International student mobility literature review

To bring their understanding of patterns in students' study and work abroad up to date, HEFCE and the British Council, the UK National Agency for Erasmus, commissioned a review of international student mobility. Professor Russell King and Jill Ahrens of the University of Sussex, and Professor Allan Findlay of the University of Dundee undertook the review which includes new evidence from interviews with staff in higher education institutions (HEIs). A group of several UK stakeholders in international student mobility, including the organisations BUTEX (British Universities Transatlantic Exchange) and HEURO (the Association of UK Higher Education European Officers), and the Department for Business, Innovation and Skills (BIS) oversaw the work. The report brings together recent literature and data on student mobility. It looks at the trends in UK international students' mobility and compares these internationally. It also considers the causal factors for students' choice to spend time abroad, the socio-economic and demographic characteristics of mobile students, and the impact that time abroad has on their employability; and it highlights policy and practice in HEIs in respect of student mobility

British Students in the United States: motivations, experiences and career aspirations

Twelve years ago, the British educational press, and indeed the mainstream media, were consumed by the story of Laura Spence, a super-bright pupil from a Newcastle comprehensive school who, despite having five straight-As at ‘A level’ (the final secondary school exams), had been refused a place to read Medicine at Oxford after an interview there. General outrage at Oxford’s snobbishness ensued, with politician Gordon Brown, amongst others, weighing in with the criticism that Oxford favored applicants from the UK’s fee-paying independent schools (which include the elite but perversely named ‘public schools’), thereby excluding excellent applicants from state schools like Laura – especially if they come from deprived parts of the country with strong local accents. Laura instead went to the US to Harvard on a funded scholarship, completed her biochemistry degree there and returned to do postgraduate medical training at Cambridge – the other UK university which constitutes the top duo known collectively as ‘Oxbridge’. How typical is Laura’s story? Are there many British students who, as Oxbridge ‘rejects’, or fearful of being turned down for a place at the UK’s two most ancient and prestigious universities, apply abroad to widen their chances of success at other globally recognized institutions? Brooks and Waters (2009a) argue that there are indeed those like Laura who apply to US universities as a ‘second chance at success’; but our research suggests that there are many other explanations of the upward trend in favor of international study. Since the US is the most important destination for people from the UK studying abroad, the findings of this chapter are particularly important in producing a more robust understanding of the key drivers of international student mobility between one advanced economy and another. We suggest that there are some movers for whom study abroad is part of a carefully strategized plan of international career enhancement, while for others it is a product of their class habitus and family networks (see Bourdieu 1977). We would also argue that there are those who are looking for ‘something different’ yet, at the same time, desire a ‘knowable’ destination, familiar to them for example from film and television and without any great linguistic challenge. In the next section we describe our research project and its aims and methods. The main body of the chapter is made up of three sections which correspond to our three key research questions: about motivations for study in the US, about experiences there, and about future career plans. The conclusion emphasises the motivational and strategic nature of UK student migration to the US, targeted especially at universities perceived to be of high international standing. In terms of the link between study abroad and future career plans, fears about a putative British ‘brain drain’ are shown to be largely unfounded, since most students plan to return to the UK

Molecular Genetic Analysis of the C1-Inhibitor Gene in Hereditary Angio-Oedema

The development of recombinant DNA technology has enabled the molecular genetic basis of a number of inherited diseases to be established. This thesis describes the application of this technology to the study of hereditary Cl-inhibitor deficiency or hereditary angio-oedema (HAE). In addition, the findings of a clinical survey of HAE in Scotland are presented. Hereditary angio-oedema is an autosomal dominant disease in which there is either a quantitative (Type I HAE) or functional (Type II HAE) deficiency of Cl-inhibitor, this protein being an important inhibitor of complement system activation and an inhibitor of other serine protease dependent plasma mediator systems. In Type I HAE, which constitutes approximately 85% of cases, functionally normal Cl-inhibitor is present in the serum but at low levels. This contrasts with Type II HAE in which there are normal or sometimes elevated levels of serum Cl-inhibitor as measured by immunoassay, though most of this is in the form of a functionally inactive molecule. Clinically Type I and Type II disease cannot be distinguished since both present with recurrent attacks of subcutaneous or submucous oedema. In this study restriction fragment length polymorphism (RFLP) analysis of the Cl-inhibitor gene was carried out on genomic DNA isolated from 25 normal, unrelated individuals and on genomic DNA samples from 12 Type I HAE kindred and two Type II HAE kindred. A total of 38 restriction endonucleases were used to digest each DNA sample followed by agarose gel electrophoresis and Southern blotting of each sample onto nylon hybridisation membranes. Each digested DNA sample was then probed with a radiolabelled exon 2-8 Cl-inhibitor cDNA which represents the full protein coding sequence of the Cl-inhibitor gene. Four of the 12 Type I HAE kindred were shown to have unique disease-specific RFLPs affecting one allele of the Cl-inhibitor gene. Localisation studies clearly demonstrated that the gene mutations responsible for each RFLP affected exon 4, the 3' exon/ intron boundary of exon 6, exon 7 and exon 8 of the Cl-inhibitor gene. Family studies showed that each mutation co-segregated with the disease. Mutations affecting exon 6 and exon 8 had not been reported previously in Type I HAE. Both these mutations were small, possibly point mutations and it is highly likely that the mutation at the extreme 3' boundary of exon 6 results in loss of the donor splice site for excision of the sixth intron during RNA processing. The effect of the small exon 8 mutation is less certain. Nucleotide sequence analysis of both these mutated areas is currently being undertaken. This should help to establish their likely effects. The remaining two mutations, which were shown to be a complete exon 4 deletion and a complete exon 7 deletion, had recently been documented in Type I HAE by other investigators. No RFLPs were identified in the two Type II HAE kindred. Detection of a disease-specific RFLP in 33% of the Type I HAE kindred tested represents a significantly higher detection rate than other published studies in which 16% was the previous maximum. This increase appears to reflect the greater number of restriction enzymes employed since no other methodological differences were apparent. These results suggest that Type I HAE is likely to be due to a multiplicity of gene mutations as is seen in other genetic diseases including B-thalassaemia, haemophilia A and haemophilia B. Cl-inhibitor gene RFLPs were generated by the restriction enzymes Kpn I and Hgi AI in the normal population. The Kpn I RFLP had not been reported previously and was shown to be due to a mutation that lay approximately 10kb downstream of the Cl-inhibitor gene. The Hgi AI RFLP had already been observed in normal individuals from North America and arose due to a point mutation within the Cl-inhibitor gene itself. Both RFLPs fulfill criteria which are likely to make them useful as indirect genetic markers of the mutant Cl-inhibitor allele in those HAE families who lack a disease-specific RFLP. The clinical survey of HAE in Scotland identified a total of 46 patients which represents a disease incidence of approximately one patient per 110,000 of the population. This is the first documented attempt to calculate disease incidence in Scotland. It became evident from the survey that despite the development of more effective treatment regimes in recent years, significant disease-associated morbidity and mortality still existed within the relatively young patient population. This observation provided ample justification for studying the molecular genetics of HAE since an understanding of this aspect of the disease is central to future disease prevention in the form of prenatal diagnosis

Electrocardiographic Interpretation by Computer

journal articleBiomedical Informatic