THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY
Identifieur interne : 000077 ( PascalFrancis/Checkpoint ); précédent : 000076; suivant : 000078THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY
Auteurs : M. J. Ferris [États-Unis] ; D. Frederick-Duus [États-Unis] ; J. Fadel [États-Unis] ; C. F. Mactutus [États-Unis] ; R. M. Booze [États-Unis]Source :
- Neuroscience [ 0306-4522 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PascalFrancis, to step Corpus: 000140
- to stream PascalFrancis, to step Corpus: 000154
- to stream PascalFrancis, to step Curation: 000139
Links to Exploration step
Pascal:09-0199428Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT<sub>1-86</sub>, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY</title><author><name sortKey="Ferris, M J" sort="Ferris, M J" uniqKey="Ferris M" first="M. J." last="Ferris">M. J. Ferris</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation></author><author><name sortKey="Frederick Duus, D" sort="Frederick Duus, D" uniqKey="Frederick Duus D" first="D." last="Frederick-Duus">D. Frederick-Duus</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Fadel, J" sort="Fadel, J" uniqKey="Fadel J" first="J." last="Fadel">J. Fadel</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Mactutus, C F" sort="Mactutus, C F" uniqKey="Mactutus C" first="C. F." last="Mactutus">C. F. Mactutus</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation></author><author><name sortKey="Booze, R M" sort="Booze, R M" uniqKey="Booze R" first="R. M." last="Booze">R. M. Booze</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">09-0199428</idno><date when="2009">2009</date><idno type="stanalyst">PASCAL 09-0199428 INIST</idno><idno type="RBID">Pascal:09-0199428</idno><idno type="wicri:Area/PascalFrancis/Corpus">000140</idno><idno type="stanalyst">FRANCIS 09-0199428 INIST</idno><idno type="wicri:Area/PascalFrancis/Corpus">000154</idno><idno type="wicri:Area/PascalFrancis/Curation">000139</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000077</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000077</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT<sub>1-86</sub>, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY</title><author><name sortKey="Ferris, M J" sort="Ferris, M J" uniqKey="Ferris M" first="M. J." last="Ferris">M. J. Ferris</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation></author><author><name sortKey="Frederick Duus, D" sort="Frederick Duus, D" uniqKey="Frederick Duus D" first="D." last="Frederick-Duus">D. Frederick-Duus</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Fadel, J" sort="Fadel, J" uniqKey="Fadel J" first="J." last="Fadel">J. Fadel</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author><author><name sortKey="Mactutus, C F" sort="Mactutus, C F" uniqKey="Mactutus C" first="C. F." last="Mactutus">C. F. Mactutus</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation></author><author><name sortKey="Booze, R M" sort="Booze, R M" uniqKey="Booze R" first="R. M." last="Booze">R. M. Booze</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Caroline du Sud</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Carrier protein</term><term>Cocaine</term><term>Dopamine</term><term>Human immunodeficiency virus</term><term>Microdialysis</term><term>Nerve ending</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Virus immunodéficience humaine</term><term>Protéine transport</term><term>Dopamine</term><term>Cocaïne</term><term>Terminaison nerveuse</term><term>Microdialyse</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0306-4522</s0></fA01><fA02 i1="01"><s0>NRSCDN</s0></fA02><fA03 i2="1"><s0>Neuroscience</s0></fA03><fA05><s2>159</s2></fA05><fA06><s2>4</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT<sub>1-86</sub>, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY</s1></fA08><fA11 i1="01" i2="1"><s1>FERRIS (M. J.)</s1></fA11><fA11 i1="02" i2="1"><s1>FREDERICK-DUUS (D.)</s1></fA11><fA11 i1="03" i2="1"><s1>FADEL (J.)</s1></fA11><fA11 i1="04" i2="1"><s1>MACTUTUS (C. F.)</s1></fA11><fA11 i1="05" i2="1"><s1>BOOZE (R. M.)</s1></fA11><fA14 i1="01"><s1>Department of Psychology, Program in Behavioral Neuroscience, University of South Carolina</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine</s1><s2>Columbia, SC 29208</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA20><s1>1292-1299</s1></fA20><fA21><s1>2009</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>17194</s2><s5>354000186798120110</s5></fA43><fA44><s0>0000</s0><s1>© 2009 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>09-0199428</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neuroscience</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>-Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurode-generation in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.</s0></fC01><fC02 i1="01" i2="X"><s0>002A25</s0></fC02><fC02 i1="02" i2="X"><s0>002B02B02</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Virus immunodéficience humaine</s0><s2>NW</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Human immunodeficiency virus</s0><s2>NW</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Human immunodeficiency virus</s0><s2>NW</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Protéine transport</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Carrier protein</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Proteína transportador</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Dopamina</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Cocaïne</s0><s2>NK</s2><s2>FR</s2><s2>FX</s2><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Cocaine</s0><s2>NK</s2><s2>FR</s2><s2>FX</s2><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Cocaína</s0><s2>NK</s2><s2>FR</s2><s2>FX</s2><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Terminaison nerveuse</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Nerve ending</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Terminación nerviosa</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Microdialyse</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Microdialysis</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Microdiálisis</s0><s5>06</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Lentivirus</s0><s2>NW</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Lentivirus</s0><s2>NW</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Lentivirus</s0><s2>NW</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Retroviridae</s0><s2>NW</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Retroviridae</s0><s2>NW</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Retroviridae</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Virus</s0><s2>NW</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Catécholamine</s0><s5>20</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Catecholamine</s0><s5>20</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Catecolamina</s0><s5>20</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Neurotransmetteur</s0><s5>21</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Neurotransmitter</s0><s5>21</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Neurotransmisor</s0><s5>21</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Substance toxicomanogène</s0><s5>22</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Drug of abuse</s0><s5>22</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sustancia toxicomanógena</s0><s5>22</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Stimulant SNC</s0><s5>23</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>CNS stimulant</s0><s5>23</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Estimulante SNC</s0><s5>23</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Psychotrope</s0><s2>FX</s2><s5>24</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Psychotropic</s0><s2>FX</s2><s5>24</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Psicotropo</s0><s2>FX</s2><s5>24</s5></fC07><fN21><s1>145</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>Caroline du Sud</li></region><settlement><li>Columbia (Caroline du Sud)</li></settlement><orgName><li>Université de Caroline du Sud</li></orgName></list><tree><country name="États-Unis"><region name="Caroline du Sud"><name sortKey="Ferris, M J" sort="Ferris, M J" uniqKey="Ferris M" first="M. J." last="Ferris">M. J. Ferris</name></region><name sortKey="Booze, R M" sort="Booze, R M" uniqKey="Booze R" first="R. M." last="Booze">R. M. Booze</name><name sortKey="Booze, R M" sort="Booze, R M" uniqKey="Booze R" first="R. M." last="Booze">R. M. Booze</name><name sortKey="Fadel, J" sort="Fadel, J" uniqKey="Fadel J" first="J." last="Fadel">J. Fadel</name><name sortKey="Frederick Duus, D" sort="Frederick Duus, D" uniqKey="Frederick Duus D" first="D." last="Frederick-Duus">D. Frederick-Duus</name><name sortKey="Mactutus, C F" sort="Mactutus, C F" uniqKey="Mactutus C" first="C. F." last="Mactutus">C. F. Mactutus</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/StressCovidV1/Data/PascalFrancis/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000077 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Checkpoint/biblio.hfd -nk 000077 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= StressCovidV1
|flux= PascalFrancis
|étape= Checkpoint
|type= RBID
|clé= Pascal:09-0199428
|texte= THE HUMAN IMMUNODEFICIENCY VIRUS-1-ASSOCIATED PROTEIN, TAT1-86, IMPAIRS DOPAMINE TRANSPORTERS AND INTERACTS WITH COCAINE TO REDUCE NERVE TERMINAL FUNCTION : A NO-NET-FLUX MICRODIALYSIS STUDY
}}
| This area was generated with Dilib version V0.6.33. |  |