159 research outputs found
Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic Ancestry
Background: Individuals of African descent in the United States suffer disproportionately from diseases with a metabolic etiology (obesity, metabolic syndrome, and diabetes), and from the pathological consequences of these disorders (hypertension and cardiovascular disease). Methodology/Principal Findings: Using a combination of genetic/genomic and bioinformatics approaches, we identified a large number of genes that were both differentially expressed between American subjects self-identified to be of either African or European ancestry and that also contained single nucleotide polymorphisms that distinguish distantly related ancestral populations. Several of these genes control the metabolism of simple carbohydrates and are direct targets for the SREBP1, a metabolic transcription factor also differentially expressed between our study populations. Conclusions/Significance: These data support the concept of stable patterns of gene transcription unique to a geographic ancestral lineage. Differences in expression of several carbohydrate metabolism genes suggest both genetic and transcriptional mechanisms contribute to these patterns and may play a role in exacerbating the disproportionate levels o
4. National Support for Behavioral Science
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/67094/2/10.1177_000276425800100504.pd
Class Is Not Dead! It Has Been Buried Alive
By means of a reanalysis of the most relevant data source—the International
Social Mobility and Politics File—this article criticizes the newly grown consensus
in political sociology that class voting has declined since World War II. An
increase in crosscutting cultural voting, rooted in educational differences rather
than a decline in class voting, proves responsible for the decline of traditional
class-party alignments. Moreover, income differences have not become less but
more consequential for voting behavior during this period. It is concluded that the
new consensus has been built on quicksand. Class is not dead—it has been buried
alive under the increasing weight of cultural voting, systematically misinterpreted
as a decline in class voting because of the widespread application of the so-called
Alford index
Evaluation of cytochrome P450-derived eicosanoids in humans with stable atherosclerotic cardiovascular disease
Preclinical and genetic epidemiologic studies suggest that modulating cytochrome P450 (CYP)-mediated arachidonic acid metabolism may have therapeutic utility in the management of coronary artery disease (CAD). However, predictors of inter-individual variation in CYP-derived eicosanoid metabolites in CAD patients have not been evaluated to date. Therefore, the primary objective was to identify clinical factors that influence CYP epoxygenase, soluble epoxide hydrolase (sEH), and CYP ω-hydroxylase metabolism in patients with established CAD
Tobacco use induces anti-apoptotic, proliferative patterns of gene expression in circulating leukocytes of Caucasian males
Abstract Background Strong epidemiologic evidence correlates tobacco use with a variety of serious adverse health effects, but the biological mechanisms that produce these effects remain elusive. Results We analyzed gene transcription data to identify expression spectra related to tobacco use in circulating leukocytes of 67 Caucasian male subjects. Levels of cotinine, a nicotine metabolite, were used as a surrogate marker for tobacco exposure. Significance Analysis of Microarray and Gene Set Analysis identified 109 genes in 16 gene sets whose transcription levels were differentially regulated by nicotine exposure. We subsequently analyzed this gene set by hyperclustering, a technique that allows the data to be clustered by both expression ratio and gene annotation (e.g. Gene Ontologies). Conclusion Our results demonstrate that tobacco use affects transcription of groups of genes that are involved in proliferation and apoptosis in circulating leukocytes. These transcriptional effects include a repertoire of transcriptional changes likely to increase the incidence of neoplasia through an altered expression of genes associated with transcription and signaling, interferon responses and repression of apoptotic pathways
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