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Institution

Université libre de Bruxelles

EducationBrussels, Belgium
About: Université libre de Bruxelles is a education organization based out in Brussels, Belgium. It is known for research contribution in the topics: Population & Breast cancer. The organization has 24974 authors who have published 56969 publications receiving 2084303 citations. The organization is also known as: ULB.


Papers
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Journal ArticleDOI
TL;DR: Letrozole after tamoxifen is well-tolerated and improves both disease- free and distant disease-free survival but not overall survival, except in node-positive patients.
Abstract: BACKGROUND: Most recurrences in women with breast cancer receiving 5 years of adjuvant tamoxifen occur after 5 years. The MA.17 trial, which was designed to determine whether extended adjuvant therapy with the aromatase inhibitor letrozole after tamoxifen reduces the risk of such late recurrences, was stopped early after an interim analysis showed that letrozole improved disease-free survival. This report presents updated findings from the trial. METHODS: Postmenopausal women completing 5 years of tamoxifen treatment were randomly assigned to a planned 5 years of letrozole (n = 2593) or placebo (n = 2594). The primary endpoint was disease-free survival (DFS); secondary endpoints included distant disease-free survival, overall survival, incidence of contralateral tumors, and toxic effects. Survival was examined using Kaplan-Meier analysis and log-rank tests. Planned subgroup analyses included those by axillary lymph node status. All statistical tests were two-sided. RESULTS: After a median follow-up of 30 months (range = 1.5-61.4 months), women in the letrozole arm had statistically significantly better DFS and distant DFS than women in the placebo arm (DFS: hazard ratio [HR] for recurrence or contralateral breast cancer = 0.58, 95% confidence interval [CI] = 0.45 to 0.76; P

1,065 citations

Journal ArticleDOI
TL;DR: This review addresses the transition from physiology to pathology, namely how and why the physiological UPR evolves to a proapoptotic ER stress response and which defenses are triggered by beta-cells against these challenges.
Abstract: Accumulating evidence suggests that endoplasmic reticulum (ER) stress plays a role in the pathogenesis of diabetes, contributing to pancreatic beta-cell loss and insulin resistance. Components of the unfolded protein response (UPR) play a dual role in beta-cells, acting as beneficial regulators under physiological conditions or as triggers of beta-cell dysfunction and apoptosis under situations of chronic stress. Novel findings suggest that "what makes a beta-cell a beta-cell", i.e., its enormous capacity to synthesize and secrete insulin, is also its Achilles heel, rendering it vulnerable to chronic high glucose and fatty acid exposure, agents that contribute to beta-cell failure in type 2 diabetes. In this review, we address the transition from physiology to pathology, namely how and why the physiological UPR evolves to a proapoptotic ER stress response and which defenses are triggered by beta-cells against these challenges. ER stress may also link obesity and insulin resistance in type 2 diabetes. High fat feeding and obesity induce ER stress in liver, which suppresses insulin signaling via c-Jun N-terminal kinase activation. In vitro data suggest that ER stress may also contribute to cytokine-induced beta-cell death. Thus, the cytokines IL-1beta and interferon-gamma, putative mediators of beta-cell loss in type 1 diabetes, induce severe ER stress through, respectively, NO-mediated depletion of ER calcium and inhibition of ER chaperones, thus hampering beta-cell defenses and amplifying the proapoptotic pathways. A better understanding of the pathways regulating ER stress in beta-cells may be instrumental for the design of novel therapies to prevent beta-cell loss in diabetes.

1,063 citations

Journal ArticleDOI
TL;DR: Variations in mortality between countries suggest the need for national and international strategies to improve care for patients undergoing inpatient non-cardiac surgery.

1,056 citations

Journal ArticleDOI
TL;DR: Experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue are reviewed, providing insight into the rate‐limiting adjustments that constrain muscle function during fatiguing contractions.
Abstract: Much is known about the physiological impairments that can cause muscle fatigue. It is known that fatigue can be caused by many different mechanisms, ranging from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor command in the motor cortex, and that there is no global mechanism responsible for muscle fatigue. Rather, the mechanisms that cause fatigue are specific to the task being performed. The development of muscle fatigue is typically quantified as a decline in the maximal force or power capacity of muscle, which means that submaximal contractions can be sustained after the onset of muscle fatigue. There is even evidence that the duration of some sustained tasks is not limited by fatigue of the principal muscles. Here we review experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue. Selected comparisons of tasks, groups of individuals and interventions with the task-failure approach can provide insight into the rate-limiting adjustments that constrain muscle function during fatiguing contractions.

1,050 citations

Journal ArticleDOI
TL;DR: An update on the effects of mineral deficiencies on the expression of genes involved in primary metabolism in the shoot, the evidence for increased carbohydrate concentrations and altered biomass allocation between shoot and root, and the consequences of these changes on the growth and morphology of the plant root system are presented.

1,022 citations


Authors

Showing all 25206 results

NameH-indexPapersCitations
Karl J. Friston2171267217169
Yi Chen2174342293080
David Miller2032573204840
Jing Wang1844046202769
H. S. Chen1792401178529
Jie Zhang1784857221720
Jasvinder A. Singh1762382223370
D. M. Strom1763167194314
J. N. Butler1722525175561
Andrea Bocci1722402176461
Bradley Cox1692150156200
Marc Weber1672716153502
Hongfang Liu1662356156290
Guenakh Mitselmakher1651951164435
Yang Yang1642704144071
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023119
2022411
20213,194
20203,051
20192,751
20182,609