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Träfflista för sökning "WFRF:(Holmes Elaine) srt2:(2015-2019)"

Sökning: WFRF:(Holmes Elaine) > (2015-2019)

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1.
  • Grafton, Ben, et al. (författare)
  • Confusing procedures with process when appraising the impact of cognitive bias modification on emotional vulnerability
  • 2017
  • Ingår i: British Journal of Psychiatry. - : CAMBRIDGE UNIV PRESS. - 0007-1250 .- 1472-1465. ; 211:5, s. 266-271
  • Tidskriftsartikel (refereegranskat)abstract
    • If meta-analysis is to provide valuable answers, then it is critical to ensure clarify about the questions being asked. Here, we distinguish two important questions concerning cognitive bias modification research that are not differentiated in the meta-analysis recently published by Cristea et al (2015) in this journal: (1) do the varying procedures that investigators have employed with the intention of modifying cognitive bias, on average, significantly impact emotional vulnerability?; and (2) does the process of successfully modifying cognitive bias, on average, significantly impact emotional vulnerability? We reanalyse the data from Cristea et al to address this latter question. Our new analyses demonstrate that successfully modifying cognitive bias does significantly alter emotional vulnerability. We revisit Cristea et al's conclusions in light of these findings.
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2.
  • Vorkas, Panagiotis A., et al. (författare)
  • Perturbations in fatty acid metabolism and apoptosis are manifested in calcific coronary artery disease : An exploratory lipidomic study
  • 2015
  • Ingår i: International Journal of Cardiology. - : Elsevier. - 0167-5273 .- 1874-1754. ; 197, s. 192-199
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Controversy exists concerning the beneficial or harmful effects of the presence of ectopic calcification in the coronary arteries. Additionally, further elucidation of the exact pathophysiological mechanism is needed. In this study, we sought to identify metabolic markers of vascular calcification that could assist in understanding the disease, monitoring its progress and generating hypotheses describing its pathophysiology. Methods: Untargeted lipid profiling and complementary modeling strategies were employed to compare serum samples from patients with different levels of calcific coronary artery disease (CCAD) based on their calcium score (CS). Subsequently, patients were divided into three groups: no calcification (NC; CS = 0; n = 26), mild calcification (MC; CS: 1-250; n = 27) and severe (SC; CS > 250; n = 17). Results: Phosphatidylcholine levels were found to be significantly altered in the disease states (p = 0.001-0.04). Specifically, 18-carbon fatty acyl chain (FAC) phosphatidylcholines were detected in lower levels in the SC group, while 20:4 FAC lipid species were detected in higher concentrations. A statistical trend was observed with phosphatidylcholine lipids in the MC group, showing the same tendency as with the SC group. We also observed several sphingomyelin signals present at lower intensities in SC when compared with NC or MC groups (p = 0.000001-0.01). Conclusions: This is the first lipid profiling study reported in CCAD. Our data demonstrate dysregulations of phosphatidylcholine lipid species, which suggest perturbations in fatty acid elongation/desaturation. The altered levels of the 18-carbon and 20:4 FAC lipids may be indicative of disturbed inflammation homeostasis. The marked sphingomyelin dysregulation in SC is consistent with profound apoptosis as a potential mechanism of CCAD. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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