Research Topics
| Julien OchalaSummaryAffiliation: Uppsala University Country: Sweden Publications
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Detail Information
Publications
Nemaline myopathy-related skeletal muscle α-actin (ACTA1) mutation, Asp286Gly, prevents proper strong myosin binding and triggers muscle weaknessJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, Uppsala University, Sweden
PLoS ONE 7:e45923. 2012..To counterbalance such negative events, future potential therapeutic strategies may focus on the inappropriate actin-actin interface or myosin binding...
Congenital myopathy-causing tropomyosin mutations induce thin filament dysfunction via distinct physiological mechanismsJulien Ochala
Department of Neuroscience, Uppsala University, Uppsala, Sweden
Hum Mol Genet 21:4473-85. 2012..Therefore, administration of troponin activators may constitute a promising therapeutic approach in the future...
Maintenance of muscle mass, fiber size, and contractile function in mice lacking the Z-disc protein myotilinJulien Ochala
Department of Clinical Neurophysiology, Uppsala University Hospital, Sweden
Ups J Med Sci 114:235-41. 2009..Myotilin location and interactions with other Z-disc proteins are clearly defined, but its role in the regulation of muscle structure and function remains unknown. The present study aims at investigating this specific role of myotilin...
Disrupted myosin cross-bridge cycling kinetics triggers muscle weakness in nebulin-related myopathyJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, Uppsala University Hospital, Entrance 85, 3rd Floor, SE 751 85 Uppsala, Sweden
FASEB J 25:1903-13. 2011..To reverse such a negative cascade of events, future potential therapeutic interventions should, therefore, focus on the triggering component, the altered myosin cross-bridge cycling kinetics...
Diaphragm muscle weakness in an experimental porcine intensive care unit modelJulien Ochala
Department of Neuroscience, Uppsala University, Uppsala, Sweden
PLoS ONE 6:e20558. 2011..Unexpectedly, sepsis, CS or NMBA have no significant additive effects, suggesting that mechanical ventilation and sedation are the triggering factors leading to diaphragm weakness in the intensive care unit...
EMD 57033 partially reverses ventilator-induced diaphragm muscle fibre calcium desensitisationJulien Ochala
Department of Clinical Neurophysiology, Uppsala University Hospital, Uppsala, Sweden
Pflugers Arch 459:475-83. 2010..Thus, EMD 57033 partly restored the Ca(2+) activation of cells, reducing VIDD. This finding offers a strong basis for evaluating the effect of Ca(2+) sensitisers on diaphragm function in vivo...
A myopathy-linked tropomyosin mutation severely alters thin filament conformational changes during activationJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, Uppsala University, Uppsala, Sweden
Proc Natl Acad Sci U S A 107:9807-12. 2010....
Factors underlying the early limb muscle weakness in acute quadriplegic myopathy using an experimental ICU porcine modelJulien Ochala
Department of Neuroscience, Uppsala University, Uppsala, Sweden
PLoS ONE 6:e20876. 2011..These results suggest that the rapid declines in CMAP amplitude and in force generation capacity are triggered by independent mechanisms with significant clinical and therapeutic implications...
Mechanisms underlying the sparing of masticatory versus limb muscle function in an experimental critical illness modelSudhakar Aare
Department of Neuroscience, Clinical Neurophysiology, Uppsala University, Uppsala, Sweden
Physiol Genomics 43:1334-50. 2011..spinal nerve innervated muscles during exposure to the ICU intervention...
Effects of a preferential myosin loss on Ca2+ activation of force generation in single human skeletal muscle fibresJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, University Hospital, Uppsala, Sweden
Exp Physiol 93:486-95. 2008..Thus, a change in Ca(2+) activation of the contractile apparatus in patients with preferential myosin loss is proposed as an additional factor contributing to the muscle function impairment in these patients...
Effects of a R133W beta-tropomyosin mutation on regulation of muscle contraction in single human muscle fibresJulien Ochala
Department of Clinical Neurophysiology, Uppsala University Hospital, Entrance 85, 3rd Floor, SE 751 85 Uppsala, Sweden
J Physiol 581:1283-92. 2007....
A myopathy-related actin mutation increases contractile functionJohan Lindqvist
Department of Neuroscience, Clinical Neurophysiology, Uppsala University, Sweden
Acta Neuropathol 123:739-46. 2012..Overall, at the cell level, these divergent mechanisms conduct to an improved steady-state force production. Such results provide new surprising scientific insights and crucial information for future therapeutic strategies...
Preferential skeletal muscle myosin loss in response to mechanical silencing in a novel rat intensive care unit model: underlying mechanismsJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, Uppsala University, Uppsala, Sweden
J Physiol 589:2007-26. 2011....
Defective regulation of contractile function in muscle fibres carrying an E41K beta-tropomyosin mutationJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, University Hospital, Entrance 85, 3rd Floor, SE 751 85 Uppsala, Sweden
J Physiol 586:2993-3004. 2008....
Ca2+ sensitizers: An emerging class of agents for counterbalancing weakness in skeletal muscle diseases?Julien Ochala
Department of Clinical Neurophysiology, Uppsala University Hospital, Sweden
Neuromuscul Disord 20:98-101. 2010..Therefore, in the future, under certain conditions, these agents may represent an emerging class of agents to enhance the quality of life of patients suffering from skeletal muscle weakness...
Gene expression and muscle fiber function in a porcine ICU modelVaruna C Banduseela
Department of Clinical Neurophysiology, Uppsala University Hospital, SE 751 85 Uppsala, Sweden
Physiol Genomics 39:141-59. 2009..To our knowledge, this is the first study that isolates the effect of immobilization and mechanical ventilation in an ICU condition from various other cofactors...
Thin filament proteins mutations associated with skeletal myopathies: defective regulation of muscle contractionJulien Ochala
Department of Neuroscience, Clinical Neurophysiology, University Hospital, Entrance 85, SE 751 85, Uppsala, Sweden
J Mol Med (Berl) 86:1197-204. 2008..With an enhanced understanding of the cellular and molecular mechanisms underlying muscle weakness in patients carrying such mutations, better therapy strategies can be developed to improve the quality of life...
Sparing of muscle mass and function by passive loading in an experimental intensive care unit modelGuillaume Renaud
Department of Neuroscience, Clinical Neurophysiology, University Hospital, Entrance 85, 3rd Floor, SE 751 85 Uppsala, Sweden
J Physiol 591:1385-402. 2013....
