970 research outputs found
Anomalous monism and mental causality : on the debate of Donald Davidson’s philosophy of the mental
No full textThe English version of the first chapter of Erwin Rogler and Gerhard Preyer: Materialismus, anomaler Monismus und mentale Kausalität. Zur gegenwärtigen Philosophie des Mentalen bei Donald Davidson und David Lewis (2001) "Anomaler Monismus und Mentale Kausalität. Ein Beitrag zur Debatte über Donald Davidsons Philosophie des Mentalen" is a contribution to the current debates on the philosophy of the mental and mental causality initiated from Donald Davidson's philosophy with his article "Mental Events" (1970). It is the intent of the English version to give a response to the controversy among American, British and Australian philosophers in the context of a global exchange of ideas on problems understanding the mental. Contents 1. Preliminary Remarks 2. The Critique of Property-Epiphenomenalism and Counterarguments (a) The Enlargement of Nomological Reasoning (b) The Counterfactual Analysis (c) Supervenient Causality 3. Are Mental Properties real or unreal (fictive)? Abstract Things and events are fundamental entities in Davidson's ontology. Less distinct is the ontological status of properties, especially of mental types. Despite of some eliminative allusions there are weighty reasons to understand Davidson's philosophy of mind as including intentional realism. With it, the question of mental causality arises. There are two striking solutions to this problem: the epiphenomenalism of mental properties and the downward causation of mental events. Davidson cannot accept either. He claims to justify the mental as supervenient causality in order to thus integrate it into physicalism (his version of monism). But his argument at best proves the explanatory, not the causal relevance of mental properties. For this and for other reasons, Davidson fails the aspired synthesis of a sufficiently strong physicalism and the autonomy of the mental; a project whose realization is anyhow hard to achieve
Inklusive Immaterialgüterrechte
No full textAnna Rogler leistet einen Beitrag zu einer angemessenen »Exklusivitäts- und Zugangskultur« im Immaterialgüterrecht. Eines der grundsätzlichen Probleme im Kontext von Immaterialgüterrechten ist die generelle Abwägung zwischen einem angemessenen Schutz der Rechteinhaber und der Zugangsfreiheit der Allgemeinheit zu eigentumsrechtlich geschützten Gütern. Die Autorin zeigt hierzu die gegenwärtige Forschung rund um inklusive (Immaterialgüter-) Rechte auf und überprüft in dem Kontext Konzepte, wie die Public Domain, Copyleft-Lizenzen sowie das inklusive Patentsystem auf den Grad der Inklusion. Anschließend stellt die Autorin die Idee von inklusiven Rechten in einen rechtsphilosophischen Kontext und sucht innerhalb der Eigentumstheorien von John Locke und Immanuel Kant nach einer rechtstheoretischen Rechtfertigung. In dem Zusammenhang wird von Anna Rogler erstmalig eine Definition für inklusive (Immaterialgüter-) Rechte vorgeschlagen.»Inclusive Intellectual Property Rights«The author's aim is to contribute to an appropriate »exclusivity and access culture« in intellectual property law. One of the fundamental problems in the context of intellectual property rights is the general balance between adequate protection of right holders and freedom of access for the general public to proprietary rights. For this, the author shows the current research in relation to inclusive (intellectual property) rights and examines concepts, such as the public domain, copyleft licenses as well as the inclusive patent system on the degree of inclusion.Anna Rogler then puts this into a jurisprudential context and, within the property theories of John Locke and Immanuel Kant, looks for a theoretical justification for the concept of inclusive rights. In this context, the author proposes a definition for inclusive (intellectual property) rights
sj-docx-1-tag-10.1177_17562848231179335 – Supplemental material for Because I’m happy – positive affect and its predictive value for future disease activity in patients with inflammatory bowel diseases: a retrospective cohort study
No full textSupplemental material, sj-docx-1-tag-10.1177_17562848231179335 for Because I’m happy – positive affect and its predictive value for future disease activity in patients with inflammatory bowel diseases: a retrospective cohort study by Brian M. Lang, Martina Ledergerber, Sebastian Bruno Ulrich Jordi, Niklas Krupka, Luc Biedermann, Philipp Schreiner, Pascal Juillerat, Jacqueline Wyss, Stephan R. Vavricka, Jonas Zeitz, Roland von Känel, Gerhard Rogler, Niko Beerenwinkel and Benjamin Misselwitz in Therapeutic Advances in Gastroenterology</p
Supplemental Material1 - Supplemental material for Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease
No full textSupplemental material, Supplemental Material1 for Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease by Philipp Schreiner, Bahtiyar Yilmaz, Jean-Benoît Rossel, Yannick Franc, Benjamin Misselwitz, Michael Scharl, Jonas Zeitz, Pascal Frei, Thomas Greuter, Stephan R Vavricka, Valérie Pittet, Alexander Siebenhüner, Pascal Juillerat, Roland von Känel, Andrew J Macpherson, Gerhard Rogler, Luc Biedermann and on behalf of the Swiss IBD Cohort Study Group in United European Gastroenterology Journal</p
Supplemental Material2 - Supplemental material for Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease
No full textSupplemental material, Supplemental Material2 for Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease by Philipp Schreiner, Bahtiyar Yilmaz, Jean-Benoît Rossel, Yannick Franc, Benjamin Misselwitz, Michael Scharl, Jonas Zeitz, Pascal Frei, Thomas Greuter, Stephan R Vavricka, Valérie Pittet, Alexander Siebenhüner, Pascal Juillerat, Roland von Känel, Andrew J Macpherson, Gerhard Rogler, Luc Biedermann and on behalf of the Swiss IBD Cohort Study Group in United European Gastroenterology Journal</p
Supplemental Material3 - Supplemental material for Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease
No full textSupplemental material, Supplemental Material3 for Vegetarian or gluten-free diets in patients with inflammatory bowel disease are associated with lower psychological well-being and a different gut microbiota, but no beneficial effects on the course of the disease by Philipp Schreiner, Bahtiyar Yilmaz, Jean-Benoît Rossel, Yannick Franc, Benjamin Misselwitz, Michael Scharl, Jonas Zeitz, Pascal Frei, Thomas Greuter, Stephan R Vavricka, Valérie Pittet, Alexander Siebenhüner, Pascal Juillerat, Roland von Känel, Andrew J Macpherson, Gerhard Rogler, Luc Biedermann and on behalf of the Swiss IBD Cohort Study Group in United European Gastroenterology Journal</p
New therapeutic avenues for treatment of fibrosis: can we learn from other diseases?
No full textCrohn's disease (CD) is characterized by the frequent occurrence of complications, such as fibrotic strictures and subsequently the need for CD-related surgery. Chronic or recurrent inflammation is generally regarded to be a necessary precondition for the initiation of intestinal fibrosis. In this view, fibrosis is a pathologically augmented healing response to inflammation-induced mucosal tissue destruction and injury. At present, there are no approved or effective medical therapies aimed specifically at fibrosis or stricture in IBD. Indirect benefits may occur from anti-inflammatory therapies, although there is no consensus on this. Therapy for fibrosis is complicated by the fact that a wound-healing response is essential in CD and ulcerative colitis. Several pharmaceutical companies are now working on the therapy of fibrosis in other diseases. Strategies interfering with TGF-β expression and activation are promising. Pirfenidone has been studied in several clinical trials. Further therapeutic options are second-generation and wide-spectrum tyrosine kinase inhibitors. These inhibit growth factor receptor signaling, thus reducing fibrosis in animal models and some patients with tumor-associated fibrosis. At present, the development of antifibrotic therapies takes place in other diseases such as lung and liver fibrosis. This is partially due to a lack of experimental models for gut fibrosis and the fact that reliable readouts (MRI, serum markers) in patients are lacking. It will be important to test the above-mentioned newly available treatment strategies in IBD to profit from progress in other fibrotic diseases
Resolution of inflammation in inflammatory bowel disease
No full textTreatment of inflammatory bowel disease at present mainly targets mediators of inflammation to stop or suppress pro-inflammatory processes. Typical examples are steroids, suppression of T cells by thioguanine nucleotides, or antibodies against cytokines such as tumour necrosis factor, interleukin 12, or interleukin 23. In addition to suppression of inflammation, development of therapeutic strategies that support resolution of inflammation or that actively resolve inflammation might be desirable. Resolution of inflammation is now seen as an active process involving specific mediators (eg, lipid mediators or specific cytokines) that is mandatory to restore organ function and completely shut down inflammation. The molecular pathways involved in resolution of inflammation have been investigated in recent years and could be adopted in treatment strategies for inflammatory bowel disease. Among these approaches are anti-integrin strategies and means to produce or locally increase restitution or resolution factors, such as restoration of the activity of transforming growth factor-β by anti-SMAD7 antisense oligonucleotides. The potential role of inflammation-resolving lipid mediators (eg, resolvins), however, still warrants further study and clinical development. This Review focuses on the specific role of active resolution of inflammation in inflammatory bowel disease pathophysiology. Potential therapeutic targets based on these pathways are also discussed
Crohn's disease: Fistulising disease--a problem shared is a problem halved?
No full textAn international consensus on the classification, diagnosis and multidisciplinary treatment of perianal fistulising Crohn's disease has recently been published. The statement is an important starting point to address the many problems we still have with the clinical classification and treatment of fistulising Crohn's disease
The effects of NOD2/CARD15 mutations on the function of the intestinal barrier
No full textAbstractNOD2 variants have been identified to be a susceptibility factor for Crohn's disease. The NOD2 protein is an intracellular sensor of the bacterial wall product muramyl dipeptide (MDP) and activates the transcription factor NF-kappaB upon MDP-binding. NOD2 variants are associated with reduced NF-kappaB activation and reduced production of epithelial derived antibacterial peptides such as defensins. A reduced expression of defensins is described and found in patients with Crohn's disease and ulcerative colitis especially when NOD2 variants are present. Furthermore recent evidence from mouse models suggests that the ability of intestinal epithelial cells to activate NF-kappaB upon bacterial stimulation protects from mucosal inflammation.Taken together these data indicate that NOD2 mediated NF-kappaB activation, subsequent induction of anti-microbial peptides such as defensins and induction of cytokine expression are essential for the function of the intestinal barrier and for the prevention of bacterial translocation. The data indicate why a defect in the induction of this acute defense response is associated with chronic inflammation. Invading bacteria that cannot be readily detected and eliminated may start a backup mechanism of inflammation finally resulting in chronic inflammatory reaction followed by further impairment of the mucosal barrier
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