Fairness in Algorithmic Decision Making: An Excursion Through the Lens of Causality

As virtually all aspects of our lives are increasingly impacted by algorithmic decision making systems, it is incumbent upon us as a society to ensure such systems do not become instruments of unfair discrimination on the basis of gender, race, ethnicity, religion, etc. We consider the problem of determining whether the decisions made by such systems are discriminatory, through the lens of causal models. We introduce two definitions of group fairness grounded in causality: fair on average causal effect (FACE), and fair on average causal effect on the treated (FACT). We use the Rubin-Neyman potential outcomes framework for the analysis of cause-effect relationships to robustly estimate FACE and FACT. We demonstrate the effectiveness of our proposed approach on synthetic data. Our analyses of two real-world data sets, the Adult income data set from the UCI repository (with gender as the protected attribute), and the NYC Stop and Frisk data set (with race as the protected attribute), show that the evidence of discrimination obtained by FACE and FACT, or lack thereof, is often in agreement with the findings from other studies. We further show that FACT, being somewhat more nuanced compared to FACE, can yield findings of discrimination that differ from those obtained using FACE.Comment: 7 pages, 2 figures, 2 tables.To appear in Proceedings of the International Conference on World Wide Web (WWW), 201

Skeletal maturation in relation to ethnic background in children of school age: The Generation R Study

Ethnicity is a well-established determinant of pediatric maturity, but the underlying genetic and environmental contributions to these ethnic differences are poorly comprehended. We aimed to evaluate the influence of ethnicity on skeletal age (SA), an assessment of pediatric maturation widely used in clinical settings. We included children from the Generation R Study, a multiethnic population-based pregnancy cohort, assessed at a mean age of 9.78 (±0.33) years. SA was evaluated by a trained observer on hand DXA scans using the Greulich and Pyle method. Ethnic background was defined as geographic ancestry (questionnaire-based assessment) (N = 5325) and genetic ancestry (based on admixture analysis) (N = 3413). Associations between the ethnic background and SA were investigated separately in boys and girls, using linear regression models adjusted for age, height and BMI. Based on geographic ancestry, 84% of the children were classified as European, 6% as Asian and 10% as African. Children of European background had on average younger SA than those of Asian or African descent. Asian boys had 0.46 (95% CI 0.26–0.66, p-value < 0.0001) and African boys 0.36 years (95% CI 0.20–0.53, p-value < 0.0001) older SA as compared to European boys. Similarly, Asian girls showed 0.64 (95% CI 0.51–0.77, p-value < 0.0001) and African girls 0.38 years (95% CI 0.27–0.48, p-value < 0.0001) older SA as compared to European girls. A similar pattern was observed in the analysis with genetically-defined ancestry. Furthermore, an increase in the proportion of Asian or African component was associated with older SA in both boys (log[Non-European/European]proportion = 0.10, 95% CI 0.06–0.13, p-value < 0.0001) and girls (log[Non-European/European]proportion = 0.06, 95% CI 0.04–0.08, p-value < 0.0001). In summary, children of Asian and African backgrounds have on average older SA as compared to children of European descent, partially explained by a genetic com

Ancestry and dental development: A geographic and genetic perspective

Objective: In this study, we investigated the influence of ancestry on dental development in the Generation R Study. Methods: Information on geographic ancestry was available in 3,600 children (1,810 boys and 1,790 girls, mean age 9.81±0.35 years) and information about genetic ancestry was available in 2,786 children (1,387 boys and 1,399 girls, mean age 9.82±0.34 years). Dental development was assessed in all children using the Demirjian method. The associations of geographic ancestry (Cape Verdean, Moroccan, Turkish, Dutch Antillean, Surinamese Creole and Surinamese Hindustani vs Dutch as the reference group) and genetic content of ancestry (European, African or Asian) with dental development was analyzed using linear regression models. Results: In a geographic perspective of ancestry, Moroccan (β=0.18; 95% CI: 0.07, 0.28), Turkish (β=0.22; 95% CI: 0.12, 0.32), Dutch Antillean (β=0.27; 95% CI: 0.12, 0.41), and Surinamese Creole (β=0.16; 95% CI: 0.03, 0.30) preceded Dutch children in dental development. Moreover, in a genetic perspective of ancestry, a higher proportion of European ancestry was associated with decelerated dental development (β=-0.32; 95% CI: -.44, -.20). In contrast, a higher proportion of African ancestry (β=0.29; 95% CI: 0.16, 0.43) and a higher proportion of Asian ancestry (β=0.28; 95% CI: 0.09, 0.48) were associated with accelerated dental development. When investigating only European children, these effect estimates increased to twice as large in absolute value. Conclusion: Based on a geographic and genetic perspective, differences in dental development exist in a population of heterogeneous ancestry and should be considered when describing the physiological growth in children

Resistance Training Volume Enhances Muscle Hypertrophy but Not Strength in Trained Men

Purpose: The purpose of this study was to evaluate muscular adaptations between low-, moderate-, and high-volume resistance training protocols in resistance-trained men. Methods: Thirty-four healthy resistance-trained men were randomly assigned to one of three experimental groups: a low-volume group performing one set per exercise per training session (n = 11), a moderate-volume group performing three sets per exercise per training session (n = 12), or a high-volume group performing five sets per exercise per training session (n = 11). Training for all routines consisted of three weekly sessions performed on nonconsecutive days for 8 wk. Muscular strength was evaluated with one repetition maximum (RM) testing for the squat and bench press. Upper-body muscle endurance was evaluated using 50% of subjects bench press 1RM performed to momentary failure. Muscle hypertrophy was evaluated using B-mode ultrasonography for the elbow flexors, elbow extensors, mid-thigh, and lateral thigh. Results: Results showed significant preintervention to postintervention increases in strength and endurance in all groups, with no significant between-group differences. Alternatively, while all groups increased muscle size in most of the measured sites from preintervention to postintervention, significant increases favoring the higher-volume conditions were seen for the elbow flexors, mid-thigh, and lateral thigh. Conclusions: Marked increases in strength and endurance can be attained by resistance-trained individuals with just three 13-min weekly sessions over an 8-wk period, and these gains are similar to that achieved with a substantially greater time commitment. Alternatively, muscle hypertrophy follows a dose–response relationship, with increasingly greater gains achieved with higher training volumes. Ke

LiFT: A Scalable Framework for Measuring Fairness in ML Applications

Many internet applications are powered by machine learned models, which are usually trained on labeled datasets obtained through either implicit / explicit user feedback signals or human judgments. Since societal biases may be present in the generation of such datasets, it is possible for the trained models to be biased, thereby resulting in potential discrimination and harms for disadvantaged groups. Motivated by the need for understanding and addressing algorithmic bias in web-scale ML systems and the limitations of existing fairness toolkits, we present the LinkedIn Fairness Toolkit (LiFT), a framework for scalable computation of fairness metrics as part of large ML systems. We highlight the key requirements in deployed settings, and present the design of our fairness measurement system. We discuss the challenges encountered in incorporating fairness tools in practice and the lessons learned during deployment at LinkedIn. Finally, we provide open problems based on practical experience.Comment: Accepted for publication in CIKM 202

Calcium-Activated Potassium Channels BK and IK1 Are Functionally Expressed in Human Gliomas but Do Not Regulate Cell Proliferation

Gliomas are morbid brain tumors that are extremely resistant to available chemotherapy and radiology treatments. Some studies have suggested that calcium-activated potassium channels contribute to the high proliferative potential of tumor cells, including gliomas. However, other publications demonstrated no role for these channels or even assigned them antitumorogenic properties. In this work we characterized the expression and functional contribution to proliferation of Ca2+-activated K+ channels in human glioblastoma cells. Quantitative RT-PCR detected transcripts for the big conductance (BK), intermediate conductance (IK1), and small conductance (SK2) K+ channels in two glioblastoma-derived cell lines and a surgical sample of glioblastoma multiforme. Functional expression of BK and IK1 in U251 and U87 glioma cell lines and primary glioma cultures was verified using whole-cell electrophysiological recordings. Inhibitors of BK (paxilline and penitrem A) and IK1 channels (clotrimazole and TRAM-34) reduced U251 and U87 proliferation in an additive fashion, while the selective blocker of SK channels UCL1848 had no effect. However, the antiproliferative properties of BK and IK1 inhibitors were seen at concentrations that were higher than those necessary to inhibit channel activity. To verify specificity of pharmacological agents, we downregulated BK and IK1 channels in U251 cells using gene-specific siRNAs. Although siRNA knockdowns caused strong reductions in the BK and IK1 current densities, neither single nor double gene silencing significantly affected rates of proliferation. Taken together, these results suggest that Ca2+-activated K+ channels do not play a critical role in proliferation of glioma cells and that the effects of pharmacological inhibitors occur through their off-target actions

Reactive oxygen species and small-conductance calcium-dependent potassium channels are key mediators of inflammation-induced hypotension and shock

Septic shock is associated with life-threatening vasodilation and hypotension. To cause vasodilation, vascular endothelium may release nitric oxide (NO), prostacyclin (PGI2), and the elusive endothelium-derived hyperpolarizing factor (EDHF). Although NO is critical in controlling vascular tone, inhibiting NO in septic shock does not improve outcome, on the contrary, precipitating the search for alternative therapeutic targets. Using a hyperacute tumor necrosis factor (TNF)-induced shock model in mice, we found that shock can develop independently of the known vasodilators NO, cGMP, PGI2, or epoxyeicosatrienoic acids. However, the antioxidant tempol efficiently prevented hypotension, bradycardia, hypothermia, and mortality, indicating the decisive involvement of reactive oxygen species (ROS) in these phenomena. Also, in classical TNF or lipopolysaccharide-induced shock models, tempol protected significantly. Experiments with (cell-permeable) superoxide dismutase or catalase, N-acetylcysteine and apocynin suggest that the ROS-dependent shock depends on intracellular \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$^\bullet {\hbox{OH}}$$\end{document} radicals. Potassium channels activated by ATP (KATP) or calcium (KCa) are important mediators of vascular relaxation. While NO and PGI2-induced vasodilation involves KATP and large-conductance BKCa channels, small-conductance SKCa channels mediate vasodilation induced by EDHF. Interestingly, also SKCa inhibition completely prevented the ROS-dependent shock. Our data thus indicate that intracellular \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$^\bullet {\hbox{OH}}$$\end{document} and SKCa channels represent interesting new therapeutic targets for inflammatory shock. Moreover, they may also explain why antioxidants other than tempol fail to provide survival benefit during shock