63 research outputs found

    The Sultan's Jew

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    Der Text stellt die deutsche Übersetzung einer von Ramdane Mesbah Idrissi auf Arabisch verfassten Rezension dar. Idrissi bespricht die im Jahr 2011 bei 'Editions & Impression Bouregreg' in Rabat/Marokko erschienene arabische Übersetzung von Daniel J. Schroeters 'The Sultan's Jew. Morocco and the Sephardi world' (Stanford/CA: Stanford University Press 2002). Schroeter ist Professor für Zeitgeschichte an der Universität Minnesota in den USA und ausgewiesener Experte für die Geschichte des marokkanischen Judentums und seiner internationalen Verflechtung, insbesondere im 18. Jahrhundert. Der Rezensent Ramdane Mesbah Idrissi aus Kénitra in Marokko ist ein pensionierter Schulinspektor, der aus dem Französischen ins Arabische übersetzt hat und zurzeit einen eigenen Blogg unterhält. Die arabische Übersetzung von Schroeters 'The Sultan's Jew' wurde von Khalid Ben-al-Srhir, Professor für Zeitgeschichte an der Universität Mohammed V. in Rabat-Agdal, besorgt. Idrissis auf Arabisch verfasste Rezension wurde von Friedhelm Hoffmann, Tübingen, ins Deutsche übertragen.This is the German translation of a review of the Arabic translation of Daniel J. Schroeter's 'The Sultan's Jew. Moroco and the Sephardi World' (Stanford/CA 2002), which was published in 2011 in Rabat/Morocco by 'Editions & Impression Bouregreg'. Ramdane Mesbah Idrissi wrote his review in Arabic and published it on his personal blog. This was afterwards translated from Arabic to German by Friedhelm Hoffmann, Tübingen. Background information in Arabic on Ramdane Mesbah Idrissi's review is provided on page VI of the document

    Soluble NgR Fusion Protein Modulates the Proliferation of Neural Progenitor Cells via the Notch Pathway

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    NogoA, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein are CNS myelin molecules that bind to the neuronal Nogo-66 receptor (NgR) and inhibit axon growth. The NgR antagonist, soluble NgR1-Fc protein (sNgR-Fc), facilitates axon regeneration by neutralizing the inhibitory effects of myelin proteins in experimental models of CNS injury. Here we aim to investigate the effect of sNgR-Fc on the proliferation of neural progenitor cells (NPCs). The hippocampus cells of embryonic rats were isolated and cultured in vitro. The expression of nestin, βIII-Tubulin, GFAP and Nogo-A on these cells was observed using immunocytochemistry. In order to investigate the effect on proliferation of NPCs, sNgR-Fc, MAG-Fc chimera and Notch1 blocker were added respectively. The total cell number for the proliferated NPCs was counted. BrdU was applied and the rate of proliferating cells was examined. The level of Notch1 was analyzed using Western blotting. We identified that NogoA is expressed in NPCs. sNgR-Fc significantly enhanced the proliferation of NPCs in vitro as indicated by BrdU labeling and total cell count. This proliferation effect was abolished by the administration of MAG suggesting specificity. In addition, we demonstrate that sNgR-Fc is a potent activator for Notch1 and Notch1 antagonist reversed the effect of sNgR-Fc on NPC proliferation. Our results suggest that sNgR-Fc may modulate Nogo activity to induce NPC proliferation via the Notch pathway

    Genetic architecture of subcortical brain structures in 38,851 individuals

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    Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease

    Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence

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    About one-third of people with major depressive disorder (MDD) fail at least two antidepressant drug trials at 1 year. Together with clinical and experimental evidence indicating that the pathophysiology of MDD is multifactorial, this observation underscores the importance of elucidating mechanisms beyond monoaminergic dysregulation that can contribute to the genesis and persistence of MDD. Oxidative stress and neuroinflammation are mechanistically linked to the presence of neurovascular dysfunction with blood-brain barrier (BBB) hyperpermeability in selected neurological disorders, such as stroke, epilepsy, multiple sclerosis, traumatic brain injury, and Alzheimer’s disease. In contrast to other major psychiatric disorders, MDD is frequently comorbid with such neurological disorders and constitutes an independent risk factor for morbidity and mortality in disorders characterized by vascular endothelial dysfunction (cardiovascular disease and diabetes mellitus). Oxidative stress and neuroinflammation are implicated in the neurobiology of MDD. More recent evidence links neurovascular dysfunction with BBB hyperpermeability to MDD without neurological comorbidity. We review this emerging literature and present a theoretical integration between these abnormalities to those involving oxidative stress and neuroinflammation in MDD. We discuss our hypothesis that alterations in endothelial nitric oxide levels and endothelial nitric oxide synthase uncoupling are central mechanistic links in this regard. Understanding the contribution of neurovascular dysfunction with BBB hyperpermeability to the pathophysiology of MDD may help to identify novel therapeutic and preventative approaches

    Neuroinflammation and psychiatric illness

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