49 research outputs found

    Cognitive assessment using ERP in child and adolescent psychiatry: Difficulties and opportunities

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    Event related potentials (ERPs) represent powerful tools to investigate cognitive functioning in child and adolescent psychiatry. So far, the available body of research has largely focused on advancements in analysis methods, with little attention given to the perspective of assessment. The aim of this brief report is to provide recommendations for cognitive ERPs assessment that can be applied across diagnostic categories in child and adolescent psychiatry research. First, we discuss major issues for ERPs testing using examples from common psychiatric disorders. We conclude by summing up our recommendations for methodological standards and highlighting the potential role of ERPs in the field

    EEG Biomarkers in Children and Adolescents With Feeding and Eating Disorders: Current Evidence and Future Directions

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    Introduction: Electroencephalography (EEG) represents a powerful tool to detect abnormal neural dynamics in child and adolescent psychiatry. Feeding and Eating Disorders (FEDs), such as anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and avoidant restrictive food intake disorder (ARFID) onset in childhood and adolescence. EEG has rarely been used to examine cortical brain activity in children and adolescents with FEDs. This review aims to summarize EEG findings in FEDs amongst children and adolescents, and to highlight areas deserving further research. / Methods: We searched the literature for EEG studies on children and adolescents with FEDs using Google Scholar, PsycINFO, Medline, and PubMed. / Results: Twelve studies were identified, the majority focusing on AN (N = 10). The identified studies suggest reduced action monitoring control (preparatory waves, N200, P300), specific perceptual-cognitive styles to body/face perception (late positive potentials/early posterior negativity), as well as fundamental changes in posterior theta oscillations in AN. Behavioral traits of BN/BED (i.e., loss of control eating, emotional eating), and AN seem to be associated with an increased attentional reactivity (P300) to visual food stimuli. / Conclusion: Electroencephalography research in children and adolescents with FEDs is limited and mostly focused on AN. While EEG abnormalities seem consistent with a reduced top-down control and attentional allocation deficits in AN, altered attention specific to food cues emerges across FEDs. Overcoming conventional EEG analyses, and investigating spatial properties (i.e., electrical neuroimaging), will enhance our understanding of FEDs neurobiology

    Temporal dynamics of cognitive flexibility in adolescents with anorexia nervosa: A high-density EEG study

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    Impairment in cognitive flexibility is a core symptom of anorexia nervosa (AN) and is associated with treatment resistance. Nevertheless, studies on the neural basis of cognitive flexibility in adolescent AN are rare. This study aimed to investigate brain networks underlying cognitive flexibility in adolescents with AN. To address this aim, participants performed a Dimensional Change Card Sorting task during high-density electroencephalography (EEG) recording. Anxiety was measured with the State–Trait Anxiety Inventory. Data were collected on 22 girls with AN and 23 controls. Evoked responses were investigated using global-spatial analysis. Adolescents with AN showed greater overall accuracy, fewer switch trial errors and reduced inverse efficiency switch cost relative to controls, although these effects disappeared after adjusting for trait and state anxiety. EEG results indicated augmented early visual orienting processing (P100) and subsequent impaired attentional mechanisms to task switching (P300b) in subjects with AN. During task switching, diminished activations in subjects with AN were identified in the posterior cingulate, calcarine sulcus and cerebellum, and task repetitions induced diminished activations in a network involving the medial prefrontal cortex, and several posterior regions, compared with controls. No significant associations were found between measures of cognitive flexibility and anxiety in the AN group. Findings of this study suggest atypical neural mechanisms underlying cognitive flexibility in adolescents with AN. More importantly, our findings suggest that different behavioural profiles in AN could relate to differences in anxiety levels. Future research should investigate the efficacy of cognitive training to rebalance brain networks of cognitive flexibility in AN

    Forensic tools for the diagnosis of electrocution death: Case study and literature review

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    Diagnosis of death by electrocution may be difficult when electric marking is not visible or unclear. Accordingly, the body of a man who appeared to have died from accidental electrocution was carefully forensically analysed. Macroscopic and microscopic analysis of the current mark was carried out using a variable-pressure scanning electron microscope equipped with energy dispersive X-ray microanalyser to highlight skin metallisation, indicating the presence of iron and zinc. The histological findings of electrocution myocardial damage were supported by the results of biochemical analysis which demonstrated the creatine kinase-MB and cardiac troponin I elevation. The effects of electric current flow were also highlighted by perforations of endothelial surface of a pulmonary artery using scanning electron microscope, and all the results were analysed by the main tools suggested in the literature

    Silencing of the XAF1 gene by promoter hypermethylation in cancer cells and reactivation to TRAIL-sensitization by IFN-β

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    BACKGROUND: XIAP-associated factor 1 (XAF1) is a putative tumor suppressor that exerts its proapoptotic effects through both caspase-dependent and – independent means. Loss of XAF1 expression through promoter methylation has been implicated in the process of tumorigenesis in a variety of cancers. In this report, we investigated the role of basal xaf1 promoter methylation in xaf1 expression and assessed the responsiveness of cancer cell lines to XAF1 induction by IFN-β. METHODS: We used the conventional bisulfite DNA modification and sequencing method to determine the methylation status in the CpG sites of xaf1 promoter in glioblastoma (SF539, SF295), neuroblastoma (SK-N-AS) and cervical carcinoma (HeLa) cells. We analysed the status and incidence of basal xaf1 promoter methylation in xaf1 expression in non-treated cells as well as under a short or long exposure to IFN-β. Stable XAF1 glioblastoma knock-down cell lines were established to characterize the direct implication of XAF1 in IFN-β-mediated sensitization to TRAIL-induced cell death. RESULTS: We found a strong variability in xaf1 promoter methylation profile and responsiveness to IFN-β across the four cancer cell lines studied. At the basal level, aberrant promoter methylation was linked to xaf1 gene silencing. After a short exposure, the IFN-β-mediated reactivation of xaf1 gene expression was related to the degree of basal promoter methylation. However, in spite of continued promoter hypermethylation, we find that IFN-β induced a transient xaf1 expression, that in turn, was followed by promoter demethylation upon a prolonged exposure. Importantly, we demonstrated for the first time that IFN-β-mediated reactivation of endogenous XAF1 plays a critical role in TRAIL-induced cell death since XAF1 knock-down cell lines completely lost their IFN-β-mediated TRAIL sensitivity. CONCLUSION: Together, these results suggest that promoter demethylation is not the sole factor determining xaf1 gene induction under IFN-β treatment. Furthermore, our study provides evidence that XAF1 is a crucial interferon-stimulated gene (ISG) mediator of IFN-induced sensitization to TRAIL in cancer

    Coevolution between a Family of Parasite Virulence Effectors and a Class of LINE-1 Retrotransposons

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    Parasites are able to evolve rapidly and overcome host defense mechanisms, but the molecular basis of this adaptation is poorly understood. Powdery mildew fungi (Erysiphales, Ascomycota) are obligate biotrophic parasites infecting nearly 10,000 plant genera. They obtain their nutrients from host plants through specialized feeding structures known as haustoria. We previously identified the AVRk1 powdery mildew-specific gene family encoding effectors that contribute to the successful establishment of haustoria. Here, we report the extensive proliferation of the AVRk1 gene family throughout the genome of B. graminis, with sequences diverging in formae speciales adapted to infect different hosts. Also, importantly, we have discovered that the effectors have coevolved with a particular family of LINE-1 retrotransposons, named TE1a. The coevolution of these two entities indicates a mutual benefit to the association, which could ultimately contribute to parasite adaptation and success. We propose that the association would benefit 1) the powdery mildew fungus, by providing a mechanism for amplifying and diversifying effectors and 2) the associated retrotransposons, by providing a basis for their maintenance through selection in the fungal genome

    Italian Guidelines in diagnosis and treatment of alopecia areata

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    Alopecia areata (AA) is an organ-specific autoimmune disorder that targets anagen phase hair follicles. The course is unpredictable and current available treatments have variable efficacy. Nowadays, there is relatively little evidence on treatment of AA from well-designed clinical trials. Moreover, none of the treatments or devices commonly used to treat AA are specifically approved by the Food and Drug Administration. The Italian Study Group for Cutaneous Annexial Disease of the Italian Society of dermatology proposes these Italian guidelines for diagnosis and treatment of Alopecia Areata deeming useful for the daily management of the disease. This article summarizes evidence-based treatment associated with expert-based recommendations

    Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

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    Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

    Loco-Regional Treatments for Hepatocellular Carcinoma in People Living with HIV

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    Hepatocellular carcinoma (HCC) accounts for approximately 75–90% of primary liver cancers and is the sixth most common cancer and the third leading cause of cancer-related deaths worldwide. In the HIV-positive population, the risk of HCC is approximately four times higher than in the general population, with higher cancer-specific mortality than in HIV-negative patients. In most cases, HCC diagnosis is made in patients younger than the HIV-negative population and in the intermediate-advanced stage, thus limiting the therapeutic possibilities. Treatment choice in HIV-positive patients with HCC is subject to cancer staging, liver function and health status, as for HIV-negative and non-HIV-negative HCC patients. There are relatively few studies on the efficacy and safety in HIV-positive patients to date in loco-regional treatments for HCC. So far, literature shows that curative treatments such as radiofrequency ablation (RFA) have no significant differences in overall survival between HIV-positive and HIV-negative patients, as opposed to palliative treatments such as TACE, where there is a significant difference in overall survival. Although it can be assumed that the most recently discovered loco-regional therapies are applicable to HIV-positive patients with HCC in the same way as HIV-negative patients, further studies are needed to confirm this hypothesis. The purpose of our review is to evaluate these treatments, their efficacy, effectiveness, safety and their applicability to HIV-positive patients

    Towards robust biomarkers of psychosocial interventions

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