Institution
University of Düsseldorf
Education•Düsseldorf, Germany•
About: University of Düsseldorf is a education organization based out in Düsseldorf, Germany. It is known for research contribution in the topics: Population & Diabetes mellitus. The organization has 25225 authors who have published 49155 publications receiving 1946434 citations.
Topics: Population, Diabetes mellitus, Transplantation, Gene, Medicine
Papers published on a yearly basis
Papers
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Christian Fuchsberger1, Christian Fuchsberger2, Jason Flannick3, Jason Flannick4 +346 more•Institutions (77)
TL;DR: In this paper, the authors performed whole-genome sequencing in 2,657 European individuals with and without diabetes, and exome sequencing for 12,940 individuals from five ancestry groups.
Abstract: The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of the heritability of this disease. Here, to test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole-genome sequencing in 2,657 European individuals with and without diabetes, and exome sequencing in 12,940 individuals from five ancestry groups. To increase statistical power, we expanded the sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support the idea that lower-frequency variants have a major role in predisposition to type 2 diabetes.
866 citations
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TL;DR: An updated review of local and systemic adverse effects upon administration of topical corticosteroids, including the latest FDA report on the safety of such steroids in children, is provided.
Abstract: Topical corticosteroids were introduced into medicine about 50 years ago. They represent a significant milestone in dermatologic therapy. Despite encouragement to report observed adverse drug reactions, the clinical practice of reporting is poor and incomplete. Likewise, adverse effects and safety of topical corticosteroids are neglected in the medical literature. The authors provide an updated review of their adverse-effect profile. Children are more prone to the development of systemic reactions to topically applied medication because of their higher ratio of total body surface area to body weight. Cutaneous adverse effects occur regularly with prolonged treatment and are dependent on the chemical nature of the drug, the vehicle, and the location of its application. The most frequent adverse effects include atrophy, striae, rosacea, perioral dermatitis, acne, and purpura. Those that occur with lower frequency include hypertrichosis, pigmentation alterations, delayed wound healing, and exacerbation of skin infections. Of particular interest is the rate of contact sensitization against corticosteroids, which is considerably higher than generally believed. Systemic reactions such as hyperglycemia, glaucoma, and adrenal insufficiency have also been reported to follow topical application. The authors provide an updated review of local and systemic adverse effects upon administration of topical corticosteroids, including the latest FDA report on the safety of such steroids in children. Learning objective At the completion of this learning activity, participants should be familiar with topical corticosteroids and their proper use.
865 citations
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TL;DR: In this paper, a review gives an overview on recent progress in the understanding of the photoprotective role of the xanthophylls zeaxanthin and lutein with emphasis on the NPQ processes associated with photosystem II of higher plants.
865 citations
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University of California, Los Angeles1, University of North Carolina at Chapel Hill2, Bangor University3, University of Maryland, Baltimore4, United States Department of Veterans Affairs5, University of Düsseldorf6, University of Pennsylvania7, University of California, Berkeley8, Vanderbilt University9, University of Medicine and Dentistry of New Jersey10, National Institutes of Health11
TL;DR: A consensus-building meeting on social cognition in schizophrenia was held at the National Institute of Mental Health in March 2006, and agreement was reached on several points, including definitions of terms, the significance of social cognition for schizophrenia research, and suggestions for future research directions.
Abstract: Social cognition has become a high priority area for the study of schizophrenia. However, despite developments in this area, progress remains limited by inconsistent terminology and differences in the way social cognition is measured. To address these obstacles, a consensus-building meeting on social cognition in schizophrenia was held at the National Institute of Mental Health in March 2006. Agreement was reached on several points, including definitions of terms, the significance of social cognition for schizophrenia research, and suggestions for future research directions. The importance of translational interdisciplinary research teams was emphasized. The current article presents a summary of these discussions.
860 citations
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TL;DR: These experiments provide the first direct demonstration that Fto is functionally involved in energy homeostasis by the control of energy expenditure, and leads to postnatal growth retardation and a significant reduction in adipose tissue and lean body mass.
Abstract: Variations in the human FTO gene have been linked to obesity-related traits in several genome-wide association studies. A functional correlation is now reported between Fto, the equivalent gene in the mouse, and obesity. In Fto-deficient mice there is postnatal growth retardation and a lean phenotype with high energy expenditure and reduced fat accumulation. This suggests that Fto/FTO is involved in homeostasis via the control of energy expenditure. This study shows that mice lacking the Fto gene do not grow properly after birth, and have less adipose tissue and lean body mass. This is due to increased energy expenditure and systemic sympathetic activation, even though these mice move less and eat lots. Several independent, genome-wide association studies have identified a strong correlation between body mass index and polymorphisms in the human FTO gene1,2,3,4. Common variants in the first intron define a risk allele predisposing to obesity, with homozygotes for the risk allele weighing approximately 3 kilograms more than homozygotes for the low risk allele1. Nevertheless, the functional role of FTO in energy homeostasis remains elusive. Here we show that the loss of Fto in mice leads to postnatal growth retardation and a significant reduction in adipose tissue and lean body mass. The leanness of Fto-deficient mice develops as a consequence of increased energy expenditure and systemic sympathetic activation, despite decreased spontaneous locomotor activity and relative hyperphagia. Taken together, these experiments provide, to our knowledge, the first direct demonstration that Fto is functionally involved in energy homeostasis by the control of energy expenditure.
854 citations
Authors
Showing all 25575 results
Name | H-index | Papers | Citations |
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Karl J. Friston | 217 | 1267 | 217169 |
Roderick T. Bronson | 169 | 679 | 107702 |
Stanley B. Prusiner | 168 | 745 | 97528 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Monique M.B. Breteler | 159 | 546 | 93762 |
Thomas Meitinger | 155 | 716 | 108491 |
Karl Zilles | 138 | 692 | 72733 |
Ruben C. Gur | 136 | 741 | 61312 |
Alexis Brice | 135 | 870 | 83466 |
Michael Schmitt | 134 | 2007 | 114667 |
Michael Weller | 134 | 1105 | 91874 |
Helmut Sies | 133 | 670 | 78319 |
Peter T. Fox | 131 | 622 | 83369 |
Yuri S. Kivshar | 126 | 1845 | 79415 |
Markus M. Nöthen | 125 | 943 | 83156 |