Explore the vast range of titles available.

This book explores the many ways in which a military Scottish identity was reinvented and forged overseas amongst Scotland's diaspora from the late nineteenth century to the present day. It provides case studies from North America, South Africa, Australia and New Zealand.

Confusion has long existed on the subject of Vilhjalmur Stefansson's citizenship. A Canadian (that is, a British subject) by birth, Stefansson was brought up and educated in the United States. When his father became an American citizen in 1887, according to the laws of the time Stefansson too became an American. Dual citizenship was not then permitted by either the British or the American laws. Therefore, Stefansson was no longer a British subject. After he took command of the government sponsored Canadian Arctic Expedition in 1913, Stefansson was careful to give the impression that his status had never changed. Although Stefansson swore an oath of allegiance to King George V in May 1913, he did not take the other steps that would have been required to restore him to being Canadian. But, by an American act passed in 1907, this oath meant the loss of Stefansson's American citizenship. In the 1930s American officials informed Stefansson that he must apply for naturalisation in order to regain it. From 1913 until he received his American citizenship papers in 1937, Stefansson was a man without a country.

It is widely believed among historians that in 1920, the Danish explorer Knud Rasmussen and the Danish government challenged Canada's sovereignty over Ellesmere Island. This paper draws on a wide range of Canadian and British government files and private papers to contest this view. It demonstrates that Prime Minister Arthur Meighen and others in Ottawa were initially convinced by Vilhjalmur Stefansson that Denmark harboured territorial ambitions in the north, but most realised in the spring of 1921 that they had been mistaken. However, one civil servant, J. B. Harkin, stubbornly maintained his belief in the Danish threat. After Mackenzie King's Liberals came to power, Harkin was able to obtain a hearing for his views. It was largely due to Harkin's persistence that the first Eastern Arctic Patrol went north in 1922.

This fascinating tale of the rivalries and intrigues that played out as Canada secured the Arctic illuminates an under-explored era in Canadian foreign policy.

A growing number of endurance athletes have considered switching from a traditional high-carbohydrate/low-fat (HCLF) to a low-carbohydrate/high-fat (LCHF) eating pattern for health and performance reasons. However, few studies have examined how LCHF diets affect blood lipid profiles in highly-trained runners. In a randomized and counterbalanced, cross-over design, athletes (n = 7 men; VO2max: 61.9 ± 6.1 mL/kg/min) completed six weeks of two, ad libitum, LCHF (6/69/25% en carbohydrate/fat/protein) and HCLF (57/28/15% en carbohydrate/fat/protein) diets, separated by a two-week washout. Plasma was collected on days 4, 14, 28, and 42 during each condition and analyzed for: triglycerides (TG), LDL-C, HDL-C, total cholesterol (TC), VLDL, fasting glucose, and glycated hemoglobin (HbA1c). Capillary blood beta-hydroxybutyrate (BHB) was monitored during LCHF as a measure of ketosis. LCHF lowered plasma TG, VLDL, and TG/HDL-C (all p < 0.01). LCHF increased plasma TC, LDL-C, HDL-C, and TC/HDL-C (all p < 0.05). Plasma glucose and HbA1c were unaffected. Capillary BHB was modestly elevated throughout the LCHF condition (0.5 ± 0.05 mmol/L). Healthy, well-trained, normocholesterolemic runners consuming a LCHF diet demonstrated elevated circulating LDL-C and HDL-C concentrations, while concomitantly decreasing TG, VLDL, and TG/HDL-C ratio. The underlying mechanisms and implications of these adaptive responses in cholesterol should be explored.

The autism spectrum disorders (ASDs) are a group of conditions characterized by impairments in reciprocal social interaction and communication, and the presence of restricted and repetitive behaviors1. Individuals with an ASD vary greatly in cognitive development, which can range from above average to intellectual disability (ID)2. While ASDs are known to be highly heritable (~90%)3, the underlying genetic determinants are still largely unknown. Here, we analyzed the genome-wide characteristics of rare (<1% frequency) copy number variation (CNV) in ASD using dense genotyping arrays. When comparing 996 ASD individuals of European ancestry to 1,287 matched controls, cases were found to carry a higher global burden of rare, genic CNVs (1.19 fold, P= 0.012), especially so for loci previously implicated in either ASD and/or intellectual disability (1.69 fold, P= 3.4×10−4). Among the CNVs, there were numerous de novo and inherited events, sometimes in combination in a given family, implicating many novel ASD genes like SHANK2, SYNGAP1, DLGAP2 and the X-linked DDX53-PTCHD1 locus. We also discovered an enrichment of CNVs disrupting functional gene-sets involved in cellular proliferation, projection and motility, and GTPase/Ras signaling. Our results reveal many new genetic and functional targets in ASD that may lead to final connected pathways.