University of Kiel

About: University of Kiel is a education organization based out in Kiel, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 27816 authors who have published 57114 publications receiving 2061802 citations. The organization is also known as: Christian Albrechts University & Christian-Albrechts-Universität zu Kiel.

Estimation of agent-based models: the case of an asymmetric herding model

Abstract: The behavioral origins of the stylized facts of financial returns have been addressed in a growing body of agent-based models of financial markets. While the traditional efficient market viewpoint explains all statistical properties of returns by similar features of the news arrival process, the more recent behavioral finance models explain them as imprints of universal patterns of interaction in these markets. In this paper we contribute to this literature by introducing a very simple agent-based model in which the ubiquitous stylized facts (fat tails, volatility clustering) are emergent properties of the interaction among traders. The simplicity of the model allows us to estimate the underlying parameters, since it is possible to derive a closed form solution for the distribution of returns. We show that the tail shape characterizing the fatness of the unconditional distribution of returns can be directly derived from some structural variables that govern the traders' interactions, namely the herding propensity and the autonomous switching tendency.

Magmatic and amagmatic seafloor generation at the ultraslow-spreading Gakkel ridge, Arctic Ocean

Abstract: A high-resolution mapping and sampling study of the Gakkel ridge was accomplished during an international ice-breaker expedition to the high Arctic and North Pole in summer 2001. For this slowest-spreading endmember of the global mid-ocean-ridge system, predictions were that magmatism should progressively diminish as the spreading rate decreases along the ridge, and that hydrothermal activity should be rare. Instead, it was found that magmatic variations are irregular, and that hydrothermal activity is abundant. A 300-kilometre-long central amagmatic zone, where mantle peridotites are emplaced directly in the ridge axis, lies between abundant, continuous volcanism in the west, and large, widely spaced volcanic centres in the east. These observations demonstrate that the extent of mantle melting is not a simple function of spreading rate: mantle temperatures at depth or mantle chemistry (or both) must vary significantly along-axis. Highly punctuated volcanism in the absence of ridge offsets suggests that first-order ridge segmentation is controlled by mantle processes of melting and melt segregation. The strong focusing of magmatic activity coupled with faulting may account for the unexpectedly high levels of hydrothermal activity observed.

p38 Mitogen-Activated Protein Kinase Is Activated and Linked to TNF-α Signaling in Inflammatory Bowel Disease

Abstract: Inflammatory bowel diseases (IBD)--Crohn's disease and ulcerative colitis--are relapsing chronic inflammatory disorders which involve genetic, immunological, and environmental factors. The regulation of TNF-alpha, a key mediator in the inflammatory process in IBD, is interconnected with mitogen-activated protein kinase pathways. The aim of this study was to characterize the activity and expression of the four p38 subtypes (p38alpha-delta), c-Jun N-terminal kinases (JNKs), and the extracellular signal-regulated kinases (ERK)1/2 in the inflamed intestinal mucosa. Western blot analysis revealed that p38alpha, JNKs, and ERK1/2 were significantly activated in IBD, with p38alpha showing the most pronounced increase in kinase activity. Protein expression of p38 and JNK was only moderately altered in IBD patients compared with normal controls, whereas ERK1/2 protein was significantly down-regulated. Immunohistochemical analysis of inflamed mucosal biopsies localized the main expression of p38alpha to lamina propria macrophages and neutrophils. ELISA screening of the supernatants of Crohn's disease mucosal biopsy cultures showed that incubation with the p38 inhibitor SB 203580 significantly reduced secretion of TNF-alpha. In vivo inhibition of TNF-alpha by a single infusion of anti-TNF-alpha Ab (infliximab) resulted in a highly significant transient increase of p38alpha activity during the first 48 h after infusion. A significant infliximab-dependent p38alpha activation was also observed in THP-1 myelomonocytic cells. In human monocytes, infliximab enhanced TNF-alpha gene expression, which could be inhibited by SB 203580. In conclusion, p38alpha signaling is involved in the pathophysiology of IBD.