scispace - formally typeset
Search or ask a question

Showing papers by "Fiona S. L. Brinkman published in 2014"


Journal ArticleDOI
TL;DR: It is thought that the prevailing focus on an individual’s genes and biology insufficiently incorporates the important role of environmental factors in disease etiology and health, and it will require a fundamental change to the current research agenda and public health policies to emphasize the role of the social and physical environments and related epigenetic changes.
Abstract: The brave new world envisioned by proponents of personalized medicine has attracted considerable interest and investment during the past decade or so. The excitement is understandable because personalized medicine promises to drastically improve individual health and make more efficient use of existing resources, changing both health care and public health for the better. Improved use of resources is becoming particularly important, as many national healthcare schemes are straining to maintain affordable health care of acceptable quality under the combined pressures of rising costs, an aging population and the increasing prevalence of many chronic and common diseases. Although not a panacea for all these problems, personalized medicine could theoretically reduce healthcare costs, as an individual’s genetic or other biological information could be used to make better or earlier diagnoses of disease, apply cheaper, preventive measures to decrease disease risk, and make more efficient use of therapeutic options. However, there remains a considerable gap between theory and reality, and we think that the prevailing focus on an individual’s genes and biology insufficiently incorporates the important role of environmental factors in disease etiology and health. Including these factors in our approach to personalized medicine and population health should bring that theory closer to reality. However, it will require a fundamental change to the current research agenda and public health policies to emphasize the role of the social and physical environments and related epigenetic changes.

39 citations


Journal ArticleDOI
TL;DR: It is argued that there is benefit to regarding the global human microbiome as a collective good (i.e., a Microbial Commons) and the situation where each individual benefits from overexploitation of a public resource.
Abstract: Many studies have shown how the human gut microbiome can be altered by diet, antibiotics, and other factors. All of these factors can contribute to dysbiosis, where the services typically provided by symbiotic microflora are disrupted because of shifts in function or diversity. Just as humans have impacted many large animal species in the environment, drastic changes in human lifestyle over the past century may have altered the global pool of human-associated microbes; if so, these shifts may pose substantial threats to individual and public health. Hardin (1) defined “The Tragedy of the Commons” as a situation where each individual benefits from overexploitation of a public resource, and we argue that there is benefit to regarding the global human microbiome as a collective good (i.e., a Microbial Commons).

19 citations


Journal ArticleDOI
TL;DR: The present report is the first to describe norovirus GI.6 infection in patients with the G428A nonsense mutation in FUT2; this cluster of cases suggests that the G 428A mutation inFUT2 may not confer resistance to norov virusGI.6.
Abstract: BACKGROUND: The availability of direct-to-consumer personalized genetic testing has enabled the public to access and interpret their own genetic information. Various genetic traits can be determined including resistance to norovirus through a nonsense mutation (G428A) in the FUT2 gene. Although this trait is believed to confer resistance to the most dominant norovirus genotype (GII.4), the spectrum of resistance to other norovirus strains is unknown. The present report describes a cluster of symptomatic norovirus GI.6 infection in a family identified to have norovirus resistance through personalized genetic testing.

7 citations


Book ChapterDOI
TL;DR: It is described here how the Pseudomonas Genome Database and other bioinformatics resources can be leveraged to help PseUDomonas researchers "mine" Pseudomanas genomes, and associated genome-scale data, to facilitate new discovery.
Abstract: Pseudomonas species were targeted early for genomic studies since they were noted for their diverse metabolic capacity, ability to inhabit a wide range of environments and hosts, and include notable human and agriculturally relevant pathogens As more genomes are sequenced, the power of genome-scale analyses are increasing and a wide range of analyses are now possible The Pseudomonas Genome database has contributed to this effort by providing peer-reviewed, continually updated annotations of the Pseudomonas aeruginosa PAO1 reference strain genome plus integrated data and analyses of related Pseudomonas species Analyses are now available via multiple resources to facilitate identification and characterization of drug targets, virulence factors, regulatory elements, genomic islands, genome rearrangements, orthologs, single nucleotide polymorphisms, and multiple other gene/protein-based analyses from gene expression to protein structure We describe here how the Pseudomonas Genome Database and other bioinformatics resources can be leveraged to help Pseudomonas researchers "mine" Pseudomonas genomes, and associated genome-scale data, to facilitate new discovery

3 citations


Journal ArticleDOI
TL;DR: AERO OWL file: http://purl.obolibrary.org/obo/aero.owl Melanie Courtot: mcourtot@gmail.com Effective automated classification using ontology-based annotation: experience with analysis of adverse event reports Melanie CourtOT.
Abstract: AERO OWL file: http://purl.obolibrary.org/obo/aero.owl Melanie Courtot: mcourtot@gmail.com Effective automated classification using ontology-based annotation: experience with analysis of adverse event reports Melanie Courtot1, Alan Ruttenberg2 , William W.L. Hsiao3, Fiona S.L. Brinkman4 and Ryan R. Brinkman1,5 1 BC Cancer Agency, Vancouver, BC, Canada, 2 School of Dental Medicine, University at Buffalo, Buffalo, NY, USA, 3 Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada, 4 Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC, Canada, 5 Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada