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- ItemAcesso aberto (Open Access)Dengue: muscle biopsy findings in 15 patients(Academia Brasileira de Neurologia - ABNEURO, 1993-06-01) Malheiros, Suzana Maria Fleury [UNIFESP]; Oliveira, Acary Souza Bulle [UNIFESP]; Schmidt, Beny [UNIFESP]; Lima, J.g. Camargo [UNIFESP]; Gabbai, Alberto Alain [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Dengue is known to produce a syndrome involving muscles, tendons and joints. The hallmark of this syndrome is severe myalgia but includes fever, cutaneous rash, and headache. The neuromuscular aspects of this infection are outlined only in isolated reports, and the muscle histopathological features during myalgia have not been described. In order to ascertain the actual neuromuscular involvement in dengue and better comprehend the histological nature of myalgia, we performed a clinical and neurological evaluation, a serum CPK level and a muscle biopsy (with histochemistry) in 15 patients (4 males), median age 23 years (range 14-47) with classic dengue fever, serologically confirmed, during the bra-zilian dengue epidemics from September 1986 to March 1987. All patients had a history of fever, headache and severe myalgia. Upon examination 4 had a cutaneous rash, 3 had fever, and 3 a small hepatomegaly. The neurological examination was unremarkable in all and included a manual muscle test. CPK was mildly elevated in only 3 patients. Muscle biopsy revealed a light to moderate perivascular mononuclear infiltrate in 12 patients and lipid accumulation in 11. Mild mitochondrial proliferation was seen in 3, few central nuclei in 3, rare foci of myonecrosis in 3, and 2 patients had type grouping. Dengue in our patients, produced myalgia but no detectable muscle weakness or other neuromuscular involvement. The main histopathological correlation with myalgia seems to be a perivascular mononuclear infiltrate and lipid accumulation.
- ItemSomente MetadadadosEffects of respiratory muscle unloading on leg muscle oxygenation and blood volume during high-intensity exercise in chronic heart failure(Amer Physiological Soc, 2008-06-01) Borghi-Silva, Audrey [UNIFESP]; Carrascosa, Claudia [UNIFESP]; Oliveira, Cristino Carneiro [UNIFESP]; Barroco, Adriano C. [UNIFESP]; Berton, Danilo C. [UNIFESP]; Vilaca, Debora [UNIFESP]; Lira-Filho, Edgar B. [UNIFESP]; Ribeiro, Dirceu [UNIFESP]; Nery, Luiz Eduardo [UNIFESP]; Neder, J. Alberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Blood flow requirements of the respiratory muscles (RM) increase markedly during exercise in chronic heart failure (CHF). We reasoned that if the RM could subtract a fraction of the limited cardiac output (QT) from the peripheral muscles, RM unloading would improve locomotor muscle perfusion. Nine patients with CHF ( left ventricle ejection fraction = 26 +/- 7%) undertook constant-work rate tests (70-80% peak) receiving proportional assisted ventilation (PAV) or sham ventilation. Relative changes (Delta%) in deoxy-hemoglobyn, oxi-Hb ([O(2)Hb]), tissue oxygenation index, and total Hb ([Hb(TOT)], an index of local blood volume) in the vastus lateralis were measured by near infrared spectroscopy. in addition, QT was monitored by impedance cardiography and arterial O-2 saturation by pulse oximetry (SpO(2)). There were significant improvements in exercise tolerance (Tlim) with PAV. Blood lactate, leg effort/Tlim and dyspnea/Tlim were lower with PAV compared with sham ventilation (P < 0.05). There were no significant effects of RM unloading on systemic O-2 delivery as QT and SpO2 at submaximal exercise and at Tlim did not differ between PAV and sham ventilation (P > 0.05). Unloaded breathing, however, was related to enhanced leg muscle oxygenation and local blood volume compared with sham, i.e., higher Delta[O(2)Hb]% and Delta[Hb(TOT)]%, respectively (P < 0.05). We conclude that RM unloading had beneficial effects on the oxygenation status and blood volume of the exercising muscles at similar systemic O-2 delivery in patients with advanced CHF. These data suggest that blood flow was redistributed from respiratory to locomotor muscles during unloaded breathing.
- ItemSomente MetadadadosEstudo da fibrose no músculo esquelético mediada por receptores de angiotensina e tratamento do músculo lesionado por prp e terapia gênica(Universidade Federal de São Paulo (UNIFESP), 2015-12-17) Stilhano, Roberta Sessa [UNIFESP]; Han, Sang Won Han [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)process, which frequently occurs in cases of deeper muscle injury, leads to imperfect tissue regeneration. The current therapies have a low efficacy for prevention or treatment of the complications caused by fibrosis, such as atrophy, contraction and pain followed by functional loss and post-traumatic fibrosis. Hypertension is a contributing factor in fibrosis, and angiotensin II (Ang II), which is the main responsible for vasoconstriction, seems to trigger signaling fibrosis. There is communication between TGFB1 and Ang II signaling pathway in cardiac muscle. In parallel, there is a discordant discussion of GM-CSF role in skeletal muscle fibrosis. To better understand the fibrotic process occurring after injury in skeletal muscle, first of all, we established a muscle injury model followed by suture, which produces a deep lesion developing fibrosis largely muscle. To evaluate the possible role of the AT1 and GM-CSF in promoting fibrosis, multiple vectors were constructed, including, Lv-mirAT1a expressing a microRNA to silence the expression of AT1a protein and Lv-GM-CSF expressing GM-CSF. Considering that the injection of lentiviral solution in skeletal muscle may not be efficient for transduction of these vectors and cause leakage to other tissues, an alginate hydrogel was formulated for carrying lentivetores. The animals treated with alginate hydrogel loaded with Lv-GM-CSF and Lv-mirAT1a drastically reduced muscle fibrosis. Thus, it was inferred that the AT1a should participate in the fibrotic process of skeletal muscle and its inhibition is a good strategy for reducing post-injury fibrosis. On the other hand, the effect of the expression of GM-CSF in the control of fibrosis varied depending on the inflammatory progression, or its expression and the onset of inflammation-accentuated fibrosis, but expression in late stage drastically reduced fibrosis, confirming the results of our previous work. The mediators of fibrosis, such as angiotensin and growth factors are present in plasma and in sports medicine, the platelet rich plasma (PRP) is widely used to treat various types of lesions, including muscle injury. In an attempt to correlate the above studies with these factors in PRP, the molecular and cellular content of that preparation was evaluated. Two methods for preparation of PRP were established in the literature database and were named LPRP and PPRP. The main difference between the two preparations is the presence of leukocytes (LPRP) or not (PPRP), but the molecular and cellular contents thereof vary markedly PRPs. NIH3T3 cell lines (fibroblasts) and C2C12 (myoblast) grown with 1% PRP, and 10% FBS promoted cell proliferation in different patterns. The expression gene expression profile of 6 growth factors were analyzed and showed that each PRP for each cell type expression level of these genes is significantly variable. In conclusion, it was demonstrated that AT1 participates in skeletal muscle fibrosis and the inhibition of AT1 via microRNA is a good alternative to reduce fibrosis. Forced expression of GM-CSF early in the muscle injury promotes the formation of fibrosis, but their expression days later drastically reduces fibrosis. For late expression of GM-CSF via lentivetor contained in loco, the alginate hydrogel formulation with lentivetor developed here was ideal. As for PRPs, leukocytes contained in LPRP takes the PRP formation with different quality and amount of cells and molecules, hence its effect on the target cells were different.
- ItemSomente MetadadadosProgressive myopathy with a combined respiratory chain defect including Complex II(Elsevier B.V., 2008-01-15) Rodrigues, Andresa De Santi [UNIFESP]; Kiyomoto, Beatriz Hitomi [UNIFESP]; Oliveira, Acary Souza Bulle [UNIFESP]; Gabbai, Alberto Alain [UNIFESP]; Schmidt, Beny [UNIFESP]; Tengan, Celia Harumi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Biochemical defects in the respiratory chain are mostly associated with deficiencies in Complexes I, III and IV, caused by nuclear or mitochondrial DNA mutations. Combined defects including Complex II have been reported very rarely and have muscular symptoms as the main manifestation, including muscle weakness, exercise intolerance and myoglobinuria. We report a patient with a fatal progressive myopathy and muscle biopsy showing diffuse reduction in succinate dehydrogenase activity, ragged red fibers and intense lipid accumulation. Cytochrome c oxidase (COX) histochemistry demonstrated 30% of fibers with increased subsarcolemmal staining while 27% were COX negative. Western blotting analysis showed reduction in the expression of the 39 kDa subunit of Complex I, subunit II of Complex IV and the 70 kDa subunit of Complex II. Our findings suggest that the patient had a complex pattern of mitochondrial dysfunction affecting multiple respiratory chain complexes (I, II and IV) and fatty acid metabolism. This report adds a new histological pattern associated to combined deficiencies of respiratory chain with involvement of Complex II and shows that this disease may be fatal with a rapid progression. (c) 2007 Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosScaling skeletal muscle function to mass in patients with moderate-to-severe COPD(Springer, 2006-11-01) Malaguti, Carla; Nery, Luiz E.; Dal Corso, Simone; Napolis, Lara; De Fuccio, Marcelo Bicalho; Lazaretti-Castro, Marise [UNIFESP]; Neder, José Alberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); UNINOVESkeletal muscle performance and muscle mass are commonly reduced in patients with advanced chronic obstructive pulmonary disease (COPD). It is currently unclear, however, whether negative changes in muscle structure and function are proportionately related to each other in these patients. in a cross-sectional study, 39 patients (post-bronchodilator FEV1 = 49.7 +/- 15.5% pred) and 17 controls were submitted to knee isokinetic dynamometry [peak torque (PT), isometric strength (IS), and total work (TW)] and dual energy X-ray absorptiometry for the evaluation of leg muscle mass (LMM). Muscle function (F) was normalised for LMM by using ratio standards (F center dot LMM-1), power function ratios (F center dot LMM-b, where b is usually not equal 1), and analysis of covariance (ANCOVA). Patients with COPD presented with reduced PT, IS, TW, and LMM as compared to controls: there were significant linear correlations among these variables in both groups (P < 0.05). Ratio standards of PT center dot LMM-1 and TW center dot LMM-1 were, on average, 14% lower in patients than controls (P < 0.01). the coefficients for allometric correction of IS and TW were significantly higher in patients as compared to controls (0.975 vs. 0.603 and 1.471 vs. 0.824, respectively, P < 0.05), i.e. more LMM was needed to generate a given functional output in patients than normal subjects. in addition, adjusted means of muscle function variables by ANCOVA were 11-18% lower for patients than controls with LMM as the covariate (P < 0.05). We conclude that factors other than simple atrophy (i.e. mass-independent mechanisms) might play a role in explaining the COPD-related skeletal muscle dysfunction.
- ItemSomente MetadadadosUltrastructural features of the myotendinous junction of the sternomastoid muscle in Wistar rats: From newborn to aging(Wiley-Blackwell, 2012-09-01) Ciena, Adriano Polican; Yokomizo de Almeida, Sonia Regina; Bolina, Cristina de Sousa; Bolina-Matos, Regina de Sousa; Grassi Rici, Rose Eli; Pereira Da Silva, Marcelo Cavenaghi [UNIFESP]; Miglino, Maria Angelica; Watanabe, Ii-Sei; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)The myotendinous junction (MTJ) is a major area for transmitting force from the skeletal muscle system and acts in joint position and stabilization. This study aimed to use transmission electron microscopy to describe the ultrastructural features of the MTJ of the sternomastoid muscle in Wistar rats from newborn to formation during adulthood and possible changes with aging. Ultrastructural features of the MTJ from the newborn group revealed pattern during development with interactions between muscle cells and extracellular matrix elements with thin folds in the sarcolemma and high cellular activity evidenced through numerous oval mitochondria groupings. the adult group had classical morphological features of the MTJ, with folds in the sarcolemma forming long projections called finger-like processes and sarcoplasmic invaginations. Sarcomeres were aligned in series, showing mitochondria near the Z line in groupings between collagen fiber bundles. the old group had altered finger-like processes, thickened in both levels of sarcoplasmic invaginations and in central connections with the lateral junctions. We conclude that the MTJ undergoes intense activity from newborn to its formation during adulthood. With increasing age, changes to the MTJ were observed in the shapes of the invaginations and finger-like processes due to hypoactivity, potentially compromising force transmission and joint stability. Microsc. Res. Tech. 75:12921296, 2012. (C) 2012 Wiley Periodicals, Inc.