Hey Everyone! Yes, you can send mail to Justin now. The address on the previous post was in fact correct, but it has not really been tested by me yet. He is at Camp Bucca and might even have a day off in a day or two. I will let you know how that goes!
First, the good news: My proposal is scheduled for June 4 at 10:00 in 5C201 of the HSC. Yay! It is finally going to happen. Below is the copy of the posting....
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ANNOUCEMENT OF DISSERTATION PROPOSAL
Cognitive Impairment in the mdx Mouse
Allison R. Hollingsworth Deming, M.A.
Committee:
Alice M. Young, Ph.D., Chair
Roman Taraban, Ph.D.
Michael O’Boyle, Ph.D.
Gregory Schrimsher, M.D., Ph.D.
Wednesday, June 4, 2008
10:00 AM
5C201 Health Sciences Center
Dystrophin, part of the dystrophin-glycoprotein complex (DGC), is one of the longest and most complex proteins in the body. It serves a critical function for structural integrity and calcium regulation in muscle cells, and is related to multiple disorders of the musculature known as dystrophinopathies. The most common dystrophinopathy, Duchenne Muscular Dystrophy (DMD), is caused by an early stop exon in the gene transcription process that leads to lower levels of free circulating dystrophin as well as some of the smaller dystrophin isoforms at the neuromuscular gap junction. Those affected with DMD suffer from rapid muscle decline and eventually death around the age of 20 to 30, as well as several marked cognitive deficits in the areas of reading comprehension, attention, working memory, intelligence scores, and overall academic achievement. The murine model of DMD, the mdx mouse, has been studied for years to better understand how dystrophin affects the musculature in DMD patients, but not their cognitive deficits. As it is not possible to measure all reported deficits using the mdx mouse, we will focus on the component processes of attention, working memory, and spatial memory in three studies involving the mdx mouse and the control C57BL/10 over a period of four months. During this time the decline in musculature will also be monitored. We expect that the mdx mouse will show impaired learning and a lower asymptote on all tasks, along with possible decline is performance over the lifespan. While it is expected that this cognitive decline will be correlated with decline in the musculature, we predict that purely cognitive decline will also be present. If these predictions are correct it is possible that the mdx mouse could be used as the human analog for future cognitive studies of DMD.
Cognitive Impairment in the mdx Mouse
Allison R. Hollingsworth Deming, M.A.
Committee:
Alice M. Young, Ph.D., Chair
Roman Taraban, Ph.D.
Michael O’Boyle, Ph.D.
Gregory Schrimsher, M.D., Ph.D.
Wednesday, June 4, 2008
10:00 AM
5C201 Health Sciences Center
Dystrophin, part of the dystrophin-glycoprotein complex (DGC), is one of the longest and most complex proteins in the body. It serves a critical function for structural integrity and calcium regulation in muscle cells, and is related to multiple disorders of the musculature known as dystrophinopathies. The most common dystrophinopathy, Duchenne Muscular Dystrophy (DMD), is caused by an early stop exon in the gene transcription process that leads to lower levels of free circulating dystrophin as well as some of the smaller dystrophin isoforms at the neuromuscular gap junction. Those affected with DMD suffer from rapid muscle decline and eventually death around the age of 20 to 30, as well as several marked cognitive deficits in the areas of reading comprehension, attention, working memory, intelligence scores, and overall academic achievement. The murine model of DMD, the mdx mouse, has been studied for years to better understand how dystrophin affects the musculature in DMD patients, but not their cognitive deficits. As it is not possible to measure all reported deficits using the mdx mouse, we will focus on the component processes of attention, working memory, and spatial memory in three studies involving the mdx mouse and the control C57BL/10 over a period of four months. During this time the decline in musculature will also be monitored. We expect that the mdx mouse will show impaired learning and a lower asymptote on all tasks, along with possible decline is performance over the lifespan. While it is expected that this cognitive decline will be correlated with decline in the musculature, we predict that purely cognitive decline will also be present. If these predictions are correct it is possible that the mdx mouse could be used as the human analog for future cognitive studies of DMD.
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So there it is...now onto the house pictures I was sent. I guess it was a bit muddy, so there are only ones of the outside.
2 comments:
Yay on all fronts!
Congrats! Looks like a nice house.
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