MovDisordV3, PascalFrancis, Corpus, bibRecord, 001E40

Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism

Identifieur interne : 001E40 ( PascalFrancis/Corpus ); précédent : 001E39; suivant : 001E41

Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism

Auteurs : Antonio L. Jr Teixeira ; Melissa M. Guimaraes ; Marco Aurélio Romano-Silva ; Francisco Cardoso

Source :

Movement disorders [ 0885-3185 ] ; 2005.

RBID : Pascal:05-0387178

Descripteurs français

Pascal (Inist)
- Système nerveux pathologie, Chorée Sydenham, Streptococcie, Homme, Intracellulaire, Calcium, Complément, Noyau gris central, Streptococcus.

English descriptors

KwdEn :
- Basal ganglion, Calcium, Complement, Human, Intracellular, Nervous system diseases, Streptococcal infection, Streptococcus, Sydenham chorea.

Abstract

The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca²⁺ levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca²⁺ levels determined by SC patients sera correlated directly with the enzyme-linked immunosorbent assay optical density values for anti-basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`02`	`1`		`@1 GUIMARAES (Melissa M.)`
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C01	`01`		`ENG`	@0 The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca²⁺ levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca²⁺ levels determined by SC patients sera correlated directly with the enzyme-linked immunosorbent assay optical density values for anti-basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction.
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C03	`06`	`X`	`FRE`	`@0 Calcium @2 NC @2 FR @5 11`
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C07	`06`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 37`
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N21				`@1 269`
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Format Inist (serveur)

NO :	PASCAL 05-0387178 INIST
ET :	Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism
AU :	TEIXEIRA (Antonio L. JR); GUIMARAES (Melissa M.); ROMANO-SILVA (Marco Aurélio); CARDOSO (Francisco)
AF :	Movement Disorders Clinic, Hospital das Clinicas, Universidade Federal de Minas Gerais/Belo Horizonte/Brésil (1 aut., 4 aut.); Laboratory of Neuropharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais/Belo Horizonte/Brésil (2 aut., 3 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 7; Pp. 843-845; Bibl. 14 ref.
LA :	Anglais
EA :	The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca²⁺ levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca²⁺ levels determined by SC patients sera correlated directly with the enzyme-linked immunosorbent assay optical density values for anti-basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction.
CC :	002B17; 002B17F; 002A25L
FD :	Système nerveux pathologie; Chorée Sydenham; Streptococcie; Homme; Intracellulaire; Calcium; Complément; Noyau gris central; Streptococcus
FG :	Bactériose; Infection; Streptococcaceae; Micrococcales; Bactérie; Extrapyramidal syndrome; Maladie inflammatoire; Système nerveux central pathologie; Encéphale pathologie; Système nerveux central
ED :	Nervous system diseases; Sydenham chorea; Streptococcal infection; Human; Intracellular; Calcium; Complement; Basal ganglion; Streptococcus
EG :	Bacteriosis; Infection; Streptococcaceae; Micrococcales; Bacteria; Extrapyramidal syndrome; Inflammatory disease; Central nervous system disease; Cerebral disorder; Central nervous system
SD :	Sistema nervioso patología; Corea Sydenham; Estreptococia; Hombre; Intracelular; Calcio; Complemento; Núcleo basal; Streptococcus
LO :	INIST-20953.354000132363110100
ID :	05-0387178

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Pascal:05-0387178

Le document en format XML

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<front><div type="abstract" xml:lang="en">The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca<sup>2+</sup>
 levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca<sup>2+</sup>
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 levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca<sup>2+</sup>
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<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Complemento</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Noyau gris central</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>13</s5>
</fC03>
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<s2>NS</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Streptococcus</s0>
<s2>NS</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Streptococcus</s0>
<s2>NS</s2>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Bactériose</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Bacteriosis</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Bacteriosis</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Streptococcaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Streptococcaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Streptococcaceae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Micrococcales</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Micrococcales</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Micrococcales</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Bactérie</s0>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Bacteria</s0>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Bacteria</s0>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Maladie inflammatoire</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Inflammatory disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Enfermedad inflamatoria</s0>
<s5>38</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>41</s5>
</fC07>
<fN21><s1>269</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 05-0387178 INIST</NO>
<ET>Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism</ET>
<AU>TEIXEIRA (Antonio L. JR); GUIMARAES (Melissa M.); ROMANO-SILVA (Marco Aurélio); CARDOSO (Francisco)</AU>
<AF>Movement Disorders Clinic, Hospital das Clinicas, Universidade Federal de Minas Gerais/Belo Horizonte/Brésil (1 aut., 4 aut.); Laboratory of Neuropharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais/Belo Horizonte/Brésil (2 aut., 3 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 7; Pp. 843-845; Bibl. 14 ref.</SO>
<LA>Anglais</LA>
<EA>The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody-mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement-inactivated serum from SC patients was associated with a significant increase in Ca<sup>2+</sup>
 levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca<sup>2+</sup>
 levels determined by SC patients sera correlated directly with the enzyme-linked immunosorbent assay optical density values for anti-basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction.</EA>
<CC>002B17; 002B17F; 002A25L</CC>
<FD>Système nerveux pathologie; Chorée Sydenham; Streptococcie; Homme; Intracellulaire; Calcium; Complément; Noyau gris central; Streptococcus</FD>
<FG>Bactériose; Infection; Streptococcaceae; Micrococcales; Bactérie; Extrapyramidal syndrome; Maladie inflammatoire; Système nerveux central pathologie; Encéphale pathologie; Système nerveux central</FG>
<ED>Nervous system diseases; Sydenham chorea; Streptococcal infection; Human; Intracellular; Calcium; Complement; Basal ganglion; Streptococcus</ED>
<EG>Bacteriosis; Infection; Streptococcaceae; Micrococcales; Bacteria; Extrapyramidal syndrome; Inflammatory disease; Central nervous system disease; Cerebral disorder; Central nervous system</EG>
<SD>Sistema nervioso patología; Corea Sydenham; Estreptococia; Hombre; Intracelular; Calcio; Complemento; Núcleo basal; Streptococcus</SD>
<LO>INIST-20953.354000132363110100</LO>
<ID>05-0387178</ID>
</server>
</inist>
</record>

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	Movement Disorders (revue)
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Movement Disorders (revue)

Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism

Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement-independent mechanism

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