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Institution

International Centre for Diarrhoeal Disease Research, Bangladesh

FacilityDhaka, 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.


Papers
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Journal ArticleDOI
TL;DR: Peer counselling can effectively increase the initiation and duration of exclusive breastfeeding and recommend incorporation of peer counsellors in mother and child health programmes in developing countries.

411 citations

Journal ArticleDOI
TL;DR: There are many promising measures that might be pursued: establishment of goals for improved coverage in the poor, rather than in entire populations, and use of those goals to direct planning toward the needs of the disadvantaged.

407 citations

Journal ArticleDOI
TL;DR: The importance of separating biological or behavioural interventions from the delivery systems required to put them in place is highlighted, and the need to tailor delivery strategies to the stage of health-system development is discussed.

404 citations

Journal ArticleDOI
TL;DR: It is estimated that childhood undernutrition may have its origins in the foetal period, suggesting a need to intervene early, ideally during pregnancy, with interventions known to reduce FGR and preterm birth.
Abstract: Background Low- and middle-income countries continue to experience a large burden of stunting; 148 million children were estimated to be stunted, around 30–40% of all children in 2011. In many of these countries, foetal growth restriction (FGR) is common, as is subsequent growth faltering in the first 2 years. Although there is agreement that stunting involves both prenatal and postnatal growth failure, the extent to which FGR contributes to stunting and other indicators of nutritional status is uncertain. Methods Using extant longitudinal birth cohorts (n = 19) with data on birthweight, gestational age and child anthropometry (12–60 months), we estimated study-specific and pooled risk estimates of stunting, wasting and underweight by small-for-gestational age (SGA) and preterm birth. Results We grouped children according to four combinations of SGA and gestational age: adequate size-for-gestational age (AGA) and preterm; SGA and term; SGA and preterm; and AGA and term (the reference group). Relative to AGA and term, the OR (95% confidence interval) for stunting associated with AGA and preterm, SGA and term, and SGA and preterm was 1.93 (1.71, 2.18), 2.43 (2.22, 2.66) and 4.51 (3.42, 5.93), respectively. A similar magnitude of risk was also observed for wasting and underweight. Low birthweight was associated with 2.5–3.5-fold higher odds of wasting, stunting and underweight. The population attributable risk for overall SGA for outcomes of childhood stunting and wasting was 20% and 30%, respectively. Conclusions This analysis estimates that childhood undernutrition may have its origins in the foetal period, suggesting a need to intervene early, ideally during pregnancy, with interventions known to reduce FGR and preterm birth.

402 citations

Journal ArticleDOI
Didier Menard1, Nimol Khim1, Johann Beghain, Ayola A. Adegnika2, Ayola A. Adegnika3, Mohammad Shafiul-Alam4, Olukemi K. Amodu5, Ghulam Rahim-Awab6, Ghulam Rahim-Awab7, Céline Barnadas8, Céline Barnadas9, Céline Barnadas10, Antoine Berry, Yap Boum11, Yap Boum12, Maria Dorina Bustos13, Jun Cao14, Jun Hu Chen15, Louis Collet, Liwang Cui16, Garib Das Thakur, Alioune Dieye1, Alioune Dieye17, Djibrine Djalle1, Monique A. Dorkenoo18, Carole E. Eboumbou-Moukoko19, Fe Espino20, Thierry Fandeur, Maria de Fátima Ferreira-da-Cruz21, Abebe A. Fola10, Abebe A. Fola22, Hans-Peter Fuehrer, Abdillahi Mohamed Hassan13, Sócrates Herrera, Bouasy Hongvanthong, Sandrine Houzé, Maman Laminou Ibrahim, Mohammad Jahirul-Karim, Lubin Jiang23, Shigeyuki Kano1, Wasif Ali-Khan4, Maniphone Khanthavong, Peter G. Kremsner3, Marcus V. G. Lacerda21, Rithea Leang, Mindy Leelawong24, Mei Li15, Khin Lin, Jean Baptiste Mazarati, Sandie Menard, Isabelle Morlais25, Hypolite Muhindo-Mavoko26, Hypolite Muhindo-Mavoko27, Lise Musset1, Kesara Na-Bangchang28, Michael Nambozi, Karamoko Niaré29, Harald Noedl30, Jean-Bosco Ouédraogo, Dylan R. Pillai31, Bruno Pradines, Bui Quang-Phuc, Michael Ramharter2, Michael Ramharter30, Milijaona Randrianarivelojosia1, Jetsumon Sattabongkot7, Abdiqani Sheikh-Omar, Kigbafori D. Silué32, Sodiomon B. Sirima, Colin J. Sutherland33, Din Syafruddin34, Rachida Tahar, Lin Hua Tang15, Offianan Andre Toure1, Patrick Tshibangu-Wa-Tshibangu26, Inès Vigan-Womas1, Marian Warsame, Lyndes Wini35, Sedigheh Zakeri1, Saorin Kim1, Rotha Eam1, Laura Berne1, Chanra Khean1, Sophy Chy1, Malen Ken1, Kaknika Loch1, Lydie Canier1, Valentine Duru1, Eric Legrand1, Jean Christophe Barale, Barbara H. Stokes36, Judith Straimer36, Benoit Witkowski1, David A. Fidock36, Christophe Rogier1, Pascal Ringwald, Frédéric Ariey37, Odile Mercereau-Puijalon 
TL;DR: In this article, the authors analyzed the K13-propeller sequence polymorphism in 14,037 samples collected in 59 countries in which malaria is endemic and identified 108 nonsynonymous K13 mutations, which showed marked geographic disparity in their frequency and distribution.
Abstract: BACKGROUND: Recent gains in reducing the global burden of malaria are threatened by the emergence of Plasmodium falciparum resistance to artemisinins. The discovery that mutations in portions of a P. falciparum gene encoding kelch (K13)-propeller domains are the major determinant of resistance has provided opportunities for monitoring such resistance on a global scale. METHODS: We analyzed the K13-propeller sequence polymorphism in 14,037 samples collected in 59 countries in which malaria is endemic. Most of the samples (84.5%) were obtained from patients who were treated at sentinel sites used for nationwide surveillance of antimalarial resistance. We evaluated the emergence and dissemination of mutations by haplotyping neighboring loci. RESULTS: We identified 108 nonsynonymous K13 mutations, which showed marked geographic disparity in their frequency and distribution. In Asia, 36.5% of the K13 mutations were distributed within two areas--one in Cambodia, Vietnam, and Laos and the other in western Thailand, Myanmar, and China--with no overlap. In Africa, we observed a broad array of rare nonsynonymous mutations that were not associated with delayed parasite clearance. The gene-edited Dd2 transgenic line with the A578S mutation, which expresses the most frequently observed African allele, was found to be susceptible to artemisinin in vitro on a ring-stage survival assay. CONCLUSIONS: No evidence of artemisinin resistance was found outside Southeast Asia and China, where resistance-associated K13 mutations were confined. The common African A578S allele was not associated with clinical or in vitro resistance to artemisinin, and many African mutations appear to be neutral. (Funded by Institut Pasteur Paris and others.).

398 citations


Authors

Showing all 3121 results

NameH-indexPapersCitations
Stanley Falkow13434962461
Myron M. Levine12378960865
Roger I. Glass11647449151
Robert F. Breiman10547343927
Harry B. Greenberg10043334941
Barbara J. Stoll10039042107
Andrew M. Prentice9955046628
Robert H. Gilman9690343750
Robert E. Black9220156887
Johan Ärnlöv9138690490
Juan Jesus Carrero8952266970
John D. Clemens8950628981
William A. Petri8550726906
Toshifumi Hibi8280828674
David A. Sack8043723320
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20235
202234
2021494
2020414
2019391
2018334