B-decay form factors from QCD sum rules

Im Standardmodell wird CP-Verletzung über eine einzige komplexe Phase in der unitären 3 × 3 CKM-Matrix, die Übergänge zwischen den verschiedenen Quarksorten beschreibt, implementiert. Üblicherweise wird die Unitarität dieser Matrix durch ein Dreieck in der komplexen &#961; - &#951;-Ebene veranschaulicht, so daß eine Verifikation auf das Messen der Winkel und Seitenlängen hinausläuft. Dies geschieht, indem Observable aus schwachen Zerfällen zu diesen in Beziehung gesetzt werden. Besonderes Interesse wurde dabei den Zerfällen von Mesonen mit einem schweren <i>b</i>-Quark zuteil, da allein aus diesen alle benötigten Parameter des sogenannten Unitaritätsdreieckes bestimmt werden können. Dabei treten hadronische Matrixelemente in den theoretischen Rechnungen auf, die nicht mittels störungstheoretischer Methoden berechnet werden können. In dieser Arbeit werden eine Reihe solcher Matrixelemente, sogenannte Formfaktoren, über zwei Ansätze im Rahmen der Lichtkegelsummenregeln berechnet. Einer, dessen Grundlagen im Laufe dieser Arbeit gelegt wurde, nutzt eine Korrelationsfunktion mit einem B-Meson, der andere mit dem leichten Meson im Endzustand auf der Massenschale. Ersterer ermöglicht es, verschiedene Endzustände durch eine einfache Änderung der Dirac-Struktur des entsprechenden Stroms zu berücksichtigen, birgt jedoch den Nachteil, daß nicht auf den Formalismus der Twistentwicklung des Zweiteren zurückgegriffen werden kann. Höhere Fockzustände des B-Mesons konnten berücksichtigt werden, indem die ersten Modelle für Dreiteilchenverteilungsamplituden hergeleitet wurden. Trotz fehlender &#945;_s-Korrekturen zeigt sich bereits eine hinreichende numerische Übereinstimmung mit weiter entwickelten Methoden. Im zweiten Ansatz wurden alle bekannten Korrekturen, insbesondere die bisher noch nicht überprüften &#945;_s-Beiträge zu Twist drei, neu berechnet und so |V_ub| mit konkurrenzfähiger Genauigkeit erhalten. <br /><br /> <a href=\u27http://dokumentix.ub.uni-siegen.de/opus/volltexte/incoming/2008/334/pdf/abstract.pdf\u27> Zusammenfassung (PDF-Dokument)</a>In the Standard Model of particle physics there is only one source of CP-violation. Namely, a single complex phase in the unitary 3 × 3 CKM-Matrix governing flavor transitions in the weak interaction. The unitarity is usually visualized by a triangle in the complex &#961; - &#951;-plane. Therefore testing this framework comes down to measuring weak decays, relating observables to sides and angles of this so called Unitarity Triangle(UT). Particular interest in this respect is payed to decays of mesons containing a heavy <i>b</i>-quark, giving the opportunity to alone determine all parameters of the UT. Doing this is far from easy. Besides tedious experimental measurements the theoretical calculations are plagued by hadronic quantities which cannot be determined by perturbation theory. In this work several of these quantities so called form factors are computed using the well known method of light cone sum rules(LCSR). Two different setups have been used. One, established in this work, utilizing a correlation function with an on-shell B-Meson and one following the traditional calculation by taking the light meson on-shell. Both using light cone expansion in the respective on-shell mesons distribution amplitudes. While the first approach allows to calculate a whole bunch of phenomenologically interesting quantities by just changing Dirac-structures of the relevant currents it has the drawback that it does not have access to the well developed twist expansion of the latter. To incorporate higher Fock-state contributions the first models for three-particle distribution amplitudes of the B-Meson have been derived. &#945;_s-corrections remain out of the scope of this work. Nevertheless does a comparison with more sophisticated methods show an encouraging numerical agreement. In the second setup all known corrections especially the never verified &#945;_s-corrections to Twist three terms have been recalculated and a competitive result for the CKM-matrixelement |V_ub| was obtained. <br /><br /> <a href=\u27http://dokumentix.ub.uni-siegen.de/opus/volltexte/incoming/2008/334/pdf/abstract.pdf\u27> Abstract (PDF-Dokument)</a

Form Factors from Light-Cone Sum Rules with B-Meson Distribution Amplitudes

New sum rules for $B\to \pi,K$ and $B\to \rho,K^*$ form factors are derived from the correlation functions expanded near the light-cone in terms of B-meson distribution amplitudes. The contributions of quark-antiquark and quark-antiquark-gluon components in the B meson are taken into account. Models for the B-meson three-particle distribution amplitudes are suggested, based on QCD sum rules in HQET. Employing the new light-cone sum rules we calculate the form factors at small momentum transfers, including $SU(3)_{fl}$ violation effects. The results agree with the predictions of the conventional light-cone sum rules.Comment: 32 pages, 7 figures, the discussion of numerical results extended, two references added, version to be published in Phys.Rev.

Fgfr1 signalling in the development of a sexually selected trait in vertebrates, the sword of swordtail fish

<p>Abstract</p> <p>Background</p> <p>One of Darwin's chosen examples for his idea of sexual selection through female choice was the "sword", a colourful extension of the caudal fin of male swordtails of the genus <it>Xiphophorus</it>. Platyfish, also members of the genus <it>Xiphophorus</it>, are thought to have arisen from within the swordtails, but have secondarily lost the ability to develop a sword. The sustained increase of testosterone during sexual maturation initiates sword development in male swordtails. Addition of testosterone also induces sword-like fin extensions in some platyfish species, suggesting that the genetic interactions required for sword development may be dormant, rather than lost, within platyfish. Despite considerable interest in the evolution of the sword from a behavioural or evolutionary point of view, little is known about the developmental changes that resulted in the gain and secondary loss of the sword. Up-regulation of <it>msxC </it>had been shown to characterize the development of both swords and the gonopodium, a modified anal fin that serves as an intromittent organ, and prompted investigations of the regulatory mechanisms that control <it>msxC </it>and sword growth.</p> <p>Results</p> <p>By comparing both development and regeneration of caudal fins in swordtails and platyfish, we show that <it>fgfr1 </it>is strongly up-regulated in developing and regenerating sword and gonopodial rays. Characterization of the fin overgrowth mutant <it>brushtail </it>in a platyfish background confirmed that fin regeneration rates are correlated with the expression levels of <it>fgfr1 </it>and <it>msxC</it>. Moreover, <it>brushtail </it>re-awakens the dormant mechanisms of sword development in platyfish and activates <it>fgfr1/msxC</it>-signalling. Although both genes are co-expressed in scleroblasts, expression of <it>msxC </it>in the distal blastema may be independent of <it>fgfr1</it>. Known regulators of Fgf-signalling in teleost fins, <it>fgf20a </it>and <it>fgf24</it>, are transiently expressed only during regeneration and thus not likely to be required in developing swords.</p> <p>Conclusion</p> <p>Our data suggest that Fgf-signalling is involved upstream of <it>msxC </it>in the development of the sword and gonopodium in male swordtails. Activation of a gene regulatory network that includes <it>fgfr1 </it>and <it>msxC </it>is positively correlated with fin ray growth rates and can be re-activated in platyfish to form small sword-like fin extensions. These findings point towards a disruption between the <it>fgfr1/msxC </it>network and its regulation by testosterone as a likely developmental cause for sword-loss in platyfish.</p

Retinoic Acid Is Involved in the Metamorphosis of the Anal Fin into an Intromittent Organ, the Gonopodium, in the Green Swordtail (Xiphophorus hellerii)

In poeciliid fish the male anal fin has been transformed into a gonopodium, an intromittent organ required for internal fertilization. Elevated testosterone levels induce metamorphosis of a subset of anal fin rays to grow and form the specialized terminal structures of the gonopodium. The molecular mechanisms underlying these processes are largely unknown. Here, we investigated whether retinoic acid (RA) signaling is involved in gonopodium development in the swordtail Xiphophorus hellerii. We showed that aldh1a2, a RA synthesizing enzyme, and the RA receptors, rar-ga and rar-gb, are expressed in anal fins during metamorphosis. aldh1a2 expression is regulated by testosterone in a concentration-dependent manner and is up-regulated in both hormone-induced and naturally developing gonopodia. Androgen receptor (ar), a putative regulator of gonopodial development, is co-expressed with aldh1a2 and the RA receptors in gonopodial rays. Importantly, experimental increase of RA signaling promoted growth of the gonopodium and increased the number of new segments. Based on gene expression analyses and pharmacological manipulation of gonopodium development, we show that the RA signaling pathway is activated in response to androgen signaling and promotes fin ray growth and development during the metamorphosis of the anal fin into the gonopodium

BB-Meson Distribution Amplitude from the B→πB\to \pi Form Factor

Employing the light-cone sum rule approach in QCD, we relate the $B$-meson distribution amplitude to the $B\to \pi$ form factor at zero momentum transfer. In leading order, the sum rule is converted into a simple expression for the inverse moment $\lambda_B$ of the distribution amplitude $\phi_{+}^B$. Using as an input the $B\to\pi$ form factor calculated from the light-cone sum rule in terms of pion distribution amplitudes, we obtain an estimate: $\lambda_B =460 \pm 160$ MeV. We investigate how this result is modified by the $B$-meson three-particle distribution amplitudes.Comment: 11 pages, 1 figure, version to appear in Phys.Lett.

Ectopic Expression of Neurogenin 2 Alone is Sufficient to Induce Differentiation of Embryonic Stem Cells into Mature Neurons

Recent studies show that combinations of defined key developmental transcription factors (TFs) can reprogram somatic cells to pluripotency or induce cell conversion of one somatic cell type to another. However, it is not clear if single genes can define a cell̀s identity and if the cell fate defining potential of TFs is also operative in pluripotent stem cells in vitro. Here, we show that ectopic expression of the neural TF Neurogenin2 (Ngn2) is sufficient to induce rapid and efficient differentiation of embryonic stem cells (ESCs) into mature glutamatergic neurons. Ngn2-induced neuronal differentiation did not require any additional external or internal factors and occurred even under pluripotency-promoting conditions. Differentiated cells displayed neuron-specific morphology, protein expression, and functional features, most importantly the generation of action potentials and contacts with hippocampal neurons. Gene expression analyses revealed that Ngn2-induced in vitro differentiation partially resembled neurogenesis in vivo, as it included specific activation of Ngn2 target genes and interaction partners. These findings demonstrate that a single gene is sufficient to determine cell fate decisions of uncommitted stem cells thus giving insights into the role of key developmental genes during lineage commitment. Furthermore, we present a promising tool to improve directed differentiation strategies for applications in both stem cell research and regenerative medicine

Molekulare Grundlagen der Entwicklung des Schwertes, eines sexuell selektierten Merkmales im Genus Xiphophorus

The sword, a colourful extension of the ventral caudal fin of male swordtails of the genus Xiphophorus was one of Darwin's chosen examples for his idea of sexual selection. Experiments in X. helleri have shown that (1) the total length of the sword is an important criterion during mate choice and (2) the females have a preference for a specific pattern of differently coloured stripes. Besides its role in the process of sexual selection the sword has an interesting evolutionary history. Only males of swordtail species develop a sword, whereas males of platyfish, another group within the genus Xiphophorus, are swordless. One scenario suggests a sworded common ancestor of all Xiphophorus species and a secondary loss of the sword in platyfish during evolution. It remains elusive which molecular events preceded the loss of the sword in platyfish, since the genetic network that controls sword development is poorly understood. Data from interspecies crosses suggests that multiple loci control sword development. In addition, testosterone was identified as sufficient factor to induce sword development in immature fish, which indicates that sword development is controlled by androgen signalling. Recent work also identified the homeobox transcription factor msxC as another potential candidate, since it was shown to be up-regulated in growing sword rays. Up-regulation of msxC has also been found in the developing gonopodium, the modified male anal fin that is also induced by exogenous testosterone. The gonopodium is evolutionary older than the sword and it was assumed that the genetic network controlling gonopodium development was partly co-opted for the sword.In chapter I we focussed on Fgf signalling that has been shown to regulate msxC expression during caudal fin regeneration. Both sword development and fin regeneration are characterized by elevated outgrowth of fin rays, which is likely controlled by a conserved genetic network. We showed that fgfr1 is specifically up-regulated in developing swords, which presents first evidence that fgfr1 is involved in sword development. A similar pattern was also observed in the developing gonopodium. fgfr1 is spatial-temporally co-expressed with msxC both in the sword and the gonopodium, which might indicate a putative interaction between both genes. Interestingly, in the ventral caudal fin rays of testosterone treated platyfish, fgfr1 and msxC are only up-regulated after prolonged hormone treatment. This points towards a disruption between the fgfr1/msxC network and its regulation by testosterone as a likely developmental cause for sword-loss in platyfish. Finally, we demonstrated that fgfr1 and msxC activation is correlated with fin ray growth rates by employing the X. maculatus brushtail mutant that exhibits excessive growth of the median caudal fin rays.Only a subset of the genes involved in sword development can be targeted by candidate gene approaches (e.g. as performed in chapter I), because prior knowledge about gene function is needed to select appropriate candidates. In chapter II we employed the suppression subtractive hybridisation (SSH) technique to bypass this limitation, because this method can be applied to isolate genes that are differentially expressed in swords and gonopodia compared to juvenile fins without ab initio knowledge of gene identity or function. In this study we identified 128 different sequences with significant similarity to known genes. We showed that four of these sequences with similarity to rack1, dusp1, klf2 and tmsb a-like are specifically up-regulated in induced swords and/or gonopodia. In parallel, we also showed that these genes are strongly expressed during fin regeneration. Therefore these four genes are interesting candidates to further analyse their role in both sword development and fin regeneration.The anal fin of male Xiphophorus fishes is modified into an intromittant organ, the gonopodium. The gonopodium is formed during sexual maturation by a subset of three anal fin rays, the 3-4-5 complex. These three rays are modified in terms of ray length, segment thickness and different distal structures like blades, claws, spines, hooks and serraes. Therefore, the mature gonopodium exhibits a strong proximo-distal polarity due to the smaller terminal segments and terminal structures. Gonopodium development is thought to proceed in two phases. During the first phase, low levels of testosterone promote ray outgrowth, whereas high levels of testosterone induce the formation of terminal structures during the second phase. Shh, androgen and probably Fgf signalling are involved in gonopodium development.In chapter 3 we tested the role of retinoic acid (RA) signalling during gonopodium development, for two reasons. RA signalling is essential for paired appendage development in vertebrates and it provides positional information along the proximodistal axis in developing and regenerating limbs. Therefore, RA signalling might either play a general role in gonopodium development or specific role in establishing the proximo-distal polarity within the gonopodium. RA, a small lipophilic, diffusible molecule is synthesised by retinaldehyde dehydrogenases (Aldh1as) and stimulates gene expression through binding to two types of receptors, retinoic acid receptors (RARs) and retinoic X receptors (RXRs). In this study we showed that aldh1a2, a RA synthesising enzyme, and two RA receptors, rarg-a and rarg-b, are expressed in developing gonopodia. Inhibiting RA synthesis with DEAB increases the length of newly formed terminal segments, whereas the segment length decreases when RA signalling is overactivated by exogenous all-trans RA. Both the expression and the functional data present first evidence that RA signalling is involved in gonopodium development. Finally, we showed that androgen receptors b (arb), a putative regulator up-stream of RA signalling is co-expressed with aldh1a2 in the distal mesenchyme of the gononopodial rays. Interestingly, developing swords lack the distal expression domain of both aldh1a2 and arb, whereas the two rars are similarly expressed in developing swords and gonopodia. This might point towards an interaction between these two genes

Light-Cone Sum Rule Approach for Baryon Form Factors

We present the state-of-the-art of the light-cone sum rule approach to Baryon form factors. The essence of this approach is that soft Feynman contributions are calculated in terms of small transverse distance quantities using dispersion relations and duality. The form factors are thus expressed in terms of nucleon wave functions at small transverse separations, called distribution amplitudes, without any additional parameters. The distribution amplitudes, therefore, can be extracted from the comparison with the experimental data on form factors and compared to the results of lattice QCD simulations

Identification of novel genes involved in the development of the sword and gonopodium in swordtail fish

Male sword tail fish of the genus Xiphophorus develop a sword, a colourful extension of the caudal fin, that evolved by sexual selection through female choice. Swords and gonopodia, an intromittent organ developing from the male anal fin, can be prematurely induced by exogenous testosterone, offering the opportunity to examine the identity and expression profiles of genes required during various stages of fin metamorphosis. Here, we employed suppression subtractive hybridisation to identify genes specifically up-regulated during two early stages of sword and gonopodium development. We identified 128 different sequences with significant similarity to known genes and characterized the rack 1, dusp1, klf2, and tmsβ-like genes as specifically up-regulated in developing as well as regenerating fin rays of the sword and gonopodium. We show that some of these genes follow distinct expression profiles in swords and gonopodia, suggesting differences in the genetic networks underlying the development of anal and caudal fin modifications

Enrichment of FGF8-expressing cells from neurally induced human pluripotent stem cell cultures

In early vertebrate development, organizer regions-groups of cells that signal to and thereby influence neighboring cells by secreted morphogens-play pivotal roles in the establishment and maintenance of cell identities within defined tissue territories. The midbrain-hindbrain organizer drives regionalization of neural tissue into midbrain and hindbrain territories with fibroblast growth factor 8 (FGF8) acting as a key morphogen. This organizer has been extensively studied in chicken, mouse, and zebrafish. Here, we demonstrate the enrichment of FGF8-expressing cells from human pluripotent stem cells (hPSCs), cultured as attached embryoid bodies using antibodies that recognize "Similar Expression to Fgf" (SEF) and Frizzled proteins. The arrangement of cells in embryoid body subsets of these cultures and the gene expression profile of the FGF8-expressing population show certain similarities to the midbrain-hindbrain organizer in animal models. In the embryonic chick brain, the enriched cell population induces formation of midbrain structures, consistent with FGF8-organizing capability