Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Alyssa B Becker"'
Autor:
Arnulf H Koeppen, R Liane Ramirez, Alyssa B Becker, Sarah T Bjork, Sonia Levi, Paolo Santambrogio, Patrick J Parsons, Pamela C Kruger, Karl X Yang, Paul J Feustel, Joseph E Mazurkiewicz
Publikováno v:
PLoS ONE, Vol 10, Iss 3, p e0116396 (2015)
Friedreich ataxia (FA) is an autosomal recessive disease with a complex neurological phenotype, but the most common cause of death is heart failure. This study presents a systematic analysis of 15 fixed and 13 frozen archival autopsy tissues of FA he
Externí odkaz:
https://doaj.org/article/b701158d15db466b802bee797fea0330
Autor:
Alyssa B. Becker, Lanlin Chen, Bo Ning, Song Hu, John A. Hossack, Alexander L. Klibanov, Brian H. Annex, Brent A. French
Publikováno v:
Ultrasound Med Biol
Mouse models are critical in developing new therapeutic approaches to treat peripheral arterial disease (PAD). Despite decades of research and numerous clinical trials, the efficacy of available therapies is limited. This may suggest shortcomings in
Publikováno v:
Journal of Neuropathology & Experimental Neurology. 76:969-977
Dorsal root ganglia, dorsal roots (DR), and dorsal root entry zones (DREZ) are vulnerable to frataxin deficiency in Friedreich ataxia (FA). A previously unrecognized abnormality is the intrusion of astroglial tissue into DR. Segments of formalin-fixe
Autor:
Patrick J. Parsons, Arnulf H. Koeppen, Alyssa B. Becker, Paul J. Feustel, Karl X. Yang, Pamela C. Kruger
Publikováno v:
The American Journal of Cardiology. 118:127-131
Cardiomyopathy is a frequent cause of death in patients with Friedreich ataxia (FA), and a characteristic pathological feature is the focal accumulation of iron (Fe) in cardiomyocytes. This restricted localization of the metal contrasts with the diff
Autor:
Michele L. Yang, Peter Bauer, Jiang Qian, Arnulf H. Koeppen, Alyssa B. Becker, Benjamin B. Gelman
In a small percentage of patients with Friedreich ataxia (FA), the pathogenic mutation is compound heterozygous, consisting of a guanine-adenine-adenine (GAA) trinucleotide repeat expansion in one allele, and a deletion, point mutation, or insertion
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7dec9fb1310ffa9f48cd9fa1f46c57f6
https://europepmc.org/articles/PMC5901083/
https://europepmc.org/articles/PMC5901083/
Autor:
Benjamin B. Gelman, Arnulf H. Koeppen, Paul J. Feustel, Alyssa B. Becker, Joseph E. Mazurkiewicz
Publikováno v:
Journal of the neurological sciences. 367
Friedreich ataxia (FRDA) is an autosomal recessive disorder with a complex clinical and neuropathological phenotype, but the most frequent cause of death is cardiomyopathy. The principal autopsy findings in FRDA hearts are concentric hypertrophy, enl
Autor:
Paul J. Feustel, R. Liane Ramirez, Alyssa B. Becker, Joseph E. Mazurkiewicz, Arnulf H. Koeppen
Atrophy of large neurons in the dentate nucleus (DN) is an important pathologic correlate of neurologic disability in patients with Friedreich ataxia (FA). Thinning of the DN was quantified in 29 autopsy cases of FA and 2 carriers by measuring the th
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f88ac4bf5d12fe300fc82e66ef026f47
https://europepmc.org/articles/PMC4294979/
https://europepmc.org/articles/PMC4294979/
Publikováno v:
Journal of Neuropathology & Experimental Neurology. :nlw111
After Friedreich's description in 1877, depletion of myelinated fibers in the dorsal columns, dorsal spinocerebellar and lateral corticospinal tracts, and neuronal loss in the dorsal nuclei of Clarke columns were considered unique and essential neuro
Publikováno v:
Acta Neuropathologica Communications
Introduction Dorsal root ganglia (DRG) are highly vulnerable to frataxin deficiency in Friedreich ataxia (FA), an autosomal recessive disease due to pathogenic homozygous guanine-adenine-adenine trinucleotide repeat expansions in intron 1 of the FXN