Institution
Medical Research Council
Government•London, United Kingdom•
About: Medical Research Council is a government organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Malaria. The organization has 16430 authors who have published 19150 publications receiving 1475494 citations.
Papers published on a yearly basis
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TL;DR: Overall, it is shown that socioeconomic status, gender, age, parity, physical inactivity, and increased energy, fat, and sugar intake are powerful predictors of overweight and/or obesity.
Abstract: This review illustrates the outcomes of the nutrition transition in Sub-Saharan Africa (SSA) and its association with overweight and obesity; the relationship with the double burden of malnutrition is also explored. We describe the increase in overweight in nearly all Sub-Saharan African countries and present data on associated increased gross domestic product, and availability of energy, protein, fat, and sugar at country national levels. Predictors of overweight are described by means of various studies undertaken in SSA, and dietary intakes of numerous countries are presented. Overall, we show that socioeconomic status, gender, age, parity, physical inactivity, and increased energy, fat, and sugar intake are powerful predictors of overweight and/or obesity. The urgency for health interventions in countries in the early stages of the nutrition transition is emphasized, particularly in view of the fact that fat intake is still less than 30% of energy intake in nearly all Sub-Saharan African countries.
302 citations
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Medical Research Council1, Erasmus University Rotterdam2, University of Eastern Finland3, Imperial College London4, University of Lausanne5, University of Gothenburg6, deCODE genetics7, Boston University8, Broad Institute9, Boston Children's Hospital10, Wellcome Trust Sanger Institute11, Cedars-Sinai Medical Center12, University of Maryland, Baltimore13, Washington University in St. Louis14, University College London15, Reykjavík University16, University of Helsinki17, National Institutes of Health18, King's College London19, Karolinska Institutet20, University of Washington21, University of Edinburgh22, University of Texas Southwestern Medical Center23, Harvard University24, Malmö University25, Lund University26, University of Cambridge27, Wake Forest University28, Uppsala University29, GlaxoSmithKline30, Newcastle University31, Spanish National Research Council32, University of Iceland33, Science for Life Laboratory34, Pacific Biosciences35, Sage Bionetworks36, University of Split37, United States Department of Veterans Affairs38, Albert Einstein College of Medicine39, Ludwig Maximilian University of Munich40
TL;DR: In this paper, a meta-analysis of associations between similar to 2.5 million SNPs and body fat percentage from 36,626 individuals and followed up the 14 most significant independent loci in 39,576 individuals.
Abstract: Genome-wide association studies have identified 32 loci influencing body mass index, but this measure does not distinguish lean from fat mass. To identify adiposity loci, we meta-analyzed associations between similar to 2.5 million SNPs and body fat percentage from 36,626 individuals and followed up the 14 most significant (P < 10(-6)) independent loci in 39,576 individuals. We confirmed a previously established adiposity locus in FTO (P = 3 x 10(-26)) and identified two new loci associated with body fat percentage, one near IRS1 (P = 4 x 10(-11)) and one near SPRY2 (P = 3 x 10(-8)). Both loci contain genes with potential links to adipocyte physiology. Notably, the body-fat-decreasing allele near IRS1 is associated with decreased IRS1 expression and with an impaired metabolic profile, including an increased visceral to subcutaneous fat ratio, insulin resistance, dyslipidemia, risk of diabetes and coronary artery disease and decreased adiponectin levels. Our findings provide new insights into adiposity and insulin resistance.
301 citations
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TL;DR: The method should be useful for making aggregation-resistant proteins and for helping to identify features that promote or prevent protein aggregation, including those responsible for misfolding diseases.
Abstract: We describe a method for selecting aggregation-resistant proteins by heat denaturation. This is illustrated with antibody heavy chain variable domains (dAbs), which are prone to aggregate. The dAbs were displayed multivalently at the infective tip of filamentous bacteriophage, and heated transiently to induce unfolding and to promote aggregation of the dAbs. After cooling, the dAbs were selected for binding to protein A (a ligand common to these folded dAbs). Phage displaying dAbs that unfold reversibly were thereby enriched with respect to those that do not. From a repertoire of phage dAbs, six dAbs were characterized after selection; they all resisted aggregation, and were soluble, well expressed in bacteria and could be purified in good yields. The method should be useful for making aggregation-resistant proteins and for helping to identify features that promote or prevent protein aggregation, including those responsible for misfolding diseases.
301 citations
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TL;DR: Evidence is presented in 5 of 8 affected families that mutation at this locus results in the Okihiro syndrome phenotype, and the human SALL4 gene on chromosome 20q13-q13.2 is characterized.
Abstract: Okihiro syndrome refers to the association of forearm malformations with Duane syndrome of eye retraction. Based on the reported literature experience, clinical diagnosis of the syndrome can be elusive, owing to the variable presentation in families reported. Specifically, there is overlap of clinical features with other conditions, most notably Holt-Oram syndrome, a condition resulting from mutation of the TBX5 locus and Townes-Brocks syndrome, known to be caused by mutations in the SALL1 gene. Arising from our observation of several malformations in Okihiro syndrome patients which are also described in Townes-Brocks syndrome, we postulated that Okihiro syndrome might result from mutation of another member of the human SALL gene family. We have characterized the human SALL4 gene on chromosome 20q13.13-q13.2. Moreover, we have identified literature reports of forelimb malformations in patients with cytogenetically identifiable abnormalities of this region. We here present evidence in 5 of 8 affected families that mutation at this locus results in the Okihiro syndrome phenotype.
301 citations
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28 Nov 2000TL;DR: In this article, the authors described methods for the production of anti-self antibodies and antibody fragments, being antibodies or fragments of a particular species of mammal which bind self antigens of that species.
Abstract: Methods are disclosed for the production of anti-self antibodies and antibody fragments, being antibodies or fragments of a particular species of mammal which bind self antigens of that species. Methods comprise providing a library of replicable genetic display packages (rgdps), such as filamentous phage, each rgdp displaying at its surface a member of a specific binding pair which is an antibody or antibody fragment, and each rgdp containing nucleic acid sequence derived from a species of mammal. The nucleic acid sequence in each rgdp encodes a polypeptide chain which is a component part of the sbp member displayed at the surface of that rgdp. Anti-self antibody fragments are selected by binding with a self antigen from the said species of mammal. The displayed antibody fragments may be scFv, Fd, Fab or any other fragment which has the capability of binding antigen. Nucleic acid libraries used may be derived from a rearranged V-gene sequences of unimmunised mammal. Synthetic or artificial libraries are described and shown to be useful.
301 citations
Authors
Showing all 16441 results
Name | H-index | Papers | Citations |
---|---|---|---|
Shizuo Akira | 261 | 1308 | 320561 |
Trevor W. Robbins | 231 | 1137 | 164437 |
Richard A. Flavell | 231 | 1328 | 205119 |
George Davey Smith | 224 | 2540 | 248373 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
Cyrus Cooper | 204 | 1869 | 206782 |
Martin White | 196 | 2038 | 232387 |
Frank E. Speizer | 193 | 636 | 135891 |
Michael Rutter | 188 | 676 | 151592 |
Richard Peto | 183 | 683 | 231434 |
Terrie E. Moffitt | 182 | 594 | 150609 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Chris D. Frith | 173 | 524 | 130472 |
Phillip A. Sharp | 172 | 614 | 117126 |
Avshalom Caspi | 170 | 524 | 113583 |