Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets / Merel C. POSTEMA in Journal of Child Psychology and Psychiatry, 62-10 (October 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1202-1219 Titre : Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets Type de document : Texte imprimé et/ou numérique Auteurs : Merel C. POSTEMA, Auteur ; Martine HOOGMAN, Auteur ; Sara AMBROSINO, Auteur ; Philip ASHERSON, Auteur ; Tobias BANASCHEWSKI, Auteur ; Cibele E. BANDEIRA, Auteur ; Alexandr BARANOV, Auteur ; Claiton H.D. BAU, Auteur ; Sarah BAUMEISTER, Auteur ; Ramona BAUR-STREUBEL, Auteur ; Mark A. BELLGROVE, Auteur ; Joseph BIEDERMAN, Auteur ; Janita B. BRALTEN, Auteur ; Daniel BRANDEIS, Auteur ; Silvia BREM, Auteur ; Jan K. BUITELAAR, Auteur ; Geraldo F. BUSATTO, Auteur ; Francisco Xavier CASTELLANOS, Auteur ; Mara CERCIGNANI, Auteur ; Tiffany M. CHAIM-AVANCINI, Auteur ; Kaylita C. CHANTILUKE, Auteur ; Anastasia CHRISTAKOU, Auteur ; David COGHILL, Auteur ; Annette CONZELMANN, Auteur ; Ana I. CUBILLO, Auteur ; Renata B. CUPERTINO, Auteur ; Patrick DE ZEEUW, Auteur ; Alysa E. DOYLE, Auteur ; Sarah DURSTON, Auteur ; Eric A. EARL, Auteur ; Jeffery N. EPSTEIN, Auteur ; Thomas ETHOFER, Auteur ; Damien A. FAIR, Auteur ; Andreas J. FALLGATTER, Auteur ; Stephen V. FARAONE, Auteur ; Thomas FRODL, Auteur ; Matt C. GABEL, Auteur ; Tinatin GOGBERASHVILI, Auteur ; Eugenio H. GREVET, Auteur ; Jan HAAVIK, Auteur ; Neil A. HARRISON, Auteur ; Catharina A. HARTMAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Sarah HOHMANN, Auteur ; Marie F. HØVIK, Auteur ; Terry L. JERNIGAN, Auteur ; Bernd KARDATZKI, Auteur ; Georgii KARKASHADZE, Auteur ; Clare KELLY, Auteur ; Gregor KOHLS, Auteur ; Kerstin KONRAD, Auteur ; Jonna KUNTSI, Auteur ; Luisa LÁZARO, Auteur ; Sara LERA-MIGUEL, Auteur ; Klaus-Peter LESCH, Auteur ; Mario R. LOUZA, Auteur ; Astri J. LUNDERVOLD, Auteur ; Charles B MALPAS, Auteur ; Paulo MATTOS, Auteur ; Hazel MCCARTHY, Auteur ; Leyla NAMAZOVA-BARANOVA, Auteur ; Rosa NICOLAU, Auteur ; Joel T. NIGG, Auteur ; Stephanie E. NOVOTNY, Auteur ; Eileen OBERWELLAND WEISS, Auteur ; Ruth L. O'GORMAN TUURA, Auteur ; Jaap OOSTERLAAN, Auteur ; Bob ORANJE, Auteur ; Yannis PALOYELIS, Auteur ; Paul PAULI, Auteur ; Felipe A. PICON, Auteur ; Kerstin J. PLESSEN, Auteur ; J. Antoni RAMOS-QUIROGA, Auteur ; Andreas REIF, Auteur ; Liesbeth RENEMAN, Auteur ; Pedro G.P. ROSA, Auteur ; Katya RUBIA, Auteur ; Anouk SCHRANTEE, Auteur ; Lizanne SCHWEREN, Auteur ; Jochen SEITZ, Auteur ; Philip SHAW, Auteur ; Tim J. SILK, Auteur ; Norbert SKOKAUSKAS, Auteur ; Juan C. SOLIVA VILA, Auteur ; Michael C. STEVENS, Auteur ; Gustavo SUDRE, Auteur ; Leanne TAMM, Auteur ; Fernanda TOVAR-MOLL, Auteur ; Theo G.M. VAN ERP, Auteur ; Alasdair VANCE, Auteur ; Oscar VILARROYA, Auteur ; Yolanda VIVES-GILABERT, Auteur ; Georg G. VON POLIER, Auteur ; Susanne WALITZA, Auteur ; Yuliya N. YONCHEVA, Auteur ; Marcus V. ZANETTI, Auteur ; Georg C. ZIEGLER, Auteur ; David C. GLAHN, Auteur ; Neda JAHANSHAD, Auteur Année de publication : 2021 Article en page(s) : p.1202-1219 Langues : Anglais (eng) Mots-clés : Attention-deficit  brain asymmetry  brain laterality  hyperactivity disorder  large-scale data  structural MRI Index. décimale : PER Périodiques Résumé : Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from ?0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait. En ligne : https://doi.org/10.1111/jcpp.13396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=462 [article] Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets [Texte imprimé et/ou numérique] / Merel C. POSTEMA, Auteur ; Martine HOOGMAN, Auteur ; Sara AMBROSINO, Auteur ; Philip ASHERSON, Auteur ; Tobias BANASCHEWSKI, Auteur ; Cibele E. BANDEIRA, Auteur ; Alexandr BARANOV, Auteur ; Claiton H.D. BAU, Auteur ; Sarah BAUMEISTER, Auteur ; Ramona BAUR-STREUBEL, Auteur ; Mark A. BELLGROVE, Auteur ; Joseph BIEDERMAN, Auteur ; Janita B. BRALTEN, Auteur ; Daniel BRANDEIS, Auteur ; Silvia BREM, Auteur ; Jan K. BUITELAAR, Auteur ; Geraldo F. BUSATTO, Auteur ; Francisco Xavier CASTELLANOS, Auteur ; Mara CERCIGNANI, Auteur ; Tiffany M. CHAIM-AVANCINI, Auteur ; Kaylita C. CHANTILUKE, Auteur ; Anastasia CHRISTAKOU, Auteur ; David COGHILL, Auteur ; Annette CONZELMANN, Auteur ; Ana I. CUBILLO, Auteur ; Renata B. CUPERTINO, Auteur ; Patrick DE ZEEUW, Auteur ; Alysa E. DOYLE, Auteur ; Sarah DURSTON, Auteur ; Eric A. EARL, Auteur ; Jeffery N. EPSTEIN, Auteur ; Thomas ETHOFER, Auteur ; Damien A. FAIR, Auteur ; Andreas J. FALLGATTER, Auteur ; Stephen V. FARAONE, Auteur ; Thomas FRODL, Auteur ; Matt C. GABEL, Auteur ; Tinatin GOGBERASHVILI, Auteur ; Eugenio H. GREVET, Auteur ; Jan HAAVIK, Auteur ; Neil A. HARRISON, Auteur ; Catharina A. HARTMAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Sarah HOHMANN, Auteur ; Marie F. HØVIK, Auteur ; Terry L. JERNIGAN, Auteur ; Bernd KARDATZKI, Auteur ; Georgii KARKASHADZE, Auteur ; Clare KELLY, Auteur ; Gregor KOHLS, Auteur ; Kerstin KONRAD, Auteur ; Jonna KUNTSI, Auteur ; Luisa LÁZARO, Auteur ; Sara LERA-MIGUEL, Auteur ; Klaus-Peter LESCH, Auteur ; Mario R. LOUZA, Auteur ; Astri J. LUNDERVOLD, Auteur ; Charles B MALPAS, Auteur ; Paulo MATTOS, Auteur ; Hazel MCCARTHY, Auteur ; Leyla NAMAZOVA-BARANOVA, Auteur ; Rosa NICOLAU, Auteur ; Joel T. NIGG, Auteur ; Stephanie E. NOVOTNY, Auteur ; Eileen OBERWELLAND WEISS, Auteur ; Ruth L. O'GORMAN TUURA, Auteur ; Jaap OOSTERLAAN, Auteur ; Bob ORANJE, Auteur ; Yannis PALOYELIS, Auteur ; Paul PAULI, Auteur ; Felipe A. PICON, Auteur ; Kerstin J. PLESSEN, Auteur ; J. Antoni RAMOS-QUIROGA, Auteur ; Andreas REIF, Auteur ; Liesbeth RENEMAN, Auteur ; Pedro G.P. ROSA, Auteur ; Katya RUBIA, Auteur ; Anouk SCHRANTEE, Auteur ; Lizanne SCHWEREN, Auteur ; Jochen SEITZ, Auteur ; Philip SHAW, Auteur ; Tim J. SILK, Auteur ; Norbert SKOKAUSKAS, Auteur ; Juan C. SOLIVA VILA, Auteur ; Michael C. STEVENS, Auteur ; Gustavo SUDRE, Auteur ; Leanne TAMM, Auteur ; Fernanda TOVAR-MOLL, Auteur ; Theo G.M. VAN ERP, Auteur ; Alasdair VANCE, Auteur ; Oscar VILARROYA, Auteur ; Yolanda VIVES-GILABERT, Auteur ; Georg G. VON POLIER, Auteur ; Susanne WALITZA, Auteur ; Yuliya N. YONCHEVA, Auteur ; Marcus V. ZANETTI, Auteur ; Georg C. ZIEGLER, Auteur ; David C. GLAHN, Auteur ; Neda JAHANSHAD, Auteur . - 2021 . - p.1202-1219. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1202-1219 Mots-clés : Attention-deficit  brain asymmetry  brain laterality  hyperactivity disorder  large-scale data  structural MRI Index. décimale : PER Périodiques Résumé : Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from ?0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait. En ligne : https://doi.org/10.1111/jcpp.13396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=462

Association of a functional variant of the nitric oxide synthase 1 gene with personality, anxiety, and depressiveness / Triin KURRIKOFF in Development and Psychopathology, 24-4 (November 2012)  

Public ISBD [article]  inDevelopment and Psychopathology > 24-4 (November 2012) . - p.1225-1235 Titre : Association of a functional variant of the nitric oxide synthase 1 gene with personality, anxiety, and depressiveness Type de document : Texte imprimé et/ou numérique Auteurs : Triin KURRIKOFF, Auteur ; Klaus-Peter LESCH, Auteur ; Evelyn KIIVE, Auteur ; Kenn KONSTABEL, Auteur ; Sabine HERTERICH, Auteur ; Toomas VEIDEBAUM, Auteur ; Andreas REIF, Auteur ; Jaanus HARRO, Auteur Année de publication : 2012 Article en page(s) : p.1225-1235 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : A functional promoter polymorphism of the nitric oxide synthase 1 gene first exon 1f variable number tandem repeat (NOS1 ex1f-VNTR) is associated with impulsivity and related psychopathology. Facets of impulsivity are strongly associated with personality traits; maladaptive impulsivity with neuroticism; and adaptive impulsivity with extraversion. Both high neuroticism and low extraversion predict anxiety and depressive symptoms. The aim of the present study was to evaluate the effect of the NOS1 ex1f-VNTR genotype and possible interaction with environmental factors on personality, anxiety, and depressiveness in a population-representative sample. Short allele carriers had higher neuroticism and anxiety than individuals with the long/long (l/l) genotype. Male short/short homozygotes also had higher extraversion. In the face of environmental adversity, females with a short allele had higher scores of neuroticism, anxiety, and depressiveness compared to the l/l genotype. Males were more sensitive to environmental conditions when they had the l/l genotype and low extraversion. In conclusion, the NOS1 ex1f-VNTR influences personality and emotional regulation dependent on gender and environment. Together with previous findings on the effect of the NOS1 genotype on impulse control, these data suggest that NOS1 should be considered another plasticity gene, because its variants are associated with different coping strategies. En ligne : http://dx.doi.org/10.1017/S0954579412000661 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=182 [article] Association of a functional variant of the nitric oxide synthase 1 gene with personality, anxiety, and depressiveness [Texte imprimé et/ou numérique] / Triin KURRIKOFF, Auteur ; Klaus-Peter LESCH, Auteur ; Evelyn KIIVE, Auteur ; Kenn KONSTABEL, Auteur ; Sabine HERTERICH, Auteur ; Toomas VEIDEBAUM, Auteur ; Andreas REIF, Auteur ; Jaanus HARRO, Auteur . - 2012 . - p.1225-1235. Langues : Anglais (eng) in Development and Psychopathology > 24-4 (November 2012) . - p.1225-1235 Index. décimale : PER Périodiques Résumé : A functional promoter polymorphism of the nitric oxide synthase 1 gene first exon 1f variable number tandem repeat (NOS1 ex1f-VNTR) is associated with impulsivity and related psychopathology. Facets of impulsivity are strongly associated with personality traits; maladaptive impulsivity with neuroticism; and adaptive impulsivity with extraversion. Both high neuroticism and low extraversion predict anxiety and depressive symptoms. The aim of the present study was to evaluate the effect of the NOS1 ex1f-VNTR genotype and possible interaction with environmental factors on personality, anxiety, and depressiveness in a population-representative sample. Short allele carriers had higher neuroticism and anxiety than individuals with the long/long (l/l) genotype. Male short/short homozygotes also had higher extraversion. In the face of environmental adversity, females with a short allele had higher scores of neuroticism, anxiety, and depressiveness compared to the l/l genotype. Males were more sensitive to environmental conditions when they had the l/l genotype and low extraversion. In conclusion, the NOS1 ex1f-VNTR influences personality and emotional regulation dependent on gender and environment. Together with previous findings on the effect of the NOS1 genotype on impulse control, these data suggest that NOS1 should be considered another plasticity gene, because its variants are associated with different coping strategies. En ligne : http://dx.doi.org/10.1017/S0954579412000661 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=182

SLC2A3 single-nucleotide polymorphism and duplication influence cognitive processing and population-specific risk for attention-deficit/hyperactivity disorder / Sören MERKER in Journal of Child Psychology and Psychiatry, 58-7 (July 2017)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 58-7 (July 2017) . - p.798-809 Titre : SLC2A3 single-nucleotide polymorphism and duplication influence cognitive processing and population-specific risk for attention-deficit/hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : Sören MERKER, Auteur ; Andreas REIF, Auteur ; Georg C. ZIEGLER, Auteur ; Heike WEBER, Auteur ; Ute MAYER, Auteur ; Ann-Christine EHLIS, Auteur ; Annette CONZELMANN, Auteur ; Stefan JOHANSSON, Auteur ; Clemens MÜLLER-REIBLE, Auteur ; Indrajit NANDA, Auteur ; Thomas HAAF, Auteur ; Reinhard ULLMANN, Auteur ; Marcel ROMANOS, Auteur ; Andreas J. FALLGATTER, Auteur ; Paul PAULI, Auteur ; Tatyana STREKALOVA, Auteur ; Charline JANSCH, Auteur ; Alejandro ARIAS-VASQUEZ, Auteur ; Jan HAAVIK, Auteur ; Marta RIBASES, Auteur ; Josep Antoni RAMOS-QUIROGA, Auteur ; Jan K. BUITELAAR, Auteur ; Barbara FRANKE, Auteur ; Klaus-Peter LESCH, Auteur Article en page(s) : p.798-809 Langues : Anglais (eng) Mots-clés : Attention-deficit/hyperactivity disorder  glucose transporter  SLC2A3  single-nucleotide polymorphisms  duplication  copy number variants  energy homeostasis  frontostriatal network Index. décimale : PER Périodiques Résumé : Background Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder with profound cognitive, behavioral, and psychosocial impairments with persistence across the life cycle. Our initial genome-wide screening approach for copy number variants (CNVs) in ADHD implicated a duplication of SLC2A3, encoding glucose transporter-3 (GLUT3). GLUT3 plays a critical role in cerebral glucose metabolism, providing energy for the activity of neurons, which, in turn, moderates the excitatory–inhibitory balance impacting both brain development and activity-dependent neural plasticity. We therefore aimed to provide additional genetic and functional evidence for GLUT3 dysfunction in ADHD. Methods Case–control association analyses of SLC2A3 single-nucleotide polymorphisms (SNPs) and CNVs were conducted in several European cohorts of patients with childhood and adult ADHD (SNP, n = 1,886 vs. 1,988; CNV, n = 1,692 vs. 1,721). These studies were complemented by SLC2A3 expression analyses in peripheral cells, functional EEG recordings during neurocognitive tasks, and ratings of food energy content. Results Meta-analysis of all cohorts detected an association of SNP rs12842 with ADHD. While CNV analysis detected a population-specific enrichment of SLC2A3 duplications only in German ADHD patients, the CNV + rs12842 haplotype influenced ADHD risk in both the German and Spanish cohorts. Duplication carriers displayed elevated SLC2A3 mRNA expression in peripheral blood cells and altered event-related potentials reflecting deficits in working memory and cognitive response control, both endophenotypic traits of ADHD, and an underestimation of energy units of high-caloric food. Conclusions Taken together, our results indicate that both common and rare SLC2A3 variation impacting regulation of neuronal glucose utilization and energy homeostasis may result in neurocognitive deficits known to contribute to ADHD risk. En ligne : http://dx.doi.org/10.1111/jcpp.12702 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=316 [article] SLC2A3 single-nucleotide polymorphism and duplication influence cognitive processing and population-specific risk for attention-deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / Sören MERKER, Auteur ; Andreas REIF, Auteur ; Georg C. ZIEGLER, Auteur ; Heike WEBER, Auteur ; Ute MAYER, Auteur ; Ann-Christine EHLIS, Auteur ; Annette CONZELMANN, Auteur ; Stefan JOHANSSON, Auteur ; Clemens MÜLLER-REIBLE, Auteur ; Indrajit NANDA, Auteur ; Thomas HAAF, Auteur ; Reinhard ULLMANN, Auteur ; Marcel ROMANOS, Auteur ; Andreas J. FALLGATTER, Auteur ; Paul PAULI, Auteur ; Tatyana STREKALOVA, Auteur ; Charline JANSCH, Auteur ; Alejandro ARIAS-VASQUEZ, Auteur ; Jan HAAVIK, Auteur ; Marta RIBASES, Auteur ; Josep Antoni RAMOS-QUIROGA, Auteur ; Jan K. BUITELAAR, Auteur ; Barbara FRANKE, Auteur ; Klaus-Peter LESCH, Auteur . - p.798-809. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 58-7 (July 2017) . - p.798-809 Mots-clés : Attention-deficit/hyperactivity disorder  glucose transporter  SLC2A3  single-nucleotide polymorphisms  duplication  copy number variants  energy homeostasis  frontostriatal network Index. décimale : PER Périodiques Résumé : Background Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder with profound cognitive, behavioral, and psychosocial impairments with persistence across the life cycle. Our initial genome-wide screening approach for copy number variants (CNVs) in ADHD implicated a duplication of SLC2A3, encoding glucose transporter-3 (GLUT3). GLUT3 plays a critical role in cerebral glucose metabolism, providing energy for the activity of neurons, which, in turn, moderates the excitatory–inhibitory balance impacting both brain development and activity-dependent neural plasticity. We therefore aimed to provide additional genetic and functional evidence for GLUT3 dysfunction in ADHD. Methods Case–control association analyses of SLC2A3 single-nucleotide polymorphisms (SNPs) and CNVs were conducted in several European cohorts of patients with childhood and adult ADHD (SNP, n = 1,886 vs. 1,988; CNV, n = 1,692 vs. 1,721). These studies were complemented by SLC2A3 expression analyses in peripheral cells, functional EEG recordings during neurocognitive tasks, and ratings of food energy content. Results Meta-analysis of all cohorts detected an association of SNP rs12842 with ADHD. While CNV analysis detected a population-specific enrichment of SLC2A3 duplications only in German ADHD patients, the CNV + rs12842 haplotype influenced ADHD risk in both the German and Spanish cohorts. Duplication carriers displayed elevated SLC2A3 mRNA expression in peripheral blood cells and altered event-related potentials reflecting deficits in working memory and cognitive response control, both endophenotypic traits of ADHD, and an underestimation of energy units of high-caloric food. Conclusions Taken together, our results indicate that both common and rare SLC2A3 variation impacting regulation of neuronal glucose utilization and energy homeostasis may result in neurocognitive deficits known to contribute to ADHD risk. En ligne : http://dx.doi.org/10.1111/jcpp.12702 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=316

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