672 resultados para Skeletal-muscles
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A piomiosite tropical é uma infecção primária dos músculos, que ocorre principalmente em países tropicais. Inicialmente, suas manifestações são leves e inespecíficas, o que dificulta o diagnóstico. A história natural dessa doença costuma ser benigna, com raras complicações. Essa apresentação descreve quatro casos de piomiosite, com manifestações e complicações peculiares.
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In 1956, Africanized bees began to spread in the American continent from southern Brazil, where original African bees mated with European bees. A few years later, in 1990, these Africanized bees reached the United States and were found in Texas. Currently, these hybrid bees are found in several North American states and will probably reach the Canadian border in the future. Although the presence of Africanized bees had produced positive effects on Brazilian economy, including improvement in crop pollination and in honey production, turning Brazil into a major exporter, the negative impacts-such as swarming, aggressive behavior, and the ability to mass attack-resulted in serious and fatal envenomation with humans and animals. Victims of bee attacks usually develop a severe envenomation syndrome characterized by the release of a large amount of cytokines [interleukins (IL) IL-1, IL-6, IL-8], and tumor necrosis factor (TNF). Subsequently, such cytokines produce an acute inflammatory response that triggers adverse effects on skeletal muscles; bone marrow; hepatic and renal functions; and cardiovascular, central nervous, and immune systems. Finally, the aim of the present review is to study historical characteristics and current status of Africanized bees' spread, the composition of their venom, the impact of the bees on the Brazilian economy and ecology, and clinical aspects of their stings including immune response, and to suggest a protocol for bee sting management since there is no safe and effective antivenom available.
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Carcaças bovinas resfriadas rapidamente podem apresentar uma contração muscular conhecida como encurtamento pelo frio. Esse fenômeno, prejudicial à textura da carne, ocorre principalmente nas fibras musculares oxidativas. O objetivo deste trabalho foi disponibilizar uma ferramenta analítica para distinguir essas fibras e determinar com maior precisão a contração do tecido muscular pela mensuração do comprimento dos sarcômeros. Amostras do músculo Longissimus dorsi de 12 novilhas nelore foram coletadas. As amostras obtidas de uma das meias-carcaças foram submetidas a uma refrigeração rápida, e as amostras provenientes da outra meia-carcaça à refrigeração lenta. Foi testado um método analítico, baseado na técnica de coloração por Nicotinamida Adenina Dinucleotídeo - Tetrazolium Redutase (NADH-TR), para mensurar, por microscopia, o comprimento dos sarcômeros das fibras vermelhas. Foram determinadas as velocidades de queda de pH e temperatura, a área do olho de lombo (AOL) e a força de cisalhamento. Os resultados demonstraram que a temperatura é o principal fator responsável pelo comprimento do sarcômero quando a velocidade de resfriamento é rápida, sendo essa influência menor quando a queda de temperatura é mais lenta. Desta forma, demonstrou-se que a técnica de coloração com NADH-TR é capaz de detectar a ocorrência do encurtamento pelo frio nos músculos esqueléticos de bovinos.
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The activities of the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LD), creatine kinase (CK), amylase (AMS) and angiotensin converting enzyme (ACE) have been used to assess the toxic effects of xenobiotics that have hypoglycaemic action in hepatic, pancreatic, renal and muscle tissue. Using a validated experimental model of diabetes mellitus in rats, we ascertained whether this syndrome itself affected the serum activities of these enzymes over a 53-day period. Levels of hepatic enzymes AST, ALT and ALP were higher in the streptozotocin (STZ)diabetic rats (group D), but were controlled by insulin therapy (group DI). AMS was reduced in group D and unchanged in group DI rats. Proteinuria was detected 1 day after STZ administation and partially controlled by insulin (group DI); its early presence in group D rats, and the lack of any change in serum ACE in this group, indicates that proteinuria is the better marker for microangiopathy. Microscopic examination of liver, kidney, heart and skeletal muscles (soleus and extensor digitorum longus) revealed various alterations in group D rat tissues, which were less pronounced in group DI. The liver, pancreas and kidney tissue-damage was consistent with the altered serum levels of AST, ALT, ALP and AMS and proteinuria. We conclude that: (i) rigorous control is required when these serum-enzyme levels are used as indicators of tissue toxicity in experimental diabetes, and (ii) LD, CK and bilirubin serum levels, which are unaffected by diabetes, can be used when testing effects of xenobiotics on tissues.
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The morphological and structural alterations that occur in the neuromuscular junctions of the denervated rat diaphragm were studied. Fifteen adult male albino rats (Rattus norvegicus) aged about 60 days and with a mean weight of 200 g were used. Chronically denervated diaphragms were obtained and the animals were sacrificed after 4, 8 and 12 weeks of denervation. The left antimere of the diaphragm was denervated by section of the phrenic nerve and the right antimere was used as control. Each antimere was divided into three fragments: one was used for histochemical (nonspecific esterase) and morphometric study of neuromuscular junctions, and the other two were used for transmission and scanning electron microscopy (SEM) analysis. Histochemical analysis of the diaphragm neuromuscular junctions after denervation showed only small changes in junction morphology. However, these junctions became smaller and elongated and presented less visible contours with increasing time of denervation. Ultrastructural analysis of neuromuscular junctions after 12 weeks showed more or less organized junctional folds on the muscle fiber surface. The junctional cytoplasm exhibited important alterations such as mitochondrial degeneration and the presence of numerous filaments. SEM revealed the presence of deep primary synaptic grooves with peripheral excavations which housed the nerve terminal boutons and exhibited internally the secondary synaptic clefts present among the junctional folds of the sarcolemma. This study showed that some of the morphological changes demonstrated in other denervated striated skeletal muscles are not repeated at the same intensity or in the same temporal pattern in the rat diaphragm.
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O músculo estriado esquelético é formado pela associação de fibras musculares com a matriz extracelular. Esse tecido possui alta plasticidade e o conhecimento das características morfológicas, da miogênese, e da dinâmica do crescimento é importante para o entendimento da morfofisiologia bem como para a seleção de animais visando a melhoria na produção de carne. A maioria dos músculos estriados originam-se de células precursoras do mesoderma a partir dos somitos do embrião e o controle da diferenciação ocorre pela ação de fatores indutores ou inibidores. Um grupo de fatores transcricionais, pertencentes à família MyoD tem um papel central na diferenciação muscular. Coletivamente chamados de Fatores de Regulação Miogênica (MRFs), são conhecidos quatro tipos: MyoD, myf-5, miogenina e MRF4. Esses fatores ligam-se à seqüências de DNA conhecidas como Ebox (CANNTG) na região promotora de vários genes músculo-específicos, levando à expressão dos mesmos. As células embrionárias com potencial para diferenciação em células musculares (células precursoras miogênicas) expressam MyoD e Myf-5 e são denominadas de mioblastos. Essas células proliferam, saem do ciclo celular, expressam miogenina e MRF4, que regulam a fusão e a diferenciação da fibra muscular. Uma população de mioblastos que se diferencia mais tardiamente, as células miossatélites, são responsáveis pelo crescimento muscular no período pós natal, que pode ocorrer por hiperplasia e hipertrofia das fibras. As células satélites quiescentes não expressam os MRFs, porém, sob a ação de estímulos como fatores de crescimento ou citocinas, ocorre a ativação desse tipo celular que prolifera e expressa os MRFs de maneira similar ao que ocorre com as células precursoras miogênicas durante a miogênese. Os mecanismos de crescimento muscular são regulados pela expressão temporal dos (MRFs), que controlam a expressão dos genes relacionados com o crescimento muscular.
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A total of 222 dogs were examined by blood smear examination and Hepatozoon canis infection was detected in 13 dogs (5.9%). Five H. canis-infected dogs were necropsied to observe tissue stages in the organs. Fragments of spleen, liver, lungs, heart, kidneys, lymph nodes, bone marrow and skeletal muscles were used to made touch-impression smears. No macroscopic lesions were found in the organs. Two dogs had gamonts within polymorphonuclear cells and schizonts in various stages of development within the spleen and the bone marrow. Nevertheless, no mature meronts were found.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Duchenne muscular dystrophy is a lethal genetic disease characterized by progressive muscle degeneration that usually had been used the Golden Retriever as a model for studying the disease (GRMD - Golden Retriever Muscular Dystrophy). A total of 16 male dystrophic Golden Retrievers dogs between 5 to 51 months of age were examined in the present study. The animals were classified as dystrophic according to two simultaneous complementary criteria: genotypic analysis and serum creatine kinase levels. The macroscopic abnormalities of the different organs and tissues and histopathological features were described using hematoxylin-eosin. The lesions in the skeletal muscles associated with the digestive problems resulted in cachexia with different intensities in all the dystrophic dogs. Cardiac muscle involvement was found in 87,5% of the GRMD dogs resulting, however, in cardiac failure in only 18,8% of the animals. The musculature of the diaphragm was hypertrophic in all affected animals resulting in progressive respiratory muscle weakness and at later stages in respiratory failure (81,25%). The liver abnormalities found in dystrophic dogs were originated mainly from heart disease and developed progressively. Hyperemia of mucosa and granular material indicated changes in the functioning and emptying of bladder. The germinative lineage cells presented moderate to severe degeneration probably due to degeneration of the scrotum and cremaster muscle which prevented the proper thermo-regulation of the testicle. Our results highlight the fact that there is significant impairment of the cardiac, respiratory and skeletal muscle systems in GRMD dogs since the age of five months. In addition, significant alterations of the gastrointestinal tract, urinary and reproductive systems are indicating the presence of degenerative lesions in the smooth musculature.
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The present study had the objective of evaluating calcium accumulations in muscle fibers and their correlation with the canine muscular dystrophy. After the deaths of the animals (13 dystrophic and 3 non-dystrophic), samples of the skeletal muscles were collected. The material was stained with hematoxylin-eosin, Gomori's modified trichrome and alizarin red S technique (pH 4.3). The histopathological changes were analyzed and the proportions of calcium-positive (CPF) and negative muscle fibers were evaluated. Histopathological changes such as muscle fiber diameter changes, necrosis, hyalinization, presence of inflammatory infiltrate and fatty atrophy were identified in all the dystrophic muscles. Statistically significant differences in numbers of CPF between dystrophic muscles and non-dystrophics were observed for the masseter (6%), brachial biceps (5%) and triceps, sartorius and femoral biceps (4%) muscles. The identifying calcium is of interest as a parameter for helping in diagnostic screening.
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Although canine visceral leishmaniasis (CVL) has been extensively studied, muscular damage due to Leishmania (Leishmania) infantum chagasi infection remains to be fully established. The aim of this study was to describe the electromyographic and histological changes, as well as search for the presence of amastigote forms of Leishmania spp, CD3+ T-lymphocytes, macrophages and IgG in skeletal muscles of dogs with visceral leishmaniasis (VL). Four muscles (triceps brachial, extensor carpi radialis, biceps femoris and gastrocnemius) from a total of 17 naturally infected and six healthy dogs were used in this study. Electromyographic alterations such as fibrillation potentials, positive sharp waves and complex repetitive discharges were observed in, at least, three muscles from all infected dogs. Myocyte necrosis and degeneration were the most frequent muscular injury seen, followed by inflammatory reaction, fibrosis and variation in muscle fibers size. Immunohistochemistry in muscle samples revealed amastigote forms in 4/17 (23. 53%), IgG in 12/17 (70. 58%), CD3+ T-lymphocytes in 16/17 (94. 12%) and macrophages in 17/17 (100%) dogs. Statistically positive correlation was observed between: inflammatory infiltrate (p=0. 0305) and CD3+ immunoreaction (p=0. 0307) in relation to the number of amastigote forms; inflammatory infiltrate (p=0. 0101) and macrophage immunoreaction (p=0. 0127) in relation to the amount of CD3+; and inflammatory infiltrate (p=0. 0044) and degeneration/necrosis (p<0. 0001) in relation to the presence of macrophages. Our results suggest that different mechanisms contribute to the development of myocytotoxicity, including celular and humoral immune responses and direct muscular injury by the parasite. Nevertheless, the catabolic nature of the disease can probably interact with other factors, but cannot be incriminated as the only responsible for myositis.
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The aim of this study was to evaluate the electromyographic and histopathological changes in skeletal muscles of dogs naturally infected by L. infantum. Twenty five mixed breed adult dogs with parasitological, molecular and serological diagnosis were selected. The evaluated muscles were: triceps brachial, extensor carpi radialis, biceps femoris and gastrocnemius. One dog had locomotor clinical signs with hind limbs paresis associated with severe muscle atrophy. Twenty-three (92%) had some type of muscular change, and in 22 (88%) such changes were directly identified by electromyography. Even without any clinical signs of the disease, 10 (40%) dogs had electromyographic and histopathological changes. Leishmania antigens were detected in muscles of four (16%) dogs. The electromyographic evaluation indicated the occurrence of chronic polymyositis in 13 (52%) dogs, the presence of both acute and chronic muscle inflammation four (16%), acute myopathy in two (8%) and absence of electromyographic abnormalities in three (12%) dogs. The most frequently observed histopathological changes were degeneration and necrosis of myofibers and inflammatory infiltration observed in 12 (48%) dogs. Other changes were decreased diameter of muscle fibers in 15 (60%) and peri or endomysial fibrosis in 14 (56%) animals. The changes observed in the present study showed that even in the absence of clinical signs, most dogs infected by Leishmania infantum have chronic polymyositis.
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Aim: Chronic exposure to intermittent hypoxia commonly induces the activation of sympathetic tonus and the disruption of glucose homoeostasis. However, the effects of exposure to acute intermittent hypoxia (AIH) on glucose homoeostasis are not yet fully elucidated. Herein, we evaluated parameters related to glucose metabolism in rats exposed to AIH. Methods: Male adult rats were submitted to 10 episodes of hypoxia (6% O2, for 45 s) interspersed with 5-min intervals of normoxia (21%), while the control (CTL) group was kept in normoxia. Results: Acute intermittent hypoxia rats presented higher fasting glycaemia, normal insulinaemia, increased lactataemia and similar serum lipid levels, compared to controls (n = 10, P < 0.05). Additionally, AIH rats exhibited increased glucose tolerance (GT) (n = 10, P < 0.05) and augmented insulin sensitivity (IS) (n = 10, P < 0.05). The p-Akt/Akt protein ratio was increased in the muscle, but not in the liver and adipose tissue of AIH rats (n = 6, P < 0.05). The elevated glycaemia in AIH rats was associated with a reduction in the hepatic glycogen content (n = 10, P < 0.05). Moreover, the AIH-induced increase in blood glucose concentration, as well as reduced hepatic glycogen content, was prevented by prior systemic administration of the β-adrenergic antagonist (P < 0.05). The effects of AIH on glycaemia and Akt phosphorylation were transient and not observed after 60 min. Conclusions: We suggest that AIH induces an increase in blood glucose concentration as a result of hepatic glycogenolysis recruitment through sympathetic activation. The augmentation of GT and IS might be attributed, at least in part, to increased β-adrenergic sympathetic stimulation and Akt protein activation in skeletal muscles, leading to a higher glucose availability and utilization. © 2013 Scandinavian Physiological Society.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)