| 1. |
- Lexell, Jan, et al.
(författare)
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What is the cause of the ageing atrophy? : number, size and proportion of different fiber types studied in whole vastus lateralis muscle from 15- to 83-year-old men
- 1988
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Ingår i: Journal of the Neurological Sciences. - 0022-510X .- 1878-5883. ; 84:2-3, s. 275-294
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Tidskriftsartikel (refereegranskat)abstract
- In order to study the effects of increasing age on the human skeletal muscle, cross-sections (15 micron) of autopsied whole vastus lateralis muscle from 43 previously physically healthy men between 15 and 83 years of age were prepared and examined. The data obtained on muscle area, total number, size, proportion and distribution of type 1 (slow-twitch) and type 2 (fast-twitch) fibers were analysed using multivariate regression. The results show that the ageing atrophy of this muscle begins around 25 years of age and thereafter accelerates. This is caused mainly by a loss of fibers, with no predominant effect on any fiber type, and to a lesser extent by a reduction in fiber size, mostly of type 2 fibers. The results also suggest the occurrence of several other age-related adaptive mechanisms which could influence fiber sizes and fiber number, as well as enzyme histochemical fiber characteristics
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| 2. |
- Strigård, Karin, et al.
(författare)
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Modulation of experimental allergic neuritis in rats by in vivo treatment with monoclonal anti T cell antibodies.
- 1988
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Ingår i: Journal of the Neurological Sciences. - 0022-510X .- 1878-5883. ; 83:2-3
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Tidskriftsartikel (refereegranskat)abstract
- Monoclonal antibodies (MCA) to different T lymphocyte cell surface antigens have been used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves of the antibody-treated rats. Several MCA, W3/13 (pan T cell reactive), W3/25 (anti-rat CD4), Ox 8 (anti-rat CD8) as well as Ox 6 (anti-Ia) partly prevented clinical signs of EAN when given shortly before expected onset of disease, whereas W3/13 and Ox 8 given at the height of disease did not further affect disease development. However, Ox 19 (anti-rat CD5) given at the same time as immunization partly prevented clinical signs of EAN, while Ox 19 given shortly before expected onset of disease or during height of disease drastically exaggerated disease symptoms. Immunohistochemical studies after Ox 8 or Ox 19 treatment showed a complete absence of staining for the respective antibodies, while staining was preserved with the other MCA. It is concluded that: (1) Ox 8 positive "suppressor/cytotoxic" T lymphocytes do not exert any suppressive effects on EAN during the now investigated phases of disease, and that (2) anti T lymphocyte antibodies (here Ox 19) may exert opposite effects on autoimmune disease when given at different phases of disease development. This may have implications for potential therapeutic trials of MCA therapy for putative autoimmune demyelinating diseases in man.
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