61 research outputs found
Discovery of an Allosteric Binding Site in Kinetoplastid Methionyl-tRNA Synthetase
- Author
- Publication venue
- 'American Chemical Society (ACS)'
- Publication date
- 08/05/2020
- Field of study
PROGNOSTIC IMPLICATION OF THE MITRAL VALVE TENTING GEOMETRY IN PATIENTS WITH DILATED CARDIOMYOPATHY: TRANSTHORACIC REAL-TIME 3D ECHOCARDIOGRAPHIC STUDY
- Author
- Christiaans Imke
- de Boer Rudolf A.
- Deprez Ronald H. Lekanne Dit
- Groeneweg Judith A.
- Hauer Richard N. W.
- Jongbloed Jan D. H.
- Nannenberg Eline A.
- Pinto Yigal M.
- Post Jan G.
- Tan Hanno L.
- van den Berg Maarten P.
- van der Zwaag Paul A.
- van Rijsingen Ingrid A. W.
- van Tintelen J. Peter
- Wilde Arthur A. M.
- Zwinderman Aeilko H.
- Publication venue
- American College of Cardiology Foundation. Published by Elsevier Inc.
- Publication date
- 12/03/2013
- Field of study
BACKGROUND: The pathogenic phospholamban R14del mutation causes dilated and arrhythmogenic right ventricular cardiomyopathies and is associated with an increased risk of malignant ventricular arrhythmias and end-stage heart failure. We performed a multicentre study to evaluate mortality, cardiac disease outcome, and risk factors for malignant ventricular arrhythmias in a cohort of phospholamban R14del mutation carriers. METHODS AND RESULTS: Using the family tree mortality ratio method in a cohort of 403 phospholamban R14del mutation carriers, we found a standardized mortality ratio of 1.7 (95% confidence interval, 1.4-2.0) with significant excess mortality starting from the age of 25 years. Cardiological data were available for 295 carriers. In a median follow-up period of 42 months, 55 (19%) individuals had a first episode of malignant ventricular arrhythmias and 33 (11%) had an end-stage heart failure event. The youngest age at which a malignant ventricular arrhythmia occurred was 20 years, whereas for an end-stage heart failure event this was 31 years. Independent risk factors for malignant ventricular arrhythmias were left ventricular ejection fraction <45% and sustained or nonsustained ventricular tachycardia with hazard ratios of 4.0 (95% confidence interval, 1.9-8.1) and 2.6 (95% confidence interval, 1.5-4.5), respectively. CONCLUSIONS: Phospholamban R14del mutation carriers are at high risk for malignant ventricular arrhythmias and end-stage heart failure, with left ventricular ejection fraction <45% and sustained or nonsustained ventricular tachycardia as independent risk factors. High mortality and a poor prognosis are present from late adolescence. Genetic and cardiac screening is, therefore, advised from adolescence onwards
Effect of Functional Capacity Evaluation information on the judgment of physicians about physical work ability in the context of disability claims
- Author
- AM Kelly
- B Patel
- C Anagnostis
- CA Bodian
- DG Altman
- DL Hart
- DP Gross
- DP Gross
- EJ Gallagher
- EW Ehrich
- G Zanoli
- H Wind
- Haije Wind
- J Rainville
- JR Lyth
- Judith K. Sluiter
- LN Matheson
- M Baldwin
- MF Reneman
- MH Liang
- Monique H. W. Frings-Dresen
- MT Duruöz
- OP Krief
- P. Paul F. M. Kuijer
- PJ Scott
- PM Brooks
- PR Oesch
- RB Post
- S Brouwer
- S Brouwer
- TS Carey
- V Gouttebarge
- V Gouttebarge
- VIH Kwa
- Vincent Gouttebarge
- W Zinn
- Publication venue
- Springer-Verlag
- Publication date
- 01/01/2009
- Field of study
Purpose To test whether Functional Capacity Evaluation (FCE) information lead insurance physicians (IPs) to change their judgment about the physical work ability of claimants with musculoskeletal disorders (MSDs). Methods Twenty-seven IPs scored twice the physical work ability of two claimants for 12 specified activities, using a visual analogue scale. One claimant performed an FCE, the other served as a control. Outcome measure was the difference between experimental and control group in number of shifts in the physical work ability for the total of 12 specified activities. Results The IPs changed their judgment about the work ability 141 times when using FCE information compared to 102 times when not using this information (P-value = 0.001), both in the direction of more and less ability. Conclusions The IPs change their judgment of the physical work ability of claimants with MSDs in the context of disability claim procedures more often when FCE information is provide
Thyroid-stimulating hormone and free thyroxine fail to predict the severity and clinical course of hyperemesis gravidarum : A prospective cohort study
- Author
- Bais Joke M J
- Bremer Henk A
- Grooten Iris J
- Heidema Wieteke M
- Huisjes Anjoke
- Kleiverda Gunilla
- Koot Marjette H
- Kuppens Simone M
- Langenveld Josje
- Mol Ben W
- Naaktgeboren Christiana
- Nijsten Kelly
- Painter Rebecca C
- Papatsonis Dimitri
- Pelinck Marie-José
- Pernet Paula J
- Rijnders Robbert J
- Ris-Stalpers Carrie
- Roseboom Tessa J
- Scheepers Hubertina C J
- Siegelaar Sarah E
- van der Ham David P
- van der Made Flip
- van der Post Joris A M
- van Laar Judith O E H
- van Rheenen-Flach Leonie
- Vogelvang Tatjana
- Publication venue
- 'Wiley'
- Publication date
- 01/01/2021
- Field of study
Funding information: This prospective cohort study was supported by a research grant from North West Hospital Group, Alkmaar, the Netherlands (Grant number: 2013T085) and by a research grant from the Amsterdam Reproduction and Development (AR&D) Research Institute, Amsterdam UMC, the Netherlands (Project number: 23346). ACKNOWLEDGMENTS We thank Dr. J.P. Bestwick (employed at Queen Mary University of London, London, UK) and Professor Dr. J.H. Lazarus (employed at Cardiff School of Medicine, Cardiff, UK) for providing TSH medians from their study in the UK. Dr. J.P. Bestwick and Professor Dr. Lazarus have nothing to disclose.Peer reviewedPublisher PD
From national monopoly to Multinational Corporation: how regulation shaped the road towards telecommunications internationalization
- Author
- Antonelli C.
- Bauer J.
- Bureau Van Dijk. (undated)
- Calvo Á.
- Calvo Á.
- Clifton J.
- Clifton J.
- Clifton J.
- Clifton J.
- Committee of Enquiry on the Post Office
- Comín F.
- Comín F.
- Comín F.
- Daniel Díaz-Fuentes
- Dunning J.
- Florio M.
- Francisco Comín
- Guillén M.
- Gálvez L.
- Hertner P.
- Judith Clifton
- Ledbetter R.
- Lipartito K.
- Little D.
- López S.
- Millward R.
- Noam E.
- OECD
- OECD
- OECD
- OECD
- OECD
- OECD
- OECD
- Parker D.
- Puig N.
- Ramamurti R.
- Rodriguez M.
- Schröter H.
- Sobel R.
- Tascón Fernández J.
- Turner C.
- UNCTAD
- UNCTAD
- Wilkins M.
- Zeitlin J.
- Álvaro A.
- Álvaro A.
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2011
- Field of study
One of the consequences of major regulatory reform of the telecommunications sector from the end of the 1970s – particularly, privatization, liberalization and deregulation – was the establishment of a new business environment which permitted former national telecommunications monopolies to expand abroad. From the 1990s, a number of these firms, particularly those based in Europe, joined the rankings of the world’s leading Multinational Corporations. Their internationalization was uneven, however: while some firms internationalised strongly, others ventured abroad much slower. This article explores how the regulatory framework within which telecommunications incumbents evolved over the long-term shaped their subsequent, uneven, paths to internationalization. Two case studies representing ´maximum variation´ are selected: Telefónica, whose early and unrelenting expansion transformed it into one of the world’s most international of Multinational Corporations, and BT, whose overseas ventures failed and, with eroding domestic market share, forced the firm to partially retreat, becoming the least international of the large European incumbents. Long-term ownership, access to capital, management style and exposure to liberalization strongly influenced firms’ approaches to internationalizatio
Germline MBD4-deficiency causes a multi-tumor predisposition syndrome
- Author
- Adams David J.
- Arbe-Barnes Edward H.
- Arnedo-Pac Claudia
- Bajel Ashish
- Buchanan Daniel D.
- Caravagna Giulio
- Cheadle Jeremy P.
- Chegwidden Laura
- Chew Edward
- Christie Michael
- Chubb Daniel
- Church David
- Clendenning Mark
- Cross William
- Curley Helen
- de Voer Richarda M.
- Deltas Constantinos
- Dimovski Aleksandar J.
- Dymerska Dagmara
- Flensburg Christoffer
- Fostira Florentia
- Frangou Anna
- Galavotti Sara
- Georgiou Demetra
- Goldberg Yael
- Graham Trevor
- Green Andrew
- Grolleman Judith E.
- Gruber Andreas J.
- Hoogerbrugge Nicoline
- Houlston Richard
- Jansen Erik A.M.
- Jenkins Mark A.
- Kinnersley Ben
- Koelzer Viktor H.
- Kuiper Roland P.
- Lander Nicola
- Ligtenberg Marjolijn J.L.
- Lopez-Bigas Nuria
- Lubinski Jan
- Mahmood Khalid
- Majewski Ian J.
- Martin Lynn
- Noyvert Boris
- Pagan Judith
- Palles Claire
- Ponte Clara Ruiz
- Power Derek G.
- Rivas Andres Dacal
- Roberts Andrew W.
- Sampson Julian R.
- Sanders Mathijs
- Sherwood Kitty
- Sottoriva Andrea
- Taylor Jenny C.
- Thomas Huw
- Thomas Laura E.
- Tomlinson Ian P.M.
- Truscott Rebekah
- Turnbull Clare
- van der Biezen Simone A.M.
- van der Post Rachel S.
- van Wezel Tom
- Vreede Lilian
- Wedge David
- Weitz Jürgen
- West Hannah D.
- Whalley Celina
- Winship Ingrid M.
- Publication venue
- Publication date
- 01/01/2022
- Field of study
We report an autosomal recessive, multi-organ tumor predisposition syndrome, caused by bi-allelic loss-of-function germline variants in the base excision repair (BER) gene MBD4. We identified five individuals with bi-allelic MBD4 variants within four families and these individuals had a personal and/or family history of adenomatous colorectal polyposis, acute myeloid leukemia, and uveal melanoma. MBD4 encodes a glycosylase involved in repair of G:T mismatches resulting from deamination of 5′-methylcytosine. The colorectal adenomas from MBD4-deficient individuals showed a mutator phenotype attributable to mutational signature SBS1, consistent with the function of MBD4. MBD4-deficient polyps harbored somatic mutations in similar driver genes to sporadic colorectal tumors, although AMER1 mutations were more common and KRAS mutations less frequent. Our findings expand the role of BER deficiencies in tumor predisposition. Inclusion of MBD4 in genetic testing for polyposis and multi-tumor phenotypes is warranted to improve disease management
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
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- A. -G. Wu
- A. C. Ma
- A. K. Au
- Abdel-Aziz A. K.
- Abdelfatah S.
- Abdellatif M.
- Abdoli A.
- Abel S.
- Abeliovich H.
- Abildgaard M. H.
- Abudu Y. P.
- Acevedo-Arozena A.
- Adamopoulos I. E.
- Adeli K.
- Adolph T. E.
- Adornetto A.
- Aflaki E.
- Agam G.
- Agarwal A.
- Aggarwal B. B.
- Agnello M.
- Agostinis P.
- Agrewala J. N.
- Agrotis A.
- Aguilar P. V.
- Ahmad S. T.
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- Ahumada-Castro U.
- Aits S.
- Aizawa S.
- Akkoc Y.
- Akoumianaki T.
- Akpinar H. A.
- Al-Abd A. M.
- Al-Akra L.
- Al-Gharaibeh A.
- Alaoui-Jamali M. A.
- Alberti S.
- Alcocer-Gomez E.
- Alessandri C.
- Ali M.
- Alim Al-Bari M. A.
- Aliwaini S.
- Alizadeh J.
- Almacellas E.
- Almasan A.
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- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
- Author
- Abdel-Aziz AK
- Abdelfatah S
- Abdellatif M
- Abdoli A
- Abel S
- Abeliovich H
- Abildgaard MH
- Abudu YP
- Acevedo-Arozena A
- Adamopoulos IE
- Adeli K
- Adolph TE
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- Aflaki E
- Agam G
- Agarwal A
- Aggarwal BB
- Agnello M
- Agostinis P
- Agrewala JN
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- Ahmed ZM
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- Akkoc Y
- Akoumianaki T
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- Alim Al-Bari MA
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- Alizadeh J
- Almacellas E
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- Alonso GD
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- Altieri DC
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- Ambrosio S
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- Zhivotovsky B
- Zhong Q
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- Zhu B
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- Zhu H
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- Zhu W-G
- Zhu Y
- Zhu Y
- Zhuang H
- Zhuang X
- 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
- Álvarez ÉMC
- Ávalos Y
- Önal G
- Üstün S
- Čolić M
- Đokić J
- Žerovnik 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
Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease
- Author
- Abecasis Gonçalo R.
- Adair Linda S.
- Adeyemo Adebowale
- Adrienne Cupples L.
- Ala-Korpela Mika
- Alexander Myriam
- Altshuler David
- Amin Najaf
- Andrade Mariza de
- Arfan Ikram M.
- Arking Dan E.
- Arora Pankaj
- Artigas Maria Soler
- Aspelund Thor
- Asselbergs Folkert W.
- Aulchenko Yurii
- Bakker Stephan J. L.
- Ballantyne Christie
- Bandinelli Stefania
- Barroso Inês
- Basu Saonli
- Baumert Jens
- Becker Diane M.
- Becker Lewis C.
- Beckmann Jacques S.
- Beilby John P.
- Bergman Richard N.
- Bergmann Sven
- Bevan Steve
- Bielak Lawrence F.
- Bis Joshua C.
- Blankenberg Stefan
- Bochud Murielle
- Boehm Bernhard O.
- Boehnke Michael
- Boerwinkle Eric
- Bonnycastle Lori L.
- Borecki Ingrid B.
- Bornstein Stefan R.
- Bots Michiel L.
- Bragg-Gresham Jennifer L.
- Brand Eva
- Brand Stefan-Martin
- Braund Peter S.
- Brown Morris J.
- Burgess Stephen
- Burton Paul R.
- Cambien Francois
- Campbell Harry
- Carter Angela M.
- Casas Juan P.
- Caulfield Mark J.
- Chakravarti Aravinda
- Chambers John C.
- Chandak Giriraj R.
- Chang Yen-Pei C.
- Charchar Fadi J.
- Chasman Daniel I.
- Chaturvedi Nish
- Chen Ming-Huei
- Cheng Yu-Ching
- Chilukoti Ravi Kumar
- Cho Yoon Shin
- Clarke Robert
- Collins Francis S.
- Collins Rory
- Connell John M.
- Cooper Jackie A.
- Cooper Matthew N.
- Cooper Richard S.
- Coresh Josef
- Corsi Anna Maria
- Couper David J.
- Cunningham Julie
- Cushman Mary
- D'Agostino Ralph B.
- Dahgam Santosh
- Danesh John
- Day Ian N. M.
- Dehghan Abbas
- Deloukas Panos
- Demirkan Ayse
- Demissie Serkalem
- Denniff Matthew
- Ding Jingzhong
- Dominiczak Anna F.
- Dong Yanbin
- Doumatey Ayo
- Dreisbach Albert W.
- Duijn Cornelia van
- Dörr Marcus
- Ehret Georg B.
- Eicher John D.
- Eiriksdottir Gudny
- Elias-Smale Suzette E.
- Elliott Paul
- Elosua Roberto
- Emilsson Valur
- Erdmann Jeanette
- Erich Wichmann H.
- Eriksson Per
- Ernst Florian
- Eyheramendy Susana
- Farrall Martin
- Fava Cristiano
- Feitosa Mary F.
- Ferrucci Luigi
- Folkersen Lasse
- Folsom Aaron R.
- Forrester Terrence
- Fowkes F. Gerald R.
- Fox Caroline S.
- Fox Ervin R.
- Franceschini Nora
- Franco-Cereceda Anders
- Franzosi Maria Grazia
- Frayling Timothy M.
- Galan Pilar
- Ganesh Santhi K.
- Garcia Melissa
- Gaunt Tom R.
- Gieger Christian
- Glazer Nicole L.
- Go Min Jin
- Goel Anuj
- Goodall Alison H.
- Grant Peter J.
- Grobbee Diederick E.
- Groop Leif
- Grässler Jürgen
- Guarrera Simonetta
- Gudnason Vilmundur
- Guo Xiuqing
- Gyllensten Ulf B.
- Hadley David
- Halperin Eran
- Hamsten Anders
- Han Bok-Ghee
- Hardy Rebecca
- Harris Tamara B.
- Hartikainen Anna-Liisa
- Hayward Caroline
- Heath Simon
- Heckbert Susan R.
- Hedblad Bo
- Heiss Gerardo
- Hercberg Serge
- Hernandez Dena
- Herrington David M.
- Hicks Andrew A.
- Hillege Hans L.
- Hilton Gina
- Hingorani Aroon D.
- Hoffman Bolton Judith A.
- Hoffmann Udo
- Hofman Albert
- Homuth Georg
- Hopewell Jemma C.
- Howard Philip
- Howard Timothy D.
- Huang Jie
- Huffman Jennifer E.
- Humphries Steve E.
- Hunt Steven C.
- Hveem Kristian
- Hwang Shih-Jen
- Igl Wilmar
- Ikram Mohammad A.
- Illig Thomas
- Isaacs Aaron
- Islam Muhammad
- Iwai Naoharu
- Jackson Anne U.
- Jafar Tazeen H.
- Janipalli Charles S.
- Johnson Andrew D.
- Johnson Toby
- Järvelin Marjo-Riitta
- Kangas Antti J.
- Karakas Mahir
- Kardia Sharon L.
- Kathiresan Sekar
- Kavousi Maryam
- Kettunen Johannes
- Khaw Kay-Tee
- Kim Hyung-Lae
- Kinra Sanjay
- Kita Yoshikuni
- Kivimaki Mika
- Kleber Marcus E.
- Klopp Norman
- Koenig Wolfgang
- Kooner Jaspal S.
- Kraja Aldi T.
- Krestin Gabriel P.
- Kroemer Heyo K.
- Kuh Diana
- Kulkarni Smita R.
- Kumar M. V. Kranthi
- Kumari Meena
- Kuusisto Johanna
- Kuznetsova Tatiana
- Kähönen Mika
- Köttgen Anna
- Laakso Markku
- Laan Maris
- Laitinen Jaana
- Lakatta Edward G.
- Langefeld Carl D.
- Larson Martin G.
- Lathrop Mark
- Launer Lenore
- Launer Lenore J.
- Lawlor Debbie A.
- Lawrence Robert W.
- Lee Jong-Young
- Lee Nanette R.
- Lehtimäki Terho
- Levy Daniel
- Li Xia
- Li Yali
- Linda Kao Wen Hong
- Liu Yongmei
- Lohman Kurt
- Lohman Kurt K.
- Longstreth W. T.
- Loos Ruth J. F.
- Luan Jian'an
- Lucas Gavin
- Ludwig Barbara
- Lundmark Per
- Lyytikäinen Leo-Pekka
- Lüdemann Jan
- Mangino Massimo
- Mani K. Radha
- Markus Hugh S.
- Marmot Michael G.
- Massaro Joseph M.
- Matijevic Nena
- Mattace-Raso Francesco U. S.
- Matullo Giuseppe
- McArdle Wendy L.
- McKenzie Colin A.
- McKnight Barbara
- Meigs James B.
- Meisinger Christa
- Meitinger Thomas
- Melander Olle
- Meneton Pierre
- Meschia James F.
- Miki Tetsuro
- Milaneschi Yuri
- Mitchell Braxton D.
- Mohlke Karen L.
- Moore Jason H.
- Mooser Vincent
- Morange Pierre-Emmanuel
- Morken Mario A.
- Morris Richard W.
- Morrison Alanna C.
- Mosley Thomas H.
- Munroe Patricia B.
- Murabito Joanne M.
- Mychaleckyj Josyf C.
- März Winfried
- Müller-Nurasyid Martina
- Münzel Thomas
- Najjar Samer
- Nalls Michael
- Nalls Michael A.
- Nambi Vijay
- Narisu Narisu
- Navis Gerjan
- Navis Gerjan J.
- Newman Anne B.
- Newton-Cheh Christopher
- Nguyen Khanh-Dung Hoang
- Nilsson Peter
- North Kari
- Nyberg Fredrik
- O'Connell Jeffrey R.
- O'Donnell Christopher J.
- O'Leary Daniel H.
- O'Reilly Paul F.
- Ogihara Toshio
- Ohkubo Takayoshi
- Okamura Tomonori
- Olden Matthias
- Ong Rick Twee-Hee
- Ongen Halit
- Onland-Moret N. Charlotte
- Oostra Ben
- Oostra Ben A.
- Org Elin
- Orru Marco
- Oudkerk Matthijs
- Oudot-Mellakh Tiphaine
- Palmas Walter
- Palmen Jutta
- Palmer Lyle J.
- Palmer Nicholette D.
- Parker Alex N.
- Parsa Afshin
- Pattaro Cristian
- Peden John F.
- Peltonen Leena
- Perola Markus
- Peters Annette
- Petrovic Katja E.
- Peyser Patricia A.
- Pihur Vasyl
- Platou Carl G. P.
- Plump Andrew
- Polak Joseph F.
- Polasek Ozren
- Post Wendy S.
- Prabhakaran Dorairaj
- Pramstaller Peter P.
- Prokopenko Inga
- Province Michael A.
- Psaty Bruce M.
- Raffel Leslie J.
- Raitakari Olli
- Rao Dabeeru C.
- Rasheed Asif
- Rathmann Wolfgang
- Reilly Muredach P.
- Rettig Rainer
- Ricceri Fulvio
- Rice Kenneth
- Rice Kenneth M.
- Ridker Paul M.
- Rivadeneira Fernando
- Rosengren Annika
- Rotimi Charles
- Rotter Jerome I.
- Rudan Igor
- Rudock Megan E.
- Sabater-Lleal Maria
- Salako Tunde
- Saleheen Danish
- Salomaa Veikko
- Samani Nilesh J.
- Sanna Serena
- Schillert Arne
- Schmidt Helena
- Schmidt Reinhold
- Schminke Ulf
- Schnabel Renate B.
- Schrijvers Elisabeth M. C.
- Schwartz Stephen M.
- Schwarz Peter E. H.
- Scott James
- Scott Laura J.
- Scuteri Angelo
- Seedorf Udo
- Sehmi Joban S.
- Seielstad Mark
- Seissler Jochen
- Sennblad Bengt
- Seshadri Sudha
- Sharma Pankaj
- Shaw-Hawkins Sue
- Shen Haiqing
- Shi Gang
- Shin So-Youn
- Shrine Nick R. G.
- Shriner Daniel
- Shuldiner Alan R.
- Shyong Tai E.
- Sigurdsson Sigurdur
- Sijbrands Eric J. G.
- Silbernagel Günther
- Silveira Angela
- Sim Xueling
- Singleton Andrew
- Siscovick David S.
- Sitzer Matthias
- Sjögren Marketa
- Smith Albert V.
- Smith George Davey
- Smith Nicholas L.
- Smith Shelly
- Snieder Harold
- Soininen Pasi
- Song Ci
- Soranzo Nicole
- Spector Timothy D.
- Staessen Jan A.
- Stančáková Alena
- Steinle Nanette I.
- Stoegerer Eva-Maria
- Strachan David P.
- Strawbridge Rona J.
- Stringham Heather M.
- Sun Yan V.
- Swift Amy J.
- Syvänen Ann-Christine
- Sõber Siim
- Tabara Yasuharu
- Talmud Philippa J.
- Tanaka Toshiko
- Tang Weihong
- Taylor Andrew
- Taylor Kent
- Tayo Bamidele
- Terzic Janos
- Teumer Alexander
- Thelle Dag S.
- Thiery Joachim
- Thorsson Bolli
- Tobin Martin D.
- Tofler Geoffrey H.
- Tomaszewski Maciej
- Tracy Russell P.
- Tregouet David
- Tripathy Vikal
- Truong Vinh
- Tukiainen Taru
- Tuomilehto Jaakko
- Tzoulaki Ioanna
- Uda Manuela
- Ueshima Hirotsugu
- Uiterwaal Cuno S. P. M.
- Uitterlinden Andre
- Uitterlinden Andre G.
- Umemura Satoshi
- Usala Gianluca
- van der Harst Pim
- van der Lugt Aad
- van der Schouw Yvonne T.
- van Duijn Cornelia M.
- van Gilst Wiek H.
- Vartiainen Erkki
- Vasan Ramachandran S.
- Veldre Gudrun
- Verwoert Germaine C.
- Viigimaa Margus
- Viikari Jorma
- Vinay D. G.
- Vineis Paolo
- Vitart Veronique
- Voight Benjamin F.
- Vollenweider Peter
- Völker Uwe
- Völzke Henry
- Wagenknecht Lynne E.
- Wain Louise V.
- Wang Thomas J.
- Wang Xiaoling
- Wareham Nicholas J.
- Watkins Hugh
- Weder Alan B.
- Whincup Peter H.
- White Charles C.
- Wichmann H. -Erich
- Wiggins Kerri L.
- Wild Philipp S.
- Wild Sarah H.
- Williams Frances M. K.
- Williams Scott M.
- Wilson James F.
- Winkelmann Bernhard R.
- Witteman Jacqueline
- Witteman Jacqueline C. M.
- Wolf Philip A.
- Wong Andrew
- Wong Tien Y.
- Wright Alan F.
- Wu Ying
- Würtz Peter
- Yajnik Chittaranjan S.
- Yanek Lisa R.
- Yang Qiong
- Yao Jie
- Young J. Hunter
- Zelenika Diana
- Zeller Tanja
- Zhai Guangju
- Zhang Feng
- Zhang Qunyuan
- Zhang Weihua
- Zhao Jing Hua
- Zhu Haidong
- Zhu Xiaofeng
- Ziegler Andreas
- Zitting Paavo
- Zukowska-Szczechowska Ewa
- Öhrvik John
- Publication venue
- 'Ovid Technologies (Wolters Kluwer Health)'
- Publication date
- 01/01/2017
- Field of study
Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction
Integrated genomic approaches implicate osteoglycin (Ogn) in the regulation of left ventricular mass
- Author
- B Schroen
- B Schroen
- BC Berk
- BH Lorell
- Blanche Schroen
- C Cerutti
- Chris Kiesewetter
- D Zhang
- DJ de Koning
- Dudley J Pennell
- E Birney
- E Petretto
- Elena S Tasheva
- Enrico Petretto
- ES Tasheva
- ES Tasheva
- G Passador-Gurgel
- Gary W Conrad
- GS Wang
- H Hirota
- H Kresse
- Han Lu
- HH Goring
- Ian Grieve
- J Hashimoto
- J Yoshioka
- Jonathan Mangion
- Judith Fischer
- Lolita M Corpuz
- M Hoshijima
- M Pravenec
- Mande K Kumaran
- Matthew Benson
- MD Cheitlin
- Megan D Webb
- Michal Pravenec
- N Hubner
- Norbert Hubner
- Phillip J Muckett
- Prakash P Punjabi
- RB Devereux
- Rizwan Sarwar
- SA Cook
- SA Cook
- Sanjay K Prasad
- SD Caruthers
- Stuart A Cook
- T Oka
- TD O'Connell
- Theodore W Kurtz
- Timothy J Aitman
- VG Tusher
- Vladimir Kren
- WS Post
- Yigal M Pinto
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2008
- Field of study
Left ventricular mass (LVM) and cardiac gene expression are complex traits regulated by factors both intrinsic and extrinsic to the heart. To dissect the major determinants of LVM, we combined expression quantitative trait locus1 and quantitative trait transcript (QTT) analyses of the cardiac transcriptome in the rat. Using these methods and in vitro functional assays, we identified osteoglycin (Ogn) as a major candidate regulator of rat LVM, with increased Ogn protein expression associated with elevated LVM. We also applied genome-wide QTT analysis to the human heart and observed that, out of 22,000 transcripts, OGN transcript abundance had the highest correlation with LVM. We further confirmed a role for Ogn in the in vivo regulation of LVM in Ogn knockout mice. Taken together, these data implicate Ogn as a key regulator of LVM in rats, mice and humans, and suggest that Ogn modifies the hypertrophic response to extrinsic factors such as hypertension and aortic stenosi
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