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.
Topics: Population, Malaria, Plasmodium falciparum, Medicine, Plasmodium vivax
Papers published on a yearly basis
Papers
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TL;DR: The pivotal factor leading to the declining efficacy of the artemisinin-based combination on the Thailand–Myanmar border (mefloquine–artesunate) to a clinically unacceptable level is the increasing local prevalence of K13 mutations superimposed onto a long-standing background of Pfmdr1 amplification.
Abstract: Background. Deployment of mefloquine–artesunate (MAS3) on the Thailand–Myanmar border has led to a sustained reduction in falciparum malaria, although antimalarial efficacy has declined substantially in recent years. The role of Plasmodium falciparum K13 mutations (a marker of artemisinin resistance) in reducing treatment efficacy remains controversial.
Methods. Between 2003 and 2013, we studied the efficacy of MAS3 in 1005 patients with uncomplicated P. falciparum malaria in relation to molecular markers of resistance.
Results. Polymerase chain reaction (PCR)–adjusted cure rates declined from 100% in 2003 to 81.1% in 2013 as the proportions of isolates with multiple Pfmdr1 copies doubled from 32.4% to 64.7% and those with K13 mutations increased from 6.7% to 83.4%. K13 mutations conferring moderate artemisinin resistance (notably E252Q) predominated initially but were later overtaken by propeller mutations associated with slower parasite clearance (notably C580Y). Those infected with both multiple Pfmdr1 copy number and a K13 propeller mutation were 14 times more likely to fail treatment. The PCR-adjusted cure rate was 57.8% (95% confidence interval [CI], 45.4, 68.3) compared with 97.8% (95% CI, 93.3, 99.3) in patients with K13 wild type and Pfmdr1 single copy. K13 propeller mutation alone was a strong risk factor for recrudescence (P = .009). The combined population attributable fraction of recrudescence associated with K13 mutation and Pfmdr1 amplification was 82%.
Conclusions. The increasing prevalence of K13 mutations was the decisive factor for the recent and rapid decline in efficacy of artemisinin-based combination (MAS3) on the Thailand–Myanmar border.
171 citations
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TL;DR: In this paper, a systematic review used "science mapping" as a means of understanding the evolution of research in educational administration (EA), and the review sought to document the size, growth trajectory, and an...
Abstract: This systematic review used “science mapping” as a means of understanding the evolution of research in educational administration (EA). The review sought to document the size, growth trajectory, an...
171 citations
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TL;DR: In endemic areas the screening tests described offer a cheap, simple, and accurate means of presumptively identifying Ps pseudomallei from clinical specimens and may also help to delineate the geographical distribution of melioidosis.
Abstract: The API 20NE kit and a simple screening system involving Gram's stain, the oxidase reaction, colistin and gentamicin resistance, and colonial characteristics on a differential agar medium, were used to test 400 strains of Pseudomonas pseudomallei. The API kit identified 390 (97.5%) strains correctly on first testing and all but one of the remainder on second testing. Only one strain was initially misidentified (as Ps cepacia). The screening system was 100% accurate in identifying Ps pseudomallei. In non-endemic areas the API 20NE kit may be used to identify sporadic imported strains of Ps pseudomallei. Such kits may also help to delineate the geographical distribution of melioidosis. In endemic areas the screening tests described offer a cheap, simple, and accurate means of presumptively identifying Ps pseudomallei from clinical specimens.
171 citations
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TL;DR: The genetic and functional data both suggest that the homozygous AE1 G701D mutation causes recessively transmitted dRTA in this kindred with apparently normal erythroid anion transport.
Abstract: The AE1 gene encodes band 3 Cl-/HCO3- exchangers that are expressed both in the erythrocyte and in the acid-secreting, type A intercalated cells of the kidney. Kidney AE1 contributes to urinary acidification by providing the major exit route for HCO3- across the basolateral membrane. Several AE1 mutations cosegregate with dominantly transmitted nonsyndromic renal tubular acidosis (dRTA). However, the modest degree of in vitro hypofunction exhibited by these dRTA-associated mutations fails to explain the disease phenotype in light of the normal urinary acidification associated with the complete loss-of-function exhibited by AE1 mutations linked to dominant spherocytosis. We report here novel AE1 mutations linked to a recessive syndrome of dRTA and hemolytic anemia in which red cell anion transport is normal. Both affected individuals were triply homozygous for two benign mutations M31T and K56E and for the loss-of-function mutation, G701D. AE1 G701D loss-of-function was accompanied by impaired trafficking to the Xenopus oocyte surface. Coexpression with AE1 G701D of the erythroid AE1 chaperonin, glycophorin A, rescued both AE1-mediated Cl- transport and AE1 surface expression in oocytes. The genetic and functional data both suggest that the homozygous AE1 G701D mutation causes recessively transmitted dRTA in this kindred with apparently normal erythroid anion transport.
170 citations
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Ifakara Health Institute1, Medical Research Council2, University of Khartoum3, Columbia University4, University of Cape Town5, National Institute of Malaria Research6, Mahidol University7, Eijkman Institute for Molecular Biology8, Democratic Republic of the Congo Ministry of Health9, Karolinska Institutet10, Sanofi S.A.11, University of Montpellier12, University of Tübingen13, Kenya Medical Research Institute14, Radboud University Nijmegen15, University of London16
TL;DR: AS-MQ and AL are more effective than DP and AS-AQ FDC in preventing gametocytaemia shortly after treatment, suggesting that then on-artemisinin partner drug or the timing of artemisin in dosing are important determinants of post-treatment gametocyte dynamics.
Abstract: Background: Gametocytes are responsible for transmission of malaria from human to mosquito. Artemisinin combination therapy (ACT) reduces post-treatment gametocyte carriage, dependent upon host, parasite and pharmacodynamic factors. The gametocytocidal properties of antimalarial drugs are important for malaria elimination efforts. An individual patient clinical data meta-analysis was undertaken to identify the determinants of gametocyte carriage and the comparative effects of four ACTs: artemether-lumefantrine (AL), artesunate/amodiaquine (AS-AQ), artesunate/mefloquine (AS-MQ), and dihydroartemisinin-piperaquine (DP). Methods: Factors associated with gametocytaemia prior to, and following, ACT treatment were identified in multivariable logistic or Cox regression analysis with random effects. All relevant studies were identified through a systematic review of PubMed. Risk of bias was evaluated based on study design, methodology, and missing data. Results: The systematic review identified 169 published and 9 unpublished studies, 126 of which were shared with the WorldWide Antimalarial Resistance Network (WWARN) and 121 trials including 48,840 patients were included in the analysis. Prevalence of gametocytaemia by microscopy at enrolment was 12.1 % (5887/48,589), and increased with decreasing age, decreasing asexual parasite density and decreasing haemoglobin concentration, and was higher in patients without fever at presentation. After ACT treatment, gametocytaemia appeared in 1.9 % (95 % CI, 1.7-2.1) of patients. The appearance of gametocytaemia was lowest after AS-MQ and AL and significantly higher after DP (adjusted hazard ratio (AHR), 2.03; 95 % CI, 1.24-3.12; P = 0.005 compared to AL) and AS-AQ fixed dose combination (FDC) (AHR, 4.01; 95 % CI, 2.40-6.72; P <0.001 compared to AL). Among individuals who had gametocytaemia before treatment, gametocytaemia clearance was significantly faster with AS-MQ (AHR, 1.26; 95 % CI, 1.00-1.60; P = 0.054) and slower with DP (AHR, 0.74; 95 % CI, 0.63-0.88; P = 0.001) compared to AL. Both recrudescent (adjusted odds ratio (AOR), 9.05; 95 % CI, 3.74-21.90; P <0.001) and new (AOR, 3.03; 95 % CI, 1.66-5.54; P <0.001) infections with asexual-stage parasites were strongly associated with development of gametocytaemia after day 7. Conclusions: AS-MQ and AL are more effective than DP and AS-AQ FDC in preventing gametocytaemia shortly after treatment, suggesting that then on-artemisinin partner drug or the timing of artemisinin dosing are important determinants of post-treatment gametocyte dynamics
170 citations
Authors
Showing all 23819 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |