Zobrazeno 1 - 10
of 48
pro vyhledávání: '"Chainllie Young"'
Publikováno v:
Neurobiology of Disease, Vol 33, Iss 1, Pp 111-118 (2009)
Although a wide range of developmental disabilities following fetal alcohol exposure are observed clinically, the molecular factors that determine the severity of these sequelae remain undefined. In mice exposed to ethanol, deletion of adenylyl cycla
Externí odkaz:
https://doaj.org/article/0ed1565e4f594d29903647294f43b944
Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain
Publikováno v:
Neurobiology of Disease, Vol 31, Iss 3, Pp 355-360 (2008)
Transient exposure of immature animals during the brain growth spurt period to ethanol triggers neuroapoptosis in the developing brain. Here we report that lithium, when administered in a single, well-tolerated dose to infant mice, suppresses spontan
Externí odkaz:
https://doaj.org/article/fc103b4dfe374360866f5189ff34618e
Autor:
Chainllie Young, John W. Olney
Publikováno v:
Neurobiology of Disease, Vol 22, Iss 3, Pp 548-554 (2006)
Exposure of infant rats or mice to ethanol on a single occasion during the period of rapid synaptogenesis can cause extensive apoptotic neurodegeneration throughout the developing CNS. Prior studies were designed to assess the effects of large doses
Externí odkaz:
https://doaj.org/article/8b6d0a40313945a9b1dd07bd156f0d0a
Autor:
Chainllie Young, Kevin A. Roth, Barbara J. Klocke, Tim West, David M. Holtzman, Joann Labruyere, Yue-Qin Qin, Krikor Dikranian, John W. Olney
Publikováno v:
Neurobiology of Disease, Vol 20, Iss 2, Pp 608-614 (2005)
Acute, transient exposure to ethanol causes a widespread pattern of caspase-3 activation and neuroapoptosis in the developing rodent brain. To determine whether caspase-3 activation is an essential step in ethanol-induced developmental neuroapoptosis
Externí odkaz:
https://doaj.org/article/ddbf78aae8964682938b87f19d085287
Autor:
David F. Wozniak, Richard E. Hartman, Maureen P. Boyle, Sherri K. Vogt, Ashley R. Brooks, Tatyana Tenkova, Chainllie Young, John W. Olney, Louis J. Muglia
Publikováno v:
Neurobiology of Disease, Vol 17, Iss 3, Pp 403-414 (2004)
Administration of ethanol to rodents during the synaptogenesis period induces extensive apoptotic neurodegeneration in the developing brain. This neurotoxicity may explain the reduced brain mass and neurobehavioral disturbances in human Fetal Alcohol
Externí odkaz:
https://doaj.org/article/6c70138f8bec4e86bd3a85dd522ca8d7
Autor:
Chainllie Young1, Vesna Jevtovic-Todorovic2, Yue-Qin Qin1, Tatyana Tenkova1, Haihui Wang1, Labruyere, Joann1, Olney, John W.1 olneyj@psychiatry.wustl.edu
Publikováno v:
British Journal of Pharmacology. Sep2005, Vol. 146 Issue 2, p189-197. 9p.
Ethanol causes and lithium prevents neuroapoptosis and suppression of pERK in the infant mouse brain
Publikováno v:
Neurobiology of Disease, Vol 31, Iss 3, Pp 355-360 (2008)
Transient exposure of immature animals during the brain growth spurt period to ethanol triggers neuroapoptosis in the developing brain. Here we report that lithium, when administered in a single, well-tolerated dose to infant mice, suppresses spontan
Publikováno v:
Journal of Neurosurgical Anesthesiology. 20:21-28
Drugs that suppress neuronal activity, including general anesthetics used in pediatric and obstetric medicine, trigger neuroapoptosis in the developing rodent brain. Exposure of infant rats for 6 hours to a combination of anesthetic drugs (midazolam,
Autor:
Paul Saftig, John W. Olney, John J. Shacka, Kevin A. Roth, Chainllie Young, Barbara J. Klocke, Yasuo Uchiyama, Masahiro Shibata
Publikováno v:
The Journal of Neuroscience. 27:2081-2090
Neuronal ceroid lipofuscinosces/Batten disease (NCL) is a devastating group of neurodegenerative diseases caused by genetic disruptions in lysosomal function. Cathepsin D (CD) is a major lysosomal protease, and mutations in CD that render it enzymati
Autor:
John W. Olney, Chainllie Young
Publikováno v:
Neurobiology of Disease, Vol 22, Iss 3, Pp 548-554 (2006)
Exposure of infant rats or mice to ethanol on a single occasion during the period of rapid synaptogenesis can cause extensive apoptotic neurodegeneration throughout the developing CNS. Prior studies were designed to assess the effects of large doses