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  • Wahlin, Åke, et al. (författare)
  • How health and biological age influence chronological age and sex differences in cognitive aging: Moderating, mediating, or both?
  • 2006
  • Ingår i: Psychology and Aging. - 0882-7974. ; 21:2, s. 318-332
  • Tidskriftsartikel (refereegranskat)abstract
    • Much research on cognitive competence in normal older adults has documented age and sex differences. We used cross-sectional data from the Victoria Longitudinal Study (n=386; age 61-95 years) to examine how health and biological age influence age and sex differences in cognitive aging. We found evidence for both moderating and mediating influences. Age differences were moderated by health status, such that the negative effects of age were most pronounced among participants of relatively better health. Sex differences were moderated by health and were pronounced among participants reporting comparatively poorer health. Although health mediated a notable amount of age-related cognitive variation, BioAge mediated considerably more variance, even after statistical control for differences in health. A complex pattern emerged for the mediation of sex differences: whereas BioAge accounted for sex-related variation in cognitive performance, health operated to suppress these differences. Overall, both health and BioAge predicted cognitive variation independently of chronological age.
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208.
  • Wickramasinghe, S N, et al. (författare)
  • Observations on two members of the Swedish family with congenital dyserythropoietic anaemia, type III
  • 1993
  • Ingår i: European Journal of Haematology. - 0902-4441 .- 1600-0609. ; 50, s. 213-221
  • Tidskriftsartikel (refereegranskat)abstract
    • Two affected individuals of the Swedish family with CDA, type III, in which the disease is transmitted as an autosomal dominant character, were studied. Both cases displayed features hitherto undescribed in this family but described in patients with CDA, type III, in whom the inheritance may have been as an autosomal recessive character. Such features were: (a) haemosiderinuria, (b) grossly disorganised erythroblast nuclei, (c) differences in the ultrastructural appearances of individual nuclei within the same multinucleate erythroblast and (d) intraerythroblastic inclusions resembling precipitated globin chains. In both cases the giant mononucleate erythroblasts and the multinucleate erythroblasts had total DNA contents up to 28c (1c = haploid DNA content) and 48c respectively, and some DNA synthesising bi- and multinucleate erythroblasts contained one or more nuclei which were unlabelled with 3H-thymidine. These findings are similar to those in patients with the autosomal recessive type of disease. Thus no major phenotypic differences are yet apparent between cases of CDA, type III, with different patterns of inheritance. Analysis of the surface erythrocyte proteins of the 2 Swedish CDA, type III, patients with monoclonal antibodies recognising Band 3, glycophorins A, B, C and D, Rh, CD44, CD47, CD55, CD58, CD59, Lutheran, Kell, LW and acetylcholinesterase did not reveal any gross abnormality of expression of these proteins. A slightly altered expression of blood group antigens A and H was revealed by the lectins Dolichos biflorus and Ulex europaeus and the Mr of Band 3 as judged by SDS polyacrylamide gel electrophoresis was also slightly reduced, suggesting that there may be minor alterations in the degree of N-glycosylation of some red cell membrane constituents.
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