Institution
International Centre for Diarrhoeal Disease Research, Bangladesh
Facility•Dhaka, Bangladesh•
About: International Centre for Diarrhoeal Disease Research, Bangladesh is a facility organization based out in Dhaka, Bangladesh. It is known for research contribution in the topics: Population & Vibrio cholerae. The organization has 3103 authors who have published 5238 publications receiving 226880 citations. The organization is also known as: SEATO Cholera Research Laboratory & Bangladesh International Centre for Diarrhoeal Disease Research.
Topics: Population, Vibrio cholerae, Cholera, Diarrhea, Health care
Papers published on a yearly basis
Papers
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University of Oxford1, Hanoi Medical University2, Mahidol University3, International Centre for Diarrhoeal Disease Research, Bangladesh4, University of Health and Allied Sciences5, Eduardo Mondlane University6, University of the Witwatersrand7, University of KwaZulu-Natal8, Vietnam Academy of Science and Technology9, Umeå University10
TL;DR: In this paper, the authors compared community-based antibiotic access and use practices across communities in low-income and middle-income countries to identify contextually specific targets for interventions to improve antibiotic use practices.
88 citations
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TL;DR: The ecosystem comprising the aquatic environment, V. cholerae, genetic elements mediating gene transfer, and the mammalian host appears to support the clustering of critical virulence genes in a proper combination leading to the origination of new V. Cholerae strains with epidemic potential.
Abstract: Toxigenic Vibrio cholerae is the etiological agent of cholera, an acute dehydrating diarrhea that occurs in epidemic form in many developing countries. Although V. cholerae is a human pathogen, aquatic ecosystems are major habitats of Vibrio species, which includes both pathogenic and nonpathogenic strains that vary in their virulence gene content. V. cholerae belonging to the 01 and 0139 serogroups is commonly known to carry a set of virulence genes necessary for pathogenesis in humans. Recent studies have indicated that virulence genes or their homologues are also dispersed among environmental strains of V. cholerae belonging to diverse serogroups, which appear to constitute an environmental reservoir of virulence genes. Although the definitive roles of the virulence-associated factors in the environment, and the environmental selection pressures for V. cholerae-carrying virulence genes or their homologues is not clear, the potential for origination of new epidemic strains from environmental progenitors seems real. It is likely that the aquatic environment harbors different virulence-associated genes scattered among environmental vibrios, which possess a lower virulence potential than the epidemic strains. The ecosystem comprising the aquatic environment, V. cholerae, genetic elements mediating gene transfer, and the mammalian host appears to support the clustering of critical virulence genes in a proper combination leading to the origination of new V. cholerae strains with epidemic potential.
88 citations
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TL;DR: The rationale for the microbiologic assays chosen and methodologies used to accomplish the MAL-ED goals are described, including harmonized protocols to test for a diverse range of enteropathogens and maximum laboratory throughput and minimum cost.
Abstract: A central hypothesis of The Etiology, Risk Factors and Interactions of Enteric Infections and Malnutrition and the Consequences for Child Health and Development (MAL-ED) study is that enteropathogens contribute to growth faltering. To examine this question, the MAL-ED network of investigators set out to achieve 3 goals: (1) develop harmonized protocols to test for a diverse range of enteropathogens, (2) provide quality-assured and comparable results from 8 global sites, and (3) achieve maximum laboratory throughput and minimum cost. This paper describes the rationale for the microbiologic assays chosen and methodologies used to accomplish the 3 goals.
88 citations
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TL;DR: These results challenge the common assumption that flooding, precipitation extremes and high temperatures will consistently increase temporary migration and are consistent with a livelihoods interpretation of environmental migration in which households draw on a range of strategies to cope with environmental variability.
Abstract: Mass migration is one of the most concerning potential outcomes of global climate change. Recent research into environmentally induced migration suggests that relationship is much more complicated than originally posited by the 'environmental refugee' hypothesis. Climate change is likely to increase migration in some cases and reduce it in others, and these movements will more often be temporary and short term than permanent and long term. However, few large-sample studies have examined the evolution of temporary migration under changing environmental conditions. To address this gap, we measure the extent to which temperature, precipitation, and flooding can predict temporary migration in Matlab, Bangladesh. Our analysis incorporates high-frequency demographic surveillance data, a discrete time event history approach, and a range of sociodemographic and contextual controls. This approach reveals that migration declines immediately after flooding but quickly returns to normal. In contrast, optimal precipitation and high temperatures have sustained positive effects on temporary migration that persist over one to two year periods. Building on previous studies of long-term migration, these results challenge the common assumption that flooding, precipitation extremes and high temperatures will consistently increase temporary migration. Instead, our results are consistent with a livelihoods interpretation of environmental migration in which households draw on a range of strategies to cope with environmental variability.
88 citations
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TL;DR: The results suggest that girls as compared to boys may be genetically more vulnerable to environmental exposures influencing the immunological processes towards coeliac disease.
Abstract: In the mid 1980s the incidence of coeliac disease in Swedish children below 2 years of age increased threefold within a few years, and after a 10-year high incidence period returned equally rapidly to the previous level. Analysing the epidemic with respect to any change in female to male ratio over time, or shift in age at diagnosis, may increase the understanding of coeliac disease aetiology. In a population-based incidence study of childhood coeliac disease, 2151 cases (811 boys/1340 girls) were diagnosed from 1973 to 1997. Incidence rates and relative risks (RRs) were calculated by gender, age at diagnosis and calendar time. Cumulative incidences by age and gender were calculated for different birth cohorts. A twofold higher risk (RR: 1.9, 95% confidence interval (CI) 1.7-2.1) for coeliac disease in girls as compared to boys prevailed throughout the epidemic. Further, during the post-epidemic period there was an upward shift in age at diagnosis. So far, however, a majority of the cases diagnosed at older ages belong to birth cohorts of the epidemic period, i.e. cohorts that already had a high coeliac disease risk before 2 years of age. Our results suggest that girls as compared to boys may be genetically more vulnerable to environmental exposures influencing the immunological processes towards coeliac disease. Further, an increased risk for coeliac disease during the first years of life due to, for example, unfavourable infant dietary habits, may result in an increased total childhood risk for coeliac disease. A longer follow-up, even into adulthood, is needed to determine whether or not the lifetime risk has changed.
88 citations
Authors
Showing all 3121 results
Name | H-index | Papers | Citations |
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Stanley Falkow | 134 | 349 | 62461 |
Myron M. Levine | 123 | 789 | 60865 |
Roger I. Glass | 116 | 474 | 49151 |
Robert F. Breiman | 105 | 473 | 43927 |
Harry B. Greenberg | 100 | 433 | 34941 |
Barbara J. Stoll | 100 | 390 | 42107 |
Andrew M. Prentice | 99 | 550 | 46628 |
Robert H. Gilman | 96 | 903 | 43750 |
Robert E. Black | 92 | 201 | 56887 |
Johan Ärnlöv | 91 | 386 | 90490 |
Juan Jesus Carrero | 89 | 522 | 66970 |
John D. Clemens | 89 | 506 | 28981 |
William A. Petri | 85 | 507 | 26906 |
Toshifumi Hibi | 82 | 808 | 28674 |
David A. Sack | 80 | 437 | 23320 |