Neurochemical Alterations in Spinocerebellar Ataxia Type 1 and their Correlations with Clinical Status
Identifieur interne : 000948 ( PascalFrancis/Checkpoint ); précédent : 000947; suivant : 000949Neurochemical Alterations in Spinocerebellar Ataxia Type 1 and their Correlations with Clinical Status
Auteurs : Gülin Öz [États-Unis] ; Diane Hutter [États-Unis] ; Ivan Tkac [États-Unis] ; H. Brent Clark [États-Unis] ; Myron D. Gross [États-Unis] ; HONG JIANG [États-Unis] ; Lynn E. Eberly [États-Unis] ; Khalaf O. Bushara [États-Unis] ; Christopher M. Gomez [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2010.
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- Pascal (Inist)
English descriptors
Abstract
Robust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy (1H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N-acetylaspartate + N-acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo-inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate-glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo-inositol, and glutamate levels were discernible in individual spectra and the tNAA/ myo-inositol ratio in the cerebellar hemipheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo-inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo-inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F2-isoprostanes as a marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that 1H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients.
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Gross</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Laboratory Medicine and Pathology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Hong Jiang" sort="Hong Jiang" uniqKey="Hong Jiang" last="Hong Jiang">HONG JIANG</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurology, University of Chicago</s1><s2>Chicago, Illinois</s2><s3>USA</s3><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Eberly, Lynn E" sort="Eberly, Lynn E" uniqKey="Eberly L" first="Lynn E." last="Eberly">Lynn E. 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Gomez</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurology, University of Chicago</s1><s2>Chicago, Illinois</s2><s3>USA</s3><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">10-0376238</idno><date when="2010">2010</date><idno type="stanalyst">PASCAL 10-0376238 INIST</idno><idno type="RBID">Pascal:10-0376238</idno><idno type="wicri:Area/PascalFrancis/Corpus">000A16</idno><idno type="wicri:Area/PascalFrancis/Curation">002303</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000948</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Neurochemical Alterations in Spinocerebellar Ataxia Type 1 and their Correlations with Clinical Status</title><author><name sortKey="Oz, Gulin" sort="Oz, Gulin" uniqKey="Oz G" first="Gülin" last="Öz">Gülin Öz</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Center for MR Research, Department of Radiology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Hutter, Diane" sort="Hutter, Diane" uniqKey="Hutter D" first="Diane" last="Hutter">Diane Hutter</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Center for MR Research, Department of Radiology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Tkac, Ivan" sort="Tkac, Ivan" uniqKey="Tkac I" first="Ivan" last="Tkac">Ivan Tkac</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Center for MR Research, Department of Radiology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Clark, H Brent" sort="Clark, H Brent" uniqKey="Clark H" first="H. Brent" last="Clark">H. Brent Clark</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Laboratory Medicine and Pathology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Gross, Myron D" sort="Gross, Myron D" uniqKey="Gross M" first="Myron D." last="Gross">Myron D. Gross</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Laboratory Medicine and Pathology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Hong Jiang" sort="Hong Jiang" uniqKey="Hong Jiang" last="Hong Jiang">HONG JIANG</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurology, University of Chicago</s1><s2>Chicago, Illinois</s2><s3>USA</s3><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Eberly, Lynn E" sort="Eberly, Lynn E" uniqKey="Eberly L" first="Lynn E." last="Eberly">Lynn E. Eberly</name><affiliation wicri:level="2"><inist:fA14 i1="04"><s1>Division of Biostatistics, School of Public Health, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Bushara, Khalaf O" sort="Bushara, Khalaf O" uniqKey="Bushara K" first="Khalaf O." last="Bushara">Khalaf O. Bushara</name><affiliation wicri:level="2"><inist:fA14 i1="05"><s1>Department of Neurology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author><author><name sortKey="Gomez, Christopher M" sort="Gomez, Christopher M" uniqKey="Gomez C" first="Christopher M." last="Gomez">Christopher M. Gomez</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Department of Neurology, University of Chicago</s1><s2>Chicago, Illinois</s2><s3>USA</s3><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Illinois</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cerebellum</term><term>Nervous system diseases</term><term>Spinocerebellar ataxia</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Pathologie du système nerveux</term><term>Ataxie spinocérébelleuse</term><term>Cervelet</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Robust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy (<sup>1</sup>H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N-acetylaspartate + N-acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo-inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate-glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo-inositol, and glutamate levels were discernible in individual spectra and the tNAA/ myo-inositol ratio in the cerebellar hemipheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo-inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo-inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F<sub>2</sub>-isoprostanes as a marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that <sup>1</sup>H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>25</s2></fA05><fA06><s2>9</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Neurochemical Alterations in Spinocerebellar Ataxia Type 1 and their Correlations with Clinical Status</s1></fA08><fA11 i1="01" i2="1"><s1>ÖZ (Gülin)</s1></fA11><fA11 i1="02" i2="1"><s1>HUTTER (Diane)</s1></fA11><fA11 i1="03" i2="1"><s1>TKAC (Ivan)</s1></fA11><fA11 i1="04" i2="1"><s1>CLARK (H. Brent)</s1></fA11><fA11 i1="05" i2="1"><s1>GROSS (Myron D.)</s1></fA11><fA11 i1="06" i2="1"><s1>HONG JIANG</s1></fA11><fA11 i1="07" i2="1"><s1>EBERLY (Lynn E.)</s1></fA11><fA11 i1="08" i2="1"><s1>BUSHARA (Khalaf O.)</s1></fA11><fA11 i1="09" i2="1"><s1>GOMEZ (Christopher M.)</s1></fA11><fA14 i1="01"><s1>Center for MR Research, Department of Radiology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Laboratory Medicine and Pathology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Department of Neurology, University of Chicago</s1><s2>Chicago, Illinois</s2><s3>USA</s3><sZ>6 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="04"><s1>Division of Biostatistics, School of Public Health, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>7 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Neurology, Medical School, University of Minnesota</s1><s2>Minneapolis, Minnesota</s2><s3>USA</s3><sZ>8 aut.</sZ></fA14><fA20><s1>1253-1261</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000191760240210</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>41 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>10-0376238</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Robust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy (<sup>1</sup>H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N-acetylaspartate + N-acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo-inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate-glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo-inositol, and glutamate levels were discernible in individual spectra and the tNAA/ myo-inositol ratio in the cerebellar hemipheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo-inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo-inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F<sub>2</sub>-isoprostanes as a marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that <sup>1</sup>H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A03</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Ataxie spinocérébelleuse</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Spinocerebellar ataxia</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Ataxia spinocerebelosa</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Cervelet</s0><s5>10</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Cerebellum</s0><s5>10</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Cerebelo</s0><s5>10</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Maladie héréditaire</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Genetic disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Encéphale</s0><s5>41</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Encephalon</s0><s5>41</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>42</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system</s0><s5>42</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>42</s5></fC07><fN21><s1>242</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li><li>Minnesota</li></region></list><tree><country name="États-Unis"><region name="Minnesota"><name sortKey="Oz, Gulin" sort="Oz, Gulin" uniqKey="Oz G" first="Gülin" last="Öz">Gülin Öz</name></region><name sortKey="Bushara, Khalaf O" sort="Bushara, Khalaf O" uniqKey="Bushara K" first="Khalaf O." last="Bushara">Khalaf O. Bushara</name><name sortKey="Clark, H Brent" sort="Clark, H Brent" uniqKey="Clark H" first="H. Brent" last="Clark">H. Brent Clark</name><name sortKey="Eberly, Lynn E" sort="Eberly, Lynn E" uniqKey="Eberly L" first="Lynn E." last="Eberly">Lynn E. Eberly</name><name sortKey="Gomez, Christopher M" sort="Gomez, Christopher M" uniqKey="Gomez C" first="Christopher M." last="Gomez">Christopher M. Gomez</name><name sortKey="Gross, Myron D" sort="Gross, Myron D" uniqKey="Gross M" first="Myron D." last="Gross">Myron D. Gross</name><name sortKey="Hong Jiang" sort="Hong Jiang" uniqKey="Hong Jiang" last="Hong Jiang">HONG JIANG</name><name sortKey="Hutter, Diane" sort="Hutter, Diane" uniqKey="Hutter D" first="Diane" last="Hutter">Diane Hutter</name><name sortKey="Tkac, Ivan" sort="Tkac, Ivan" uniqKey="Tkac I" first="Ivan" last="Tkac">Ivan Tkac</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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