Institution
University of Gothenburg
Education•Gothenburg, Sweden•
About: University of Gothenburg is a education organization based out in Gothenburg, Sweden. It is known for research contribution in the topics: Population & Poison control. The organization has 23855 authors who have published 65241 publications receiving 2606327 citations. The organization is also known as: Göteborg University & Gothenburg University.
Topics: Population, Poison control, Health care, Implant, Dementia
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the authors argue for restraint in the use of spinal-fusion surgery and for controlled trials to define more clearly the associated benefits and the indications of spinal fusions.
Abstract: The use of spinal-fusion surgery is increasing rapidly in the United States. Most of these expensive, complex procedures are now being done for back pain and degenerative disease. Spinal fusions require long operations and are associated with an increase in the rate of complications, particularly in older patients. The benefits of surgery may be only modest, and pain relief is affected by many factors besides the anatomy. The authors of this article argue for restraint in the use of spinal-fusion surgery and for controlled trials to define more clearly the associated benefits and the indications.
558 citations
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TL;DR: In this article, the authors analyzed the transcriptional response to osmotic shock in the yeast Saccharomyces cerevisiae and found that the mRNA level of 186 genes increased at least 3-fold after a shift to NaCl or sorbitol whereas that of more than 100 genes was at least 1.5-fold diminished.
557 citations
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University of Newcastle1, Florey Institute of Neuroscience and Mental Health2, University of Gothenburg3, University of Wisconsin-Madison4, University of Bonn5, Washington University in St. Louis6, University of Alabama at Birmingham7, Royal Netherlands Academy of Arts and Sciences8, Utrecht University9, University of Amsterdam10, University of California11
TL;DR: It is argued that targeting astrocytes may represent an effective therapeutic strategy for Alexander disease, neurotrauma, stroke, epilepsy and Alzheimer’s disease as well as other neurodegenerative diseases.
Abstract: The neurone-centred view of the past disregarded or downplayed the role of astroglia as a primary component in the pathogenesis of neurological diseases. As this concept is changing, so is also the perceived role of astrocytes in the healthy and diseased brain and spinal cord. We have started to unravel the different signalling mechanisms that trigger specific molecular, morphological and functional changes in reactive astrocytes that are critical for repairing tissue and maintaining function in CNS pathologies, such as neurotrauma, stroke, or neurodegenerative diseases. An increasing body of evidence shows that the effects of astrogliosis on the neural tissue and its functions are not uniform or stereotypic, but vary in a context-specific manner from astrogliosis being an adaptive beneficial response under some circumstances to a maladaptive and deleterious process in another context. There is a growing support for the concept of astrocytopathies in which the disruption of normal astrocyte functions, astrodegeneration or dysfunctional/maladaptive astrogliosis are the primary cause or the main factor in neurological dysfunction and disease. This review describes the multiple roles of astrocytes in the healthy CNS, discusses the diversity of astroglial responses in neurological disorders and argues that targeting astrocytes may represent an effective therapeutic strategy for Alexander disease, neurotrauma, stroke, epilepsy and Alzheimer's disease as well as other neurodegenerative diseases.
557 citations
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TL;DR: In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10−8 and, consistent with the winner's curse, its effect size in the replication sample was much smaller.
Abstract: Although autism spectrum disorders (ASDs) have a substantial genetic basis, most of the known genetic risk has been traced to rare variants, principally copy number variants (CNVs). To identify common risk variation, the Autism Genome Project (AGP) Consortium genotyped 1558 rigorously defined ASD families for 1 million single-nucleotide polymorphisms (SNPs) and analyzed these SNP genotypes for association with ASD. In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P < 5 × 10(-8). When a smaller replication sample was analyzed, the risk allele at rs4141463 was again over-transmitted; yet, consistent with the winner's curse, its effect size in the replication sample was much smaller; and, for the combined samples, the association signal barely fell below the P < 5 × 10(-8) threshold. Exploratory analyses of phenotypic subtypes yielded no significant associations after correction for multiple testing. They did, however, yield strong signals within several genes, KIAA0564, PLD5, POU6F2, ST8SIA2 and TAF1C.
554 citations
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TL;DR: Improved liver function was reflected by normal concentrations of prothrombin complex and in decreased activities of alkaline phosphatase and gamma-glutamyltransferase in serum, and this type of treatment may offer an alternative to liver transplantation in hereditary tyrosinaemia.
553 citations
Authors
Showing all 24120 results
Name | H-index | Papers | Citations |
---|---|---|---|
Peter J. Barnes | 194 | 1530 | 166618 |
Luigi Ferrucci | 193 | 1601 | 181199 |
Richard H. Friend | 169 | 1182 | 140032 |
Napoleone Ferrara | 167 | 494 | 140647 |
Timothy A. Springer | 167 | 669 | 122421 |
Anders Björklund | 165 | 769 | 84268 |
Hua Zhang | 163 | 1503 | 116769 |
Kaj Blennow | 160 | 1845 | 116237 |
Leif Groop | 158 | 919 | 136056 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Johan G. Eriksson | 156 | 1257 | 123325 |
Naveed Sattar | 155 | 1326 | 116368 |
Paul Elliott | 153 | 773 | 103839 |
Claude Bouchard | 153 | 1076 | 115307 |
Hakon Hakonarson | 152 | 968 | 101604 |