Zobrazeno 1 - 10
of 17
pro vyhledávání: '"David W Donley"'
Publikováno v:
PLoS ONE, Vol 16, Iss 5, p e0250606 (2021)
Huntington's disease (HD) is a neurodegenerative disorder caused by a dominant CAG-repeat expansion in the huntingtin gene. Microglial activation is a key feature of HD pathology, and is present before clinical disease onset. The kynurenine pathway (
Externí odkaz:
https://doaj.org/article/09f6d8fb20fd4f8f8e9c185b729c4aa6
Publikováno v:
PLoS ONE, Vol 11, Iss 9, p e0162404 (2016)
Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a polyglutamine-repeat expansion in the huntingtin protein. Activation of the kynurenine pathway of tryptophan degradation is implicated in the pathogenesis of HD. Indole
Externí odkaz:
https://doaj.org/article/f3393d3dc7904f608e20d1a6a882998a
Publikováno v:
NER
Neuroscience is a highly interdisciplinary field, but more collaboration among STEM disciplines is needed to advance undergraduate neuroscience education. This paper reports the development of code-based virtual laboratories to cross-foster ideas fro
Autor:
Deiter C, Jenkins T, Chopra, Marley Realing, David W. Donley, Jonathan H. Fox, Hersch S, Jason P. Gigley, Campbell R
Toxoplasma gondii causes a prevalent neuroinvasive protozoal pathogen that in immune competent individuals results in latent infection characterized by intra-cellular parasite cysts in brain. Despite life-long infection, the role of latent toxoplasmo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::21aff03fdf4be5439a99f9fc2e29b4db
Huntington’s disease (HD) is a progressive neurodegenerative disease that affects the striatum and cerebral cortex. It is caused by a dominant CAG trinucleotide expansion in exon 1 of theHTTgene. Mutant huntingtin protein (mHtt) is expressed in neu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9775a26ad0eb144dc177af6c08cb851e
Publikováno v:
PLoS ONE
PLoS ONE, Vol 16, Iss 5, p e0250606 (2021)
PLoS ONE, Vol 16, Iss 5, p e0250606 (2021)
Huntington’s disease (HD) is a neurodegenerative disorder caused by a dominant CAG-repeat expansion in the huntingtin gene. Morphologic activation of microglia is a key marker of neuroinflammation that is present before clinical onset in HD patient
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbcea615713bf31a5e6ae7e6c42ed391
https://doi.org/10.1101/550905
https://doi.org/10.1101/550905
Publikováno v:
PLoS ONE
PLoS ONE, Vol 11, Iss 9, p e0162404 (2016)
PLoS ONE, Vol 11, Iss 9, p e0162404 (2016)
Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a polyglutamine-repeat expansion in the huntingtin protein. Activation of the kynurenine pathway of tryptophan degradation is implicated in the pathogenesis of HD. Indole
Autor:
Kathleen A. Taylor, Kenneth G. Saag, Steven Boonen, Gail P. Dalsky, Elizabeth Shane, David W. Donley, Fernando Marin, Robert Marcus
Publikováno v:
New England Journal of Medicine. 357:2028-2039
Bisphosphonates are, at present, recommended for patients who have-or are at risk of developing-glucocorticoid-induced osteoporosis. Effective treatment, however, remains challenging. One alternative is once-a-day anabolic therapy with teriparatide,
Autor:
Tony M. Keaveny, Javier San Martin, Paul F. Hoffmann, Bruce H. Mitlak, Emmett V. Glass, David W. Donley
Publikováno v:
Journal of Bone and Mineral Research. 22:149-157
FE modeling was used to estimate the biomechanical effects of teriparatide and alendronate on lumbar vertebrae. Both treatments enhanced predicted vertebral strength by increasing average density. This effect was more pronounced for teriparatide, whi
Autor:
Louis Georges Ste-Marie, Yanfei L. Ma, J. Christopher Gallagher, Erik Fink Eriksen, Gail P Dalsky, Qingqiang Zeng, David W. Donley, Robert Marcus
Publikováno v:
Journal of Bone and Mineral Research. 21:855-864
Transiliac bone biopsies were obtained from 55 women treated with teriparatide or placebo for 12–24 months. We report direct evidence that modeling bone formation at quiescent surfaces was present only in teriparatide-treated patients and bone form