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Rezensionen zu: Band 1: Gilbert Crispin : Religionsgespräche mit einem Juden und einem Heiden, Lateinisch-Deutsch, übersetzt und eingeleitet von Karl Werner Wilhelm und Gerhard Wilhelmi, Freiburg / Basel / Wien 2005, Herder Verlag, ISBN 3-451-28506-1, 197 Seiten, 32 Euro. Band 2: Ibn Sab'in : Die Sizilianischen Fragen ; Arabisch-Deutsch, übersetzt und eingeleitet von Anna Akasoy, Freiburg / Basel / Wien 2005, Herder Verlag, ISBN 3-451-28505-3, 252 Seiten, 34 Euro. Band 4: Johannes Duns Scotus : Pariser Vorlesungen über Wissen und Kontingenz ; Lateinisch-Deutsch, übersetzt und eingeleitet von Joachim R. Söder, Freiburg/ Basel / Wien 2005, Herder Verlag, ISBN 3-451-28686-6, 215 Seiten, 29,50 Euro.
Vascular occlusive diseases are one of the leading mortality causes in westernised countries. Occlusions of one of the major arteries can be overcome without devastating consequences provided a timely induction of compensating collateral arteries occurs. Perhaps the most outstanding feature of collateral vessel growth is the proliferation of smooth muscle cells (SMCs). Understanding the molecular mechanisms and identifying key molecular players of SMC proliferation would contribute significantly to the development of efficient therapies to intervene with all processes involving neointima formation, including collateral growth. mRNA and protein coding for co-transcription factor Egr1 were found to be up-regulated in growing collateral vessels 6, 12 or 24 hours following femoral artery ligation in mice. Since Egr1 is required for SMC proliferation in vitro and in vivo and likely to be implicated in the initiation of collateral artery growth, the key signalling mediators regulating Egr1 expression specifically in proliferating vascular SMCs were investigated. Northern blot and Western blot analysis revealed a strong up-regulation of Egr1 within 2 hours of stimulation with PDGF-AB and FGF-2. These two potent SMC mitogens involved in neointima formation were used to stimulate vascular SMCs not only to delineate the regulators of Egr1 expression but also to identify additional key mediators of SMC proliferation. FGF-2 but not PDGF-AB led to a drastic reduction of desmin amount in proliferating SMCs, correlating closely with the phenotypic modulation of SMCs in vivo. Both growth factors triggered a dramatic increase in DNA-synthesis rate with a concomitant loss of p27 exp Kip1. Stimulation with PDGF-AB and FGF-2 triggered a rapid and transient activation of PDGFRβ and FGFR1 respectively, thus providing the basis for activation of down-stream targets. Analysis of an array of signalling pathways demonstrated a strong activation of the Ras-Raf-MEK-ERK cascade in response to both factors as measured by the level of phosphorylation of prominent members MEK, ERK1/2 and c-Myc. SAPK/JNK and p38, which also belong to the superfamily of MAP kinases, did not become activated following stimulation with either PDGF-AB or FGF-2. The analysis of various PKC isoforms identified PKCδ and PKCθ to be the key mediators of PDGF-AB- and FGF-2-induced mitogenesis in proliferating SMCs. Whereas PDGF-AB potently stimulated PKB/Akt with concomitant GSK3β phosphorylation, FGF-2-induced inactivation of GSK3β was independent of PKB/Akt. Specific inhibition in order to evaluate the contribution of individual pathways to Egr1 expression and vascular SMC proliferation revealed that inhibition of the Raf-MEK-ERK module by UO126 completely abolished DNA-synthesis and Egr1 expression without a compensation by alternative pathways. Surprisingly, inhibition of PI3K led to a switch to the mitogenic RafMEK-ERK signalling cascade which resulted in an augmented Egr1 expression. In conclusion, in porcine vascular SMCs, activation of the Ras-Raf-MEK-ERK signalling module appears to be the main prerequisite for Egr1 expression and DNA synthesis induction in response to PDGF-AB and FGF-2 whereas related kinases SAPK/JNK and p38 play no significant role. Inhibition of the PI3K-Akt cascade represents an alternative way to activate ERK1/2 and induce Egr1 expression. Whereas MEK is the central regulator of mitogenic effects in proliferating vascular SMCs, the PI3K-Akt pathway most likely exerts survival function. Inactivation of MEK by its specific inhibitors identified hyperphosphorylation as ayet unknown mechanism of kinase inhibition.
Cette recherche retrace l’histoire de la fondation des musées en France englobant les périodes du Directoire, du Consulat et de l’Empire. Cette création des musées se fait à travers des envois gouvernementaux de tableaux à plusieurs villes périphériques. Elle est intimement liée au dit « Décret Chaptal », l’arrêté consulaire du 14 fructidor an IX (1er septembre 1801) qui lance quinze envois dans différentes villes dont Bruxelles, Genève et Mayence, alors considérées comme parties intégrantes du territoire national. Ma thèse est présentée en trois parties, pour valoriser le rôle singulier de Chaptal. Le dépouillement des archives fournit un récit détaillé des prémices de cette politique, de la conception du texte et de la mise en œuvre de cet arrêté avant, pendant et après le Ministère Chaptal. Leur analyse ouvre des perspectives nouvelles sur la politique muséologique initiée par Chaptal dans la continuité des Lumières.
Background: Prolonged Grief Disorder (PGD) is a distinct syndrome that follows bereavement. It is different from other mental disorders and is characterized by symptoms such as yearning for the bereaved, or intense emotional pain or distress. Violent loss is one major risk factor for the development of PGD.
Objectives: PGD has been studied in different populations, mostly in small samples, with only a few of them being representative. Although research highlighted that traumatic experiences paired with challenges related to migration make refugees particularly vulnerable to PGD, PGD has only rarely been studied in refugees. Thus, this article a) examines the prevalence of PGD in female refugees in Germany according to the criteria proposed by Prigerson and colleagues in 2009, and b) associates PGD with other common psychopathology (e.g. anxiety, depression, somatization and trauma).
Method: A total of 106 female refugees were assessed for bereavement and PGD. Of these 106 individuals, 85 were interviewed using the Prolonged Grief Disorder Scale (PG-13). Symptoms of anxiety and depression were assessed by the Hopkins Symptom Checklist-25 (HSCL-25), somatization was assessed by the Somatization Subscale of the Symptom-Checklist-90 (SCL-90), and the number of witnessed and experienced trauma was assessed by the Posttraumatic Diagnostic Scale (PDS/HTQ).
Results: Ninety of the 106 participants had experienced bereavement, and among those, 9.41% met criteria for PGD. The most frequent PGD symptoms were bitterness, longing or yearning for the bereaved, and lack of acceptance of the loss. Furthermore, grief symptoms were significantly associated with symptoms of depression, anxiety, somatization, and the number of experienced traumatic events.
Conclusion: The PGD prevalence rate found corresponds with previous studies, demonstrating that prevalence rates for PGD are especially high in refugees. High prevalence rates of bereavement as well as PGD highlight the need for assessment and specifically tailored treatment of PGD in refugees. PGD goes along with significant psychopathology, which further emphasizes the need for treatment.