No abstract
Research is a core function of cultural heritage organisations. Inevitably, the undertaking of research by galleries, libraries, archives and museums (the GLAM sector) leads to the creation of vast quantities of research data. Yet despite growing recognition that research data must be managed if it is to be exploited effectively, and in spite of increasing understanding of research data management practices and needs, particularly in the higher education sector, knowledge of research data management in cultural heritage organisations remains extremely limited. This paper represents an attempt to address the limited awareness of research data management in the cultural heritage sector. It presents the results of a data management audit conducted at Historic Royal Palaces (HRP) in 2018. The study reveals that research data management at HRP is underdeveloped, while highlighting some causes for optimism. The results of the study are compared to the results of similar studies conducted in UK higher education institutions (HEIs), highlighting the many discrepancies in the ways that research data is managed at HRP and in the HE sector. Recognition of these differences and similarities, it is argued, is necessary for the development of better research data management practices and tools for the heritage sector.
Reduced nephron number is linked with chronic kidney disease and adult onset hypertension. Defects in the formation of nephrons are a major factor in determining nephron number. Multiple genome wide association studies have strongly linked SHROOM3 with altered kidney function and chronic kidney disease. Yet, the role of SHROOM3 in kidney function and nephron formation is not known. We utilized Shroom3‐/‐ and Shroom3+/‐ mutant mice containing a gene trap β‐galactosidase reporter to analyze Shroom3 expression. LacZ expression localized shroom3 to cap mesenchyme and podocytes throughout kidney development. LacZ expression was only observed in the collecting ducts after E15.5. LacZ expression was maintained in the podocyte and collecting ducts in mature kidneys. Immunohistochemistry using a Shroom3 antibody confirmed the dynamic spatial and temporal expression pattern. Histological analysis of kidneys from Shroom3‐/‐ mice demonstrated numerous condensed and cystic glomeruli at E13.5. Abnormal glomeruli demonstrated markedly reduced expression of the podocyte markers Wilms’ Tumor Suppressor‐1 (Wt‐1) and Nephrin in Shroom3‐/‐ mice at E13.5 and E14.5. Glomerular counting at E18.5 demonstrated a 1.6‐fold reduction in glomerular number in Shroom3‐/‐ mice when compared to wild type (n=3). Analysis of postnatal Shroom3 +/‐ mice revealed focal segmental glomerulosclerosis (FSGS), glomerular hypercellularity, and hydronephrosis. Postnatal expression of Wt‐1 was similar to wild‐type mice but nephrin expression was virtually absent. In summary Shroom3 exhibits a dynamic expression pattern and the absence of Shroom3 leads to early defects in nephrogenesis resulting in reduced glomerular number and postnatal glomerular diseases. We conclude that Shroom3 is required for nephron formation or maintenance.
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