Liquidity risk meets economic capital and RAROC: a framework for measuring liquidity risk in banks

Liquidity risk is a crucial and inherent feature of the business model of banks. While banks and regulators use sophisticated mathematical methods to measure a bank's solvency risk, they use relatively simple tools for a bank's liquidity risk such as coverage ratios, sensitivity analyses, and scenario analyses. In this thesis we present a more rigorous framework that allows us to measure a bank's liquidity risk within the standard economic capital and RAROC setting. In particular, we introduce the concept of liquidity cost profiles as a quantification of a bank's illiquidity at balance sheet level, which leads subsequently to the concept of liquidity-adjusted risk measures defined on the vector space of balance sheet positions under liquidity call functions. We study the model-free effects of adding, scaling, and mixing balance sheets. In particular, we show that convexity and positive super-homogeneity of the underlying risk measures is preserved in terms of positions under the liquidity adjustment, given certain moderate conditions are met, while coherence is not, reflecting the common idea that size does matter in the face of liquidity risk.\ud We also show that a liquidity-adjustment of the well-known Euler capital allocation principle is possible without losing the soundness property that justifies the principle. However, it is in general not possible to combine soundness with the total allocation property for both the numerator and the denominator in liquidity-adjusted RAROC. Liquidity-adjusted risk measures could be a useful addition to banking regulation and bank management as they capture essential features of a bank's liquidity risk, can be combined with existing risk management systems, possess reasonable properties under portfolio manipulations, and lead to an intuitive risk ranking of banks

The Impact of Country-of-Origin on the Liability-of-Foreignness in the Acceptance of Products in the Global Marketplace

Upon entering a foreign market, multinational corporations (MNCs) encounter business environments that are far more diverse and complex that what they are attuned to experiencing in their home market. MNCs face inherent encumbrances due to spatial distance, unfamiliarity with the local environment, differential treatment by the host country, and costs imposed by the homecountry environment, pertaining to the construct liability of foreignness (LOF). While prior research empirically demonstrated LOF’s existence at firm level of analysis with respect to various costs (e.g. survival, revenue, labor lawsuits, profitability), surprisingly little empirical work has been conducted on marketing derived costs, particularly at the individual level of analysis. This article elucidates LOF as marketing derived costs due to divides in understanding consumers’ perception of respective market offerings that impact both the firm’s external and internal environments as a measure of negative stigmatization. Drawing upon well-established streams of research from the international management and marketing literature, a conceptual framework of the impact of COO on individual LOF by extending previous work on COO effects under stigmatization theory was introduced. Propositions and recommendations to stimulate future research are offered. The authors discuss future research directions and managerial implications

Protein Kinase D2 Is an Essential Regulator of Murine Myoblast Differentiation

Muscle differentiation is a highly conserved process that occurs through the activation of quiescent satellite cells whose progeny proliferate, differentiate, and fuse to generate new myofibers. A defined pattern of myogenic transcription factors is orchestrated during this process and is regulated via distinct signaling cascades involving various intracellular signaling pathways, including members of the protein kinase C (PKC) family. The protein kinase D (PKD) isoenzymes PKD1, -2, and -3, are prominent downstream targets of PKCs and phospholipase D in various biological systems including mouse and could hence play a role in muscle differentiation. In the present study, we used a mouse myoblast cell line (C2C12) as an in vitro model to investigate the role of PKDs, in particular PKD2, in muscle stem cell differentiation. We show that C2C12 cells express all PKD isoforms with PKD2 being highly expressed. Furthermore, we demonstrate that PKD2 is specifically phosphorylated/activated during the initiation of mouse myoblast differentiation. Selective inhibition of PKCs or PKDs by pharmacological inhibitors blocked myotube formation. Depletion of PKD2 by shRNAs resulted in a marked inhibition of myoblast cell fusion. PKD2-depleted cells exhibit impaired regulation of muscle development-associated genes while the proliferative capacity remains unaltered. Vice versa forced expression of PKD2 increases myoblast differentiation. These findings were confirmed in primary mouse satellite cells where myotube fusion was also decreased upon inhibition of PKDs. Active PKD2 induced transcriptional activation of myocyte enhancer factor 2D and repression of Pax3 transcriptional activity. In conclusion, we identify PKDs, in particular PKD2, as a major mediator of muscle cell differentiation in vitro and thereby as a potential novel target for the modulation of muscle regeneration

Environmentally sustainable food consumption : a review and research agenda from a goal-directed perspective

The challenge of convincing people to change their eating habits toward more environmentally sustainable food consumption (ESFC) patterns is becoming increasingly pressing. Food preferences, choices and eating habits are notoriously hard to change as they are a central aspect of people's lifestyles and their socio-cultural environment. Many people already hold positive attitudes toward sustainable food, but the notable gap between favorable attitudes and actual purchase and consumption of more sustainable food products remains to be bridged. The current work aims to (1) present a comprehensive theoretical framework for future research on ESFC, and (2) highlight behavioral solutions for environmental challenges in the food domain from an interdisciplinary perspective. First, starting from the premise that food consumption is deliberately or unintentionally directed at attaining goals, a goal-directed framework for understanding and influencing ESFC is built. To engage in goal-directed behavior, people typically go through a series of sequential steps. The proposed theoretical framework makes explicit the sequential steps or hurdles that need to be taken for consumers to engage in ESFC. Consumers need to positively value the environment, discern a discrepancy between the desired versus the actual state of the environment, opt for action to reduce the experienced discrepancy, intend to engage in behavior that is expected to bring them closer to the desired end state, and act in accordance with their intention. Second, a critical review of the literature on mechanisms that underlie and explain ESFC (or the lack thereof) in high-income countries is presented and integrated into the goal-directed framework. This contribution thus combines a top-down conceptualization with a bottom-up literature review; it identifies and discusses factors that might hold people back from ESFC and interventions that might promote ESFC; and it reveals knowledge gaps as well as insights on how to encourage both short- and long-term ESFC by confronting extant literature with the theoretical framework. Altogether, the analysis yields a set of 33 future research questions in the interdisciplinary food domain that deserve to be addressed with the aim of fostering ESFC in the short and long term

Die Proteinkinase D2 als kritischer Parameter während der Skelettmuskeldifferenzierung

The developement of every multicellular organism occurs through the highly conserved mechanism of genetic programs orchestrated by genes that coordinate cell growth, proliferation, differentiation, migration and apoptosis. This is regulated by signal transduction cascades mediated by kinases such as protein kinases or phospholipases. Muscle cell differentiation is regulated by the activation of a defined pattern of myogenic transcription factors involving members of the protein kinase C (PKC), Protein kinase D (PKD) or phospholipase D families. The protein kinase D (PKD) isoenzymes PKD1, -2, and -3 are prominent downstream targets of PKCs and PLDs in various biological systems. Recent data suggest that PKDs and PKCs also play an important role in muscle cell differentiation. Hence the influence of PKDs and PKCs was examined by establishing the model of C2C12 cells as a known in vitro model for muscle cell differentiation. PKD expression could be demonstrated in C2C12 cells with PKD2 being highly expressed. Furthermore the activation of PKD2 at the beginning of muscle cell differentiation could be observed and inihibited by using pharmacological inhibitors. Depletion of PKD2 by shRNA resulted in a marked inhibition of satellite cell fusion. Furthermore, an activation of myocyte enhancer factor 2D, a key transcription factor for muscle cell differentiation in satellite cells by PKD2 could be observed. In conclusion, the PKD family, especially PKD2 can be seen as a major mediator of muscle cell differentiation in vitro and thereby as a potential novel target for the modulation of muscle regeneration