balance parental resource allocation and it plays an important role in growth. The placenta, as the interface between mother and fetus, is central to prenatal growth control. The expression of genes subject to parental allelic expression bias has, over the years, been shown to be essential for the normal development and physiology of the placenta. In this review we also discuss the significance of genes that lack conservation of imprinting between mice and humans, genes whose imprinted expression is often placental-specific. Finally, we illustrate the importance of imprinting in the postnatal human in terms of several human imprinting disorders, with consideration of the brain as a key organ for imprinted gene expression after birth
Sub-Telomere Directed Gene Expression during Initiation of Invasive Aspergillosis
- Author
- A Hayashi
- A Markaryan
- A Mullbacher
- A Schaffner
- AL Hughes
- AM Calvo
- Andrew McDonagh
- BJ Howlett
- Brendan P. Cormack
- C Kupfahl
- C Maerker
- CP Bracken
- CS Chim
- D Deprost
- D Komagata
- DA Hosack
- Dan Chen
- Darius Armstrong-James
- DJ Cove
- E Bignell
- EK Shwab
- Elaine Bignell
- F Tekaia
- G Lau
- G Pontecorvo
- GK Smyth
- GM Gersuk
- Gregory May
- Gustavo Goldman
- HJ Pel
- Hubertus Haas
- IA Hansen
- IY Adamson
- J Heitman
- J Pardo
- J Robin
- JA Sugui
- JA Sugui
- JC Panepinto
- JD Barry
- JE Galagan
- Jonathan Crabtree
- JP Latge
- JW Bok
- JW Bok
- K Jaton-Ogay
- Ken Haynes
- M Hensel
- M Machida
- M Rohlfs
- M Schrettl
- M Schrettl
- MA Davis
- MA Penalva
- Markus Schrettl
- ME Cardenas
- ML Farman
- MR Branco
- N Keller
- Natalie D. Fedorova
- ND Fedorova
- NM Donofrio
- NP Keller
- O Ibrahim-Granet
- Omar Loss
- OS Zmeili
- PA De Las
- PE Kolattukudy
- RA Cramer Jr
- RC Summerbell
- RM Perrin
- RM Tuder
- S Krappmann
- S Krappmann
- S Lonial
- S Maiya
- S Spikes
- S Teichert
- S Thewes
- Stanley Kim
- Timothy Cairns
- V Nygaard
- V Nygaard
- W Blyth
- WC Nierman
- William C. Nierman
- Yan Yu
- YC Chang
- YG Amaar
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2008
- Field of study
Aspergillus fumigatus is a common mould whose spores are a
component of the normal airborne flora. Immune dysfunction permits developmental
growth of inhaled spores in the human lung causing aspergillosis, a significant
threat to human health in the form of allergic, and life-threatening invasive
infections. The success of A. fumigatus as a pathogen is unique
among close phylogenetic relatives and is poorly characterised at the molecular
level. Recent genome sequencing of several Aspergillus species
provides an exceptional opportunity to analyse fungal virulence attributes
within a genomic and evolutionary context. To identify genes preferentially
expressed during adaptation to the mammalian host niche, we generated multiple
gene expression profiles from minute samplings of A. fumigatus
germlings during initiation of murine infection. They reveal a highly
co-ordinated A. fumigatus gene expression programme, governing
metabolic and physiological adaptation, which allows the organism to prosper
within the mammalian niche. As functions of phylogenetic conservation and
genetic locus, 28% and 30%, respectively, of the
A. fumigatus subtelomeric and lineage-specific gene
repertoires are induced relative to laboratory culture, and physically clustered
genes including loci directing pseurotin, gliotoxin and siderophore biosyntheses
are a prominent feature. Locationally biased A. fumigatus gene
expression is not prompted by in vitro iron limitation, acid,
alkaline, anaerobic or oxidative stress. However, subtelomeric gene expression
is favoured following ex vivo neutrophil exposure and in
comparative analyses of richly and poorly nourished laboratory cultured
germlings. We found remarkable concordance between the A.
fumigatus host-adaptation transcriptome and those resulting from
in vitro iron depletion, alkaline shift, nitrogen
starvation and loss of the methyltransferase LaeA. This first transcriptional
snapshot of a fungal genome during initiation of mammalian infection provides
the global perspective required to direct much-needed diagnostic and therapeutic
strategies and reveals genome organisation and subtelomeric diversity as
potential driving forces in the evolution of pathogenicity in the genus
Aspergillus
A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)
- Author
- Abbott TE
- Abdallah RI
- Abdel-Aal IR
- Abdelmonem SA
- Abdo WF
- Abellan AN
- Abellán AN
- Abellán AN
- Abellán AN
- Abrams ST
- Ackerley C
- Acuña M
- Adda M
- Adhikari NK
- Adriano G
- Adrie C
- Affatato R
- Affatato R
- Afonso-Rivero D
- Agarossi A
- Agarwal LK
- Ageeva T
- Agrawal R
- Aguayo-DeHoyos E
- Aguilar AL
- Aguilar-Alonso E
- Aguilar-Alonso E
- Aguilar-Alonso E
- Aguirregabyria M
- Ahmadnia E
- Ahn C
- Ahn JY
- Ahn JY
- Ahn MY
- Ahn MY
- Aitken LM
- Akalaev R
- Akbarzadeh A
- Akcan-Arikan A
- Akhlagh SH
- Akhtar N
- AKI Research Group
- Akiduki N
- Akin S
- Akizuki N
- Akkoc T
- Ala-Kokko T
- Alanio A
- Albaiceta GM
- Albaladejo P
- Alberto F
- Albuisson E
- Alcala MA
- Alcázar L
- Aldabo-Pallas T
- Aldana NN
- Aldecoa C
- Alegría L
- Alejandro R
- Alejo GC
- Alejos RM
- Alexandrova E
- Algarte R
- Algarte R
- Algieri I
- Algora-Weber A
- Alhamdi Y
- Aliaga FA
- Aliberti S
- Alkan A
- Almudena PM
- Almudevar PM
- Almudevar PM
- Almudévar PM
- Altıntas ND
- Alvarez J
- Alves SC
- Alzola LM
- Amargianitakis V
- Amaro R
- Amato MB
- Ambler M
- Amerongen MP
- Amininejad T
- Amor LL
- Amorim V
- Anand RK
- Andersen LW
- Andersson S
- Andoh K
- Andrade AH
- Andrade AH
- Andrade AH
- Andrade G
- Andreis DT
- Andreis DT
- Annane D
- Antonelli M
- Antoniadou A
- Antonio C
- Antonucci E
- Antón DG
- Anzueto A
- Appiani F
- Aquevedo A
- Aragon C
- Araujo NJ
- Araujo VF
- ARIAM registry of adult cardiac surgery
- ARIAM-ANDALUCIA
- Arias CC
- Arias N
- Arias-Verdu MD
- Arias-Verdu MD
- Arias-Verdu MD
- Armaganidis A
- Arora MK
- Arora N
- Arrigo M
- Arslantas MK
- Artiguenave M
- Aslanian P
- Aspide R
- Asyralyyeva G
- Ataman S
- Ataman S
- Atchade E
- Atchade E
- Atchasiri S
- Athapattu P
- Atkins G
- Aublanc M
- Aublanc M
- Augustin P
- Augustin P
- Auquier P
- Avilés-Jurado FX
- Avramidis V
- Ayala LY
- Aydin M
- Azevedo JC
- Azevedo JR
- Aznar GP
- Babalis D
- Babini G
- Bachli EB
- Bader A
- Bader A
- Baena J
- Baidya DK
- Baikova VN
- Bakker J
- Balcázar LC
- Balcázar LC
- Baldassarri R
- Baldwin CE
- Balik M
- Ball I
- Ballin A
- Balsera B
- Banderas-Bravo ME
- Banderas-Bravo ME
- Bandert A
- Bangstad IL
- Baptista N
- Baquero JD
- Barbadillo S
- Barberet G
- Barberet G
- Barberet G
- Barbier J
- Barcenilla F
- Barea-Mendoza JA
- Barinas OD
- Baron AV
- Barrachina LG
- Barral M
- Basile-Filho A
- Bassi GL
- Bates D
- Battistini M
- Bauer M
- Bauer PR
- Baumstarck K
- Baumstarck K
- Bawin M
- Bazan N
- Bañeras J
- Beane A
- Beduneau G
- Beduneau G
- Beduneau G
- Beeharry SD
- Beerepoot M
- Begzjav T
- Beishuizen A
- Bell C
- Belletti A
- Bellissimo-Rodrigues F
- Belloli A
- Bellomo R
- Bellver BQ
- Belmonte R
- Ben-Hamouda N
- Bendel S
- Bendel S
- Benyamina M
- Beretta S
- Berg R
- Bergantino B
- Berghmans J
- Bernal FF
- Berric A
- Berrutti D
- Berthelsen RE
- Bertini P
- Bertini P
- Berto MB
- Besevli SG
- Bestle MH
- Bettex D
- Bettex DA
- Beunders R
- Bhasin D
- Bhattal MK
- Bhide S
- Bianchi I
- Bianchi I
- Bianzina S
- Bianzina S
- Bianzina S
- Bishop J
- Bissenova N
- Bisso MC
- Blans MJ
- Blobner M
- Bloomer MJ
- Blot K
- Blot S
- Blot S
- Boa F
- Bobi Q
- Bodingbauer M
- Bodí M
- Boer C
- Bogossian E
- Bonet S
- Bonn M
- Bonnet M
- Borges FK
- Bouadma L
- Boucekine M
- Bougouin W
- Bourenne J
- Boyd JG
- Boyd JG
- Bozbay S
- Bozza F
- Bradac O
- Brandon RA
- Brandon RB
- Braschi A
- Braschi A
- Braschi A
- Brasseur A
- Brasseur A
- Brasseur A
- Braune S
- Brazzi L
- Breitkreutz R
- Brianti R
- Brioni M
- Brochard L
- Brochard L
- Brochard L
- Brock N
- Brody DL
- Brook R
- Brousseau C
- Brown K
- Brugger SC
- Brugger SC
- Bruno F
- Bruno K
- Brusasco C
- Brusasco C
- Brusasco C
- Bruyere O
- Bucknall T
- Buddi S
- Buise M
- Buitinck SH
- Buranavanich P
- Bureau C
- Burle JF
- Burtin P
- Busico M
- Butler MB
- Butrov AV
- Caballero CH
- Caballero J
- Cabello JT
- Cabello JT
- Cabrera AR
- Cabrera JL
- Cabrera JL
- Cabrini L
- Cairus C
- Cakin O
- Caliskan K
- Calpe P
- Calvo CP
- Calvo SA
- Camargo M
- Cambronero JA
- Cameron C
- Campbell R
- Campelo FA
- Campelo FA
- Campos LM
- Cannesson M
- CAPCRI Study
- Capellier G
- Carbonara M
- Cardellino S
- Cardenas CL
- Cariou A
- Cariou A
- Carlesso E
- Carmona AF
- Carmona SA
- Carmona SA
- Carmona SA
- Carmona SA
- Carone M
- Carpio D
- Carratalá A
- Carreira MM
- Carrero-Gómez F
- Carreño ER
- Carreño R
- Carvalho JP
- Carvalho KV
- Casals XN
- Casals XN
- Cassina T
- Castañeda DP
- Castellana D
- Castellanos A
- Castellanos A
- Castillo-Lorente E
- Castillo-Lorente E
- Catalan M
- Catalán RM
- Catena E
- Catena E
- Cauwenberghs H
- Cavalcanti D
- Cavalheiro AM
- Cavalier E
- Cavicchi FZ
- Cavicchi FZ
- Cengiz M
- Ceriani R
- Cermelli S
- Cerović O
- Cha YS
- Chabanne R
- Chacon-Alves S
- Champigneulle B
- Champigneulle B
- Chan KC
- Chan KK
- Chan WS
- Chang CH
- Chang WY
- Chao A
- Chao A
- Chao AS
- Chao HC
- Chaouat M
- Charitidou E
- Charpentier C
- Charpentier J
- Charron C
- Chatelon J
- Chaudhari HK
- Chaussard M
- Chavanon O
- Chaves S
- Chelly J
- Chemam S
- Chen CM
- Chen CM
- Chen CW
- Chen CW
- Chen GQ
- Chen L
- Chen YS
- Chen YS
- Chen YS
- Cheng CC
- Cheng CC
- Cheng CC
- Cheng CC
- Cheng KC
- Cheng YJ
- Chernyshuk S
- Chevret S
- Chhor V
- Chiang CC
- Chiang CH
- Chiang CH
- Chiang CH
- Chiappa C
- Chiou KR
- Chiou KR
- Chiou KR
- Chiu LC
- Chiumello D
- Chiurazzi C
- Chiurazzi C
- Cho Y
- Cho YJ
- Cho YJ
- Choi JY
- Choi JY
- Choi KS
- Choi S
- Choi YJ
- Choi YY
- Chok L
- Cholkraisuwat J
- Cholley B
- Chondropoulos S
- Chou W
- Chouris I
- Chouvarda I
- Christopher KB
- Chrétien JM
- Chrétien JM
- Chrétien JM
- Chumaev A
- Chung CR
- Churchill K
- Chytas A
- Cinel I
- Cinnella G
- Citerio G
- Citerio G
- Clavel M
- Clemente EA
- Clermont G
- Cleyet M
- Cohen Y
- Colaprico A
- Colino L
- Collange O
- Colombo A
- Colombo A
- Colson P
- Combes A
- Concha P
- Connolly B
- Constan A
- Constan A
- Constan A
- Conte V
- Conti G
- Conti G
- Contreras KM
- Contreras MR
- Cook DJ
- Coombs M
- Cordeiro CP
- Cordero M
- Cordolcini V
- Cordovilla-Guardia S
- Cordón J
- Corona A
- Corona A
- Corradi F
- Corradi F
- Corradi F
- Correa-Chamorro E
- Corte FD
- Cortes ML
- Corzo L
- Coss-Bu JA
- Coss-Bu JA
- Costa MI
- Costa RC
- Costa RC
- Costa RC
- Costanzo E
- Cotoia A
- Cottini SR
- Cottle D
- Cotton H
- Cotton H
- Courant P
- Cowan R
- Creagh-Brown B
- Cressoni M
- Creteur J
- Creteur J
- Creteur J
- Creteur J
- Creteur J
- Creteur J
- Creteur J
- Creteur J
- Crimella F
- Cron N
- Cuellar AI
- Cui N
- Cunha MM
- Curiel-Balsera E
- Curiel-Balsera E
- Curinga M
- Curtis A
- Cuthbertson BH
- Cutuli SL
- Câmara M
- D'Arsigny C
- da Silva SL
- da Silva VZ
- Daga-Ruiz D
- Dalhuisen A
- Dalorzo M
- Damas P
- Dambrosio M
- Damås JK
- Das Neves A
- David H
- Davis C
- Davis P
- Day A
- de Abreu MG
- De Backer A
- De Brito-Ashurst I
- De Cassai A
- De Freitas FF
- De Gasperi A
- de Hoyos EA
- De la Calle-Pedrosa N
- de la Fuente MV
- De La Fuente-Martos C
- De La Fuente-Martos C
- De La Rica AS
- De la Torre MA
- De Maglie M
- De Maglie M
- de Molina FJ
- De Morton N
- de Oca Sandoval MA
- De Pascale G
- De Rosa S
- De Sanctis F
- De Silva AP
- De Sousa I
- de Vera AP
- de Wilde W
- De Zani D
- Deblier I
- DeBrunnar R
- Del Arco A
- Del Moral OL
- Del Olmo R
- Del Rosario CG
- Del Sorbo L
- Delgado CP
- Delgado MJ
- Delgado-Amaya M
- Demirkiran O
- Demoule A
- Denehy L
- Der Kinderen EP
- Descotte E
- Deshpande K
- Desmard M
- Desmard M
- Deveugele M
- Deye N
- Di Bello F
- Di Giancamillo M
- Di Gravio V
- Di Gregorio A
- Di Mussi R
- Di Rosso R
- Diaz DD
- Diaz P
- Dilek M
- Dilly MP
- Dima E
- Dimitroulakis K
- Dimitrov BD
- Dimitrov BD
- Dimopoulou IK
- Dinh A
- Divatia JV
- Dixon J
- Doganci M
- Doglia JA
- Doherty P
- Dolset RA
- Dominguez JP
- Domínguez JP
- Donald CL
- Donnino M
- Doorduin J
- Dorent R
- Dos Reis Miranda D
- Dos Santos HP
- Dougall PC
- Doyle J
- Doyle J
- Drover J
- Duarte R
- Dubois EA
- Dubrawski A
- Dubó S
- Dudas G
- Dudoignon E
- Dumas F
- Dunthorne E
- Duran N
- Durand M
- Durovray JD
- Durrant J
- Duzgun M
- Díaz E
- Díaz JJ
- Díaz M
- Díaz PV
- Dünser MW
- E Silva ZC
- E YY
- Ebeling G
- Echeverri JE
- Echeverría JG
- Ediboglu O
- Ediboglu O
- Egea-Guerero JJ
- Egginton JS
- Egi M
- El Adawy AS
- El Hamid MA
- El Hossainy R
- El Sayed E
- El Sayed F
- El Sayed I
- El-Hamamsy M
- El-Keraie A
- Eladawy S
- Elbers PW
- Elgendy M
- Eliet J
- Emmanuel J
- Emmerich M
- Encina B
- Endacott R
- Endacott R
- Engelberts D
- ENVIN-HELICS Study Group
- Erb J
- Erdogan M
- Eroles AA
- Escalada SH
- Escalada SH
- Escoval A
- Escribá A
- Escórcio S
- Eslami S
- Espinasse F
- Espinel E
- Estagnasie P
- Esteban A
- Estella A
- Estenssoro E
- Evelein-Brugman S
- Facchin F
- Faivre V
- Fang M
- Fanzaghi P
- Farias P
- Faulds MC
- Fave G
- Feehan A
- Feijoo AM
- Feliot E
- Ferez MA
- Fernandes MJ
- Fernandes N
- Fernandez NG
- Fernandez R
- Fernandez-Zamora MD
- Fernández IF
- Fernández L
- Fernández MV
- Fernández PA
- Fernández-Barat L
- Fernández-Mondéjar E
- Fernández-Ortega JF
- Ferraz AB
- Ferrero-Calleja J
- Ferri F
- Ferry A
- Ferré A
- Ferrón FR
- Ferrón FR
- Fiks T
- Fiks T
- Fileković S
- Filho CA
- Filho CA
- Filho CA
- Filipe E
- FINNRESUSCI Study Group
- Fischer G
- Fleischmann E
- Fless K
- Floccard B
- Flowers E
- Follin A
- Follin A
- Fong KY
- Fontaiña LP
- Fontana V
- Fontenot T
- Forel JM
- Forni L
- Forni L
- Forni LG
- Forni LG
- Forni LG
- Fournel E
- Fox B
- Franchi P
- Francioni JE
- Francioni JE
- Franco JF
- Frantzeskaki F
- Frantzeskaki F
- Frat JP
- Frat JP
- Frat JP
- Freile MT
- Frenzel T
- Frigeni B
- Frithiof R
- Fritz C
- FROG ICU Investigators
- Fromentin M
- Frontera PR
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- Fumagalli F
- Fumagalli F
- Fumis RR
- Fushimi K
- Gabán-Díez Á
- Gadgil S
- Gaide-Chevronnay L
- Gainnier M
- Gaite FB
- Gaizauskas E
- Gajic O
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- Gallego-Corpa AI
- Gameiro J
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- Gando S
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- Garcia-Delgado M
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- García MF
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- Garnacho-Montero J
- Garrido BB
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- Garrouste M
- Gaspard N
- Gasparovic V
- Gattinoni L
- Gaudard P
- Gavranovic Z
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- Gordon M
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- Gorjup V
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- Gottlieb J
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- Granillo JF
- Grassi L
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- Hassanin H
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- Hayashi K
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- Hirayama T
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- Kleinpell R
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- Olaechea P
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- Álvarez JT
- Álvarez-Lerma F
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2016
- Field of study
Meeting abstrac
The global burden of cancer attributable to risk factors, 2010-19: a systematic analysis for the Global Burden of Disease Study 2019
- Author
- Aali A
- Ab Khan M
- Abbas Q
- Abbasi B
- Abbasi-Kangevari M
- Abbasi-Kangevari Z
- Abbastabar H
- Abd-Elsalam S
- Abdelmasseh M
- Abdelwahab AA
- Abdoli G
- Abdulkader RS
- Abdulkadir HA
- AbdulmuhsinMohammad K
- Abedi A
- Abegaz KH
- Abidi H
- Aboagye RG
- Abolhassani H
- Absalan A
- Abtew YD
- Abu-Gharbieh E
- Achappa B
- Acheson AR
- Acuna JM
- Addison D
- Addo IY
- Adegboye OA
- Adesina MA
- Adnan M
- Adnani QES
- Advani SM
- Afrin S
- Afzal MS
- Aggarwal M
- Ahinkorah BO
- Ahmad AR
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- Ahmadi S
- Ahmed H
- Ahmed LA
- Ahmed MB
- Aiman W
- Ajami M
- Akalu GT
- Akbarzadeh-Khiavi M
- Aklilu A
- Akonde M
- Akunna CJ
- Al Hamad H
- Al Montasir A
- Al-Hanawi MK
- Al-Maweri SAA
- Al-Raddadi RM
- Al-Rifai RHH
- Al-Sabah SK
- Al-Tammemi AB
- Alahdab F
- Alanezi FM
- Alanzi TM
- Alessy SA
- Algammal AM
- Alhassan RK
- Ali AH
- Ali BA
- Ali HA
- Ali L
- Ali SS
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- Alipour V
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- Alkhayyat M
- Almustanyir S
- Alonso N
- Alqalyoobi S
- Altawalah H
- Alvis-Guzman N
- Amare F
- Ameyaw EK
- Amirzade-Iranaq MH
- Amu H
- Amusa GA
- Ancuceanu R
- Anderson JA
- Animut YA
- Anoushiravani A
- Anoushirvani AA
- Ansari-Moghaddam A
- Ansha MG
- Antony B
- Antwi MH
- Anwar SL
- Anwer R
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- Aremu O
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- Birega MGB
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- Buchanan CM
- Bulamu NB
- Bustamante-Teixeira MT
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- Camera LA
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- Demisse B
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- Dessalegni SAA
- Dessie G
- Desta AA
- Dewan SMR
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- Diao N
- Diaz D
- Digesa LE
- Dixit SG
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- Dongarwar D
- dos Santos WM
- Driscoll TR
- Dsouza HL
- Durojaiye OC
- Edalati S
- Eghbalian F
- Ehsani-Chimeh E
- Eini E
- Ekerija MA
- Ekholuenetale M
- Ekundayo TC
- Ekwueme DU
- El Tantawi M
- El-Huneidi W
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- Elbarazi I
- Elghazaly H
- Elhadi M
- Emamian MH
- Enyew DB
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- Eshrati B
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- Fahimi S
- Fakhradiyev IR
- Faraon EJA
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- Fasanmi AO
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- Gaal PA
- Gad MM
- Gadanya MA
- Gaipov A
- Galehdar N
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- Gebremichael MA
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- Gela YY
- Gemeda BNB
- Getachew M
- Getachew ME
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- Ghafourifard M
- Ghamari S-H
- Ghassemi F
- Ghimire A
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- Gizaw ATT
- Glasbey JC
- Godos J
- Goel A
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- Golitaleb M
- Gorini G
- Goulart BNG
- Grosso G
- Guadie HA
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- Guerra MR
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- Gupta VK
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- Halboub ES
- Halimi A
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- Haro JM
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- Henrikson HJ
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- Househ M
- Huang J
- Hugo FN
- Humayun A
- Hussain S
- Hussein NR
- Hwang B-F
- Ibitoye SE
- Iftikhar PM
- Ikuta KS
- Ilesanmi OS
- Ilic IM
- Ilic MD
- Immurana M
- Innos K
- Iranpour P
- Irham LM
- Isfahani HM
- Islam MS
- Islam RM
- Islami F
- Ismail NE
- Isola G
- Iwagami M
- Jabbari SHY
- Jafari AA
- Jaiswal A
- Jakovljevic M
- Jalili M
- Jalilian S
- Jamshidi E
- Jang S-I
- Jani CT
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- Javaheri T
- Jayarajah UU
- Jayaram S
- Jazayeri SB
- Jebai R
- Jemal B
- Jeong W
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- Jindal HA
- John-Akinola YO
- Jonas JB
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- Jozwiak JJ
- Julian GS
- Kabir A
- Kacimi SEO
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- Kanno GG
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- Kar SS
- Karanth SD
- Karaye IM
- Karch A
- Karimi A
- Kashani HRK
- Kassa BG
- Katoto PDMC
- Kauppila JH
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- Publication venue
- Publication date
- 20/08/2022
- Field of study
Pan-cancer analysis of whole genomes
- Author
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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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- Y. uz
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- Y. yc
- ya Al-Ahmadie
- Yachida
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- z ah
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- zd Gershenwald
- Zenklusen
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- zf Ghossein
- Zhang
- Zhang
- Zhang
- Zhang
- Zhang
- Zhang
- Zhang H. b
- Zhao
- Zheng
- Zhou
- Zhou
- Zhu
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- zi zj
- zm Jayaseelan
- Zou
- Zou
- zt Kim
- zw Lewis
- Ó. A. th
- Ø. 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
Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019
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- Abbafati C
- Abbas KM
- Abbasi M
- Abbasi-Kangevari M
- Abbasifard M
- Abbastabar H
- Abd El Razek HM
- Abd El Razek MM
- Abd-Allah F
- Abdelalim A
- Abdollahi M
- Abdollahpour I
- Abdulkader RS
- Abdullah KH
- Abedi A
- Abedi P
- Abegaz KH
- Abolhassani H
- Abosetugn AE
- Aboyans V
- Abrams EM
- Abreu LG
- Abrigo MRM
- Abu Haimed AK
- Abu-Gharbieh E
- Abu-Raddad LJ
- Abualhasan A
- Abushouk AI
- Acebedo A
- Ackerman IN
- Adabi M
- Adair T
- Adamu AA
- Adebayo OM
- Adedeji IA
- Adekanmbi V
- Adelson JD
- Adeoye AM
- Adetokunboh OO
- Adham D
- Advani SM
- Afarideh M
- Afshari M
- Afshin A
- Agardh EE
- Agarwal G
- Agasthi P
- Agesa KM
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- Aghamir SMK
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- Akalu TY
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- Albertson SB
- Alcalde-Rabanal JE
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- Woldu G
- Wolfe CDA
- Wondmeneh TG
- Wondmieneh AB
- Wool EE
- Wozniak SS
- Wu A-M
- Wu C
- Wu J
- Wunrow HY
- Xie Y
- Xu G
- Xu R
- Yadgir S
- Yamada T
- Yamagishi K
- Yaminfirooz M
- Yano Y
- Yaya S
- Yazdi-Feyzabadi V
- Yearwood JA
- Yeheyis TY
- Yeshitila YG
- Yilgwan CS
- Yilma MT
- Yip P
- Yonemoto N
- Yoon S-J
- York HW
- Younis MZ
- Younker TP
- Yousefi B
- Yousefi Z
- Yousefifard M
- Yousefinezhadi T
- Yousuf AY
- Yu C
- Yu Y
- Yuan C-W
- Yuce D
- Yusefzadeh H
- Zadey S
- Zahabi SS
- Zaidi SS
- Zaki L
- Zaki MES
- Zakzuk J
- Zamani M
- Zamanian M
- Zandian H
- Zangeneh A
- Zarafshan H
- Zastrozhin MS
- Zewdie KA
- Zhang J
- Zhang Y
- Zhang Z-J
- Zhao JT
- Zhao X-JG
- Zhao Y
- Zheleva B
- Zheng P
- Zhou M
- Zhu C
- Ziapour A
- Zimsen SRM
- Zlavog BS
- Zodpey S
- Publication venue
- 'Elsevier BV'
- Publication date
- 17/10/2020
- Field of study
Five insights from the Global Burden of Disease Study 2019
- Author
- Abbafati C
- Abbas KM
- Abbasi M
- Abbasi-Kangevari M
- Abbasifard M
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- 01/01/2020
- Field of study
The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a rules-based synthesis of the available evidence on levels and trends in health outcomes, a diverse set of risk factors, and health system responses. GBD 2019 covered 204 countries and territories, as well as first administrative level disaggregations for 22 countries, from 1990 to 2019. Because GBD is highly standardised and comprehensive, spanning both fatal and non-fatal outcomes, and uses a mutually exclusive and collectively exhaustive list of hierarchical disease and injury causes, the study provides a powerful basis for detailed and broad insights on global health trends and emerging challenges. GBD 2019 incorporates data from 281 586 sources and provides more than 3.5 billion estimates of health outcome and health system measures of interest for global, national, and subnational policy dialogue. All GBD estimates are publicly available and adhere to the Guidelines on Accurate and Transparent Health Estimate Reporting. From this vast amount of information, five key insights that are important for health, social, and economic development strategies have been distilled. These insights are subject to the many limitations outlined in each of the component GBD capstone papers.Peer reviewe
Prostate Cancer Induced by Loss of Apc Is Restrained by TGFβ Signaling
- Author
- A Chytil
- A Di Cristofano
- A Suzuki
- AA Aitchison
- Bryce M. Paschal
- BT MacDonald
- C Jeronimo
- C-H Heldin
- David Wotton
- ER Fearon
- F Rodier
- Glen A. Bjerke
- H Clevers
- H Ikushima
- H Jakel
- H Sun
- H Suzuki
- H Wang
- H Zhao
- HB Pearson
- Henry F. Frierson Jr.
- HJ Voeller
- IY Kim
- J Kim
- J Massague
- J Massague
- J Massague
- J Massagué
- JC Francis
- K Taniguchi
- Karolina Pietrzak
- Kin Mang Lau
- KJ Bruxvoort
- KJ Cheung
- KJ Pienta
- KM Yamada
- L Bartholin
- L Levy
- M Ittmann
- M Kuraguchi
- MM Shen
- MP Myers
- MT Galgano
- P Cairns
- P Friedl
- P Roy-Burman
- PK Majumder
- PL Dahia
- Q Eastman
- RH Williams
- SE Powers
- SI Wang
- SW Fine
- T Maehama
- Tiffany A. Melhuish
- V Stambolic
- WH Tu
- X Wu
- X Wu
- X Yu
- Y Chen
- Y Guo
- Y Zhang
- Z Ding
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- 01/01/2014
- Field of study
Recent work with mouse models of prostate cancer (CaP) has shown that inactivation of TGFβ signaling in prostate epithelium can cooperate with deletion of the Pten tumor suppressor to drive locally aggressive cancer and metastatic disease. Here, we show that inactivating the TGFβ pathway by deleting the gene encoding the TGFβ type II receptor (Tgfbr2) in combination with a deletion of the Apc tumor suppressor gene specifically in mouse prostate epithelium, results in the rapid onset of invasive CaP. Micro-metastases were observed in the lymph nodes and lungs of a proportion of the double mutant mice, whereas no metastases were observed in Apc single mutant mice. Prostate-specific Apc;Tgfbr2 mutants had a lower frequency of metastasis and survived significantly longer than Pten;Tgfbr2 double mutants. However, all Apc;Tgfbr2 mutants developed invasive cancer by 30 weeks of age, whereas invasive cancer was rarely observed in Apc single mutant animals, even by one year of age. Further comparison of the Pten and Apc models of CaP revealed additional differences, including adenosquamous carcinoma in the Apc;Tgfbr2 mutants that was not seen in the Pten model, and a lack of robust induction of the TGFβ pathway in Apc null prostate. In addition to causing high-grade prostate intra-epithelial neoplasia (HGPIN), deletion of either Pten or Apc induced senescence in affected prostate ducts, and this restraint was overcome by loss of Tgfbr2. In summary, this work demonstrates that TGFβ signaling restrains the progression of CaP induced by different tumor suppressor mutations, suggesting that TGFβ signaling exerts a general tumor suppressive effect in prostate.This work was supported by a Program Project Grant from the National Cancer Institute (2P01CA104106 to B. Paschal and D. Wotton), and by a pilot grant from the UVA Cancer Center (funded from the CCSG P30 CA44579, the James and Rebecca CraigFoundation, and UVA Women's Oncology fund) to D. Wotton. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We thank Sharon Birdsall for technical assistance, Anindya Dutta and Dan
Gioeli for helpful discussions, and Chun-Song Yang for advice and
reagent
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