Preisbildungsprozess von Neuemissionen am Neuen Markt: Identifizierung von Ineffizienzen und Handlungsempfehlungen für die Gestaltung zukünftiger Börsengänge an ein Wachstumssegment

Die vorliegende Dissertation beschäftigt sich mit der Frage, welche Lehren aus dem Experiment Neuer Markt bezüglich des Börsengangs von Wachstumsunternehmen gezogen werden können. Anhand empirischer Untersuchungen zum Underpricing und zur langfristigen Kursperformance wird der Preisbildungsprozess hinsichtlich seiner Qualität beurteilt. Ob die Erwartungen der mit der Unternehmensbewertung befassten Analysten der Konsortialbanken an die Börsenkandidaten rational waren, wird anhand eines Abgleichs der zum Zeitpunkt des Gangs an den Neuen Markt abgegebenen Gewinnschätzungen mit der ex-post tatsächlich eingetretenen Entwicklung untersucht

Untersuchung einer Wasserstoff‐π Wechselwirkung in einem eingeschlossenen Wassermolekül im Festkörper

Der Nachweis und die Charakterisierung von eingeschlossenen Wassermolekülen in chemischen Gebilden und Biomakromolekülen ist weiterhin eine Herausforderung für feste Materialien. Wir präsentieren hier Protonen-detektierte Festkörper-Kernspinresonanzspektroskopie (NMR) Experimente bei Rotationsfrequenzen von 100 kHz um den magischen Winkel und bei hohen statischen Magnetfeldstärken (28.2 T), die den Nachweis eines einzelnen Wassermoleküls ermöglichen, das im Calix[4]aren-Hohlraum eines Lanthan-Komplexes durch eine Kombination von drei Arten nicht-kovalenter Wechselwirkungen fixiert ist. Die Protonenresonanzen des Wassers werden bei einer chemischen Verschiebung nahe Null ppm nachgewiesen, was wir durch quantenchemische Berechnungen bestätigen. Berechnungen mit der Dichtefunktionaltheorie zeigen, wie empfindlich der Wert der chemischen Verschiebung der Protonen auf Wasserstoff-π-Wechselwirkungen reagiert. Unsere Studie unterstreicht, wie sich die Protonen-detektierte Festkörper NMR zur Methode der Wahl für die Untersuchung schwacher nicht-kovalenter Wechselwirkungen entwickelt, die einen ganzen Zweig molekularer Erkennungsvorgänge in der Chemie und Biologie bestimmen

Writing in Britain and Ireland, c. 400 to c. 800

No abstract available

Discerning apical and basolateral properties of HT-29/B6 and IPEC-J2 cell layers by impedance spectroscopy, mathematical modeling and machine learning.

Quantifying changes in partial resistances of epithelial barriers in vitro is a challenging and time-consuming task in physiology and pathophysiology. Here, we demonstrate that electrical properties of epithelial barriers can be estimated reliably by combining impedance spectroscopy measurements, mathematical modeling and machine learning algorithms. Conventional impedance spectroscopy is often used to estimate epithelial capacitance as well as epithelial and subepithelial resistance. Based on this, the more refined two-path impedance spectroscopy makes it possible to further distinguish transcellular and paracellular resistances. In a next step, transcellular properties may be further divided into their apical and basolateral components. The accuracy of these derived values, however, strongly depends on the accuracy of the initial estimates. To obtain adequate accuracy in estimating subepithelial and epithelial resistance, artificial neural networks were trained to estimate these parameters from model impedance spectra. Spectra that reflect behavior of either HT-29/B6 or IPEC-J2 cells as well as the data scatter intrinsic to the used experimental setup were created computationally. To prove the proposed approach, reliability of the estimations was assessed with both modeled and measured impedance spectra. Transcellular and paracellular resistances obtained by such neural network-enhanced two-path impedance spectroscopy are shown to be sufficiently reliable to derive the underlying apical and basolateral resistances and capacitances. As an exemplary perturbation of pathophysiological importance, the effect of forskolin on the apical resistance of HT-29/B6 cells was quantified

Paracellular transport of phosphate along the intestine

Inorganic phosphate (P) is crucial for many biological functions, such as energy metabolism, signal transduction, and pH buffering. Efficient systems must exist to ensure sufficient supply for the body of P from diet. Previous experiments in humans and rodents suggest that two pathways for the absorption of P exist, an active transcellular P transport and a second paracellular pathway. Whereas the identity, role, and regulation of active P transport have been extensively studied, much less is known about the properties of the paracellular pathway. In Ussing chamber experiments, we characterized paracellular intestinal P permeabilities and fluxes. Dilution potential measurements in intestinal cell culture models demonstrated that the tight junction is permeable to P, with monovalent P having a higher permeability than divalent P. These findings were confirmed in rat and mouse intestinal segments by use of Ussing chambers and a combination of dilution potential measurements and fluxes of radiolabeled P. Both techniques yielded very similar results, showing that paracellular P fluxes were bidirectional and that P permeability was ~50% of the permeability for Na or Cl. P fluxes were a function of the concentration gradient and P species (mono- vs. divalent P). In mice lacking the active transcellular P transport component sodium-dependent P transporter NaPi-IIb, the paracellular pathway was not upregulated. In summary, the small and large intestines have a very high paracellular P permeability, which may favor monovalent P fluxes and allow efficient uptake of P even in the absence of active transcellular P uptake. The paracellular permeability for phosphate is high along the entire axis of the small and large intestine. There is a slight preference for monovalent phosphate. Paracellular phosphate fluxes do not increase when transcellular phosphate transport is genetically abolished. Paracellular phosphate transport may be an important target for therapies aiming to reduce intestinal phosphate absorption

Applicability of 2PI under conditions of altered R^ap or R^bl.

<p><b>A)</b> Nyquist plot of HT-29/B6 impedance spectrum after the application of forskolin. Arrows indicate estimates of R^sub (see inset) and R^T using the three methods, M1 (light grey), M2 (dark grey) and ANN (black). R^T = R^epi+R^sub. <b>B,C)</b> 2PI: Plotting epithelial conductance G^epi = 1/R^epi (♦, in the absence; ♦, in the presence of forskolin; ⋄, after EGTA application) against transepithelial fluorescein flux allows estimate of transcellular conductance, G^trans<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062913#pone.0062913-Krug1" target="_blank">[5]</a>. (B) Experiment without forskolin application. G^trans equals y-intercept (arrow) of the linear regression (grey line, G^trans = 0.64 mS/cm²). (C) G^trans in the presence of forskolin is obtained from the y-intercept (black arrow) of the linear regression (black line, G^trans = 1.69 mS/cm²). Shifting the linear regression to pass through the values obtained before the application of forskolin (grey line) allows estimate of G^trans in the absence of forskolin (grey arrow, G^trans = 0.65 mS/cm²). <b>D)</b> Comparison of R^trans values obtained from 30 experiments (15 without and 15 with forskolin or nystatin application, black and grey bars, respectively), using the three methods to estimate R^epi. Four experiments (three without and one with nystatin application) yielded negative or unreasonably high R^trans values when evaluated with methods M1 and M2. <b>E)</b> Same as (D) but after omission of these four experiments. Remaining estimates from experiments without forskolin or nystatin application were very similar for all three methods, estimates from experiments with forskolin or nystatin application showed lowest variance when evaluated by ANN.</p

Nyquist diagrams and equivalent electrical circuits.

<p><b>A)</b> Nyquist diagram of an impedance spectrum calculated for circuits depicted in (C) and (D). Data points, •, were calculated using 42 different frequencies between 1.3 Hz to 16 kHz. x-intercepts at low frequencies (f→0) correspond to the total epithelial resistance (R^T, also called “TER”). x-intercepts at high frequencies (f→∞) correspond to the subepithelial resistance, R^sub, as under these conditions the reactance of the membrane capacitor (1/(ω·C^epi)) approaches zero and thus short-circuits R^epi. Note that circuits (C) and (D) always yield semicircular spectra. <b>B)</b> Example for a Nyquist diagram of a non-semicircular impedance spectrum calculated for the circuit depicted in (E). Data points, <b>▴</b>, were calculated using 42 different frequencies between 1.3 Hz to 16 kHz. Spectra calculated for this model are the sum of two semicircles. Again, x-intercepts at low frequencies (f→0) correspond to the total epithelial resistance (R^T), x-intercepts at high frequencies (f→∞) correspond to the subepithelial resistance, R^sub. <b>C-E)</b> Equivalent electric circuits of epithelia. Components contributing to Repi are drawn in red, R^sub is highlighted in blue. Components contributing to R^T (sum of R^epi and R^sub) are joint by grey lines. <b>C)</b> Simplest form of an equivalent electric circuit describing epithelial and subepithelial resistance (R^epi, R^sub) and epithelial capacitance (C^epi). <b>D)</b> Equivalent electric circuit as in (C), but R^epi consists of two resistors in parallel, the transcellular (R^trans) and the paracellular resistance (R^para). <b>E)</b> Equivalent electric circuit as in (D), but the transcellular pathway is devided into an apical and a basolateral RC unit (R^ap, C^ap and R^bl, C^bl, respectively). </p