Optimal Central Counterparty Risk Management

In order to protect themselves against the potential losses in case of a participant's default and to contain systemic risk, central counterparties (CCPs) need to maintain sufficient financial resources. Typically, these financial resources consist of margin requirements and contributions to a collective default fund. Based on a stylized model of CCP risk management, this article analyzes the main factors affecting the trade-off between margins and default fund. The optimal balance between these two risk management instruments is found to depend on collateral costs, participants' default probability, and the extent to which margin requirements are associated with risk-mitigating incentives. Given the increasing role of CCPs in financial markets in general and for financial stability in particular, these considerations are not only important for CCPs themselves, but also for financial regulators.Central counterparty, margin requirements, default fund, financial stability, incentives

Magnetic Resonance Imaging Studies of Angiogenesis and Stem Cell Implantations in Rodent Models of Cerebral Lesions

Molecular biology and stem cell research have had an immense impact on our understanding of neurological diseases, for which little or no therapeutic options exist today. Manipulation of the underlying disease-specific molecular and cellular events promises more efficient therapy. Angiogenesis, i.e. the regrowth of new vessels from an existing vascular network, has been identified as a key contributor for the progression of tumor and, more recently, for regeneration after stroke. Donation of stem cells has proved beneficial to treat cerebral lesions. However, before angiogenesis-targeted and stem cell therapies can safely be used in patients, underlying biological processes need to be better understood in animal models. Noninvasive imaging is essential in order to follow biological processes or stem cell fate in both space and time. We optimized steady state contrast enhanced magnetic resonance imaging (SSCE MRI) to monitor vascular changes in rodent models of tumor and stroke. A modification of mathematical modeling of MR signal from the vascular network allowed for the first time simultaneous measurements of relaxation time T2 and SSCE MRI derived blood volume, vessel size, and vessel density. Limitations of SSCE MRI in tissues with high blood volume and non-cylindrically shaped vessels were explored. SSCE MRI detected angiogenesis and response to anti-angiogenic treatment in two rodent tumor models. In both tumor models, reduction of blood volume in small vessels and a shift towards larger vessels was observed upon treatment. After stroke, decreased vessel density and increased vessel size was found, which was most pronounced one week after the infarct. This is in agreement with two initial, recently published clinical studies. Overall, very little signs of angiogenesis were found. Furthermore, superparamagnetic iron oxide (SPIO) labels were used to study neural stem cells (NSCs) in vivo with MRI. SPIO labeling revealed a decrease in volume of intracerebral grafts over 4 months, assessed by T2* weighted MRI. Since SPIO labels are challenging to quantify and their MR contrast can easily be confounded, we explored the potential of in vivo 19F MRI of 19F labeled NSCs. Hardware was developed for in vitro and in vivo 19F MRI. NSCs were labeled with little effect on cell function and in vivo detection limits were determined at ~10,000 cells within 1 h imaging time. A correction for the inhomogeneous magnetic field profile of surface coils was validated in vitro and applied for both sensitive and quantitative in vivo cell imaging. As external MRI labels do not provide information on NSC function we combined 19F MRI with bioluminescence imaging (BLI). The BLI signal allowed quantification of viable cells whereas 19F MRI provided graft location and density in 3D over 4 weeks both in the healthy and stroke brain. A massive decrease in number of viable cells was detected independent of the microenvironment. This indicates that functional recovery reported in many studies of NSC implantation after stroke, is rather due to release of factors by NSCs than direct tissue replacement. In light of these indirect effects, combination of the imaging methods developed in this dissertation with other functional and structural imaging methods is suggested in order to further elucidate interactions of NSCs with the vasculature

Monetary transmission and bank lending in Germany

This paper analyses the role of bank lending in the monetary transmission process in Germany. We follow a sectoral approach by distinguishing corporate lending and household lending. We find that banks respond to a monetary contraction by adjusting their securities holdings, rather than reducing their loans portfolio. Most lending categories even show an increase following a monetary tightening. The main implication of our results is that a bank lending channel is not an important transmission mechanism. On the contrary, by insulating their loans portfolio from monetary shocks, banks are more likely to weaken than to strengthen the impact of monetary policy.

Monetary transmission and bank lending in Germany

This paper analyses the role of bank lending in the monetary transmission process in Germany. We follow a sectoral approach by distinguishing corporate lending and household lending. We find that banks respond to a monetary contraction by adjusting their securities holdings, rather than reducing their loans portfolio. Most lending categories even show an increase following a monetary tightening. The main implication of our results is that a bank lending channel is not an important transmission mechanism. On the contrary, by insulating their loans portfolio from monetary shocks, banks are more likely to weaken than to strengthen the impact of monetary policy

Literalität und Geschlecht. Zum subjektiv wahrgenommenen und in Leistungstests ermittelten schriftsprachlichen Leistungsvermögen von Jungen und Mädchen

Das vermeintliche Defizit schriftsprachlichen Leistungsvermögens von Jungen gegenüber Mädchen wird in diesem Beitrag überprüft. Anhand einer Zusammenschau empirischer Untersuchungen wird dem Aspekt nachgegangen, inwieweit sich Jungen und Mädchen in den eigenen Einschätzungen ihrer Fähigkeiten zur Bewältigung von schriftsprachlichen (Lesen und Schreiben) Anforderungen unterscheiden. Darüber hinaus werden Befunde aufgezeigt, die geschlechtsspezifische Testleistungsdifferenzen anzeigen. Insgesamt ergibt sich das Bild, dass, unabhängig vom Geschlecht, "je höher die eigene Fähigkeit eingeschätzt wird, desto höher ist die Anstrengung, bevorstehende Aufgaben zu meistern, und je erfolgreicher die Bearbeitung erfolgt [...], desto stärker ist die Zuversicht, bei neuen Herausforderungen zu reüssieren". Deshalb, so die Autorin, ist es "gefährlich", allzuschnell aus Befunden einer empirischen Studie die Notwendigkeit einer besonderen Lese- und Schreibförderung für Jungen abzuleiten. (DIPF/Orig.

MR Elastography-Based Assessment of Matrix Remodeling at Lesion Sites Associated With Clinical Severity in a Model of Multiple Sclerosis

Magnetic resonance imaging (MRI) with gadolinium based contrast agents (GBCA) is routinely used in the clinic to visualize lesions in multiple sclerosis (MS). Although GBCA reveal endothelial permeability, they fail to expose other aspects of lesion formation such as the magnitude of inflammation or tissue changes occurring at sites of blood-brain barrier (BBB) disruption. Moreover, evidence pointing to potential side effects of GBCA has been increasing. Thus, there is an urgent need to develop GBCA-independent imaging tools to monitor pathology in MS. Using MR-elastography (MRE), we previously demonstrated in both MS and the animal model experimental autoimmune encephalomyelitis (EAE) that inflammation was associated with a reduction of brain stiffness. Now, using the relapsing-remitting EAE model, we show that the cerebellum-a region with predominant inflammation in this model-is especially prone to loss of stiffness. We also demonstrate that, contrary to GBCA-MRI, reduction of brain stiffness correlates with clinical disability and is associated with enhanced expression of the extracellular matrix protein fibronectin (FN). Further, we show that FN is largely expressed by activated astrocytes at acute lesions, and reflects the magnitude of tissue remodeling at sites of BBB breakdown. Therefore, MRE could emerge as a safe tool suitable to monitor disease activity in MS

Microglia as target for anti-inflammatory approaches to prevent secondary brain injury after subarachnoid hemorrhage (SAH)

Background: Microglia-driven cerebral spreading inflammation is a key contributor to secondary brain injury after SAH. Genetic depletion or deactivation of microglia has been shown to ameliorate neuronal cell death. Therefore, clinically feasible anti-inflammatory approaches counteracting microglia accumulation or activation are interesting targets for SAH treatment. Here, we tested two different methods of interference with microglia-driven cerebral inflammation in a murine SAH model: (i) inflammatory preconditioning and (ii) pharmacological deactivation. Methods: 7T-MRI-controlled SAH was induced by endovascular perforation in four groups of C57Bl/6 mice: (i) Sham-operation, (ii) SAH naive, (iii) SAH followed by inflammatory preconditioning (LPS intraperitoneally), and (iv) SAH followed by pharmacological microglia deactivation (colony-stimulating factor-1 receptor-antagonist PLX3397 intraperitoneally). Microglia accumulation and neuronal cell death (immuno-fluorescence), as well as activation status (RT-PCR for inflammation-associated molecules from isolated microglia) were recorded at day 4 and 14. Toll-like receptor4 (TLR4) status was analyzed using FACS. Results: Following SAH, significant cerebral spreading inflammation occurred. Microglia accumulation and pro-inflammatory gene expression were accompanied by neuronal cell death with a maximum on day 14 after SAH. Inflammatory preconditioning as well as PLX3397-treatment resulted in significantly reduced microglia accumulation and activation as well as neuronal cell death. TLR4 surface expression in preconditioned animals was diminished as a sign for receptor activation and internalization. Conclusions: Microglia-driven cerebral spreading inflammation following SAH contributes to secondary brain injury. Two microglia-focused treatment strategies, (i) inflammatory preconditioning with LPS and (ii) pharmacological deactivation with PLX3397, led to significant reduction of neuronal cell death. Increased internalization of inflammation-driving TLR4 after preconditioning leaves less receptor molecules on the cell surface, providing a probable explanation for significantly reduced microglia activation. Our findings support microglia-focused treatment strategies to overcome secondary brain injury after SAH. Delayed inflammation onset provides a valuable clinical window of opportunity