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: In this area of low malaria transmission, early diagnosis and treatment with combined artesunate and me floquine has reduced the incidence of P. falciparum malaria and halted the progression of mefloquine resistance.
523 citations
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University of Turin1, Mayo Clinic2, Linköping University3, Osaka University4, Karolinska University Hospital5, The Catholic University of America6, Mahidol University7, University of Sydney8, University of Birmingham9, Fudan University10, University of Antwerp11, Marmara University12, Greifswald University Hospital13, Sungkyunkwan University14, Hunan Normal University15, University of Hawaii at Manoa16, Kyoto Prefectural University of Medicine17
TL;DR: In a systematic review and meta-analysis, Giovanni Musso and colleagues examine the association between non-alcoholic fatty liver disease and chronic kidney disease and finds no clear link between the two.
Abstract: Background: Chronic kidney disease (CKD) is a frequent, under-recognized condition and a risk factor for renal failure and cardiovascular disease. Increasing evidence connects non-alcoholic fatty liver disease (NAFLD) to CKD. We conducted a meta-analysis to determine whether the presence and severity of NAFLD are associated with the presence and severity of CKD. Methods and Findings: English and non-English articles from international online databases from 1980 through January 31, 2014 were searched. Observational studies assessing NAFLD by histology, imaging, or biochemistry and defining CKD as either estimated glomerular filtration rate (eGFR) ,60 ml/min/1.73 m 2 or proteinuria were included. Two reviewers extracted studies independently and in duplicate. Individual participant data (IPD) were solicited from all selected studies. Studies providing IPD were combined with studies providing only aggregate data with the two-stage method. Main outcomes were pooled using random-effects models. Sensitivity and subgroup analyses were used to explore sources of heterogeneity and the effect of potential confounders. The influences of age, whole-body/abdominal obesity, homeostasis model of insulin resistance (HOMA-IR), and duration of follow-up on effect estimates were assessed by meta-regression. Thirty-three studies (63,902 participants, 16 population-based and 17 hospital-based, 20 cross-sectional, and 13 longitudinal) were included. For 20 studies (61% of included studies, 11 cross-sectional and nine longitudinal, 29,282 participants), we obtained IPD. NAFLD was associated with an increased risk of prevalent (odds ratio [OR] 2.12, 95% CI 1.69– 2.66) and incident (hazard ratio [HR] 1.79, 95% CI 1.65–1.95) CKD. Non-alcoholic steatohepatitis (NASH) was associated with a higher prevalence (OR 2.53, 95% CI 1.58–4.05) and incidence (HR 2.12, 95% CI 1.42–3.17) of CKD than simple steatosis. Advanced fibrosis was associated with a higher prevalence (OR 5.20, 95% CI 3.14–8.61) and incidence (HR 3.29, 95% CI 2.30– 4.71) of CKD than non-advanced fibrosis. In all analyses, the magnitude and direction of effects remained unaffected by diabetes status, after adjustment for other risk factors, and in other subgroup and meta-regression analyses. In crosssectional and longitudinal studies, the severity of NAFLD was positively associated with CKD stages. Limitations of analysis are the relatively small size of studies utilizing liver histology and the suboptimal sensitivity of ultrasound and biochemistry for NAFLD detection in population-based studies. Conclusion: The presence and severity of NAFLD are associated with an increased risk and severity of CKD. Please see later in the article for the Editors’ Summary.
520 citations
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TL;DR: Biochemical and cellular evidence is provided that artemisinins are potent inhibitors of Plasmodium falciparum phosphatidylinositol-3-kinase (PfPI3K), revealing an unexpected mechanism of action and present PI3P as the key mediator of art Artemisinin resistance and the sole PfPI3k as an important target for malaria elimination.
Abstract: Artemisinins are the cornerstone of anti-malarial drugs. Emergence and spread of resistance to them raises risk of wiping out recent gains achieved in reducing worldwide malaria burden and threatens future malaria control and elimination on a global level. Genome-wide association studies (GWAS) have revealed parasite genetic loci associated with artemisinin resistance. However, there is no consensus on biochemical targets of artemisinin. Whether and how these targets interact with genes identified by GWAS, remains unknown. Here we provide biochemical and cellular evidence that artemisinins are potent inhibitors of Plasmodium falciparum phosphatidylinositol-3-kinase (PfPI3K), revealing an unexpected mechanism of action. In resistant clinical strains, increased PfPI3K was associated with the C580Y mutation in P. falciparum Kelch13 (PfKelch13), a primary marker of artemisinin resistance. Polyubiquitination of PfPI3K and its binding to PfKelch13 were reduced by the PfKelch13 mutation, which limited proteolysis of PfPI3K and thus increased levels of the kinase, as well as its lipid product phosphatidylinositol-3-phosphate (PI3P). We find PI3P levels to be predictive of artemisinin resistance in both clinical and engineered laboratory parasites as well as across non-isogenic strains. Elevated PI3P induced artemisinin resistance in absence of PfKelch13 mutations, but remained responsive to regulation by PfKelch13. Evidence is presented for PI3P-dependent signalling in which transgenic expression of an additional kinase confers resistance. Together these data present PI3P as the key mediator of artemisinin resistance and the sole PfPI3K as an important target for malaria elimination.
515 citations
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University of Genoa1, Nova Southeastern University2, Nippon Medical School3, The Catholic University of America4, University of Tennessee Health Science Center5, Seconda Università degli Studi di Napoli6, University of Montpellier7, National Institutes of Health8, Erasmus University Rotterdam9, University of Colorado Denver10, Federal University of Paraná11, University of Aberdeen12, University of Missouri–Kansas City13, University of Zurich14, University of Turku15, National University of Singapore16, Mahidol University17, Humboldt University of Berlin18
TL;DR: “Raising public awareness about sublingual immunotherapy”, as a need for patients, and strategies to increase awareness of allergen immunotherapy (AIT) among patients, the medical community, all healthcare stakeholders, and public opinion are reported in detail.
515 citations
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TL;DR: The results suggest that one mechanism of cell membrane damage is the increase in membrane permeability due to the presence of oxidized lipids.
514 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 |