The Credit Rating Industry: Competition and Regulation

This study provides a comprehensive analysis of credit rating economics and draws conclusions on the nature of regulation. It starts with an overview of the credit rating industry and introduces a framework that structures multiple rating agency functions. At the heart of the credit rating business model lies the reputation mechanism, which is analyzed in detail. Despite several frictions in the process that give rise to entry barriers and market power, the quality assuring function of the reputation mechanism is very robust � contrary to the fear of many. After analyzing the reputation mechanism, the study takes a wider look at the industry and identifies the forces behind credit rating supply and demand. The structure of demand is dependent on the relation between the �information value� and the �license value� attached to ratings because they are used in �rating-based regulations�. On the supply side the question is whether the high industry concentration is a �natural� result of market forces or whether it is the result of state interference. Aspects such as economies of scale, switching costs, and market segmentation are discussed. From an industrial organization perspective competition in the credit rating industry is limited. A comprehensive review of potential reasons for regulating the credit rating industry reveals that there are only few compelling arguments despite the large number of different aspects discussed by practitioners and researchers. In general, the reputation mechanism and competition should be strengthened. Specifically, the study discusses five regulatory areas: the use of rating-based regulation, competition, official recognition, civil liability, and implementation methods. The regulatory approaches of the EU under the Capital Requirements Directive of 2005 and the USA under the Credit Rating Agency Reform Act of 2006 are contrasted against an optimal regulatory regime. The study closes with a summary and a tabular literature review

MERRILL: Micromagnetic Earth Related Robust Interpreted Language Laboratory

Complex magnetic domain structures and the energy barriers between them are responsible for pseudo-single-domain phenomena in rock magnetism and contribute significantly to the magnetic remanence of paleomagnetic samples. This article introduces MERRILL, an open source software package for three-dimensional micromagnetics optimized and designed for the calculation of such complex structures. MERRILL has a simple scripting user interface that requires little computational knowledge to use but provides research strength algorithms to model complex, inhomogeneous domain structures in magnetic materials. It uses a finite element/boundary element numerical method, optimally suited for calculating magnetization structures of local energy minima (LEM) in irregular grain geometries that are of interest to the rock and paleomagnetic community. MERRILL is able to simulate the magnetic characteristics of LEM states in both single grains, and small assemblies of interacting grains, including saddle-point paths between nearby LEMs. Here the numerical model is briefly described, and an overview of the scripting language and available commands is provided. The open source nature of the code encourages future development of the model by the scientific community

Telomerase and pluripotency factors jointly regulate stemness in pancreatic cancer stem cells

To assess the role of telomerase activity and telomere length in pancreatic CSCs we used different CSC enrichment methods (CD133, ALDH, sphere formation) in primary patient-derived pancreatic cancer cells. We show that CSCs have higher telomerase activity and longer telomeres than bulk tumor cells. Inhibition of telomerase activity, using genetic knockdown or pharmacological inhibitor (BIBR1532), resulted in CSC marker depletion, abrogation of sphere formation in vitro and reduced tumorigenicity in vivo. Furthermore, we identify a positive feedback loop between stemness factors (NANOG, OCT3/4, SOX2, KLF4) and telomerase, which is essential for the self-renewal of CSCs. Disruption of the balance between telomerase activity and stemness factors eliminates CSCs via induction of DNA damage and apoptosis in primary patient-derived pancreatic cancer samples, opening future perspectives to avoid CSC-driven tumor relapse. In the present study, we demonstrate that telomerase regulation is critical for the “stemness” maintenance in pancreatic CSCs and examine the effects of telomerase inhibition as a potential treatment option of pancreatic cancer. This may significantly promote our understanding of PDAC tumor biology and may result in improved treatment for pancreatic cancer patientsThis research was funded by a Max Eder Fellowship of the German Cancer Aid (111746), a German Cancer Aid Priority Program ‘Translational Oncology’ 70112505, by a Collaborative Research Centre grant (316249678—SFB 1279) of the German Research Foundation, and by a Hector Foundation Cancer Research grant (M65.1) to P.C.H., B.S.J. is supported by a Rámon y Cajal Merit Award (RYC- 2012-12104) from the Ministerio de Economía y Competitividad, Spain and a Coordinated grant (GC16173694BARB) from the Fundación Asociación Española Contra el Cáncer (AECC). K.W. is supported by a Baustein 3.2 by Ulm University

Stability of equidimensional pseudo-single-domain magnetite over billion-year timescales

Interpretations of paleomagnetic observations assume that naturally occurring magnetic particles can retain their primary magnetic recording over billions of years. The ability to retain a magnetic recording is inferred from laboratory measurements, where heating causes demagnetization on the order of seconds. The theoretical basis for this inference comes from previous models that assume only the existence of small, uniformly magnetized particles, whereas the carriers of paleomagnetic signals in rocks are usually larger, nonuniformly magnetized particles, for which there is no empirically complete, thermally activated model. This study has developed a thermally activated numerical micromagnetic model that can quantitatively determine the energy barriers between stable states in nonuniform magnetic particles on geological timescales. We examine in detail the thermal stability characteristics of equidimensional cuboctahedral magnetite and find that, contrary to previously published theories, such nonuniformly magnetized particles provide greater magnetic stability than their uniformly magnetized counterparts. Hence, nonuniformly magnetized grains, which are commonly the main remanence carrier in meteorites and rocks, can record and retain high-fidelity magnetic recordings over billions of years

The magnetic structure and palaeomagnetic recording fidelity of sub-micron greigite (Fe3S4)

We present the results of a finite-element micromagnetic model of View the MathML source to View the MathML source greigite (Fe3S4) grains with a variety of equant morphologies. This grain size range covers the magnetic single-domain (SD) to pseudo single-domain (PSD) transition, and possibly also the PSD to multi-domain (MD) transition. The SD–PSD threshold d0 is determined to be View the MathML source depending on grain shape. The nudged elastic-band method was used to determine the room temperature energy barriers between stable states and thus the blocking volumes. It is found that, in the absence of interparticle magnetostatic interactions, the magnetisation of equant SD greigite is not stable on a geological scale and only PSD grains View the MathML source can be expected to carry a stable magnetisation over billion-year timescales, i.e., all non-interacting SD particles are essentially superparamagnetic. We further identify a mechanism for the PSD to multi-domain (MD) transition, which is of a continuous nature from PSD nucleation up to View the MathML source, when structures typical of MD behaviour like closure domains begin to form

The Inflammatory Kinase MAP4K4 Promotes Reactivation of Kaposi's Sarcoma Herpesvirus and Enhances the Invasiveness of Infected Endothelial Cells

Kaposi's sarcoma (KS) is a mesenchymal tumour, which is caused by Kaposi's sarcoma herpesvirus (KSHV) and develops under inflammatory conditions. KSHV-infected endothelial spindle cells, the neoplastic cells in KS, show increased invasiveness, attributed to the elevated expression of metalloproteinases (MMPs) and cyclooxygenase-2 (COX-2). The majority of these spindle cells harbour latent KSHV genomes, while a minority undergoes lytic reactivation with subsequent production of new virions and viral or cellular chemo- and cytokines, which may promote tumour invasion and dissemination. In order to better understand KSHV pathogenesis, we investigated cellular mechanisms underlying the lytic reactivation of KSHV. Using a combination of small molecule library screening and siRNA silencing we found a STE20 kinase family member, MAP4K4, to be involved in KSHV reactivation from latency and to contribute to the invasive phenotype of KSHV-infected endothelial cells by regulating COX-2, MMP-7, and MMP-13 expression. This kinase is also highly expressed in KS spindle cells in vivo. These findings suggest that MAP4K4, a known mediator of inflammation, is involved in KS aetiology by regulating KSHV lytic reactivation, expression of MMPs and COX-2, and, thereby modulating invasiveness of KSHV-infected endothelial cells. © 2013 Haas et al