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Articles by T Lund
Total Records ( 2 ) for T Lund
  T Lund , K. B Christensen , M Vaez , M Labriola , M Josephson , E Villadsen and M. Voss

Aim: To investigate potential differences in sickness absence among public sector employees in Sweden and Denmark, and to what extent a difference was associated with age, gender, physical and psychosocial work environment exposures, lifestyle factors, self-rated health or work ability. Methods: In 2000, two cross-sectional samples of 8562 public sector employees in Sweden and Denmark were surveyed. The study outcome, self-reported number of sick-leave days the year preceding interview, was dichotomized into 7 days or less, and more than 7 days. Chi square test was used to analyse distribution of dependent and independent variables in the two sub-cohorts. Stratified logistic regression analysis was performed to identify causes for absence within the two sub-cohorts, and logistic regression analysis was performed to study differences in sickness absence levels between the two sub-cohorts. Results: More subjects from the Swedish study population reported more than 7 days of sickness absence. Factors associated with sickness absence were largely similar in the two countries. The difference in absence level between Sweden and Denmark was not associated with differences in age, gender, skill level, lifestyle, psychosocial or physical work environment, musculoskeletal symptoms or self-rated health, whereas work ability score decreased the difference in sickness absence level. Conclusion: The results could indicate an increased retention of employees with health problems in the Swedish labour market compared with the Danish labour market. A possible explanation for the differences in sickness absence ascertained in this study could be due to differences in the sickness insurance legislation.

  D. R Brims , J Qian , I Jarchum , L Mikesh , E Palmieri , U. A Ramagopal , V. N Malashkevich , R. J Chaparro , T Lund , M Hattori , J Shabanowitz , D. F Hunt , S. G Nathenson , S. C Almo and T. P. DiLorenzo

Type 1 diabetes (T1D) is an autoimmune disease characterized by T cell-mediated destruction of insulin-producing pancreatic β cells. In both humans and the non-obese diabetic (NOD) mouse model of T1D, class II MHC alleles are the primary determinant of disease susceptibility. However, class I MHC genes also influence risk. These findings are consistent with the requirement for both CD4+ and CD8+ T cells in the pathogenesis of T1D. Although a large body of work has permitted the identification of multiple mechanisms to explain the diabetes-protective effect of particular class II MHC alleles, studies examining the protective influence of class I alleles are lacking. Here, we explored this question by performing biochemical and structural analyses of the murine class I MHC molecule H-2Kwm7, which exerts a diabetes-protective effect in NOD mice. We have found that H-2Kwm7 molecules are predominantly occupied by the single self-peptide VNDIFERI, derived from the ubiquitous protein histone H2B. This unexpected finding suggests that the inability of H-2Kwm7 to support T1D development could be due, at least in part, to the failure of peptides from critical β-cell antigens to adequately compete for binding and be presented to T cells. Predominant presentation of a single peptide would also be expected to influence T-cell selection, potentially leading to a reduced ability to select a diabetogenic CD8+ T-cell repertoire. The report that one of the predominant peptides bound by T1D-protective HLA-A*31 is histone derived suggests the potential translation of our findings to human diabetes-protective class I MHC molecules.

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