'Levelling up' social mobility? Comparing the social and spatial mobility for university graduates across districts of Britain.

Social and spatial mobility have been subject to substantial recent sociological and policy debate. Complementing other recent work, in this paper we explore these patterns in relation to higher education. Making use of high-quality data from the higher education statistics agency (HESA), we ran a set of multilevel models to test whether the local authority areas where young people grow up influence social and spatial mobility into a higher professional or managerial job on graduation. We found entry to these patterns reflect pre-existing geographies of wealth and income, with more affluent rural and suburban areas in South-East England having higher levels of entry to these occupations. Graduates clustered from major cities tended to be spatially immobile and those from peripheral areas further away from these cities show a higher density of long-distance moves following graduation. We also explored the intersection between social and spatial mobility for graduates with the economic geography of Britain, showing that access to high-class occupations is not necessarily associated with long-distance moves across most British districts. Our evidence further suggests that the 'London effect', where working-class students have higher school attainment than their peers elsewhere, may not continue through to graduate employment.

Ten years' experience of enzyme infusion therapy of Norrbottnian (type 3) Gaucher disease.

AIM: To study the long-term effects of enzyme replacement therapy on the neurological signs of chronic neuronopathic Gaucher disease and to evaluate some biochemical parameters for monitoring the treatment. METHODS: Eight patients from the Norrbottnian cohort were followed during 10 y of treatment. They were followed with regular clinical observations, biochemical tests and psychometric testing. RESULTS: After the start of treatment, their general well-being improved and was stable during the follow-up. In three of the patients there were some indications of slow neurological deterioration. The mean results of psychometric testing did not decrease. Glucosylceramide and chitotriosidase levels were useful in monitoring the treatment. The chemokine CCL18 also seems to be a useful parameter for future monitoring. CONCLUSIONS: Enzyme replacement therapy seems to slow down further neurological and mental deterioration in mild chronic neuronopathic (type 3) Gaucher disease.

Lack of correlation between the reduction of serum immunoglobulin concentration and the CTG repeat expansion in patients with type 1 dystrophia [correction of Dystrofia] myotonica.

The length of the CTG repeat in the 3' untranslated region of the DMPK gene is considered to be associated with clinical severity in type 1 Dystrofia Myotonica (DM1) and has also been suggested to correlate with the degree of deficiency of IgG noted in these patients. Total serum level of IgG and IgG subclasses was therefore measured in 61 Swedish patients with DM1, the largest number of patients investigated to date in this respect. Almost half (44%) of the DM1 patients showed a serum concentration of IgG below the normal range. Deficiency of IgG1, IgG2 or IgG3 was noted in 26%, 7% and 20% of the patients, respectively. As transcription of genes 3' of the DMPK gene on chromosome 19 is reduced in DM1 patients, a decreased expression of the alpha chain of the receptor involved in IgG catabolism, FcRn, may theoretically be responsible for the low serum IgG in DM1 patients. No correlation was however found between the number of CTG repeats, levels of FcRn transcripts in either muscle tissue or lymphocytes and serum IgG levels.

Abnormal release of incretins and cortisol after oral glucose in subjects with insulin-resistant myotonic dystrophy.

OBJECTIVE: Although the incretins, gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), as well as glucagon and cortisol, are known to influence islet function, the role of these hormones in conditions of insulin resistance and development of type 2 diabetes is unknown. An interesting model for the study of hormonal perturbations accompanying marked insulin resistance without concomitant diabetes is myotonic dystrophy (DM1). DESIGN: The work was carried out in an out-patient setting. METHODS: An oral glucose tolerance test was performed in 18 males with DM1 and 18 controls to examine the release of incretins and counter-regulatory hormones. Genetic analyses were also performed in patients. RESULTS: We found that the increment in GLP-1 after oral glucose was significantly greater in patients, while there was no significant difference in GIP or glucagon responses between patients and controls, although long CTG repeat expansions were associated with a more pronounced GIP response. Interestingly, the GLP-1 response to oral glucose correlated with the insulin response in patients but not in controls whereas, in controls, the insulin response closely correlated with the GIP response. Furthermore, cortisol and ACTH levels increased paradoxically in patients after glucose; this was more pronounced in patients with long CTG repeat expansions. CONCLUSIONS: This study showed that the GLP-1 and ACTH/cortisol responses to oral glucose are abnormal in insulin-resistant DM1 patients and that CTG triplet repeats are linked to GIP release. These abnormalities may contribute both to the severe insulin resistance and hyperinsulinemia in DM1 and to the preservation of adequate islet function, enabling glucose tolerance to be normal in spite of this marked insulin resistance in DM1.