Institution
University of Southern Denmark
Education•Odense, Syddanmark, Denmark•
About: University of Southern Denmark is a education organization based out in Odense, Syddanmark, Denmark. It is known for research contribution in the topics: Population & Randomized controlled trial. The organization has 11928 authors who have published 37918 publications receiving 1258559 citations. The organization is also known as: SDU.
Papers published on a yearly basis
Papers
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University of Melbourne1, University of Otago2, Australian Institute of Health and Welfare3, University of Oslo4, Simon Fraser University5, University of Sydney6, Oswaldo Cruz Foundation7, Cayetano Heredia University8, University of Chile9, Interamerican University of Puerto Rico10, Umeå University11, Aga Khan University12, University of Southern Denmark13, Central University of Venezuela14, Prince of Songkla University15, Peking Union Medical College16, Tibet University17, International Institute for Population Sciences18, Indian Council of Medical Research19, University of Hawaii at Manoa20, University of Nigeria, Nsukka21, Mahidol University22
TL;DR: Taking into account the UN Sustainable Development Goals, this study recommends that national governments develop targeted policy responses to Indigenous health, improving access to health services, and Indigenous data within national surveillance systems.
649 citations
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TL;DR: The analysis provides a high-confidence set of proteins present in human urinary proteome and provides a useful reference for comparing datasets obtained using different methodologies and may prove useful in biomarker discovery in the future.
Abstract: Urine is a desirable material for the diagnosis and classification of diseases because of the convenience of its collection in large amounts; however, all of the urinary proteome catalogs currently being generated have limitations in their depth and confidence of identification. Our laboratory has developed methods for the in-depth characterization of body fluids; these involve a linear ion trap-Fourier transform (LTQ-FT) and a linear ion trap-orbitrap (LTQ-Orbitrap) mass spectrometer. Here we applied these methods to the analysis of the human urinary proteome. We employed one-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis and reverse phase high-performance liquid chromatography for protein separation and fractionation. Fractionated proteins were digested in-gel or in-solution, and digests were analyzed with the LTQ-FT and LTQ-Orbitrap at parts per million accuracy and with two consecutive stages of mass spectrometric fragmentation. We identified 1543 proteins in urine obtained from ten healthy donors, while essentially eliminating false-positive identifications. Surprisingly, nearly half of the annotated proteins were membrane proteins according to Gene Ontology (GO) analysis. Furthermore, extracellular, lysosomal, and plasma membrane proteins were enriched in the urine compared with all GO entries. Plasma membrane proteins are probably present in urine by secretion in exosomes. Our analysis provides a high-confidence set of proteins present in human urinary proteome and provides a useful reference for comparing datasets obtained using different methodologies. The urinary proteome is unexpectedly complex and may prove useful in biomarker discovery in the future.
647 citations
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TL;DR: Depletion of CD38(+) immunosuppressive cells, which is associated with an increase in T-helper cells, cytotoxic T cells, T-cell functional response, and TCR clonality, represents possible additional mechanisms of action for daratumumab and deserves further exploration.
646 citations
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TL;DR: It is concluded that, as early development (in utero and during the first years of postnatal life) is particularly sensitive to developmental disruption by nutritional factors or environmental chemical exposures, with potentially adverse consequences for health later in life, both research and disease prevention strategies should focus more on these vulnerable life stages.
Abstract: This White Paper highlights the developmental period as a plastic phase, which allows the organism to adapt to changes in the environment to maintain or improve reproductive capability in part through sustained health. Plasticity is more prominent prenatally and during early postnatal life, i.e., during the time of cell differentiation and specific tissue formation. These developmental periods are highly sensitive to environmental factors, such as nutrients, environmental chemicals, drugs, infections and other stressors. Nutrient and toxicant effects share many of the same characteristics and reflect two sides of the same coin. In both cases, alterations in physiological functions can be induced and may lead to the development of non-communicable conditions. Many of the major diseases – and dysfunctions – that have increased substantially in prevalence over the last 40 years seem to be related in part to developmental factors associated with either nutritional imbalance or exposures to environmental chemicals. The Developmental Origins of Health and Disease (DOHaD) concept provides significant insight into new strategies for research and disease prevention and is sufficiently robust and repeatable across species, including humans, to require a policy and public health response. This White Paper therefore concludes that, as early development (in utero and during the first years of postnatal life) is particularly sensitive to developmental disruption by nutritional factors or environmental chemical exposures, with potentially adverse consequences for health later in life, both research and disease prevention strategies should focus more on these vulnerable life stages.
646 citations
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TL;DR: A meta-analysis of nine genome-wide association studies and a follow-up of 29 independent loci found three newly implicated loci to be associated with type 2 diabetes: GIPR, ADCY5 and VPS13C.
Abstract: Glucose levels 2 h after an oral glucose challenge are a clinical measure of glucose tolerance used in the diagnosis of type 2 diabetes. We report a meta-analysis of nine genome-wide association studies (n = 15,234 nondiabetic individuals) and a follow-up of 29 independent loci (n = 6,958-30,620). We identify variants at the GIPR locus associated with 2- h glucose level (rs10423928, beta (s.e.m.) = 0.09 (0.01) mmol/l per A allele, P = 2.0 x 10(-15)). The GIPR A-allele carriers also showed decreased insulin secretion (n = 22,492; insulinogenic index, P = 1.0 x 10(-17); ratio of insulin to glucose area under the curve, P = 1.3 x 10(-16)) and diminished incretin effect (n = 804; P = 4.3 x 10(-4)). We also identified variants at ADCY5 (rs2877716, P = 4.2 x 10(-16)), VPS13C (rs17271305, P = 4.1 x 10(-8)), GCKR (rs1260326, P = 7.1 x 10(-11)) and TCF7L2 (rs7903146, P = 4.2 x 10(-10)) associated with 2-h glucose. Of the three newly implicated loci (GIPR, ADCY5 and VPS13C), only ADCY5 was found to be associated with type 2 diabetes in collaborating studies (n = 35,869 cases, 89,798 controls, OR = 1.12, 95% CI 1.09-1.15, P = 4.8 x 10(-18)).
645 citations
Authors
Showing all 12150 results
Name | H-index | Papers | Citations |
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Paul M. Ridker | 233 | 1242 | 245097 |
George Davey Smith | 224 | 2540 | 248373 |
Matthias Mann | 221 | 887 | 230213 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Gang Chen | 167 | 3372 | 149819 |
Jun Wang | 166 | 1093 | 141621 |
Harvey F. Lodish | 165 | 782 | 101124 |
Jens J. Holst | 160 | 1536 | 107858 |
Rajesh Kumar | 149 | 4439 | 140830 |
J. Fraser Stoddart | 147 | 1239 | 96083 |
Debbie A Lawlor | 147 | 1114 | 101123 |
Børge G. Nordestgaard | 147 | 1047 | 95530 |
Oluf Pedersen | 135 | 939 | 106974 |
Rasmus Nielsen | 135 | 556 | 84898 |
Torben Jørgensen | 135 | 883 | 86822 |