Dépouillements

Cover essay in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.251 Titre : Cover essay Type de document : Texte imprimé et/ou numérique Article en page(s) : p.251 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9038-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Cover essay [Texte imprimé et/ou numérique] . - p.251. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.251 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9038-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Choline transporter gene variation is associated with attention-deficit hyperactivity disorder / B. A. ENGLISH in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.252-63 Titre : Choline transporter gene variation is associated with attention-deficit hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : B. A. ENGLISH, Auteur ; M. K. HAHN, Auteur ; I. R. GIZER, Auteur ; M. MAZEI-ROBISON, Auteur ; A. STEELE, Auteur ; D. M. KURNIK, Auteur ; M. A. STEIN, Auteur ; Irwin D. WALDMAN, Auteur ; R. D. BLAKELY, Auteur Article en page(s) : p.252-63 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The neurotransmitter acetylcholine (ACh) plays a critical role in brain circuits mediating motor control, attention, learning and memory. Cholinergic dysfunction is associated with multiple brain disorders including Alzheimer's Disease, addiction, schizophrenia and Attention-Deficit Hyperactivity Disorder (ADHD). The presynaptic choline transporter (CHT, SLC5A7) is the major, rate-limiting determinant of ACh production in the brain and periphery and is consequently upregulated during tasks that require sustained attention. Given the contribution of central cholinergic circuits to the control of movement and attention, we hypothesized that functional CHT gene variants might impact risk for ADHD. We performed a case-control study, followed by family-based association tests on a separate cohort, of two purportedly functional CHT polymorphisms (coding variant Ile89Val (rs1013940) and a genomic SNP 3' of the CHT gene (rs333229), affording both a replication sample and opportunities to reduce potential population stratification biases. Initial genotyping of pediatric ADHD subjects for two purportedly functional CHT alleles revealed a 2-3 fold elevation of the Val89 allele (n = 100; P = 0.02) relative to healthy controls, as well as a significant decrease of the 3'SNP minor allele in Caucasian male subjects (n = 60; P = 0.004). In family based association tests, we found significant overtransmission of the Val89 variant to children with a Combined subtype diagnosis (OR = 3.16; P = 0.01), with an increased Odds Ratio for a haplotype comprising both minor alleles. These studies show evidence of cholinergic deficits in ADHD, particularly for subjects with the Combined subtype, and, if replicated, may encourage further consideration of cholinergic agonist therapy in the disorder. En ligne : http://dx.doi.org/10.1007/s11689-009-9033-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Choline transporter gene variation is associated with attention-deficit hyperactivity disorder [Texte imprimé et/ou numérique] / B. A. ENGLISH, Auteur ; M. K. HAHN, Auteur ; I. R. GIZER, Auteur ; M. MAZEI-ROBISON, Auteur ; A. STEELE, Auteur ; D. M. KURNIK, Auteur ; M. A. STEIN, Auteur ; Irwin D. WALDMAN, Auteur ; R. D. BLAKELY, Auteur . - p.252-63. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.252-63 Index. décimale : PER Périodiques Résumé : The neurotransmitter acetylcholine (ACh) plays a critical role in brain circuits mediating motor control, attention, learning and memory. Cholinergic dysfunction is associated with multiple brain disorders including Alzheimer's Disease, addiction, schizophrenia and Attention-Deficit Hyperactivity Disorder (ADHD). The presynaptic choline transporter (CHT, SLC5A7) is the major, rate-limiting determinant of ACh production in the brain and periphery and is consequently upregulated during tasks that require sustained attention. Given the contribution of central cholinergic circuits to the control of movement and attention, we hypothesized that functional CHT gene variants might impact risk for ADHD. We performed a case-control study, followed by family-based association tests on a separate cohort, of two purportedly functional CHT polymorphisms (coding variant Ile89Val (rs1013940) and a genomic SNP 3' of the CHT gene (rs333229), affording both a replication sample and opportunities to reduce potential population stratification biases. Initial genotyping of pediatric ADHD subjects for two purportedly functional CHT alleles revealed a 2-3 fold elevation of the Val89 allele (n = 100; P = 0.02) relative to healthy controls, as well as a significant decrease of the 3'SNP minor allele in Caucasian male subjects (n = 60; P = 0.004). In family based association tests, we found significant overtransmission of the Val89 variant to children with a Combined subtype diagnosis (OR = 3.16; P = 0.01), with an increased Odds Ratio for a haplotype comprising both minor alleles. These studies show evidence of cholinergic deficits in ADHD, particularly for subjects with the Combined subtype, and, if replicated, may encourage further consideration of cholinergic agonist therapy in the disorder. En ligne : http://dx.doi.org/10.1007/s11689-009-9033-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Convergent genetic linkage and associations to language, speech and reading measures in families of probands with Specific Language Impairment / M. L. RICE in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.264-82 Titre : Convergent genetic linkage and associations to language, speech and reading measures in families of probands with Specific Language Impairment Type de document : Texte imprimé et/ou numérique Auteurs : M. L. RICE, Auteur ; S. D. SMITH, Auteur ; J. GAYAN, Auteur Article en page(s) : p.264-82 Langues : Anglais (eng) Mots-clés : Gene associations  Gene linkage  Language impairments  Language, reading, speech phenotypes  Specific language impairment Index. décimale : PER Périodiques Résumé : UNLABELLED: We analyzed genetic linkage and association of measures of language, speech and reading phenotypes to candidate regions in a single set of families ascertained for SLI. Sib-pair and family-based analyses were carried out for candidate gene loci for Reading Disability (RD) on chromosomes 1p36, 3p12-q13, 6p22, and 15q21, and the speech-language candidate region on 7q31 in a sample of 322 participants ascertained for Specific Language Impairment (SLI). Replication or suggestive replication of linkage was obtained in all of these regions, but the evidence suggests that the genetic influences may not be identical for the three domains. In particular, linkage analysis replicated the influence of genes on chromosome 6p for all three domains, but association analysis indicated that only one of the candidate genes for reading disability, KIAA0319, had a strong effect on language phenotypes. The findings are consistent with a multiple gene model of the comorbidity between language impairments and reading disability and have implications for neurocognitive developmental models and maturational processes. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9031-x) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9031-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Convergent genetic linkage and associations to language, speech and reading measures in families of probands with Specific Language Impairment [Texte imprimé et/ou numérique] / M. L. RICE, Auteur ; S. D. SMITH, Auteur ; J. GAYAN, Auteur . - p.264-82. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.264-82 Mots-clés : Gene associations  Gene linkage  Language impairments  Language, reading, speech phenotypes  Specific language impairment Index. décimale : PER Périodiques Résumé : UNLABELLED: We analyzed genetic linkage and association of measures of language, speech and reading phenotypes to candidate regions in a single set of families ascertained for SLI. Sib-pair and family-based analyses were carried out for candidate gene loci for Reading Disability (RD) on chromosomes 1p36, 3p12-q13, 6p22, and 15q21, and the speech-language candidate region on 7q31 in a sample of 322 participants ascertained for Specific Language Impairment (SLI). Replication or suggestive replication of linkage was obtained in all of these regions, but the evidence suggests that the genetic influences may not be identical for the three domains. In particular, linkage analysis replicated the influence of genes on chromosome 6p for all three domains, but association analysis indicated that only one of the candidate genes for reading disability, KIAA0319, had a strong effect on language phenotypes. The findings are consistent with a multiple gene model of the comorbidity between language impairments and reading disability and have implications for neurocognitive developmental models and maturational processes. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9031-x) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9031-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Autistic behavior in boys with fragile X syndrome: social approach and HPA-axis dysfunction / J. E. ROBERTS in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.283-91 Titre : Autistic behavior in boys with fragile X syndrome: social approach and HPA-axis dysfunction Type de document : Texte imprimé et/ou numérique Auteurs : J. E. ROBERTS, Auteur ; M. A. CLARKE, Auteur ; K. ALCORN, Auteur ; J. C. CARTER, Auteur ; A. C. LONG, Auteur ; W. E. KAUFMANN, Auteur Article en page(s) : p.283-91 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The primary goal of this study was to examine environmental and neuroendocrine factors that convey increased risk for elevated autistic behavior in boys with Fragile X syndrome (FXS). This study involves three related analyses: (1) examination of multiple dimensions of social approach behaviors and how they vary over time, (2) investigation of mean levels and modulation of salivary cortisol levels in response to social interaction, and (3) examination of the relationship of social approach and autistic behaviors to salivary cortisol. Poor social approach and elevated baseline and regulation cortisol are discernible traits that distinguish boys with FXS and ASD from boys with FXS only and from typically developing boys. In addition, blunted cortisol change is associated with increased severity of autistic behaviors only within the FXS and ASD group. Boys with FXS and ASD have distinct behavioral and neuroendocrine profiles that differentiate them from those with FXS alone and typically developing boys. En ligne : http://dx.doi.org/10.1007/s11689-009-9028-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Autistic behavior in boys with fragile X syndrome: social approach and HPA-axis dysfunction [Texte imprimé et/ou numérique] / J. E. ROBERTS, Auteur ; M. A. CLARKE, Auteur ; K. ALCORN, Auteur ; J. C. CARTER, Auteur ; A. C. LONG, Auteur ; W. E. KAUFMANN, Auteur . - p.283-91. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.283-91 Index. décimale : PER Périodiques Résumé : The primary goal of this study was to examine environmental and neuroendocrine factors that convey increased risk for elevated autistic behavior in boys with Fragile X syndrome (FXS). This study involves three related analyses: (1) examination of multiple dimensions of social approach behaviors and how they vary over time, (2) investigation of mean levels and modulation of salivary cortisol levels in response to social interaction, and (3) examination of the relationship of social approach and autistic behaviors to salivary cortisol. Poor social approach and elevated baseline and regulation cortisol are discernible traits that distinguish boys with FXS and ASD from boys with FXS only and from typically developing boys. In addition, blunted cortisol change is associated with increased severity of autistic behaviors only within the FXS and ASD group. Boys with FXS and ASD have distinct behavioral and neuroendocrine profiles that differentiate them from those with FXS alone and typically developing boys. En ligne : http://dx.doi.org/10.1007/s11689-009-9028-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

Novel copy number variants in children with autism and additional developmental anomalies / L. K. DAVIS in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.292-301 Titre : Novel copy number variants in children with autism and additional developmental anomalies Type de document : Texte imprimé et/ou numérique Auteurs : L. K. DAVIS, Auteur ; K. J. MEYER, Auteur ; D. S. RUDD, Auteur ; A. L. LIBRANT, Auteur ; E. A. EPPING, Auteur ; V. C. SHEFFIELD, Auteur ; T. H. WASSINK, Auteur Article en page(s) : p.292-301 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism is a neurodevelopmental disorder characterized by three core symptom domains: ritualistic-repetitive behaviors, impaired social interaction, and impaired communication and language development. Recent studies have highlighted etiologically relevant recurrent copy number changes in autism, such as 16p11.2 deletions and duplications, as well as a significant role for unique, novel variants. We used Affymetrix 250K GeneChip Microarray technology (either NspI or StyI) to detect microdeletions and duplications in a subset of children from the Autism Genetic Resource Exchange (AGRE). In order to enrich our sample for potentially pathogenic CNVs we selected children with autism who had additional features suggestive of chromosomal loss associated with developmental disturbance (positive criteria filter) but who had normal cytogenetic testing (negative criteria filter). We identified families with the following features: at least one child with autism who also had facial dysmorphology, limb or digit abnormalities, or ocular abnormalities. To detect changes in copy number we used a publicly available program, Copy Number Analyser for GeneChip(R) (CNAG) Ver. 2.0. We identified novel deletions and duplications on chromosomes 1q24.2, 3p26.2, 4q34.2, and 6q24.3. Several of these deletions and duplications include new and interesting candidate genes for autism such as syntaxin binding protein 5 (STXBP5 also known as tomosyn) and leucine rich repeat neuronal 1 (LRRN1 also known as NLRR1). Lastly, our data suggest that rare and potentially pathogenic microdeletions and duplications may have a substantially higher prevalence in children with autism and additional developmental anomalies than in children with autism alone. En ligne : http://dx.doi.org/10.1007/s11689-009-9013-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Novel copy number variants in children with autism and additional developmental anomalies [Texte imprimé et/ou numérique] / L. K. DAVIS, Auteur ; K. J. MEYER, Auteur ; D. S. RUDD, Auteur ; A. L. LIBRANT, Auteur ; E. A. EPPING, Auteur ; V. C. SHEFFIELD, Auteur ; T. H. WASSINK, Auteur . - p.292-301. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.292-301 Index. décimale : PER Périodiques Résumé : Autism is a neurodevelopmental disorder characterized by three core symptom domains: ritualistic-repetitive behaviors, impaired social interaction, and impaired communication and language development. Recent studies have highlighted etiologically relevant recurrent copy number changes in autism, such as 16p11.2 deletions and duplications, as well as a significant role for unique, novel variants. We used Affymetrix 250K GeneChip Microarray technology (either NspI or StyI) to detect microdeletions and duplications in a subset of children from the Autism Genetic Resource Exchange (AGRE). In order to enrich our sample for potentially pathogenic CNVs we selected children with autism who had additional features suggestive of chromosomal loss associated with developmental disturbance (positive criteria filter) but who had normal cytogenetic testing (negative criteria filter). We identified families with the following features: at least one child with autism who also had facial dysmorphology, limb or digit abnormalities, or ocular abnormalities. To detect changes in copy number we used a publicly available program, Copy Number Analyser for GeneChip(R) (CNAG) Ver. 2.0. We identified novel deletions and duplications on chromosomes 1q24.2, 3p26.2, 4q34.2, and 6q24.3. Several of these deletions and duplications include new and interesting candidate genes for autism such as syntaxin binding protein 5 (STXBP5 also known as tomosyn) and leucine rich repeat neuronal 1 (LRRN1 also known as NLRR1). Lastly, our data suggest that rare and potentially pathogenic microdeletions and duplications may have a substantially higher prevalence in children with autism and additional developmental anomalies than in children with autism alone. En ligne : http://dx.doi.org/10.1007/s11689-009-9013-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia / S. S. MOY in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.302-12 Titre : Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia Type de document : Texte imprimé et/ou numérique Auteurs : S. S. MOY, Auteur ; H. T. GHASHGHAEI, Auteur ; R. J. NONNEMAN, Auteur ; J. M. WEIMER, Auteur ; Y. YOKOTA, Auteur ; D. LEE, Auteur ; C. LAI, Auteur ; D. W. THREADGILL, Auteur ; E. S. ANTON, Auteur Article en page(s) : p.302-12 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Growth factor Neuregulin 1 (NRG1) plays an essential role in development and organization of the cerebral cortex. NRG1 and its receptors, ERBB3 and ERBB4, have been implicated in genetic susceptibility for schizophrenia. Disease symptoms include asociality and altered social interaction. To investigate the role of NRG1-ERBB signaling in social behavior, mice heterozygous for an Nrg1 null allele (Nrg1+/-), and mice with conditional ablation of Erbb3 or Erbb4 in the central nervous system, were evaluated for sociability and social novelty preference in a three-chambered choice task. Results showed that deficiencies in NRG1 or ERBB3 significantly enhanced sociability. All of the mutant groups demonstrated a lack of social novelty preference, in contrast to their respective wild-type controls. Effects of NRG1, ERBB3, or ERBB4 deficiency on social behavior could not be attributed to general changes in anxiety-like behavior, activity, or loss of olfactory ability. Nrg1+/- pups did not exhibit changes in isolation-induced ultrasonic vocalizations, a measure of emotional reactivity. Overall, these findings provide evidence that social behavior is mediated by NRG1-ERBB signaling. En ligne : http://dx.doi.org/10.1007/s11689-009-9017-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia [Texte imprimé et/ou numérique] / S. S. MOY, Auteur ; H. T. GHASHGHAEI, Auteur ; R. J. NONNEMAN, Auteur ; J. M. WEIMER, Auteur ; Y. YOKOTA, Auteur ; D. LEE, Auteur ; C. LAI, Auteur ; D. W. THREADGILL, Auteur ; E. S. ANTON, Auteur . - p.302-12. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.302-12 Index. décimale : PER Périodiques Résumé : Growth factor Neuregulin 1 (NRG1) plays an essential role in development and organization of the cerebral cortex. NRG1 and its receptors, ERBB3 and ERBB4, have been implicated in genetic susceptibility for schizophrenia. Disease symptoms include asociality and altered social interaction. To investigate the role of NRG1-ERBB signaling in social behavior, mice heterozygous for an Nrg1 null allele (Nrg1+/-), and mice with conditional ablation of Erbb3 or Erbb4 in the central nervous system, were evaluated for sociability and social novelty preference in a three-chambered choice task. Results showed that deficiencies in NRG1 or ERBB3 significantly enhanced sociability. All of the mutant groups demonstrated a lack of social novelty preference, in contrast to their respective wild-type controls. Effects of NRG1, ERBB3, or ERBB4 deficiency on social behavior could not be attributed to general changes in anxiety-like behavior, activity, or loss of olfactory ability. Nrg1+/- pups did not exhibit changes in isolation-induced ultrasonic vocalizations, a measure of emotional reactivity. Overall, these findings provide evidence that social behavior is mediated by NRG1-ERBB signaling. En ligne : http://dx.doi.org/10.1007/s11689-009-9017-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

Variable phenotypic expression of a MECP2 mutation in a family / K. AUGENSTEIN in Journal of Neurodevelopmental Disorders, 1-4 (December 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.313 Titre : Variable phenotypic expression of a MECP2 mutation in a family Type de document : Texte imprimé et/ou numérique Auteurs : K. AUGENSTEIN, Auteur ; J. B. LANE, Auteur ; A. HORTON, Auteur ; C. SCHANEN, Auteur ; A. K. PERCY, Auteur Article en page(s) : p.313 Langues : Anglais (eng) Mots-clés : Dystonia  Mecp2  Male  Mutation  Phenotype-genotype  Rett syndrome  X chromosome inactivation Index. décimale : PER Périodiques Résumé : We report a three generation family in which five members, three females and two males, demonstrate a 44 bp deletion (1164-1207del44) in the MECP2 gene associated with Rett syndrome, leading to a truncation of the C-terminus of the protein. Two of the three females and both males do not meet RTT criteria whereas the youngest female has classic RTT. Both males demonstrated a clear pattern of progressive involvement including dystonia. The transmitting females do not demonstrate features of RTT as a result of unbalanced X chromosome inactivation (XCI) and were only identified as carriers following the evaluation of the affected males and the girl with classic RTT. As such, accurate assessment of the precise frequency of MECP2 mutations in carrier females with mild cognitive impairment or borderline cognitive function will be under-represented unless an affected offspring is recognized. Strategies for accurate diagnosis in such instances should be considered carefully. En ligne : http://dx.doi.org/10.1007/s11689-009-9034-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Variable phenotypic expression of a MECP2 mutation in a family [Texte imprimé et/ou numérique] / K. AUGENSTEIN, Auteur ; J. B. LANE, Auteur ; A. HORTON, Auteur ; C. SCHANEN, Auteur ; A. K. PERCY, Auteur . - p.313. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-4 (December 2009) . - p.313 Mots-clés : Dystonia  Mecp2  Male  Mutation  Phenotype-genotype  Rett syndrome  X chromosome inactivation Index. décimale : PER Périodiques Résumé : We report a three generation family in which five members, three females and two males, demonstrate a 44 bp deletion (1164-1207del44) in the MECP2 gene associated with Rett syndrome, leading to a truncation of the C-terminus of the protein. Two of the three females and both males do not meet RTT criteria whereas the youngest female has classic RTT. Both males demonstrated a clear pattern of progressive involvement including dystonia. The transmitting females do not demonstrate features of RTT as a result of unbalanced X chromosome inactivation (XCI) and were only identified as carriers following the evaluation of the affected males and the girl with classic RTT. As such, accurate assessment of the precise frequency of MECP2 mutations in carrier females with mild cognitive impairment or borderline cognitive function will be under-represented unless an affected offspring is recognized. Strategies for accurate diagnosis in such instances should be considered carefully. En ligne : http://dx.doi.org/10.1007/s11689-009-9034-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342