A re-appraisal of the career and reputation of William Laud, Archbishop of Canterbury, with specific reference to Scotland 1633-1640

William Laud, Archbishop of Canterbury (1633-1645) has gained a reputation as a figure of controversy, from his days as a fellow at St John’s College, Oxford during the early years of the reign of James I, through to the height of his career as senior ecclesiastical adviser to Charles I in the 1630s. Laud was associated with the most innovatory and increasingly unpopular religious policies implemented by Charles I in three separate kingdoms. However, while Laud’s contribution to English and Irish religious policy has been well documented, his role in Scotland remains one of the least explored aspects of his career. As a result, his intervention in the Scottish church appears to be more cautious than it was in either England or Ireland. This thesis, therefore, seeks to construct a comprehensive account of all Laud’s interventions in and associations with Scotland from after the coronation visit in June 1633 until his house arrest in December 1640 in the opening weeks of the Long Parliament. A detailed analysis of Laud’s contribution to some of the most high profile policies put in place under Charles I in Scotland will demonstrate that where evidence of Laud’s involvement exists, it was overt and authoritarian, but that the extant evidence is often fragmented and incomplete, particularly when compared with the evidence for England and Ireland. While recent historiography has seen a shift in emphasis towards the ‘British’ dimension to Caroline religion, the focus of this thesis will be primarily on Scotland, and Scottish policy itself. In the process, it offers an untapped case study from which to examine William Laud, Charles I and their working partnership

A re-appraisal of the career and reputation of William Laud, Archbishop of Canterbury, with specific reference to Scotland 1633-1640

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Reduction of nitrate in water over supported nickel catalysts toward purification of polluted groundwater [an abstract of dissertation and a summary of dissertation review]

Prader–Willi syndrome (PWS), a neurodevelopmental disorder caused by loss of paternal gene expression from 15q11–q13, is characterised by growth retardation, hyperphagia and obesity. However, as single gene mutation mouse models for this condition display an incomplete spectrum of the PWS phenotype, we have characterised the metabolic impairment in a mouse model for ‘full’ PWS, in which deletion of the imprinting centre (IC) abolishes paternal gene expression from the entire PWS cluster. We show that PWS-ICdel mice displayed postnatal growth retardation, with reduced body weight, hyperghrelinaemia and marked abdominal leanness; proportionate retroperitoneal, epididymal/omental and inguinal white adipose tissue (WAT) weights being reduced by 82%, 84% and 67%, respectively. PWS-ICdel mice also displayed a 48% reduction in proportionate interscapular brown adipose tissue (isBAT) weight with significant ‘beiging’ of abdominal WAT, and a 2°C increase in interscapular surface body temperature. Maintenance of PWS-ICdel mice under thermoneutral conditions (30°C) suppressed the thermogenic activity in PWS-ICdel males, but failed to elevate the abdominal WAT weight, possibly due to a normalisation of caloric intake. Interestingly, PWS-ICdel mice also showed exaggerated food hoarding behaviour with standard and high-fat diets, but despite becoming hyperphagic when switched to a high-fat diet, PWS-ICdel mice failed to gain weight. This evidence indicates that, unlike humans with PWS, loss of paternal gene expression from the PWS cluster in mice results in abdominal leanness. Although reduced subcutaneous insulation may lead to exaggerated heat loss and thermogenesis, abdominal leanness is likely to arise from a reduced lipid storage capacity rather than increased energy utilisation in BAT