bluuebunny/crossref_metadata_2025_split huggingface dataset:
Somatische Komorbidität bei Schizophrenie: Unentdeckt und unbehandelt?
Authors: Wobrock T. , Falkai P. , Hasan A. 
Published: September 2018

ZusammenfassungSomatische Begleiterkrankungen bei schizophren Erkrankten sind sehr häufig und eine wesentliche Ursache für die erhöhte Mortalität dieser schweren psychiatrischen Erkrankung. Diese Komorbiditäten umfassen eine Vielzahl von Erkrankungsgruppen, wobei das metabolische Syndrom, die koronare Herzkrankheit und Infektionskrankheiten die führenden Entitäten zu sein scheinen. Körperliche Begleiterkrankungen werden jedoch oft nicht erkannt, obwohl eine Vielzahl an wissenschaftlichen Publikationen die enorme Bedeutung dieser Erkrankungen für den Gesamtbehandlungsplan der Schizophrenie dokumentiert. Diese Übersichtsarbeit gibt eine kurze Einführung in dieses wichtige Thema und stellt anhand des metabolischen Syndroms, des Typ-2-Diabetes und der koronaren Herzkrankheit die Risiken zusätzlicher somatischer Erkrankungen dar. Darüber hinaus erfolgt eine Übersicht über andere somatische Erkrankungen bei Schizophrenie und es werden mögliche Ursachen dieser Komorbiditäten diskutiert. Zusammenfassend müssen Psychiater, Hausärzte und alle in der Behandlung der Schizophrenie involvierten Personen die Bedeutung und das Auftreten somatischer Erkrankung erkennen, um in Zukunft eine Reduktion der Mortalität zu ermöglichen.
Pregabalin – Update der klinischen Daten
Authors: Volz H.-P. 
Published: September 2018

ZusammenfassungPregabalin ist ein Modulator spannungsabhȨngiger Kalzium-KanȨle und besitzt eine Zulassung fɒr die Therapie peripherer und zentraler neuropathischer Schmerzen, als Zusatzmedikation (add-on) bei partiellen epileptischen AnfȨllen und fɒr die Therapie der Generalisierten AngststɆrung (Generalized Anxiety Disorder [GAD]). Die wichtigsten klinischen Studien hierzu wurden in einer ersten Publikation in dieser Zeitschrift (15) dargestellt. Nun werden einige, seinerzeit nur kurz oder ɒberhaupt nicht behandelte Publikationen zu folgenden Themen erɆrtert: 1. Vergleich Pregabalin vs. Venlafaxin retardiert vs. Placebo (6); 2. Vergleich Pregabalin vs. Placebo bei Ȩlteren GAD-Patienten (11); 3. Pregabalin als „add-on舠 bei Therapie- resistenten GAD-Patienten (13); 4. Pregabalin vs. Placebo beim Ausschleichen von Benzodiazepinen (4); 5. Meta-Analyse pharmakotherapeutischer Interventionen bei GAD (5).
Neurobiology of severe psychiatric disorders – new approaches in the molecular research landscape
Authors: Reich-Erkelenz D. , Schmitt A. , Gruber O. , Dechent P. , Brockmöller J. , Tzvetkov M. , Fischer A. , Bickeböller H. , Rossner M. , Nave K.-A. , Falkai P. , Schulze T. G. 
Published: September 2018

SummaryOver many years, intensive research into the molecular biological basis of psychosis (schizophrenia, bipolar disorder) has been conducted via complementary approaches of clinical and molecular biological techniques and strategies, be it linkage analyses, candidate gene association studies, pharmacogenetics, neuroimaging, or further neurobiological investigations in post-mortem tissue and animal models for risk factors of the diseases.However, since these approaches could not successfully explain the very heterogeneous disease pattern of schizophrenia or its overlapping spectra with bipolar disorder, we are in the need of a new perspective. Biological psychiatric research has largely focused on cross-sectional data sets without focusing on a phenotype of utmost relevance: the longitudinal course. Large-scale and systematic studies on the genetic and neurobiological underpinnings of the course of psychosis within a framework are lacking. To fill this gap, we are currently establishing such a framework via the DFG funded Clinical Research Group “Genotype-phenotype relationships and neurobiology of the longitudinal course of psychosis”. Here we will establish large cohorts with this phenotype of interest that is longitudinal in nature and also includes information on functional parameters and environmental factors.
Die Rolle von Qualitätsindikatoren in der psychiatrischen Qualitätssicherung und aktueller Stand der Entwicklung von Qualitätsindikatoren
Authors: Zielasek J. , Großimlinghaus I. , Janssen B. , Wobrock T. , Falkai P. , Reich-Erkelenz D. , Riesbeck M. , Gaebel W. 
Published: September 2018

ZusammenfassungDie Entwicklung von sektorenübergreifenden Qualitätsindikatoren für die Versorgung von Menschen mit psychischen Störungen wurde durch den Gemeinsamen Bundesausschuss auf den Weg gebracht. Wir beschreiben diese aktuelle Entwicklung und informieren über den Stand des Projektes zur Entwicklung von Qualitätsindikatoren durch die DGPPN für vier häufige psychische Störungen: Schizophrenie, Demenzen, Alkoholabhängigkeit und unipolare Depressionen.
Schulenorientierte versus Störungsorientierte Psychotherapien in der Psychiatrie
Authors: Berger M. , Hohagen F. 
Published: September 2018

ZusammenfassungDie frühe Phase der Psychotherapieentwicklungen war ganz geprägt von den großen Schulen der Psychoanalyse, Tiefenpsychologie und Verhaltenstherapie. Dementsprechend waren auch die Zulassungsprinzipien der so genannten Richtlinienpsychotherapie ganz auf die Psychotherapieschulen zugeschnitten. In den letzten Dekaden hat sich in der psychotherapeutischen Forschung und Praxis dagegen in weiten Bereichen eine störungsfokussierte Psychotherapie mehr und mehr durchgesetzt, welche, fokussiert auf die psychopathologischen aber auch pathogenetischen Besonderheiten verschiedener konkreter Störungsbilder, psychotherapeutische Elemente aus den unterschiedlichen Schultraditionen symptomzentriert integriert.In diesem Artikel wird diese Entwicklung exemplarisch nachgezeichnet und auf die Notwendigkeit hingewiesen, dass diese Entwicklungen in der psychotherapeutischen Praxis auch ihre Entsprechung im gesundheitspolitischen Zulassungsreglementarium finden sollte.
Modulare Psychotherapie – Rationale und Grundprinzipien
Authors: Bohus M. , Herpertz S. C. , Falkai P. 
Published: September 2018

ZusammenfassungDie Weiterentwicklung der Psychotherapie hat in den letzten Jahren unerwartet Tempo aufgenommen, doch in der Praxis kommt diese kaum an. Wie sollen Therapeuten die Orientierung behalten, wenn jedes Jahr Dutzende von neuen, evidenzbasierten störungsspezifischen Therapien auf den Markt kommen? Wie können experimentell entwickelte therapeutische Strategien in die tägliche Praxis integriert werden, und wie sollte die Aus- und Weiterbildung in Psychotherapie organisiert werden? Modulare Psychotherapie will Antwort geben auf diese Fragen. Dabei ist Modulare Psychotherapie keine neue Schule, sondern ein duales Organisationsprinzip: Einerseits eine pragmatische Gliederung der derzeit etablierten therapeutischen Strategien und Interventionen und andererseits eine Handreichung in Form von Heurismen, die vorgibt, welche dieser Strategien im Einzelfall zur Anwendung kommen sollten. Die Modulare Psychotherapie erhebt folgerichtig den Anspruch, die Enge der therapeutischen Schulen zu verlassen und den Redundanzen der störungsspezifischen Konzepte einen entsprechenden Rahmen zu geben. Didaktisch gliedert sich die Modulare Psychotherapie in sechs Komponenten: Theoretische Grundlagen; Therapeutische Basiskompetenzen; Therapeutische Interventionen; Störungsspezifische Kompetenzen; Behandlungsheurismen und evaluative Kompetenzen. Was die Aus- und Weiterbildung anbelangt, so arbeitet die DGPPN derzeit an einer Neuausrichtung der Facharztweiterbildung Psychiatrie und Psychotherapie und orientiert sich an den Grundideen der Modularen Psychotherapie.
IL-33 promotes recovery from acute colitis by inducing miR-320 to stimulate epithelial restitution and repair
Authors: Lopetuso Loris R. , De Salvo Carlo , Pastorelli Luca , Rana Nitish , Senkfor Henry N. , Petito Valentina , Di Martino Luca , Scaldaferri Franco , Gasbarrini Antonio , Cominelli Fabio , Abbott Derek W. , Goodman Wendy A. , Pizarro Theresa T. 
Published: September 2018

Significance
We clarify that the normal, inherent function of IL-33 following acute, resolving colitis is protection, inducing proliferation and restitution of ST2L-bearing intestinal epithelial cells (IECs). Importantly, this response occurs in otherwise healthy, immunocompetent C57BL/6J (B6) mice and may be different in other models possessing genetic and/or immunologic abnormalities that predispose to colitis, similar to patients with inflammatory bowel disease. Mechanistically, although the molecular processes responsible for control of microRNA (miR) biogenesis in response to challenge remain largely unknown, we report that IL-33 augments epithelial miR-320, which increases IEC proliferation and wound closure that is significantly diminished upon specific miR-320 inhibition. This study provides the rationale for the potential therapeutic use of either IL-33 or miR-320A to obtain optimal gut mucosal healing and the resolution of inflammation.
Behavior of homing endonuclease gene drives targeting genes required for viability or female fertility with multiplexed guide RNAs
Authors: Oberhofer Georg , Ivy Tobin , Hay Bruce A. 
Published: September 2018

Significance
Homing endonuclease gene (HEG)-based gene drive can bring about population suppression when genes required for viability or fertility are targeted. However, these strategies are vulnerable to failure through mechanisms that create alleles resistant to cleavage but that retain wild-type gene function. We show that resistance allele creation can be prevented through the use of guide RNAs designed to cleave a gene at four target sites. However, homing rates were modest, and the HEGs were unstable during homing. In addition, use of a promoter active in the female germline resulted in levels of HEG carryover that compromised the viability or fertility of HEG-bearing heterozygotes, thereby preventing drive. We propose strategies that can help to overcome these problems in next-generation HEG systems.
Control of CCND1 ubiquitylation by the catalytic SAGA subunit USP22 is essential for cell cycle progression through G1 in cancer cells
Authors: Gennaro Victoria J. , Stanek Timothy J. , Peck Amy R. , Sun Yunguang , Wang Feng , Qie Shuo , Knudsen Karen E. , Rui Hallgeir , Butt Tauseef , Diehl J. Alan , McMahon Steven B. 
Published: September 2018

Significance
The deubiquitylase USP22 is frequently overexpressed in cancer and contributes to tumorigenesis by driving cell cycle progression. Current models define USP22 as functional mediator of gene regulation and chromatin modification, working within the SAGA transcriptional cofactor complex. Here we report a catalytic role for USP22 distinct from its well-characterized transcription regulatory capacity. USP22 directly stabilizes the essential G1-cyclin, CCND1, protecting it from proteasome-mediated degradation via deubiquitylation. Our findings reveal a pathway that regulates CCND1, while also raising the possibility that simulteously targeting USP22 may allow the use of less toxic doses of the new wave of cancer therapies that target the cyclin/CDK complex. Finally, these results provide a mechanistic explanation for the effects of USP22 in cancer cell cycle control.
Effects of protein size, thermodynamic stability, and net charge on cotranslational folding on the ribosome
Authors: Farías-Rico José Arcadio , Ruud Selin Frida , Myronidi Ioanna , Frühauf Marie , von Heijne Gunnar 
Published: September 2018

SignificanceThere is increasing interest to understand how proteins fold as they are synthesized on the ribosome. However, we still lack basic knowledge such as how protein size, net charge, and thermodynamic stability impact cotranslational folding. Here, we have studied eight proteins of increasing size and provide a comprehensive picture of how the location in the ribosome exit tunnel where a protein folds correlates with protein size. Moreover, we demonstrate that the force exerted on the nascent chain by protein folding varies linearly with the thermodynamic stability of the folded state, and that the ribosome environment disfavors folding of domains of high net-negative charge. These findings establish important basic facts about cotranslational folding.
Praxis, symbol and language
Authors: Sinha Chris 
Published: September 2018

AbstractThis article focuses on the interweaving of constructive praxis with communication inontogenesis, inphylogenesisand in biocultural niche evolution (ecogenesis), within anEvoDevoSocioframework. I begin by discussing the nature of symbolization, its evolution from communicative signaling and its elaboration into semantic systems. I distinguish between thesymbol-readyand thelanguage-readybrain, leading to a discussion of linguistic conceptualization and itsdual groundingin organism and language system. There follows an outline account of the interpenetration in the human biocultural niche-complex ofsemiosphereandtechnosphere,mediated by the evolution of the niche of infancy. Symbolization (the foundation of the semiosphere) is by definition normative; the normative character of the technosphere is demonstrated by the interrelations in human development between affordance, action schema and canonical functional object schema. A model of the neuro-computational implementation of dual grounding is proposed.
Relating the evolution of Music-Readiness and Language-Readiness within the context of comparative neuroprimatology
Authors: Seifert Uwe 
Published: September 2018

AbstractLanguage- and music-readiness are demonstrated as related within comparative neuroprimatology by elaborating three hypotheses concerning music-readiness (MR): The (musicological) rhythm-first hypothesis (MR-1), the combinatoriality hypothesis (MR-2), and the socio-affect-cohesion hypothesis (MR-3). MR-1 states that rhythm precedes evolutionarily melody and tonality. MR-2 states that complex imitation and fractionation within the expanding spiral of the mirror system/complex imitation hypothesis (MS/CIH) lead to the combinatorial capacities of rhythm necessary for building up a musical lexicon and complex structures; and rhythm, in connection with repetition and variation, scaffolds both musical form and content. MR-3 states that music’s main evolutionary function is to self-induce affective states in individuals to cope with distress; rhythm, in particular isochrony, provides a temporal framework to support movement synchronization, inducing shared affective states in group members, which in turn enhances group cohesion. This document reviews current behavioural and neurocognitive research relevant to the comparative neuroprimatology of music-readiness. It further proposes to extend MS/CIH through the evolution of the relationship of the language- and music-ready brain, by comparing “affective rhythm” and prosody – i.e. by comparatively approaching the language- and music-emotion link in neuroprimatology.
Social manipulation, turn-taking and cooperation in apes
Authors: Rossano Federico 
Published: September 2018

AbstractThis paper outlines how the focus on how communicative signals might emerge and how the capacity to interpret them might develop, does not yet explain what type of motivation is required to actually deal with those signals. Without the consistent production of appropriate responses to the production of communicative signals, there would be no point in producing any signal. If language is a tool to accomplish things with others, we need to understand what would lead to cooperation. The first step consists in avoiding the blind belief that all cooperation requires some prosocial attitude. A great deal of cooperation can occur while each participant in the interaction is selfishly attempting to maximize their own benefits or minimizing damaging consequences.I describe how different types of turn-taking can be achieved via different levels of cognitive complexity and how interpretive turn-taking requires a great deal of cognitive abilities that great apes possess. Finally, I provide empirical evidence of social manipulation in non-human primates. Given our awareness of the occurrence of social manipulation during cooperation among human adults, it seems necessary to reconsider to what degree human communication and language evolution require unique prosocial motivations.
Why do we want to talk?
Authors: Semendeferi Katerina 
Published: September 2018

Abstract
Cognitive and emotional processes are now known to be intertwined and thus the limbic system that underlies emotions is important for human brain evolution, including the evolution of circuits supporting language. The neural substrates of limbic functions, like motivation, attention, inhibition, evaluation, detection of emotional stimuli and others have changed over time. Even though no new, added structures are present in the human brain compared to nonhuman primates, evolution tweaks existing structural systems with possible functional implications. Empirical comparative neuroanatomical evidence is presented here in support of such changes in the limbic system, including the amygdala and the orbitofrontal cortex. Given their possible functional significance, these alterations may further enable and enhance human interest and motivation to communicate beyond what is seen in other primates living in complex social groups. The argument here is that even though emotion processing is likely needed for increased social complexity independent of language, the reason why humans want to talk may be related in part to the enhancement of socioemotional processes resulting from the reorganization and rewiring of underlying neural systems some of which are interconnected to the language areas. Neurodevelopmental disorders in humans affecting both language and sociability fuel such arguments.
Inhibition of TLR9-NF-κB-mediated sterile inflammation improves pressure overload-induced right ventricular dysfunction in rats
Authors: Yoshida Keimei , Abe Kohtaro , Ishikawa Mariko , Saku Keita , Shinoda-Sakamoto Masako , Ishikawa Tomohito , Watanabe Takanori , Oka Masahiko , Sunagawa Kenji , Tsutsui Hiroyuki 
Published: September 2018

AbstractAimsRecent accumulating evidence suggests that sterile inflammation plays a crucial role in the progression of various cardiovascular diseases. However, its contribution to right ventricular (RV) dysfunction remains unknown. The aim of this study was to elucidate whether toll-like receptor 9 (TLR9)-NF-κB-mediated sterile inflammation plays a critical role in the pathogenesis of RV dysfunction.Methods and resultsWe performed main pulmonary artery banding (PAB) in rats to induce RV pressure overload and dysfunction. On Day 14 after PAB, the pressure overload impaired RV function as indicated by increased RV end-diastolic pressure concomitant with macrophage infiltration and fibrosis, as well as maximal activation of NF-κB and TLR9. Short-term administration (days 14–16 after PAB) of a specific TLR9 inhibitor, E6446, or an NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC) significantly attenuated NF-κB activation. Furthermore, long-term administration of E6446 (treatment: days 14–28) or PDTC (prevention: days −1 to 28; treatment: days 14 to 28) improved RV dysfunction associated with mitigated macrophage infiltration and fibrosis in right ventricle and decreased serum brain natriuretic peptide levels.ConclusionInhibition of TLR9-NF-κB pathway-mediated sterile inflammation improved PAB-induced RV dysfunction in rats. This pathway plays a major role in the progression of pressure overload-induced RV dysfunction and is potentially a novel therapeutic target for the disorder.
Modern physics in the museum
Authors: Boyle Alison 
Published: September 2018

Abstract
This paper examines how modern physics was collected and displayed in the UK over the (long) twentieth century, focusing on the national collections in the Science Museum, London. The emergence and establishment of modern physics roughly overlaps with the development of distinct science and technology museums. This provides an opportunity to explore how collections are shaped in response to scientists’ own narratives of their professional identities, institutional or political priorities, and how certain aspects of the material culture of a scientific area can become closely intertwined with its public image. By tracing the movement of a well-known artefact of modern physics – a cathode-ray tube used by J. J. Thomson in his ‘electron’ experiments – I show how collection boundaries could be porous, although overall collection framings persisted.
Elites and emulators: The evolution of Iraqi Kurdish asylum migration to Europe
Authors: Paasche Erlend 
Published: September 2018

AbstractResearch on migration’s internal dynamics has focused on labour migration and drawn heavily on cumulative causation theory. It is often believed that pioneer labour migrants of middling socioeconomic selectivity facilitate the migration of others in their networks by reducing the costs and risks of migration through practical assistance. Expanding migrant networks can allow for labour migration to grow although macrostructural conditions change. For asylum migration in the context of armed conflict, the mechanisms whereby migration grows may very well differ. For one thing, pioneer asylum migrants in such contexts are often social elites. What is the relationship between the movement of these elites and that of subsequent asylum migrants? This article traces the evolution of Iraqi Kurdish asylum migration to Europe from its inception by elite pioneer migrants to its continuation by non-elites, during four decades of altered contextual conditions. The analysis is based on 106 semi-structured interviews with Iraqi Kurdish migrants. An evolving interplay between exogenous and endogenous dynamics is observed, and so are commonalities with the social processes that underpin labour migration. The basic principles of cumulative causation seem to be operating, yet there is little to indicate that established migrants functioned as ‘bridgeheads’ for newcomers. The empirical analysis feeds into a concluding conceptual discussion in which I argue that, compared to labour migration, asylum migration from conflict-affected areas may be relatively less driven by the interpersonal networks that reduce costs and risks, and relatively more driven by what the article coins ‘emulation’, the observational learning of migration.