Добірка наукової літератури з теми "Skeletal muscle biopsy samples"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Skeletal muscle biopsy samples".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "Skeletal muscle biopsy samples"
Kurt, YaseminGulcan, Bulent Kurt, Omer Ozcan, Turgut Topal, Abdullah Kilic, Tuba Muftuoglu, Cengizhan Acikel, et al. "Preservative solution for skeletal muscle biopsy samples." Annals of Indian Academy of Neurology 18, no. 2 (2015): 187. http://dx.doi.org/10.4103/0972-2327.150601.
Повний текст джерелаWendling, P. S., S. J. Peters, G. J. Heigenhauser, and L. L. Spriet. "Variability of triacylglycerol content in human skeletal muscle biopsy samples." Journal of Applied Physiology 81, no. 3 (September 1, 1996): 1150–55. http://dx.doi.org/10.1152/jappl.1996.81.3.1150.
Повний текст джерелаBraga, Sérgio De Almeida, Felipe Gomes Ferreira Padilha, and Ana Maria Reis Ferreira. "Needle muscle biopsy: technique validation and histological and histochemical methods for evaluating canine skeletal muscles." Semina: Ciências Agrárias 38, no. 2 (May 2, 2017): 765. http://dx.doi.org/10.5433/1679-0359.2017v38n2p765.
Повний текст джерелаParker, Kenneth C., Ronan J. Walsh, Mohammad Salajegheh, Anthony A. Amato, Bryan Krastins, David A. Sarracino, and Steven A. Greenberg. "Characterization of Human Skeletal Muscle Biopsy Samples Using Shotgun Proteomics†." Journal of Proteome Research 8, no. 7 (July 6, 2009): 3265–77. http://dx.doi.org/10.1021/pr800873q.
Повний текст джерелаSoderlund, K., and E. Hultman. "Effects of delayed freezing on content of phosphagens in human skeletal muscle biopsy samples." Journal of Applied Physiology 61, no. 3 (September 1, 1986): 832–35. http://dx.doi.org/10.1152/jappl.1986.61.3.832.
Повний текст джерелаGüttsches, Anne-Katrin, Robert Rehmann, Anja Schreiner, Marlena Rohm, Johannes Forsting, Martijn Froeling, Martin Tegenthoff, Matthias Vorgerd, and Lara Schlaffke. "Quantitative Muscle-MRI Correlates with Histopathology in Skeletal Muscle Biopsies." Journal of Neuromuscular Diseases 8, no. 4 (July 30, 2021): 669–78. http://dx.doi.org/10.3233/jnd-210641.
Повний текст джерелаBraund, K. G., and K. A. Amling. "Muscle Biopsy Samples for Histochemical Processing: Alterations Induced by Storage." Veterinary Pathology 25, no. 1 (January 1988): 77–82. http://dx.doi.org/10.1177/030098588802500111.
Повний текст джерелаGraham, T. E., B. Wolfe, and J. K. Barclay. "Active skeletal muscle metabolism and tension production: the influence of biopsies." Canadian Journal of Physiology and Pharmacology 71, no. 3-4 (March 1, 1993): 241–46. http://dx.doi.org/10.1139/y93-038.
Повний текст джерелаConstantin-Teodosiu, D., G. Cederblad, and E. Hultman. "PDC activity and acetyl group accumulation in skeletal muscle during isometric contraction." Journal of Applied Physiology 74, no. 4 (April 1, 1993): 1712–18. http://dx.doi.org/10.1152/jappl.1993.74.4.1712.
Повний текст джерелаBerthon, Phanélie M., Richard A. Howlett, George J. F. Heigenhauser, and Lawrence L. Spriet. "Human skeletal muscle carnitine palmitoyltransferase I activity determined in isolated intact mitochondria." Journal of Applied Physiology 85, no. 1 (July 1, 1998): 148–53. http://dx.doi.org/10.1152/jappl.1998.85.1.148.
Повний текст джерелаДисертації з теми "Skeletal muscle biopsy samples"
Pillitteri, Paul J. "Regeneration of Rat Skeletal Muscle Following a Muscle Biopsy." Ohio University / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1118087917.
Повний текст джерелаLaurentino, Gilberto Candido. "Treinamento de força com oclusão vascular: adaptações neuromusculares e moleculares." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/39/39132/tde-13082010-103300/.
Повний текст джерелаIt has been demonstrated that low intensity training associated to vascular occlusion (LIO) promotes similar gains in strength and muscle mass when compared to high intensity strength training (HI). The aim of the present study was to evaluate the effect of three different training programs on skeletal muscle hypertrophy and atrophy related gene expression. Twenty nine young male, with no previous experience in strength training were randomly allocated in three groups: low intensity strength training (i.e. 20% - 1-RM) (LI); low intensity strength training associated to vascular occlusion (i.e. 20% - 1-RM) (LIO); high intensity strength training (HI) (i.e. 80% - 1-RM). One-way ANOVA was used to assess differences in % delta change values of 1-RM and cross sectional area (CSA) of the quadriceps femoris. Mixed model analysis was used to compare myostatin (MSTN), folistatyn-3 (FLST-3), SMAD-7 e GASP-1 changes between groups pre and post training. Results demonstrated similar increases in strength and muscle hypertrophy for LIO and HI groups. Moreover, such increases were significantly greater when compared to LI. These results may be, at least in part, explained by a significant decrease in MSTN mRNA expression in LIO (45%) and HI (41%) when compared to LI (16%); additionally, SMAD-7; FLST-3 and GASP-1 mRNA expression were significantly increased. In conclusion, LIO training promotes similar gains than HI training. The results may be explained by changes in MSTN and related genes mRNA expression
Widman, Lars. "Skeletal muscle potassium and magnesium in diuretic treated patients : effects of potassium - sparing diuretics of magnesium supplementation." Doctoral thesis, Umeå universitet, Medicin, 1988. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-100556.
Повний текст джерелаMüller-Witt, Adriane [Verfasser]. "Heat shock protein 72 expression in skeletal muscle samples from cachectic- and non-cachectic-pancreatic cancer patients / Adriane Müller-Witt." Ulm : Universität Ulm. Medizinische Fakultät, 2015. http://d-nb.info/1066305412/34.
Повний текст джерелаGitiaux, Cyril. "Role of vascular plasticity in muscle remodeling in the child." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T005/document.
Повний текст джерелаSkeletal muscle is highly vascularised. Beyond oxygen and nutriment supply, new functions for vessels have been recently identified, through the interactions that vessel cells (endothelial cells) establish with muscle cells, particularly with muscle stem cells (satellite cells). These latter closely interact with endothelial cells for their expansion and their differentiation, then with periendothelial cells for their self-renewal and return to quiescence. During skeletal muscle regeneration endothelial cells reciprocally interact with myogenic cells by direct contact or by releasing soluble factors to promote both myogenesis and angiogenesis processes. Skeletal muscle regeneration typically occurs as a result of a trauma or disease, such as congenital or myopathies. To better understand the role of vessel plasticity in tissue remodeling, we took advantage of two muscular disorders that could be considered as paradigmatic situations of regenerating skeletal muscle in the child: Juvenile Dermatomyositis (JDM), the most frequent inflammatory myopathy and Duchenne Muscular Dystrophy (DMD), the most common type of muscular dystrophy. Although these two muscular disorders share, at the tissue level, similar mechanisms of necrosis-inflammation, they differ regarding the vessel domain. In JDM patients, microvascular changes consist in a destruction of endothelial cells assessed by focal capillary loss. This capillary bed destruction is transient. The tissue remodeling is efficient and muscle may progressively recover its function. By contrast, in DMD, despite an increase of vessels density in an attempt to improve the muscle perfusion, the muscle function progressively alters with age. We identified clinical and pathological markers of severity and predictive factors for poor clinical outcome in JDM by computing a comprehensive initial and follow-up clinical data set with deltoid muscle biopsy alterations controlled by age-based analysis of the deltoid muscle capillarization. We demonstrated that JDM can be divided into two distinctive clinical subgroups. The severe clinical presentation and outcome are linked to vasculopathy. Furthermore, a set of simple predictors (CMAS<34, gastrointestinal involvement, muscle endomysial fibrosis at disease onset) allow early recognition of patients needing rapid therapeutic escalation with more potent drugs. We studied in vitro the specific cell interactions between myogenic cells issued from JDM and DMD patients and normal endothelial cells to explore whether myogenic cells participate to the vessel remodeling observed in the two pathologies. We demonstrated that MPCs possessed angiogenic properties depending on the pathological environment. In DMD, MPCs promoted the development of establishment of an anarchic, although strong, EC stimulation, leading to the formation of weakly functional vessels. In JDM, MPCs enhanced the vessel reconstruction via the secretion of proangiogenic factors. This functional analysis was supported by the transcriptomic analysis consistent with a central vasculopathy in JDM including a strong and specific response to an inflammatory environment. On the contrary, DMD cells presented an unbalanced homeostasis with deregulation of several processes including muscle and vessel development with attempts to recover neuromuscular system by MPCs. To summarize, our data should allow the definition of new functions of vessel cells in skeletal muscle remodelling during muscle pathologies of the child that will open the way to explore new therapeutic options and to gain further insights in the pathogenesis of these diseases
Guardia, Paolo Gadioli La. "Inibição, por sinvastatina, da respiração mitocondrial de biopsias de musculo esqueletico e figado de ratos." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311233.
Повний текст джерелаDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicaas
Made available in DSpace on 2018-08-15T19:15:54Z (GMT). No. of bitstreams: 1 Guardia_PaoloGadioliLa_M.pdf: 2017398 bytes, checksum: 71295ad7aacb6f016fb0abb80fd36bf9 (MD5) Previous issue date: 2010
Resumo: Inibidores da 3-hidroxi-3-metilglutaril-CoA redutase (estatinas) são fármacos utilizados para diminuir os níveis plasmáticos de colesterol e são, geralmente, seguros e bem tolerados. Ocasionalmente esses fármacos induzem miotoxicidade, como miopatia e rabdomiólise, e hepatotoxicidade. Neste trabalho investigou-se o mecanismo, in vitro e in vivo, pelo qual as estatinas atuam sobre a respiração mitocondrial de biópsias de músculo esquelético e de fígado de ratos. A incubação (1 hora) de biópsias permeabilizadas de músculo sóleo (2-3 mg) com doses crescentes de sinvastatina reduziu a velocidade de respiração mitocondrial estimulada por ADP ou FCCP de forma dose-dependente e significativa (p<0,05). A inibição causada por 1 |iM de sinvastatina nas velocidades de respiração estimuladas por ADP e FCCP foi de respectivamente cerca de 25% e 27%. Em contraste, não houve alteração significativa na velocidade de respiração de repouso. O efeito de 1|iM de sinvastatina foi inibido pela incubação concomitante com 100 |uM de mevalonato (produto da enzima HMG-CoA redutase), ou 10 |JM de coenzima Q10 (um outro produto da via de síntese do colesterol). A redução na velocidade de respiração também foi inibida pela incubação concomitante com 1 mM de L-carnitina. A incubação com sinvastatina aumentou de forma significativa (p<0,05) a produção de lactato pelas biópsias musculares em cerca de 26%, efeito protegido pela incubação concomitante com mevalonato ou coenzima Q10 ou L-carnitina na mesma concentração descrita anteriormente. Por outro lado, esta mesma concentração de sinvastatina não provocou efeito algum sobre as velocidades de respiração de mitocôndrias isoladas de músculo de ratos. A incubação (1 hora) de biópsias hepáticas (2-3 mg) com doses crescentes de sinvastatina reduziu a respiração mitocondrial estimulada por ADP ou FCCP, sem alterar a respiração de repouso. Sinvastatina (5 uM) inibiu significativamente (p<0,05) a respiração estimulada por ADP e FCCP em cerca de 24% e 29% respectivamente. Esta inibição não foi sensível a 100 |iM de mevalonato ou 10 |iM de coenzima Q10 ou 1 mM de L-carnitina. Biópsias de músculo sóleo de ratos tratados durante 15 dias com 100 mg / kg (gavagem) de sinvastatina apresentaram velocidades de consumo de oxigênio reduzidas em todos os estados respiratórios. Este efeito foi inibido pela administração concomitante de L-carnitina 200 mg / kg (gavagem).
Abstract: 3-Hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are safe and well-tolerated therapeutic drugs, that occasionally induce myotoxicity such as myopathy and rhabdomyolysis, and hepatotocixity. Here, we investigated in vitro and in vivo the mechanisms of statin-induced toxicity on mitochondrial respiration of rat skeletal muscle and liver biopsies. One hour incubation of permeabilized soleus muscle biopsies (2-3 mg) with increasing doses of simvastatin (1 to 40 |iM) reduced ADP- or FCCP-stimulated mitochondrial respiration rate in a dose-dependent manner. The inhibition of ADP- or FCCP-stimulated mitochondrial respiration rate by simvastatin 1 |iM was 25% and 27%, respectively. No changes in rest respiration rate was observed. Simvastatin (1 |JM) inhibition of muscle respiration was prevented by coincubation with 100 |JM mevalonate, 10 |JM coenzyme Q10 or 1 mM L-carnitine. Simvastatin (1 |JM) also increased lactate production in muscle biopsies by 26%; this effect was prevented by the coincubation with mevalonate, coenzyme Q10 or L-carnitine. At the same concentration, simvastatin did not inhibit the respiration of isolated skeletal muscle mitochondria suggesting that simvastatin effect on mitochondrial respiration is not direct. Incubation (1 hour) of liver biopsies (2-3 mg) with increasing doses of simvastatin reduced ADP- or FCCP-stimulated mitochondrial respiration rate without changes in rest respiration rate. The lowest simvastatin concentration able to reduce liver biopsies respiration rates was 5 |JM, which promoted 24% and 29% inhibition in ADP- or FCCP-stimulated respiration rates, respectively. This was not modified by mevalonate, coenzyme Q10 or L-carnitine. Soleus muscle biopsies from rats treated during 15 days with simvastatin (100 mg/kg, p.o.) presented L-carnite sensitive inhibition of oxygen consumption rate in all respiratory states.
Mestrado
Medicina Experimental
Mestre em Fisiopatologia Médica
Breda, Ana Paula. "Avaliação da musculatura estriada de membros inferiores na limitação funcional ao exercício em pacientes com hipertensão arterial pulmonar." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5150/tde-20072011-145309/.
Повний текст джерелаIntroduction: Pulmonary arterial hypertension (PAH) is a relentlessly progressive disease that leads to right heart failure and death. Despite advances in pharmacological treatment, prognosis is still poor with survival rates of 86%, 70% and 55% at 1, 3 and 5 years, respectively. Progressive dyspnea and exercise intolerance are the main clinical manifestations and reflect the impairment of right ventricular function. Peripheral skeletal muscle also seems to be a major determinant of functional limitation, as the reduction of oxygen supply and changes in extraction and utilization of oxygen by the muscle are directly associated to exercise tolerance. There are two potential mechanisms involved in the regulation of oxygen supply and therefore in exercise capacity: central (as a function of heart, lung and autonomic nervous system function) and peripheral (associated to peripheral blood flow and skeletal muscle function). Patients with PAH usually present low cardiac output and exacerbated adrenergic state. The combination of these features might result in changes of peripheral skeletal muscle and structure. However, there is no robust information that clearly clarifies whether the muscle involvement is an independent factor for exercise limitation. Objectives: (1) Characterize the role of the peripheral muscles in functional limitation in patients with PAH. (2) Address the role of the peripheral muscle system as an independent factor in exercise limitation in PAH. Materials and methods: Sixteen PAH patients were prospectively compared to 10 control individuals in terms of demographic data, health related quality of life and exercise limitation, assessed by six-minute walk test, cardiopulmonary test, isokinetic dynamometry and maximum respiratory pressure measurements. PAH patients also were submitted to vastus lateralis biopsy in order to assess structural changes. Results: PAH patients presented poorer quality of life (p <0.001), lower percentage of fat free mass (p = 0.044), lower respiratory muscle strength (p <0.001), lower resistance and strength of the extensor of the thigh (p = 0.017 and 0.012, respectively) and greater functional limitation demonstrated by the six-minute walk distance (p <0.001) and at the cardiopulmonary exercise test (p <0.001 for VO2max/kg), as compared to the control group. These findings of reduced muscle strength and function are in agreement with the findings of reduced percentage of Type I fibers at the muscle biopsy. The oxygen consumption correlated to the function of respiratory muscles and of extensor muscles of the thigh (endurance and strength) as well as to the proportion of oxidative fibers (Type I). The cardiac output also correlated with VO2. A bivariate model demonstrated that muscle function is an independent predictor of maximum oxygen consumption, even correcting for the hemodynamic profile. Conclusion: (1) PAH patients present functional and structural changes in peripheral skeletal muscles, and (2) these changes determine overall exercise capacity limitation, independently of the hemodynamic pattern
Книги з теми "Skeletal muscle biopsy samples"
Atlas of skeletal muscle pathology. Lancaster: MTP Press, 1985.
Знайти повний текст джерелаPipitone, Nicolo. Imaging of skeletal muscle. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0014.
Повний текст джерелаMammen, Andrew L., and Jessica R. Nance. Evaluation of hyperCKaemia. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0007.
Повний текст джерелаChinoy, Hector, and Robert G. Cooper. Polymyositis and dermatomyositis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0124.
Повний текст джерелаJadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.
Повний текст джерелаJadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.
Повний текст джерелаHall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.
Повний текст джерелаЧастини книг з теми "Skeletal muscle biopsy samples"
Ferguson, Richard A., and Natalie F. Shur. "Skeletal muscle biopsy." In Sport and Exercise Physiology Testing Guidelines, 205–11. 5th ed. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003045267-32.
Повний текст джерелаFerguson, Richard A., and Natalie F. Shur. "Skeletal muscle biopsy." In Sport and Exercise Physiology Testing Guidelines: Volume I – Sport Testing, 118–24. 5th ed. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003045281-22.
Повний текст джерелаBurns, Dennis K. "Skeletal Muscle Biopsy Evaluation." In A Case-Based Guide to Neuromuscular Pathology, 3–48. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-25682-1_1.
Повний текст джерелаWeidenheim, Karen M. "Optimizing the Skeletal Muscle Biopsy." In Histopathology, 397–410. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1050-2_24.
Повний текст джерелаGaspar, Balan Louis, Rakesh Kumar Vasishta, and Bishan Dass Radotra. "A Beginner’s Approach to Skeletal Muscle Biopsy." In Myopathology, 283–84. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1462-9_16.
Повний текст джерелаTurner, Daniel C., Andreas M. Kasper, Robert A. Seaborne, Alexander D. Brown, Graeme L. Close, Mark Murphy, Claire E. Stewart, Neil R. W. Martin, and Adam P. Sharples. "Exercising Bioengineered Skeletal Muscle In Vitro: Biopsy to Bioreactor." In Methods in Molecular Biology, 55–79. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8897-6_5.
Повний текст джерелаJuel, Carsten. "Membrane Transport in Human Skeletal Muscle." In Muscle Biopsy. InTech, 2012. http://dx.doi.org/10.5772/31425.
Повний текст джерелаCapel, Frederic, Valentin Barquissau, Ruddy Richard, and Beatrice Morio. "Evaluation of Mitochondrial Functions and Dysfunctions in Muscle Biopsy Samples." In Muscle Biopsy. InTech, 2012. http://dx.doi.org/10.5772/30705.
Повний текст джерелаLejay, A., A. L. Charles, J. Zoll, J. Bouitbir, F. Thaveau, F. Piquard, and B. Geny. "Skeletal Muscle Mitochondrial Function in Peripheral Arterial Disease: Usefulness of Muscle Biopsy." In Muscle Biopsy. InTech, 2012. http://dx.doi.org/10.5772/31674.
Повний текст джерелаGherardi, Romain, Anthony A. Amato, Hart G. Lidov, and Umberto De Girolami. "Pathology of Skeletal Muscle." In Escourolle and Poirier's Manual of Basic Neuropathology, 299–340. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190675011.003.0012.
Повний текст джерелаТези доповідей конференцій з теми "Skeletal muscle biopsy samples"
Jalal, M., JA Campbell, J. Wadsley, and AD Hopper. "OWE-29 Can digital skeletal muscle index predict palliative chemotherapy uptake before patients undergo endoscopic pancreatic biopsy?" In British Society of Gastroenterology Annual Meeting, 17–20 June 2019, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-bsgabstracts.289.
Повний текст джерелаPerez, Matheus Moreira, David Feder, Beatriz da Costa Aguiar Alves, Fernando Luiz Affonso Fonseca, and Alzira Alves de Siqueira Carvalho. "myoMIR and gene expression in myofibrillar myopathy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.662.
Повний текст джерелаAthayde, Natália Merten, and Alzira Alves de Siqueira Carvalho. "The heart of myofibrillary myopathy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.457.
Повний текст джерелаAhmed, Amira, Huda Farah, Omnia Ahmed, Dina Elsayegh, Abdelrahman Elgamal, and Nasser Moustafa Rizk. "Profile Of Oxidative Stress Genes In Response To Obesity Treatment." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0150.
Повний текст джерела