Le contrôle de la discrimination raciale au Canada

This article is divided into four parts: the first is a brief survey of race relations in Canada before the enactment of anti-discrimination legislation; the next two parts are devoted to an outline of the scope of this legislation and of the administration and enforcement of it ; finally, the last part suggests some current and possible future developments to make it more effective. Prior to the nineteenth century both the French and the British settlers in the colonies that have become a part of Canada had slaves. Slavery was not, however, very extensive due to lack of large agricultural holdings. At the end of the eighteenth century the legislature in Upper Canada and some judges in Lower Canada limited its expansion and helped to end its practice. The British Imperial Emancipation Act of 1833 brought it to an end. In the next few decades, up to the American Civil War, some Canadians helped run-away slaves from the slave-holding states in the United States, while others actively discouraged them from coming. By the end of the nineteenth century a new source of racial tension arose on the West Coast between the newer immigrants from Asia and the older immigrants from Europe. The result was the enactment of numerous discriminatory laws by the legislature of British Columbia and subsequently, on a lesser scale, by the other western provinces. Most of these remained on the statute books until after World War II. None of these laws were held invalid by the courts on the basis of their discriminatory nature. In addition, both the common law and the Civil Code were interpreted as not prohibiting private discrimination, except by hotel-keepers and common carriers. The change from this situation started in the I930's with a few specific legislative prohibitions of discrimination in specific instances. In the 1940's Ontario, with respect to signs and advertisements and Saskatchewan, with respect to a whole range of activities, enacted legislation prohibiting discrimination, enforcing their prohibitions with penal sanctions. The 1950's saw the introduction of fair employment and fair accommodation practices acts. By the I960's these were being consolidated into comprehensive human rights codes administered by human rights commissions. This trend has continued up to this year, with the result that all eleven jurisdictions have commissions charged with enforcing antidiscrimination codes or acts. The usual, but not invariable, procedure is the laying of a complaint, the investigation of it by the commission staff, an attempt to bring about a settlement and finally, failing that, a hearing before an adjudicative tribunal to determine whether an act of discrimination did occur and, if so, what redress is appropriate. In concluding, three suggestions are made regarding measures that could be taken to strengthen the effectiveness of anti-discrimination legislation: (I) contract compliance; (2) greater independence for the commissions from the government; and (3) giving the legislation paramountcy over other statutes

Ways for Insuring the Protection of Minorities

La première question qui se pose est celle de définir ce que sont les droits des minorités. L'auteur l'aborde en examinant la reconnaissance qu'ont reçue ces droits dans le passé, à travers les traités internationaux, les constitutions d'autres pays ainsi que l'expérience canadienne. Il s'attarde sur la distinction à faire entre « droits individuels » et « droits de minorités ». L'essence de cette distinction se situe surtout dans le fait que la protection des groupes minoritaires exige une action positive du gouvernement tandis que celle des droits individuels ne nécessite aucune intervention

AdS Description of Induced Higher-Spin Gauge Theory

We study deformations of three-dimensional large N CFTs by double-trace operators constructed from spin s single-trace operators of dimension \Delta. These theories possess UV fixed points, and we calculate the change of the 3-sphere free energy \delta F= F_{UV}- F_{IR}. To describe the UV fixed point using the dual AdS_4 space we modify the boundary conditions on the spin s field in the bulk; this approach produces \delta F in agreement with the field theory calculations. If the spin s operator is a conserved current, then the fixed point is described by an induced parity invariant conformal spin s gauge theory. The low spin examples are QED_3 (s=1) and the 3-d induced conformal gravity (s=2). When the original CFT is that of N conformal complex scalar or fermion fields, the U(N) singlet sector of the induced 3-d gauge theory is dual to Vasiliev's theory in AdS_4 with alternate boundary conditions on the spin s massless gauge field. We test this correspondence by calculating the leading term in \delta F for large N. We show that the coefficient of (1/2)\log N in \delta F is equal to the number of spin s-1 gauge parameters that act trivially on the spin s gauge field. We discuss generalizations of these results to 3-d gauge theories including Chern-Simons terms and to theories where s is half-integer. We also argue that the Weyl anomaly a-coefficients of conformal spin s theories in even dimensions d, such as that of the Weyl-squared gravity in d=4, can be efficiently calculated using massless spin s fields in AdS_{d+1} with alternate boundary conditions. Using this method we derive a simple formula for the Weyl anomaly a-coefficients of the d=4 Fradkin-Tseytlin conformal higher-spin gauge fields. Similarly, using alternate boundary conditions in AdS_3 we reproduce the well-known central charge c=-26 of the bc ghosts in 2-d gravity, as well as its higher-spin generalizations.Comment: 62 pages, 1 figure; v2 refs added, minor improvements; v3 refs added, minor improvement

Perspectives on Exertional Rhabdomyolysis

© 2017, The Author(s). Exertional (exercise-induced) rhabdomyolysis is a potentially life threatening condition that has been the subject of research, intense discussion, and media attention. The causes of rhabdomyolysis are numerous and can include direct muscle injury, unaccustomed exercise, ischemia, extreme temperatures, electrolyte abnormalities, endocrinologic conditions, genetic disorders, autoimmune disorders, infections, drugs, toxins, and venoms. The objective of this article is to review the literature on exertional rhabdomyolysis, identify precipitating factors, and examine the role of the dietary supplement creatine monohydrate. PubMed and SPORTDiscus databases were searched using the terms rhabdomyolysis, muscle damage, creatine, creatine supplementation, creatine monohydrate, and phosphocreatine. Additionally, the references of papers identified through this search were examined for relevant studies. A meta-analysis was not performed. Although the prevalence of rhabdomyolysis is low, instances still occur where exercise is improperly prescribed or used as punishment, or incomplete medical history is taken, and exertional rhabdomyolysis occurs. Creatine monohydrate does not appear to be a precipitating factor for exertional rhabdomyolysis. Healthcare professionals should be able to recognize the basic signs of exertional rhabdomyolysis so prompt treatment can be administered. For the risk of rhabdomyolysis to remain low, exercise testing and prescription must be properly conducted based on professional standards

The effect of endurance exercise on both skeletal muscle and systemic oxidative stress in previously sedentary obese men

Background: Obesity is associated with low-grade systemic inflammation, in part because of secretion of proinflammatory cytokines, resulting into peripheral insulin resistance (IR). Increased oxidative stress is proposed to link adiposity and chronic inflammation. The effects of endurance exercise in modulating these outcomes in insulin-resistant obese adults remain unclear. We investigated the effect of endurance exercise on markers of oxidative damage (4-hydroxy-2-nonenal (4-HNE), protein carbonyls (PCs)) and antioxidant enzymes (superoxide dismutase (SOD), catalase) in skeletal muscle; urinary markers of oxidative stress (8-hydroxy-2-deoxyguanosine (8-OHdG), 8-isoprostane); and plasma cytokines (C-reactive protein (CRP), interleukin-6 (IL-6), leptin, adiponectin). Methods: Age- and fitness-matched sedentary obese and lean men (n=9 per group) underwent 3 months of moderate-intensity endurance cycling training with a vastus lateralis biopsy, 24-h urine sample and venous blood samples taken before and after the intervention. Results: Obese subjects had increased levels of oxidative damage: 4-HNE (+37% P⩽0.03) and PC (+63% P⩽0.02); evidence of increased adaptive response to oxidative stress because of elevated levels of copper/zinc SOD (Cu/ZnSOD) protein content (+84% P⩽0.01); increased markers of inflammation: CRP (+737% P⩽0.0001) and IL-6 (+85% P⩽0.03), and these correlated with increased markers of obesity; and increased leptin (+262% P⩽0.0001) with lower adiponectin (−27% P⩽0.01) levels vs lean controls. Training reduced 4-HNE (−10% P⩽0.04), PC (−21% P⩽0.05), 8-isoprostane (−26% P⩽0.02) and leptin levels (−33% P⩽0.01); had a tendency to decrease IL-6 levels (−21% P=0.07) and IR (−17% P=0.10); and increased manganese SOD (MnSOD) levels (+47% P⩽0.01). Conclusion: Endurance exercise reduced skeletal muscle-specific and systemic oxidative damage while improving IR and cytokine profile associated with obesity, independent of weight loss. Hence, exercise is a useful therapeutic modality to reduce risk factors associated with the pathogenesis of IR in obesity

Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes

There is evidence that female athletes may be more susceptible to exercise-induced arterial hypoxemia and expiratory flow limitation and have greater increases in operational lung volumes during exercise relative to men. These pulmonary limitations may ultimately lead to greater levels of diaphragmatic fatigue in women. Accordingly, the purpose of this study was to determine whether there are sex differences in the prevalence and severity of exercise-induced diaphragmatic fatigue in 38 healthy endurance-trained men (n = 19; maximal aerobic capacity = 64.0 ± 1.9 ml·kg–1·min–1) and women (n = 19; maximal aerobic capacity = 57.1 ± 1.5 ml·kg–1·min–1). Transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures. Inspiratory pressure-time products of the diaphragm and esophagus were calculated as the product of breathing frequency and the Pdi and esophageal pressure time integrals, respectively. Cervical magnetic stimulation was used to measure potentiated Pdi twitches (Pdi,tw) before and 10, 30, and 60 min after a constant-load cycling test performed at 90% of peak work rate until exhaustion. Diaphragm fatigue was considered present if there was a 15% reduction in Pdi,tw after exercise. Diaphragm fatigue occurred in 11 of 19 men (58%) and 8 of 19 women (42%). The percent drop in Pdi,tw at 10, 30, and 60 min after exercise in men (n = 11) was 30.6 ± 2.3, 20.7 ± 3.2, and 13.3 ± 4.5%, respectively, whereas results in women (n = 8) were 21.0 ± 2.1, 11.6 ± 2.9, and 9.7 ± 4.2%, respectively, with sex differences occurring at 10 and 30 min (P < 0.05). Men continued to have a reduced contribution of the diaphragm to total inspiratory force output (pressure-time product of the diaphragm/pressure-time product of the esophagus) during exercise, whereas diaphragmatic contribution in women changed very little over time. The findings from this study point to a female diaphragm that is more resistant to fatigue relative to their male counterparts