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- Löscher, W N, et al.
(författare)
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Electromyographic responses of the human triceps surae and force tremor during sustained submaximal isometric plantar flexion.
- 1994
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Ingår i: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 152:1, s. 73-82
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Tidskriftsartikel (refereegranskat)abstract
- The objective was to investigate electromyographic activity (EMG) and isometric force tremor (IFT) changes during a sustained sub-maximal isometric contraction in two muscles acting upon the same joint but differing in muscle fibre composition. Surface and intra-muscular EMG activity from the gastrocnemius and soleus muscles and IFT were recorded during an exhausting isometric plantar flexion (30% of maximal voluntary contraction). Surface EMG amplitude (RMS) of both gastrocnemius and soleus muscles increased significantly over time. Gastrocnemius EMG RMS increased in a non-linear fashion while soleus EMG RMS increased linearly. A significant linear decrease of surface EMG mean power frequency (MPF) was observed over time for both muscles. The decrease in gastrocnemius MPF was significantly greater than that for soleus. Intra-muscular EMG results showed similar trends. Correlations of intramuscular EMG RMS and MPF with time were, however, characterized by lower correlation coefficients than those from the surface EMG. Isometric force tremor RMS significantly increased non-linearly with duration of contraction, while IFT MPF showed a significant linear decrease with time. Changes in surface EMG RMS were correlated to changes seen in IFT RMS, in particular, for the predominantly fast twitch gastrocnemius muscle. Correlation coefficients of surface EMG MPF and IFT MPF were lower than RMS correlations. The associated changes in IFT and EMG with fatigue indicate alterations in motor unit firing rate, recruitment and synchronization. The muscle specificity of the EMG and IFT changes suggests a coupling to muscle fibre type composition, although differences in the relative force contribution of each muscle could also affect the results.
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| 2. |
- Squitieri, F, et al.
(författare)
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DNA haplotype analysis of Huntington disease reveals clues to the origins and mechanisms of CAG expansion and reasons for geographic variations of prevalence.
- 1994
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Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 3:12, s. 2103-14
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Tidskriftsartikel (refereegranskat)abstract
- This study of allelic association using three intra- and two extragenic markers within 150 kb of the Huntington disease (HD) mutation has provided evidence for linkage disequilibrium for four of five markers. Haplotype analysis of 67 HD families using markers in strong linkage disequilibrium with HD identified two haplotypes underlying 77.6% of HD chromosomes. Normal chromosomes with these two haplotypes had a mean number of CAG repeats significantly larger than and an altered distribution of CAG repeats compared with other normal chromosomes. Furthermore, haplotype analysis of five new mutation families reveals that HD has arisen on these same two chromosomal haplotypes. These findings suggest that HD arises more frequently on chromosomes with specific DNA haplotypes and higher CAG repeat lengths. We then studied CAG and CCG repeat lengths in the HD gene on 896 control chromosomes from different ancestries to determine whether the markedly reduced frequency of HD in Finland, Japan, China and African Blacks is associated with an altered frequency of DNA haplotypes and subsequently lower CAG lengths on control chromosomes compared to populations of Western European descent. The results show a highly significant inverse relationship between CAG and CCG repeat lengths. In populations with lowered prevalence rates of HD, CAG repeat lengths are smaller and the distribution of CCG alleles is markedly different from Western European populations. These findings suggest that, in addition to European emigration, new mutations make a contribution to geographical variation of prevalence rates and is consistent with a multistep model of HD developing from normal chromosomes with higher CAG repeat lengths.
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