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AIMS AND METHOD: Workplace violence and aggression toward healthcare staff has a significant impact on the individual, causing self-blame, isolation and burnout. Timely and appropriate support can mitigate harm, but there is little research into how this should be delivered. We conducted multi-speciality peer groups for London doctors in postgraduate training (DPT), held over a 6-week period. Pre- and post-group burnout questionnaires and semi-structured interviews were used to evaluate peer support. Thematic analysis and descriptive statistical methods were used to describe the data. RESULTS: We found four themes: (a) the experience and impact of workplace violence and aggression on DPT, (b) the experience of support following incidents of workplace violence and aggression, (c) the impact and experience of the peer groups and (d) future improvements to support. DPTs showed a reduction in burnout scores. CLINICAL IMPLICATIONS: Peer groups are effective support for DPT following workplace violence and aggression. Embedding support within postgraduate training programmes would improve access and availability.
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BACKGROUND: Neurobiological research frequently implicates inflammatory and neurogenic components with core aspects of bipolar disorder. Even in periods of symptom remission (euthymia), individuals with bipolar disorder experience cognitive impairments, which are increasingly being proposed as an outcome for interventions; identifying biomarkers associated with cognitive impairment in people with bipolar disorder could advance progress in this therapeutic field through identifying biological treatment targets. AIMS: We aimed to identify proteomic biomarker correlates of cognitive impairment in individuals with euthymic bipolar disorder. METHOD: Forty-four adults with a bipolar disorder diagnosis in euthymia underwent a battery of cognitive assessments and provided blood for biomarkers. We examined a comprehensive panel of inflammatory and trophic proteins as putative cross-sectional predictors of cognition, conceptualised according to recommended definitions of clinically significant cognitive impairment (binary construct) and global cognitive performance (continuous measure). RESULTS: A total of 48% of the sample met the criteria for cognitive impairment. Adjusting for potentially important covariates, regression analyses identified lower levels of three proteins as significantly and independently associated with cognitive deficits, according to both binary and continuous definitions (interleukin-7, vascular endothelial growth factor C and placental growth factor), and one positively correlated with (continuous) global cognitive performance (basic fibroblast growth factor). CONCLUSIONS: This study identifies four candidate markers of cognitive impairment in bipolar disorder, none of which have been previously compared with cognitive function in participants with bipolar disorder. Pending replication in larger samples and support from longitudinal studies, these markers could have implications for treating cognitive dysfunction in this patient population.
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Our current clinical approach to visual hallucinations is largely derived from work carried out by Georges de Morsier in the 1930s. Now, almost a century after his influential papers, we have the research tools to further explore the ideas he put forward. In this review, we address de Morsier's proposal that visual hallucinations in all clinical conditions have a similar neurological mechanism by comparing structural imaging studies of susceptibility to visual hallucinations in Parkinson's disease, Alzheimer's disease, Dementia with Lewy bodies and schizophrenia. Systematic review of the literature was undertaken using PubMed searches. A total of 18 studies across conditions were identified reporting grey matter differences between patients with and without visual hallucinations. Grey matter changes were categorised into brain regions relevant to current theories of visual hallucinations. The distribution of cortical atrophy supports de Morsier's premise that visual hallucinations are invariably linked to aberrant activity within visual thalamo-cortical networks. Further work is required to determine by what mechanism these networks become predisposed to spontaneous activation, and whether the frontal lobe and hippocampal changes identified are present in all conditions. The findings have implications for the development of effective treatments for visual hallucinations.
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Corteza Cerebral/patología , Alucinaciones/etiología , Alucinaciones/patología , Enfermedad por Cuerpos de Lewy/complicaciones , Enfermedad de Parkinson/complicaciones , Trastornos del Conocimiento/etiología , Humanos , Imagen por Resonancia MagnéticaRESUMEN
We report genetic aberrations that activate the ERK/MAP kinase pathway in 100% of posterior fossa pilocytic astrocytomas, with a high frequency of gene fusions between KIAA1549 and BRAF among these tumours. These fusions were identified from analysis of focal copy number gains at 7q34, detected using Affymetrix 250K and 6.0 SNP arrays. PCR and sequencing confirmed the presence of five KIAA1549-BRAF fusion variants, along with a single fusion between SRGAP3 and RAF1. The resulting fusion genes lack the auto-inhibitory domains of BRAF and RAF1, which are replaced in-frame by the beginning of KIAA1549 and SRGAP3, respectively, conferring constitutive kinase activity. An activating mutation of KRAS was identified in the single pilocytic astrocytoma without a BRAF or RAF1 fusion. Further fusions and activating mutations in BRAF were identified in 28% of grade II astrocytomas, highlighting the importance of the ERK/MAP kinase pathway in the development of paediatric low-grade gliomas.