Hostility, negative emotional valence, sadness, rumination to sadness and cardiovascular reactivity

The study's first goal investigated what type of thoughts and underlying emotions are exactly experienced by high versus low hostile participants following an anger provoking interpersonal stressor. Results revealed that high compared to low hostile participants experienced overall significantly more inferred thoughts of negative emotional valence; emotions that they did not express in a direct manner. It was suggested, that high hostiles might be high on the trait of Negative Affectivity. When specific emotion categories were analyzed, results revealed that high compared to low hostile individuals experienced overall more sad-inferred thoughts; sad thoughts that they did not express in a direct manner. Furthermore, the study found that high compared to low hostile participants ruminate more to sadness. The combined results of more sad-inferred thoughts and significantly more rumination to sadness, lends support to the interpretation, that high hostile individuals may be vulnerable for the development of sustained depressed mood and perhaps even depression. These results are important given that depression, even milder depressive symptoms have been found to be independent risk factors for cardiovascular disease in general and coronary heart disease in particular. This study did not find associations between cardiovascular reactivity and hostility or rumination to sadness. The absence of an association between hostility and cardiovascular reactivity is, however, consistent with the specific emotion category results found in this study. Research suggests that it is the high hostile's propensity to experience more frequent and more intense emotions in the anger category that is directly linked to heightened cardiovascular reactivity. This study did not find that anger-thoughts and anger intensities were significantly higher for high compared to low hostile participants following the anger provoking interpersonal stressor. It was suggested that the lack of heightened cardiovascular reactivity to interpersonal stress is due to the finding that the high hostile participants in this study did not experience more frequent and intense anger

A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer’s disease risk (AD). The role of PLCG2 in immune system signaling suggests it may also protect against other neurodegenerative diseases and possibly associates with longevity. We studied the effect of the rs72824905-G on seven neurodegenerative diseases and longevity, using 53,627 patients, 3,516 long-lived individuals and 149,290 study-matched controls. We replicated the association of rs72824905-G with reduced AD risk and we found an association with reduced risk of dementia with Lewy bodies (DLB) and frontotemporal dementia (FTD). We did not find evidence for an effect on Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) risks, despite adequate sample sizes. Conversely, the rs72824905-G allele was associated with increased likelihood of longevity. By-proxy analyses in the UK Biobank supported the associations with both dementia and longevity. Concluding, rs72824905-G has a protective effect against multiple neurodegenerative diseases indicating shared aspects of disease etiology. Our findings merit studying the PLCγ2 pathway as drug-target.Fil:  van der Lee, Sven J.. Vrije Universiteit Amsterdam; Países BajosFil: Conway, Olivia J.. Mayo Clinic Cancer Center; Estados UnidosFil: Jansen, Iris. Vrije Universiteit Amsterdam; Países BajosFil: Carrasquillo, Minerva M.. Mayo Clinic Cancer Center; Estados UnidosFil: Kleineidam, Luca. Universitat Bonn; Alemania. German Center for Neurodegenerative Diseases; Alemania. University Hospital Cologne; AlemaniaFil: van den Akker, Erik. Leiden University. Leiden University Medical Center; Países Bajos. Delft University of Technology; Países BajosFil: Hernández, Isabel. Universitat Internacional de Catalunya; España. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; EspañaFil: van Eijk, Kristel R.. University of Utrecht; Países BajosFil: Stringa, Najada. Vrije Universiteit Amsterdam; Países BajosFil: Chen, Jason A.. University of California at Los Angeles; Estados UnidosFil: Zettergren, Anna. University of Gothenburg; SueciaFil: Andlauer, Till F. M.. Max Planck Institute of Psychiatry; Alemania. Universitat Technical Zu Munich; Alemania. German Competence Network Multiple Sclerosis; AlemaniaFil: Diez Fairen, Monica. University Hospital Mutua de Terrassa; España. Fundacio per la Recerca Biomedica I Social Mutua Terrassa; EspañaFil: Simon Sanchez, Javier. Deutsches Zentrum für Neurodegenerative Erkrankungen; Alemania. Eberhard Karls Universität Tübingen; AlemaniaFil: Lleó, Alberto. Universitat Autònoma de Barcelona; España. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; EspañaFil: Zetterberg, Henrik. Sahlgrenska University Hospital; Suecia. University of Gothenburg; Suecia. University College London; Estados UnidosFil: Nygaard, Marianne. University of Southern Denmark; DinamarcaFil: Blauwendraat, Cornelis. National Institute of Neurological Disorders and Stroke; Estados UnidosFil: Savage, Jeanne E.. Vrije Universiteit Amsterdam; Países BajosFil: Mengel From, Jonas. University of Southern Denmark; DinamarcaFil: Moreno Grau, Sonia. Universitat Internacional de Catalunya; EspañaFil: Wagner, Michael. Universitat Bonn; Alemania. Deutsches Zentrum für Neurodegenerative Erkrankungen; AlemaniaFil: Fortea, Juan. Universitat Autònoma de Barcelona; España. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; EspañaFil: Keogh, Michael J.. University of Newcastle; Reino Unido. University of Cambridge; Reino UnidoFil: Blennow, Kaj. Sahlgrenska University Hospital; Suecia. University of Gothenburg; SueciaFil: Skoog, Ingmar. University of Gothenburg; SueciaFil: Friese, Manuel A.. German Competence Network Multiple Sclerosis; Alemania. Universitätsklinikum Hamburg‐Eppendorf; AlemaniaFil: Pletnikova, Olga. University Johns Hopkins; Estados UnidosFil: Zulaica, Miren. Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas ; España. Instituto Biodonostia; EspañaFil: Dalmasso, Maria Carolina. University Hospital Cologne; Alemania. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentin

Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity.

The IPDGC (The International Parkinson Disease Genomics Consortium) and EADB (Alzheimer Disease European DNA biobank) are listed correctly as an author to the article, however, they were incorrectly listed more than once

Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

The IPDGC (The International Parkinson Disease Genomics Consortium) and EADB (Alzheimer Disease European DNA biobank) are listed correctly as an author to the article, however, they were incorrectly listed more than once

Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

The IPDGC (The International Parkinson Disease Genomics Consortium) and EADB (Alzheimer Disease European DNA biobank) are listed correctly as an author to the article, however, they were incorrectly listed more than once

Work-Life-Balance für junge Mütter. Neue Bildungsansätze und bildungspolitische Reformbedarfe zur Förderung von Kompetenz und Partizipation

Der Beitrag nimmt [die Problematik der Work-Life-Balance für junge Mütter] aus theoretischer und empirischer Perspektive auf. Es werden vier Zugänge gewählt: Der erste Schritt zeigt statistische Befunde zur sozioökonomischen Situation junger Mütter auf, die in einem zweiten Schritt mit der Darstellung von biografischen Dispositionen und subjektiven Perspektiven junger Mütter zu Motiven, zu Leitbildern und zu Strategien der Alltagsgestaltung verbunden werden. Ein dritter Strang thematisiert Bildungsentwürfe und Entwicklungen im Bereich der Ausbildung, wobei insbesondere Perspektiven neuer Zeitmodelle in den Blick geraten. In einem vierten Schritt werden Anforderungen an Kinderbetreuung und Qualitätsentwicklung diskutiert. In der Gesamtperspektive besteht ein doppeltes Ziel: Ansätze zur Schaffung von Bildungs- und Partizipationsräumen für junge Mütter und ihre Kinder aufzuzeigen sowie neue gesellschaftliche und pädagogische Konzepte zur Überwindung von Geschlechtertypisierungen und zur Realisierung von Work-Life-Balance auch für junge Mütter anzuregen. (DIPF/Orig.