نتایج جستجو برای: mitochondrial myopathy

تعداد نتایج: 143464  

2014
Alessandra Zulian Francesca Tagliavini Erika Rizzo Camilla Pellegrini Francesca Sardone Nicoletta Zini Nadir Mario Maraldi Spartaco Santi Cesare Faldini Luciano Merlini Valeria Petronilli Paolo Bernardi Patrizia Sabatelli

Ullrich congenital muscular dystrophy and Bethlem myopathy are caused by mutations in collagen VI (ColVI) genes, which encode an extracellular matrix protein; yet, mitochondria play a major role in disease pathogenesis through a short circuit caused by inappropriate opening of the permeability transition pore, a high-conductance channel, which causes a shortage in ATP production. We find that m...

Journal: :Journal of neurology, neurosurgery, and psychiatry 1987
M P Carey K Poulton C Hawkins R P Murphy

A case of carnitine palmitoyl transferase deficiency presenting in a 72 year old woman with the clinical picture of ophthalmoplegia plus other muscle weakness is reported. Histological and ultrastructural examination showed the features of a mitochondrial myopathy.

Journal: :Brain : a journal of neurology 2012
Tanja Taivassalo Karen Ayyad Ronald G Haller

Human skeletal muscle respiratory chain defects restrict the ability of working muscle to extract oxygen from blood, and result in a hyperkinetic circulation during exercise in which oxygen delivery is excessive relative to oxygen uptake and oxygen levels within contracting muscle are abnormally high. To investigate the role of the muscle microcirculation in this anomalous circulatory response ...

2012
P Sabatelli E Palma A Angelin S Squarzoni A Urciuolo C Pellegrini T Tiepolo P Bonaldo F Gualandi L Merlini P Bernardi NM Maraldi

Collagen VI myopathies (Ullrich congenital muscular dystrophy (UCMD), Bethlem myopathy (BM), and myosclerosis myopathy) share a common pathogenesis, that is, mitochondrial dysfunction due to deregulation of the permeability transition pore (PTP). This effect was first identified in the Col6a1(-/-) mouse model and then in muscle cell cultures from UCMD and BM patients; the normalizing effect of ...

2013
Rojeen Shahni Yehani Wedatilake Maureen A Cleary Keith J Lindley Keith R Sibson Shamima Rahman

Nuclear-encoded disorders of mitochondrial translation are clinically and genetically heterogeneous. Genetic causes include defects of mitochondrial aminoacyl-tRNA synthetases, and factors required for initiation, elongation and termination of protein synthesis as well as ribosome recycling. We report on a new case of myopathy, lactic acidosis and sideroblastic anemia (MLASA) syndrome caused by...

2017
Majid Alfadhel Marwan Nashabat Qais Abu Ali Khalid Hundallah

Iron_sulfur clusters (ISCs) are known to play a major role in various protein functions. Located in the mitochondria, cytosol, endoplasmic reticulum and nucleus, they contribute to various core cellular functions. Until recently, only a few human diseases related to mitochondrial ISC biogenesis defects have been described. Such diseases include Friedreich ataxia, combined oxidative phosphorylat...

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