Comparison between the Psychopathy Checklist-Revised and the Comprehensive Assessment of Psychopathic Personality in a representative sample of Spanish prison inmates

In the field of psychopathy, there is an ongoing debate about the core traits that define the disorder, and that therefore must be present to some extent in all psychopaths. The main controversy of this debate concerns criminal behaviour, as some researchers consider it a defining trait, while others disagree. Using a representative sample of 204 Spanish convicted inmates incarcerated at the Pereiro de Aguiar Penitentiary in Ourense, Spain, we tested two competing models, the Psychopathy Checklist-Revised (PCL-R), which includes criminal behaviour items, versus the Comprehensive Assessment of Psychopathic Personality (CAPP), which does not. We used two different PCL-R models, one that includes criminal items and another that does not. PCL-R factors, facets, and testlets from both models and CAPP dimensions were correlated and compared. Two different PCL-R cut-off scores, 25 or more and 30 or more, were used for the analysis. Overall, a strong correlation was found between PCL-R and CAPP scores in the whole sample, but as scores increased and inmates became more psychopathic, the correlations weakened. All these data indicate that psychopathy, understood to mean having high scores on the PCL-R and CAPP, is a multidimensional entity, and inmates can develop the disorder and then receive the diagnosis through different dimensions. The CAPP domains showed better correlations when compared with the PCL-R factors from both models, showing that an instrument for the assessment of psychopathy without a criminal dimension is valuable for clinical assessment and research purposes.publishedVersio

Consensus of experts from the Spanish Pharmacogenetics and Pharmacogenomics Society and the Spanish Society of Medical Oncology for the genotyping of DPYD in cancer patients who are candidates for treatment with fluoropyrimidines

5-Fluorouracil (5-FU) and oral fluoropyrimidines, such as capecitabine, are widely used in the treatment of cancer, especially gastrointestinal tumors and breast cancer, but their administration can produce serious and even lethal toxicity. This toxicity is often related to the partial or complete deficiency of the dihydropyrimidine dehydrogenase (DPD) enzyme, which causes a reduction in clearance and a longer half-life of 5-FU. It is advisable to determine if a DPD deficiency exists before administering these drugs by genotyping DPYD gene polymorphisms. The objective of this consensus of experts, in which representatives from the Spanish Pharmacogenetics and Pharmacogenomics Society and the Spanish Society of Medical Oncology participated, is to establish clear recommendations for the implementation of genotype and/or phenotype testing for DPD deficiency in patients who are candidates to receive fluoropyrimidines. The genotyping of DPYD previous to treatment classifies individuals as normal, intermediate, or poor metabolizers. Normal metabolizers do not require changes in the initial dose, intermediate metabolizers should start treatment with fluoropyrimidines at doses reduced to 50%, and poor metabolizers are contraindicated for fluoropyrimidines

Smoking cessation improves clinical outcome in severe mental disorders and is modulated by genetic variability at CHRNA5 gene

Smoking has been traditionally tolerated for patients with mental disorders due to its hypothesized self-medication function (Schroeder and Morris, 2010).[...

Adolescent subthreshold-depression and anxiety: psychopathology, functional impairment and increased suicide risk

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Life-time prevalence and psychosocial correlates of adolescent direct self-injurious behavior: A comparative study of findings in 11 European countries

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Function of glutathione peroxidases in legume root nodules

© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.[EN] Glutathione peroxidases (Gpxs) are antioxidant enzymes not studied so far in legume nodules, despite the fact that reactive oxygen species are produced at different steps of the symbiosis. The function of two Gpxs that are highly expressed in nodules of the model legume Lotus japonicus was examined. Gene expression analysis, enzymatic and nitrosylation assays, yeast cell complementation, in situ mRNA hybridization, immunoelectron microscopy, and LjGpx-green fluorescent protein (GFP) fusions were used to characterize the enzymes and to localize each transcript and isoform in nodules. The LjGpx1 and LjGpx3 genes encode thioredoxin-dependent phospholipid hydroperoxidases and are differentially regulated in response to nitric oxide (NO) and hormones. LjGpx1 and LjGpx3 are nitrosylated in vitro or in plants treated with S-nitrosoglutathione (GSNO). Consistent with the modification of the peroxidatic cysteine of LjGpx3, in vitro assays demonstrated that this modification results in enzyme inhibition. The enzymes are highly expressed in the infected zone, but the LjGpx3 mRNA is also detected in the cortex and vascular bundles. LjGpx1 is localized to the plastids and nuclei, and LjGpx3 to the cytosol and endoplasmic reticulum. Based on yeast complementation experiments, both enzymes protect against oxidative stress, salt stress, and membrane damage. It is concluded that both LjGpxs perform major antioxidative functions in nodules, preventing lipid peroxidation and other oxidative processes at different subcellular sites of vascular and infected cells. The enzymes are probably involved in hormone and NO signalling, and may be regulated through nitrosylation of the peroxidatic cysteine essential for catalytic function.AS and PBS were the recipients of predoctoral (Formacion de Personal Investigador) and postdoctoral (Marie Curie) contracts, respectively. We thank Martin Crespi for help with in situ RNA hybridization and Simon Avery for sharing the yeast mutant and for helpful advice. This work was supported by Ministerio de Economia y Competitividad-Fondo Europeo de Desarrollo Regional (AGL2011-24524 and AGL2014-53717-R). The UMR1136 is supported by a grant overseen by the French National Research Agency (ANR) as part of the 'Investissements d'Avenir' programme (ANR-11-LABX-0002-01, Lab of Excellence ARBRE). MM and KJD acknowledge support within SPP1710. The proteomic analysis was performed in the CSIC/UAB Proteomics Facility of IIBB-CSIC that belongs to ProteoRed, PRB2-ISCIII, supported by grant PT13/0001.Matamoros, MA.; Saiz Andres, A.; Peñuelas, M.; Bustos-Sanmamed, P.; Mulet Salort, JM.; Barja, MV.; Rouhier, N.... (2015). Function of glutathione peroxidases in legume root nodules. Journal of Experimental Botany. 66(10):2979-2990. https://doi.org/10.1093/jxb/erv066S297929906610Astier, J., Kulik, A., Koen, E., Besson-Bard, A., Bourque, S., Jeandroz, S., … Wendehenne, D. (2012). Protein S-nitrosylation: What’s going on in plants? Free Radical Biology and Medicine, 53(5), 1101-1110. doi:10.1016/j.freeradbiomed.2012.06.032Avery, A. M., & Avery, S. V. (2001). Saccharomyces cerevisiaeExpresses Three Phospholipid Hydroperoxide Glutathione Peroxidases. Journal of Biological Chemistry, 276(36), 33730-33735. doi:10.1074/jbc.m105672200Avsian-Kretchmer, O., Gueta-Dahan, Y., Lev-Yadun, S., Gollop, R., & Ben-Hayyim, G. (2004). 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TAp73 is one of the genes responsible for the lack of response to chemotherapy depending on B-Raf mutational status

<p>Abstract</p> <p>Background</p> <p>Although there have been many studies on the p73 gene, some of its functions still remain unclear. There is little research on the relationship between p73 gene transcription and its protein expression and the response to certain drugs such as oxaliplatin and cetuximab, which are drugs currently used in colorectal cancer.</p> <p>The purpose of this study was to evaluate the impact of TAp73 expression on oxaliplatin and cetuximab-based chemotherapy in colorectal cancer cell lines with different K-Ras and B-Raf mutational status.</p> <p>Methods</p> <p>TAp73 was analyzed in three colorectal tumor cell lines HT-29, SW-480 and Caco-2. mRNA TAp73 was determined using Real time PCR; TAp73 protein by immunoblotting and cell viability was analyzed by the MTT method.</p> <p>Results</p> <p>We found that mRNA and TAp73 protein were decreased in cells treated with oxaliplatin (in monotherapy or combined with cetuximab) when B-Raf is mutated. This was statistically significant and was also associated with higher cell viability after the treatment.</p> <p>Conclusions</p> <p>Here, for the first time we report, that there is a signaling loop between B-Raf activation and p73 function.</p> <p>Low expression of TAp73 in colorectal cancer cell lines with mutated B-Raf may be involved in the lack of response to oxaliplatin in monotherapy or combined with cetuximab.</p

Replicated evidence that endophenotypic expression of schizophrenia polygenic risk is greater in healthy siblings of patients compared to controls, suggesting gene-environment interaction. The EUGEI study

Background First-degree relatives of patients with psychotic disorder have higher levels of polygenic risk (PRS) for schizophrenia and higher levels of intermediate phenotypes. Methods We conducted, using two different samples for discovery (n = 336 controls and 649 siblings of patients with psychotic disorder) and replication (n = 1208 controls and 1106 siblings), an analysis of association between PRS on the one hand and psychopathological and cognitive intermediate phenotypes of schizophrenia on the other in a sample at average genetic risk (healthy controls) and a sample at higher than average risk (healthy siblings of patients). Two subthreshold psychosis phenotypes, as well as a standardised measure of cognitive ability, based on a short version of the WAIS-III short form, were used. In addition, a measure of jumping to conclusion bias (replication sample only) was tested for association with PRS. Results In both discovery and replication sample, evidence for an association between PRS and subthreshold psychosis phenotypes was observed in the relatives of patients, whereas in the controls no association was observed. Jumping to conclusion bias was similarly only associated with PRS in the sibling group. Cognitive ability was weakly negatively and non-significantly associated with PRS in both the sibling and the control group. Conclusions The degree of endophenotypic expression of schizophrenia polygenic risk depends on having a sibling with psychotic disorder, suggestive of underlying gene–environment interaction. Cognitive biases may better index genetic risk of disorder than traditional measures of neurocognition, which instead may reflect the population distribution of cognitive ability impacting the prognosis of psychotic disorder