Institution
McGill University
Education•Montreal, 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.
Topics: Population, Poison control, Health care, Cancer, Receptor
Papers published on a yearly basis
Papers
More filters
••
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
••
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
••
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
••
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
••
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
Name | H-index | Papers | Citations |
---|---|---|---|
Karl J. Friston | 217 | 1267 | 217169 |
Yi Chen | 217 | 4342 | 293080 |
Yoshua Bengio | 202 | 1033 | 420313 |
Irving L. Weissman | 201 | 1141 | 172504 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Lewis C. Cantley | 196 | 748 | 169037 |
Martin White | 196 | 2038 | 232387 |
Michael Marmot | 193 | 1147 | 170338 |
Michael A. Strauss | 185 | 1688 | 208506 |
Alan C. Evans | 183 | 866 | 134642 |
Douglas R. Green | 182 | 661 | 145944 |
David A. Weitz | 178 | 1038 | 114182 |
David L. Kaplan | 177 | 1944 | 146082 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Feng Zhang | 172 | 1278 | 181865 |