Pattern formation. Spiral cracks without twisting.
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Biomedical subjects
Publications and source records attributed to L Józsa.
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The Achilles tendon is the strongest tendon in the human body. Because most Achilles tendon injuries take place in sports and there has been an common upsurge in sporting activities, the number and incidence of the Achilles tendon overuse injuries and complete ruptures have increased in the industrialized countries during the last decades. The most common clinical diagnosis of Achilles overuse injuries is tendinopathy, which is characterized by a combination of pain and swelling in the Achilles tendon accompanied by impaired ability to perform strenuous activities. Most patients with Achilles tendon injury respond favorably to conservative treatment and only those who fail to respond to carefully followed nonoperative treatment should undergo surgery for repair. A complete rupture of the Achilles tendon usually occurs in sports that require jumping, running, and quick turns. Although histopathologic studies have shown that ruptured Achilles tendons include clear degenerative changes before the rupture, many of the Achilles tendon ruptures occur suddenly without any preceding signs or symptoms. Neither conservative nor operative treatment is a treatment of choice for the ruptured Achilles tendon. It is generally accepted that surgery should be performed on ruptured Achilles tendons in young, physically active patients and in those patients for whom the diagnosis or the treatment of the rupture has been delayed, whereas the results of conservative treatment are an acceptable outcome in older patients with sedentary lifestyles. Many important issues still remain unanswered concerning the cause, pathogenesis, diagnosis, and management of the Achilles tendon disorders. Only when these issues have been solved by well-controlled studies can tailored treatment protocols be created.
The authors studied the dental calculus of 20 mummies with ligth microscopy, polarized ligth microscopy and scanning electron microscopy. Gram positive bacteria could be detected in all preparates, while Gram negative bacteria in 12 and fungi only in 3 dental calculus was visible. Animal food remains within five, and plant remains in all dental calculus were identified. Anorgic element and cell debris were seen in all preparates.
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The effect of Achilles tenotomy on resting blood flow of rat gastrocnemius muscle and Achilles tendon was studied by radioactive microspheres. Tenotomy produced an immediate, marked decrease in both intramuscular and intratendinous blood flow and it remained significantly lowered at both sites till the end of the observation period, i.e., day 18 after tenotomy. The decrease in the resting blood flow was more rapid and pronounced in the Achilles tendon than in the gastrocnemius muscle. Although the blood flow of the Achilles tendon started to recover after the 4th postoperative day, it was still 33% (statistically not significant) lower than that in the controls 18 days after tenotomy. In the gastrocnemius muscle, the 18-day deficit was 38% (p < 0.001), respectively. The results indicate that after division of a rat Achilles tendon the resting blood flow to the gastrocnemius muscle and Achilles tendon is not adequately restored, remaining at a significantly lowered level even 18 days after tenotomy.
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Since a tendon is a living tissue, it is not a surprise that tendon shows the capacity to adapt its structure and mechanical properties to the functional demands of the entire muscle-tendon unit. However, compared with muscle, the experimental knowledge of the effects of strength or endurance-type training on tendon tissue is scarce and clinical human experiments are completely lacking (1). Research should, however, be able to improve the true understanding of the biomechanical, functional, morphological and biochemical changes that occur in tendons due to training and physical activity, since understanding of the basic physiology of a tissue is the key to understanding its pathological processes (1, 2). Compared with muscle tissue, the metabolic turnover of tendon tissue is many times slower due to poorer vascularity and circulation (1, 3). The adaptive responses of tendons to training are therefore also slower than those in muscles, but they may finally be considerable if the time frame is long enough (3, 4).
Tendon injuries and other tendon disorders represent a common diagnostic and therapeutic challenge in sports medicine, resulting in chronic and long-lasting problems. Tissue degeneration is a common finding in many sports-related tendon complaints. In the great majority of spontaneous tendon ruptures, chronic degenerative changes are seen at the rupture site of the tendon (1). Systemic diseases and diseases specifically deteriorating the normal structure of the tendon (i.e. foreign bodies, and metabolic, inherited and infectious tendon diseases) are only rarely the cause of tendon pathology. Inherited diseases, such as various hereditary diseases with disturbed collagen metabolism and characteristic pathological structural alterations (Ehlers-Danlos syndrome, Marfani syndrome, homocystinuria (ochronosis)), represent approximately 1% of the causes of chronic tendon complaints (2), whereas foreign bodies are somewhat more common and are found in less than 10% of all chronic tendon problems (1). Rheumatoid arthritis and sarcoidosis are typical systemic diseases that cause chronic inflammation in tendon and peritendinous tissues. Altogether, these 'specific' disorders represented less than 2% of the pathological alterations found in the histological analysis of more than 1000 spontaneously ruptured tendons (1, 3, 4). In this material, degenerative changes were seen in a great majority of the tendons, indicating that a spontaneous tendon rupture is a typical clinical end-state manifestation of a degenerative process in the tendon tissue. The role of overuse in the pathogenesis of chronic tendon injuries and disorders is not completely understood. It has been speculated that when tendon is overused it becomes fatigued and loses its basal reparative ability, the repetitive microtraumatic processes thus overwhelming the ability of the tendon cells to repair the fiber damage. The intensive repetitive activity, which often is eccentric by nature, may lead to cumulative microtrauma which further weakens the collagen cross-linking, non-collagenous matrix, and vascular elements of the tendon. Overuse has also been speculated to cause chronic tendon problems, by disturbing the micro- and macrovasculature of the tendon and resulting in insufficiency in the local blood circulation. Decreased blood flow simultaneous with an increased activity may result in local tissue hypoxia, impaired nutrition and energy metabolism, and together these factors are likely to play an important role in the sequence of events leading to tendon degeneration (4). A sedentary lifestyle has been proposed as a main reason for poor basal circulation of the tendon, and presumably is at least partly responsible for the high number of tendon problems in people with a sedentary lifestyle who occasionally take part in high physical activity sports events.
A spontaneous rupture of a tendon may be defined as a rupture that occurs during movement and activity, that should not and usually does not damage the involved musculotendinous units (1). Spontaneous tendon ruptures were uncommon before the 1950s. Böhler found only 25 Achilles tendon ruptures in Wien between 1925 and 1948 (2). Mösender & Klatnek treated 20 Achilles tendon ruptures between 1953 and 1956, but 105 ruptures between 1964 and 1967 (3). Lawrence et al. found only 31 Achilles tendon ruptures in Boston during a period of 55 years (1900-1954) (4). During the recent decades tendon ruptures have, however, become relatively common in developed countries, especially in Europe and North America. A high incidence of tendon ruptures has been reported in Austria, Denmark, Finland, Germany. Hungary, Sweden, Switzerland and the USA; somewhat lower incidences have been reported in Canada, France, Great Britain and Spain. On the other hand, Greece, Japan, the Netherlands and Portugal have reported a clearly lower incidence. Interestingly, Achilles tendon ruptures are a rarity in developing countries, especially in Africa and East-Asia (5). In many developed countries, the increases in the rupture incidence have been dramatic. In the National Institute of Traumatology in Budapest, Hungary, the number of patients with an Achilles tendon rupture increased 285% in men and 500% in women between two successive 7-year periods, 1972-1978 and 1979-1985 (5).
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Effect of free and forced remobilization on the mineral content and distribution of the mineral content in the formerly immobilized bones of the extremities was examined. Authors performed after plaster immobilization free and forced (on production line) remobilization in rats. After the 3 weeks immobilization and the following 8 weeks remobilization the mineral content of the bones of the extremities, formerly in plaster, and the density of the mineral did not reach the parameters of the bones of the free extremities.
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So-called amianthoid fibres were identified in 17 of 460 tendons (3.7%) after spontaneous rupture. These tendons belonged to 10 men and 7 women with an age-range from 18 to 67 years. In 445 postmortem control tendons taken of accidentally killed previously healthy persons amianthoid fibres were not found. Ultrastructurally the tendineal amianthoid fibres differ from normal tendon collagen fibrils in many respects. Their diameter (600-1400 nm) is many times larger than that of native collagen fibrils (20-120 nm). The fibre profile is often irregular and the cross-sectioned fibres have a homogeneous granular appearance. In longitudinal sections, the amianthoid fibres are frequently disintegrated and outspread, and some of the fibres have lost their periodicity. In addition, some of the fibres are angulated and show nonparallel organization. Occasionally the amianthoid fibres are calcified.
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