<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-09-21T06:30:41Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/45835" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/45835</identifier><datestamp>2022-01-13T07:54:36Z</datestamp><setSpec>com_1721.1_7582</setSpec><setSpec>com_1721.1_7581</setSpec><setSpec>col_1721.1_131024</setSpec></header><metadata><dim:dim xmlns:dim="http://www.dspace.org/xmlns/dspace/dim" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
   <dim:field mdschema="dc" element="contributor" qualifier="advisor" lang="en_US">Myron Spector.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Jennings, Edward B., III (Edward Bernard)</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="other" lang="en_US">Massachusetts Institute of Technology. Dept. of Mechanical Engineering.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="department">Massachusetts Institute of Technology. Department of Mechanical Engineering</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2009-06-30T16:24:03Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2009-06-30T16:24:03Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="copyright" lang="en_US">2008</dim:field>
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   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">319602950</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (S.B.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2008.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Includes bibliographical references (leaf 28).</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">Healing by contraction is responsible for scarring in adults. Embryos heal by regeneration but the mechanism is unknown. Alpha-smooth muscle actin ([alpha]-SMA) is the protein responsible for contraction, thus determining if it is present in embryos which heal by regeneration will further our knowledge about the causes of regenerative healing. This thesis experimentally determined the presence of [alpha]-SMA in these cell types by the following procedure. Embryonic and mesenchymal stem cells of various species were cultured and seeded into collagen scaffolds. Contractile behavior was determined by measuring the diameter change of the scaffolds over time. Alpha-smooth muscle actin presence was determined by immunohistochemical evaluation. This study found that while all the cell types displayed alpha smooth muscle actin presence in monolayer, not every cell type contracted when seeded into the collagen scaffolds designed to mimic the in vivo environment. Specifically, the embryonic stem cells did not contract. Upon staining, the embryonic stem cell seeded scaffolds and several of the mesenchymal stem cell seeded scaffolds, which did contract, did not stain positive for [alpha]-SMA. These results imply that the embryonic scaffolds did not generate actin filament bundles, and that several of the mesenchymal stem cell seeded scaffolds were imaged after [alpha]-SMA expression in them ceased.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Edward B. Jennings, III.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="degree" lang="en_US">S.B.</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="extent" lang="en_US">33 leaves</dim:field>
   <dim:field mdschema="dc" element="language" qualifier="iso" lang="en_US">eng</dim:field>
   <dim:field mdschema="dc" element="publisher" lang="en_US">Massachusetts Institute of Technology</dim:field>
   <dim:field mdschema="dc" element="rights" lang="en_US">M.I.T. theses are protected by 
copyright. They may be viewed from this source for any purpose, but 
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   <dim:field mdschema="dc" element="rights" qualifier="uri" lang="en_US">http://dspace.mit.edu/handle/1721.1/7582</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">Mechanical Engineering.</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">Determining alpha-smooth muscle actin expression in embryonic and mesenchymal stem cells of assorted mammals seeded in collagen scaffolds in vitro</dim:field>
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   	&lt;Title>Determining alpha-smooth muscle actin expression in embryonic and mesenchymal stem cells of assorted mammals seeded in collagen scaffolds in vitro&lt;/Title>
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   	&lt;PublicationDate>2008&lt;/PublicationDate>
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   	&lt;Abstract>Healing by contraction is responsible for scarring in adults. Embryos heal by regeneration but the mechanism is unknown. Alpha-smooth muscle actin ([alpha]-SMA) is the protein responsible for contraction, thus determining if it is present in embryos which heal by regeneration will further our knowledge about the causes of regenerative healing. This thesis experimentally determined the presence of [alpha]-SMA in these cell types by the following procedure. Embryonic and mesenchymal stem cells of various species were cultured and seeded into collagen scaffolds. Contractile behavior was determined by measuring the diameter change of the scaffolds over time. Alpha-smooth muscle actin presence was determined by immunohistochemical evaluation. This study found that while all the cell types displayed alpha smooth muscle actin presence in monolayer, not every cell type contracted when seeded into the collagen scaffolds designed to mimic the in vivo environment. Specifically, the embryonic stem cells did not contract. Upon staining, the embryonic stem cell seeded scaffolds and several of the mesenchymal stem cell seeded scaffolds, which did contract, did not stain positive for [alpha]-SMA. These results imply that the embryonic scaffolds did not generate actin filament bundles, and that several of the mesenchymal stem cell seeded scaffolds were imaged after [alpha]-SMA expression in them ceased.&lt;/Abstract>
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