171 research outputs found

    Dealer Intermediation and Price Behavior in the Aftermarket for New Bond Issues

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    We study trading and prices in newly issued municipal bonds. Municipals, which trade in decentralized, broker-dealer markets, are underpriced when issued, but unlike equities the average price rises slowly over a period of several days. We document high levels of price dispersion in newly issued bonds, and show that the average drift upward in price is because of changes in the mix of trades over time. While large trades occur at prices close to the reoffering yield, and close to each other, small trades occur at a wide range of prices almost simultaneously. Some small investors appear to be informed about the status of the issue, and trade on attractive terms. Others appear uninformed, and broker/dealers are able to discriminate between them.

    Pilot study of the relationship between psychotic manifestations and living environment

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    The study of subclinical psychotic manifestations (quantitative schizotypy) represents clinical and public health issues. These manifestations are more common than schizophrenia or depression, but rarely identified while it impacts the quality of life. Screening schizotypy in the general population would make it possible to propose prevention strategies. The objectives of the present research is to better understand the determinants and mechanisms of schizotypy in order to identify population..

    Interplay Between Childhood Physical Abuse and Familial Risk in the Onset of Psychotic Disorders

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    Background: Childhood abuse is considered one of the main environmental risk factors for the development of psychotic symptoms and disorders. However, this association could be due to genetic factors influencing exposure to such risky environments or increasing sensitivity to the detrimental impact of abuse. Therefore, using a large epidemiological case-control sample, we explored the interplay between a specific form of childhood abuse and family psychiatric history (a proxy for genetic risk) in the onset of psychosis. Methods: Data were available on 172 first presentation psychosis cases and 246 geographically matched controls from the Aetiology and Ethnicity of Schizophrenia and Other Psychoses study. Information on childhood abuse was obtained retrospectively using the Childhood Experience of Care and Abuse Questionnaire and occurrence of psychotic and affective disorders in first degree relatives with the Family Interview for Genetic Studies. Results: Parental psychosis was more common among psychosis cases than unaffected controls (adjusted OR = 5.96, 95% CI: 2.09–17.01, P = .001). Parental psychosis was also associated with physical abuse from mothers in both cases (OR = 3.64, 95% CI: 1.06–12.51, P = .040) and controls (OR = 10.93, 95% CI: 1.03–115.90, P = .047), indicative of a gene-environment correlation. Nevertheless, adjusting for parental psychosis did not measurably impact on the abuse-psychosis association (adjusted OR = 3.31, 95% CI: 1.22–8.95, P= .018). No interactions were found between familial liability and maternal physical abuse in determining psychosis caseness. Conclusions: This study found no evidence that familial risk accounts for associations between childhood physical abuse and psychotic disorder nor that it substantially increases the odds of psychosis among individuals reporting abuse

    Trading on Algos

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    Abstract This paper studies the impact of algorithmic trading (AT) on asset prices. We find that the heterogeneity of algorithmic traders across stocks generates predictable patterns in stock returns. A trading strategy that exploits the AT return predictability generates a monthly risk-adjusted performance between 50-130 basis points for the period 1999 to 2012. We find that stocks with lower AT have higher returns, after controlling for standard market-, size-, book-to-market-, momentum, and liquidity risk factors. This effect survives the inclusion of many cross-sectional return predictors and is statistically and economically significant. Return predictability is stronger among stocks with higher impediments to trade and higher predatory/opportunistic algorithmic traders. Our paper is the first to study and establish a strong link between algorithmic trading and asset prices

    Autistic and Schizotypal Traits and Global Functioning in Bipolar I Disorder

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    Objective: To determine the expression of autistic and positive schizotypal traits in a large sample of adults with bipolar I disorder (BD-I), and the effect of co-occurring autistic and positive schizotypal traits on global functioning in BD-I. Method: Autistic and positive schizotypal traits were self-assessed in 797 individuals with BD-I recruited by the Bipolar Disorder Research Network. Differences in global functioning (rated using the Global Assessment Scale) during lifetime worst depressive and manic episodes (GASD and GASM respectively) were calculated in groups with high/low autistic and positive schizotypal traits. Regression analyses assessed the interactive effect of autistic and positive schizotypal traits on global functioning. Results: 47.2% (CI=43.7-50.7%) showed clinically significant levels of autistic traits, and 23.22% (95% CI=20.29-26.14) showed clinically significant levels of positive schizotypal traits. In the worst episode of mania, the high autistic, high positive schizotypal group had better global functioning compared to the other groups. Individual differences analyses showed that high levels of co-occurring traits were associated with better global functioning in both mood states. Limitations: Autistic and schizotypal traits were assessed using self-rated questionnaires. Conclusions: Expression of autistic and schizotypal traits in adults with BD-I is prevalent, and may be important to predict illness aetiology, prognosis, and diagnostic practices in this population. Future work should focus on replicating these findings in independent samples, and on the biological and/or psychosocial mechanisms underlying better global functioning in those who have high levels of both autistic and positive schizotypal traits

    The p250GAP Gene Is Associated with Risk for Schizophrenia and Schizotypal Personality Traits

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    BACKGROUND: Hypofunction of the glutamate N-Methyl-d-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia. p250GAP is a brain-enriched NMDA receptor-interacting RhoGAP. p250GAP is involved in spine morphology, and spine morphology has been shown to be altered in the post-mortem brains of patients with schizophrenia. Schizotypal personality disorder has a strong familial relationship with schizophrenia. Several susceptibility genes for schizophrenia have been related to schizotypal traits. METHODS: We first investigated the association of eight linkage disequilibrium-tagging single-nucleotide polymorphisms (SNPs) that cover the p250GAP gene with schizophrenia in a Japanese sample of 431 schizophrenia patients and 572 controls. We then investigated the impact of the risk genetic variant in the p250GAP gene on schizotypal personality traits in 180 healthy subjects using the Schizotypal Personality Questionnaire. RESULTS: We found a significant difference in genotype frequency between the patients and the controls in rs2298599 (χ(2) = 17.6, p = 0.00015). The minor A/A genotype frequency of rs2298599 was higher in the patients (18%) than in the controls (9%) (χ(2) = 15.5, p = 0.000083). Moreover, we found that subjects with the rs2298599 risk A/A genotype, compared with G allele carriers, had higher scores of schizotypal traits (F(1,178) = 4.08, p = 0.045), particularly the interpersonal factor (F(1,178) = 5.85, p = 0.017). DISCUSSION: These results suggest that a genetic variation in the p250GAP gene might increase susceptibility not only for schizophrenia but also for schizotypal personality traits. We concluded that the p250GAP gene might be a new candidate gene for susceptibility to schizophrenia

    Anhedonia in schizophrenia and major depression: state or trait?

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    <p>Abstract</p> <p>Background</p> <p>In schizophrenia and major depressive disorder, anhedonia (a loss of capacity to feel pleasure) had differently been considered as a premorbid personological trait or as a main symptom of their clinical picture. The aims of this study were to examine the pathological features of anhedonia in schizophrenic and depressed patients, and to investigate its clinical relations with general psychopathology (negative, positive, and depressive dimensions).</p> <p>Methods</p> <p>A total of 145 patients (80 schizophrenics and 65 depressed subjects) were assessed using the Physical Anhedonia Scale and the Social Anhedonia Scale (PAS and SAS, respectively), the Scales for the Assessment of Positive and Negative Symptoms (SAPS and SANS, respectively), the Calgary Depression Scale for Schizophrenics (CDSS), and the Hamilton Depression Rating Scale (HDRS). The statistical analysis was performed in two steps. First, the schizophrenic and depressed samples were dichotomised into 'anhedonic' and 'normal hedonic' subgroups (according to the 'double (PAS/SAS) cut-off') and were compared on the general psychopathology scores using the Mann-Whitney Z test. Subsequently, for the total schizophrenic and depressed samples, Spearman correlations were calculated to examine the relation between anhedonia ratings and the other psychopathological parameters.</p> <p>Results</p> <p>In the schizophrenic sample, anhedonia reached high significant levels only in 45% of patients (n = 36). This 'anhedonic' subgroup was distinguished by high scores in the disorganisation and negative dimensions. Positive correlations of anhedonia with disorganised and negative symptoms were also been detected. In the depressed sample, anhedonia reached high significant levels in only 36.9% of subjects (n = 24). This 'anhedonic' subgroup as distinguished by high scores in the depression severity and negative dimensions. Positive correlations of anhedonia with depressive and negative symptoms were also been detected.</p> <p>Conclusion</p> <p>In the schizophrenic sample, anhedonia seems to be a specific subjective psychopathological experience of the negative and disorganised forms of schizophrenia. In the depressed sample, anhedonia seems to be a specific subjective psychopathological experience of those major depressive disorder forms with a marked clinical depression severity.</p

    The continuity of effect of schizophrenia polygenic risk score and patterns of cannabis use on transdiagnostic symptom dimensions at first-episode psychosis: findings from the EU-GEI study

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    Diagnostic categories do not completely reflect the heterogeneous expression of psychosis. Using data from the EU-GEI study, we evaluated the impact of schizophrenia polygenic risk score (SZ-PRS) and patterns of cannabis use on the transdiagnostic expression of psychosis. We analysed first-episode psychosis patients (FEP) and controls, generating transdiagnostic dimensions of psychotic symptoms and experiences using item response bi-factor modelling. Linear regression was used to test the associations between these dimensions and SZ-PRS, as well as the combined effect of SZ-PRS and cannabis use on the dimensions of positive psychotic symptoms and experiences. We found associations between SZ-PRS and (1) both negative (B = 0.18; 95%CI 0.03–0.33) and positive (B = 0.19; 95%CI 0.03–0.35) symptom dimensions in 617 FEP patients, regardless of their categorical diagnosis; and (2) all the psychotic experience dimensions in 979 controls. We did not observe associations between SZ-PRS and the general and affective dimensions in FEP. Daily and current cannabis use were associated with the positive dimensions in FEP (B = 0.31; 95%CI 0.11–0.52) and in controls (B = 0.26; 95%CI 0.06–0.46), over and above SZ-PRS. We provide evidence that genetic liability to schizophrenia and cannabis use map onto transdiagnostic symptom dimensions, supporting the validity and utility of the dimensional representation of psychosis. In our sample, genetic liability to schizophrenia correlated with more severe psychosis presentation, and cannabis use conferred risk to positive symptomatology beyond the genetic risk. Our findings support the hypothesis that psychotic experiences in the general population have similar genetic substrates as clinical disorders

    Handedness as a neurodevelopmental marker in schizophrenia: Results from the FACE-SZ cohort

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    Objectives: High rates of non-right-handedness (NRH) including mixed-handedness have been reported in neurodevelopmental disorders. In schizophrenia (SZ), atypical handedness has been inconsistently related to impaired features. We aimed to determine whether SZ subjects with NRH and mixed-handedness had poorer clinical and cognitive outcomes compared to their counterparts. Methods: 667 participants were tested with a battery of neuropsychological tests, and assessed for laterality using the Edinburg Handedness Inventory. Clinical symptomatology was assessed. Learning disorders and obstetrical complications were recorded. Biological parameters were explored. Results: The prevalence of NRH and mixed-handedness was high (respectively, 42.4% and 34.1%). In the multivariable analyses, NRH was associated with cannabis use disorder (p = 0.045). Mixed-handedness was associated with positive symptoms (p = 0.041), current depressive disorder (p = 0.005)), current cannabis use (p = 0.024) and less akathisia (p = 0.019). A history of learning disorder was associated with NRH. No association was found with cognition, trauma history, obstetrical complications, psychotic symptoms, peripheral inflammation. Conclusions: Non-right and mixed-handedness are very high in patients with SZ, possibly reflecting a neurodevelopmental origin. NRH is associated with learning disorders and cannabis use. Mixed-handedness is associated with positive symptoms, current depressive disorder, cannabis use and less akathisia. However, this study did not confirm greater cognitive impairment in these patients. © 2021 Informa UK Limited, trading as Taylor & Francis Group.Sorbonne Universités à Paris pour l'Enseignement et la RechercheFondaMental-Cohorte
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