Killing the Messenger: The Misuse of Disparate Impact Theory to Challenge High-Stakes Educational Tests

There are two basic theoretical models for addressing claims of discrimination: disparate treatment and disparate impact. The disparate treatment model attempts to expose and punish intentional discrimination; the disparate impact model seeks to eliminate policies that, while neutral on their face, disproportionately harm members of a protected class. Since 1991, Title VII of the Civil Rights Act of 1964, which prohibits discrimination in employment, has expressly permitted plaintiffs to challenge employment practices with a disproportionate impact on certain protected groups. By contrast, Title VI, which prohibits discrimination by federally assisted programs including most schools, does not explicitly authorize claims of disparate impact. Many commentators and activists have long sought to expand the disparate impact doctrine\u27s reach to the education context. In- deed, in recent years it has become fashionable to use the disparate impact model to challenge as discriminatory high-stakes educational tests on which the average black or Latino student scores lower than the average white student. The national groundswell of support for higher educational standards and greater educational accountability has raised questions as to whether federal antidiscrimination law should prohibit standardized tests used to deter- mine whether a student will graduate from high school or be promoted to the next grade level when the use of such tests results in lower pass rates for black and Latino students. This Article examines the claim that standardized educational tests discriminate against minority students and considers whether the disparate impact model should be applied to educational testing. After reviewing the arguments for and against applying the disparate impact model of employment discrimination to the educational testing context, the Article concludes that claims of discrimination in educational testing should be limited to claims of intentional discrimination. Because the standardized tests used by primary and secondary schools can just as easily be understood as a tool for remedying inequality as a tool for exacerbating inequality, educational policymakers should be permitted to use their discretion in deciding whether and how to employ such tests in the absence of an intent to discriminate. In other words, because testing policies necessarily impose both costs and benefits on minority test-takers and communities, they are inappropriate targets of the disparate impact doctrine

Deep Phenotyping of Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS) is a disabling disorder, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available. We used rigorous criteria to recruit PI-ME/CFS participants with matched controls to conduct deep phenotyping. Among the many physical and cognitive complaints, one defining feature of PI-ME/CFS was an alteration of effort preference, rather than physical or central fatigue, due to dysfunction of integrative brain regions potentially associated with central catechol pathway dysregulation, with consequences on autonomic functioning and physical conditioning. Immune profiling suggested chronic antigenic stimulation with increase in naïve and decrease in switched memory B-cells. Alterations in gene expression profiles of peripheral blood mononuclear cells and metabolic pathways were consistent with cellular phenotypic studies and demonstrated differences according to sex. Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention

Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome

Abstract Post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS) is a disabling disorder, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available. We used rigorous criteria to recruit PI-ME/CFS participants with matched controls to conduct deep phenotyping. Among the many physical and cognitive complaints, one defining feature of PI-ME/CFS was an alteration of effort preference, rather than physical or central fatigue, due to dysfunction of integrative brain regions potentially associated with central catechol pathway dysregulation, with consequences on autonomic functioning and physical conditioning. Immune profiling suggested chronic antigenic stimulation with increase in naïve and decrease in switched memory B-cells. Alterations in gene expression profiles of peripheral blood mononuclear cells and metabolic pathways were consistent with cellular phenotypic studies and demonstrated differences according to sex. Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention

Apixaban versus warfarin in patients with atrial fibrillation

BACKGROUND: Vitamin K antagonists are highly effective in preventing stroke in patients with atrial fibrillation but have several limitations. Apixaban is a novel oral direct factor Xa inhibitor that has been shown to reduce the risk of stroke in a similar population in comparison with aspirin. METHODS: In this randomized, double-blind trial, we compared apixaban (at a dose of 5 mg twice daily) with warfarin (target international normalized ratio, 2.0 to 3.0) in 18,201 patients with atrial fibrillation and at least one additional risk factor for stroke. The primary outcome was ischemic or hemorrhagic stroke or systemic embolism. The trial was designed to test for noninferiority, with key secondary objectives of testing for superiority with respect to the primary outcome and to the rates of major bleeding and death from any cause. RESULTS: The median duration of follow-up was 1.8 years. The rate of the primary outcome was 1.27% per year in the apixaban group, as compared with 1.60% per year in the warfarin group (hazard ratio with apixaban, 0.79; 95% confidence interval [CI], 0.66 to 0.95; P<0.001 for noninferiority; P = 0.01 for superiority). The rate of major bleeding was 2.13% per year in the apixaban group, as compared with 3.09% per year in the warfarin group (hazard ratio, 0.69; 95% CI, 0.60 to 0.80; P<0.001), and the rates of death from any cause were 3.52% and 3.94%, respectively (hazard ratio, 0.89; 95% CI, 0.80 to 0.99; P = 0.047). The rate of hemorrhagic stroke was 0.24% per year in the apixaban group, as compared with 0.47% per year in the warfarin group (hazard ratio, 0.51; 95% CI, 0.35 to 0.75; P<0.001), and the rate of ischemic or uncertain type of stroke was 0.97% per year in the apixaban group and 1.05% per year in the warfarin group (hazard ratio, 0.92; 95% CI, 0.74 to 1.13; P = 0.42). CONCLUSIONS: In patients with atrial fibrillation, apixaban was superior to warfarin in preventing stroke or systemic embolism, caused less bleeding, and resulted in lower mortality. Copyright © 2011 Massachusetts Medical Society. All rights reserved