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Sökning: WFRF:(Kavanagh D)

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  • Jaffee, E. M., et al. (författare)
  • Future cancer research priorities in the USA: a Lancet Oncology Commission
  • 2017
  • Ingår i: Lancet Oncology. - 1470-2045. ; 18:11, s. E653-E706
  • Forskningsöversikt (refereegranskat)abstract
    • We are in the midst of a technological revolution that is providing new insights into human biology and cancer. In this era of big data, we are amassing large amounts of information that is transforming how we approach cancer treatment and prevention. Enactment of the Cancer Moonshot within the 21st Century Cures Act in the USA arrived at a propitious moment in the advancement of knowledge, providing nearly US$ 2 billion of funding for cancer research and precision medicine. In 2016, the Blue Ribbon Panel (BRP) set out a roadmap of recommendations designed to exploit new advances in cancer diagnosis, prevention, and treatment. Those recommendations provided a high-level view of how to accelerate the conversion of new scientific discoveries into effective treatments and prevention for cancer. The US National Cancer Institute is already implementing some of those recommendations. As experts in the priority areas identified by the BRP, we bolster those recommendations to implement this important scientific roadmap. In this Commission, we examine the BRP recommendations in greater detail and expand the discussion to include additional priority areas, including surgical oncology, radiation oncology, imaging, health systems and health disparities, regulation and financing, population science, and oncopolicy. We prioritise areas of research in the USA that we believe would accelerate efforts to benefit patients with cancer. Finally, we hope the recommendations in this report will facilitate new international collaborations to further enhance global efforts in cancer control.
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  • Huckins, Laura M., et al. (författare)
  • Gene expression imputation across multiple brain regions provides insights into schizophrenia risk
  • 2019
  • Ingår i: Nature genetics. - 1546-1718. ; 51:4, s. 659-
  • Tidskriftsartikel (refereegranskat)abstract
    • Transcriptomic imputation approaches combine eQTL reference panels with large-scale genotype data in order to test associations between disease and gene expression. These genic associations could elucidate signals in complex genome-wide association study (GWAS) loci and may disentangle the role of different tissues in disease development. We used the largest eQTL reference panel for the dorso-lateral prefrontal cortex (DLPFC) to create a set of gene expression predictors and demonstrate their utility. We applied DLPFC and 12 GTEx-brain predictors to 40,299 schizophrenia cases and 65,264 matched controls for a large transcriptomic imputation study of schizophrenia. We identified 413 genic associations across 13 brain regions. Stepwise conditioning identified 67 non-MHC genes, of which 14 did not fall within previous GWAS loci. We identified 36 significantly enriched pathways, including hexosaminidase-A deficiency, and multiple porphyric disorder pathways. We investigated developmental expression patterns among the 67 non-MHC genes and identified specific groups of pre- and postnatal expression.
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  • Ripke, Stephan, et al. (författare)
  • Biological insights from 108 schizophrenia-associated genetic loci
  • 2014
  • Ingår i: Nature. - 0028-0836. ; 511:7510, s. 421-427
  • Tidskriftsartikel (refereegranskat)abstract
    • Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia.
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7.
  • Akbarian, S, et al. (författare)
  • The PsychENCODE project
  • 2015
  • Ingår i: Nature neuroscience. - 1546-1726. ; 18:12, s. 1707-1712
  • Tidskriftsartikel (refereegranskat)
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8.
  • Marshall, Christian R., et al. (författare)
  • Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects
  • 2017
  • Ingår i: Nature Genetics. - 1061-4036. ; 49:1, s. 27-35
  • Tidskriftsartikel (refereegranskat)abstract
    • Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (odds ratio (OR) = 1.11, P = 5.7 x 10(-15)), which persisted after excluding loci implicated in previous studies (OR = 1.07, P = 1.7 x 10(-6)). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 x 10(-11)) and neurobehavioral phenotypes in mouse (OR = 1.18, P = 7.3 x 10(-5)). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by nonallelic homologous recombination.
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9.
  • Newnham, D. A., et al. (författare)
  • Observations and Modeling of Increased Nitric Oxide in the Antarctic Polar Middle Atmosphere Associated With Geomagnetic Storm-Driven Energetic Electron Precipitation
  • 2018
  • Ingår i: Journal of Geophysical Research - Space Physics. - 2169-9380. ; 123:7, s. 6009-6025
  • Tidskriftsartikel (refereegranskat)abstract
    • Nitric oxide (NO) produced in the polar middle and upper atmosphere by energetic particle precipitation depletes ozone in the mesosphere and, following vertical transport in the winter polar vortex, in the stratosphere. Medium-energy electron (MEE) ionization by 30-1,000 keV electrons during geomagnetic storms may have a significant role in mesospheric NO production. However, questions remain about the relative importance of direct NO production by MEE at altitudes similar to 60-90 km versus indirect NO originating from auroral ionization above 90 km. We investigate potential drivers of NO variability in the southern-hemisphere mesosphere and lower thermosphere during 2013-2014. Contrasting geomagnetic activity occurred during the two austral winters, with more numerous moderate storms in the 2013 winter. Ground-based millimeter-wave observations of NO from Halley, Antarctica, are compared with measurements by the Solar Occultation For Ice Experiment (SOFIE) spaceborne spectrometer. NO partial columns over the altitude range 65-140 km from the two observational data sets show large day-to-day variability and significant disagreement, with Halley values on average 49% higher than the corresponding SOFIE data. SOFIE NO number densities, zonally averaged over geomagnetic latitudes -59 degrees to -65 degrees, are up to 3 x 10(8)/cm(3) higher in the winter of 2013 compared to 2014. Comparisons with a new version of the Whole Atmosphere Community Climate Model, which includes detailed D-region ion chemistry (WACCM-SIC) and MEE ionization rates, show that the model underestimates NO in the winter lower mesosphere whereas thermospheric abundances are too high. This indicates the need to further improve and verify WACCM-SIC with respect to MEE ionization, thermospheric NO chemistry, and vertical transport.
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10.
  • Sabado, R.L., et al. (författare)
  • In vitro priming recapitulates in vivo HIV-1 specific T cell responses, revealing rapid loss of virus reactive CD4+ T cells in acute HIV-1 infection
  • 2009
  • Ingår i: PLoS ONE. - 1932-6203. ; 4:1, s. e4256
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The requirements for priming of HIV-specific T cell responses initially seen in infected individuals remain to be defined. Activation of T cell responses in lymph nodes requires cell-cell contact between T cells and DCs, which can give concurrent activation of T cells and HIV transmission. Methodology: The study aim was to establish whether DCs pulsed with HIV-1 could prime HIV-specific T cell responses and to characterize these responses. Both infectious and aldrithiol-2 inactivated noninfectious HIV-1 were compared to establish efficiencies in priming and the type of responses elicited. Findings: Our findings show that both infectious and inactivated HIV-1 pulsed DCs can prime HIV-specific responses from na�ve T cells. Responses included several CD4+ and CD8+ T cell epitopes shown to be recognized in vivo by acutely and chronically infected individuals and some CD4+ T cell epitopes not identified previously. Follow up studies of acute and recent HIV infected samples revealed that these latter epitopes are among the earliest recognized in vivo, but the responses are lost rapidly, presumably through activation-induced general CD4+ T cell depletion which renders the newly activated HIV-specific CD4+ T cells prime targets for elimination. Conclusion: Our studies highlight the ability of DCs to efficiently prime na�ve T cells and induce a broad repertoire of HIV-specific responses and also provide valuable insights to the pathogenesis of HIV-1 infection in vivo.
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