15 research outputs found

    Manual / Issue 1 / Hand in Hand

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    Manual, a journal about art and its making. Hand in Hand. The inaugural issue of The Manual, a twice-yearly publication by the RISD Museum. The theme of this first issue is “hand in hand,” a phrase first recorded in the 16th century. Its early usage described the clasping of palm to palm, but the term has since come to encompass more than this literal meaning. To be hand in hand is also to be connected, joined, concurrent, well matched. Thumb through these pages to find rigorous, imaginative musings as artists and academics make solid contact, gesture wildly, and put their fingers on the pulse of new ideas. In your grasp, an open invitation to explore objects and materials, and the meanings and makings of things. Softcover, 48 pages. Published 2013 by the RISD Museum. Proceeds from RISD Museum publications support the work of the museum. Manual 1 (Hand in Hand) contributors include Sheila Bonde, Robert Brinkerhoff, Kate Irvin, James McShane, Maureen C. O’Brien, and Elizabeth A. Williams.https://digitalcommons.risd.edu/risdmuseum_journals/1000/thumbnail.jp

    Investigation of hospital discharge cases and SARS-CoV-2 introduction into Lothian care homes

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    Background The first epidemic wave of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in Scotland resulted in high case numbers and mortality in care homes. In Lothian, over one-third of care homes reported an outbreak, while there was limited testing of hospital patients discharged to care homes. Aim To investigate patients discharged from hospitals as a source of SARS-CoV-2 introduction into care homes during the first epidemic wave. Methods A clinical review was performed for all patients discharges from hospitals to care homes from 1st March 2020 to 31st May 2020. Episodes were ruled out based on coronavirus disease 2019 (COVID-19) test history, clinical assessment at discharge, whole-genome sequencing (WGS) data and an infectious period of 14 days. Clinical samples were processed for WGS, and consensus genomes generated were used for analysis using Cluster Investigation and Virus Epidemiological Tool software. Patient timelines were obtained using electronic hospital records. Findings In total, 787 patients discharged from hospitals to care homes were identified. Of these, 776 (99%) were ruled out for subsequent introduction of SARS-CoV-2 into care homes. However, for 10 episodes, the results were inconclusive as there was low genomic diversity in consensus genomes or no sequencing data were available. Only one discharge episode had a genomic, time and location link to positive cases during hospital admission, leading to 10 positive cases in their care home. Conclusion The majority of patients discharged from hospitals were ruled out for introduction of SARS-CoV-2 into care homes, highlighting the importance of screening all new admissions when faced with a novel emerging virus and no available vaccine

    SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

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    Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant

    Genetic ancestry, skin reflectance and pigmentation genotypes in association with serum vitamin D metabolite balance

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    BACKGROUND: Lower serum vitamin D (25(OH)D) among individuals with African ancestry is attributed primarily to skin pigmentation. However, the influence of genetic polymorphisms controlling for skin melanin content has not been investigated. Therefore, we investigated differences in non-summer serum vitamin D metabolites according to self-reported race, genetic ancestry, skin reflectance and key pigmentation genes (SLC45A2 and SLC24A5). MATERIALS AND METHODS: Healthy individuals reporting at least half African American or half European American heritage were frequency matched to one another on age (+/− 2 years) and sex. 176 autosomal ancestry informative markers were used to estimate genetic ancestry. Melanin index was measured by reflectance spectrometry. Serum vitamin D metabolites (25(OH)D(3), 25(OH)D(2) and 24,25(OH)(2)D(3)) were determined by high performance liquid chromatography (HPLC) tandem mass spectrometry. Percent 24,25(OH)(2)D(3) was calculated as a percent of the parent metabolite (25(OH)D(3)). Stepwise and backward selection regression models were used to identify leading covariates. RESULTS: Fifty African Americans and 50 European Americans participated in the study. Compared with SLC24A5 111(Thr) homozygotes, individuals with the SLC24A5 111(Thr/Ala) and 111(Ala/Ala) genotypes had respectively lower levels of 25(OH)D(3) (23.0 and 23.8 nmol/L lower, p-dominant=0.007), and percent 24,25(OH)(2)D(3) (4.1 and 5.2 percent lower, p-dominant=0.003), controlling for tanning bed use, vitamin D/fish oil supplement intake, race/ethnicity, and genetic ancestry. Results were similar with melanin index adjustment, and were not confounded by glucocorticoid, oral contraceptive, or statin use. CONCLUSIONS: The SLC24A5 111(Ala) allele was associated with lower serum vitamin 25(OH)D(3) and lower percent 24,25(OH)(2)D(3), independently from melanin index and West African genetic ancestry
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