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   <dim:field mdschema="dc" element="contributor" qualifier="advisor" lang="en_US">Jacqueline A. Lees.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Eipper-Mains, Marcie A., 1979-</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="other" lang="en_US">Massachusetts Institute of Technology. Dept. of Biology.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="department">Massachusetts Institute of Technology. Department of Biology</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2005-09-27T18:46:43Z</dim:field>
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   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Biology, 2004.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Includes bibliographical references (leaves [54]-[66]).</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">The development of the immune system is a highly dynamic process, characterized by quickly and frequently changing cell types and numbers. The orchestration of cell growth and proliferation and also of cell death is a necessarily complex process, taking cues from a wide variety of sources. The nematode Caenorhabditus elegans has provided an elegant and simple model of the control of programmed cell death, or apoptosis, in metazoans. Apoptosis in mammals is regulated by pathways related to but more intricate than metazoans. Several key features define the onset of apoptosis in any given cell; these include DNA fragmentation and chromatin condensation, "blebbing" of the plasma membrane, and subsequent phagocytosis of the resulting cell fragments by adjacent cells (Kerr et al. 1972 and Wyllie et al. 1980).</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Marcie A. Eipper-Mains.</dim:field>
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   <dim:field mdschema="dc" element="subject" lang="en_US">Biology.</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">The role of the Bcl-2 family in proliferation and apoptosis and in mediating the development of lymphatic diseases</dim:field>
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   	&lt;Title>The role of the Bcl-2 family in proliferation and apoptosis and in mediating the development of lymphatic diseases&lt;/Title>
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   	&lt;Abstract>The development of the immune system is a highly dynamic process, characterized by quickly and frequently changing cell types and numbers. The orchestration of cell growth and proliferation and also of cell death is a necessarily complex process, taking cues from a wide variety of sources. The nematode Caenorhabditus elegans has provided an elegant and simple model of the control of programmed cell death, or apoptosis, in metazoans. Apoptosis in mammals is regulated by pathways related to but more intricate than metazoans. Several key features define the onset of apoptosis in any given cell; these include DNA fragmentation and chromatin condensation, &amp;quot;blebbing&amp;quot; of the plasma membrane, and subsequent phagocytosis of the resulting cell fragments by adjacent cells (Kerr et al. 1972 and Wyllie et al. 1980).&lt;/Abstract>
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