Browsing by Author "Inserm"

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    Acute dengue virus 2 infection in Gabonese patients is associated with an early innate immune response, including strong interferon alpha production
    (2010-12-17) Pierre Becquart; Nadia Wauquier; Dieudonné Nkoghe; Angélique Ndjoyi-Mbiguino; Cindy Padilla; Marc Souris; Eric M. Leroy; Centre International de Recherches Medicales de Franceville; Maladies Infectieuses et Vecteurs : Ecologie, Genetique, Evolution et Controle; Inserm; Université des Sciences de la Santé; Emergence des Pathologies Virales; Mahidol University
    Background: Dengue is now a leading cause of morbidity and mortality throughout the tropics. We conducted the first ex vivo study of dengue fever (DF) in African patients infected during the first Gabonese dengue virus 2 (DENV-2) outbreak in 2007, in order to investigate cytokine production, including the antiviral cytokine IFN-α, reported to be a potent inhibitor of DENV replication in vitro.Methods: Levels of 50 cytokines, chemokines and growth factors were measured in plasma from 36 patients with DENV-2 infection, and in uninfected controls, using Luminex multiplex technology. The results were interpreted according to the day of sampling after symptom onset. PBMC from six patients were also studied for T lymphocyte cell surface marker expression by flow cytometry.Results: Acute DENV-2 infection elicited high levels of several pro-inflammatory cytokines (IL-6 and IL-17), chemokines (MIF, RANTES, IP-10 and MCP-1) and growth factors (G-CSF, GM-CSF and VEGF-A). We also observed high levels of IFN-α for the first time in adult DF patients, and CD4+ and CD8+ T cell activation at symptom onset.Conclusion: Acute DENV-2 infection in African patients elicits a strong innate response involving IFN-α production, as well as an adaptive immune response. © 2010 Becquart et al; licensee BioMed Central Ltd.
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    Alcohol, tobacco and breast cancer - Collaborative reanalysis of individual data from 53 epidemiological studies, including 58 515 women with breast cancer and 95 067 women without the disease
    (2002-11-18) N. Hamajima; K. Hirose; K. Tajima; T. Rohan; E. E. Calle; C. W. Heath; R. J. Coates; J. M. Liff; R. Talamini; N. Chantarakul; S. Koetsawang; D. Rachawat; A. Morabia; L. Schuman; W. Stewart; M. Szklo; C. Bain; F. Schofield; V. Siskind; P. Band; A. J. Coldman; R. P. Gallagher; T. G. Hislop; P. Yang; L. M. Kolonel; A. M.Y. Nomura; J. Hu; K. C. Johnson; Y. Mao; S. De Sanjosé; N. Lee; P. Marchbanks; H. W. Ory; H. B. Peterson; H. G. Wilson; P. A. Wingo; K. Ebeling; D. Kunde; P. Nishan; J. L. Hopper; G. Colditz; V. Gajalakshmi; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; M. Ewertz; H. O. Adami; L. Bergkvist; C. Magnusson; I. Persson; J. Chang-Claude; C. Paul; D. C.G. Skegg; G. F.S. Spears; P. Boyle; T. Evstifeeva; J. R. Daling; W. B. Hutchinson; K. Malone; E. A. Noonan; J. L. Stanford; D. B. Thomas; N. S. Weiss; E. White; N. Andrieu; A. Brêmond; F. Clavel; B. Gairard; J. Lansac; L. Piana; R. Renaud; A. Izquierdo; P. Viladiu; H. R. Cuevas; P. Ontiveros; A. Palet; S. B. Salazar; N. Aristizabal; A. Cuadros; L. Tryggvadottir; H. Tulinius; A. Bachelot; M. G. Lê; J. Peto; S. Franceschi; F. Lubin; B. Modan; E. Ron; Y. Wax; G. D. Friedman; R. A. Hiatt; F. Levi; T. Bishop; Cancer Research UK; Aichi Cancer Center Hospital and Research Institute; Albert Einstein College of Medicine of Yeshiva University; American Cancer Society; Emory University; IRCCS Centro Di Riferimento Oncologico Aviano; Mahidol University; Johns Hopkins University; University of Queensland; British Columbia Cancer Agency; University of Hawaii System; Canadian Cancer Registries Epidemiology Research Group; Catalan Oncology Institute; Centers for Disease Control and Prevention; Max Delbruck Center for Molecular Medicine; University of Melbourne; Brigham and Women's Hospital; Cancer Institute India; Chiang Mai University; Chulalongkorn University; Kraeftens Bekaempelse; Karolinska Institutet; German Cancer Research Center; University of Otago; Istituto Europeo di Oncologia; Fred Hutchinson Cancer Research Center; Inserm; Girona Cancer Registry; Hospital General de Mexico; Hospital Universitario; Icelandic Cancer Society; Institut de Cancerologie Gustave Roussy; London School of Hygiene & Tropical Medicine; International Agency for Research on Cancer; Chaim Sheba Medical Center Israel; Kaiser Permanente; Institut Universitaire de Medecine Sociale et Preventive Lausanne; Onkoloski institut Ljubljana; Loma Linda University Adventist Health Sciences Center; Skånes universitetssjukhus; Maastricht University; University of the Philippines Manila; Istituto di Ricerche Farmacologiche Mario Negri; Fondazione IRCCS Istituto Nazionale dei Tumori, Milan; Istituto di Statistica Medica e Biometria; Nairobi Centre for Research in Reproduction; National Cancer Institute; National Institute of Child Health and Human Development; National University of Singapore; The Netherlands Cancer Institute; NEW JERSEY STATE DEPT OF HEALTH; New South Wales Cancer Council; Columbia University Medical Center; Ontario Cancer Treatment and Research Foundation; Clinical Trial Service Unit; Radiation Effects Research Foundation Hiroshima; Royal College of General Practitioners' Oral Contraception Study; Universidad de Costa Rica; Medical Center of Fudan University; Shanghai Institute of Planned Parenthood Research; Tianjin Cancer Institute and Hospital; Universitetet i Tromso; Vanderbilt University; University of Athens Medical School; Universidad de Chile; University of Edinburgh; University of Minnesota School of Public Health; The University of North Carolina at Chapel Hill; University of Nottingham; University of Southern California; University of Wisconsin; Organisation Mondiale de la Sante
    Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58 515 women with invasive breast cancer and 95 067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P<0.00001) for an intake of 35-44 g per day alcohol, and 1.46 (1.33-1.61, P<0.00001) for ≥45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% Cl 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1% per 10 g per day, P<0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22255 women with breast cancer and 40832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers=1.03, 95% Cl 0.98-1.07, and for current smokers=0.99, 0.92-1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has littte or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver. © 2002 Cancer Research UK.
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    Allergic rhinitis and its impact on asthma in Asia Pacific and the ARIA update 2008
    (2012-01-01) Ruby Pawankar; Chaweewan Bunnag; Nikolai Khaltaev; Jean Bousquet; Nippon Medical School; Mahidol University; Inserm
    The prevalence of allergic diseases such as allergic rhinitis (AR) and asthma are markedly increasing to epidemic proportions worldwide as societies adopt Western lifestyles. An estimated 300 million persons worldwide have asthma, about 50% of whom live in developing countries, and about 400 million people suffer from AR. AR has a marked impact on quality of life, socially, at school, and in the workplace and is a huge socioeconomic burden. Thus, there was clearly a need for a global evidence-based guideline not only for managing AR but also highlighting the interactions between the upper and lower airways including diagnosis, epidemiology, common risk factors, management, and prevention. The Allergic Rhinitis and its Impact on Asthma (ARIA) document was first published in 2001 as a state-of-the-art document for the specialist, the general practitioner, and other health care professionals. Subsequent research and increasing knowledge have resulted in the ARIA 2008 update. The present review summarizes the ARIA update with particular emphasis on the current status of AR and asthma in Asia Pacific. Copyright © 2012 by World Allergy Organization.
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    Analysis of published PKD1 gene sequence variants [3]
    (2007-04-01) Alexander M. Gout; David Ravine; Peter C. Harris; Sandro Rossetti; Dorien Peters; Martijn Breuning; Elizabeth Petri Henske; Akio Koizumi; Sumiko Inoue; Yoshiko Shimizu; Wanna Thongnoppakhun; Pa Thai Yenchitsomanus; Constantinos Deltas; Richard Sandford; Roser Torra; Alberto E. Turco; Steve Jeffery; Michel Fontes; Stefan Somlo; Laszlo M. Furu; Yvo M. Smulders; Bernard Mercier; Claude Ferec; Stéphane Burtey; York Pei; Luba Kalaydjieva; Nadja Bogdanova; Marie McCluskey; Lee Jung Geon; C. H. Wouters; Jana Reiterova; Jitka Stekrová; Jose L. San Millan; Gianluca Aguiari; Laura Del Senno; Walter and Eliza Hall Institute of Medical Research; University of Melbourne; University of Western Australia Faculty of Medicine and Dentistry; Western Australian Institute for Medical Research; Mayo Clinic College of Medicine; Leiden University Medical Center - LUMC; Fox Chase Cancer Center; Kyoto University; Kyorin University; Mahidol University; University of Cyprus; Addenbrooke's Hospital; Fundacio Puigvert; Universita degli Studi di Verona; St George's University of London; Inserm; Yale University School of Medicine; VU University Medical Center; Centre Hospitalier Universitaire de Brest; University of Toronto; Westfalische Wilhelms-Universitat Munster; Edith Cowan University, Joondalup; Seoul National University; Erasmus University Medical Center; Charles University; Hospital Ramo; University of Ferrara
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    Anti-IFN-γ autoantibodies are strongly associated with HLA-DR∗15:02/16:02 and HLA-DQ∗05:01/05:02 across Southeast Asia
    (2016-03-01) Cheng Lung Ku; Chia Hao Lin; Su Wei Chang; Chen Chung Chu; Jasper F.W. Chan; Xiao Fei Kong; Chen Hsiang Lee; Emily A. Rosen; Jing Ya Ding; Wen I. Lee; Jacinta Bustamante; Torsten Witte; Han Po Shih; Chen Yen Kuo; Ploenchan Chetchotisakd; Sasisopin Kiertiburanakul; Yupin Suputtamongkol; Kwok Yung Yuen; Jean Laurent Casanova; Steven M. Holland; Rainer Doffinger; Sarah K. Browne; Chih Yu Chi; Chang Gung University; China Medical University Taichung; The University of Hong Kong; Rockefeller University; National Institute of Allergy and Infectious Diseases; Chang Gung Memorial Hospital; Inserm; Universite Paris Descartes; Medizinische Hochschule Hannover (MHH); Khon Kaen University; Faculty of Medicine, Ramathibodi Hospital, Mahidol University; Mahidol University; Howard Hughes Medical Institute; Hopital Necker Enfants Malades; Addenbrooke's Hospital; National Institute for Health Research; China Medical University Hospital Taichung; Mackay Memorial Hospital Taiwan
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    An assessment of interactions between global health initiatives and country health systems
    (2009-01-01) Badara Samb; Tim Evans; Mark Dybul; Rifat Atun; Jean Paul Moatti; Sania Nishtar; Anna Wright; Francesca Celletti; Justine Hsu; Jim Yong Kim; Ruairi Brugha; Asia Russell; Carissa Etienne; Susna De; Takondwa Mwase; Wenjuan Wang; Jenna Wright; Lola Daré; Jean François Delfraissy; François Boillot; Pierre Miege; Xiulan Zhang; Joseph Rhatigan; Rebecca Weintraub; Sok Pun; C. Abé; Carlos Caceres; Mamadou Camara; Benjamin Coriat; Cristina D’Almeida; Julia Aleshkina; Gulgun Murzalieva; John Kadzandira; N. Hammami; Victor Mwapasa; Ketevan Chkhatarashvili; Eric Buch; Katabaro Miti; Claudes Kamenga; Marthe Sylvie Essengue Elouma; Nina Schwalbe; Alan Greenberg; Seble Frehywot; Anne Markus; Lieve Goeman; Alia Khan; Jael Amati; Esther Mwaura-Muiru; Louise C. Ivers; Andrew Ellner; Aaron Shakow; Nicole C. Kley; Alec Irwin; Erin Sullivan; Brook Baker; Jennifer Cohn; Paul Davis; Jamila Headley; Patricia Siplon; Clare Dickinson; Mark Pearson; Catriona Waddington; Sylvie Boyer; Fred Eboko; Fabienne Orsi; Bernard Larouzé; Guillaume Le Loup; Phillimon Ndubani; Joseph Simbaya; Marleen Boelaert; Anna Cavalli; Gorik Ooms; Marjan Pirard; Katja Polman; Wim Van Damme; Monique Van Dormael; Peter Vermeiren; Waranya Teokul; Riitta Dlodlo; Paula Fujiwara; Sandrine Ruppol; Stefano Vella; Tetyana Semigina; Elizabeth Corbett; Peter Godfrey-Faussett; Neil Spicer; Gill Walt; Abt Associates, Inc.; African Council for Sustainable Health Development; Agence Nationale de Recherche sur le Sida et les Hépatites Virales; Alter Santé Internationale et Développement; Beijing Normal University; Brigham and Women's Hospital; Catholic Relief Services; Catholic University of Central African States; Cayetano Heredia University; Universite Paris 13; Centre for Health System Development; University of Malawi; Child Welfare Scheme; University of Malawi College of Medicine; Curatio International Foundation; Universiteit van Pretoria; Family Health International; Gavi; George Washington University; German Technical Cooperation; Global AIDS Alliance; GROOTS; Harvard Medical School; Harvard School of Public Health; Health Gap; Heartfile Pakistan; HLSP Institute; Imperial College London; Inserm; University of Zambia; Prins Leopold Instituut voor Tropische Geneeskunde; ; International Union Against Tuberculosis and Lung Disease; Istituto Superiore Di Sanita, Rome; National University of Kyiv-Mohyla Academy; London School of Hygiene & Tropical Medicine; Mahidol University; Medecins Sans Frontieres, Brussels; Ministry of Foreign Affairs; Ministry of Health; Ministry of Public Health Cameroon; Ministry of Health; Thailand Ministry of Public Health; Royal College of Surgeons in Ireland; Georgetown University; Organisation Mondiale de la Sante
    © 2009,Lancet Publishing Group. All rights reserved. Since 2000,the emergence of several large disease-specific global health initiatives (GHIs) has changed the way in which international donors provide assistance for public health. Some critics have claimed that these initiatives burden health systems that are already fragile in countries with few resources,whereas others have asserted that weak health systems prevent progress in meeting disease-specific targets. So far,most of the evidence for this debate has been provided by speculation and anecdotes. We use a review and analysis of existing data,and 15 new studies that were submitted to WHO for the purpose of writing this Report to describe the complex nature of the interplay between country health systems and GHIs. We suggest that this Report provides the most detailed compilation of published and emerging evidence so far,and provides a basis for identification of the ways in which GHIs and health systems can interact to mutually reinforce their effects. On the basis of the findings,we make some general recommendations and identify a series of action points for international partners,governments,and other stakeholders that will help ensure that investments in GHIs and country health systems can fulfil their potential to produce comprehensive and lasting results in disease-specific work,and advance the general public health agenda. The target date for achievement of the health-related Millennium Development Goals is drawing close,and the economic downturn threatens to undermine the improvements in health outcomes that have been achieved in the past few years. If adjustments to the interactions between GHIs and country health systems will improve efficiency,equity,value for money,and outcomes in global public health,then these opportunities should not be missed.
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    Asthma and atopic dermatitis are associated with increased risk of clinical Plasmodium falciparum malaria
    (2013-09-09) Magali Herrant; Cheikh Loucoubar; Hubert Bassène; Bronner Gonçalves; Sabah Boufkhed; Fatoumata Diene Sarr; Arnaud Fontanet; Adama Tall; Laurence Baril; Odile Mercereau-Puijalon; Salaheddine Mécheri; Anavaj Sakuntabhai; Richard Paul; CNRS Centre National de la Recherche Scientifique; Institut Pasteur de Dakar; Inserm; Universite Paris 7- Denis Diderot; Unite de Recherche sur les Maladies Infectieuses et Tropicales emergentes; Institut Pasteur, Paris; Conservatoire National des Arts et Metiers; Mahidol University
    Objectives: To assess the impact of atopy and allergy on the risk of clinical malaria. Design: A clinical and immunological allergy crosssectional survey in a birth cohort of 175 children from 1 month to 14 years of age followed for up to 15 years in a longitudinal open cohort study of malaria in Senegal. Malaria incidence data were available for 143 of these children (aged 4 months to 14 years of age) for up to 15 years. Mixed-model regression analysis was used to determine the impact of allergy status on malaria incidence, adjusting for age, gender, sickle-cell trait and force of infection. Main outcome measures: Asthma, allergic rhinoconjunctivitis and atopic dermatitis status, the number of clinical Plasmodium falciparum malaria episodes since birth and associated parasite density. Results: 12% of the children were classified as asthmatic and 10% as having atopic dermatitis. These groups had respectively a twofold (OR 2.12 95%; CI 1.46 to 3.08; p=8×10-5) and threefold (OR 3.15; 1.56 to 6.33; p=1.3×10-3) increase in the risk of clinical P falciparum malaria once older than the age of peak incidence of clinical malaria (3-4 years of age). They also presented with higher P falciparum parasite densities (asthma: mean 105.3 parasites/ μL±SE 41.0 vs 51.3±9.7; p=6.2×10-3. Atopic dermatitis: 135.4 ±70.7 vs 52.3±11.0; p=0.014). There was no effect of allergy on the number of non-malaria clinical presentations. Individuals with allergic rhinoconjunctivitis did not have an increased risk of clinical malaria nor any difference in parasite densities. Conclusions: These results demonstrate that asthma and atopic dermatitis delay the development of clinical immunity to P falciparum. Despite the encouraging decrease in malaria incidence rates in Africa, a significant concern is the extent to which the increase in allergy will exacerbate the burden of malaria. Given the demonstrated antiparasitic effect of antihistamines, administration to atopic children will likely reduce the burden of clinical malaria in these children, increase the efficacy of first-line treatment antimalarials and alleviate the non-infectious consequences of atopy.
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    Author Correction: The temporal dynamics and infectiousness of subpatent Plasmodium falciparum infections in relation to parasite density (Nature Communications, (2019), 10, 1, (1433), 10.1038/s41467-019-09441-1)
    (2019-12-01) Hannah C. Slater; Amanda Ross; Ingrid Felger; Natalie E. Hofmann; Leanne Robinson; Jackie Cook; Bronner P. Gonçalves; Anders Björkman; Andre Lin Ouedraogo; Ulrika Morris; Mwinyi Msellem; Cristian Koepfli; Ivo Mueller; Fitsum Tadesse; Endalamaw Gadisa; Smita Das; Gonzalo Domingo; Melissa Kapulu; Janet Midega; Seth Owusu-Agyei; Cécile Nabet; Renaud Piarroux; Ogobara Doumbo; Safiatou Niare Doumbo; Kwadwo Koram; Naomi Lucchi; Venkatachalam Udhayakumar; Jacklin Mosha; Alfred Tiono; Daniel Chandramohan; Roly Gosling; Felista Mwingira; Robert Sauerwein; Richard Paul; Eleanor M. Riley; Nicholas J. White; Francois Nosten; Mallika Imwong; Teun Bousema; Chris Drakeley; Lucy C. Okell; University of Health and Allied Sciences, Ghana; Wellcome Trust Centre for Human Genetics; Papua New Guinea Institute of Medical Research; University of Dar Es Salaam; National Institute for Medical Research Tanga; Institut Pasteur de Dakar; Armauer Hansen Research Institute; Addis Ababa University; London School of Hygiene & Tropical Medicine; PATH Seattle; Walter and Eliza Hall Institute of Medical Research; University of Melbourne; University of Edinburgh, Roslin Institute; University of California, San Francisco; Universitat Basel; Swiss Tropical and Public Health Institute (Swiss TPH); Centers for Disease Control and Prevention; University of Notre Dame; Karolinska University Hospital; University of Ghana; Imperial College London; Mahidol University; Nuffield Department of Clinical Medicine; Burnet Institute; Radboud University Nijmegen Medical Centre; Institut Pasteur, Paris; Inserm; Mnazi Mmoja Hospital; University of Sciences; Institute for Disease Modeling; Centre National de Recherche et de Formation sur le Paludisme
    © 2019, The Author(s). An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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    Biodiversity conservation in Southeast Asia: Challenges in a Changing Environment
    (2017-07-28) Serge Morand; Claire Lajaunie; Rojchai Satrawaha; CNRS Centre National de la Recherche Scientifique; Kasetsart University; Mahidol University; Inserm; Maha Sarakham University
    © 2018 S. Morand, C. Lajaunie and R. Satrawaha. All Rights Reserved. Southeast Asia is highly diversified in terms of socio-ecosystems and biodiversity, but is undergoing dramatic environmental and social changes. These changes characterize the recent period and can be illustrated by the effects of the Green Revolution in the late 1960s and 1970s, to the globalization of trade and increasing agronomic intensification over the past decade. Biodiversity Conservation in Southeast Asia provides theoretical overviews and challenges for applied research in living resource management, conservation ecology, health ecology and conservation planning in Southeast Asia. Five key themes are addressed: origin and evolution of Southeast Asian biodiversity; challenges in conservation biology; ecosystem services and biodiversity; managing biodiversity and living resources; policy, economics and governance of biodiversity. Detailed case studies are included from Thailand and the Lower Mekong Basin, while other chapters address cross-cutting themes applicable to the whole Southeast Asia region. This is a valuable resource for academics and students in the areas of ecology, conservation, environmental policy and management, Southeast Asian studies and sustainable development.
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    Biological, immunological and functional properties of two novel multi-variant chimeric recombinant proteins of CSP antigens for vaccine development against Plasmodium vivax infection
    (2017-10-01) Samaneh H. Shabani; Sedigheh Zakeri; Ali H. Salmanian; Jafar Amani; Akram A. Mehrizi; Georges Snounou; François Nosten; Chiara Andolina; Yousef Mourtazavi; Navid D. Djadid; Pasteur Institute of Iran; Zanjan University of Medical Sciences; National Institute for Genetic Engineering and Biotechnology Iran; Baqiyatallah University of Medical Sciences; Inserm; Mahidol University; Nuffield Department of Clinical Medicine
    © 2017 Elsevier Ltd The circumsporozoite protein (CSP) of the malaria parasite Plasmodium vivax is a major pre-erythrocyte vaccine candidate. The protein has a central repeat region that belongs to one of repeat families (VK210, VK247, and the P. vivax-like). In the present study, computer modelling was employed to select chimeric proteins, comprising the conserved regions and different arrangements of the repeat elements (VK210 and VK247), whose structure is similar to that of the native counterparts. DNA encoding the selected chimeras (named CS127 and CS712) were synthetically constructed based on E. coli codons, then cloned and expressed. Mouse monoclonal antibodies (mAbs; anti-Pv-210-CDC and −Pv-247-CDC), recognized the chimeric antigens in ELISA, indicating correct conformation and accessibility of the B-cell epitopes. ELISA using IgG from plasma samples collected from 221 Iranian patients with acute P. vivax showed that only 49.32% of the samples reacted to both CS127 and CS712 proteins. The dominant subclass for the two chimeras was IgG1 (48% of the positive responders, OD492 = 0.777 ± 0.420 for CS127; 48.41% of the positive responders, OD492 = 0.862 ± 0.423 for CS712, with no statistically significant difference P > 0.05; Wilcoxon signed ranks test). Binding assays showed that both chimeric proteins bound to immobilized heparan sulphate and HepG2 hepatocyte cells in a concentration-dependent manner, saturable at 80 μg/mL. Additionally, anti-CS127 and −CS712 antibodies raised in mice recognized the native protein on the surface of P. vivax sporozoite with high intensity, confirming the presence of common epitopes between the recombinant forms and the native proteins. In summary, despite structural differences at the molecular level, the expression levels of both chimeras were satisfactory, and their conformational structure retained biological function, thus supporting their potential for use in the development of vivax-based vaccine.
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    Biology of Zika virus infection in human skin cells
    (2015-01-01) Rodolphe Hamel; Ophélie Dejarnac; Sineewanlaya Wichit; Peeraya Ekchariyawat; Aymeric Neyret; Natthanej Luplertlop; Manuel Perera-Lecoin; Pornapat Surasombatpattana; Loïc Talignani; Frédéric Thomas; Van Mai Cao-Lormeau; Valérie Choumet; Laurence Briant; Philippe Desprès; Ali Amara; Hans Yssel; Dorothée Missé; Maladies Infectieuses et Vecteurs : Ecologie, Genetique, Evolution et Controle; Inserm; CNRS Centre National de la Recherche Scientifique; Mahidol University; Prince of Songkla University; Institut Louis Malarde; Institut Pasteur, Paris; Universite de La Reunion
    © 2015, American Society for Microbiology. Zika virus (ZIKV) is an emerging arbovirus of the Flaviviridae family, which includes dengue, West Nile, yellow fever, and Japanese encephalitis viruses, that causes a mosquito-borne disease transmitted by the Aedes genus, with recent outbreaks in the South Pacific. Here we examine the importance of human skin in the entry of ZIKV and its contribution to the induction of antiviral immune responses. We show that human dermal fibroblasts, epidermal keratinocytes, and immature dendritic cells are permissive to the most recent ZIKV isolate, responsible for the epidemic in French Polynesia. Several entry and/or adhesion factors, including DC-SIGN, AXL, Tyro3, and, to a lesser extent, TIM-1, permitted ZIKV entry, with a major role for the TAM receptor AXL. The ZIKV permissiveness of human skin fibroblasts was confirmed by the use of a neutralizing antibody and specific RNA silencing. ZIKV induced the transcription of Toll-like receptor 3 (TLR3), RIG-I, and MDA5, as well as several interferonstimulated genes, including OAS2, ISG15, and MX1, characterized by strongly enhanced beta interferon gene expression. ZIKV was found to be sensitive to the antiviral effects of both type I and type II interferons. Finally, infection of skin fibroblasts resulted in the formation of autophagosomes, whose presence was associated with enhanced viral replication, as shown by the use of Torin 1, a chemical inducer of autophagy, and the specific autophagy inhibitor 3-methyladenine. The results presented herein permit us to gain further insight into the biology of ZIKV and to devise strategies aiming to interfere with the pathology caused by this emerging flavivirus.
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    Body fluid proteomics for biomarker discovery: Lessons from the past hold the key to success in the future
    (2007-12-01) David M. Good; Visith Thongboonkerd; Jan Novak; Jean Loup Bascands; Joost P. Schanstra; Joshua J. Coon; Anna Dominiczak; Harald Mischak; University of Wisconsin Madison; Mahidol University; University of Alabama at Birmingham; Inserm; Universite Paul Sabatier Toulouse III; University of Glasgow; Mosaiques Diagnostics and Therapeutics AG
    Sparked by the article from Lescuyer and colleagues in a recent issue, we aim here to further encourage interest in and discussion of clinically relevant biomarker research. We express our view on proteomics for biomarker discovery by addressing multiple relevant issues, including the inherent differences between biological fluids (and how these differences affect current analytical approaches) and experimental design to maximize the efficiency of moving from the bench to the bedside. Herein, we also include suggestions for definition of the term "biomarker", based on the use of a set of universal characterization/validation requirements, and illustrate several recent examples of successful transitions of benchtop proteomic studies work to clinical practice. © 2007 American Chemical Society.
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    Breast cancer and hormonal contraceptives: Collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies
    (1996-06-22) E. E. Calle; C. W. Heath; H. L. Miracle-McMahill; R. J. Coates; J. M. Liff; S. Franceschi; R. Talamini; N. Chantarakul; S. Koetsawang; D. RachawatRachawat; A. Morabia; L. Schuman; W. Stewart; M. Szklo; C. Bain; F. Schofield; V. Siskind; P. Band; A. J. Coldman; R. P. Gallagher; T. G. Hislop; P. Yang; S. W. Duffy; L. M. Kolonel; A. M.Y. Nomura; M. W. Oberle; H. W. Ory; H. B. Peterson; H. G. Wilson; P. A. Wingo; K. Ebeling; D. Kunde; P. Nishan; G. Colditz; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; A. J. McMichael; T. Rohan; M. Ewertz; C. Paul; D. C.G. Skegg; P. Boyle; M. Evstifeeva; J. R. Daling; K. Malone; E. A. Noonan; J. L. Stanford; D. B. Thomas; N. S. Weiss; E. White; N. Andrieu; A. Brêmond; F. Clavel; B. Gairard; J. Lansac; L. Piana; R. Renaud; S. R.P. Fine; H. R. Cuevas; P. Ontiveros; A. Palet; S. B. Salazar; N. Aristizabel; A. Cuadros; A. Bachelot; M. G. Lê; J. Deacon; J. Peto; C. N. Taylor; E. Alfandary; B. Modan; E. Ron; G. D. Friedman; R. A. Hiatt; T. Bishop; J. Kosmelj; M. Primic-Zakelj; B. Ravnihar; J. Stare; W. L. Beeson; G. Fraser; D. S. Allen; R. D. Bulbrook; J. Cuzick; I. S. Fentiman; J. L. Hayward; D. Y. Wang; R. L. Hanson; M. C. Leske; M. C. Mahoney; P. C. Nasca; A. O. Varma; A. L. Weinstein; American Cancer Society; Emory University; IRCCS Centro Di Riferimento Oncologico Aviano; Mahidol University; Johns Hopkins University; University of Queensland; British Colombia Cancer Agency; MRC Biostatistics Unit; University of Hawaii System; Centers for Disease Control and Prevention; Central Institute of Cancer Research; Brigham and Women's Hospital; Chiang Mai University; Chulalongkorn University; Food Science Australia; Kraeftens Bekaempelse; University of Otago; Istituto Europeo di Oncologia; Fred Hutchinson Cancer Research Center; Inserm; Holly Lodge; Hospital General de Mexico; Hospital Universitario; Institut de Cancerologie Gustave Roussy; The Institute of Cancer Research, London; Israel Chaim Sheba Medical Center; Kaiser Permanente; Cancer Research UK; Onkoloski institut Ljubljana; Loma Linda University Adventist Health Sciences Center; Skånes universitetssjukhus; Maastricht University; University of the Philippines Manila; Istituto 'Mario Negri'; Divisione di Statistica Medica e Biometria; Istituto di Statistica Medica e Biometria; Nairobi Centre for Research in Reproduction; National Cancer Institute; National Institute of Child Health and Human Development; National University of Singapore; The Netherlands Cancer Institute; NEW JERSEY STATE DEPT OF HEALTH; Columbia University Medical Center; Ontario Cancer Treatment and Research Foundation; Clinical Trial Service Unit; University of Costa Rica; Medical Center of Fudan University; Shanghai Institute of Planned Parenthood Research; Tianjin Cancer Institute and Hospital; Universitetet i Tromso; Universidad de Chile; University of Edinburgh; The University of North Carolina at Chapel Hill; University of Nottingham; University of Southern California; Uppsala Universitet; University of Wisconsin; Organisation Mondiale de la Sante
    Background: The Collaborative Group on Hormonal Factors in Breast Cancer has brought together and reanalysed the worldwide epidemiological evidence on the relation between breast cancer risk and use of hormonal contraceptives. Methods: Individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 studies conducted in 25 countries were collected, checked, and analysed centrally. Estimates of the relative risk for breast cancer were obtained by a modification of the Mantel-Haenszel method. All analyses were stratified by study, age at diagnosis, parity, and, where appropriate, the age a woman was when her first child was born, and the age she was when her risk of conception ceased. Findings: The results provide strong evidence for two main conclusions. First, while women are taking combined oral contraceptives and in the 10 years after stopping there is a small increase in the relative risk of having breast cancer diagnosed (relative risk [95% Cl] in current users 1·24 [1·15-1·33], 2p<0·00001; 1-4 years after stopping 1·6 [1·08-1·23], 2p=0·00001; 5-9 years after stopping 1·07 [1·02-1·13], 2p=0·009). Second, there is no significant excess risk of having breast cancer diagnosed 10 or more years after stopping use (relative risk 1·01 [0·96-1·05], NS). The cancers diagnosed in women who had used combined oral contraceptives were less advanced clinically than those diagnosed in women who had never used these contraceptives: for ever-users compared with never-users, the relative risk for tumours that had spread beyond the breast compared with localised tumours was 0·88 (0·81-0·95; 2p=0·002). There was no pronounced variation in the results for recency of use between women with different background risks of breast cancer, including women from different countries and ethnic groups, women with different reproductive histories, and those with or without a family history of breast cancer. The studies included in this collaboration represent about 90% of the epidemiological information on the topic, and what is known about the other studies suggests that their omission has not materially affected the main conclusions. Other features of hormonal contraceptive use such as duration of use, age at first use, and the dose and type of hormone within the contraceptives had little additional effect on breast cancer risk, once recency of use had been taken into account. Women who began use before age 20 had higher relative risks of having breast cancer diagnosed while they were using combined oral contraceptives and in the 5 years after stopping than women who began use at older ages, but the higher relative risks apply at ages when breast cancer is rare and, for a given duration of use, earlier use does not result in more cancers being diagnosed than use beginning at older ages. Because breast cancer incidence rises steeply with age, the estimated excess number of cancers diagnosed in the period between starting use and 10 years after stopping increases with age at last use: for example, among 10 000 women from Europe or North America who used oral contraceptives from age 16 to 19, from age 20 to 24, and from age 25 to 29, respectively, the estimated excess number of cancers diagnosed up to 10 years after stopping use is 0·5 (95% Cl 0·3-0·7), 1·5 (0·7-2·3), and 4·7 (2·7-6·7). Up to 20 years after cessation of use the difference between ever-users and never-users is not so much in the total number of cancers diagnosed, but in their clinical presentation, with the breast cancers diagnosed in ever-users being less advanced clinically than those diagnosed in never-users. The relation observed between breast cancer risk and hormone exposure is unusual, and it is not possible to infer from these data whether it is due to an earlier diagnosis of breast cancer in ever-users, the biological effects of hormonal contraceptives, or a combination of reasons. Interpretation: Women who are currently using combined oral contraceptives or have used them in the past 10 years are at a slightly increased risk of having breast cancer diagnosed, although the additional cancers diagnosed tend to be localised to the breast. There is no evidence of an increase in the risk of having breast cancer diagnosed 10 or more years after cessation of use, and the cancers diagnosed then are less advanced clinically than the cancers diagnosed in never-users.
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    Breast cancer and hormone replacement therapy: Collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer
    (1997-10-11) E. E. Calle; C. W. Heath; R. J. Coates; J. M. Liff; S. Franceschi; R. Talamini; N. Chantarakul; S. Koetsawang; D. Rachawat; A. Morabia; L. Schuman; W. Stewart; M. Szklo; C. Bain; F. Schofield; V. Siskind; P. Band; A. J. Coldman; R. P. Gallagher; T. G. Hislop; P. Yang; S. W. Duffy; L. M. Kolonel; A. M.Y. Nomura; M. W. Oberle; H. W. Ory; H. B. Peterson; H. G. Wilson; P. A. Wingo; K. Ebeling; D. Kunde; P. Nishan; G. Colditz; N. Martin; T. Pardthaisong; S. Silpisornkosol; C. Theetranont; B. Boosiri; S. Chutivongse; P. Jimakorn; P. Virutamasen; C. Wongsrichanalai; A. J. McMichael; T. Rohan; M. Ewertz; C. Paul; D. C.G. Skegg; G. F.S. Spears; P. Boyle; M. Evstifeeva; J. R. Daling; W. B. Hutchinson; K. Malone; E. A. Noonan; J. L. Stanford; D. B. Thomas; N. S. Weiss; E. White; N. Andrieu; A. Bràmond; F. Clavel; B. Gairard; J. Lansac; L. Piana; R. Renaud; S. R.P. Fine; H. R. Cuevas; P. Ontiveros; A. Palet; S. B. Salazar; N. Aristizabel; A. Cuadros; A. Bachelot; M. G. Lê; J. Deacon; J. Peto; C. N. Taylor; E. Alfandary; B. Modan; E. Ron; G. D. Friedman; R. A. Hiatt; T. Bishop; J. Kosmelj; M. Primic-Zakelj; B. Ravnihar; J. Stare; W. L. Beeson; G. Fraser; R. D. Bulbrook; J. Cuzick; I. S. Fentiman; J. L. Hayward; D. Y. Wang; R. L. Hanson; M. C. Leske; M. C. Mahoney; P. C. Nasca; A. O. Varma; A. L. Weinstein; American Cancer Society; Emory University; IRCCS Centro Di Riferimento Oncologico Aviano; Mahidol University; Johns Hopkins University; University of Queensland; British Colombia Cancer Agency; MRC Biostatistics Unit; University of Hawaii System; Centers for Disease Control and Prevention; Central Institute of Cancer Research; Harvard Medical School; Chiang Mai University; Chulalongkorn University; Food Science Australia; Kraeftens Bekaempelse; University of Otago; Istituto Europeo di Oncologia; Fred Hutchinson Cancer Research Center; Inserm; Holly Lodge; Hospital General de Mexico; Hospital Universitario; Institut de Cancerologie Gustave Roussy; The Institute of Cancer Research, London; Israel Chaim Sheba Medical Center; Kaiser Permanente; Cancer Research UK; Onkoloski institut Ljubljana; Loma Linda University Adventist Health Sciences Center; Long Island Breast Cancer Study; Skånes universitetssjukhus; Maastricht University; University of the Philippines Manila; Istituto 'Mario Negri'; Divisione di Statistica Medica e Biometria; Istituto di Statistica Medica e Biometria; Nairobi Centre for Research in Reproduction; National Cancer Institute; National Institute of Child Health and Human Development; National University of Singapore; The Netherlands Cancer Institute; NEW JERSEY STATE DEPT OF HEALTH; Columbia University Medical Center; Ontario Cancer Treatment and Research Foundation; Clinical Trial Service Unit; Royal College of General Practitioners Oral Contraception Study; University of Costa Rica; Medical Center of Fudan University; Shanghai Institute of Planned Parenthood Research; Tianjin Cancer Institute and Hospital; Universitetet i Tromso; Universidad de Chile; University of Edinburgh; The University of North Carolina at Chapel Hill; University of Nottingham; University of Southern California; University of Wisconsin; Organisation Mondiale de la Sante; Karolinska Institutet; Institut Universitaire de Medecine Sociale et Preventive Lausanne; London School of Hygiene & Tropical Medicine; Radiation Effects Research Foundation Hiroshima; University of Athens Medical School
    Background. The Collaborative Group on Hormonal Factors in Breast Cancer has brought together and reanalysed about 90% of the worldwide epidemiological evidence on the relation between risk of breast cancer and use of hormone replacement therapy (HRT). Methods. Individual data on 52,705 women with breast cancer and 108,411 women without breast cancer from 51 studies in 21 countries were collected, checked, and analysed centrally. The main analyses are based on 53,865 postmenopausal women with a known age at menopause, of whom 17,830 (33%) had used HRT at some time. The median age at first use was 48 years, and 34% of ever-users had used HRT for 5 years or longer. Estimates of the relative risk of breast cancer associated with the use of HRT were obtained after stratification of all analyses by study, age at diagnosis, time since menopause, body-mass index, parity, and the age a woman was when her first child was born. Findings. Among current users of HRT or those who ceased use 1-4 years previously, the relative risk of having breast cancer diagnosed increased by a factor of 1.023 (95% CI 1.011-1.036; 2p = 0.0002) for each year of use; the relative risk was 1.35 (1.21-1.49; 2p = 0.00001) for women who had used HRT for 5 years or longer (average duration of use in this group 11 years). This increase is comparable with the effect on breast cancer of delaying menopause, since among never-users of HRT the relative risk of breast cancer increases by a factor of 1.028 (95% CI 1.021-1.034) for each year older at menopause. 5 or more years after cessation of HRT use, there was no significant excess of breast cancer overall or in relation to duration of use. These main findings did not vary between individual studies. Of the many factors examined that might affect the relation between breast cancer risk and use of HRT, only a woman's weight and body-mass index had a material effect: the increase in the relative risk of breast dancer associated with long durations of use in current and recent users was greater for women of lower than of higher weight or body-mass index. There was no marked variation in the results according to hormonal type or dose but little information was available about long durations of use of any specific preparation. Cancers diagnosed in women who had ever used HRT tended to be less advanced clinically than those diagnosed in never-users. In North America and Europe the cumulative incidence of breast cancer between the ages of 50 and 70 in never-users of HRT is about 45 per 1000 women. The cumulative excess numbers of breast cancers diagnosed between these ages per 1000 women who began use of HRT at age 50 and used it for 5, 10, and 15 years, respectively, are estimated to be 2 (95% CI 1-3), 6 (3-9), and 12 (5-20). Whether HRT affects mortality from breast cancer is not known. Interpretation. The risk of having breast cancer diagnosed is increased in women using HRT and increases with increasing duration of use. This effect is reduced after cessation of use of HRT and has largely, if not wholly, disappeared after about 5 years. These findings should be considered in the context of the benefits and other risks associated with the use of HRT.
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    Changes in genome organization of parasite-specific gene families during the Plasmodium transmission stages
    (2018-12-01) Evelien M. Bunnik; Kate B. Cook; Nelle Varoquaux; Gayani Batugedara; Jacques Prudhomme; Anthony Cort; Lirong Shi; Chiara Andolina; Leila S. Ross; Declan Brady; David A. Fidock; Francois Nosten; Rita Tewari; Photini Sinnis; Ferhat Ay; Jean Philippe Vert; William Stafford Noble; Karine G. Le Roch; Département de Mathématiques et Applications; Institut Curie; Mines ParisTech; Columbia University in the City of New York; University of California, Riverside; Columbia University Medical Center; University of Oxford; University of California, Berkeley; University of Texas Health Science Center at San Antonio; University of Washington, Seattle; University of Nottingham; La Jolla Institute for Allergy and Immunology; Mahidol University; Johns Hopkins Bloomberg School of Public Health; Inserm; Berkeley Global Science Institute
    © 2018 The Author(s). The development of malaria parasites throughout their various life cycle stages is coordinated by changes in gene expression. We previously showed that the three-dimensional organization of the Plasmodium falciparum genome is strongly associated with gene expression during its replication cycle inside red blood cells. Here, we analyze genome organization in the P. falciparum and P. vivax transmission stages. Major changes occur in the localization and interactions of genes involved in pathogenesis and immune evasion, host cell invasion, sexual differentiation, and master regulation of gene expression. Furthermore, we observe reorganization of subtelomeric heterochromatin around genes involved in host cell remodeling. Depletion of heterochromatin protein 1 (PfHP1) resulted in loss of interactions between virulence genes, confirming that PfHP1 is essential for maintenance of the repressive center. Our results suggest that the three-dimensional genome structure of human malaria parasites is strongly connected with transcriptional activity of specific gene families throughout the life cycle.
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    Chloroquine resistant vivax malaria in a pregnant woman on the western border of Thailand
    (2011-05-09) Marcus J. Rijken; Mac Hteld E Boel; Bruce Russell; Mallika Imwong; Mara L. Leimanis; Aung Pyae Phyo; Atis Muehlenbachs; Niklas Lindegardh; Rose McGready; Laurent Rénia; Georges Snounou; Pratap Singhasivanon; François Nosten; Shoklo Malaria Research Unit; Agency for Science, Technology and Research, Singapore; Mahidol University; University of Washington, Seattle; Nuffield Department of Clinical Medicine; Inserm; Universite Pierre et Marie Curie
    Chloroquine (CQ) resistant vivax malaria is spreading. In this case, Plasmodium vivax infections during pregnancy and in the postpartum period were not satisfactorily cleared by CQ, despite adequate drug concentrations. A growth restricted infant was delivered. Poor susceptibility to CQ was confirmed in-vitro and molecular genotyping was strongly suggestive of true recrudescence of P. vivax. This is the first clinically and laboratory confirmed case of two high-grade CQ resistant vivax parasite strains from Thailand. © 2011 Rijken et al; licensee BioMed Central Ltd.
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    Clinical proteomics: A need to define the field and to begin to set adequate standards
    (2007-02-01) Harald Mischak; Rolf Apweiler; Rosamonde E. Banks; Mark Conaway; Joshua Coon; Anna Dominiczak; Jochen H.H. Ehrich; Danilo Fliser; Mark Girolami; Henning Hermjakob; Denis Hochstrasser; Joachim Jankowski; Bruce A. Julian; Walter Kolch; Ziad A. Massy; Christian Neusuess; Jan Novak; Karlheinz Peter; Kasper Rossing; Joost Schanstra; O. John Semmes; Dan Theodorescu; Visith Thongboonkerd; Eva M. Weissinger; Jennifer E. Van Eyk; Tadashi Yamamoto; Mosaiques Diagnostics and Therapeutics AG; European Bioinformatics Institute; St James's University Hospital; University of Virginia; University of Wisconsin Madison; University of Glasgow; Medizinische Hochschule Hannover (MHH); Charité – Universitätsmedizin Berlin; Universite de Geneve; University of Alabama at Birmingham; Beatson Institute for Cancer Research; Inserm; University of Aalen; Baker Heart and Diabetes Institute; Steno Diabetes Center; Eastern Virginia Medical School; Mahidol University; Johns Hopkins University; Niigata University School of Medicine; CHU Amiens Picardie
    The aim of this manuscript is to initiate a constructive discussion about the definition of clinical proteomics, study requirements, pitfalls and (potential) use. Furthermore, we hope to stimulate proposals for the optimal use of future opportunities and seek unification of the approaches in clinical proteomic studies. We have outlined our collective views about the basic principles that should be considered in clinical proteomic studies, including sample selection, choice of technology and appropriate quality control, and the need for collaborative interdisciplinary efforts involving clinicians and scientists. Furthermore, we propose guidelines for the critical aspects that should be included in published reports. Our hope is that, as a result of stimulating discussion, a consensus will be reached amongst the scientific community leading to guidelines for the studies, similar to those already published for mass spectrometric sequencing data. We contend that clinical proteomics is not just a collection of studies dealing with analysis of clinical samples. Rather, the essence of clinical proteomics should be to address clinically relevant questions and to improve the state-of-the-art, both in diagnosis and in therapy of diseases. © 2007 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.
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    Common variants at 12q15 and 12q24 are associated with infant head circumference
    (2012-05-01) H. Rob Taal; Beate St Pourcain; Elisabeth Thiering; Shikta Das; Dennis O. Mook-Kanamori; Nicole M. Warrington; Marika Kaakinen; Eskil Kreiner-Møller; Jonathan P. Bradfield; Rachel M. Freathy; Frank Geller; Mònica Guxens; Diana L. Cousminer; Marjan Kerkhof; Nicholas J. Timpson; M. Arfan Ikram; Lawrence J. Beilin; Klaus Bønnelykke; Jessica L. Buxton; Pimphen Charoen; Bo Lund Krogsgaard Chawes; Johan Eriksson; David M. Evans; Albert Hofman; John P. Kemp; Cecilia E. Kim; Norman Klopp; Jari Lahti; Stephen J. Lye; George Mcmahon; Frank D. Mentch; Martina Müller-Nurasyid; Paul F. O'reilly; Inga Prokopenko; Fernando Rivadeneira; Eric A.P. Steegers; Jordi Sunyer; Carla Tiesler; Hanieh Yaghootkar; Myriam Fornage; Albert V. Smith; Sudha Seshadri; Reinhold Schmidt; Stéphanie Debette; Henri A. Vrooman; Sigurdur Sigurdsson; Stefan Ropele; Laura H. Coker; W. T. Longstreth; Wiro J. Niessen; Anita L. Destefano; Alexa Beiser; Alex P. Zijdenbos; Erasmus University Medical Center; University of Bristol; Helmholtz Center Munich German Research Center for Environmental Health; Imperial College London; Weill Cornell Medicine-Qatar; University of Western Australia Faculty of Medicine and Dentistry; University of Toronto; Oulun Yliopisto; Kobenhavns Universitet; The Children's Hospital of Philadelphia; University of Exeter; Statens Serum Institut; Centre de Recerca en Epidemiologia Ambiental, Barcelona; Hospital del Mar; CIBER Epidemiologia Y Salud Publica; Helsingin Yliopisto; University of Groningen, University Medical Center Groningen; Netherlands Consortium for Healthy Ageing (NCHA); Mahidol University; National Institute for Health and Welfare; Medizinische Hochschule Hannover (MHH); Ludwig-Maximilians-Universitat Munchen; Klinikum der Universitat Munchen; University of Oxford; Wellcome Trust Centre for Human Genetics; Universitat Pompeu Fabra; German Center for Neurodgenerative Diseases (DZNE); Boston University School of Medicine; Boston University School of Public Health; Inserm; University of Texas School of Public Health; Icelandic Research Institute; University of Iceland; National Institute on Aging; University of Mississippi Medical Center; Framingham Heart Study; European Bioinformatics Institute; University of Pennsylvania; Center for Public Health Research (CSISP); Centre National de Genotypage; Fondation Jean Dausset - CEPH; Ontario Institute for Cancer Research; Broad Institute; Wellcome Trust Sanger Institute; London School of Hygiene & Tropical Medicine; University of California, Davis; Churchill Hospital; Centro de Regulacion Genomica; Health Protection Agency; The University of North Carolina at Chapel Hill; Ita-Suomen yliopisto; Vrije Universiteit Amsterdam; UCL; King's College London; National University of Singapore; Universitat Duisburg-Essen; Children's Hospital Boston; Harvard Medical School; University of Southampton; Institut for Sygdomsforebyggelse; University of Copenhagen, Faculty of Health Sciences; University of Edinburgh; University Hospital of Tampere; Tampereen Yliopisto; University of Tartu; Children's Hospital of Iowa; Harokopio University; Mid Sweden University, Ostersund; Turun yliopisto; St George's University of London; Harvard Pilgrim Health Care Institute; Universitat Potsdam; Charité – Universitätsmedizin Berlin; MRC Epidemiology Unit; University of Dundee; Singapore Eye Research Institute; Medizinische Universitat Graz; Wake Forest University School of Medicine; University of Washington, Seattle; Delft University of Technology; Universite de Montreal; Mayo Clinic; Leiden University Medical Center - LUMC
    To identify genetic variants associated with head circumference in infancy, we performed a meta-analysis of seven genome-wide association studies (GWAS) (N = 10,768 individuals of European ancestry enrolled in pregnancy and/or birth cohorts) and followed up three lead signals in six replication studies (combined N = 19,089). rs7980687 on chromosome 12q24 (P = 8.1 × 10 -9 ) and rs1042725 on chromosome 12q15 (P = 2.8 × 10 -10 ) were robustly associated with head circumference in infancy. Although these loci have previously been associated with adult height, their effects on infant head circumference were largely independent of height (P = 3.8 × 10 -7 for rs7980687 and P = 1.3 × 10 -7 for rs1042725 after adjustment for infant height). A third signal, rs11655470 on chromosome 17q21, showed suggestive evidence of association with head circumference (P = 3.9 × 10 -6 ). SNPs correlated to the 17q21 signal have shown genome-wide association with adult intracranial volume, Parkinson's disease and other neurodegenerative diseases, indicating that a common genetic variant in this region might link early brain growth with neurological disease in later life. © 2012 Nature America, Inc. All rights reserved.
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    Corrigendum to “Unambiguous determination of Plasmodium vivax reticulocyte invasion by flow cytometry” [Int. J. Parasitol. 46 (2016) 31–39] (S0020751915002246)(10.1016/j.ijpara.2015.08.003))
    (2017-03-01) Jee Sun Cho; Bruce Russell; Varakorn Kosaisavee; Rou Zhang; Yves Colin; Olivier Bertrand; Rajesh Chandramohanadas; Cindy S. Chu; Francois Nosten; Laurent Renia; Benoit Malleret; Yong Loo Lin School of Medicine; A-Star, Singapore Immunology Network; Inserm; Institut National de la Transfusion Sanguine; Universite Paris 7- Denis Diderot; Singapore University of Technology and Design; Mahidol University; Nuffield Department of Clinical Medicine
    © 2017 The authors regret to inform about an error in the original publication of this article. The last name and the affiliation of the author Varakorn Kosaisavee was incorrect. The correct name and the affiliation is as above. The authors would like to apologise for any inconvenience caused.
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    Darapladib for preventing ischemic events in stable coronary heart disease
    (2014-01-01) Harvey D. White; Claes Held; Ralph Stewart; Elizabeth Tarka; Rebekkah Brown; Richard Y. Davies; Andrzej Budaj; Robert A. Harrington; P. Gabriel Steg; Diego Ardissino; Paul W. Armstrong; Alvaro Avezum; Philip E. Aylward; Alfonso Bryce; Hong Chen; Ming Fong Chen; Ramon Corbalan; Anthony J. Dalby; Nicolas Danchin; Robbert J. De Winter; Stefan Denchev; Rafael Diaz; Moses Elisaf; Marcus D. Flather; Assen R. Goudev; Christopher B. Granger; Liliana Grinfeld; Judith S. Hochman; Steen Husted; Hyo Soo Kim; Wolfgang Koenig; Ales Linhart; Eva Lonn; José López-Sendón; Athanasios J. Manolis; Emile R. Mohler; José C. Nicolau; Prem Pais; Alexander Parkhomenko; Terje R. Pedersen; Daniel Pella; Marco A. Ramos-Corrales; Mikhail Ruda; Mátyás Sereg; Saulat Siddique; Peter Sinnaeve; Peter Smith; Piyamitr Sritara; Henk P. Swart; Rody G. Sy; Tamio Teramoto; Hung Fat Tse; David Watson; W. Douglas Weaver; Robert Weiss; Margus Viigimaa; Dragos Vinereanu; Junren Zhu; Christopher P. Cannon; Lars Wallentin; University of Auckland; Akademiska Sjukhuset; GlaxoSmithKline, USA; Duke University Medical Center; Szpital Grochowski, Warszawa; Stanford University; Inserm; Universite Paris 7- Denis Diderot; Universite Paris Descartes; Royal Brompton Hospital; Universita degli Studi di Parma; University of Alberta; McMaster University, Faculty of Health Sciences; Instituto Dante Pazzanese de Cardiologia; Instituto do Coracao do Hospital das Clinicas; Flinders University; Cardiogolf/Clinica El Golf; Peking University; National Taiwan University Hospital; Pontificia Universidad Catolica de Chile; Milpark Hospital; Academic Medical Centre, University of Amsterdam; University Hospital Alexandrovska; Etudios Cardiologica Latin America, Rosario; University of Ioannina, School of Medicine; Norwich Medical School; Norfolk and Norwich University Hospital NHS Trust; Universidad de Buenos Aires; NYU Langone Medical Center; Hospital Unit West; Seoul National University Hospital; Universitat Ulm; Veobecna Fakultni Nemocnice V Praze; Charles University; Hospital Universitario La Paz; Asklepeion Hospital; University of Pennsylvania; St. Johns Medical College; National Scientific Center M.D. Strazhesko Institute of Cardiology; Universitetet i Oslo; Pavol Jozef Safarik University in Kosice; San Jose Satelite Hospital; National Medical Research Center of Cardiology, Moscow; St. George's Hospital; Shaikh Zayed Postgraduate Medical Institute; KU Leuven– University Hospital Leuven; Mahidol University; St. Antonius Ziekenhuis; University of the Philippines Manila; Teikyo Academic Research Center; The University of Hong Kong; Henry Ford Heart and Vascular Institute; Maine Research Associates; Tallinn University of Technology; Universitatea de Medicina si Farmacie Carol Davila din Bucuresti; Fudan University; Brigham and Women's Hospital
    BACKGROUND: Elevated lipoprotein-associated phospholipase A2 activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A2. METHODS: In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization). RESULTS: During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P = 0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P = 0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P = 0.02). CONCLUSIONS: In patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. Copyright © 2014 Massachusetts Medical Society.