Institution
Mahidol University
Education•Bangkok, Nakhon Pathom, Thailand•
About: Mahidol University is a education organization based out in Bangkok, Nakhon Pathom, Thailand. It is known for research contribution in the topics: Population & Malaria. The organization has 23758 authors who have published 39761 publications receiving 878781 citations.
Papers published on a yearly basis
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TL;DR: In this paper, the authors presented a catalog of hard Fermi-LAT sources (2FHLs) in the 50 GeV-2 TeV energy range and found that 86% of the sources can be associated with counterparts at other wavelengths, of which the majority are active galactic nuclei and the rest (11%) are Galactic sources.
Abstract: We present a catalog of sources detected above 50 GeV by the Fermi-Large Area Telescope (LAT) in 80 months of data. The newly delivered Pass 8 event-level analysis allows the detection and characterization of sources in the 50 GeV–2 TeV energy range. In this energy band, Fermi-LAT has detected 360 sources, which constitute the second catalog of hard Fermi-LAT sources (2FHL). The improved angular resolution enables the precise localization of point sources (~1farcm7 radius at 68% C. L.) and the detection and characterization of spatially extended sources. We find that 86% of the sources can be associated with counterparts at other wavelengths, of which the majority (75%) are active galactic nuclei and the rest (11%) are Galactic sources. Only 25% of the 2FHL sources have been previously detected by Cherenkov telescopes, implying that the 2FHL provides a reservoir of candidates to be followed up at very high energies. This work closes the energy gap between the observations performed at GeV energies by Fermi-LAT on orbit and the observations performed at higher energies by Cherenkov telescopes from the ground.
296 citations
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296 citations
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University of Leicester1, University of Melbourne2, Walter and Eliza Hall Institute of Medical Research3, Brigham and Women's Hospital4, GlaxoSmithKline5, Mahidol University6, University of Arizona7, University of Oxford8, University of British Columbia9, University of Cambridge10, Imperial College London11, Greifswald University Hospital12, University of Edinburgh13, University of Liverpool14, Sir Charles Gairdner Hospital15, Swiss Tropical and Public Health Institute16, Science for Life Laboratory17, University of Helsinki18, University of Tampere19, University of Bergen20, Johns Hopkins University21, Laval University22, University Medical Center Groningen23, Icahn School of Medicine at Mount Sinai24, Anschutz Medical Campus25, Peking University26, Uppsala University27, Wellcome Trust Centre for Human Genetics28, Merck & Co.29, University of Aberdeen30, University of Münster31, University of Nottingham32, University of Dundee33, Autonomous University of Barcelona34, VA Boston Healthcare System35, University of California, San Francisco36, Princeton University37, Turku University Hospital38, University of Split39, University of Basel40, University of Western Australia41, Wellcome Trust Sanger Institute42, St George's, University of London43, National Institute for Health Research44
TL;DR: In this paper, a genome-wide association study in 400,102 individuals of European ancestry was conducted to define 279 lung function signals, 139 of which are new and the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups.
Abstract: Reduced lung function predicts mortality and is key to the diagnosis of chronic obstructive pulmonary disease (COPD). In a genome-wide association study in 400,102 individuals of European ancestry, we define 279 lung function signals, 139 of which are new. In combination, these variants strongly predict COPD in independent populations. Furthermore, the combined effect of these variants showed generalizability across smokers and never smokers, and across ancestral groups. We highlight biological pathways, known and potential drug targets for COPD and, in phenome-wide association studies, autoimmune-related and other pleiotropic effects of lung function-associated variants. This new genetic evidence has potential to improve future preventive and therapeutic strategies for COPD.
295 citations
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TL;DR: The exo-E415G SNP and plasmepsin 2-3 amplification are markers of piperquine resistance and dihydroartemisinin-piperaquine failures in Cambodia, and can help monitor the spread of these phenotypes into other countries of the Greater Mekong subregion, and elucidate the mechanism of p Piperaquine resistance.
Abstract: Summary Background As the prevalence of artemisinin-resistant Plasmodium falciparum malaria increases in the Greater Mekong subregion, emerging resistance to partner drugs in artemisinin combination therapies seriously threatens global efforts to treat and eliminate this disease. Molecular markers that predict failure of artemisinin combination therapy are urgently needed to monitor the spread of partner drug resistance, and to recommend alternative treatments in southeast Asia and beyond. Methods We did a genome-wide association study of 297 P falciparum isolates from Cambodia to investigate the relationship of 11 630 exonic single-nucleotide polymorphisms (SNPs) and 43 copy number variations (CNVs) with in-vitro piperaquine 50% inhibitory concentrations (IC 50 s), and tested whether these genetic variants are markers of treatment failure with dihydroartemisinin–piperaquine. We then did a survival analysis of 133 patients to determine whether candidate molecular markers predicted parasite recrudescence following dihydroartemisinin–piperaquine treatment. Findings Piperaquine IC 50 s increased significantly from 2011 to 2013 in three Cambodian provinces (2011 vs 2013 median IC 50 s: 20·0 nmol/L [IQR 13·7–29·0] vs 39·2 nmol/L [32·8–48·1] for Ratanakiri, 19·3 nmol/L [15·1–26·2] vs 66·2 nmol/L [49·9–83·0] for Preah Vihear, and 19·6 nmol/L [11·9–33·9] vs 81·1 nmol/L [61·3–113·1] for Pursat; all p≤10 −3 ; Kruskal-Wallis test). Genome-wide analysis of SNPs identified a chromosome 13 region that associates with raised piperaquine IC 50 s. A non-synonymous SNP (encoding a Glu415Gly substitution) in this region, within a gene encoding an exonuclease, associates with parasite recrudescence following dihydroartemisinin–piperaquine treatment. Genome-wide analysis of CNVs revealed that a single copy of the mdr1 gene on chromosome 5 and a novel amplification of the plasmepsin 2 and plasmepsin 3 genes on chromosome 14 also associate with raised piperaquine IC 50 s. After adjusting for covariates, both exo-E415G and plasmepsin 2–3 markers significantly associate (p=3·0 × 10 −8 and p=1·7 × 10 −7 , respectively) with decreased treatment efficacy (survival rates 0·38 [95% CI 0·25–0·51] and 0·41 [0·28–0·53], respectively). Interpretation The exo-E415G SNP and plasmepsin 2–3 amplification are markers of piperaquine resistance and dihydroartemisinin–piperaquine failures in Cambodia, and can help monitor the spread of these phenotypes into other countries of the Greater Mekong subregion, and elucidate the mechanism of piperaquine resistance. Since plasmepsins are involved in the parasite's haemoglobin-to-haemozoin conversion pathway, targeted by related antimalarials, plasmepsin 2–3 amplification probably mediates piperaquine resistance. Funding Intramural Research Program of the US National Institute of Allergy and Infectious Diseases, National Institutes of Health, Wellcome Trust, Bill & Melinda Gates Foundation, Medical Research Council, and UK Department for International Development.
295 citations
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TL;DR: In this paper, the authors delineated sequential steps of the autophagic pathway necessary to control intracellular M. tuberculosis and found that an accessory autophagy-targeting molecule p62 (A170 or SQSTM1) was required for mycobactericidal activity.
294 citations
Authors
Showing all 23819 results
Name | H-index | Papers | Citations |
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Nicholas J. White | 161 | 1352 | 104539 |
Pete Smith | 156 | 2464 | 138819 |
Randal J. Kaufman | 140 | 491 | 79527 |
Kevin Marsh | 128 | 567 | 55356 |
Barry M. Trost | 124 | 1635 | 79501 |
John R. Perfect | 119 | 573 | 52325 |
Jon Clardy | 116 | 983 | 56617 |
François Nosten | 114 | 777 | 50823 |
Paul Turner | 114 | 1099 | 61390 |
Paul Kubes | 109 | 393 | 41022 |
Ian M. Adcock | 107 | 660 | 42380 |
Peter H. Verburg | 107 | 464 | 34254 |
Guozhong Cao | 104 | 694 | 41625 |
Carol L. Shields | 102 | 1424 | 46800 |
Nicholas P. J. Day | 102 | 708 | 50588 |