Institution
Stockholm University
Education•Stockholm, Sweden•
About: Stockholm University is a education organization based out in Stockholm, Sweden. It is known for research contribution in the topics: Population & Context (language use). The organization has 21052 authors who have published 62567 publications receiving 2725859 citations. The organization is also known as: University of Stockholm & Stockholms universitet.
Topics: Population, Context (language use), Galaxy, Supernova, Catalysis
Papers published on a yearly basis
Papers
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TL;DR: In this paper, structural and diffusion tensor imaging (DTI) revealed a heterogeneous set of differences associated with cognitive decline in aging, and suggested that increased activation is either caused by structural disruption or is a compensatory response to such disruption.
Abstract: To explore neural correlates of cognitive decline in aging, we used longitudinal behavioral data to identify two groups of older adults (n = 40) that differed with regard to whether their performance on tests of episodic memory remained stable or declined over a decade. Analysis of structural and diffusion tensor imaging (DTI) revealed a heterogeneous set of differences associated with cognitive decline. Manual tracing of hippocampal volume showed significant reduction in those older adults with a declining memory performance as did DTI-measured fractional anisotropy in the anterior corpus callosum. Functional magnetic resonance imaging during incidental episodic encoding revealed increased activation in left prefrontal cortex for both groups and additional right prefrontal activation for the elderly subjects with the greatest decline in memory performance. Moreover, mean DTI measures in the anterior corpus callosum correlated negatively with activation in right prefrontal cortex. These results demonstrate that cognitive decline is associated with differences in the structure as well as function of the aging brain, and suggest that increased activation is either caused by structural disruption or is a compensatory response to such disruption.
404 citations
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TL;DR: In this paper, the authors examined three dimensions of vulnerability (exposure, sensitivity, and adaptive capacity) of 29 coastal communities across five western Indian Ocean countries to the impacts of coral bleaching on fishery returns, and developed a novel, network-based approach to examine sensitivity to changes in the fishery that incorporates linkages between fishery and non-fishery occupations.
Abstract: Coral reefs support the livelihood of millions of people especially those engaged in marine fisheries activities Coral reefs are highly vulnerable to climate change induced stresses that have led to substantial coral mortality over large spatial scales Such climate change impacts have the potential to lead to declines in marine fish production and compromise the livelihoods of fisheries dependent communities Yet few studies have examined social vulnerability in the context of changes specific to coral reef ecosystems In this paper, we examine three dimensions of vulnerability (exposure, sensitivity, and adaptive capacity) of 29 coastal communities across five western Indian Ocean countries to the impacts of coral bleaching on fishery returns A key contribution is the development of a novel, network-based approach to examining sensitivity to changes in the fishery that incorporates linkages between fishery and non-fishery occupations We find that key sources of vulnerability differ considerably within and between the five countries Our approach allows the visualization of how these dimensions of vulnerability differ from site to site, providing important insights into the types of nuanced policy interventions that may help to reduce vulnerability at a specific location To complement this, we develop framework of policy actions thought to reduce different aspects of vulnerability at varying spatial and temporal scales Although our results are specific to reef fisheries impacts from coral bleaching, this approach provides a framework for other types of threats and different social-ecological systems more broadly
404 citations
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TL;DR: It was found that highly purified LPS did not stimulate the IMD pathway, however, lipid A, the active portion of LPS in mammals, activated melanization in the silkworm Bombyx morii, and the IMd pathway was remarkably sensitive to polymeric and monomeric gram-negative peptidoglycan.
404 citations
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TL;DR: It is reported that TDP1 is sequestered into multi-protein single-strand break repair (SSBR) complexes by direct interaction with DNA ligase IIIα and that these complexes are catalytically inactive in SCAN1 cells, and implicate this process in the maintenance of genetic integrity in post-mitotic neurons.
Abstract: Spinocerebellar ataxia with axonal neuropathy-1 (SCAN1) is a neurodegenerative disease that results from mutation of tyrosyl phosphodiesterase 1 (TDP1). In lower eukaryotes, Tdp1 removes topoisomerase 1 (top1) peptide from DNA termini during the repair of double-strand breaks created by collision of replication forks with top1 cleavage complexes in proliferating cells. Although TDP1 most probably fulfils a similar function in human cells, this role is unlikely to account for the clinical phenotype of SCAN1, which is associated with progressive degeneration of post-mitotic neurons. In addition, this role is redundant in lower eukaryotes, and Tdp1 mutations alone confer little phenotype. Moreover, defects in processing or preventing double-strand breaks during DNA replication are most probably associated with increased genetic instability and cancer, phenotypes not observed in SCAN1 (ref. 8). Here we show that in human cells TDP1 is required for repair of chromosomal single-strand breaks arising independently of DNA replication from abortive top1 activity or oxidative stress. We report that TDP1 is sequestered into multi-protein single-strand break repair (SSBR) complexes by direct interaction with DNA ligase IIIalpha and that these complexes are catalytically inactive in SCAN1 cells. These data identify a defect in SSBR in a neurodegenerative disease, and implicate this process in the maintenance of genetic integrity in post-mitotic neurons.
404 citations
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TL;DR: In this article, the authors explore several possible explanations for the skill complementarity of broadband internet and find that broadband adoption in firms complements skilled workers in executing non-routine abstract tasks, and substitutes for unskilled workers in performing routine tasks.
Abstract: Does adoption of broadband internet in firms enhance labor productivity and increase wages? Is this technological change skill biased or factor neutral? We combine several Norwegian data sets to answer these questions. A public program with limited funding rolled out broadband access points and provides plausibly exogenous variation in the availability and adoption of broadband internet in firms. Our results suggest that broadband internet improves (worsens) the labor market outcomes and productivity of skilled (unskilled) workers. We explore several possible explanations for the skill complementarity of broadband internet. We find suggestive evidence that broadband adoption in firms complements skilled workers in executing nonroutine abstract tasks, and substitutes for unskilled workers in performing routine tasks. Taken together, our findings have important implications for the ongoing policy debate over government investment in broadband infrastructure to encourage productivity and wage growth.
404 citations
Authors
Showing all 21326 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hongjie Dai | 197 | 570 | 182579 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Richard S. Ellis | 169 | 882 | 136011 |
Stanley B. Prusiner | 168 | 745 | 97528 |
Anders Björklund | 165 | 769 | 84268 |
Yang Yang | 164 | 2704 | 144071 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Bengt Winblad | 153 | 1240 | 101064 |
Zhenwei Yang | 150 | 956 | 109344 |
Marvin Johnson | 149 | 1827 | 119520 |
Jan-Åke Gustafsson | 147 | 1058 | 98804 |
Markus Ackermann | 146 | 610 | 71071 |
Hans-Olov Adami | 145 | 908 | 83473 |
Markku Kulmala | 142 | 1487 | 85179 |
Kjell Fuxe | 142 | 1479 | 89846 |