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  • 1
    ISSN: 0022-2828
    Keywords: Na^+-linked Ca^2^+-overload; Blood perfused heart; Ischemia-reperfusion
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 20 (1988), S. 753-762 
    ISSN: 0022-2828
    Keywords: Calcium distribution ; Cardiomyopathic hamster ; Cytochemistry ; Mitochondria ; Sarcolemma
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 16 (1984), S. 30 
    ISSN: 0022-2828
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-4919
    Keywords: ischemia ; dedifferentiation ; apoptosis ; chronic hibernating myocardium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Left ventricular biopsies from 21 patients with clinically diagnosed chronic hibernating myocardium (CHM) were examined by light- and electron microscopy. A mean of 27% of cardiomyocytes were structurally altered and were characterized as hibernating, because of reduced amount of myofibrils and increased glycogen content. Electron microscopy of these cells showed reduction of T-tubules and numerous small mitochondria, but few changes associated with degeneration, acute ischemia or apoptosis. The structural changes found in CHM are reminiscent of dedifferentiation rather than degeneration. The expression patterns of some structural proteins show resemblance with those in embryonic cardiomyocytes. Histochemically, mitochondrial NADH-oxidase and proton translocating ATPase activities were absent, whereas cytochrome c activity was present. Intracellular calcium distribution indicated normally bound sarcolemmal calcium and absence of excess mitochondrial calcium accumulation. Nuclear chromatin ranged from normal to dispersed with only a few nuclei that were clumped. These results suggest that cardiomyocytes from human CHM hearts are structurally altered, but viable, and lack morphologic and cytochemical characteristics suggestive of apoptosis or acute ischemia.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 43 (1975), S. 257-267 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The development of alkaline phosphatase during invasion and encystment of Trichinella spiralis in rat skeletal muscle fibres was studied at the ultrastructural level. On day 14 after infection, the enzymatic activity is found in proliferating parts of the T-tubular system and in parts of the plasmalemma. In cells, in which a strong hyperplasia of this system is noted, AIPase is present in the abundant network of stratified and concentric membranes from which a large number of pinocytic vesicles arise. From day 50 till 1 year after infection the enzyme activity was invariably present in the matrix surrounding the larvae and was confined to the enormous amounts of cytoplasmic membranes. The possible functional significance of this enzyme in the matrix, in view of its peculiar localization in the immediate vicinity of the parasite, is discussed. In the presence of 0.1 mM of the levamisole analogue, compound R 30402, which is a stereospecific inhibitor of AIPase, the activity is completely lost.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 44 (1975), S. 277-280 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A levamisole analogue, the l-p-bromotetramisole is introduced as a potent inhibitor of non-specific alkaline phosphatase. Complete inhibition is achieved cytochemically at a concentration of 0.1 mM in various rat tissues except the intestine, which is not affected. The d-p-bromotetramisole does not influence the alkaline phosphatase activities. Since no effect of the inhibitor is seen on the activities of specific phosphatases, this drug is recommended also as an additive for specific phosphatase media in order to yield the specific activity only.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1435-1803
    Keywords: ischemia ; cardiacmuscle ; calcium ; cytochemistry ; ultrastructural study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of Ca2+ in the pathogenesis leading to ischemic myocardial cell death is still controversial. To gain insight into this phenomenon a cytochemical procedure, the phosphate pyroantimonate method, was used to localize different subcellular Ca2+-pools at the ultrastructural level. After 45 min of left anterior descending coronary artery (LAD) occlusion, the coronary arteries were perfused with triphenyltetrazoliumchloride staining (TTC) to identify viable ischemic and infarcted tissue. In non-ischemic tissue, Ca2+-deposits were confined to the sarcolemma, sarcolemma-derived vesicles, transverse tubules, and intercalated disks. In infarcted tissue (TTC-negative), the sarcolemma lost its Ca2+-binding capacity and mitochondria were either overloaded with Ca2+-precipitate or they contained amorphous densities. In viable ischemic areas (determined with the TTC-technique) the sarcolemma was virtually devoid of Ca2+-deposits. Mitochondria in this area frequently showed clumping of the cristae, associated with an accumulation of Ca2+-precipitate in between the clustered cristae. The results of this study indicate that Ca2+-shifts occur in ischemic myocardial cells before the occurrence of other ultrastructural signs of irreversible injury which, therefore, narrows the possibility that Ca2+-overload is only a consequence of ischemic cell death.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular histology 25 (1993), S. 312-318 
    ISSN: 1573-6865
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The structural correlates of ‘chronic hibernating myocardium’ in man consist of myocardial cells which transformed from a functional state (rich in contractile material) to a surviving state (poor in contractile material, rich in glycogen). Since the calcium-handling organelles such as SR, sarcolemma and mitochondria underwent structural changes in cells so affected, the distribution of calcium was investigated in biopsies obtained from ‘hibernating’ areas. The material was processed for microscopic localization of total calcium (laser microprobe mass analysis, LAMMA) and of exchangeable calcium (phosphate-pyroantimonate precipitation method, PPA). Subcellular distribution of total calcium as assessed by LAMMA revealed that in the structurally affected cells the areas in which sarcomeres were replaced by glycogen contained significantly more calcium than all other areas probed such as mitochondria, remaining sarcomeres at the cell periphery and subcellular areas of normally structured cells. Calcium precipitate, obtained after PPA assessment, was localized at the sarcolemma but was virtually absent in the mitochondria of affected cells. The high calcium content in the myolytic areas of affected cells most probably belongs to a pool of bound calcium. The observations that calcium is retained at the sarcolemma and that mitochondria are devoid of precipitate favour the hypothesis that cells structurally affected as such are not ischaemic and are still able to regulate their calcium homeostasis.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-6865
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The cytochemical localization of NADH-oxidase, a possible source of oxygen derived toxic species was studied in the isolated working rabbit heart subjected to normothermic global ischaemia. The activity of this oxidase could be important for the damage observed during ischaemia, when cellular defence mechanisms against free radicals are depleted. In non-ischaemic myocardium only small amounts of the NADH-oxidase reaction product were present in the mitochondria. Although the reaction product could already be observed after 45 min of incubation, prolonged incubation times up to 2 h were necessary to clearly define these reactive sites. The reaction product is substrate dependent and is not affected by cyanide. Exposure of the hearts to ischaemia resulted in an alteration of the enzyme activity depending on the degree of ischaemic damage. In ultrastructurally slightly altered areas a high degree of cytochemical study supports the hypothesis that hydrogen peroxide and oxygen radicals produced in the mitochondria by NADH-oxidase activity may contribute to the mitochondrial damage observed during ischaemia when NADH is no longer oxidized by the respiratory chain and cellular defence mechanisms are impaired.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular histology 8 (1976), S. 301-317 
    ISSN: 1573-6865
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Synopsis The demonstration of non-lysosomal acid phosphatase has been the subject of a number of recent investigations. In the present study we compared the enzyme activities in rat liver and kidney that are revealed after incubation in the presence of either β-glycerophosphate,p-nitrophenylphosphate or phenylphosphate at varying pH. As seen by others, the activity towardsp-nitrophenylphosphate at pH 5–6 was confined to lysosomes, Golgi apparatus, endoplasmic reticulum (ER), nuclear envelope and plasmalemma. The reactivity of the plasmalemma and the ER was increased at pH 7. The ER of Küpffer cells in the liver stained intensely in contrast to the ER of the parenchymal cells, which stained only weakly. In the presence of NaF, all sites except the plasmalemma became negative. Addition of a levamisole-analogue,l-p-bromotetramisole, which is a specific inhibitor of alkaline phosphatase, resulted in the disappearance of the plasmalemmal activity whereas the activity at the other sites appeared unaltered. The rather unusual locations of activities with so-called non-specific substrates were further compared with those obtained with specific substrates such as glucose-6-phosphate and thiamine pyrophosphate. The possible implication of these data in relation to the specificity of marker-enzymes for subcellular organelles is discussed.
    Type of Medium: Electronic Resource
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