Institution
Uppsala University
Education•Uppsala, Sweden•
About: Uppsala University is a education organization based out in Uppsala, Sweden. It is known for research contribution in the topics: Population & Gene. The organization has 36485 authors who have published 107509 publications receiving 4220668 citations. The organization is also known as: Uppsala universitet & uu.se.
Topics: Population, Gene, Context (language use), Thin film, Receptor
Papers published on a yearly basis
Papers
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TL;DR: Gene-based analyses identified further biologically plausible loci, suggesting that additional loci beyond those reaching genome-wide significance are likely to represent real associations and further functional analysis of these newly discovered loci will further improve the understanding of glycemic control.
Abstract: Through genome-wide association meta-analyses of up to 133,010 individuals of European ancestry without diabetes, including individuals newly genotyped using the Metabochip, we have increased the number of confirmed loci influencing glycemic traits to 53, of which 33 also increase type 2 diabetes risk (q < 0.05). Loci influencing fasting insulin concentration showed association with lipid levels and fat distribution, suggesting impact on insulin resistance. Gene-based analyses identified further biologically plausible loci, suggesting that additional loci beyond those reaching genome-wide significance are likely to represent real associations. This conclusion is supported by an excess of directionally consistent and nominally significant signals between discovery and follow-up studies. Functional analysis of these newly discovered loci will further improve our understanding of glycemic control.
753 citations
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University of Kentucky1, Mayo Clinic2, University of Pennsylvania3, Rush University Medical Center4, Illinois Institute of Technology5, Uppsala University6, Newcastle University7, University of Cambridge8, University of Southern California9, University of Minnesota10, University of Sydney11, University of California, Irvine12, University of Washington13, Medical University of Vienna14, Emory University15, Stanford University16, University of California, San Diego17, University of California, San Francisco18, Harvard University19, University of Texas Southwestern Medical Center20
TL;DR: A recently recognized brain disorder that mimics the clinical features of Alzheimer’s disease: Limbic-predominant Age-related TDP-43 Encephalopathy (LATE).
Abstract: We describe a recently recognized disease entity, limbic-predominant age-related TDP-43 encephalopathy (LATE). LATE neuropathological change (LATE-NC) is defined by a stereotypical TDP-43 proteinopathy in older adults, with or without coexisting hippocampal sclerosis pathology. LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-type dementia in retrospective autopsy studies. LATE is distinguished from frontotemporal lobar degeneration with TDP-43 pathology based on its epidemiology (LATE generally affects older subjects), and relatively restricted neuroanatomical distribution of TDP-43 proteinopathy. In community-based autopsy cohorts, ∼25% of brains had sufficient burden of LATE-NC to be associated with discernible cognitive impairment. Many subjects with LATE-NC have comorbid brain pathologies, often including amyloid-β plaques and tauopathy. Given that the 'oldest-old' are at greatest risk for LATE-NC, and subjects of advanced age constitute a rapidly growing demographic group in many countries, LATE has an expanding but under-recognized impact on public health. For these reasons, a working group was convened to develop diagnostic criteria for LATE, aiming both to stimulate research and to promote awareness of this pathway to dementia. We report consensus-based recommendations including guidelines for diagnosis and staging of LATE-NC. For routine autopsy workup of LATE-NC, an anatomically-based preliminary staging scheme is proposed with TDP-43 immunohistochemistry on tissue from three brain areas, reflecting a hierarchical pattern of brain involvement: amygdala, hippocampus, and middle frontal gyrus. LATE-NC appears to affect the medial temporal lobe structures preferentially, but other areas also are impacted. Neuroimaging studies demonstrated that subjects with LATE-NC also had atrophy in the medial temporal lobes, frontal cortex, and other brain regions. Genetic studies have thus far indicated five genes with risk alleles for LATE-NC: GRN, TMEM106B, ABCC9, KCNMB2, and APOE. The discovery of these genetic risk variants indicate that LATE shares pathogenetic mechanisms with both frontotemporal lobar degeneration and Alzheimer's disease, but also suggests disease-specific underlying mechanisms. Large gaps remain in our understanding of LATE. For advances in prevention, diagnosis, and treatment, there is an urgent need for research focused on LATE, including in vitro and animal models. An obstacle to clinical progress is lack of diagnostic tools, such as biofluid or neuroimaging biomarkers, for ante-mortem detection of LATE. Development of a disease biomarker would augment observational studies seeking to further define the risk factors, natural history, and clinical features of LATE, as well as eventual subject recruitment for targeted therapies in clinical trials.
753 citations
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TL;DR: It is proposed that astrocyte-derived PDGF is crucial for the control of myelination in the developing central nervous system.
751 citations
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University of Saskatchewan1, Centre for Environment, Fisheries and Aquaculture Science2, Natural History Museum3, University of Rhode Island4, Sewanee: The University of the South5, Academy of Sciences of the Czech Republic6, National Institutes of Health7, Saint Petersburg State University8, University of Salzburg9, Centre national de la recherche scientifique10, Mississippi State University11, Science for Life Laboratory12, Uppsala University13, Charles University in Prague14, Spanish National Research Council15, Kaiserslautern University of Technology16, University of Duisburg-Essen17, University of Oslo18, Dalhousie University19, Pierre-and-Marie-Curie University20, American Museum of Natural History21, University of Michigan22, University of Warsaw23, University of São Paulo24, University of Paris25, University of British Columbia26, University of Guelph27, Royal Botanic Garden Edinburgh28, Kyungpook National University29, University of Geneva30, University of Alabama31, Pompeu Fabra University32, Edinburgh Napier University33, University of Arkansas34, Hosei University35, Oklahoma State University–Stillwater36, Chinese Academy of Sciences37
TL;DR: It is confirmed that eukaryotes form at least two domains, the loss of monophyly in the Excavata, robust support for the Haptista and Cryptista, and suggested primer sets for DNA sequences from environmental samples that are effective for each clade are provided.
Abstract: This revision of the classification of eukaryotes follows that of Adl et al., 2012 [J. Euk. Microbiol. 59(5)] and retains an emphasis on protists. Changes since have improved the resolution of many ...
750 citations
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TL;DR: The functions of hemocytes in innate immune response are reviewed with emphasized on their roles in coagulation, melanization and opsonization.
749 citations
Authors
Showing all 36854 results
Name | H-index | Papers | Citations |
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Zhong Lin Wang | 245 | 2529 | 259003 |
Lewis C. Cantley | 196 | 748 | 169037 |
Darien Wood | 160 | 2174 | 136596 |
Kaj Blennow | 160 | 1845 | 116237 |
Christopher J. O'Donnell | 159 | 869 | 126278 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Peter G. Schultz | 156 | 893 | 89716 |
Frederik Barkhof | 154 | 1449 | 104982 |
Deepak L. Bhatt | 149 | 1973 | 114652 |
Svante Pääbo | 147 | 407 | 84489 |
Jan-Åke Gustafsson | 147 | 1058 | 98804 |
Hans-Olov Adami | 145 | 908 | 83473 |
Hermann Kolanoski | 145 | 1279 | 96152 |
Kjell Fuxe | 142 | 1479 | 89846 |
Jan Conrad | 141 | 826 | 71445 |