Die Auswirkungen der Subprime-Krise auf den deutschen LBO-Markt für Small- und MidCaps

Since summer 2007 the Subprime credit crisis has been affecting the international financial markets. One of the consequences of the crisis was the collapse of the market for large-sized leveraged buyout transactions in late 2007 and early 2008. The goal of this Working Paper is to examine to what extent also small and mid-sized LBO deals in Germany were affected by the market turbulences. After illustrating the aspects of the crisis which are relevant for this topic, six hypotheses regarding potential consequences of the crisis on the German LBO market for Small-and MidCaps were set up. To verify these hypotheses a survey among the market participants, namely financing banks and LBO investors, was conducted in May and June 2008

Die Auswirkungen der Subprime-Krise auf den deutschen LBO-Markt für Small- und MidCaps

Since summer 2007 the Subprime credit crisis has been affecting the international financial markets. One of the consequences of the crisis was the collapse of the market for large-sized leveraged buyout transactions in late 2007 and early 2008. The goal of this Working Paper is to examine to what extent also small and mid-sized LBO deals in Germany were affected by the market turbulences. After illustrating the aspects of the crisis which are relevant for this topic, six hypotheses regarding potential consequences of the crisis on the German LBO market for Small-and MidCaps were set up. To verify these hypotheses a survey among the market participants, namely financing banks and LBO investors, was conducted in May and June 2008. --LBO,Subprime,Krise,KMU,Buyout,Leveraged Buyout,Finanzinvestoren,Private Equity

Characterisation of a functional rat hepatocyte spheroid model.

Many in vitro liver cell models, such as 2D systems, that are used to assess the hepatotoxic potential of xenobiotics suffer major limitations arising from a lack of preservation of physiological phenotype and metabolic competence. To circumvent some of these limitations there has been increased focus on producing more representative 3D models. Here we have used a novel approach to construct a size-controllable 3D hepatic spheroid model using freshly isolated primary rat hepatocytes (PRH) utilising the liquid-overlay technique whereby PRH spontaneously self-assemble in to 3D microtissues. This system produces viable spheroids with a compact in vivo-like structure for up to 21 days with sustained albumin production for the duration of the culture period. F-actin was seen throughout the spheroid body and P-glycoprotein (P-gp) and multidrug resistance-associated protein 2 (MRP2) transporters had polarised expression on the canalicular membrane of hepatocytes within the spheroids upon formation (day 3). The MRP2 transporter was able to functionally transport 5 μM 5-chloromethylfluorescein diacetate (CMFDA) substrates into these canalicular structures. These PRH spheroids display in vivo characteristics including direct cell-cell contacts, cellular polarisation, 3D cellular morphology, and formation of functional secondary structures throughout the spheroid. Such a well-characterised system could be readily exploited for pre-clinical and non-clinical repeat-dose investigations and could make a significant contribution to replace, reduce and refine the use of animals for applied research

The Cdc42 GEF Intersectin 2 controls mitotic spindle orientation to form the lumen during epithelial morphogenesis

Epithelial organs are made of tubes and cavities lined by a monolayer of polarized cells that enclose the central lumen. Lumen formation is a crucial step in the formation of epithelial organs. The Rho guanosine triphosphatase (GTPase) Cdc42, which is a master regulator of cell polarity, regulates the formation of the central lumen in epithelial morphogenesis. However, how Cdc42 is regulated during this process is still poorly understood. Guanine nucleotide exchange factors (GEFs) control the activation of small GTPases. Using the three-dimensional Madin–Darby canine kidney model, we have identified a Cdc42-specific GEF, Intersectin 2 (ITSN2), which localizes to the centrosomes and regulates Cdc42 activation during epithelial morphogenesis. Silencing of either Cdc42 or ITSN2 disrupts the correct orientation of the mitotic spindle and normal lumen formation, suggesting a direct relationship between these processes. Furthermore, we demonstrated this direct relationship using LGN, a component of the machinery for mitotic spindle positioning, whose disruption also results in lumen formation defects.This work was supported by grants from the Human Frontier Science Program (HFSP-CDA 00011/2009) and Marie Curie (IRG-209382) to F. Martín- Belmonte, National Institutes of Health grants (R01 DK067153 and R01 DK074398) to K. Mostov, and grants from the Ministerio de Ciencia e Innovación to F. Martín-Belmonte (BFU2008-01916) and M.A. Alonso (BFU2006- 01925) and to F. Martín-Belmonte and M.A. Alonso (CONSOLIDER CSD2009-00016). An institutional grant from the Fundación Ramón Areces to the Centro de Biología Molecular Severo Ochoa is also acknowledged.Peer reviewe