| 1. |
- Lexell, Jan, et al.
(författare)
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The occurrence of fibre-type grouping in healthy human muscle: a quantitative study of cross-sections of whole vastus lateralis from men between 15 and 83 years
- 1991
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Ingår i: Acta Neuropathologica. - 1432-0533 .- 0001-6322. ; 81:4, s. 377-381
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Tidskriftsartikel (refereegranskat)abstract
- Methods that objectively assess the muscle fibre-type arrangement may improve the detection of fibre-type grouping, a diagnostic sign of a denervation and reinnervation process. To distinguish between a diseased and a normal muscle, there is a need for quantitative data on the fibre-type arrangement in healthy human muscles at different ages. In this study, cross-sections were prepared of whole autopsied vastus lateralis muscle from 24 previously physically healthy men, aged 15 to 83 years. The arrangements of type 1 and type 2 fibers were assessed in terms of the number of enclosed fibres in individual fascicles throughout each muscle. Recent improvements to the enclosed fibre method were used to define measures of randomness which facilitated the combination of several sample areas and the quantification of the fibre-type arrangements. Segregation was typical for young muscles, randomness was most common between 30 and 50 years of age, while some fibre-type grouping was considered "normal" in old muscles. The arrangements of type 1 and type 2 fibres were quantitatively similar, irrespective of the age of the individual. The results imply that the fibre population changes considerably during a lifetime, and that it undergoes a continuous denervation and reinnervation process with normal ageing. Because of its importance, age should be accommodated in the analysis of a muscle sample, irrespective of the statistical model and method used.
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| 2. |
- Agardh, Carl-David, et al.
(författare)
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The influence of hypothermia on hypoglycemia-induced brain damage in the rat
- 1992
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 83:4, s. 379-385
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Tidskriftsartikel (refereegranskat)abstract
- The effects of hypothermia on hypoglycemic brain damage were studied in rats after a 30-min period of hypoglycemic coma, defined as cessation of spontaneous EEG activity. The rats were either normothermic (37 degrees C) or moderately hypothermic (33 degrees C). Morphological brain damage was evaluated after various periods of recovery. Hypothermic animals with halothane anesthesia never resumed spontaneous respiration, thus requiring artificial ventilation during recovery (maximally 8 h). In contrast, when isoflurane was used as the anesthetic agent, all animals survived and were examined after 1 week of recovery. There was a tendency towards gradually higher arterial plasma glucose levels during hypoglycemia with lower body temperature. The time period from insulin injection until isoelectric EEG appeared was gradually prolonged by hypothermia, and was shorter when isoflurane was used for anesthesia. Brain damage was examined within the neocortex, caudoputamen and hippocampus (CA1, subiculum and the tip of the dentate gyrus). Damage to neurons was found to be of two types, namely condensed dark purple neurons (pre-acidophilic) and shrunken bright red-staining neurons (acidophilic). In the neocortex, no clear influence of temperature on the degree of injury was seen. In the caudoputamen, the number of injured neurons clearly decreased at lower temperature (33 degrees C, P less than 0.001) when halothane was used, while no such difference was seen when isoflurane was used as the anesthetic agent. Likewise, a protective effect of hypothermia was seen in subiculum (P less than 0.01) when halothane, but not isoflurane was used.(ABSTRACT TRUNCATED AT 250 WORDS)
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| 3. |
- Bergstedt, Kerstin, et al.
(författare)
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Initiation of protein synthesis and heat-shock protein-72 expression in the rat brain following severe insulin-induced hypoglycemia
- 1993
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Ingår i: Acta Neuropathologica. - 0001-6322. ; 86:2, s. 145-153
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Tidskriftsartikel (refereegranskat)abstract
- Following stress such as heat shock or transient cerebral ischemia, global brain protein synthesis initiation is depressed through modulation of eucaryotic initiation factor (eIF) activities, and modification of ribosomal subunits. Concomitantly, expression of a certain class of mRNA, heat-shock protein (HSP) mRNA, is induced. Here we report that the activity of eucaryotic initiation factor-2 (eIF-2), a protein that participates in the regulation of a rate-limiting initiation step of protein synthesis, transiently decreases following insulin-induced severe hypoglycemia in the rat brain neocortex. Expression of HSP 72, a 72-kDa HSP, in surviving neurons was seen at 1-7 days of recovery following 30 min of hypoglycemic coma, but not at 1 h and 6 h of recovery. In the neocortex, HSP 72 was first seen in layer IV, and later also in surviving neurons in layer II. In the CA1 region and in the crest of dentate gyrus, HSP 72 expression was evident in cells adjacent to irreversibly damaged neurons. In the CA3 region and the hilus of dentate gyrus, HSP 72 was expressed in a few scattered neurons. In septal nucleus, HSP 72 was expressed in a lateral to medial fashion over a period of 1-3 days of recovery. We conclude that severe insulin-induced hypoglycemia induces a stress response in neurons in the recovery phase, including inhibition of protein synthesis initiation, depression of eIF-2 activity, and a delayed and prolonged expression of HSP 72 in surviving neurons. The HSP 72 expression may be a protective response to injurious stress.
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| 4. |
- Coimbra, Cicero, et al.
(författare)
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Moderate hypothermia mitigates neuronal damage in the rat brain when initiated several hours following transient cerebral ischemia
- 1994
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Ingår i: Acta Neuropathologica. - 0001-6322. ; 87:4, s. 325-331
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Tidskriftsartikel (refereegranskat)abstract
- Intraischemic moderate hypothermia generally protects the brain against ischemic cell death, while hypothermia instigated several hours into the reperfusion phase is considered to be less effective. Here we report the effect of hypothermia (32.5°-33.5°C) of 5-h duration, initiated at 2, 6, 12, 24 and 36 h into the recirculation phase following 10 min of transient cerebral ischemia, on ischemic neuronal injury in the hippocampus and striatum of the rat. Hypothermia induced at 2 h, and 6 h postischemia reduces neuronal damage in the entire hippocampal CA1 region by approximately 50%. In the lateral CA1 region hypothermia induced at 12 h postischemia, significantly mitigates necrosis. When initiated at 2 h postischemia, but not later, protection was also observed in the striatum. Hypothermia induced 24 and 36 h postischemia was ineffective. A period of hypothermia of 5 h, initiated 2 h postischemia, was required for marked neuronal protection in the CA1 region, while 3.5-h hypothermia decreased neuronal damage by approximately 10% and 30 min hypothermia was ineffective. The clinical implications of the data are that extended period of hypothermia initiated long into the recovery phase following ischemia may prove beneficial. Hypothermia protects brain regions displaying rapid as well as delayed neuronal damage, and a minimal time of hypothermia is required for effective neuronal protection. Also, strict temperature control for up to 24 h postischemia may be required for proper assessment of the efficacy of cerebro-protective drugs.
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| 5. |
- Nordborg, Claes, et al.
(författare)
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The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction
- 1991
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 82:2, s. 118-126
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Tidskriftsartikel (refereegranskat)abstract
- Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.
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