| 1. |
- Kadi, Fawzi, et al.
(författare)
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The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles
- 2004
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Ingår i: Journal of Physiology. - : Wiley. - 0022-3751 .- 1469-7793. ; 558:Pt 3, s. 1005-1012
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate the modulation of satellite cell content and myonuclear number following 30 and 90 days of resistance training and 3, 10, 30, 60 and 90 days of detraining. Muscle biopsies were obtained from the vastus lateralis of 15 young men (mean age: 24 years; range: 20-32 years). Satellite cells and myonuclei were studied on muscle cross-sections stained with a monoclonal antibody against CD56 and counterstained with Mayer's haematoxylin. Cell cycle markers CyclinD1 and p21 mRNA levels were determined by Northern blotting. Satellite cell content increased by 19% (P= 0.02) at 30 days and by 31% (P= 0.0003) at 90 days of training. Compared to pre-training values, the number of satellite cells remained significantly elevated at 3, 10 and 60 days but not at 90 days of detraining. The two cell cycle markers CyclinD1 and p21 mRNA significantly increased at 30 days of training. At 90 days of training, p21 was still elevated whereas CyclinD1 returned to pre-training values. In the detraining period, p21 and CyclinD1 levels were similar to the pre-training values. There were no significant alterations in the number of myonuclei following the training and the detraining periods. The fibre area controlled by each myonucleus gradually increased throughout the training period and returned to pre-training values during detraining. In conclusion, these results demonstrate the high plasticity of satellite cells in response to training and detraining stimuli and clearly show that moderate changes in the size of skeletal muscle fibres can be achieved without the addition of new myonuclei.
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| 2. |
- Jacobsson, Johan, et al.
(författare)
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Superoxide dismutase in CSF from amyotrophic lateral sclerosis patients with and without CuZn-superoxide dismutase mutations
- 2001
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Ingår i: Brain. - : Oxford University Press. - 0006-8950 .- 1460-2156. ; 124:7, s. 1461-1466
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Tidskriftsartikel (refereegranskat)abstract
- Mutations in CuZn-superoxide dismutase (CuZn-SOD) have been linked to familial amyotrophic lateral sclerosis (ALS), and motor neurone death is caused by the gain of a toxic property of the mutant protein. Here we determined amounts, activity and molecular forms of CuZn-SOD in CSF from ALS patients carrying the D90A and other CuZn-SOD mutations and patients without such mutations. There were no differences in amount of protein and enzymic activities of CuZn-SOD between 37 neurological controls, 54 sporadic and 12 familial ALS cases, and 10 cases homozygous for the D90A mutation. Three cases heterozygous for the A89V, S105L and G114A CuZn-SOD mutations showed low amounts of CuZn-SOD. There was no evidence for accumulation of inactive protein in any of the groups. Immunoblots showed no evidence for the presence of any precipitates or other molecular forms of CuZn-SOD with higher molecular weight in the groups. About 25% of the CuZn-SOD subunits in CSF from controls shows an N-terminal truncation. This truncated portion does not differ between controls and ALS groups not carrying CuZn-SOD mutations, but is 70% larger in samples from D90A homozygous ALS patients. The findings suggest an essentially normal amount and activity of D90A mutant CuZn-SOD in CNS tissues of ALS cases. The increased occurrence of N-terminally truncated mutant subunits may indicate a difference in degradation routes compared with the wild-type enzyme, resistance against subsequent proteolytic steps and/or a compromised downstream proteolytic machinery. Molecular fragments accumulated to a greater extent from the D90A mutant enzyme might contribute to the motor neurone degeneration. We also determined the other SOD isoenzymes: in the controls, CuZn-SOD contributed 75%, extracellular SOD 25% and Mn-SOD <5% of the total SOD activity. There was no difference in the amount of extracellular SOD between any of the groups.
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| 3. |
- Kristensen, T N, et al.
(författare)
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The increase of fluctuating asymmetry in a monoclonal strain of collembolans after chemical exposure - discussing a new method for estimating the environmental variance
- 2004
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Ingår i: Ecological Indicators. - : Elsevier BV. - 1872-7034 .- 1470-160X. ; 4:1, s. 73-81
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Tidskriftsartikel (refereegranskat)abstract
- The increasing demand for detecting and quantifying the negative effects on natural habitats caused by anthropogenic activity has led to the development of impact assessment tools. Here, we propose a monitoring method based on the concept of developmental instability (DI) estimated from fluctuating asymmetry (FA) in bilateral morphological traits in a monoclonal strain. The use of monoclonal populations conveys certain advantages over sexual populations when interpreting fluctuating asymmetry results. This is because the inherent problems of genetic heterogeneity are circumvented. Our investigation demonstrates in practice, how an estimate of the environmental component of the phenotypic variance in a population can be achieved. This estimate can be used to eliminate samples where the presence of macro environmental variance has influenced the estimated level of fluctuating asymmetry significantly. Avoiding the confounding effect due to the presence of genetic variance and controlling the environmental variance component enable a more accurate estimate of the possible detrimental effects of the putative stressing agents. We used a clonal strain of the springtail Folsomia candida exposed to three different contaminants; tributyltin, nonylphenol and bis(2-ethylhexyl)-phthalate (DEPH), in order to test the general applicability of the proposed method. The results show that the method is efficient in discriminating between environments exposed to chemical stress and control environments. However, establishing an actual dose-response relationship was only possible for one of the contaminants, nonylphenol.
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| 4. |
- Norgaard, B. L., et al.
(författare)
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Long term risk stratification of patients with acute coronary syndromes: characteristics of troponin T testing and continuous ST segment monitoring
- 2004
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Ingår i: Heart. - 1468-201X. ; 90:7, s. 739-44
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To examine the long term prognostic characteristics of troponin T testing and continuous multi-lead ST segment monitoring in combination with clinical and 12 lead ECG risk indicators in patients with acute coronary syndromes (ACS). PATIENTS AND DESIGN: Patients with suspected ACS (n = 213) were studied. Troponin T was analysed in blood samples collected during the first 12 hours after admission. Continuous vectorcardiography ST segment monitoring was performed for 24 hours and the number of ST vector magnitude episodes was registered. Patients were followed up for a median of 28 months. The end point was a composite of cardiac death and acute myocardial infarction. RESULTS: Thirty eight (18%) patients reached the composite end point. The median (interquartile range) time from study inclusion to the time of the composite end point was longer for patients predicted to be at risk by troponin T testing (n = 27) than for those predicted to be at risk by ST segment monitoring (n = 20) (8.4 (0.2-15) months v 0.3 (0.1-4.3) months, p = 0.04). Significant univariate predictors of the composite end point were age > or = 65 years, diabetes, previous myocardial infarction, congestive heart failure, use of beta blockers or diuretics at admission, 12 lead ECG ST segment depression at admission, troponin T concentration > or = 0.10 microg/l, and > or = 1 ST vector magnitude episodes. Age > or = 65 years, previous myocardial infarction, and troponin T concentration > or = 0.10 microg/l provided independent prognostic information after multivariate analysis of potential risk variables. The prognostic value of transient ischaemic episodes in ACS seems to be confined to the short term. CONCLUSIONS: Both biochemical and continuous ECG markers reflect an increased risk for patients with ACS; however, the methods exhibit different temporal risk characteristics.
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