10 research outputs found
Association of CAPN10 SNPs and Haplotypes with Polycystic Ovary Syndrome among South Indian Women
- Author
- A Gonzalez
- A Gonzalez
- A Mifsud
- B. Mohan Reddy
- C Vollmert
- D Bodhini
- DA Ehrmann
- DA Ehrmann
- DA Ehrmann
- G Villuendas
- HF Escobar-Morreale
- J Sambrook
- JC Evans
- Katragadda Anuradha
- Kudugunti Neelaveni
- L Haddad
- M Urbanek
- MN Weedon
- PG Cassell
- Pisapati V. S. Sirisha
- Robert Lafrenie
- RS Legro
- S Adak
- S Franks
- SA El Mkadem
- Shilpi Dasgupta
- SK Sreenan
- Y Horikawa
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Polycystic Ovary Syndrome (PCOS) is known to be characterized by metabolic disorder in which hyperinsulinemia and peripheral insulin resistance are central features. Given the physiological overlap between PCOS and type-2 diabetes (T2DM), and calpain 10 gene (CAPN10) being a strong candidate for T2DM, a number of studies have analyzed CAPN10 SNPs among PCOS women yielding contradictory results. Our study is first of its kind to investigate the association pattern of CAPN10 polymorphisms (UCSNP-44, 43, 56, 19 and 63) with PCOS among Indian women. 250 PCOS cases and 299 controls from Southern India were recruited for this study. Allele and genotype frequencies of the SNPs were determined and compared between the cases and controls. Results show significant association of UCSNP-44 genotype CC with PCOS (p = 0.007) with highly significant odds ratio when compared to TC (OR = 2.51, p = 0.003, 95% CI = 1.37–4.61) as well as TT (OR = 1.94, p = 0.016, 95% CI = 1.13–3.34). While the haplotype carrying the SNP-44 and SNP-19 variants (21121) exhibited a 2 fold increase in the risk for PCOS (OR = 2.37, p = 0.03), the haplotype containing SNP-56 and SNP-19 variants (11221) seems to have a protective role against PCOS (OR = 0.20, p = 0.004). Our results support the earlier evidence for a possible role of UCSNP-44 of the CAPN10 gene in the manifestation of PCOS
Advanced interatrial block: A well-defined electrocardiographic pattern with clinical arrhythmological implications
- Author
- Publication venue
- 'Oxford University Press (OUP)'
- Publication date
- 01/01/2013
- Field of study
3.050 JCR (2013) Q2, 44/125 Cardiac & cardiovascular system
Recommended from our members
Neural substrate for atrial fibrillation: implications for targeted parasympathetic blockade in the posterior left atrium
- Author
- Publication venue
- Publication date
- 01/01/2008
- Field of study
The parasympathetic (P) nervous system is thought to contribute significantly to focal atrial fibrillation (AF). Thus we hypothesized that P nerve fibers [and related muscarinic (M(2)) receptors] are preferentially located in the posterior left atrium (PLA) and that selective cholinergic blockade in the PLA can be successfully performed to alter vagal AF substrate. The PLA, pulmonary veins (PVs), and left atrial appendage (LAA) from six dogs were immunostained for sympathetic (S) nerves, P nerves, and M(2) receptors. Epicardial electrophysiological mapping was performed in seven additional dogs. The PLA was the most richly innervated, with nerve bundles containing P and S fibers (0.9 +/- 1, 3.2 +/- 2.5, and 0.17 +/- 0.3/cm(2) in the PV, PLA, and LAA, respectively, P < 0.001); nerve bundles were located in fibrofatty tissue as well as in surrounding myocardium. P fibers predominated over S fibers within bundles (P-to-S ratio = 4.4, 7.2, and 5.8 in PV, PLA, and LAA, respectively). M(2) distribution was also most pronounced in the PLA (17.8 +/- 8.3, 14.3 +/- 7.3, and 14.5 +/- 8 M(2)-stained cells/cm(2) in the PLA, PV, and LAA, respectively, P = 0.012). Left cervical vagal stimulation (VS) caused significant effective refractory period shortening in all regions, with easily inducible AF. Topical application of 1% tropicamide to the PLA significantly attenuated VS-induced effective refractory period shortening in the PLA, PV, and LAA and decreased AF inducibility by 92% (P < 0.001). We conclude that 1) P fibers and M(2) receptors are preferentially located in the PLA, suggesting an important role for this region in creation of vagal AF substrate and 2) targeted P blockade in the PLA is feasible and results in attenuation of vagal responses in the entire left atrium and, consequently, a change in AF substrate
Neural substrate for atrial fibrillation: implications for targeted parasympathetic blockade in the posterior left atrium
- Author
- Publication venue
- 'American Physiological Society'
- Publication date
- Field of study
p53 Expression in B-Cell Chronic Lymphocytic Leukemia: A Marker of Disease Progression and Poor Prognosis
- Author
- Ada Sacchi
- Aguilar-Santelises
- Aguilar-Santelises
- Cano
- Catovsky
- Cesare Guglielmi
- Cesarman
- Cheson
- Cordone
- Cuneo
- Danova
- De Re
- Dohner
- El Rouby
- Fenaux
- Francesca Mancini
- Francesca Romana Mauro
- Franco Mandelli
- French Cooperative Group on chronic lymphocytic leukemia
- Gaidano
- Gandini
- Gannon
- Garcia-Marco
- Greenblatt
- Greiner
- Hernandez
- Hollstein
- Imamura
- Inghirami
- International Workshop on Chronic Lymphocytic Leukemia
- Iole Cordone
- Keating
- Korkolopoulou
- Lane
- Lens
- Lepelley
- Levine
- Lo Coco
- Louie
- Maria Luce Vegna
- Martin
- Matsushima
- Matsushima
- Melo
- Ornella Morsilli
- Pezzella
- Piris
- Quinlan
- Reich
- Robert Foa
- Rozman
- Said
- Sander
- Sarkis
- Scott
- Serena Masi
- Sidansky
- Silvia Soddu
- Sjogren
- Sonia Giuliacci
- Thor
- Tiziana Valentini
- Villuendas
- Villuendas
- Visakorpi
- Wada
- Wattel
- Wilson
- Zoldan
- Publication venue
- 'American Society of Hematology'
- Publication date
- Field of study
MDM2 Inhibitor Nutlin-3a Induces Apoptosis and Senescence in Cutaneous T-Cell Lymphoma: Role of p53
- Author
- Agar
- Ambrosini
- Barbarotto
- Bossi
- Brady
- Caelles
- Carter
- Coll-Mulet
- Davis
- De la Cueva
- Dereure
- Drakos
- Edyta Biskup
- Efeyan
- Gartel
- Gazdar
- Gootenberg
- Hans C. Wulf
- Harris
- Hasegawa
- Haupt
- Hu
- Jin
- Kaltoft
- Kamstrup
- Kamstrup
- Kamstrup
- Kapur
- Kapur
- Kojima
- Kurosawa
- Lau
- Leroy
- Long
- Lozano
- Manfe
- Mao
- Maria R. Kamstrup
- Marrogi
- Martin-Caballero
- Nardella
- Niels Morling
- Peter Johansen
- Philipp
- Ri
- Robert Gniadecki
- Roninson
- Roninson
- Saha
- Secchiero
- Secchiero
- Shen
- Steele
- Steininger
- Thorbjørn F. Krejsgaard
- Valentina Manfé
- Vaseva
- Vassilev
- Vermeer
- Villalonga-Planells
- Villuendas
- Vogelstein
- Voltan
- Vousden
- Wada
- Wickremasinghe
- Willemze
- Wojcik
- Wollina
- Wong
- Zhu
- Zinzani
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
In Vivo Direct Molecular Imaging of Early Tumorigenesis and Malignant Progression Induced by Transgenic Expression of GFP-Met
- Author
- Ahmed
- Altstock
- Bell
- Birchmeier
- Boccaccio
- Dafna W. Kaufman
- DeVita
- Eddy Solomon
- Faletto
- Fidler
- Fukuda
- Galia Tsarfaty
- Gallego
- George F. Vande Woude
- Ghoussoub
- Gideon Y. Stein
- Gonzalez-Fernandez
- Graveel
- Hadjantonakis
- Hasebe
- Ilan Tsarfaty
- Itoh
- James H. Resau
- Jeffers
- Jin
- Kang JY Dolled-Filhart
- Kaplan
- Keren Shichrur
- Koochekpour
- Lengyel
- Li CY Shan
- Lindner
- Ma
- MacDougall
- Muller
- Nakanishi
- Nakashiro
- Okabe
- Otsuka
- Parr
- Pepperkok
- Qian
- Ren Y Cao
- Robert H. Sigler
- Rong
- Rong
- Sakata
- Sasaki
- Sawicki
- Schmidt
- Schmidt
- Seol
- Sharon Moshitch-Moshkovitz
- Sirotnak
- Steinbauer
- Takayama
- Trusolino
- Tsarfaty
- Tsarfaty
- Villuendas
- Wack
- Wang
- Wang
- Wong
- Yamashita
- Yerushalmi
- Yokoyama
- Publication venue
- 'Neoplasia Press'
- Publication date
- Field of study
Polycystic ovary syndrome
- Author
- Abbott
- Adams
- Adashi
- Adashi
- Alberti
- Asuncion
- Ayala
- Azziz
- Azziz
- Azziz
- Azziz
- Azziz
- Azziz
- Azziz
- Balen
- Balen
- Balen
- Barnes
- Beck
- Blank
- Boomsma
- Bosinski
- Boudreaux
- Bridges
- Broekmans
- Carmina
- Carmina
- Carmina
- Carmina
- Carmina
- Casper
- Chang
- Chang
- Chian
- Christin-Maitre
- Coffey
- Coffey
- Conway
- Coviello
- Crosignani
- Davies
- Davis
- De Leo
- Delvigne
- DeUgarte
- DeVane
- Dewailly
- Diamanti-Kandarakis
- Diamanti-Kandarakis
- Diamanti-Kandarakis
- Dickey
- Didier Dewailly
- Dunaif
- Dunaif
- Dunaif
- Dunaif
- Dunaif
- Ehrmann
- Ehrmann
- Ehrmann
- Ehrmann
- Ehrmann
- Ehrmann
- Ellis
- Elsenbruch
- Escobar-Morreale
- Essah
- Farquhar
- Fatemi
- Ferriman
- Ferriman
- Fogel
- Franks
- Franks
- Franks
- Gambineri
- Gilling-Smith
- Givens
- Goodarzi
- Guyatt
- Hahn
- Hahn
- Harborne
- Hardiman
- Heijnen
- Hickey
- Hickey
- Homburg
- Huber-Buchholz
- Hughes
- Hughesdon
- Ibanez
- Ibanez
- Imani
- Imani
- Jonard
- Jonard
- Jonard
- Kahn
- Kaushal
- Kelly
- Kiddy
- Knowler
- Kumar
- Lanzone
- Legro
- Legro
- Legro
- Legro
- Legro
- Legro
- Legro
- Leibel
- Lopez
- Lord
- Lucky
- Lunde
- Maciel
- Mathur
- Mifsud
- Miller
- Moll
- Moran
- Moran
- Moran
- Mulders
- Navot
- Nelson
- Nestler
- Nestler
- Nestler
- Norman
- Norman
- Norman
- Orio
- Orio
- Pache
- Pache
- Palomba
- Palomba
- Palomba
- Paradisi
- Pasquali
- Pigny
- Pugeat
- Rebar
- Rice
- Richard S Legro
- Robert J Norman
- Rodin
- Sam
- Schenker
- Shapiro
- Solomon
- Stamets
- Stein
- Stewart
- Talbott
- Taponen
- Tasali
- Theresa E Hickey
- Tsagareli
- Tucci
- Tummon
- Urbanek
- Urbanek
- van Santbrink
- van Vloten
- Vendola
- Vermeulen
- Vgontzas
- Villuendas
- Vink
- Vrbikova
- Webber
- Weil
- Welt
- Welt
- Wild
- Willis
- Willis
- Wood
- Wu
- Yildiz
- Zhang
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/01/2007
- Field of study
Copyright © 2007 Elsevier Ltd All rights reserved.Polycystic ovary syndrome is a heterogeneous endocrine disorder that affects about one in 15 women worldwide. The major endocrine disruption is excessive androgen secretion or activity, and a large proportion of women also have abnormal insulin activity. Many body systems are affected in polycystic ovary syndrome, resulting in several health complications, including menstrual dysfunction, infertility, hirsutism, acne, obesity, and metabolic syndrome. Women with this disorder have an established increased risk of developing type 2 diabetes and a still debated increased risk of cardiovascular disease. The diagnostic traits of polycystic ovary syndrome are hyperandrogenism, chronic anovulation, and polycystic ovaries, after exclusion of other conditions that cause these same features. A conclusive definition of the disorder and the importance of the three diagnostic criteria relative to each other remain controversial. The cause of polycystic ovary syndrome is unknown, but studies suggest a strong genetic component that is affected by gestational environment, lifestyle factors, or both.Robert J Norman, Didier Dewailly, Richard S Legro and Theresa E Hickeyhttp://www.elsevier.com/wps/find/journaldescription.cws_home/31066/description#descriptio
Recommended from our members
ESICM LIVES 2016: part three: Milan, Italy. 1–5 October 2016
- Author
- Abbott T. E. F.
- Abdallah R. I.
- Abdel-Aal I. R.
- Abdelmonem S. A.
- Abdo W. F.
- Abellan A. Naharro
- Abellán A. Naharro
- Abellán A. Navarro
- Abrams S. T.
- Ackerley C.
- Acuña M.
- Adda M.
- Adhikari N. K.
- Adriano G.
- Adrie C.
- Affatato R.
- Afonso-Rivero D.
- Agarossi A.
- Agarwal L. K.
- Ageeva T.
- Agrawal R.
- Aguayo-DeHoyos E.
- Aguilar A. L. Ruiz
- Aguilar-Alonso E.
- Aguirregabyria M.
- Ahmadnia E.
- Ahn C.
- Ahn J. Y.
- Ahn M. Y.
- Aitken L. M.
- Akalaev R.
- Akbarzadeh A.
- Akcan-Arikan A.
- Akhlagh S. H.
- Akhtar N.
- Akiduki N.
- Akin S.
- Akizuki N.
- Akkoc T.
- Ala-Kokko T.
- Alanio A.
- Albaiceta G. Muñiz
- Albaladejo P.
- Alberto F.
- Albuisson E.
- Alcala M. A.
- Alcázar L.
- Aldabo-Pallas T.
- Aldana N. Navarrete
- Aldecoa C.
- Alegría L.
- Alejandro R.
- Alejo G. Camarena
- Alejos R. Martínez
- Alexandrova E.
- Algarte R.
- Algieri I.
- Algora-Weber A.
- Alhamdi Y.
- Aliaga F. A.
- Aliberti S.
- Alkan A.
- Almudena P. Matía
- Almudevar P. Matia
- Almudévar P. Matía
- Altıntas N. D.
- Alvarez J.
- Alves S. Chacón
- Alzola L. Melián
- Amargianitakis V.
- Amaro R.
- Amato M. B. P.
- Ambler M.
- Amerongen M. P. van Nieuw
- Amininejad T.
- Amor L. Lopéz
- Amorim V.
- Anand R. K.
- Andersen L. W.
- Andersson S.
- Andoh K.
- Andrade A. H.
- Andrade G.
- Andreis D. T.
- Annane D.
- Antonelli M.
- Antoniadou A.
- Antonio C.
- Antonucci E.
- Antón D. González
- Anzueto A.
- Appiani F.
- Aquevedo A.
- Aragon C.
- Araujo N. J. Fernández
- Araujo V. F.
- Arias C. Castro
- Arias N.
- Arias-Verdu M. D.
- Armaganidis A.
- Arora M. K.
- Arora N.
- Arrigo M.
- Arslantas M. K.
- Artiguenave M.
- Aslanian P.
- Aspide R.
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- Ataman S.
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- Aydin M.
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- Babalis D.
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- Chan W. S.
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- da Silva V. Z. M.
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- de la Fuente M. Valdivia
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- De La Rica A. Suárez
- De la Torre M. A.
- De Maglie M.
- de Molina F. J. González
- De Morton N.
- de Oca Sandoval M. A. Montes
- De Pascale G.
- De Rosa S.
- De Sanctis F.
- De Silva A. P.
- De Sousa I.
- de Vera A. Pareja Rodríguez
- de Wilde W.
- De Zani D.
- Deblier I.
- DeBrunnar R.
- Del Arco A.
- del Moral O. Lopez
- Del Olmo R.
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- Demirkiran O.
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 18/11/2016
- Field of study
Edoxaban versus warfarin in patients with atrial fibrillation
- Author
- Abdullakutty J
- Abi-Mansour P
- Abril SB
- Accini J
- Accini M
- Acikel M
- Acikel M
- Adachi C
- Adams K
- Adams K
- Adamus J
- Adler J
- Adler P
- Agarwal D
- Aggarwal R
- Aggarwal R
- Agirov M
- Agraou B
- Ahmad A
- Ahmadpour H
- Ahuad Guerrero R
- Ajioka M
- Akhter F
- Akihisa U
- Akilli H
- Al-Maliky T
- Al-Zoebi A
- Albert L. Waldo
- Albisu J
- Albulescu P
- Alexander J
- Alexandrova L
- Alexopoulos D
- Alexopoulos D
- Alhakim M
- Aliyar P
- Allall O
- Allison J
- Allman J
- Almaraz SP
- Almeida A
- Almeida M
- Almquist A
- Aloni I
- Alsheikh T
- Altonen D
- Alvarez C
- Alvarez M
- Alvarez RF
- Amarenco P
- Amato Vincenzo de Paola A
- Ambrovic I
- Ambrovicova V
- Ameriso P
- Ameriso S
- Amin K
- Amin M
- Amuchastegui M
- Anciu M
- Anderson C
- Anderson J
- Anderson J
- Andersson R
- Andor M
- Andrade Lotufo P
- Andresen T
- Andrews A
- Angel J
- Anscombe R
- Anthony A
- Antle S
- Antman EM
- Antman EM
- Antonino M
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- Apetrei E
- Apostolovic S
- Appelros P
- Aquino M
- Arakawa S
- Araújo E
- Archibald J
- Arcocha Torres M
- Ardelean A
- Arfaoui M
- Arias J
- Armas BH
- Arneja J
- Arnold T
- Arora T
- Arora V
- Arouni A
- Arrieta M
- Arroyave C
- Arstall M
- Arutyunov G
- Asakura H
- Asensio A
- Astier L
- Ata N
- Ata N
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- Atar D
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- Atkinson C
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- Weiss R
- Weitz J
- Wessels L
- West M
- Westcott J
- Weyland K
- Wharton S
- White H
- White H
- Wierzykowski T
- Wiggers H
- Williams D
- Williams R
- Willis J
- Wilmot M
- Wilmott R
- Wilson L
- Winberg L
- Winkelmann B
- Winter K
- Witold Ruzyllo
- Witt P
- Wiviott S
- Wnetrzak-Michalska R
- Wofford E
- Wolde C
- Wollaert B
- Wood K
- Woodford T
- Worley S
- Wright A
- Wright H
- Wright J
- Wright L
- Wrobel W
- Wroblewski J
- Wu SL
- Wu WS
- Wu YW
- Wulf A
- Wulf M
- Wurow A
- Wysokinski A
- Xie J
- Xie XD
- Xu GL
- Xu JH
- Xu YM
- Xu YP
- Yagensky A
- Yagi H
- Yagi M
- Yahata A
- Yakusevich V
- Yakushin S
- Yalcin R
- Yalcin R
- Yamabe H
- Yamada T
- Yamagishi K
- Yamagishi T
- Yamaguchi A
- Yamamoto Y
- Yamano R
- Yamashina A
- Yamashita T
- Yamashita T
- Yanac Chavez P
- Yang K
- Yang Y
- Yang YJ
- Yang ZY
- Yarows S
- Yasin M
- Yasumoto S
- Yeh HI
- Yeh TC
- Yena L
- Yi J
- Yigit F
- Yigit F
- Yigit Z
- Yigit Z
- Yin YH
- Yonehara T
- York T
- Yoshida K
- Yoshida K
- Yoshino H
- Yoshioka K
- You ZG
- Young C
- Young C
- Young G
- Young K
- Yousuf K
- Yovaniniz P
- Yu B
- Yu WC
- Yuan ZY
- Yukhno E
- Yukihiro Koretsune
- Yumoto I
- Zachar A
- Zacà V
- Zajac E
- Zakhary B
- Zamlynskyy M
- Zamorano JL
- Zanotti A
- Zanwar I
- Zapanta M
- Zarandon RS
- Zarebinski M
- Zareczky P
- Zarpentin C
- Zateyshchikov D
- Zateyshchikova A
- Zeig S
- Zellner C
- Zeltser D
- Zenin S
- Zhang HQ
- Zhang P
- Zhang X
- Zhang YL
- Zhang Z
- Zhao RP
- Zhao XL
- Zharinov O
- Zheng X
- Zheng Y
- Zheng ZQ
- Zhou SX
- Zhukova N
- Zhurba S
- Zidkova E
- Zidkova E
- Ziegler K
- Zielinski M
- Zienciuk-Krajka A
- Zimmermann EB
- Zimmermann S
- Zoghi M
- Zoghi M
- Zondag M
- Zotova I
- Zubeeva G
- Zyatenkova E
- Åkerberg A
- Östberg S
- Ŝpinar J
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2013
- Field of study
Contains fulltext :
125374.pdf (publisher's version ) (Open Access)BACKGROUND: Edoxaban is a direct oral factor Xa inhibitor with proven antithrombotic effects. The long-term efficacy and safety of edoxaban as compared with warfarin in patients with atrial fibrillation is not known. METHODS: We conducted a randomized, double-blind, double-dummy trial comparing two once-daily regimens of edoxaban with warfarin in 21,105 patients with moderate-to-high-risk atrial fibrillation (median follow-up, 2.8 years). The primary efficacy end point was stroke or systemic embolism. Each edoxaban regimen was tested for noninferiority to warfarin during the treatment period. The principal safety end point was major bleeding. RESULTS: The annualized rate of the primary end point during treatment was 1.50% with warfarin (median time in the therapeutic range, 68.4%), as compared with 1.18% with high-dose edoxaban (hazard ratio, 0.79; 97.5% confidence interval [CI], 0.63 to 0.99; P<0.001 for noninferiority) and 1.61% with low-dose edoxaban (hazard ratio, 1.07; 97.5% CI, 0.87 to 1.31; P=0.005 for noninferiority). In the intention-to-treat analysis, there was a trend favoring high-dose edoxaban versus warfarin (hazard ratio, 0.87; 97.5% CI, 0.73 to 1.04; P=0.08) and an unfavorable trend with low-dose edoxaban versus warfarin (hazard ratio, 1.13; 97.5% CI, 0.96 to 1.34; P=0.10). The annualized rate of major bleeding was 3.43% with warfarin versus 2.75% with high-dose edoxaban (hazard ratio, 0.80; 95% CI, 0.71 to 0.91; P<0.001) and 1.61% with low-dose edoxaban (hazard ratio, 0.47; 95% CI, 0.41 to 0.55; P<0.001). The corresponding annualized rates of death from cardiovascular causes were 3.17% versus 2.74% (hazard ratio, 0.86; 95% CI, 0.77 to 0.97; P=0.01), and 2.71% (hazard ratio, 0.85; 95% CI, 0.76 to 0.96; P=0.008), and the corresponding rates of the key secondary end point (a composite of stroke, systemic embolism, or death from cardiovascular causes) were 4.43% versus 3.85% (hazard ratio, 0.87; 95% CI, 0.78 to 0.96; P=0.005), and 4.23% (hazard ratio, 0.95; 95% CI, 0.86 to 1.05; P=0.32). CONCLUSIONS: Both once-daily regimens of edoxaban were noninferior to warfarin with respect to the prevention of stroke or systemic embolism and were associated with significantly lower rates of bleeding and death from cardiovascular causes. (Funded by Daiichi Sankyo Pharma Development; ENGAGE AF-TIMI 48 ClinicalTrials.gov number, NCT00781391.)