| 1. |
- Underwood, J, et al.
(author)
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Validation of a Novel Multivariate Method of Defining HIV-Associated Cognitive Impairment
- 2019
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In: Open forum infectious diseases. - : Oxford University Press (OUP). - 2328-8957. ; 6:6, s. ofz198-
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Journal article (peer-reviewed)abstract
- BackgroundThe optimum method of defining cognitive impairment in virally suppressed people living with HIV is unknown. We evaluated the relationships between cognitive impairment, including using a novel multivariate method (NMM), patient– reported outcome measures (PROMs), and neuroimaging markers of brain structure across 3 cohorts.MethodsDifferences in the prevalence of cognitive impairment, PROMs, and neuroimaging data from the COBRA, CHARTER, and POPPY cohorts (total n = 908) were determined between HIV-positive participants with and without cognitive impairment defined using the HIV-associated neurocognitive disorders (HAND), global deficit score (GDS), and NMM criteria.ResultsThe prevalence of cognitive impairment varied by up to 27% between methods used to define impairment (eg, 48% for HAND vs 21% for NMM in the CHARTER study). Associations between objective cognitive impairment and subjective cognitive complaints generally were weak. Physical and mental health summary scores (SF-36) were lowest for NMM-defined impairment (P < .05).There were no differences in brain volumes or cortical thickness between participants with and without cognitive impairment defined using the HAND and GDS measures. In contrast, those identified with cognitive impairment by the NMM had reduced mean cortical thickness in both hemispheres (P < .05), as well as smaller brain volumes (P < .01). The associations with measures of white matter microstructure and brain-predicted age generally were weaker.ConclusionDifferent methods of defining cognitive impairment identify different people with varying symptomatology and measures of brain injury. Overall, NMM-defined impairment was associated with most neuroimaging abnormalities and poorer self-reported health status. This may be due to the statistical advantage of using a multivariate approach.
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| 2. |
- Hrudkova, M., et al.
(author)
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The discovery of a planetary candidate around the evolved low-mass Kepler giant star HD 175370
- 2017
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In: Monthly Notices of the Royal Astronomical Society. - : Oxford University Press (OUP). - 0035-8711 .- 1365-2966. ; 464:1, s. 1018-1028
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Journal article (peer-reviewed)abstract
- We report on the discovery of a planetary companion candidate with a minimum mass M sin i = 4.6 +/- 1.0 M-Jupiter orbiting the K2 III giant star HD 175370 (KIC 007940959). This star was a target in our programme to search for planets around a sample of 95 giant stars observed with Kepler. This detection was made possible using precise stellar radial velocity measurements of HD 175370 taken over five years and four months using the coude echelle spectrograph of the 2-m Alfred Jensch Telescope and the fibre-fed echelle spectrograph High Efficiency and Resolution Mercator Echelle Spectrograph of the 1.2-m Mercator Telescope. Our radial velocity measurements reveal a periodic (349.5 +/- 4.5 d) variation with a semi-amplitude K = 133 +/- 25 ms(-1), superimposed on a long-term trend. A low-mass stellar companion with an orbital period of similar to 88 yr in a highly eccentric orbit and a planet in a Keplerian orbit with an eccentricity e = 0.22 are the most plausible explanation of the radial velocity variations. However, we cannot exclude the existence of stellar envelope pulsations as a cause for the low-amplitude radial velocity variations and only future continued monitoring of this system may answer this uncertainty. From Kepler photometry, we find that HD 175370 is most likely a low-mass red giant branch or asymptotic giant branch star.
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| 3. |
- Gresle, MM, et al.
(author)
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Multiple sclerosis risk variants regulate gene expression in innate and adaptive immune cells
- 2020
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In: Life science alliance. - : Life Science Alliance, LLC. - 2575-1077. ; 3:7
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Journal article (peer-reviewed)abstract
- At least 200 single-nucleotide polymorphisms (SNPs) are associated with multiple sclerosis (MS) risk. A key function that could mediate SNP-encoded MS risk is their regulatory effects on gene expression. We performed microarrays using RNA extracted from purified immune cell types from 73 untreated MS cases and 97 healthy controls and then performed Cis expression quantitative trait loci mapping studies using additive linear models. We describe MS risk expression quantitative trait loci associations for 129 distinct genes. By extending these models to include an interaction term between genotype and phenotype, we identify MS risk SNPs with opposing effects on gene expression in cases compared with controls, namely, rs2256814 MYT1 in CD4 cells (q = 0.05) and rs12087340 RF00136 in monocyte cells (q = 0.04). The rs703842 SNP was also associated with a differential effect size on the expression of the METTL21B gene in CD8 cells of MS cases relative to controls (q = 0.03). Our study provides a detailed map of MS risk loci that function by regulating gene expression in cell types relevant to MS.
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