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<br>
</span><span class="style6">First Annual Dysferlin Conference</span><span class="home style11"><br>
</span><span class="style7"><br><br>
<span class="style12">July 9 - 12, 2007</span><br>
</span><br>
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<span class="style7">Sponsored by the Jain Foundation Inc.</span><br>
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<td><div align="left" class="home style4"><a href="2007summary.php"><img src="images/button_gen_sum.gif" width="79" height="40" border="0"></a> &nbsp;&nbsp;<a href="2007sci_summary.php"><img src="images/button_sci_sum.gif" width="79" height="40" border="0"></a> &nbsp;&nbsp;<a href="2007abstracts.php"><img src="images/button_speak_abs.gif" width="79" height="40" border="0"></a> &nbsp;&nbsp;<a href="2007posters.php"><img src="images/button_post_abs.gif" width="79" height="40" border="0"></a> &nbsp;&nbsp;<a href="2007program.php"><img src="images/button_conf_prog.gif" width="79" height="40" border="0"></a><a href="2007program.php"></a> &nbsp;&nbsp;<a href="shows/dysferlinconference2007.html" target="_blank"><img src="images/button_show.gif" width="79" height="40" border="0"></a><br>
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<p><span class="style10">SPEAKER ABSTRACTS </span><br><br><br>
<strong><span class="style17">Christina Jamieson, PhD</span><br>
</strong><em>University</em><em> of California at Los Angeles School of Medicine</em>&nbsp;&nbsp;<strong><br>
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<img src="images/conference/30-Jamieson.jpg" width="135"> <br>
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</span><strong>Apoptosis in dysferlin deficiency&nbsp; &nbsp;</strong><br><br>
In dysferlinopathy there is a marked increase in necrotic muscle fibers and inflammation in the muscle. Curiously, steroid treatment that works well to suppress inflammation and damage in other muscular dystrophies and muscle inflammatory diseases is not effective in reducing muscle damage in LGMD2B/MM patients and can make damage worse. We are investigating responses to the glucocorticoid and androgen classes of steroid hormones in dysferlin-deficient immune cells and muscle cells.&nbsp; We will determine whether the glucocorticoid response is defective and may contribute to the increased damage. We found that dysferlin was activated in glucocorticoid-induced apoptosis in&nbsp;T lymphocytes; therefore, we are also analyzing the role of dysferlin in apoptosis. Dysferlin is known to be involved in sarcolemma repair.&nbsp;It is thought to mediate membrane fusion between the plasma membrane and intracellular vesicles at the site of membrane damage. We propose that dysferlin may play a role in membrane blebbing and vesicle fusion events that are important for apoptosis: the process of programmed cell death in which the cell is dismantled and cleared without damage to the surrounding tissue.&nbsp; Defective apoptosis in the absence of dysferlin may, in some circumstances, result in cell death due to necrosis; that is, catastrophic, uncontrolled death that results in spilling toxic cell contents into the extracellular environment, leading to local tissue damage and inflammation.&nbsp; In addition, we are analyzing the muscle-building mechanisms of androgens and establishing screens for SARMS (Selective androgen receptor mediators) that are preferentially anabolic as protective therapy against dysferlinopathy.
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