ABSTRACT
BACKGROUND: The governance structures associated with health data are evolving in response to advances in digital technologies that enable new ways of capturing, using, and sharing different types of data. Increasingly, health data moves between different contexts such as from healthcare to research, or to commerce and marketing. Crossing these contextual boundaries has the potential to violate societal expectations about the appropriate use of health data and diminish public trust. Understanding citizens' views on the acceptability of and preferences for data use in different contexts is essential for developing information governance policies in these new contexts. METHODS: Focus group design presenting data sharing scenarios in England, Iceland, and Sweden. RESULTS: Seventy-one participants were recruited. Participants supported the need for data to help understand the observable world, improve medical research, the quality of public services, and to benefit society. However, participants consistently identified the lack of information, transparency and control as barriers to trusting organisations to use data in a way that they considered appropriate. There was considerable support for fair and transparent data sharing practices where all parties benefitted. CONCLUSION: Data governance policy should involve all stakeholders' perspectives on an ongoing basis, to inform and implement changes to health data sharing practices that accord with stakeholder views. The Findings showed that (1) data should be used for ethical purposes even when there was commercial interest; (2) data subjects and/or public institutions that provide and share data should also receive benefits from the sharing of data; (3) third parties use of data requires greater transparency and accountability than currently exists, (4) there should be greater information provided to empower data subjects.
Subject(s)
Information Dissemination , Trust , England , Focus Groups , Humans , Iceland , Information Dissemination/ethics , SwedenABSTRACT
Several copy number variants have been associated with neuropsychiatric disorders and these variants have been shown to also influence cognitive abilities in carriers unaffected by psychiatric disorders. Previously, we associated the 15q11.2(BP1-BP2) deletion with specific learning disabilities and a larger corpus callosum. Here we investigate, in a much larger sample, the effect of the 15q11.2(BP1-BP2) deletion on cognitive, structural and functional correlates of dyslexia and dyscalculia. We report that the deletion confers greatest risk of the combined phenotype of dyslexia and dyscalculia. We also show that the deletion associates with a smaller left fusiform gyrus. Moreover, tailored functional magnetic resonance imaging experiments using phonological lexical decision and multiplication verification tasks demonstrate altered activation in the left fusiform and the left angular gyri in carriers. Thus, by using convergent evidence from neuropsychological testing, and structural and functional neuroimaging, we show that the 15q11.2(BP1-BP2) deletion affects cognitive, structural and functional correlates of both dyslexia and dyscalculia.
Subject(s)
Cognition/physiology , DNA Copy Number Variations/genetics , Dyscalculia/genetics , Dyslexia/genetics , Intellectual Disability/genetics , Adolescent , Adult , Aged , Chromosome Aberrations , Chromosome Deletion , Chromosomes, Human, Pair 15/genetics , Developmental Disabilities/genetics , Female , Functional Neuroimaging/methods , Functional Neuroimaging/standards , Heterozygote , Humans , Iceland/epidemiology , Magnetic Resonance Imaging/methods , Male , Middle Aged , Neuropsychological Tests/standards , Phenotype , Temporal Lobe/anatomy & histology , Temporal Lobe/diagnostic imaging , Young AdultABSTRACT
The establishment of cell polarity in budding yeast involves assembly of actin filaments at specified cortical domains. Elucidation of the underlying mechanism requires an understanding of the machinery that controls actin polymerization and how this machinery is in turn controlled by signaling proteins that respond to polarity cues. We showed previously that the yeast orthologue of the Wiskott-Aldrich Syndrome protein, Bee1/Las17p, and the type I myosins are key regulators of cortical actin polymerization. Here, we demonstrate further that these proteins together with Vrp1p form a multivalent Arp2/3-activating complex. During cell polarization, a bifurcated signaling pathway downstream of the Rho-type GTPase Cdc42p recruits and activates this complex, leading to local assembly of actin filaments. One branch, which requires formin homologues, mediates the recruitment of the Bee1p complex to the cortical site where the activated Cdc42p resides. The other is mediated by the p21-activated kinases, which activate the motor activity of myosin-I through phosphorylation. Together, these findings provide insights into the essential processes leading to polarization of the actin cytoskeleton.
