Results 131 to 140 of about 6,956 (184)

AAV8 gene therapy for mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) in a patient's liver maintained ex situ for 9 days

Teresa Brevini, Lisa Swift, Helen Reynolds, John Ong, Richard J Stopforth, Yogeshkumar Malam, Harry V. M. Spiers, AnnaPaterson, Adam Duckworth, Arthur Kaser, Vasilis Kosmoliaptsis, Ramón Martí, Jelle van den Ameele, Gwilym James Webb, Christopher J.E. Watson, Andrew J. Butler, Fotios Sampaziotis   +16 more
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NEW HORIZONS IN THE TREATMENT OF MITOCHONDRIAL NEUROGASTROINTESTINAL ENCEPHALOMYOPATHY (MNGIE): FROM PATHOGENESIS TO THERAPIES

Dominika TRZMIEL
openalex   +1 more source

A previously diagnosed mitochondrial neurogastrointestinal encephalomyopathy patient presenting with perforated ileal diverticulitis

The Turkish Journal of Gastroenterology, 2005
Fikret AKSOY, Gökhan DEMİRAL, Tayfun BİLGİÇ, İbrahim Gürhan GÜNGÖR, Alp ÖZÇELIK   +4 more
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Liver Transplantation in Mitochondrial Neurogastrointestinal Encephalomyopathy (MNGIE): Surgical Approach and Short-term Results

Martín Huerta, Laura Vidal, Cristina Dopazo, Mar Dalmau, Mireia Caralt, Jose Andrés Molino, Concepción Gómez‐Gavara, Itxarone Bilbao   +7 more
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Brain magnetic resonance imaging findings in Mitochondrial Neurogastrointestinal Encephalomyopathy (MNGIE): A case-based review

Maria Veatriki Christodoulou, Nikoletta Anagnostou, Anastasia K. Zikou   +2 more
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Tachyduodenia in Mitochondrial Neurogastrointestinal Encephalomyopathy

Neurogastroenterology and Motility, 2011
AbstractIn a 38‐year‐old male patient diagnosed with mitochondrial neurogastrointestinal encephalomyopathy an abnormally high duodenal contraction frequency of 20 per minute was found to be present. It is speculated that this tachyduodenia is caused by a metabolic effect on Cajal cells.
A J P M Smout
exaly   +3 more sources

Mitochondrial Encephalomyopathies

Neurologic Clinics, 1990
The mitochondrial diseases present with great heterogeneity. They are often multisystemic and vary considerably in age at onset, distribution of weakness, severity, and course. Only nonthyroidal hypermetabolism has a distinctive clinical presentation. Therefore, attempts at classification have generated some controversy.
S, DiMauro, E, Bonilla, A, Lombes, S, Shanske, C, Minetti, C T, Moraes   +5 more
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Mitochondrial Encephalomyopathies

Archives of Neurology, 1993
Mitochondrial diseases are uniquely interesting from a genetic point of view because mitochondria contain their own DNA (mtDNA) and are capable of synthesizing a small but vital set of proteins, all of which are components of respiratory chain complexes.
S, DiMauro, C T, Moraes
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Succinyl-CoA Synthetase Dysfunction as a Mechanism of Mitochondrial Encephalomyopathy: More Than Just an Oxidative Energy Deficit [PDF]

International Journal of Molecular Sciences, 2023
Brett H Graham, Makayla S Lancaster
exaly   +2 more sources

Mitochondrial encephalomyopathy

2023
Mitochondrial dysfunction, especially perturbation of oxidative phosphorylation and adenosine triphosphate (ATP) generation, disrupts cellular homeostasis and is a surprisingly frequent cause of central and peripheral nervous system pathology. Mitochondrial disease is an umbrella term that encompasses a host of clinical syndromes and features caused by
Ng YS, McFarland R
openaire   +3 more sources