| 1. |
- Aspegren Kendall, Sally, 1950-, et al.
(författare)
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Differences in sensory thresholds in the skin of women with fibromyalgia syndrome : A comparison between ketamine responders and ketamine non-responders
- 2003
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Ingår i: Journal of Musculoskeletal Pain. - 1058-2452 .- 1540-7012. ; 11:2, s. 3-9
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: To compare detection and pain thresholds in the skin of female fibromyalgia patients who were either ketamine responders or ketamine nonresponders.Methods: Detection thresholds to innocuous warmth, of cold, heat or cold pain, and touch and dynamic touch sensation were determined in the skin. Pressure pain thresholds, local and widespread pain intensity, and pain duration were also registered.Results: Ketamine nonresponse was associated with more pronounced hypersensitivity for thermal pain [especially cold pain] than ketamine response.Conclusions: Blockade of N-metyl-D-aspartic acid receptors by ketamine and the recording of pain thresholds in the skin, especially for cold pain, might reveal different mechanisms of allodynia.
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| 2. |
- Henriksson, Karl-Gösta, 1928-
(författare)
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Hypersensitivity in muscle pain syndromes
- 2003
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Ingår i: Current Pain and Headache Reports. - 1531-3433 .- 1534-3081. ; 7, s. 426-432
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Tidskriftsartikel (refereegranskat)
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| 3. |
- Lindvall, Björn, 1952-, et al.
(författare)
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The expression of adhesion molecules in muscle biopsies : the LFA-1/VLA-4 ratio in polymyositis
- 2003
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Ingår i: Acta Neurologica Scandinavica. - : Hindawi Limited. - 0001-6314 .- 1600-0404. ; 107:2, s. 134-141
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Tidskriftsartikel (refereegranskat)abstract
- Objectives– The expression of three pairs of adhesion receptors and ligands was examined in 22 consecutive muscle biopsies showing morphological signs of inflammation.Material and methods– The following groups were studied: patients with polymyositis (PM) (n=7), patients with myositis that did not fulfil criteria for PM, i.e. suspected PM (n=5), patients with other diseases, with no clinical signs of inflammatory myopathy (n=6), and a small group of non-PM inflammatory myopathies (n=4). The endothelial expression of ICAM-1, VCAM-1 and E-selectin was evaluated, as was the cellular expression of LFA-1, VLA-4 and SLex. In addition, the expression of MHC class I and II was studied.Results– The ratio between the number of cells expressing LFA-1 and VLA-4 showed significant differences between the groups, with the lowest values in PM.Conclusion– The LFA-1/VLA-4 ratio should be suitable for diagnostic purposes. Our findings also indicate that the VLA-4/VCAM-1 system is important for chronic T cell inflammation in muscle, in line with findings in other “hidden” organs like joints and the central nervous system.
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| 4. |
- Tajsharghi, Homa, 1968, et al.
(författare)
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Myosin storage myopathy associated with a heterozygous missense mutation in MYH7.
- 2003
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Ingår i: Annals of neurology. - : Wiley. - 0364-5134 .- 1531-8249. ; 54:4, s. 494-500
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Tidskriftsartikel (refereegranskat)abstract
- Myosin constitutes the major part of the thick filaments in the contractile apparatus of striated muscle. MYH7 encodes the slow/beta-cardiac myosin heavy chain (MyHC), which is the main MyHC isoform in slow, oxidative, type 1 muscle fibers of skeletal muscle. It is also the major MyHC isoform of cardiac ventricles. Numerous missense mutations in the globular head of slow/beta-cardiac MyHC are associated with familial hypertrophic cardiomyopathy. We identified a missense mutation, Arg1845Trp, in the rod region of slow/beta-cardiac MyHC in patients with a skeletal myopathy from two different families. The myopathy was characterized by muscle weakness and wasting with onset in childhood and slow progression, but no overt cardiomyopathy. Slow, oxidative, type 1 muscle fibers showed large inclusions consisting of slow/beta-cardiac MyHC. The features were similar to a previously described entity: hyaline body myopathy. Our findings indicate that the mutated residue of slow/beta-cardiac MyHC is essential for the assembly of thick filaments in skeletal muscle. We propose the term myosin storage myopathy for this disease.
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