Die Schweizer Versicherungsbranche 2015 : Entwicklungen und ihre Auswirkungen auf die Soll-Kompetenzen

Die vorliegende Studie ist das Resultat aus einer Serie von Interviews, die 2010 mit rund 20 Vertreterinnen und Vertretern der Versicherungswirtschaft geführt wurden. Dabei stand die Frage im Zentrum, welche Faktoren die Schweizer Versicherungsbranche in den nächsten fünf Jahren prägen werden und was dies für die zukünftigen Soll-Kompetenzen der Mitarbeitenden bedeutet. Fünf zentrale Faktoren, die die Branche prägen werden: Die aus den Interviews gewonnenen Erkenntnisse wurden durch Expertinnen und Experten der Zürcher Hochschule für Angewandte Wissenschaften (ZHAW) zunächst zu Themenclustern verdichtet und mit bereits vorliegenden Analysen ergänzt. Aus der breiten Palette von Themen wurden anschliessend diejenigen Faktoren identifiziert, die die Branche in den nächsten Jahren prägen werden: - die Technologie - Regulierung und Recht - der brancheninterne Wettbewerb - der Vertrieb - der Kunde Drei mögliche Szenarien: Diese Faktoren – Schlüsselfaktoren genannt – können sich unterschiedlich entwickeln. In dieser Studie wurden pro Schlüsselfaktor zwei mögliche Entwicklungstrends definiert und gegenübergestellt. Anschliessend wurden diese möglichen Entwicklungstrends zu verschiedenen Szenarien gruppiert: 1. Im Basisszenario, das dem erwarteten Trend entspricht, entwickeln sich die Schlüsselfaktoren in bekannten Bahnen. 2. Im Technologieszenario wird davon ausgegangen, dass der Einsatz von Technologie einen Quantensprung erlebt. 3. Im Anpassungsszenario wird von massiv verschärften rechtlichen und regulatorischen Vorschriften bezüglich Risikofähigkeit und Transparenz ausgegangen. Strategische Optionen: Diese Szenarien unterscheiden sich nicht grundsätzlich, sondern hauptsächlich in der Radikalität der Ausprägung des einen oder anderen Schlüsselfaktors. Bewegt sich die Branche in bekannten Bahnen, zeigen sich für die Versicherer doch vielfältige strategische Möglichkeiten, sich im Wettbewerb zu positionieren. In dieser Studie stellen wir vier solcher strategischen Optionen vor und diskutieren ihre spezifischen Auswirkungen auf die zukünftigen Soll-Kompetenzen der Mitarbeitenden. Generell erwarten wir einen stärkeren Fokus auf: - Schnittstellenskills und vernetztes Handeln - Kommunikations- und Konfliktfähigkeiten - Flexibilität und Anpassungsfähigkei

IκB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-κB in the central nervous system

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, IκB kinase/nuclear factor kappa B signalling regulates peripheral myelin formation by Schwann cells, however, its role in myelin formation in the central nervous system during health and disease is largely unknown. Surprisingly, we found that brain-specific IκB kinase 2 expression is dispensable for proper myelin assembly and repair in the central nervous system, but instead plays a fundamental role for the loss of myelin in the cuprizone model. During toxic demyelination, inhibition of nuclear factor kappa B activation by conditional ablation of IκB kinase 2 resulted in strong preservation of central nervous system myelin, reduced expression of proinflammatory mediators and a significantly attenuated glial response. Importantly, IκB kinase 2 depletion in astrocytes, but not in oligodendrocytes, was sufficient to protect mice from myelin loss. Our results reveal a crucial role of glial cell-specific IκB kinase 2/nuclear factor kappa B signalling for oligodendrocyte damage during toxic demyelination. Thus, therapies targeting IκB kinase 2 function in non-neuronal cells may represent a promising strategy for the treatment of distinct demyelinating central nervous system disease

New Variant of MELAS Syndrome With Executive Dysfunction, Heteroplasmic Point Mutation in the MT-ND4 Gene (m.12015T>C; p.Leu419Pro) and Comorbid Polyglandular Autoimmune Syndrome Type 2

Background: Mitochondrial diseases are caused by dysfunctions in mitochondrial metabolic pathways. MELAS syndrome is one of the most frequent mitochondrial disorders; it is characterized by encephalopathy, myopathy, lactic acidosis, and stroke-like episodes. Typically, it is associated with a point mutation with an adenine-to-guanine transition at position 3243 of the mitochondrial DNA (mtDNA; m.3243A>G) in the mitochondrially encoded tRNA leucine 1 (MT-TL1) gene. Other point mutations are possible and the association with polyglandular autoimmune syndrome type 2 has not yet been described.Case presentation: We present the case of a 25-year-old female patient with dysexecutive syndrome, muscular fatigue, and continuous headache. Half a year ago, she fought an infection-triggered Addison crisis. As the disease progressed, she had two epileptic seizures and stroke-like episodes with hemiparesis on the right side. Cerebral magnetic resonance imaging showed a substance defect of the parieto-occipital left side exceeding the vascular territories with a lactate peak. The lactate ischemia test was clearly positive, and a muscle biopsy showed single cytochrome c oxidase-negative muscle fibers. Genetic testing of blood mtDNA revealed a heteroplasmic base exchange mutation in the mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 4 (MT-ND4) gene (m.12015T>C; p.Leu419Pro; heteroplasmy level in blood 12%, in muscle tissue: 15%). The patient suffered from comorbid autoimmune polyglandular syndrome type 2 with Hashimoto's thyroiditis, Addison's disease, and autoimmune gastritis. In addition, we found increased anti-glutamic acid decarboxylase 65, anti-partial cell, anti-intrinsic factor, and anti-nuclear antibodies.Conclusion: We present an atypical case of MELAS syndrome with predominant symptoms of a dysexecutive syndrome, two stroke-like episodes, and fast-onset fatigue. The symptoms were associated with a not yet described base and aminoacid exchange mutation in the MT-ND4 gene (m.12015T>C to p.Leu419Pro). The resulting changed protein complex in our patient is part of the respiratory chain multicomplex I and might be the reason for the mitochondriopathy. However, different simulations for pathogenetic relevance are contradictory and rather speak for a benign variant. To our knowledge this case report is the first reporting MELAS syndrome with comorbid polyglandular autoimmune syndrome type 2. Screening for autoimmune alterations in those patients is important to prevent damage to end organs

Cross-Species Single-Cell Analysis Reveals Divergence of the Primate Microglia Program

Summary Microglia, the brain-resident immune cells, are critically involved in many physiological and pathological brain processes, including neurodegeneration. Here we characterize microglia morphology and transcriptional programs across ten species spanning more than 450 million years of evolution. We find that microglia express a conserved core gene program of orthologous genes from rodents to humans, including ligands and receptors associated with interactions between glia and neurons. In most species, microglia show a single dominant transcriptional state, whereas human microglia display significant heterogeneity. In addition, we observed notable differences in several gene modules of rodents compared with primate microglia, including complement, phagocytic, and susceptibility genes to neurodegeneration, such as Alzheimer’s and Parkinson’s disease. Our study provides an essential resource of conserved and divergent microglia pathways across evolution, with important implications for future development of microglia-based therapies in humans

From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways

The human body hosts an enormous abundance and diversity of microbes, which perform a range of essential and beneficial functions. Our appreciation of the importance of these microbial communities to many aspects of human physiology has grown dramatically in recent years. We know, for example, that animals raised in a germ-free environment exhibit substantially altered immune and metabolic function, while the disruption of commensal microbiota in humans is associated with the development of a growing number of diseases. Evidence is now emerging that, through interactions with the gut-brain axis, the bidirectional communication system between the central nervous system and the gastrointestinal tract, the gut microbiome can also influence neural development, cognition and behaviour, with recent evidence that changes in behaviour alter gut microbiota composition, while modifications of the microbiome can induce depressive-like behaviours. Although an association between enteropathy and certain psychiatric conditions has long been recognized, it now appears that gut microbes represent direct mediators of psychopathology. Here, we examine roles of gut microbiome in shaping brain development and neurological function, and the mechanisms by which it can contribute to mental illness. Further, we discuss how the insight provided by this new and exciting field of research can inform care and provide a basis for the design of novel, microbiota-targeted, therapies.GB Rogers, DJ Keating, RL Young, M-L Wong, J Licinio, and S Wesseling

Praxisorientierung auf Hochschulstufe

Die Vorteile von berufsbegleitender Weiterbildung in der Versicherungsbranche liegen auf der Hand: Durch den Einsatz von erfahrenen Lehrkräften aus der Praxis und die Anwendung neuster Erkenntnisse der Forschung auf reale Fallbeispiele ergeben sich Synergien

Vermögensverwalter unter Zugzwang

Die Branche der unabhängigen Vermögensverwalter (uVV) wuchs in der Vergangenheit stetig, das Geschäft florierte. Die zunehmende Regulierungsdichte und die Relativierung des Bankkundengeheimnisses schaffen jedoch neue Voraussetzungen, die kleinere und mittlere uVV vor Probleme stellen. Der Trend geht klar in Richtung grössere Einheiten

Neuropathological evaluation of a vertebrate brain aged ~ 245 years

Multiple sclerosis (MS) is the most frequent demyelinating disease in young adults and despite significant advances in immunotherapy, disease progression still cannot be prevented. Promotion of remyelination, an endogenous repair mechanism resulting in the formation of new myelin sheaths around demyelinated axons, represents a promising new treatment approach. However, remyelination frequently fails in MS lesions, which can in part be attributed to impaired differentiation of oligodendroglial progenitor cells into mature, myelinating oligodendrocytes. The reasons for impaired oligodendroglial differentiation and defective remyelination in MS are currently unknown. To determine whether intrinsic oligodendroglial factors contribute to impaired remyelination in relapsing-remitting MS (RRMS), we compared induced pluripotent stem cell-derived oligodendrocytes (hiOL) from RRMS patients and controls, among them two monozygous twin pairs discordant for MS. We found that hiOL from RRMS patients and controls were virtually indistinguishable with respect to remyelination-associated functions and proteomic composition. However, while analyzing the effect of extrinsic factors we discovered that supernatants of activated peripheral blood mononuclear cells (PBMCs) significantly inhibit oligodendroglial differentiation. In particular, we identified CD