Common Man, Society and Religion in the 16th century/Gemeiner Mann, Gesellschaft und Religion im 16. Jahrhundert

Der zweisprachige Sammelband vereinigt zum Teil bahnbrechende Ergebnisse einer interdisziplinären Forschungstagung, deren Beiträge sozial-, wirtschafts-, kultur- und kirchengeschichtliche Aspekte der Frühneuzeit im Karpatenbogen aufgreifen. Basierend auf vielfach erstmals ausgewerteten Quellen bearbeiten die Beiträge aktuelle Fragestellungen und Forschungshorizonte zur Interdependenz von sozialen, ökonomischen, kulturellen und religiösen Phänomenen im Karpatenbogen der Frühen Neuzeit, in dem die Osmanen der international dominante politische Faktor wurden. Transformationsprozesse wurden angestoßen durch Bevölkerungs- und Militärbewegungen, ökonomische, politische und religiös-mentale Umwälzungen, die zwischen opportunistischer Anpassung und rebellierendem Widerstand oszillierten und entsprechende politische Maßnahmen und Gegenreaktionen hervorriefen. Dabei wird die bislang geltende Forschungsmeinung zur Toleranzgeschichte Siebenbürgens in Frage gestellt und völlig neu bewertet

Common Man, Society and Religion in the 16th century/Gemeiner Mann, Gesellschaft und Religion im 16. Jahrhundert

Der zweisprachige Sammelband vereinigt zum Teil bahnbrechende Ergebnisse einer interdisziplinären Forschungstagung, deren Beiträge sozial-, wirtschafts-, kultur- und kirchengeschichtliche Aspekte der Frühneuzeit im Karpatenbogen aufgreifen. Basierend auf vielfach erstmals ausgewerteten Quellen bearbeiten die Beiträge aktuelle Fragestellungen und Forschungshorizonte zur Interdependenz von sozialen, ökonomischen, kulturellen und religiösen Phänomenen im Karpatenbogen der Frühen Neuzeit, in dem die Osmanen der international dominante politische Faktor wurden. Transformationsprozesse wurden angestoßen durch Bevölkerungs- und Militärbewegungen, ökonomische, politische und religiös-mentale Umwälzungen, die zwischen opportunistischer Anpassung und rebellierendem Widerstand oszillierten und entsprechende politische Maßnahmen und Gegenreaktionen hervorriefen. Dabei wird die bislang geltende Forschungsmeinung zur Toleranzgeschichte Siebenbürgens in Frage gestellt und völlig neu bewertet

Association of circulating calprotectin with lipid profile in axial spondyloarthritis

Calprotectin (CPT) is released during inflammation, also in the context of atherosclerosis. The link between CPT and the atherosclerotic process was evaluated in several diseases. However, studies in axial spondyloarthritis (axSpA), associated with a high incidence of subclinical atherosclerosis, are scarce. Therefore, we assessed the association of CPT with subclinical atherosclerosis and metabolic risk factors in axSpA. CPT serum levels were measured by enzyme-linked immunosorbent assay in 163 axSpA patients and 63 controls. Subclinical atherosclerosis was determined in patients by carotid ultrasonography (assessing the presence/absence of carotid plaques and carotid intima-media thickness [cIMT]). Data on inflammation, disease activity, lipid profile and treatment were collected to evaluate its relationship with CPT. axSpA patients evidenced lower CPT levels than controls. CPT showed no association with plaques or cIMT in axSpA. CPT and HDL-cholesterol negatively correlated, while a positive association of CPT with the atherogenic index was disclosed. Additionally, axSpA patients with C-reactive protein values at diagnosis higher than 3?mg/L displayed higher CPT levels. Our study shows no relationship between CPT and markers of subclinical atherosclerosis in axSpA. Nevertheless, it demonstrates an association of CPT with adverse lipid profiles and inflammatory biomarkers, which could further influence on the development of atherosclerosis.We wish to thank all the patients and controls that participated in this study and Begoña Ubilla for technical assistance. FG is a recipient of a Sara Borrell post-doctoral fellowship from the Instituto de Salud Carlos III (ISCIII) (Spain), co-funded by the European Social Fund (ESF, “Investing in your future”) (grant CD15/00095). SR-M is supported by funds of the RETICS Program (RIER) RD16/0012/0009 (ISCIII, co-funded by the European Regional Development Fund, ERDF). VM is supported by funds of a Miguel Servet type I programme (grant CP16/00033) (ISCIII, co-funded by ERDF). RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the ESF (grant CP16/00033). This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors

Inflammatory Ly-6C(hi) monocytes play an important role in the development of severe transplant arteriosclerosis in hyperlipidemic recipients

Objective: Transplant arteriosclerosis (TA) restricts long-term survival of heart transplant recipients. Although the role of monocyte/macrophages is well established in native atherosclerosis, it has been studied to a much lesser extent in TA. Plasma cholesterol is the most important non-immunologic risk factor for development of TA but the underlying mechanisms are largely unknown. We hypothesized that monocyte/macrophages might play an important role in the pathogenesis of TA under hyperlipidemic conditions. Methods: We studied TA in fully mismatched arterial allografts transplanted into hyperlipidemic ApoE-/- recipients compared to wild-type controls. The recruitment of distinct monocyte populations into the grafts was tracked by in vivo labelling with fluorescent microspheres. We used antibody-mediated depletion protocols to dissect the relative contribution of T lymphocytes and monocytes to disease development. Results: In the hyperlipidemic environment the progression of TA was highly exacerbated and the inflammatory CD11b+CD115+Ly-6Chi monocytes were preferentially recruited into the neointima. The number of macrophage-derived foam cells present in the grafts strongly correlated with plasma cholesterol and disease severity. Depletion of Ly-6Chi monocytes and neutrophils significantly inhibited macrophage accumulation and disease progression. The accelerated monocyte recruitment occurs through a T cell-independent mechanism, as T cell depletion did not influence macrophage accumulation into the grafts. Conclusions: Our study identifies for the first time the involvement of inflammatory Ly-6Chi monocytes into the pathogenesis of TA, particularly in conditions of hyperlipidemia. Targeted therapies modulating the recruitment and activation of these cells could potentially delay coronary allograft vasculopathy and improve long-term survival of heart transplant recipients. © 2012 Elsevier Ireland Ltd

Tissue curvature and apicobasal mechanical tension imbalance instruct cancer morphogenesis

Tubular epithelia are a basic building block of organs and a common site of cancer occurrence. During tumorigenesis, transformed cells overproliferate and epithelial architecture is disrupted. However, the biophysical parameters that underlie the adoption of abnormal tumour tissue shapes are unknown. Here we show in the pancreas of mice that the morphology of epithelial tumours is determined by the interplay of cytoskeletal changes in transformed cells and the existing tubular geometry. To analyse the morphological changes in tissue architecture during the initiation of cancer, we developed a three-dimensional whole-organ imaging technique that enables tissue analysis at single-cell resolution. Oncogenic transformation of pancreatic ducts led to two types of neoplastic growth: exophytic lesions that expanded outwards from the duct and endophytic lesions that grew inwards to the ductal lumen. Myosin activity was higher apically than basally in wild-type cells, but upon transformation this gradient was lost in both lesion types. Three-dimensional vertex model simulations and a continuum theory of epithelial mechanics, which incorporate the cytoskeletal changes observed in transformed cells, indicated that the diameter of the source epithelium instructs the morphology of growing tumours. Three-dimensional imaging revealed that-consistent with theory predictions-small pancreatic ducts produced exophytic growth, whereas large ducts deformed endophytically. Similar patterns of lesion growth were observed in tubular epithelia of the liver and lung; this finding identifies tension imbalance and tissue curvature as fundamental determinants of epithelial tumorigenesis