Extracellular matrix and myofibrils during unloading and reloading of skeletal muscle

The aim of the study was to elucidate the effect of unloading and reloading on the collagen expression and synthesis rate of myofibrillar proteins in fast-twitch (FT) muscle in relation to changes in muscle strength and motor activity. Northern blot analysis was used for testing the specificity of cDNA probes and protein synthesis rate was measured according to incorporation of radioactive leucine into different protein fractions. Unloading depresses collagen type I and III (p<0.001), type IV (p<0.05) and reloading enhances collagen expression in fast-twitch skeletal muscle in comparison with unloading. Enhanced expression of matrix metalloproteinase-2 continued during the first week of reloading (p<0.01) and tissue inhibitor of metalloproteinase-2 during reloading (p<0.05). Changes in collagen expression in FT muscle are in good agreement with changes in myofibrillar protein synthesis during unloading and reloading. In conclusion alterations in extracellular matrix and myofibrillar apparatus in FT skeletal muscle are related to changes in muscle strength and motor activity, are significant in exercise training and determination of recovery periods in the training process as well as in athletes' rehabilitation.     

Neurodegeneration and production of the new cells in the dentate gyrus of juvenile rat hippocampus after a single administration of ethanol

Administration of ethanol during brain development induces widespread neuronal loss in various structures of the brain. Here, we show that a single administration of ethanol given during the early postnatal period can induce not only neuronal death, but also an increase in proliferation of the progenitor cells in the dentate gyrus of hippocampal formation in rats. Ethanol (1.5 or 3 g/kg, i.p.) administered to 10-day-old rats induced massive neuronal degeneration as evidenced by TUNEL assay in the dentate gyrus. The neuronal death induced by a high dose of ethanol (3 g/kg) was accompanied by an enhanced proliferation of the progenitor cells labeled by bromodeoxyuridine (BrdU, 50 mg/kg, i.p.) in dentate gyrus. One and 3 weeks following ethanol or saline administration, ethanol-treated rats still had significantly more BrdU-labeled cells than control animals. In ethanol-treated rats, a higher proportion of newly born cells acquired the phenotype of immature postmitotic neurons whereas the final differentiation into calbindin-expressing granule cells remained unchanged. The proportion of astroglial cells was also increased in ethanol-treated rats. Thus, ethanol given in high doses not only induces neurodegeneration but also initiates the process of neuro- and gliogenesis, which might be responsible for the neuronal and glial reorganization of the dentate gyrus.     

Dehydroepiandrosterone inhibits complex I of the mitochondrial respiratory chain and is neurotoxic in vitro and in vivo at high concentrations.

Dehydroepiandrosterone (DHEA) is widely used as a food supplement and considered to be relatively safe. In animal studies, however, additions of high concentrations of DHEA to the diet have led to hepatotoxicity as well as liver mitochondrial dysfunction. This study was therefore designed to find out whether DHEA is able to inhibit the respiratory activity also in neuronal mitochondria and to reveal whether this leads to functional disturbance in the brain. Using different mitochondrial substrates, we show here that DHEA suppresses the mitochondrial respiration in permeabilized neurons (half maximal inhibitory concentration 13 microM) by inhibiting complex I of the mitochondrial electron transport chain. Treatment with DHEA was associated with increased glucose expenditure in intact cultures and led to neuronal death. The latter was most prominent in hypoglycemic conditions. Mice fed with pellet containing 0.6% DHEA for 3 months showed a significant neuronal loss in the cerebral cortex and hippocampus, a slightly decreased dopamine/dihydroxyphenylacetic acid ratio, as well as motor impairment. The main conclusion of the present study is that high concentrations of DHEA inhibit complex I of the mitochondrial respiratory chain and are neurotoxic in vitro and in vivo.     

Endurance training: volume-dependent adaptational changes in myosin

The purpose of this study was to find the effect of different endurance training volumes on the composition and turnover of myosin. Sixteen-week-old male rats of the Wistar strain were divided into three different volume-based training groups. Changes in myosin heavy chain (MyHC), myosin light chain (MyLC) isoforms' composition, their synthesis rate, as well as myosin binding C-protein synthesis rate, and muscle protein degradation rate were measured. In slow-twitch (ST) soleus (Sol) muscle MyHC I isoform relative content increased and MyHC IIa isoform decreased during excessive increase in the volume of endurance training (ET). In plantaris (Pla) muscle excessive increase in ET volume decreased MyHC I and IIb isoforms, and increased MyHC IIa and IId relative content. In extensor digitorum longus (EDL) muscle the relative content of MyHC IId isoform increased during ET, but excessive increase in training volume decreased it. In Pla muscle the relative content of MyLC 1 (slow) isoform decreased during ET, but excessive increase in ET volume decreased the relative content of MyLC 3 (fast) isoform in both fast-twitch (FT) muscles. Decrease in MyHC and myosin binding C-protein synthesis rate in Pla muscle had significant correlation with ET volume (r = - 0.537, p < 0.05 and r = - 0.727, p < 0.001 subsequently). MyHC I and IIb isoforms and MyLC 3 (fast) isoform in Pla muscle and MyHC IIb, IId and MyLC 3 (fast) isoforms in EDL muscle are the most sensitive to the increase in ET volume. Excessive increase in ET volume leads to a decrease in physical working capacity. The degradation of muscle protein increased during ET in all groups.     

Registry of first-ever stroke in Tartu, Estonia, 1991 through 1993: outcome of stroke

OBJECTIVES: To provide information about the functional ability of the survivors of first-ever stroke in Estonia. PATIENTS AND METHODS: A population based epidemiological study 1991 through 1993 in Tartu. Herewith the data for 1991 and 1993 are presented. A total of 519 persons were registered; 82% of them were admitted (mean length 14 days), 66% were discharged home. RESULTS: During 6 months 41% of the patients died, the remaining 305 patients were interviewed about their living conditions, and functional ability using the Barthel ADL Index. Although 58% of patients responded to the questionnaire, no significant differences in several factors between the respondents and non-respondents were found. Thirty-eight percent of the patients were totally independent in ADL. CONCLUSION: The case-fatality rate at 6 months was high in Estonia and the proportion of totally independent patients 6 months after stroke is slightly lower compared to other studies. The short length of hospital treatment was possibly compensated by sufficient support by relatives after discharge.     

Prevalence of MS in South Estonia. Evidence of a new border of the Fennoscandian focus

A population-based study of MS was carried out in South Estonia in 1988–1989. Cases were identified from the Tartu University Hospital archives where all MS cases in South Estonia are diagnosed, from all neurologists and nursing homes of the region, and from the local Multiple Sclerosis Society. The prevalence in South Estonia is 51 per 100,000, for native Estonians 55, for Russians 29, for other nationalities 42 per 100,000. The prevalence rate in different counties was demonstrated as low as 31 per 100,000 in the County of Tartu, to 72 per 100,000 in Plva County; 55% of patients have retired because of their handicap and only 2 patients (1%) were living in nursing homes.     

Changes of sympatho-adrenal and hypothalamo-pituitary-adrenocortical system in patients with head injury

To determine the role of the sympatho-adrenal (SAS) and hypothalamo-pituitary-adrenocortical system (HPAS) after head injury, the relationship between venous blood epinephrine (E), norepinephrine (NE), adrenocorticotropic hormone (ACTH), Cortisol levels, and clinical condition was examined in 55 patients. These observations suggest that head injury causes mainly activation of the above-mentioned systems depending on the severity of trauma. An inverse correlation between the levels of E, NE and Glasgow Coma Scale score, indicating the severity of head injury was revealed. ACTH and Cortisol were similarly related to the clinical condition, although the observed correlation was less expressed. The changes in hormonal levels were present during the whole research period (1 week), although a certain shift to normalization was observed. However, catecholamines and ACTH levels in plasma were relatively low in severely head-injured patients whose CT scans revealed serious alterations in the mesencephalic-diencephalic area. At the same time their Cortisol levels obtained maximal values and their chance to survive was diminutive. The results of this study indicate that investigation of hormones of SAS and HPAS might be useful as an additional method in the complex of ordinary examinations in establishing early prognosis in patients with brain injury.