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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 comprehensive estimate of the prevalence of "cognitive impairment, no dementia" (CIND) in an elderly population of elderly Canadians and this diagnostic category includes a costly group of disorders that merit further study.

950 citations

Journal ArticleDOI
TL;DR: It is found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypers sensitivity using adaptive immune cells, likely T lymphocytes, suggesting that male mice cannot be used as proxies for females in pain research.
Abstract: A large and rapidly increasing body of evidence indicates that microglia-to-neuron signaling is essential for chronic pain hypersensitivity. Using multiple approaches, we found that microglia are not required for mechanical pain hypersensitivity in female mice; female mice achieved similar levels of pain hypersensitivity using adaptive immune cells, likely T lymphocytes. This sexual dimorphism suggests that male mice cannot be used as proxies for females in pain research.

950 citations

Journal ArticleDOI
TL;DR: In this article, the authors analyzed 8 years of precise radial velocity measurements from the Keck Planet Search, characterizing the detection threshold, selection effects, and completeness of the survey.
Abstract: . We analyze 8 years of precise radial velocity measurements from the Keck Planet Search, characterizing the detection threshold, selection effects, and completeness of the survey. We first carry out a systematic search for planets, by assessing the false-alarm probability associated with Keplerian orbit fits to the data. This allows us to understand the detection threshold for each star in terms of the number and time baseline of the observations, and the underlying “noise” from measurement errors, intrinsic stellar jitter, or additional low-mass planets. We show that all planets with orbital periods P 20 m s-1 K > 20 m s - 1 , and eccentricities e ≲ 0.6 e ≲ 0.6 have been announced, and we summarize the candidates at lower amplitudes and longer orbital periods. For the remaining stars, we calculate upper limits on the velocity amplitude of a companion. For orbital periods less than the duration of the observations, these are typically ...

949 citations

Journal ArticleDOI
18 Mar 2004-Nature
TL;DR: It is shown that Akt promotes tumorigenesis and drug resistance by disrupting apoptosis, and that disruption of Akt signalling using the mTOR inhibitor rapamycin reverses chemoresistance in lymphomas expressing Akt, but not in those with other apoptotic defects.
Abstract: Evading apoptosis is considered to be a hallmark of cancer, because mutations in apoptotic regulators invariably accompany tumorigenesis. Many chemotherapeutic agents induce apoptosis, and so disruption of apoptosis during tumour evolution can promote drug resistance. For example, Akt is an apoptotic regulator that is activated in many cancers and may promote drug resistance in vitro. Nevertheless, how Akt disables apoptosis and its contribution to clinical drug resistance are unclear. Using a murine lymphoma model, we show that Akt promotes tumorigenesis and drug resistance by disrupting apoptosis, and that disruption of Akt signalling using the mTOR inhibitor rapamycin reverses chemoresistance in lymphomas expressing Akt, but not in those with other apoptotic defects. eIF4E, a translational regulator that acts downstream of Akt and mTOR, recapitulates Akt's action in tumorigenesis and drug resistance, but is unable to confer sensitivity to rapamycin and chemotherapy. These results establish Akt signalling through mTOR and eIF4E as an important mechanism of oncogenesis and drug resistance in vivo, and reveal how targeting apoptotic programmes can restore drug sensitivity in a genotype-dependent manner.

949 citations

Journal ArticleDOI
TL;DR: By this method, no lumping of data is required, and the accuracy of the estimate of alpha (i.e., a type 1 error) depends only on the number of randomizations of the original data set.
Abstract: Significance levels obtained from a x2 contingency test are suspect when sample sizes are small. Traditionally this has meant that data must be combined. However, such an approach may obscure heterogeneity and hence potentially reduce the power of the statistical test. In this paper, we present a Monte Carlo solution to this problem: by this method, no lumping of data is required, and the accuracy of the estimate of c1 (i.e., a type 1 error) depends only on the number of randomizations of the original data set. We illustrate this technique with data from mtDNA studies, where numerous genotypes are often observed and sample sizes are relatively small.

948 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