Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice
Identifieur interne : 006166 ( Istex/Corpus ); précédent : 006165; suivant : 006167Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice
Auteurs : Susan L. Hall ; Shin-Tai Chen ; Jon E. Wergedal ; Daila S. Gridley ; Subburaman Mohan ; K. William LauSource :
- The Journal of Gene Medicine [ 1099-498X ] ; 2011-02.
English descriptors
- KwdEn :
- Bone, Bone formation, Bone formation response, Bone growth, Bone loss, Bone marrow, Bone marrow cavity, Bone marrow cells, Bone mass, Bone miner, Bone resorption, Bone surface, Cells transduced, Control group, Cortical, Cortical thickness, Endocrinology, Endosteal, Endosteal bone formation, Endosteal bone mass, Endosteum, Engraftment, Facs analysis, Femur, Gene, Gene therapy, Gene transfer strategy, Growth factor, Growth hormone, Growth plate, Hematopoietic, High levels, Igfbps, John wiley sons, Loma, Loma linda, Loma linda university school, Marrow, Marrow cavity, Marrow transplantation, Medical center, Mesenchymal, Miner, Mouse, Mrna, Mrna levels, Murine, Musculoskeletal disease center, Ndings, Nonparametric test, Osmotic lysis, Osteoblast, Osteoclast, Osteoclast surface, Osteoclastic, Osteoclastic resorption, Osteogenic, Osteogenic gene, Overexpression, Periosteal, Peripheral blood, Peripheral blood cells, Pettis memorial, Pqct, Present study, Receptor, Recipient, Recipient mice, Recipient mouse, Representative sample, Resorption, Sca1, Secondary spongiosa, Serum levels, Trabecular, Trabecular bone formation, Trabecular bone volume, Trabecular number, Trabecular separation, Transduced, Transgene, Transgenic, Transgenic mice, Transgenic mouse strains, Transgenic overexpression, Transgenic strains, Transplantation, Upper right, Viable cells, Vivo, Vivo gene transfer strategy.
- Teeft :
- Bone, Bone formation, Bone formation response, Bone growth, Bone loss, Bone marrow, Bone marrow cavity, Bone marrow cells, Bone mass, Bone miner, Bone resorption, Bone surface, Cells transduced, Control group, Cortical, Cortical thickness, Endocrinology, Endosteal, Endosteal bone formation, Endosteal bone mass, Endosteum, Engraftment, Facs analysis, Femur, Gene, Gene therapy, Gene transfer strategy, Growth factor, Growth hormone, Growth plate, Hematopoietic, High levels, Igfbps, John wiley sons, Loma, Loma linda, Loma linda university school, Marrow, Marrow cavity, Marrow transplantation, Medical center, Mesenchymal, Miner, Mouse, Mrna, Mrna levels, Murine, Musculoskeletal disease center, Ndings, Nonparametric test, Osmotic lysis, Osteoblast, Osteoclast, Osteoclast surface, Osteoclastic, Osteoclastic resorption, Osteogenic, Osteogenic gene, Overexpression, Periosteal, Peripheral blood, Peripheral blood cells, Pettis memorial, Pqct, Present study, Receptor, Recipient, Recipient mice, Recipient mouse, Representative sample, Resorption, Sca1, Secondary spongiosa, Serum levels, Trabecular, Trabecular bone formation, Trabecular bone volume, Trabecular number, Trabecular separation, Transduced, Transgene, Transgenic, Transgenic mice, Transgenic mouse strains, Transgenic overexpression, Transgenic strains, Transplantation, Upper right, Viable cells, Vivo, Vivo gene transfer strategy.
Abstract
The present study assesses the effect of the stem cell antigen‐1 positive (Sca‐1+) cell‐based human growth hormone (hGH) ex vivo gene transfer strategy on endosteal bone mass in the mouse.
Url:
DOI: 10.1002/jgm.1542
Links to Exploration step
ISTEX:C46A00C509094ACA3F0BACBAE45E1D78AB1475E4Le document en format XML
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Hall</name><affiliation><mods:affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: susan.hall1@va.gov</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence address: Musculoskeletal Disease Center (151), Jerry L. Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA.</mods:affiliation></affiliation></author><author><name sortKey="Chen, Shin Ai" sort="Chen, Shin Ai" uniqKey="Chen S" first="Shin-Tai" last="Chen">Shin-Tai Chen</name><affiliation><mods:affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Wergedal, Jon E" sort="Wergedal, Jon E" uniqKey="Wergedal J" first="Jon E." last="Wergedal">Jon E. Wergedal</name><affiliation><mods:affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Gridley, Daila S" sort="Gridley, Daila S" uniqKey="Gridley D" first="Daila S." last="Gridley">Daila S. Gridley</name><affiliation><mods:affiliation>Department of Radiation Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Mohan, Subburaman" sort="Mohan, Subburaman" uniqKey="Mohan S" first="Subburaman" last="Mohan">Subburaman Mohan</name><affiliation><mods:affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Lau, K William" sort="Lau, K William" uniqKey="Lau K" first="K. William" last="Lau">K. William Lau</name><affiliation><mods:affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The Journal of Gene Medicine</title><title level="j" type="alt">JOURNAL OF GENE MEDICINE, THE</title><idno type="ISSN">1099-498X</idno><idno type="eISSN">1521-2254</idno><imprint><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="77">77</biblScope><biblScope unit="page" to="88">88</biblScope><biblScope unit="page-count">12</biblScope><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2011-02">2011-02</date></imprint><idno type="ISSN">1099-498X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1099-498X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bone</term><term>Bone formation</term><term>Bone formation response</term><term>Bone growth</term><term>Bone loss</term><term>Bone marrow</term><term>Bone marrow cavity</term><term>Bone marrow cells</term><term>Bone mass</term><term>Bone miner</term><term>Bone resorption</term><term>Bone surface</term><term>Cells transduced</term><term>Control group</term><term>Cortical</term><term>Cortical thickness</term><term>Endocrinology</term><term>Endosteal</term><term>Endosteal bone formation</term><term>Endosteal bone mass</term><term>Endosteum</term><term>Engraftment</term><term>Facs analysis</term><term>Femur</term><term>Gene</term><term>Gene therapy</term><term>Gene transfer strategy</term><term>Growth factor</term><term>Growth hormone</term><term>Growth plate</term><term>Hematopoietic</term><term>High levels</term><term>Igfbps</term><term>John wiley sons</term><term>Loma</term><term>Loma linda</term><term>Loma linda university school</term><term>Marrow</term><term>Marrow cavity</term><term>Marrow transplantation</term><term>Medical center</term><term>Mesenchymal</term><term>Miner</term><term>Mouse</term><term>Mrna</term><term>Mrna levels</term><term>Murine</term><term>Musculoskeletal disease center</term><term>Ndings</term><term>Nonparametric test</term><term>Osmotic lysis</term><term>Osteoblast</term><term>Osteoclast</term><term>Osteoclast surface</term><term>Osteoclastic</term><term>Osteoclastic resorption</term><term>Osteogenic</term><term>Osteogenic gene</term><term>Overexpression</term><term>Periosteal</term><term>Peripheral blood</term><term>Peripheral blood cells</term><term>Pettis memorial</term><term>Pqct</term><term>Present study</term><term>Receptor</term><term>Recipient</term><term>Recipient mice</term><term>Recipient mouse</term><term>Representative sample</term><term>Resorption</term><term>Sca1</term><term>Secondary spongiosa</term><term>Serum levels</term><term>Trabecular</term><term>Trabecular bone formation</term><term>Trabecular bone volume</term><term>Trabecular number</term><term>Trabecular separation</term><term>Transduced</term><term>Transgene</term><term>Transgenic</term><term>Transgenic mice</term><term>Transgenic mouse strains</term><term>Transgenic overexpression</term><term>Transgenic strains</term><term>Transplantation</term><term>Upper right</term><term>Viable cells</term><term>Vivo</term><term>Vivo gene transfer strategy</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Bone</term><term>Bone formation</term><term>Bone formation response</term><term>Bone growth</term><term>Bone loss</term><term>Bone marrow</term><term>Bone marrow cavity</term><term>Bone marrow cells</term><term>Bone mass</term><term>Bone miner</term><term>Bone resorption</term><term>Bone surface</term><term>Cells transduced</term><term>Control group</term><term>Cortical</term><term>Cortical thickness</term><term>Endocrinology</term><term>Endosteal</term><term>Endosteal bone formation</term><term>Endosteal bone mass</term><term>Endosteum</term><term>Engraftment</term><term>Facs analysis</term><term>Femur</term><term>Gene</term><term>Gene therapy</term><term>Gene transfer strategy</term><term>Growth factor</term><term>Growth hormone</term><term>Growth plate</term><term>Hematopoietic</term><term>High levels</term><term>Igfbps</term><term>John wiley sons</term><term>Loma</term><term>Loma linda</term><term>Loma linda university school</term><term>Marrow</term><term>Marrow cavity</term><term>Marrow transplantation</term><term>Medical center</term><term>Mesenchymal</term><term>Miner</term><term>Mouse</term><term>Mrna</term><term>Mrna levels</term><term>Murine</term><term>Musculoskeletal disease center</term><term>Ndings</term><term>Nonparametric test</term><term>Osmotic lysis</term><term>Osteoblast</term><term>Osteoclast</term><term>Osteoclast surface</term><term>Osteoclastic</term><term>Osteoclastic resorption</term><term>Osteogenic</term><term>Osteogenic gene</term><term>Overexpression</term><term>Periosteal</term><term>Peripheral blood</term><term>Peripheral blood cells</term><term>Pettis memorial</term><term>Pqct</term><term>Present study</term><term>Receptor</term><term>Recipient</term><term>Recipient mice</term><term>Recipient mouse</term><term>Representative sample</term><term>Resorption</term><term>Sca1</term><term>Secondary spongiosa</term><term>Serum levels</term><term>Trabecular</term><term>Trabecular bone formation</term><term>Trabecular bone volume</term><term>Trabecular number</term><term>Trabecular separation</term><term>Transduced</term><term>Transgene</term><term>Transgenic</term><term>Transgenic mice</term><term>Transgenic mouse strains</term><term>Transgenic overexpression</term><term>Transgenic strains</term><term>Transplantation</term><term>Upper right</term><term>Viable cells</term><term>Vivo</term><term>Vivo gene transfer strategy</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">The present study assesses the effect of the stem cell antigen‐1 positive (Sca‐1+) cell‐based human growth hormone (hGH) ex vivo gene transfer strategy on endosteal bone mass in the mouse.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>recipient mice</json:string><json:string>transgenic</json:string><json:string>trabecular</json:string><json:string>endosteal</json:string><json:string>resorption</json:string><json:string>transgenic mice</json:string><json:string>transplantation</json:string><json:string>osteoclast</json:string><json:string>engraftment</json:string><json:string>endosteal bone formation</json:string><json:string>growth 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formation response</json:string><json:string>trabecular number</json:string><json:string>trabecular separation</json:string><json:string>transgenic strains</json:string><json:string>facs analysis</json:string><json:string>upper right</json:string><json:string>vivo</json:string><json:string>cortical</json:string></teeft></keywords><author><json:item><name>Susan L. Hall</name><affiliations><json:string>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</json:string><json:string>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>E-mail: susan.hall1@va.gov</json:string><json:string>Correspondence address: Musculoskeletal Disease Center (151), Jerry L. Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA.</json:string></affiliations></json:item><json:item><name>Shin‐Tai Chen</name><affiliations><json:string>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</json:string><json:string>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string></affiliations></json:item><json:item><name>Jon E. Wergedal</name><affiliations><json:string>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</json:string><json:string>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string></affiliations></json:item><json:item><name>Daila S. Gridley</name><affiliations><json:string>Department of Radiation Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string></affiliations></json:item><json:item><name>Subburaman Mohan</name><affiliations><json:string>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</json:string><json:string>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string></affiliations></json:item><json:item><name>K.‐H. William Lau</name><affiliations><json:string>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</json:string><json:string>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>bone resorption</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gene therapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>growth hormone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IGF‐I</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>marrow transplantation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sca‐1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>stem cell</value></json:item></subject><articleId><json:string>JGM1542</json:string></articleId><arkIstex>ark:/67375/WNG-TQZRBTDK-8</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>The present study assesses the effect of the stem cell antigen‐1 positive (Sca‐1+) cell‐based human growth hormone (hGH) ex vivo gene transfer strategy on endosteal bone mass in the mouse.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>30</abstractWordCount><abstractCharCount>188</abstractCharCount><keywordCount>7</keywordCount><score>7.36</score><pdfWordCount>8300</pdfWordCount><pdfCharCount>52394</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>595 x 842 pts (A4)</pdfPageSize></qualityIndicators><title>Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice</title><pmid><json:string>21322098</json:string></pmid><genre><json:string>article</json:string></genre><host><title>The Journal of Gene Medicine</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1521-2254</json:string></doi><issn><json:string>1099-498X</json:string></issn><eissn><json:string>1521-2254</json:string></eissn><publisherId><json:string>JGM</json:string></publisherId><volume>13</volume><issue>2</issue><pages><first>77</first><last>88</last><total>12</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Research Article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2011</json:string></date><geogName></geogName><orgName><json:string>PeproTech</json:string><json:string>Jerry Pettis Memorial VA Medical Center</json:string><json:string>Jackson Laboratories</json:string><json:string>Department of Radiation Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Radiation Medicine, Loma Linda University</json:string><json:string>US Government</json:string><json:string>Louis University</json:string><json:string>MJ Research/Bio-Rad, Hercules, CA, USA</json:string><json:string>Roche Diagnostics, Indianapolis</json:string><json:string>Sons, Ltd.</json:string><json:string>Loma Linda University</json:string><json:string>Jerry Pettis VA Medical Center</json:string><json:string>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Pettis Memorial VA Medical Center</json:string><json:string>Sons, Ltd</json:string><json:string>Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Roche Diagnostics, Basel, Switzerland</json:string><json:string>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</json:string><json:string>Department of Veterans Affairs</json:string><json:string>Musculoskeletal Disease Center</json:string><json:string>Miltenyi Biotec, Inc.</json:string><json:string>Pettis Memorial VA Medical Center–Musculoskeletal Disease Center</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Unit</json:string><json:string>John Wiley</json:string><json:string>Jane Barker</json:string><json:string>Rocky Hills</json:string><json:string>H. William</json:string><json:string>S. Gridley</json:string><json:string>Susan L. Hall</json:string><json:string>Jon E. Wergedal</json:string><json:string>Anil Kapoor</json:string><json:string>B.Ar</json:string><json:string>Kristy Howard</json:string><json:string>T.Ar</json:string><json:string>Carolyn Hargrave</json:string><json:string>Tai Chen</json:string></persName><placeName><json:string>San Diego</json:string><json:string>Switzerland</json:string><json:string>Valencia</json:string><json:string>San Jose</json:string><json:string>USA</json:string><json:string>Japan</json:string><json:string>CA</json:string><json:string>Auburn</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[4]</json:string><json:string>[9,12]</json:string><json:string>[54,55]</json:string><json:string>[56]</json:string><json:string>[18]</json:string><json:string>[6]</json:string><json:string>S. L. Hall et al.</json:string><json:string>[55]</json:string><json:string>[39]</json:string><json:string>[1]</json:string><json:string>[54]</json:string><json:string>[36,37,42,45,46]</json:string><json:string>[52,53]</json:string><json:string>[8,9]</json:string><json:string>[16]</json:string><json:string>[3]</json:string><json:string>[13,14]</json:string><json:string>[31]</json:string><json:string>[3,4]</json:string><json:string>[5]</json:string><json:string>[59]</json:string><json:string>[41]</json:string><json:string>[7]</json:string><json:string>[58]</json:string><json:string>[9]</json:string><json:string>[40]</json:string><json:string>[2]</json:string><json:string>[57]</json:string><json:string>[29,30]</json:string><json:string>[4,5,27]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-TQZRBTDK-8</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - medicine, research & experimental</json:string><json:string>2 - genetics & heredity</json:string><json:string>2 - biotechnology & applied microbiology</json:string></wos><scienceMetrix><json:string>1 - applied sciences</json:string><json:string>2 - enabling & strategic technologies</json:string><json:string>3 - biotechnology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Genetics(clinical)</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Pharmacology, Toxicology and Pharmaceutics</json:string><json:string>3 - Drug Discovery</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Genetics</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Molecular Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Molecular Medicine</json:string></scopus></categories><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/jgm.1542</json:string></doi><id>C46A00C509094ACA3F0BACBAE45E1D78AB1475E4</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/C46A00C509094ACA3F0BACBAE45E1D78AB1475E4/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/C46A00C509094ACA3F0BACBAE45E1D78AB1475E4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/C46A00C509094ACA3F0BACBAE45E1D78AB1475E4/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice<ref type="note" target="#fn1"></ref></title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><availability><licence>Published 2011 John Wiley & Sons, Ltd.</licence></availability><date type="published" when="2011-02"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main" xml:lang="en">Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice<ref type="note" target="#fn1"></ref></title><title level="a" type="short" xml:lang="en">Sca‐1+ cell‐based hGH gene therapy induces bone loss</title><author xml:id="author-0000" role="corresp"><persName><forename type="first">Susan L.</forename><surname>Hall</surname></persName><email>susan.hall1@va.gov</email><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Musculoskeletal Disease Center (151), Jerry L. Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA.</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Shin‐Tai</forename><surname>Chen</surname></persName><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Jon E.</forename><surname>Wergedal</surname></persName><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Daila S.</forename><surname>Gridley</surname></persName><affiliation>Department of Radiation Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Subburaman</forename><surname>Mohan</surname></persName><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">K.‐H. William</forename><surname>Lau</surname></persName><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA<address><country key="US"></country></address></affiliation></author><idno type="istex">C46A00C509094ACA3F0BACBAE45E1D78AB1475E4</idno><idno type="ark">ark:/67375/WNG-TQZRBTDK-8</idno><idno type="DOI">10.1002/jgm.1542</idno><idno type="unit">JGM1542</idno><idno type="toTypesetVersion">file:JGM.JGM1542.pdf</idno></analytic><monogr><title level="j" type="main">The Journal of Gene Medicine</title><title level="j" type="alt">JOURNAL OF GENE MEDICINE, THE</title><idno type="pISSN">1099-498X</idno><idno type="eISSN">1521-2254</idno><idno type="book-DOI">10.1002/(ISSN)1521-2254</idno><idno type="book-part-DOI">10.1002/jgm.v13.2</idno><idno type="product">JGM</idno><imprint><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="77">77</biblScope><biblScope unit="page" to="88">88</biblScope><biblScope unit="page-count">12</biblScope><publisher>John Wiley & Sons, Ltd.</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2011-02"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head>
Background
<p>The present study assesses the effect of the stem cell antigen‐1 positive (Sca‐1<hi rend="superscript">+</hi>) cell‐based human growth hormone (hGH) <hi rend="italic">ex vivo</hi> gene transfer strategy on endosteal bone mass in the mouse.</p>
Methods
<p>Sublethally irradiated recipient mice were transplanted with Sca‐1<hi rend="superscript">+</hi> cells transduced with lentiviral vectors expressing hGH or β‐galactosidase control genes. Bone parameters were assessed by micro‐computed tomography and histomorphometry.</p>
Results
<p>This hGH strategy drastically increased hGH mRNA levels in bone marrow cells and serum insulin‐like growth factor‐I (IGF‐I) (by nearly 50%, <hi rend="italic">p</hi> < 0.002) in hGH recipient mice. Femoral trabecular bone volume of the hGH mice was significantly reduced by 35% (<hi rend="italic">p</hi> < 0.002). The hGH mice also had decreased trabecular number (by 26%; <hi rend="italic">p</hi> < 0.0001), increased trabecular separation (by 38%; <hi rend="italic">p</hi> < 0.0002) and reduced trabecular connectivity density (by 64%; <hi rend="italic">p</hi> < 0.001), as well as significantly more osteoclasts (2.5‐fold; <hi rend="italic">p</hi> < 0.05) and greater osteoclastic surface per bone surface (2.6‐fold; <hi rend="italic">p</hi> < 0.01).</p>
Conclusions
<p>Targeted expression of hGH in cells of marrow cavity through the Sca‐1<hi rend="superscript">+</hi> cell‐based gene transfer strategy increased circulating IGF‐I and decreased endosteal bone mass through an increase in resorption in recipient mice. These results indicate that high local levels of hGH or IGF‐I in the bone marrow microenvironment enhanced resorption, which is consistent with previous findings in transgenic mice with targeted bone IGF‐I expression showing that high local IGF‐I expression increased bone remodeling, favoring a net bone loss. Thus, GH and/or IGF‐I would not be an appropriate transgene for use in this Sca‐1<hi rend="superscript">+</hi> cell‐based gene transfer strategy to promote endosteal bone formation. Published 2011 John Wiley & Sons, Ltd.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">bone resorption</term><term xml:id="kwd2">gene therapy</term><term xml:id="kwd3">growth hormone</term><term xml:id="kwd4">IGF‐I</term><term xml:id="kwd5">marrow transplantation</term><term xml:id="kwd6">sca‐1</term><term xml:id="kwd7">stem cell</term></keywords><keywords rend="articleCategory"><term>Research Article</term></keywords><keywords rend="tocHeading1"><term>Research Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C46A00C509094ACA3F0BACBAE45E1D78AB1475E4/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd.</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1521-2254</doi><issn type="print">1099-498X</issn><issn type="electronic">1521-2254</issn><idGroup><id type="product" value="JGM"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF GENE MEDICINE, THE">The Journal of Gene Medicine</title><title type="short">J. Gene Med.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/jgm.v13.2</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="2011-02">February 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="30" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jgm.1542</doi><idGroup><id type="unit" value="JGM1542"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Published 2011 John Wiley & Sons, Ltd.</copyright><eventGroup><event type="manuscriptReceived" date="2010-09-09"></event><event type="manuscriptRevised" date="2010-11-06"></event><event type="manuscriptAccepted" date="2010-12-07"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText mathml2tex" date="2011-03-14"></event><event type="publishedOnlineAccepted" date="2011-02-14"></event><event type="firstOnline" date="2011-03-14"></event><event type="publishedOnlineFinalForm" date="2011-03-14"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">77</numbering><numbering type="pageLast">88</numbering></numberingGroup><correspondenceTo>Musculoskeletal Disease Center (151), Jerry L. Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JGM.JGM1542.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="5"></count><count type="referenceTotal" number="59"></count></countGroup><titleGroup><title type="main" xml:lang="en">Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice<link href="#fn1"></link></title><title type="short" xml:lang="en">Sca‐1<sup>+</sup> cell‐based hGH gene therapy induces bone loss</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Susan L.</givenNames><familyName>Hall</familyName></personName><contactDetails><email>susan.hall1@va.gov</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2 #af3"><personName><givenNames>Shin‐Tai</givenNames><familyName>Chen</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2 #af3"><personName><givenNames>Jon E.</givenNames><familyName>Wergedal</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Daila S.</givenNames><familyName>Gridley</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1 #af2 #af3 #af5"><personName><givenNames>Subburaman</givenNames><familyName>Mohan</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2 #af3"><personName><givenNames>K.‐H. William</givenNames><familyName>Lau</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Radiation Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">bone resorption</keyword><keyword xml:id="kwd2">gene therapy</keyword><keyword xml:id="kwd3">growth hormone</keyword><keyword xml:id="kwd4">IGF‐I</keyword><keyword xml:id="kwd5">marrow transplantation</keyword><keyword xml:id="kwd6">sca‐1</keyword><keyword xml:id="kwd7">stem cell</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Background</title><p>The present study assesses the effect of the stem cell antigen‐1 positive (Sca‐1<sup>+</sup>) cell‐based human growth hormone (hGH) <i>ex vivo</i> gene transfer strategy on endosteal bone mass in the mouse.</p></section><section xml:id="abs1-2"><title type="main">Methods</title><p>Sublethally irradiated recipient mice were transplanted with Sca‐1<sup>+</sup> cells transduced with lentiviral vectors expressing hGH or β‐galactosidase control genes. Bone parameters were assessed by micro‐computed tomography and histomorphometry.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>This hGH strategy drastically increased hGH mRNA levels in bone marrow cells and serum insulin‐like growth factor‐I (IGF‐I) (by nearly 50%, <i>p</i> < 0.002) in hGH recipient mice. Femoral trabecular bone volume of the hGH mice was significantly reduced by 35% (<i>p</i> < 0.002). The hGH mice also had decreased trabecular number (by 26%; <i>p</i> < 0.0001), increased trabecular separation (by 38%; <i>p</i> < 0.0002) and reduced trabecular connectivity density (by 64%; <i>p</i> < 0.001), as well as significantly more osteoclasts (2.5‐fold; <i>p</i> < 0.05) and greater osteoclastic surface per bone surface (2.6‐fold; <i>p</i> < 0.01).</p></section><section xml:id="abs1-4"><title type="main">Conclusions</title><p>Targeted expression of hGH in cells of marrow cavity through the Sca‐1<sup>+</sup> cell‐based gene transfer strategy increased circulating IGF‐I and decreased endosteal bone mass through an increase in resorption in recipient mice. These results indicate that high local levels of hGH or IGF‐I in the bone marrow microenvironment enhanced resorption, which is consistent with previous findings in transgenic mice with targeted bone IGF‐I expression showing that high local IGF‐I expression increased bone remodeling, favoring a net bone loss. Thus, GH and/or IGF‐I would not be an appropriate transgene for use in this Sca‐1<sup>+</sup> cell‐based gene transfer strategy to promote endosteal bone formation. Published 2011 John Wiley & Sons, Ltd.</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>This article is a US Government work and is in the public domain in the USA.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Sca‐1+ cell‐based hGH gene therapy induces bone loss</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Stem cell antigen‐1 positive cell‐based systemic human growth hormone gene transfer strategy increases endosteal bone resorption and bone loss in mice</title></titleInfo><name type="personal"><namePart type="given">Susan L.</namePart><namePart type="family">Hall</namePart><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><affiliation>E-mail: susan.hall1@va.gov</affiliation><affiliation>Correspondence address: Musculoskeletal Disease Center (151), Jerry L. Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shin‐Tai</namePart><namePart type="family">Chen</namePart><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jon E.</namePart><namePart type="family">Wergedal</namePart><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Daila S.</namePart><namePart type="family">Gridley</namePart><affiliation>Department of Radiation Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Subburaman</namePart><namePart type="family">Mohan</namePart><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><affiliation>Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.‐H. William</namePart><namePart type="family">Lau</namePart><affiliation>Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, CA, USA</affiliation><affiliation>Department of Medicine, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><affiliation>Department of Biochemistry, Loma Linda University School of Medicine, Loma Linda, CA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>John Wiley & Sons, Ltd.</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-02</dateIssued><dateCaptured encoding="w3cdtf">2010-09-09</dateCaptured><dateValid encoding="w3cdtf">2010-12-07</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">4</extent><extent unit="tables">5</extent><extent unit="references">59</extent></physicalDescription><abstract>The present study assesses the effect of the stem cell antigen‐1 positive (Sca‐1+) cell‐based human growth hormone (hGH) ex vivo gene transfer strategy on endosteal bone mass in the mouse.</abstract><abstract>Sublethally irradiated recipient mice were transplanted with Sca‐1+ cells transduced with lentiviral vectors expressing hGH or β‐galactosidase control genes. Bone parameters were assessed by micro‐computed tomography and histomorphometry.</abstract><abstract>This hGH strategy drastically increased hGH mRNA levels in bone marrow cells and serum insulin‐like growth factor‐I (IGF‐I) (by nearly 50%, p < 0.002) in hGH recipient mice. Femoral trabecular bone volume of the hGH mice was significantly reduced by 35% (p < 0.002). The hGH mice also had decreased trabecular number (by 26%; p < 0.0001), increased trabecular separation (by 38%; p < 0.0002) and reduced trabecular connectivity density (by 64%; p < 0.001), as well as significantly more osteoclasts (2.5‐fold; p < 0.05) and greater osteoclastic surface per bone surface (2.6‐fold; p < 0.01).</abstract><abstract>Targeted expression of hGH in cells of marrow cavity through the Sca‐1+ cell‐based gene transfer strategy increased circulating IGF‐I and decreased endosteal bone mass through an increase in resorption in recipient mice. These results indicate that high local levels of hGH or IGF‐I in the bone marrow microenvironment enhanced resorption, which is consistent with previous findings in transgenic mice with targeted bone IGF‐I expression showing that high local IGF‐I expression increased bone remodeling, favoring a net bone loss. Thus, GH and/or IGF‐I would not be an appropriate transgene for use in this Sca‐1+ cell‐based gene transfer strategy to promote endosteal bone formation. Published 2011 John Wiley & Sons, Ltd.</abstract><note type="content">*This article is a US Government work and is in the public domain in the USA.</note><subject lang="en"><genre>keywords</genre><topic>bone resorption</topic><topic>gene therapy</topic><topic>growth hormone</topic><topic>IGF‐I</topic><topic>marrow transplantation</topic><topic>sca‐1</topic><topic>stem cell</topic></subject><relatedItem type="host"><titleInfo><title>The Journal of Gene Medicine</title></titleInfo><titleInfo type="abbreviated"><title>J. Gene Med.</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1099-498X</identifier><identifier type="eISSN">1521-2254</identifier><identifier type="DOI">10.1002/(ISSN)1521-2254</identifier><identifier type="PublisherID">JGM</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>77</start><end>88</end><total>12</total></extent></part></relatedItem><identifier type="istex">C46A00C509094ACA3F0BACBAE45E1D78AB1475E4</identifier><identifier type="ark">ark:/67375/WNG-TQZRBTDK-8</identifier><identifier type="DOI">10.1002/jgm.1542</identifier><identifier type="ArticleID">JGM1542</identifier><accessCondition type="use and reproduction" contentType="copyright">Published 2011 John Wiley & Sons, Ltd.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>John Wiley & Sons, Ltd.</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/C46A00C509094ACA3F0BACBAE45E1D78AB1475E4/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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