[Cardiovascular diseases in the Bible].
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Biomedical subjects
Publications and source records attributed to L Józsa.
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Thirty patients with ruptures of the Achilles tendon were studied. There were 21 men and 9 women with an average age of 36 years. Specimens from the tendon and paratenon in 24 were examined histologically. Tissue samples of 20 were studied by electron microscopy. Marked degenerative, obliterative and/or inflammatory vascular changes were found in all the ruptured tendons and their paratenon. Our findings indicate that poor vascularity play a role in the aetiology of rupture of the Achilles tendon.
Pigmented villonodular synovitis is made up of a variety of cells, including round or oval mononuclear cells, fibroblasts, synovial cells and multinucleated giant cells. The mononuclear cells were found to stain positively with anti-lysozyme, anti-alpha-1-antitrypsin, anti-alpha-1-antichymotrypsin and anti-fibronectin. Vimentin was detected in fibroblasts and in lining cells of the synovial membrane as well as in cells of acinus-like structures. The multinuclear giant cells contained lysozyme, alpha-1-antitrypsin and alpha-1-antichymotrypsin but no vimentin.
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We evaluated specimens obtained from the biopsy of spontaneously ruptured tendons in 891 patients who were treated between 1968 and 1989. The specimens, which were removed at the time of repair, included 397 Achilles tendons, 302 biceps brachii tendons, forty extensor pollicis longus tendons, eighty-two quadriceps tendons and patellar ligaments, and seventy other tendons. Age and sex-matched control specimens, from 445 tendons taken at the time of death from the cadavera of previously healthy individuals who died accidentally, also were obtained and evaluated. The histopathological analyses of the specimens included light and polarized light microscopy and scanning and transmission electron microscopy. A healthy structure was not seen in any spontaneously ruptured tendon, but two-thirds of the control tendons were structurally healthy (p less than 0.001). There were characteristic histopathological patterns in the spontaneously ruptured tendons. Most (97 per cent) of the pathological changes were degenerative; they included hypoxic degenerative tendinopathy, mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, either alone or in combination. These changes were also found in 34 per cent of the control tendons, but significantly less frequently (p less than 0.001). In the other twenty-six ruptured tendons (3 per cent), the pathological change was an intratendinous foreign body, rheumatoid tendinitis, a xanthoma, a tumor, or a tumor-like lesion such as an intratendinous ganglion. The findings clearly indicate that, at least in an urban population, degenerative changes are common in the tendons of people who are older than thirty-five years and that these changes are associated with spontaneous rupture.
The macromolecular composition and ultrastructure of the myotendineal junction (MTJ) of slow-twitch (type 1) and fast-twitch (type 2) muscle fibers were studied in the gastrocnemius-soleus-Achilles unit of the rat. Both proteoglycans and glycosaminoglycans, type III collagen, fibronectin and laminin could be detected at the MTJ. Due to membrane folding, finger-like processes were seen at the myotendineal junction. The processes of the type 1 fibers are greater in size, however, due to subdivisions, the processes of type 2 muscle fibers had a greater surface than type 1 fibers. The macromolecular composition is similar in both type 1 and type 2 muscle fibers.
The macromolecular composition and ultrastructure of the myotendineal junction (MTJ) of slow-twitch (type 1) and fast-twitch (type 2) muscle fibers were studied in the gastrocnemius-soleus-Achilles unit of the rat. Both proteoglycans and glycosaminoglycans, type III collagen, fibronectin and laminin could be detected at the MTJ. Due to membrane folding, finger-like processes were seen at the myotendineal junction. The processes of the type 1 fibers are greater in size, however, due to subdivisions, the processes of type 2 muscle fibers had a greater surface than type 1 fibers. The macromolecular composition is similar in both type 1 and type 2 muscle fibers.
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A case of a 20 year old patient with an Ehlers-Danlos syndrome is described, in which a rupture of the Achilles tendon is repaired by a segmental tendon homograft. The function of the triceps surae returned to normal gradually and the plantar flexion was even weaker after 2 years. The technique and importance of the special radiography of the soft tissue is discussed with regard to the clinical diagnosis. Radiographs, histomorphologic and histologic results illustrate the course of the healing.
The authors have studied the enzymhistochemical and ultrastructural pictures of tenocytes of adult human tendons. High succinate dehydrogenase, cytochrome oxidase, TPN-diaphorase, lactate dehydrogenase and glucose-6-phosphate dehydrogenase activity were found, as indicated both oxidativ, anaerobic and pentose-phosphate shung activity. Phosphorylase and glutamate dehydrogenase activity was medial, lipase and alcaline phosphatase activity was slight. In tenocytes well developed rough endoplasmic reticulum and GOLGI apparatus, large amount of free ribosomes were found.
The authors studied the histochemical alterations of human skeletal muscles after tenotomy and after spontaneous rupture of the tendon. Both succinate dehydrogenase (in type I fibers), and myofibrillar ATP-ase (in type 2 fibers) activity was decreased in all injured muscles. In the intact antagonists and contralateral muscles alterations were not found. The creatine phosphokinase and aldolase activity were decreased also in injured muscles. The lactate dehydrogenase activity was various both in affected and in unaffected muscles. Two weeks or more after the injury of the tendon in injured muscles the number of type 1 fibers were decreased and therefore a mathematically significant type 2 fibre predominance occurred. Atrophy involve both type 1 and type 2 fibers, but type 1 fibre atrophy was more pronunced as type 2 fibre atrophy.
The most marked changes in the human muscle following tendinous injury can be observed in the contractile components. There is a widening of the Z-membrane, dispersion of the sarcomers, a break in their continuity, and detached bundles of myofibrils are found in the sarcoplasm. A change occurs also in the proportion of different fibre types of the muscles, in the muscle with tendinous injury a predominance of type II fibre becoming apparent. Among the proteins of myofibrils a product of disintegration of a molecular weight of 31 000 can be consequently demonstrated, and in some muscles products of disintegration with a molecular weight between 90 000 and 58,000 arise.
The myofibrillar proteins and relative LC-3 content of myofibrils prepared from five different, left and right muscles of the human forearm were studied by electrophoresis in 10% SDS-polyacrylamide gels followed by densitometry. The specific K-activated ATPase activity of the myofibrillar myosin of the myofibrils was determined and the distribution of the fibre types was analyzed by histochemical methods. The qualitative pattern of the myofibrillar proteins was found to be identical in the different muscles; in the other parameters, however, a variation in a narrow range was observed. The relative LC-3 content, the ATPase activity and the type II fibre content of the right side muscles were always higher than those of the corresponding left side muscles.
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Alterations of the sceletal muscles after spontaneous rupture of the tendon were studied. It was established that after the rupture of the tendon in the muscle activity of the succinedehydrogenase, myofibrillar ATP-ase, creatinphosphokinase and aldolase markedly decreases. After the rupture of the tendon alteration of the proportion of various types of fibers may also be observed i.e. the rate of the fibres of type I considerably decreases. Electron microscopic findings indicate that alterations of the musculature are diffuse first of all elements of contractility are damaged: atrophy and rupture of them can be seen. Fibres of normal ultrastructure were not found at all, which indicates that both types of fibres I and II are equally damaged.
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