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A great number of studies have demonstrated functional abnormalities in children with attention-deficit/hyperactivity disorder (ADHD), although conflicting results have also been reported. And few studies analyzed homotopic functional connectivity between hemispheres. In this study, resting-state functional magnetic resonance imaging (MRI) data were recorded from 45 medication-naïve ADHD children and 26 healthy controls. The regional homogeneity (ReHo), degree centrality (DC) and voxel-mirrored homotopic connectivity (VMHC) values were compared between the two groups to depict the intrinsic brain activities. We found that ADHD children exhibited significantly lower ReHo and DC values in the right middle frontal gyrus and the two values correlated with each other; moreover, lower VMHC values were found in the bilateral occipital lobes of ADHD children, which was negatively related with anxiety scores of Conners' Parent Rating Scale (CPRS-R) and positively related with completed categories of Wisconsin Card Sorting Test (WCST). Our results might suggest that less spontaneous neuronal activities of the right middle frontal gyrus and the bilateral occipital lobes in ADHD children.

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The examination of copy number variation (CNV) is critical to understand the etiology of the CNV-related autism spectrum disorders (ASD). DNA samples were obtained from 64 ASD probands, which were genotyped on an Affymetrix CytoScan HD platform. qPCR or FISH were used as a validation for some novel recurrent CNVs. We further compared the clinical phenotypes of the genes in the Database of Chromosomal Imbalance and Phenotype in Humans Using Ensembl Resources (DECIPHER) database with these overlapping genes. Using vast, readily available databases with previously reported clinically relevant CNVs from human populations, the genes were evaluated using Enrichment Analysis and GO Slim Classification. By using the Ploysearch2 software, we identified the interaction relationship between significant genes and known ASD genes. A total of 29 CNVs, overlapping with 520 genes, including 315 OMIM genes, were identified. Additionally, myocyte enhancer factor 2 family (MEF2C) with two cases of CNV overlapping were also identified. Enrichment analysis showed that the 520 genes are most likely to be related to membrane components with protein-binding functions involved in metabolic processes. In the interaction network of those genes, the known ASD genes are mostly at the core position and the significant genes found in our samples are closely related to the known ASD genes. CNVs should be an independent factor to induce autism. With the strategy of our study, we could find the ASDs candidate genes by CNV data and review certain pathogenesis of this disorder. Those CNVs were associated with ASD and they may contribute to ASD by affecting the ASD-related genes.

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Objective The aim of present study was to detect methylation rate of CpG unit of brain derived neurotrophic factor (BDNF) promoter and to study the epigenetic mechanism of autism spectrum disorders (ASD).Methods Total of 12 ASD patients and 12 healthy controls were recruited.The methylation rate of CpG unit in BDNF promoter Ⅰ and Ⅳ were detected using Sequenom MassArray method.The methylation model,correlationship,evolutionary relationship of CpG units in BDNF promoter Ⅰ and Ⅳ were detected and compared between ASD patients and healthy controls.Results The methylation rate was identified in 17 and 8 CpG units in BDNF promoter][and BDNF promoter Ⅳ.A close correlation distance was detected in BDNF promoter Ⅰ CpG units 4,7,10,35,and BDNF promoter Ⅳ CpG units 11.12,14.BDNF promoter][CpG units 4,7,10,35,and BDNF promoter Ⅳ CpG units 11.12,14 could be clustered.ASD patients had a significant lower methylation rate in BDNF promoter Ⅰ CpG unit 5.6 and Ⅳ CpG units 3 and 15 compare with healthy controls (P＜0.05).Conclusions The DNA methylation rate in BDNF pronoter Ⅰ CpG unit 5.6 and Ⅳ CpG units 3 and 15 may be used as potential biomarkers of ASD.

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BACKGROUND: Methamphetamine (MA) has neurotoxic effects to central nervous system. However, as the 5-hydroxytryplamine reuptake enhancer, it is uncertain that if there are protective effects of tianeptine to the damages of 5-hydroxytryp-taminergic neurons caused by MA.OBJECTIVE: To investigate the neurotoxicity of MA and the neuroprotective effects of tianeptine as well as the acting mechanism.DESIGN: Randomized case control study based on animals.SETTING: Animal research room and pathology research room of a university.MATERIALS: The experiment was completed in the Experimental Animal Centre of Sichuan University and Molecular Pathology Laboratory of West China Hospital during June to August 2003. Totally 25 male Wistar rats were injected MA through abdominal cavity to build model. Methamphetamine was provided by National Institute for the Control of Pharmaceutical and Biological Products(NICPBP) while tianeptine was given by French Servier Company (Batch No. OE3086). The TUNEL testing kit was purchased from Boehringer Mannheim Company.INTERVENTIONS: There were one control group and four experimental groups(A, B, C, D). A group was used intraperitoneal injection of MA while B, C, D, groups were administered tianeptine 7 days, 4 days before and the same day of MA administration. Normal saline with same volume was injected into rats of control group. HE stain and silver stain were conducted after experiment to observe the morphologic changes of neurons. And TUNEL method was used to detect apoptotic cells.MAIN OUTCOME MEASURES: The HE stain and silver stain of brain tissue sections and counts of TUNEL positive neurons.RESULTS: MA could damage the axon and dendrite of neurons and the absorbance of silver positive cell was(50.74 ± 1.86) . It could also induce cell apoptosis while the apoptotic cell count every high power field was 29.26 ±4. 14. There were less apoptotic cells in the group with 7 days usage of tianeptine with the cell count of( 18.90 ± 1.60) per high power field.CONCLUSION: MA can cause neurotoxicity by inducing cell apoptosis.And giving tianeptine in advance can protect neurons.

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Objective: A double-blind and double-simulated study was used to evaluate the effects of cognitive functioning in schizophrenics receiving different antipsychotic medications. Method: Forty Patients with schizophrenia were randomly divided into quetiapine group (n=20) and chlorpromazine group (n=20). Neuropsychologiacal tests were done before treatment and in the fourth and sixth week after therapy, which included knowledge, arithmetic, digital sign, digital span, game of puzzle, logical memory visual reproduction,STROOP test, verbal fluency, score and plan time of tower of Hanoi and WCST. Twelve healthy individuals were tested in same time to study the learning effects. Double-blind and a double-simulated means was adopted in this study. Results: Marked improvement was found in patients after quetiapine treatment. While chlorpromazine do not appear to favorably affect on cognitive functioning in schizophrenics. Scores of improvement on some neuropsychological assessment of quetiapine group were higher than that of chlorpromazine group, especially in attention and executive function(P

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Objective: To investigate the effect of heroin on executive function in heroin addicts Methods: Executive function of thi rty-six heroin addicts and thirty-six normal controls was assessed with a batter y of neuropsychological evaluation instruments in Chengdu city of China The to ols include of block design test, Stroop test (C, CW), Wisconsin card sorting te st (WCST-M)Results: There were significance difference between the two groups, heroin addicts had lower score of Block design and more time spent, number of errors in Stroop test (C、CW) Further more, the addicts had more total error, perseverative err o rs and lower number of categories in WCST than control group (P