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    <title>DSpace Community: Biology</title>
    <link>http://hdl.handle.net/10090/617</link>
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      <title>Ethanol as a teratogen and zebrafish development: relation to fetal alcohol syndrome</title>
      <link>http://hdl.handle.net/10090/3784</link>
      <description>Title: Ethanol as a teratogen and zebrafish development: relation to fetal alcohol syndrome
&lt;br/&gt;
&lt;br/&gt;Authors: Webster, Lindsey
&lt;br/&gt;
&lt;br/&gt;Abstract: Neural crest cells are precursors to craniofacial elements in vertebrates. In humans,&#xD;
multiple defects, including neurological, behavioral and morphological abnormalities have been&#xD;
characterized in children born to chronic alcohol drinkers. Some of these Fetal Alcohol&#xD;
Syndrome (FAS) related defects have been observed in other vertebrates exposed to ethanol&#xD;
during development. The goal of this project is to determine how ethanol exposure affects&#xD;
development of zebrafish neural crest derivatives. With increasing exposure to ethanol, it was&#xD;
suspected that zebrafish embryos would have more severe craniofacial abnormalities due to&#xD;
abnormal neural crest cell migration, differentiation, or cell death. Zebrafish embryos were&#xD;
exposed to varying concentrations of ethanol from approximately 30% epiboly until 24 hours&#xD;
post fertilization and development was monitored. Embryos were stained with alcian blue to&#xD;
observe facial cartilage after six days of development. Cartilage length and interocular distance&#xD;
were measured. Moderate ethanol exposure resulted in increased interocular distance while&#xD;
higher ethanol concentrations led to a reduction in this distance. As ethanol dose increased, the&#xD;
length of cartilage elements decreased. These defects are consistent with some pathologies&#xD;
associated with FAS and may be due to abnormal crest development.
&lt;br/&gt;
&lt;br/&gt;Description: A thesis submitted to the&#xD;
Department of Biology&#xD;
in partial fulfillment of the&#xD;
requirements for the degree of&#xD;
Bachelor of Science. Spring Semester 2007 Thesis Advisor: Dr. Jeffrey Brown</description>
      <pubDate>Fri, 18 Jan 2008 19:50:00 GMT</pubDate>
    </item>
    <item>
      <title>Development and evolutionary history of teeth as related to the biogenic</title>
      <link>http://hdl.handle.net/10090/3782</link>
      <description>Title: Development and evolutionary history of teeth as related to the biogenic
&lt;br/&gt;
&lt;br/&gt;Authors: Song, Jin
&lt;br/&gt;
&lt;br/&gt;Description: A thesis submitted to the&#xD;
Department of Biology&#xD;
in partial fulfillment of the&#xD;
requirements for the degree of&#xD;
Bachelor of Science. Spring Semester 2007 Thesis Advisor: Dr. Hugh Jarrard</description>
      <pubDate>Fri, 18 Jan 2008 19:46:12 GMT</pubDate>
    </item>
    <item>
      <title>Introduction of lyme disease to the human population: its history, evolution, and epidemiology</title>
      <link>http://hdl.handle.net/10090/3771</link>
      <description>Title: Introduction of lyme disease to the human population: its history, evolution, and epidemiology
&lt;br/&gt;
&lt;br/&gt;Authors: Severin, Raymond S.
&lt;br/&gt;
&lt;br/&gt;Description: A thesis submitted to the&#xD;
Department of Biology&#xD;
in partial fulfillment of the&#xD;
requirements for the degree of&#xD;
Bachelor of Science. Spring Semester 2007 Thesis Advisor: Dr. Martin Connaughton</description>
      <pubDate>Fri, 18 Jan 2008 15:51:03 GMT</pubDate>
    </item>
    <item>
      <title>Effects of glucocorticoids on the development of alzheimer's disease in normal aged mice</title>
      <link>http://hdl.handle.net/10090/3770</link>
      <description>Title: Effects of glucocorticoids on the development of alzheimer's disease in normal aged mice
&lt;br/&gt;
&lt;br/&gt;Authors: Pranski, Elaine
&lt;br/&gt;
&lt;br/&gt;Abstract: In Alzheimer&amp;#8217;s disease (AD), glucocorticoid levels are elevated and levels&#xD;
of the enzyme responsible for glucocorticoid degradation are depressed. Shortterm&#xD;
glucocorticoid exposure induces the &amp;#946;-Amyloid and Tau pathologies in&#xD;
transgenic mice predisposed to AD (Green et al. 2006). The effects of chronic&#xD;
glucocorticoid administration in aged mice (Mus domesticus) on learning and&#xD;
memory were examined by the Morris water maze and &amp;#946;-amyloid and Tau&#xD;
protein levels were monitored. Twenty C57BL/6J mice were given daily injections&#xD;
of the glucocorticoid dexamethasone or a control substance for two weeks.&#xD;
Dexamethasone-treated mice showed improved performance in the Morris water&#xD;
maze in spite of increased APP and Tau accumulation. Tacrine, a reversible&#xD;
acetylcholinesterase inhibitor, was not found to alter APP levels, but may act as a&#xD;
protective agent by preventing Tau accumulation. High glucocorticoid levels may&#xD;
cause increases in AD-related protein accumulations, but over the short-term,&#xD;
these pathologies do not appear to result in the impairment of learning and&#xD;
memory of mice.
&lt;br/&gt;
&lt;br/&gt;Description: A thesis submitted to the&#xD;
Department of Biology&#xD;
in partial fulfillment of the&#xD;
requirements for the degree of&#xD;
Bachelor of Science. Spring 2007 Thesis Advisor: Dr. Jeffrey Brown</description>
      <pubDate>Fri, 18 Jan 2008 15:41:01 GMT</pubDate>
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