Logistics clusters, including inter-firm relations through community detection

This paper studies clusters in the logistics sector. Like traditional cluster research, indicators of concentration to detect co-location of employment are calculated. However, this approach is enhanced by including a quantitative analysis of the inter-firm relations between logistics companies through the use of a community detection algorithm on a microeconomic dataset of buyer-supplier relations. Combining both results in a typology of logistics clusters. Next to the big clusters characterized by employment concentration and many internal and external relations, spill-over and polycentric clusters are identified. This approach seems promising to detect in future research clusters in other sectors and place

Recent insights on Alzheimer’s disease originating from yeast models

In this review article, yeast model-based research advances regarding the role of Amyloid-? (A?), Tau and frameshift Ubiquitin UBB+1 in Alzheimer’s disease (AD) are discussed. Despite having limitations with regard to intercellular and cognitive AD aspects, these models have clearly shown their added value as a complementary model for the study of the molecular aspects of these proteins, including their interplay with AD related cellular processes such as mitochondrial dysfunction and altered proteostasis. Moreover, these yeast models have also shown their importance in translational research, e.g. in compound screenings and for AD diagnostics development. In addition to well-established Saccharomyces cerevisiae models, new upcoming Schizosaccharomyces pombe, Candida glabrata and Kluyveromyces lactis yeast models for A? and Tau are briefly described. Finally, traditional and more innovative research methodologies, e.g. for studying protein oligomerization/aggregation, are highlighted

Исследование кинетики накопления коллоидного гептасульфида рения

SummaryInflammatory cytokines are well-recognized mediators of atherosclerosis. Depending on the pathological context, type I interferons (IFNs; IFNα and IFNβ) exert either pro- or anti-inflammatory immune functions, but their exact role in atherogenesis has not been clarified. Here, we demonstrate that IFNβ enhances macrophage-endothelial cell adhesion and promotes leukocyte attraction to atherosclerosis-prone sites in mice in a chemokine-dependent manner. Moreover, IFNβ treatment accelerates lesion formation in two different mouse models of atherosclerosis and increases macrophage accumulation in the plaques. Concomitantly, absence of endogenous type I IFN signaling in myeloid cells inhibits lesion development, protects against lesional accumulation of macrophages, and prevents necrotic core formation. Finally, we show that type I IFN signaling is upregulated in ruptured human atherosclerotic plaques. Hereby, we identify type I IFNs as proatherosclerotic cytokines that may serve as additional targets for prevention or treatment