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Institution

McGill University

EducationMontreal, Quebec, Canada
About: McGill University is a education organization based out in Montreal, Quebec, Canada. It is known for research contribution in the topics: Population & Poison control. The organization has 72688 authors who have published 162565 publications receiving 6966523 citations. The organization is also known as: Royal institution of advanced learning & University of McGill College.


Papers
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Journal ArticleDOI
TL;DR: A geometric-flow-based algorithm for computing a dense oversegmentation of an image, often referred to as superpixels, which yields less undersegmentation than algorithms that lack a compactness constraint while offering a significant speedup over N-cuts, which does enforce compactness.
Abstract: We describe a geometric-flow-based algorithm for computing a dense oversegmentation of an image, often referred to as superpixels. It produces segments that, on one hand, respect local image boundaries, while, on the other hand, limiting undersegmentation through a compactness constraint. It is very fast, with complexity that is approximately linear in image size, and can be applied to megapixel sized images with high superpixel densities in a matter of minutes. We show qualitative demonstrations of high-quality results on several complex images. The Berkeley database is used to quantitatively compare its performance to a number of oversegmentation algorithms, showing that it yields less undersegmentation than algorithms that lack a compactness constraint while offering a significant speedup over N-cuts, which does enforce compactness.

1,158 citations

Journal ArticleDOI
TL;DR: These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified.
Abstract: Summary Background Genome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease. Methods We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation. Findings Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16–36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10−7). Interpretation These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data. Funding The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources).

1,152 citations

Journal ArticleDOI
25 Mar 2005-Science
TL;DR: It is found that protein production rates fluctuate over a time scale of about one cell cycle, while intrinsic noise decays rapidly, which can form a basis for quantitative modeling of natural gene circuits and for design of synthetic ones.
Abstract: The quantitative relation between transcription factor concentrations and the rate of protein production from downstream genes is central to the function of genetic networks. Here we show that this relation, which we call the gene regulation function (GRF), fluctuates dynamically in individual living cells, thereby limiting the accuracy with which transcriptional genetic circuits can transfer signals. Using fluorescent reporter genes and fusion proteins, we characterized the bacteriophage lambda promoter P_R in Escherichia coli. A novel technique based on binomial errors in protein partitioning enabled calibration of in vivo biochemical parameters in molecular units. We found that protein production rates fluctuate over a time scale of about one cell cycle, while intrinsic noise decays rapidly. Thus, biochemical parameters, noise, and slowly varying cellular states together determine the effective single-cell GRF. These results can form a basis for quantitative modeling of natural gene circuits and for design of synthetic ones.

1,152 citations

Journal ArticleDOI
TL;DR: In this article, the authors classify the effects of ecosystem service trade-offs along three axes: spatial scale, temporal scale, and reversibility, where spatial scale refers to whether the effect of the trade-off is felt locally or at a distant location, while temporal scale describes whether the effects take place relatively rapidly or slowly.
Abstract: Ecosystem service (ES) trade-offs arise from management choices made by humans, which can change the type, magnitude, and relative mix of services provided by ecosystems. Trade-offs occur when the provision of one ES is reduced as a consequence of increased use of another ES. In some cases, a trade-off may be an explicit choice; but in others, trade-offs arise without premeditation or even awareness that they are taking place. Trade-offs in ES can be classified along three axes: spatial scale, temporal scale, and reversibility. Spatial scale refers to whether the effects of the trade-off are felt locally or at a distant location. Temporal scale refers to whether the effects take place relatively rapidly or slowly. Reversibility expresses the likelihood that the perturbed ES may return to its original state if the perturbation ceases. Across all four Millennium Ecosystem Assessment scenarios and selected case study examples, trade-off decisions show a preference for provisioning, regulating, or cultural services (in that order). Supporting services are more likely to be “taken for granted.” Cultural ES are almost entirely unquantified in scenario modeling; therefore, the calculated model results do not fully capture losses of these services that occur in the scenarios. The quantitative scenario models primarily capture the services that are perceived by society as more important—provisioning and regulating ecosystem services—and thus do not fully capture tradeoffs of cultural and supporting services. Successful management policies will be those that incorporate lessons learned from prior decisions into future management actions. Managers should complement their actions with monitoring programs that, in addition to monitoring the short-term provisions of services, also monitor the long-term evolution of slowly changing variables. Policies can then be developed to take into account ES trade-offs at multiple spatial and temporal scales. Successful strategies will recognize the inherent complexities of ecosystem management and will work to develop policies that minimize the effects of ES trade-offs.

1,151 citations

Book
25 Apr 2002
TL;DR: Findings from 5 large, randomized studies of the symptomatic treatment of probable and possible vascular dementia indicate that the presence of a cholinergic deficit is not required for the anticholinesterases to produce cognitive improvement, and so the cholin allergic hypothesis is neither necessary nor sufficient to explain the effects of these drugs.
Abstract: Cerebrovascular disease is the second most common cause of acquired cognitive impairment and dementia and contributes to cognitive decline in the neurodegenerative dementias. The current narrow definitions of vascular dementia should be broadened to recognise the important part cerebrovascular disease plays in several cognitive disorders, including the hereditary vascular dementias, multi-infarct dementia, post-stroke dementia, subcortical ischaemic vascular disease and dementia, mild cognitive impairment, and degenerative dementias (including Alzheimer's disease, frontotemporal dementia, and dementia with Lewy bodies). Here we review the current state of scientific knowledge on the subject of vascular brain burden. Important non-cognitive features include depression, apathy, and psychosis. We propose use of the term vascular cognitive impairment, which is characterised by a specific cognitive profile involving preserved memory with impairments in attentional and executive functioning. Diagnostic criteria have been proposed for some subtypes of vascular cognitive impairment, and there is a pressing need to validate and further refine these. Clinical trials in vascular cognitive impairment are in their infancy but support the value of therapeutic interventions for symptomatic treatment.

1,148 citations


Authors

Showing all 73373 results

NameH-indexPapersCitations
Karl J. Friston2171267217169
Yi Chen2174342293080
Yoshua Bengio2021033420313
Irving L. Weissman2011141172504
Mark I. McCarthy2001028187898
Lewis C. Cantley196748169037
Martin White1962038232387
Michael Marmot1931147170338
Michael A. Strauss1851688208506
Alan C. Evans183866134642
Douglas R. Green182661145944
David A. Weitz1781038114182
David L. Kaplan1771944146082
Hyun-Chul Kim1764076183227
Feng Zhang1721278181865
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023342
2022998
20219,055
20208,668
20197,828
20187,237