116 research outputs found

    Therapist-client sex in psychotherapy: attitudes of professionals and students towards ethical arguments

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    Data suggest that a substantial proportion of psychotherapists engage in therapist-client sex (TCS), violating national and international ethical guidelines. The objective of our study was to find a new and effective starting point for preventive interventions.; Using an online questionnaire, this study explored professionals' attitudes toward aspects of a TCS-case example influencing the tendency to pursue colleagues' TCS, including self-interest and responsibility ascribed to clients.; A total of 421 participants expressed preferences for courses of action and rated given information in a questionnaire. Results indicate that TCS is most often condemned for its inherent carelessness towards clients, its exploitative nature, the abuse of dependency and for counteracting the inherent intention of psychotherapy. Partial responsibility for TCS was attributed to clients by 41.3% of the respondents. Although self-interest related information was rated as an acceptable reason against pursuing TCS, a strong tendency exists to confront an abusive colleague, even at the risk of own disadvantages.; In the detailed discussion ethical arguments against TCS (other than the certainly inflicted, but hardly measurable harm) are elaborated. In particular the incompatibility of TCS with a psychotherapeutic relationship, the responsibility for TCS in the asymmetrical client-therapist relationship and the legitimacy of self-protection are discussed.; Reasoning against TCS can and should be based on explicit, ethical requirements for psychotherapists. Furthermore, integrating the topic in psychotherapists' training is encouraged and a discrete procedure to report a colleague's TCS is requested

    Effects of an electronic reminder system on guideline-concordant treatment of psychotic disorders : Results from a pilot feasibility trial

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    Adherence to evidence-based guidelines is essential for the treatment outcome of psychotic disorders. Previous studies showed that IT-supported pathways are able to increase guideline adherence in psychiatric care. This paper describes a pilot study on the development of an electronic recall-reminder-system (RRS) for supporting guideline-adherent treatment in outpatient care of patients with chronic psychotic disorders and analyses its feasibility.; Guidelines were integrated in the RRS software M.E.M.O.R.E.S. Software training for the staff was provided. We compared the number of conducted vs. guideline-recommended interventions 6 months before and after implementation. Subsequently both the caregivers' and the patients' satisfaction with the RRS was evaluated.; Guideline adherence in general was low and the RRS was barely used. After its implementation a significant increase was observed in chemogram-check-ups and diagnostics regarding cardiovascular risks (esp. ECG). Both patients and professionals described problems with integrating the RRS in their daily routine and questioned the usefulness of the guidelines for chronically ill, although they basically approved its importance and usefulness.; Participants appreciated the idea of supporting guideline adherence with an IT-system, but there seemed to be major obstacles to implementation: caregivers appear to be concerned of being exposed or questioned, technical difficulties might lead to avoidance, and there seems to be a lack of knowledge and awareness about the health risks for individuals with psychotic disorders. Possibly guidelines adapted for the chronically ill would find more acceptance. Technical simplifications and better information should be considered prior to further attempts to implement IT-supported guidelines in order to increase acceptance

    Assisted dying requests from people in detention: Psychiatric, ethical, and legal considerations–A literature review

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    The principle of equivalence of care states that prisoners must have access to the same standard of health care as the general population. If, as recent court decisions suggest, assisted dying is not limited to people with a terminal physical illness or irremediable suffering, it might also be requested by people with severe mental illness in detention. Some of the countries with legal regulations on assisted dying also have recommendations on how to handle requests from prisoners. However, detention itself can lead to psychological distress and suicidality, so we must consider whether and how people in such settings can make autonomous decisions. Ethical conflicts arise with regard to an individual's free will, right to life, and physical and personal integrity and to the right of a state to inflict punishment. Furthermore, people in prison often receive insufficient mental health care. In this review, we compare different practices for dealing with requests for assisted dying from people in prison and forensic psychiatric facilities and discuss the current ethical and psychiatric issues concerning assisted dying in such settings

    Relationship between benzodiazepine prescription, aggressive behavior, and behavioral disinhibition: a retrospective study in a Swiss prison.

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    BACKGROUND Benzodiazepines are commonly prescribed in prisons amidst the controversies surrounding their potential role in causing behavioral disinhibition and aggressive behavior and their association with use and trafficking of illicit and addictive substances. The present study aimed to (1) ascertain the relationship between benzodiazepine prescription (including their dosage and duration of use) and aggressive behavior and behavioral disinhibition in prison and (2) investigate whether there was an association between benzodiazepine prescription, (including their dosage and duration of use) and using and trafficking illicit and addictive substances during imprisonment. METHODS Data were extracted from the electronic database of an "open" Swiss prison (n = 1206, 1379 measures) over a 5-year period (2010-2015). Measures included benzodiazepine prescription, duration of benzodiazepine use and mean dosage, and punishable behaviors (physical and verbal aggression, disinhibited but not directly aggressive behaviors, property damage or theft, substance-related offenses, and rule transgression). We assessed the relationship between benzodiazepine prescription and punishable behaviors after propensity score matching. Logistic regressions were also used to test the relationship of benzodiazepine use duration and dosage with punishable behaviors among participants who received benzodiazepines. RESULTS After propensity score matching, benzodiazepine prescription was not significantly associated with any punishable behavior. Among detained persons who took benzodiazepines, there was no significant association of dosage and duration of use with offenses involving illicit or addictive substance use or trafficking. CONCLUSIONS Our study did not empirically support the occurrence of increased aggressive or disinhibited behaviors or increased risk of substance abuse in detained persons who received benzodiazepines in prison. This suggests a need to reconsider restrictions in prescribing benzodiazepines in the prison setting

    PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC

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    The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) is a regulatory hub for transcription and RNA processing. Here, we identify PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a CTD reader domain that preferentially binds two phosphorylated Serine-2 marks in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length of genes. PHF3 knock-out or SPOC deletion in human cells results in increased Pol II stalling, reduced elongation rate and an increase in mRNA stability, with marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation. Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation by bridging transcription with mRNA decay

    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

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    Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

    Genome-wide association study identifies novel loci associated with circulating phospho- and sphingolipid concentrations.

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    Phospho- and sphingolipids are crucial cellular and intracellular compounds. These lipids are required for active transport, a number of enzymatic processes, membrane formation, and cell signalling. Disruption of their metabolism leads to several diseases, with diverse neurological, psychiatric, and metabolic consequences. A large number of phospholipid and sphingolipid species can be detected and measured in human plasma. We conducted a meta-analysis of five European family-based genome-wide association studies (N = 4034) on plasma levels of 24 sphingomyelins (SPM), 9 ceramides (CER), 57 phosphatidylcholines (PC), 20 lysophosphatidylcholines (LPC), 27 phosphatidylethanolamines (PE), and 16 PE-based plasmalogens (PLPE), as well as their proportions in each major class. This effort yielded 25 genome-wide significant loci for phospholipids (smallest P-value = 9.88×10(-204)) and 10 loci for sphingolipids (smallest P-value = 3.10×10(-57)). After a correction for multiple comparisons (P-value<2.2×10(-9)), we observed four novel loci significantly associated with phospholipids (PAQR9, AGPAT1, PKD2L1, PDXDC1) and two with sphingolipids (PLD2 and APOE) explaining up to 3.1% of the variance. Further analysis of the top findings with respect to within class molar proportions uncovered three additional loci for phospholipids (PNLIPRP2, PCDH20, and ABDH3) suggesting their involvement in either fatty acid elongation/saturation processes or fatty acid specific turnover mechanisms. Among those, 14 loci (KCNH7, AGPAT1, PNLIPRP2, SYT9, FADS1-2-3, DLG2, APOA1, ELOVL2, CDK17, LIPC, PDXDC1, PLD2, LASS4, and APOE) mapped into the glycerophospholipid and 12 loci (ILKAP, ITGA9, AGPAT1, FADS1-2-3, APOA1, PCDH20, LIPC, PDXDC1, SGPP1, APOE, LASS4, and PLD2) to the sphingolipid pathways. In large meta-analyses, associations between FADS1-2-3 and carotid intima media thickness, AGPAT1 and type 2 diabetes, and APOA1 and coronary artery disease were observed. In conclusion, our study identified nine novel phospho- and sphingolipid loci, substantially increasing our knowledge of the genetic basis for these traits
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