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Institution

University of British Columbia

EducationVancouver, British Columbia, Canada
About: University of British Columbia is a education organization based out in Vancouver, British Columbia, Canada. It is known for research contribution in the topics: Population & Poison control. The organization has 89939 authors who have published 209679 publications receiving 9226862 citations. The organization is also known as: UBC & The University of British Columbia.


Papers
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Journal ArticleDOI
TL;DR: It is found that, although microglia can enter the cell cycle and return to quiescence following remission, recruited monocytes vanish, and therefore do not ultimately contribute to the resident microglial pool.
Abstract: The authors examine the roles of microglia and blood-derived macrophages (which are morphologically indistinguishable) in experimental autoimmune encephalitis, a mouse model of multiple sclerosis. They discover that the transient infiltration of circulating cells is responsible for progression to paralytic disease, and that disease resolution coincides with their disappearance.

910 citations

Journal ArticleDOI
TL;DR: In this article, the authors provide a brief historical background of the development of hydraulic fracturing models for use in the petroleum and other industries, and discuss scaling laws and propagation regimes that control the growth of hydraulic fractures from the laboratory to the field scale.

909 citations

Journal ArticleDOI
Nobuyuki Hamajima, Kaoru Hirose, K. Tajima, T E Rohan1  +216 moreInstitutions (15)
TL;DR: In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis.
Abstract: Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58515 women with invasive breast cancer and 95067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19 - 1.45, P < 0.00001) for an intake of 35 - 44 g per day alcohol, and 1.46 (1.33 - 1.61, P < 0.00001) for greater than or equal to 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1 % per 10 g per day, P < 0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers= 1.03, 95% CI 0.98 - 1.07, and for current smokers=0.99, 0.92 - 1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver. (C) 2002 Cancer Research UK.

909 citations

Journal ArticleDOI
TL;DR: Once-daily sofosbuvir-velpatasvir for 12 weeks provided high rates of sustained virologic response among both previously treated and untreated patients infected with HCV genotype 1, 2, 4, 5, or 6, including those with compensated cirrhosis.
Abstract: BackgroundA simple treatment regimen that is effective in a broad range of patients who are chronically infected with the hepatitis C virus (HCV) remains an unmet medical need. MethodsWe conducted a phase 3, double-blind, placebo-controlled study involving untreated and previously treated patients with chronic HCV genotype 1, 2, 4, 5, or 6 infection, including those with compensated cirrhosis. Patients with HCV genotype 1, 2, 4, or 6 were randomly assigned in a 5:1 ratio to receive the nucleotide polymerase inhibitor sofosbuvir and the NS5A inhibitor velpatasvir in a once-daily, fixed-dose combination tablet or matching placebo for 12 weeks. Because of the low prevalence of genotype 5 in the study regions, patients with genotype 5 did not undergo randomization but were assigned to the sofosbuvir–velpatasvir group. The primary end point was a sustained virologic response at 12 weeks after the end of therapy. ResultsOf the 624 patients who received treatment with sofosbuvir–velpatasvir, 34% had HCV genotype...

909 citations

Journal ArticleDOI
10 Aug 2001-Science
TL;DR: In vivo evidence is provided for substantial release of endogenous dopamine in the striatum of PD patients in response to placebo, indicating that the placebo effect in PD is powerful and is mediated through activation of the damaged nigrostriatal dopamine system.
Abstract: The power of placebos has long been recognized for improving numerous medical conditions such as Parkinson's disease (PD). Little is known, however, about the mechanism underlying the placebo effect. Using the ability of endogenous dopamine to compete for [11C]raclopride binding as measured by positron emission tomography, we provide in vivo evidence for substantial release of endogenous dopamine in the striatum of PD patients in response to placebo. Our findings indicate that the placebo effect in PD is powerful and is mediated through activation of the damaged nigrostriatal dopamine system.

908 citations


Authors

Showing all 90682 results

NameH-indexPapersCitations
Gordon H. Guyatt2311620228631
John C. Morris1831441168413
Douglas Scott1781111185229
John R. Yates1771036129029
Deborah J. Cook173907148928
Richard A. Gibbs172889249708
Evan E. Eichler170567150409
James F. Sallis169825144836
Michael Snyder169840130225
Jiawei Han1681233143427
Michael Kramer1671713127224
Bruce L. Miller1631153115975
Peter A. R. Ade1621387138051
Marc W. Kirschner162457102145
Kaj Blennow1601845116237
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20241
2023307
20221,209
202113,228
202012,052
201910,934