Fanon’s Black Skin, White Masks on Race Consciousness

When the issue of race is approached one is either for retaining race consciousness or for working toward its abolition. There are various ways people choose to retain racial categories and various definitions and meanings of race. As well, abolitionists take on a range of stances on when and how to eliminate racial categories. Nonetheless, that one must take a stance and advocate either retention or abolition seems to be required when studying race theory or discussing racial identities in terms of questions of justice. These two positions are understood as contradictory as well as the only two options available. Using Fanon, and debates surrounding White Skin, Black Masks on this very question of race consciousness, this paper argues against expecting or requiring a clear stance on the issue or even posing it as a dilemma. Reading Fanon as employing an existential phenomenological methodology allows us to see how he exposes injustice by writing about experience and projecting a future shared community of hope and freedom without clear indication of the role our group identities might play. The paper will then show the importance of rethinking the question of perpetuating racial categories, particularly through Fanon, by analyzing three potentially liberatory projects, Critical Whiteness Studies, Indigenous Studies, and Development Studies , demonstrating how the endeavors of many practitioners who claim to already know what various identities will (should) or will not (should not) mean for us truncates these projects

A Study of the Dynamic Intersection of the Individual and the Food Environment in Three Populations.

The food environment, encompassing all of the external influences that affect a person’s diet, is a highly studied topic in public health. Many aspects of the food environment have been implicated in reducing diet quality, from food available in the home, to availability of different varieties of food outlets, to changes in the food system on a national level. However, less attention has been paid to the interaction between the individual and his/her food environment: the ways in which the effects of food environment differ by individual characteristics, and the ways in which the individual shapes the food environment to which he/she is exposed. This dissertation assesses the relationship between the individual and the food environment within 3 populations, at 3 levels of the food environment. First, we describe the creation of the Healthy Meal Index, a tool for measuring the healthfulness of meals served in the home. We describe the characteristics of the parents and children that are associated with healthier meals. We found that parental education was positively associated with meal healthfulness and that parents served healthier meals to girls than boys. Next, we assess the individual characteristics and the food environment characteristics that are associated with choice of grocery store within a population of college students. We found that males, younger students, and minorities shopped at less expensive stores. Fruit and vegetable consumption was positively associated with shopping at more expensive stores. Distance to a stores in the two lowest priced store tertiles, but not the highest, affected store choice. Finally, we assessed the interaction between changes in the food environment with different socioeconomic characteristics on obesity prevalence in a nationally representative sample of the Colombian population. We found that obesity incidence was highest in the lowest wealth index and in urban areas between 2005 and 2010. Overall, our studies provide evidence for a dynamic relationship between individuals and the food environment, in which individual characteristics shape the food environment to which one is exposed and the degree to which the food environment shapes behavior is affected by the level of restriction an individual faces.PhDNutritional SciencesUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/113300/1/nmka_1.pd

Finding measures of clinical placements quality for pre-service health services training: challenges of definition and search strategy construction

Abstract of a poster presentation that was presented at Health Services Research: Evidence-Based Practice Meeting, London, UK, 1-3 July, 2014

Finding measures of clinical placements quality for pre-service health services training: challenges of definition and search strategy construction

Abstract of a poster presentation that was presented at Health Services Research: Evidence-Based Practice Meeting, London, UK, 1-3 July, 2014

Interpreting Cancer Genomes Using Systematic Host Perturbations by Tumour Virus Proteins

Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations associated with cancer predisposition and large numbers of somatic genomic alterations. However, it remains challenging to distinguish between background, or “passenger” and causal, or “driver” cancer mutations in these datasets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. To test the hypothesis that genomic variations and tumour viruses may cause cancer via related mechanisms, we systematically examined host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways that go awry in cancer, such as Notch signalling and apoptosis. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on par with their identification through functional genomics and large-scale cataloguing of tumour mutations. Together, these complementary approaches result in increased specificity for cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate prioritization of cancer-causing driver genes so as to advance understanding of the genetic basis of human cancer

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Genome-wide identification and phenotypic characterization of seizure-associated copy number variations in 741,075 individuals

Copy number variants (CNV) are established risk factors for neurodevelopmental disorders with seizures or epilepsy. With the hypothesis that seizure disorders share genetic risk factors, we pooled CNV data from 10,590 individuals with seizure disorders, 16,109 individuals with clinically validated epilepsy, and 492,324 population controls and identified 25 genome-wide significant loci, 22 of which are novel for seizure disorders, such as deletions at 1p36.33, 1q44, 2p21-p16.3, 3q29, 8p23.3-p23.2, 9p24.3, 10q26.3, 15q11.2, 15q12-q13.1, 16p12.2, 17q21.31, duplications at 2q13, 9q34.3, 16p13.3, 17q12, 19p13.3, 20q13.33, and reciprocal CNVs at 16p11.2, and 22q11.21. Using genetic data from additional 248,751 individuals with 23 neuropsychiatric phenotypes, we explored the pleiotropy of these 25 loci. Finally, in a subset of individuals with epilepsy and detailed clinical data available, we performed phenome-wide association analyses between individual CNVs and clinical annotations categorized through the Human Phenotype Ontology (HPO). For six CNVs, we identified 19 significant associations with specific HPO terms and generated, for all CNVs, phenotype signatures across 17 clinical categories relevant for epileptologists. This is the most comprehensive investigation of CNVs in epilepsy and related seizure disorders, with potential implications for clinical practice

A first update on mapping the human genetic architecture of COVID-19

peer reviewe