Evidence that Myocardial Na/I Symporter Gene Imaging Does Not Perturb Cardiac Function
Adenoviral Na/I symporter (NIS) gene transfer has emerged as a promising method for myocardial gene imaging but concern over possible perturbation of cardiac function persists. In this study, we addressed this issue with cultured cardiac cells and serial echocardiography, creatine kinase (CK) measur...
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| Veröffentlicht in: | The Journal of nuclear medicine (1978) 2006-11, Vol.47 (11), p.1851-1857 |
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| creator | Lee, Kyung-Han Bae, Jun-Sang Lee, Sang-Chul Paik, Jin-Young Matsui, Takashi Jung, Kyung-Ho Ko, Bong-Ho Kim, Byung-Tae |
| description | Adenoviral Na/I symporter (NIS) gene transfer has emerged as a promising method for myocardial gene imaging but concern over possible perturbation of cardiac function persists. In this study, we addressed this issue with cultured cardiac cells and serial echocardiography, creatine kinase (CK) measurements, and histologic examination of rats intramyocardially injected with an adenovirus that expresses both NIS and enhanced green fluorescent protein (EGFP) (Ad.EGFP.NIS) or a control virus (Ad.EGFP).
H9C2 cardiac myoblasts differentiated into cardiomyocytes were evaluated for the effect of Ad.EGFP.NIS and Ad.EGFP infection on viable cell number and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Rats injected intramyocardially with 3 x 10(8) plaque-forming units of Ad.EGFP.NIS (n = 9) or Ad.EGFP (n = 8) underwent serial echocardiographic measurements of heart rate, left ventricular (LV) dimensions, ejection fraction (EF), and fractional shortening (FS) on the day before and on days 4 and 9 after gene transfer. Five Ad.EGFP.NIS rats also underwent repeated (123)I imaging from which ratios of cardiac to mediastinal counts (C/M ratios) were obtained. Separate rats underwent serial measurements of serum CK, myocardial myeloperoxidase assays, and microscopic assessment of inflammation.
Cultured cardiac cells showed no change in cell viability or proliferation at 4 and 9 d after Ad.EGFP.NIS or Ad.EGFP infection compared with controls. (123)I scintigraphy demonstrated high cardiac radiouptake at Ad.EGFP.NIS injection sites by days 2 and 4 (C/M ratios, 5.0 +/- 0.6 and 5.1 +/- 1.0, respectively), followed by a complete loss of uptake by day 9 (C/M ratio, 1.4 +/- 0.0). Serial echocardiography revealed no difference in heart rate, LV dimensions, or functional parameters between Ad.EGFP.NIS and Ad.EGFP groups at any given time. Mild reductions in LVEF and LVFS by day 9 compared with baseline were similar for both Ad.EGFP (88.2% +/- 6.4% vs. 79.6% +/- 5.0% for LVEF and 0.55 +/- 0.10 vs. 0.44 +/- 0.05 for LVFS) and Ad.EGFP.NIS groups (88.0% +/- 5.4% vs. 78.7% +/- 4.6% for LVEF and 0.54 +/- 0.09 vs. 0.42 +/- 0.05 for LVFS). Serial serum CK and myocardial myeloperoxidase activities were not elevated in either group, in contrast to substantial increases found after ischemia-reperfusion injury. Histology revealed similar mild inflammatory cell infiltration restricted to the injection site for both groups.
The results of this study demonstrate that my |
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H9C2 cardiac myoblasts differentiated into cardiomyocytes were evaluated for the effect of Ad.EGFP.NIS and Ad.EGFP infection on viable cell number and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Rats injected intramyocardially with 3 x 10(8) plaque-forming units of Ad.EGFP.NIS (n = 9) or Ad.EGFP (n = 8) underwent serial echocardiographic measurements of heart rate, left ventricular (LV) dimensions, ejection fraction (EF), and fractional shortening (FS) on the day before and on days 4 and 9 after gene transfer. Five Ad.EGFP.NIS rats also underwent repeated (123)I imaging from which ratios of cardiac to mediastinal counts (C/M ratios) were obtained. Separate rats underwent serial measurements of serum CK, myocardial myeloperoxidase assays, and microscopic assessment of inflammation.
Cultured cardiac cells showed no change in cell viability or proliferation at 4 and 9 d after Ad.EGFP.NIS or Ad.EGFP infection compared with controls. (123)I scintigraphy demonstrated high cardiac radiouptake at Ad.EGFP.NIS injection sites by days 2 and 4 (C/M ratios, 5.0 +/- 0.6 and 5.1 +/- 1.0, respectively), followed by a complete loss of uptake by day 9 (C/M ratio, 1.4 +/- 0.0). Serial echocardiography revealed no difference in heart rate, LV dimensions, or functional parameters between Ad.EGFP.NIS and Ad.EGFP groups at any given time. Mild reductions in LVEF and LVFS by day 9 compared with baseline were similar for both Ad.EGFP (88.2% +/- 6.4% vs. 79.6% +/- 5.0% for LVEF and 0.55 +/- 0.10 vs. 0.44 +/- 0.05 for LVFS) and Ad.EGFP.NIS groups (88.0% +/- 5.4% vs. 78.7% +/- 4.6% for LVEF and 0.54 +/- 0.09 vs. 0.42 +/- 0.05 for LVFS). Serial serum CK and myocardial myeloperoxidase activities were not elevated in either group, in contrast to substantial increases found after ischemia-reperfusion injury. Histology revealed similar mild inflammatory cell infiltration restricted to the injection site for both groups.
The results of this study demonstrate that myocardial NIS gene imaging does not cause significant myocardial injury or perturbed cardiac function, other than mild effects likely due to adenoviral vector-associated host response. Thus, this practical and convenient reporter gene strategy can be used safely for noninvasive myocardial gene imaging in living subjects.</description><identifier>ISSN: 0161-5505</identifier><identifier>EISSN: 1535-5667</identifier><identifier>PMID: 17079819</identifier><identifier>CODEN: JNMEAQ</identifier><language>eng</language><publisher>United States: Soc Nuclear Med</publisher><subject>Adenoviridae - metabolism ; Adenoviruses ; Animals ; Cardiovascular system ; Cell Survival ; Cells ; Creatine Kinase - metabolism ; Echocardiography - methods ; Gene expression ; Genes, Reporter ; Genetic Therapy - methods ; Green Fluorescent Proteins - metabolism ; Heart failure ; Humans ; Iodine Radioisotopes - pharmacology ; Kinases ; Medical imaging ; Methods ; Myocardium - metabolism ; Myocardium - pathology ; Proteins ; Radionuclide Imaging - methods ; Rats ; Rats, Sprague-Dawley ; Rodents ; Symporters - metabolism</subject><ispartof>The Journal of nuclear medicine (1978), 2006-11, Vol.47 (11), p.1851-1857</ispartof><rights>Copyright Society of Nuclear Medicine Nov 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17079819$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Kyung-Han</creatorcontrib><creatorcontrib>Bae, Jun-Sang</creatorcontrib><creatorcontrib>Lee, Sang-Chul</creatorcontrib><creatorcontrib>Paik, Jin-Young</creatorcontrib><creatorcontrib>Matsui, Takashi</creatorcontrib><creatorcontrib>Jung, Kyung-Ho</creatorcontrib><creatorcontrib>Ko, Bong-Ho</creatorcontrib><creatorcontrib>Kim, Byung-Tae</creatorcontrib><title>Evidence that Myocardial Na/I Symporter Gene Imaging Does Not Perturb Cardiac Function</title><title>The Journal of nuclear medicine (1978)</title><addtitle>J Nucl Med</addtitle><description>Adenoviral Na/I symporter (NIS) gene transfer has emerged as a promising method for myocardial gene imaging but concern over possible perturbation of cardiac function persists. In this study, we addressed this issue with cultured cardiac cells and serial echocardiography, creatine kinase (CK) measurements, and histologic examination of rats intramyocardially injected with an adenovirus that expresses both NIS and enhanced green fluorescent protein (EGFP) (Ad.EGFP.NIS) or a control virus (Ad.EGFP).
H9C2 cardiac myoblasts differentiated into cardiomyocytes were evaluated for the effect of Ad.EGFP.NIS and Ad.EGFP infection on viable cell number and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Rats injected intramyocardially with 3 x 10(8) plaque-forming units of Ad.EGFP.NIS (n = 9) or Ad.EGFP (n = 8) underwent serial echocardiographic measurements of heart rate, left ventricular (LV) dimensions, ejection fraction (EF), and fractional shortening (FS) on the day before and on days 4 and 9 after gene transfer. Five Ad.EGFP.NIS rats also underwent repeated (123)I imaging from which ratios of cardiac to mediastinal counts (C/M ratios) were obtained. Separate rats underwent serial measurements of serum CK, myocardial myeloperoxidase assays, and microscopic assessment of inflammation.
Cultured cardiac cells showed no change in cell viability or proliferation at 4 and 9 d after Ad.EGFP.NIS or Ad.EGFP infection compared with controls. (123)I scintigraphy demonstrated high cardiac radiouptake at Ad.EGFP.NIS injection sites by days 2 and 4 (C/M ratios, 5.0 +/- 0.6 and 5.1 +/- 1.0, respectively), followed by a complete loss of uptake by day 9 (C/M ratio, 1.4 +/- 0.0). Serial echocardiography revealed no difference in heart rate, LV dimensions, or functional parameters between Ad.EGFP.NIS and Ad.EGFP groups at any given time. Mild reductions in LVEF and LVFS by day 9 compared with baseline were similar for both Ad.EGFP (88.2% +/- 6.4% vs. 79.6% +/- 5.0% for LVEF and 0.55 +/- 0.10 vs. 0.44 +/- 0.05 for LVFS) and Ad.EGFP.NIS groups (88.0% +/- 5.4% vs. 78.7% +/- 4.6% for LVEF and 0.54 +/- 0.09 vs. 0.42 +/- 0.05 for LVFS). Serial serum CK and myocardial myeloperoxidase activities were not elevated in either group, in contrast to substantial increases found after ischemia-reperfusion injury. Histology revealed similar mild inflammatory cell infiltration restricted to the injection site for both groups.
The results of this study demonstrate that myocardial NIS gene imaging does not cause significant myocardial injury or perturbed cardiac function, other than mild effects likely due to adenoviral vector-associated host response. Thus, this practical and convenient reporter gene strategy can be used safely for noninvasive myocardial gene imaging in living subjects.</description><subject>Adenoviridae - metabolism</subject><subject>Adenoviruses</subject><subject>Animals</subject><subject>Cardiovascular system</subject><subject>Cell Survival</subject><subject>Cells</subject><subject>Creatine Kinase - metabolism</subject><subject>Echocardiography - methods</subject><subject>Gene expression</subject><subject>Genes, Reporter</subject><subject>Genetic Therapy - methods</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Heart failure</subject><subject>Humans</subject><subject>Iodine Radioisotopes - pharmacology</subject><subject>Kinases</subject><subject>Medical imaging</subject><subject>Methods</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Proteins</subject><subject>Radionuclide Imaging - methods</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Symporters - metabolism</subject><issn>0161-5505</issn><issn>1535-5667</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpd0EFLwzAUB_AgipvTryDBg3gpJm2SpkeZ2xzoFBxeQ5q-bhltOtNU2be3bvPi5f0vv_f4807QkPKER1yI9BQNCRU04pzwAbpo2w0hREgpz9GApiTNJM2G6GPyZQtwBnBY64Bfdo3RvrC6wgt9P8fvu3rb-AAez8ABntd6Zd0KPzbQ4kUT8Bv40Pkcj_dLBk87Z4Jt3CU6K3XVwtUxR2g5nSzHT9Hz62w-fniO1rHIQmRK4FJLAAZlriWBNC44N4IUsjAZoxAzmZRAINN5YoCxXMSGcdb7LC1lMkK3h7Nb33x20AZV29ZAVWkHTdcqISlJ-9HDm39w03Te9dVUTDPKON2j6yPq8hoKtfW21n6n_r7Vg7sDWNvV-tt6UK4zFWj_qzeuZqmiVFHJafIDSSR0mg</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Lee, Kyung-Han</creator><creator>Bae, Jun-Sang</creator><creator>Lee, Sang-Chul</creator><creator>Paik, Jin-Young</creator><creator>Matsui, Takashi</creator><creator>Jung, Kyung-Ho</creator><creator>Ko, Bong-Ho</creator><creator>Kim, Byung-Tae</creator><general>Soc Nuclear Med</general><general>Society of Nuclear Medicine</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>4T-</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>M7Z</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20061101</creationdate><title>Evidence that Myocardial Na/I Symporter Gene Imaging Does Not Perturb Cardiac Function</title><author>Lee, Kyung-Han ; Bae, Jun-Sang ; Lee, Sang-Chul ; Paik, Jin-Young ; Matsui, Takashi ; Jung, Kyung-Ho ; Ko, Bong-Ho ; Kim, Byung-Tae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h269t-cfe58a8ee4efba80e72d55c60d8dc941e2483fe0e9ab3ce44b62c454e4e97f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adenoviridae - metabolism</topic><topic>Adenoviruses</topic><topic>Animals</topic><topic>Cardiovascular system</topic><topic>Cell Survival</topic><topic>Cells</topic><topic>Creatine Kinase - metabolism</topic><topic>Echocardiography - methods</topic><topic>Gene expression</topic><topic>Genes, Reporter</topic><topic>Genetic Therapy - methods</topic><topic>Green Fluorescent Proteins - metabolism</topic><topic>Heart failure</topic><topic>Humans</topic><topic>Iodine Radioisotopes - pharmacology</topic><topic>Kinases</topic><topic>Medical imaging</topic><topic>Methods</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Proteins</topic><topic>Radionuclide Imaging - methods</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Symporters - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Kyung-Han</creatorcontrib><creatorcontrib>Bae, Jun-Sang</creatorcontrib><creatorcontrib>Lee, Sang-Chul</creatorcontrib><creatorcontrib>Paik, Jin-Young</creatorcontrib><creatorcontrib>Matsui, Takashi</creatorcontrib><creatorcontrib>Jung, Kyung-Ho</creatorcontrib><creatorcontrib>Ko, Bong-Ho</creatorcontrib><creatorcontrib>Kim, Byung-Tae</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Docstoc</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of nuclear medicine (1978)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Kyung-Han</au><au>Bae, Jun-Sang</au><au>Lee, Sang-Chul</au><au>Paik, Jin-Young</au><au>Matsui, Takashi</au><au>Jung, Kyung-Ho</au><au>Ko, Bong-Ho</au><au>Kim, Byung-Tae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence that Myocardial Na/I Symporter Gene Imaging Does Not Perturb Cardiac Function</atitle><jtitle>The Journal of nuclear medicine (1978)</jtitle><addtitle>J Nucl Med</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>47</volume><issue>11</issue><spage>1851</spage><epage>1857</epage><pages>1851-1857</pages><issn>0161-5505</issn><eissn>1535-5667</eissn><coden>JNMEAQ</coden><abstract>Adenoviral Na/I symporter (NIS) gene transfer has emerged as a promising method for myocardial gene imaging but concern over possible perturbation of cardiac function persists. In this study, we addressed this issue with cultured cardiac cells and serial echocardiography, creatine kinase (CK) measurements, and histologic examination of rats intramyocardially injected with an adenovirus that expresses both NIS and enhanced green fluorescent protein (EGFP) (Ad.EGFP.NIS) or a control virus (Ad.EGFP).
H9C2 cardiac myoblasts differentiated into cardiomyocytes were evaluated for the effect of Ad.EGFP.NIS and Ad.EGFP infection on viable cell number and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Rats injected intramyocardially with 3 x 10(8) plaque-forming units of Ad.EGFP.NIS (n = 9) or Ad.EGFP (n = 8) underwent serial echocardiographic measurements of heart rate, left ventricular (LV) dimensions, ejection fraction (EF), and fractional shortening (FS) on the day before and on days 4 and 9 after gene transfer. Five Ad.EGFP.NIS rats also underwent repeated (123)I imaging from which ratios of cardiac to mediastinal counts (C/M ratios) were obtained. Separate rats underwent serial measurements of serum CK, myocardial myeloperoxidase assays, and microscopic assessment of inflammation.
Cultured cardiac cells showed no change in cell viability or proliferation at 4 and 9 d after Ad.EGFP.NIS or Ad.EGFP infection compared with controls. (123)I scintigraphy demonstrated high cardiac radiouptake at Ad.EGFP.NIS injection sites by days 2 and 4 (C/M ratios, 5.0 +/- 0.6 and 5.1 +/- 1.0, respectively), followed by a complete loss of uptake by day 9 (C/M ratio, 1.4 +/- 0.0). Serial echocardiography revealed no difference in heart rate, LV dimensions, or functional parameters between Ad.EGFP.NIS and Ad.EGFP groups at any given time. Mild reductions in LVEF and LVFS by day 9 compared with baseline were similar for both Ad.EGFP (88.2% +/- 6.4% vs. 79.6% +/- 5.0% for LVEF and 0.55 +/- 0.10 vs. 0.44 +/- 0.05 for LVFS) and Ad.EGFP.NIS groups (88.0% +/- 5.4% vs. 78.7% +/- 4.6% for LVEF and 0.54 +/- 0.09 vs. 0.42 +/- 0.05 for LVFS). Serial serum CK and myocardial myeloperoxidase activities were not elevated in either group, in contrast to substantial increases found after ischemia-reperfusion injury. Histology revealed similar mild inflammatory cell infiltration restricted to the injection site for both groups.
The results of this study demonstrate that myocardial NIS gene imaging does not cause significant myocardial injury or perturbed cardiac function, other than mild effects likely due to adenoviral vector-associated host response. Thus, this practical and convenient reporter gene strategy can be used safely for noninvasive myocardial gene imaging in living subjects.</abstract><cop>United States</cop><pub>Soc Nuclear Med</pub><pmid>17079819</pmid><tpages>7</tpages></addata></record> |
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| subjects | Adenoviridae - metabolism Adenoviruses Animals Cardiovascular system Cell Survival Cells Creatine Kinase - metabolism Echocardiography - methods Gene expression Genes, Reporter Genetic Therapy - methods Green Fluorescent Proteins - metabolism Heart failure Humans Iodine Radioisotopes - pharmacology Kinases Medical imaging Methods Myocardium - metabolism Myocardium - pathology Proteins Radionuclide Imaging - methods Rats Rats, Sprague-Dawley Rodents Symporters - metabolism |
| title | Evidence that Myocardial Na/I Symporter Gene Imaging Does Not Perturb Cardiac Function |
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