<?xml version="1.0" encoding="UTF-8" ?>
<oai_dc:dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
<dc:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</dc:title>
<dc:creator>Pérez López, Silvia</dc:creator>
<dc:creator>Vázquez Moreno, Natalia</dc:creator>
<dc:creator>Escudero Augusto, Dolores</dc:creator>
<dc:creator>Astudillo González, Aurora</dc:creator>
<dc:creator>Alvarez Menéndez, Francisco</dc:creator>
<dc:creator>Goyache Goñi, Félix</dc:creator>
<dc:creator>Otero Hernández, Jesús</dc:creator>
<dc:subject>Muerte cerebral</dc:subject>
<dc:subject>Genes de apoptosis</dc:subject>
<dc:subject>Trasplante de corazón</dc:subject>
<dc:subject>Donador de órganos.</dc:subject>
<dc:subject>Publicado</dc:subject>
<dc:description>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</dc:description>
<dc:date>2018-03-27T11:29:42Z</dc:date>
<dc:date>2018-03-27T11:29:42Z</dc:date>
<dc:date>2008</dc:date>
<dc:type>article</dc:type>
<dc:identifier>Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</dc:identifier>
<dc:identifier>0041-1337</dc:identifier>
<dc:identifier>https://ria.asturias.es/RIA/handle/123456789/9867</dc:identifier>
<dc:language>eng</dc:language>
<dc:relation>Transplantation</dc:relation>
<dc:relation>86</dc:relation>
<dc:relation>Sí, esta versión ha sido citada</dc:relation>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</dc:rights>
<dc:format>application/pdf</dc:format>
<dc:publisher>Lippincott, Williams & Wilkins</dc:publisher>
<dc:source>977;982</dc:source>
</oai_dc:dc>
<?xml version="1.0" encoding="UTF-8" ?>
<d:DIDL schemaLocation="urn:mpeg:mpeg21:2002:02-DIDL-NS http://standards.iso.org/ittf/PubliclyAvailableStandards/MPEG-21_schema_files/did/didl.xsd">
<d:DIDLInfo>
<dcterms:created schemaLocation="http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/dcterms.xsd">2018-03-27T11:29:42Z</dcterms:created>
</d:DIDLInfo>
<d:Item id="hdl_123456789_9867">
<d:Descriptor>
<d:Statement mimeType="application/xml; charset=utf-8">
<dii:Identifier schemaLocation="urn:mpeg:mpeg21:2002:01-DII-NS http://standards.iso.org/ittf/PubliclyAvailableStandards/MPEG-21_schema_files/dii/dii.xsd">urn:hdl:123456789/9867</dii:Identifier>
</d:Statement>
</d:Descriptor>
<d:Descriptor>
<d:Statement mimeType="application/xml; charset=utf-8">
<oai_dc:dc schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
<dc:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</dc:title>
<dc:creator>Pérez López, Silvia</dc:creator>
<dc:creator>Vázquez Moreno, Natalia</dc:creator>
<dc:creator>Escudero Augusto, Dolores</dc:creator>
<dc:creator>Astudillo González, Aurora</dc:creator>
<dc:creator>Alvarez Menéndez, Francisco</dc:creator>
<dc:creator>Goyache Goñi, Félix</dc:creator>
<dc:creator>Otero Hernández, Jesús</dc:creator>
<dc:subject>Muerte cerebral</dc:subject>
<dc:subject>Genes de apoptosis</dc:subject>
<dc:subject>Trasplante de corazón</dc:subject>
<dc:subject>Donador de órganos.</dc:subject>
<dc:description>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</dc:description>
<dc:date>2018-03-27T11:29:42Z</dc:date>
<dc:date>2018-03-27T11:29:42Z</dc:date>
<dc:date>2008</dc:date>
<dc:type>article</dc:type>
<dc:identifier>Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</dc:identifier>
<dc:identifier>0041-1337</dc:identifier>
<dc:identifier>https://ria.asturias.es/RIA/handle/123456789/9867</dc:identifier>
<dc:language>eng</dc:language>
<dc:relation>Transplantation</dc:relation>
<dc:relation>86</dc:relation>
<dc:relation>Sí, esta versión ha sido citada</dc:relation>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</dc:rights>
<dc:publisher>Lippincott, Williams & Wilkins</dc:publisher>
<dc:source>977;982</dc:source>
</oai_dc:dc>
</d:Statement>
</d:Descriptor>
<d:Component id="123456789_9867_1">
</d:Component>
</d:Item>
</d:DIDL>
<?xml version="1.0" encoding="UTF-8" ?>
<dim:dim schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
<dim:field element="contributor" mdschema="dc" qualifier="author">Pérez López, Silvia</dim:field>
<dim:field element="contributor" mdschema="dc" qualifier="author">Vázquez Moreno, Natalia</dim:field>
<dim:field element="contributor" mdschema="dc" qualifier="author">Escudero Augusto, Dolores</dim:field>
<dim:field element="contributor" mdschema="dc" qualifier="author">Astudillo González, Aurora</dim:field>
<dim:field element="contributor" mdschema="dc" qualifier="author">Alvarez Menéndez, Francisco</dim:field>
<dim:field element="contributor" mdschema="dc" qualifier="author">Goyache Goñi, Félix</dim:field>
<dim:field element="contributor" mdschema="dc" qualifier="author">Otero Hernández, Jesús</dim:field>
<dim:field element="date" mdschema="dc" qualifier="accessioned">2018-03-27T11:29:42Z</dim:field>
<dim:field element="date" mdschema="dc" qualifier="available">2018-03-27T11:29:42Z</dim:field>
<dim:field element="date" mdschema="dc" qualifier="issued">2008</dim:field>
<dim:field element="identifier" lang="eng" mdschema="dc" qualifier="citation">Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</dim:field>
<dim:field element="identifier" mdschema="dc" qualifier="issn">0041-1337</dim:field>
<dim:field element="identifier" mdschema="dc" qualifier="uri">https://ria.asturias.es/RIA/handle/123456789/9867</dim:field>
<dim:field element="description" lang="eng" mdschema="dc" qualifier="abstract">Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</dim:field>
<dim:field element="language" lang="eng" mdschema="dc" qualifier="iso">eng</dim:field>
<dim:field element="publisher" lang="eng" mdschema="dc">Lippincott, Williams & Wilkins</dim:field>
<dim:field element="relation" lang="eng" mdschema="dc" qualifier="ispartof">Transplantation</dim:field>
<dim:field element="relation" lang="eng" mdschema="dc" qualifier="haspart">86</dim:field>
<dim:field element="relation" lang="eng" mdschema="dc" qualifier="isreferencedby">Sí, esta versión ha sido citada</dim:field>
<dim:field element="rights" lang="eng" mdschema="dc">http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</dim:field>
<dim:field element="source" mdschema="dc">977;982</dim:field>
<dim:field element="subject" lang="eng" mdschema="dc">Muerte cerebral</dim:field>
<dim:field element="subject" lang="eng" mdschema="dc">Genes de apoptosis</dim:field>
<dim:field element="subject" lang="eng" mdschema="dc">Trasplante de corazón</dim:field>
<dim:field element="subject" lang="eng" mdschema="dc">Donador de órganos.</dim:field>
<dim:field element="subject" lang="eng" mdschema="dc" qualifier="classification">Publicado</dim:field>
<dim:field element="title" lang="eng" mdschema="dc">A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</dim:field>
<dim:field element="type" lang="eng" mdschema="dc">article</dim:field>
</dim:dim>
<?xml version="1.0" encoding="UTF-8" ?>
<thesis schemaLocation="http://www.ndltd.org/standards/metadata/etdms/1.0/ http://www.ndltd.org/standards/metadata/etdms/1.0/etdms.xsd">
<title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</title>
<creator>Pérez López, Silvia</creator>
<creator>Vázquez Moreno, Natalia</creator>
<creator>Escudero Augusto, Dolores</creator>
<creator>Astudillo González, Aurora</creator>
<creator>Alvarez Menéndez, Francisco</creator>
<creator>Goyache Goñi, Félix</creator>
<creator>Otero Hernández, Jesús</creator>
<subject>Muerte cerebral</subject>
<subject>Genes de apoptosis</subject>
<subject>Trasplante de corazón</subject>
<subject>Donador de órganos.</subject>
<description>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</description>
<date>2018-03-27</date>
<date>2018-03-27</date>
<date>2008</date>
<type>article</type>
<identifier>Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</identifier>
<identifier>0041-1337</identifier>
<identifier>https://ria.asturias.es/RIA/handle/123456789/9867</identifier>
<language>eng</language>
<relation>Transplantation</relation>
<relation>86</relation>
<relation>Sí, esta versión ha sido citada</relation>
<rights>http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</rights>
<publisher>Lippincott, Williams & Wilkins</publisher>
<source>977;982</source>
</thesis>
<?xml version="1.0" encoding="UTF-8" ?>
<record schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
<leader>00925njm 22002777a 4500</leader>
<datafield ind1=" " ind2=" " tag="042">
<subfield code="a">dc</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Pérez López, Silvia</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Vázquez Moreno, Natalia</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Escudero Augusto, Dolores</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Astudillo González, Aurora</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Alvarez Menéndez, Francisco</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Goyache Goñi, Félix</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="720">
<subfield code="a">Otero Hernández, Jesús</subfield>
<subfield code="e">author</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="260">
<subfield code="c">2008</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="520">
<subfield code="a">Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</subfield>
</datafield>
<datafield ind1="8" ind2=" " tag="024">
<subfield code="a">Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</subfield>
</datafield>
<datafield ind1="8" ind2=" " tag="024">
<subfield code="a">0041-1337</subfield>
</datafield>
<datafield ind1="8" ind2=" " tag="024">
<subfield code="a">https://ria.asturias.es/RIA/handle/123456789/9867</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="653">
<subfield code="a">Muerte cerebral</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="653">
<subfield code="a">Genes de apoptosis</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="653">
<subfield code="a">Trasplante de corazón</subfield>
</datafield>
<datafield ind1=" " ind2=" " tag="653">
<subfield code="a">Donador de órganos.</subfield>
</datafield>
<datafield ind1="0" ind2="0" tag="245">
<subfield code="a">A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</subfield>
</datafield>
</record>
<?xml version="1.0" encoding="UTF-8" ?>
<mets ID=" DSpace_ITEM_123456789-9867" OBJID=" hdl:123456789/9867" PROFILE="DSpace METS SIP Profile 1.0" TYPE="DSpace ITEM" schemaLocation="http://www.loc.gov/METS/ http://www.loc.gov/standards/mets/mets.xsd">
<metsHdr CREATEDATE="2023-01-14T18:18:13Z">
<agent ROLE="CUSTODIAN" TYPE="ORGANIZATION">
<name>RIA</name>
</agent>
</metsHdr>
<dmdSec ID="DMD_123456789_9867">
<mdWrap MDTYPE="MODS">
<xmlData schemaLocation="http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-1.xsd">
<mods:mods schemaLocation="http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-1.xsd">
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Pérez López, Silvia</mods:namePart>
</mods:name>
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Vázquez Moreno, Natalia</mods:namePart>
</mods:name>
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Escudero Augusto, Dolores</mods:namePart>
</mods:name>
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Astudillo González, Aurora</mods:namePart>
</mods:name>
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Alvarez Menéndez, Francisco</mods:namePart>
</mods:name>
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Goyache Goñi, Félix</mods:namePart>
</mods:name>
<mods:name>
<mods:role>
<mods:roleTerm type="text">author</mods:roleTerm>
</mods:role>
<mods:namePart>Otero Hernández, Jesús</mods:namePart>
</mods:name>
<mods:extension>
<mods:dateAccessioned encoding="iso8601">2018-03-27T11:29:42Z</mods:dateAccessioned>
</mods:extension>
<mods:extension>
<mods:dateAvailable encoding="iso8601">2018-03-27T11:29:42Z</mods:dateAvailable>
</mods:extension>
<mods:originInfo>
<mods:dateIssued encoding="iso8601">2008</mods:dateIssued>
</mods:originInfo>
<mods:identifier type="citation">Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</mods:identifier>
<mods:identifier type="issn">0041-1337</mods:identifier>
<mods:identifier type="uri">https://ria.asturias.es/RIA/handle/123456789/9867</mods:identifier>
<mods:abstract>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</mods:abstract>
<mods:language>
<mods:languageTerm authority="rfc3066">eng</mods:languageTerm>
</mods:language>
<mods:accessCondition type="useAndReproduction">http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</mods:accessCondition>
<mods:subject>
<mods:topic>Muerte cerebral</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Genes de apoptosis</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Trasplante de corazón</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Donador de órganos.</mods:topic>
</mods:subject>
<mods:titleInfo>
<mods:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</mods:title>
</mods:titleInfo>
<mods:genre>article</mods:genre>
</mods:mods>
</xmlData>
</mdWrap>
</dmdSec>
<amdSec ID="FO_123456789_9867_1">
<techMD ID="TECH_O_123456789_9867_1">
<mdWrap MDTYPE="PREMIS">
<xmlData schemaLocation="http://www.loc.gov/standards/premis http://www.loc.gov/standards/premis/PREMIS-v1-0.xsd">
<premis:premis>
<premis:object>
<premis:objectIdentifier>
<premis:objectIdentifierType>URL</premis:objectIdentifierType>
<premis:objectIdentifierValue>http://172.28.36.237:8080/jspui/bitstream/123456789/9867/1/Archivo.pdf</premis:objectIdentifierValue>
</premis:objectIdentifier>
<premis:objectCategory>File</premis:objectCategory>
<premis:objectCharacteristics>
<premis:fixity>
<premis:messageDigestAlgorithm>MD5</premis:messageDigestAlgorithm>
<premis:messageDigest>f3e0c39d60a6aa660cb9ac28be6fef17</premis:messageDigest>
</premis:fixity>
<premis:size>388274</premis:size>
<premis:format>
<premis:formatDesignation>
<premis:formatName>application/pdf</premis:formatName>
</premis:formatDesignation>
</premis:format>
</premis:objectCharacteristics>
<premis:originalName>Archivo.pdf</premis:originalName>
</premis:object>
</premis:premis>
</xmlData>
</mdWrap>
</techMD>
</amdSec>
<fileSec>
<fileGrp USE="ORIGINAL">
<file ADMID="FO_123456789_9867_1" CHECKSUM="f3e0c39d60a6aa660cb9ac28be6fef17" CHECKSUMTYPE="MD5" GROUPID="GROUP_BITSTREAM_123456789_9867_1" ID="BITSTREAM_ORIGINAL_123456789_9867_1" MIMETYPE="application/pdf" SEQ="1" SIZE="388274">
</file>
</fileGrp>
</fileSec>
<structMap LABEL="DSpace Object" TYPE="LOGICAL">
<div ADMID="DMD_123456789_9867" TYPE="DSpace Object Contents">
<div TYPE="DSpace BITSTREAM">
</div>
</div>
</structMap>
</mets>
<?xml version="1.0" encoding="UTF-8" ?>
<mods:mods schemaLocation="http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-1.xsd">
<mods:name>
<mods:namePart>Pérez López, Silvia</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Vázquez Moreno, Natalia</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Escudero Augusto, Dolores</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Astudillo González, Aurora</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Alvarez Menéndez, Francisco</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Goyache Goñi, Félix</mods:namePart>
</mods:name>
<mods:name>
<mods:namePart>Otero Hernández, Jesús</mods:namePart>
</mods:name>
<mods:extension>
<mods:dateAvailable encoding="iso8601">2018-03-27T11:29:42Z</mods:dateAvailable>
</mods:extension>
<mods:extension>
<mods:dateAccessioned encoding="iso8601">2018-03-27T11:29:42Z</mods:dateAccessioned>
</mods:extension>
<mods:originInfo>
<mods:dateIssued encoding="iso8601">2008</mods:dateIssued>
</mods:originInfo>
<mods:identifier type="citation">Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</mods:identifier>
<mods:identifier type="issn">0041-1337</mods:identifier>
<mods:identifier type="uri">https://ria.asturias.es/RIA/handle/123456789/9867</mods:identifier>
<mods:abstract>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</mods:abstract>
<mods:language>
<mods:languageTerm>eng</mods:languageTerm>
</mods:language>
<mods:accessCondition type="useAndReproduction">http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</mods:accessCondition>
<mods:subject>
<mods:topic>Muerte cerebral</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Genes de apoptosis</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Trasplante de corazón</mods:topic>
</mods:subject>
<mods:subject>
<mods:topic>Donador de órganos.</mods:topic>
</mods:subject>
<mods:titleInfo>
<mods:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</mods:title>
</mods:titleInfo>
<mods:genre>article</mods:genre>
</mods:mods>
<?xml version="1.0" encoding="UTF-8" ?>
<atom:entry schemaLocation="http://www.w3.org/2005/Atom http://www.kbcafe.com/rss/atom.xsd.xml">
<atom:id>https://ria.asturias.es/RIA/handle/123456789/9867/ore.xml</atom:id>
<atom:published>2018-03-27T11:29:42Z</atom:published>
<atom:updated>2018-03-27T11:29:42Z</atom:updated>
<atom:source>
<atom:generator>RIA</atom:generator>
</atom:source>
<atom:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</atom:title>
<atom:author>
<atom:name>Pérez López, Silvia</atom:name>
</atom:author>
<atom:author>
<atom:name>Vázquez Moreno, Natalia</atom:name>
</atom:author>
<atom:author>
<atom:name>Escudero Augusto, Dolores</atom:name>
</atom:author>
<atom:author>
<atom:name>Astudillo González, Aurora</atom:name>
</atom:author>
<atom:author>
<atom:name>Alvarez Menéndez, Francisco</atom:name>
</atom:author>
<atom:author>
<atom:name>Goyache Goñi, Félix</atom:name>
</atom:author>
<atom:author>
<atom:name>Otero Hernández, Jesús</atom:name>
</atom:author>
<oreatom:triples>
<rdf:Description about="https://ria.asturias.es/RIA/handle/123456789/9867/ore.xml#atom">
<dcterms:modified>2018-03-27T11:29:42Z</dcterms:modified>
</rdf:Description>
<rdf:Description about="http://172.28.36.237:8080/jspui/bitstream/123456789/9867/1/Archivo.pdf">
<dcterms:description>ORIGINAL</dcterms:description>
</rdf:Description>
</oreatom:triples>
</atom:entry>
<?xml version="1.0" encoding="UTF-8" ?>
<qdc:qualifieddc schemaLocation="http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://dspace.org/qualifieddc/ http://www.ukoln.ac.uk/metadata/dcmi/xmlschema/qualifieddc.xsd">
<dc:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</dc:title>
<dc:creator>Pérez López, Silvia</dc:creator>
<dc:creator>Vázquez Moreno, Natalia</dc:creator>
<dc:creator>Escudero Augusto, Dolores</dc:creator>
<dc:creator>Astudillo González, Aurora</dc:creator>
<dc:creator>Alvarez Menéndez, Francisco</dc:creator>
<dc:creator>Goyache Goñi, Félix</dc:creator>
<dc:creator>Otero Hernández, Jesús</dc:creator>
<dc:subject>Muerte cerebral</dc:subject>
<dc:subject>Genes de apoptosis</dc:subject>
<dc:subject>Trasplante de corazón</dc:subject>
<dc:subject>Donador de órganos.</dc:subject>
<dcterms:abstract>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</dcterms:abstract>
<dcterms:dateAccepted>2018-03-27T11:29:42Z</dcterms:dateAccepted>
<dcterms:available>2018-03-27T11:29:42Z</dcterms:available>
<dcterms:created>2018-03-27T11:29:42Z</dcterms:created>
<dcterms:issued>2008</dcterms:issued>
<dc:type>article</dc:type>
<dc:identifier>Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</dc:identifier>
<dc:identifier>0041-1337</dc:identifier>
<dc:identifier>https://ria.asturias.es/RIA/handle/123456789/9867</dc:identifier>
<dc:language>eng</dc:language>
<dc:relation>Transplantation</dc:relation>
<dc:relation>86</dc:relation>
<dc:relation>Sí, esta versión ha sido citada</dc:relation>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</dc:rights>
<dc:publisher>Lippincott, Williams & Wilkins</dc:publisher>
<dc:source>977;982</dc:source>
</qdc:qualifieddc>
<?xml version="1.0" encoding="UTF-8" ?>
<rdf:RDF schemaLocation="http://www.openarchives.org/OAI/2.0/rdf/ http://www.openarchives.org/OAI/2.0/rdf.xsd">
<ow:Publication about="oai:http://172.28.36.237/:123456789/9867">
<dc:title>A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</dc:title>
<dc:creator>Pérez López, Silvia</dc:creator>
<dc:creator>Vázquez Moreno, Natalia</dc:creator>
<dc:creator>Escudero Augusto, Dolores</dc:creator>
<dc:creator>Astudillo González, Aurora</dc:creator>
<dc:creator>Alvarez Menéndez, Francisco</dc:creator>
<dc:creator>Goyache Goñi, Félix</dc:creator>
<dc:creator>Otero Hernández, Jesús</dc:creator>
<dc:subject>Muerte cerebral</dc:subject>
<dc:subject>Genes de apoptosis</dc:subject>
<dc:subject>Trasplante de corazón</dc:subject>
<dc:subject>Donador de órganos.</dc:subject>
<dc:description>Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</dc:description>
<dc:date>2018-03-27T11:29:42Z</dc:date>
<dc:date>2018-03-27T11:29:42Z</dc:date>
<dc:date>2008</dc:date>
<dc:type>article</dc:type>
<dc:identifier>Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</dc:identifier>
<dc:identifier>0041-1337</dc:identifier>
<dc:identifier>https://ria.asturias.es/RIA/handle/123456789/9867</dc:identifier>
<dc:language>eng</dc:language>
<dc:relation>Transplantation</dc:relation>
<dc:relation>86</dc:relation>
<dc:relation>Sí, esta versión ha sido citada</dc:relation>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</dc:rights>
<dc:publisher>Lippincott, Williams & Wilkins</dc:publisher>
<dc:source>977;982</dc:source>
</ow:Publication>
</rdf:RDF>
<?xml version="1.0" encoding="UTF-8" ?>
<metadata schemaLocation="http://www.lyncode.com/xoai http://www.lyncode.com/xsd/xoai.xsd">
<element name="dc">
<element name="contributor">
<element name="author">
<element name="none">
<field name="value">Pérez López, Silvia</field>
<field name="value">Vázquez Moreno, Natalia</field>
<field name="value">Escudero Augusto, Dolores</field>
<field name="value">Astudillo González, Aurora</field>
<field name="value">Alvarez Menéndez, Francisco</field>
<field name="value">Goyache Goñi, Félix</field>
<field name="value">Otero Hernández, Jesús</field>
</element>
</element>
</element>
<element name="date">
<element name="accessioned">
<element name="none">
<field name="value">2018-03-27T11:29:42Z</field>
</element>
</element>
<element name="available">
<element name="none">
<field name="value">2018-03-27T11:29:42Z</field>
</element>
</element>
<element name="issued">
<element name="none">
<field name="value">2008</field>
</element>
</element>
</element>
<element name="identifier">
<element name="citation">
<element name="eng">
<field name="value">Pérez López, S...[et al.].A Molecular Approach to Apoptosis in the Human Heart During Brain Death. Transplantation. 2008 ; 86 : 977-982</field>
</element>
</element>
<element name="issn">
<element name="none">
<field name="value">0041-1337</field>
</element>
</element>
<element name="uri">
<element name="none">
<field name="value">https://ria.asturias.es/RIA/handle/123456789/9867</field>
</element>
</element>
</element>
<element name="description">
<element name="abstract">
<element name="eng">
<field name="value">Background. Brain death induces changes in tissues and organs destined for transplant at the cell, molecular, and endocrine level including cell death through apoptosis. This study was designed to examine apoptotic damage in cardiac tissue obtained from brain dead donors. Methods. Fifty tissue specimens from the left ventricles of individual donors were processed to evaluate changes in the expression levels of five genes involved in apoptosis (BAX, BCL2, CASPASE 3, CYTOCHROME C, and FAS) using the real time-polymerase chain reaction technique. Expression levels were quantified by the relative standard method and results normalized to the levels recorded for the endogenous control peptidylprolyl isomerase A. The HIF1 gene was also determined to check for the possibility of hypoxic damage. Control ventricular tissue specimens were obtained from patients undergoing mitral valve replacement. Results. Using a mixed linear model it was determined that the sample type (donor vs. control patient) significantly affected (P 0.0001) expression levels of the genes examined reflected by their Ct values. Three of the genes (BAX, CASPASE 3, and FAS) showed significantly higher (Student’s t test, P 0.05) expression levels (4.89-, 7.85-, and 12.14-fold endogenous control values, respectively) in donors compared with control patients (2.31-, 2.64-, and 3.57-fold endogenous control values, respectively) indicating the activation of apoptosis during brain death. Conclusion. Our findings suggest the possibility of using antiapoptosis agents to prevent cardiac injury and improve posttransplant behavior.</field>
</element>
</element>
</element>
<element name="language">
<element name="iso">
<element name="eng">
<field name="value">eng</field>
</element>
</element>
</element>
<element name="publisher">
<element name="eng">
<field name="value">Lippincott, Williams & Wilkins</field>
</element>
</element>
<element name="relation">
<element name="ispartof">
<element name="eng">
<field name="value">Transplantation</field>
</element>
</element>
<element name="haspart">
<element name="eng">
<field name="value">86</field>
</element>
</element>
<element name="isreferencedby">
<element name="eng">
<field name="value">Sí, esta versión ha sido citada</field>
</element>
</element>
</element>
<element name="rights">
<element name="eng">
<field name="value">http://creativecommons.org/licenses/by-nc-nd/3.0/deed.es</field>
</element>
</element>
<element name="source">
<element name="none">
<field name="value">977;982</field>
</element>
</element>
<element name="subject">
<element name="eng">
<field name="value">Muerte cerebral</field>
<field name="value">Genes de apoptosis</field>
<field name="value">Trasplante de corazón</field>
<field name="value">Donador de órganos.</field>
</element>
<element name="classification">
<element name="eng">
<field name="value">Publicado</field>
</element>
</element>
</element>
<element name="title">
<element name="eng">
<field name="value">A Molecular Approach to Apoptosis in the Human Heart During Brain Death.</field>
</element>
</element>
<element name="type">
<element name="eng">
<field name="value">article</field>
</element>
</element>
</element>
<element name="bundles">
<element name="bundle">
<field name="name">ORIGINAL</field>
<element name="bitstreams">
<element name="bitstream">
<field name="name">Archivo.pdf</field>
<field name="originalName">Archivo.pdf</field>
<field name="format">application/pdf</field>
<field name="size">388274</field>
<field name="url">http://172.28.36.237:8080/jspui/bitstream/123456789/9867/1/Archivo.pdf</field>
<field name="checksum">f3e0c39d60a6aa660cb9ac28be6fef17</field>
<field name="checksumAlgorithm">MD5</field>
<field name="sid">1</field>
</element>
</element>
</element>
</element>
<element name="others">
<field name="handle">123456789/9867</field>
<field name="identifier">oai:http://172.28.36.237/:123456789/9867</field>
<field name="lastModifyDate">2020-04-08 13:12:53.709</field>
</element>
<element name="repository">
<field name="name">RIA</field>
<field name="mail">gemma.gonzalez@ricoh.es</field>
</element>
</metadata>