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La toxine botulique en 10 questions / Audrey ALAU in Déclic, 145 (Janvier-Février 2012)
[article]
Titre : La toxine botulique en 10 questions Type de document : Texte imprimé et/ou numérique Auteurs : Audrey ALAU, Auteur Année de publication : 2012 Article en page(s) : p.60-61 Langues : Français (fre) Index. décimale : PER Périodiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=150
in Déclic > 145 (Janvier-Février 2012) . - p.60-61[article] La toxine botulique en 10 questions [Texte imprimé et/ou numérique] / Audrey ALAU, Auteur . - 2012 . - p.60-61.
Langues : Français (fre)
in Déclic > 145 (Janvier-Février 2012) . - p.60-61
Index. décimale : PER Périodiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=150 Toxocariasis / C. G. H. NEWMAN in Developmental Medicine & Child Neurology, 20-2 (April 1978)
[article]
Titre : Toxocariasis Type de document : Texte imprimé et/ou numérique Auteurs : C. G. H. NEWMAN, Auteur Année de publication : 1978 Article en page(s) : p.218-220 Langues : Anglais (eng) Index. décimale : PER Périodiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=476
in Developmental Medicine & Child Neurology > 20-2 (April 1978) . - p.218-220[article] Toxocariasis [Texte imprimé et/ou numérique] / C. G. H. NEWMAN, Auteur . - 1978 . - p.218-220.
Langues : Anglais (eng)
in Developmental Medicine & Child Neurology > 20-2 (April 1978) . - p.218-220
Index. décimale : PER Périodiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=476 TPH2 G/T polymorphism is associated with hyperphagia, IQ, and internalizing problems in Prader–Willi syndrome / Elisabeth M. DYKENS in Journal of Child Psychology and Psychiatry, 52-5 (May 2011)
[article]
Titre : TPH2 G/T polymorphism is associated with hyperphagia, IQ, and internalizing problems in Prader–Willi syndrome Type de document : Texte imprimé et/ou numérique Auteurs : Elisabeth M. DYKENS, Auteur ; Elizabeth ROOF, Auteur ; Douglas BITTEL, Auteur ; Merlin G. BUTLER, Auteur Année de publication : 2011 Article en page(s) : p.580-587 Langues : Anglais (eng) Mots-clés : Behavior problems genetics intelligence internalizing disorder neurochemistry Prader–Willi syndrome Index. décimale : PER Périodiques Résumé : Background: Prader–Willi syndrome (PWS) is a genetic, neurodevelopmental disorder characterized by intellectual disabilities, growth hormone dysregulation, hyperphagia, increased risks of morbid obesity, compulsive behaviors, and irritability. As aberrant serotonergic functioning is strongly implicated in PWS, we examined associations between the PWS phenotype and polymorphisms in tryptophan hydroxylase 2 (TPH2), the rate-limiting enzyme in the biosynthesis of serotonin in the brain.
Methods: Ninety-two individuals with PWS aged 4 to 50 years (M = 21.97) were genotyped for the TPH2 G703-T polymorphism. IQ testing was conducted in offspring, and parents completed questionnaires that tapped their child’s compulsivity, hyperphagia, and other behavior problems.
Results: As expected, the frequency of G/T or T/T polymorphisms in participants with PWS (39%) was similar to rates found in the general population (38%). Compared to those with a homozygous (G/G) genotype, individuals with a T allele had significantly higher hyperphagic behavior, drive, and severity scores, and they also had a younger age of onset of hyperphagia. Those with a T allele also had higher IQ scores than their counterparts. Females with a T allele had significantly higher internalizing symptoms, primarily anxiety and depression, than all others.
Conclusions: TPH2 G/T polymorphisms, and presumed loss of enzyme function, were associated with specific aspects of the PWS phenotype. Aberrant serotonergic functioning is strongly implicated in hyperphagia in PWS, and females with TPH2 T alleles may be at higher risk for affective or mood disorders. Findings hold promise for examining other serotonin-altering genes in PWS, and for future serotonin-altering treatment trials.En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02365.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121
in Journal of Child Psychology and Psychiatry > 52-5 (May 2011) . - p.580-587[article] TPH2 G/T polymorphism is associated with hyperphagia, IQ, and internalizing problems in Prader–Willi syndrome [Texte imprimé et/ou numérique] / Elisabeth M. DYKENS, Auteur ; Elizabeth ROOF, Auteur ; Douglas BITTEL, Auteur ; Merlin G. BUTLER, Auteur . - 2011 . - p.580-587.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 52-5 (May 2011) . - p.580-587
Mots-clés : Behavior problems genetics intelligence internalizing disorder neurochemistry Prader–Willi syndrome Index. décimale : PER Périodiques Résumé : Background: Prader–Willi syndrome (PWS) is a genetic, neurodevelopmental disorder characterized by intellectual disabilities, growth hormone dysregulation, hyperphagia, increased risks of morbid obesity, compulsive behaviors, and irritability. As aberrant serotonergic functioning is strongly implicated in PWS, we examined associations between the PWS phenotype and polymorphisms in tryptophan hydroxylase 2 (TPH2), the rate-limiting enzyme in the biosynthesis of serotonin in the brain.
Methods: Ninety-two individuals with PWS aged 4 to 50 years (M = 21.97) were genotyped for the TPH2 G703-T polymorphism. IQ testing was conducted in offspring, and parents completed questionnaires that tapped their child’s compulsivity, hyperphagia, and other behavior problems.
Results: As expected, the frequency of G/T or T/T polymorphisms in participants with PWS (39%) was similar to rates found in the general population (38%). Compared to those with a homozygous (G/G) genotype, individuals with a T allele had significantly higher hyperphagic behavior, drive, and severity scores, and they also had a younger age of onset of hyperphagia. Those with a T allele also had higher IQ scores than their counterparts. Females with a T allele had significantly higher internalizing symptoms, primarily anxiety and depression, than all others.
Conclusions: TPH2 G/T polymorphisms, and presumed loss of enzyme function, were associated with specific aspects of the PWS phenotype. Aberrant serotonergic functioning is strongly implicated in hyperphagia in PWS, and females with TPH2 T alleles may be at higher risk for affective or mood disorders. Findings hold promise for examining other serotonin-altering genes in PWS, and for future serotonin-altering treatment trials.En ligne : http://dx.doi.org/10.1111/j.1469-7610.2011.02365.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121 TPH2 polymorphisms and expression in Prader-Willi syndrome subjects with differing genetic subtypes / R. S. HENKHAUS in Journal of Neurodevelopmental Disorders, 2-3 (September 2010)
[article]
Titre : TPH2 polymorphisms and expression in Prader-Willi syndrome subjects with differing genetic subtypes Type de document : Texte imprimé et/ou numérique Auteurs : R. S. HENKHAUS, Auteur ; D. C. BITTEL, Auteur ; M. G. BUTLER, Auteur Article en page(s) : p.144-8 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Prader-Willi syndrome (PWS) is a genetic imprinting disease that causes developmental and behavioral disturbances resulting from loss of expression of genes from the paternal chromosome 15q11-q13 region. In about 70% of subjects, this portion of the paternal chromosome is deleted, while 25% have two copies of the maternal chromosome 15, or uniparental maternal disomy (UPD; the remaining subjects have imprinting center defects. There are several documented physical and behavioral differences between the two major PWS genetic subtypes (deletion and UPD) indicating the genetic subtype plays a role in clinical presentation. Serotonin is known to be disturbed in PWS and affects both eating behavior and compulsion, which are reported to be abnormal in PWS. We investigated the tryptophan hydroxylase gene (TPH2), the rate-limiting enzyme in the production of brain serotonin, by analyzing three different TPH2 gene polymorphisms, transcript expression, and correlation with PWS genetic subtype. DNA and RNA from lymphoblastoid cell lines derived from 12 PWS and 12 comparison subjects were used for the determination of genetic subtype, TPH2 polymorphisms and quantitative RT-PCR analysis. A similar frequency of TPH2 polymorphisms was seen in the PWS and comparison subjects with PWS deletion subjects showing increased expression with one or more TPH2 polymorphism. Both PWS deletion and PWS UPD subjects had significantly lower TPH2 expression than control subjects and PWS deletion subjects had significantly lower TPH2 expression compared with PWS UPD subjects. PWS subjects with 15q11-q13 deletions had lower TPH2 expression compared with PWS UPD or control subjects, requiring replication and further studies to identify the cause including identification of disturbed gene interactions resulting from the deletion process. En ligne : http://dx.doi.org/10.1007/s11689-010-9051-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.144-8[article] TPH2 polymorphisms and expression in Prader-Willi syndrome subjects with differing genetic subtypes [Texte imprimé et/ou numérique] / R. S. HENKHAUS, Auteur ; D. C. BITTEL, Auteur ; M. G. BUTLER, Auteur . - p.144-8.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-3 (September 2010) . - p.144-8
Index. décimale : PER Périodiques Résumé : Prader-Willi syndrome (PWS) is a genetic imprinting disease that causes developmental and behavioral disturbances resulting from loss of expression of genes from the paternal chromosome 15q11-q13 region. In about 70% of subjects, this portion of the paternal chromosome is deleted, while 25% have two copies of the maternal chromosome 15, or uniparental maternal disomy (UPD; the remaining subjects have imprinting center defects. There are several documented physical and behavioral differences between the two major PWS genetic subtypes (deletion and UPD) indicating the genetic subtype plays a role in clinical presentation. Serotonin is known to be disturbed in PWS and affects both eating behavior and compulsion, which are reported to be abnormal in PWS. We investigated the tryptophan hydroxylase gene (TPH2), the rate-limiting enzyme in the production of brain serotonin, by analyzing three different TPH2 gene polymorphisms, transcript expression, and correlation with PWS genetic subtype. DNA and RNA from lymphoblastoid cell lines derived from 12 PWS and 12 comparison subjects were used for the determination of genetic subtype, TPH2 polymorphisms and quantitative RT-PCR analysis. A similar frequency of TPH2 polymorphisms was seen in the PWS and comparison subjects with PWS deletion subjects showing increased expression with one or more TPH2 polymorphism. Both PWS deletion and PWS UPD subjects had significantly lower TPH2 expression than control subjects and PWS deletion subjects had significantly lower TPH2 expression compared with PWS UPD subjects. PWS subjects with 15q11-q13 deletions had lower TPH2 expression compared with PWS UPD or control subjects, requiring replication and further studies to identify the cause including identification of disturbed gene interactions resulting from the deletion process. En ligne : http://dx.doi.org/10.1007/s11689-010-9051-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Trace element levels and autism spectrum disorder in a sample of Algerian children: A case-control study investigation / Belkis STAMBOULI ; Imene KADDOUR-BENKADA ; Ahmed AMZIANE ; Akli Islam CHEBLI ; Mohammed Yacine ACHOURI ; Reda DJIDJIK ; Barkahoum ALAMIR in Research in Autism Spectrum Disorders, 110 (February 2024)
[article]
Titre : Trace element levels and autism spectrum disorder in a sample of Algerian children: A case-control study investigation Type de document : Texte imprimé et/ou numérique Auteurs : Belkis STAMBOULI, Auteur ; Imene KADDOUR-BENKADA, Auteur ; Ahmed AMZIANE, Auteur ; Akli Islam CHEBLI, Auteur ; Mohammed Yacine ACHOURI, Auteur ; Reda DJIDJIK, Auteur ; Barkahoum ALAMIR, Auteur Article en page(s) : p.102287 Mots-clés : ASD Autism Metals Trace elements ICP-MS Index. décimale : PER Périodiques Résumé : The prevalence of autism has been increasing in recent years due to better screening. diagnosis. and awareness campaigns. Toxic metals are considered to be one of the environmental factors that may contribute to autism spectrum disorders (ASD). This study aimed to investigate the levels of toxic and essential trace elements in autistic children and their connection to autism. The study included 40 autistic children and 41 controls. both aged 4?9 years. The levels of toxic metals and metalloids (Arsenic. Cadmium. Chromium. Mercury. Lead) and trace elements (Copper. Iron. Selenium. Zinc) were measured in whole blood. plasma. and urine using ICP-MS multi-elemental techniques. The results showed that the concentrations of toxic and essential metals were significantly higher in autistic children compared to controls. This was demonstrated by higher levels of Cadmium. Chromium. Copper. Zinc. and Lead in blood. plasma. and urine. while plasma Iron levels were lower in autistic children. The results suggest a possible association between autism and metal exposure. but causality cannot be established. En ligne : https://doi.org/10.1016/j.rasd.2023.102287 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=520
in Research in Autism Spectrum Disorders > 110 (February 2024) . - p.102287[article] Trace element levels and autism spectrum disorder in a sample of Algerian children: A case-control study investigation [Texte imprimé et/ou numérique] / Belkis STAMBOULI, Auteur ; Imene KADDOUR-BENKADA, Auteur ; Ahmed AMZIANE, Auteur ; Akli Islam CHEBLI, Auteur ; Mohammed Yacine ACHOURI, Auteur ; Reda DJIDJIK, Auteur ; Barkahoum ALAMIR, Auteur . - p.102287.
in Research in Autism Spectrum Disorders > 110 (February 2024) . - p.102287
Mots-clés : ASD Autism Metals Trace elements ICP-MS Index. décimale : PER Périodiques Résumé : The prevalence of autism has been increasing in recent years due to better screening. diagnosis. and awareness campaigns. Toxic metals are considered to be one of the environmental factors that may contribute to autism spectrum disorders (ASD). This study aimed to investigate the levels of toxic and essential trace elements in autistic children and their connection to autism. The study included 40 autistic children and 41 controls. both aged 4?9 years. The levels of toxic metals and metalloids (Arsenic. Cadmium. Chromium. Mercury. Lead) and trace elements (Copper. Iron. Selenium. Zinc) were measured in whole blood. plasma. and urine using ICP-MS multi-elemental techniques. The results showed that the concentrations of toxic and essential metals were significantly higher in autistic children compared to controls. This was demonstrated by higher levels of Cadmium. Chromium. Copper. Zinc. and Lead in blood. plasma. and urine. while plasma Iron levels were lower in autistic children. The results suggest a possible association between autism and metal exposure. but causality cannot be established. En ligne : https://doi.org/10.1016/j.rasd.2023.102287 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=520 Traces dans la clinique psychomotrice en périnatalité: ...qualités de la rencontre pour des qualités d'être / Béatrice THIEBO in Thérapie psychomotrice et recherches, 169 (2012)
PermalinkTraces écrites du psychomotricien et traçabilité une incompatibilité? / Odile FRAND in Thérapie psychomotrice et recherches, 169 (2012)
PermalinkTraces et mémoire: comment et où se forment nos souvenirs? / Jean Christophe CASSEL in Thérapie psychomotrice et recherches, 169 (2012)
PermalinkDe traces en tracés / Anne CIANI-HOLTZ in Thérapie psychomotrice et recherches, 161 (2010)
PermalinkTracing back to the onset of abnormal head circumference growth in Italian children with autism spectrum disorder / Filippo MURATORI in Research in Autism Spectrum Disorders, 6-1 (January-March 2012)
PermalinkTracking eye movements proves informative for the study of gaze direction detection in autism / Deborah M. RIBY in Research in Autism Spectrum Disorders, 3-3 (July-September 2009)
PermalinkTracking Social Motivation Systems Deficits: The Affective Neuroscience View of Autism / Arnaud CARRE in Journal of Autism and Developmental Disorders, 45-10 (October 2015)
PermalinkTracking the Sensory Environment: An ERP Study of Probability and Context Updating in ASD / Marissa A. WESTERFIELD in Journal of Autism and Developmental Disorders, 45-2 (February 2015)
PermalinkTract-specific analyses of diffusion tensor imaging show widespread white matter compromise in autism spectrum disorder / Dinesh K. SHUKLA in Journal of Child Psychology and Psychiatry, 52-3 (March 2011)
PermalinkTraditional and Atypical Presentations of Anxiety in Youth with Autism Spectrum Disorder / Connor M. KERNS in Journal of Autism and Developmental Disorders, 44-11 (November 2014)
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