Spectral distribution for the decay tau -> nu_tau K pi

With the newly available data sets on hadronic tau decays from the B-factories BABAR and BELLE, and future data from BESIII, precise information on the decay distributions will soon become available. This calls for an improvement of the decay spectra also on the theoretical side. In this work, the distribution function for the decay tau -> nu_tau K pi will be presented with the relevant K pi vector and scalar form factors being calculated in the framework of the resonance chiral theory, also taking into account additional constraints from dispersion relations and short-distances. As a by-product the slope and curvature of the vector form factor F_+^{K pi}(s) are determined to be lambda_+^' = 25.6 10^{-3} and lambda_+^{''} = 1.31 10^{-3} respectively. From our approach it appears that it should be possible to obtain information on the low lying scalar K_0^*(800) as well as the second vector K^*(1410) resonances from the tau decay data. In particular, the exclusive branching fraction of the scalar component is found to be B[tau -> nu_tau(K pi)_{S-wave}] = (3.88 +- 0.19) 10^{-4}.Comment: 14 pages, 2 figure

Sensitivity to the Higgs sector of SUSY-seesaw models via LFV tau decays

Here we study and compare the sensitivity to the Higgs sector of the SUSY-seesaw models via the LFV tau decays: tau-> 3 mu, tau->K^{+}K^{-}, tau->mu eta and tau-> mu f_{0}. We emphasize that, at present, the two later channels are the most efficient ones to test indirectly the Higgs particles.Comment: 4 pages, 3 figures, conference SUSY09 Boston (M.Herrero

<VAP> Green Function in the Resonance Region

We analyse the three-point function of vector, axial-vector and pseudoscalar currents. In the spirit of large N_C, a resonance dominated Green function is confronted with the leading high-energy behaviour from the operator product expansion. The matching is shown to be fully compatible with a chiral resonance Lagrangian and it allows to determine some of the chiral low-energy constants of O(p^6).Comment: 13 pages, 2 figures. Published version. Results and conclusions unchange

Lepton flavour violating semileptonic tau decays in constrained MSSM-seesaw scenarios

In this work we study the Lepton Flavour Violating semileptonic $\tau$ decays: 1) $\tau \to \mu PP$ with $PP= \pi^+\pi^-, \pi^0\pi^0, K^+K^-, K^0 {\bar K}^0$; 2) $\tau \to \mu P$ with $P=\pi^0, \eta, \eta'$ and 3) $\tau \to \mu V$ with $V = \rho^0, \phi$. We work within the context of two constrained MSSM scenarios: the CMSSM and NUHM. A full one-(SUSY)loop computation is presented and the importance of the various contributions, the $\gamma$-, $Z$-, and Higgs bosons mediated ones are analysed. The hadronization of quark bilinears is performed within the chiral framework. Some discrepancies in the predicted rates for BR($\tau \to \mu \eta$), BR($\tau \to \mu \eta'$) and BR($\tau \to \mu K^+K^-$) are found with respect to previous estimates, which will be commented here. These three channels will be shown to be the most competitive ones to test simultaneously the Lepton Flavour Violation and the Higgs sector. We further present here a set of approximate formulas for all the semileptonic channels which we believe can be useful for further comparison with present and future data.Comment: 51 pages, 18 figures. Version published in JHEP06(2008)07

The PI-3-Kinase P110α Catalytic Subunit of T Lymphocytes Modulates Collagen-Induced Arthritis

The phosphatidylinositol 3-kinase (PI3K) family of enzymes plays a determinant role in inflammation and autoimmune responses. However, the implication of the different isoforms of catalytic subunits in these processes is not clear. Rheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disease that entails innate and adaptive immune response elements in which PI3K is a potential hub for immune modulation. In a mouse transgenic model with T-cell-specific deletion of p110α catalytic chain (p110α-/-ΔT), we show the modulation of collagen-induced arthritis (CIA) by this isoform of PI3K. In established arthritis, p110α-/-ΔT mice show decreased prevalence of illness than their control siblings, higher IgG1 titers and lower levels of IL-6 in serum, together with decreased ex vivo Collagen II (CII)-induced proliferation, IL-17A secretion and proportion of naive T cells in the lymph nodes. In a pre-arthritis phase, at 13 days post-Ag, T-cell-specific deletion of p110α chain induced an increased, less pathogenic IgG1/IgG2a antibodies ratio; changes in the fraction of naive and effector CD4+ subpopulations; and an increased number of CXCR5+ T cells in the draining lymph nodes of the p110α-/-ΔT mice. Strikingly, T-cell blasts in vitro obtained from non-immunized p110α-/-ΔT mice showed an increased expression of CXCR5, CD44 and ICOS surface markers and defective ICOS-induced signaling towards Akt phosphorylation. These results, plus the accumulation of cells in the lymph nodes in the early phase of the process, could explain the diminished illness incidence and prevalence in the p110α-/-ΔT mice and suggests a modulation of CIA by the p110α catalytic chain of PI3K, opening new avenues of intervention in T-cell-directed therapies to autoimmune diseases.This research was funded by Acción Estratégica en Salud Intramural (AESI) del Instituto de Salud Carlos III, grant number AESI PI16CIII/00012 to PP, and by Acción Estratégica en Salud AESI del Instituto de Salud Carlos III, grant number AES PI16/00032 to G.C.S

PI3-Kinase p110α Deficiency Modulates T Cell Homeostasis and Function and Attenuates Experimental Allergic Encephalitis in Mature Mice

Class I phosphoinositide 3-kinases (PI3K) are involved in the development of normal and autoimmune responses, including Experimental Autoimmune Encephalomyelitis (EAE), a mouse model for human multiple sclerosis (MS). Here, the role of the ubiquitously expressed class IA PI3K p110α catalytic subunits in EAE has been analyzed using a model of Cre/flox mediated T cell specific deletion of p110α catalytic chain (p110αΔT). Comparison of two month-old (young) and six month-old (mature) p110αΔT mice and their wild type (WT) counterparts indicated loss of spleen CD4+ T cells that increased with age, indicating a role of p110α in their homeostasis. In contrast, CD4+ T regulatory (Treg) cells were enhanced in mature p110αΔT mice when compared to WT mice. Since Myelin Oligodendrocyte Glycoprotein (MOG) peptide-induced EAE is dependent on, or mediated by CD4+ T cells and CD4+ T cell-derived cytokines and controlled by Treg cells, development of EAE in young and mature WT or p110αΔT mice was analyzed. EAE clinical symptoms and disease scores in six month p110αΔT mice were significantly lower than those of mature WT, or young WT and p110αΔT mice. Furthermore, ex vivo antigen activation of lymph node cells from MOG immunized mature p110αΔT mice induced significantly lower levels of IFN-γ and IL-17A than young p110αΔT or young and mature WT mice. Other cytokines including IL-2, IL-10 or TNF-α showed no significant differences between p110αΔT and WT mature mice. Our data show a lower incidence of MOG-induced EAE in mature p110αΔT mice linked to altered T cell homeostasis and lower secretion of inflammatory cytokines.This research was supported by Grants PI13/01809 (to JMR), PI13/02153 and PI16CIII/00012 (to PP) from “Acción Estratégica en Salud, Plan Estatal I+D+i”, Ministerio de Economía, Industria y Competitividad (MINECO, Spain), and by the Associazione Italiana Ricerca sul Cancro (Grant IG20714, AIRC, Milan) and Fondazione Cariplo (2017-0535) (to U.D.).S

τ−→π−π0ντ\tau^{-} \to \pi^{-} \pi^{0} \nu_\tau decay in the extended NJL model

The width of the decay $\tau^{-} \to \pi^{-} \pi^{0} \nu_\tau$ was calculated in the extended NJL model. Contact interaction of $W$ boson with pion pair as well as the contribution of the $\rho$ mesons in ground and first radial-exited states are taken into account. The sum of the contact diagram and diagram with intermediate $\rho$ meson in the ground state leads to the result which coincides with the result of the vector-dominance model. Our results are in satisfactory agreement with experimental data.Comment: 5 pages, 3 figures, 1 tabl

One-dimensional metal-organic frameworks built by coordinating 2,4,6-tris(4-pyridyl)-1,3,5-triazine linker with copper nodes : CO2 adsorption properties

Altres ajuts: acord transformatiu CRUE-CSICThe reaction between 2,4,6-tris(4-pyridyl)-1,3,5-triazine (4-tpt) and copper(II) hexafluoroacetylacetone (Cu(hfa)2) yields two different 1D metal-organic frameworks (MOFs), [(Cu(hfa)2)2(4-tpt)]n (1) and [Cu(hfa)2(4-tpt)]n (2). The Cu:4-tpt ratio in the new MOFs is determined by the reaction medium, particularly, the solvent used. The two compounds have been fully characterized, including crystal structure elucidation. [(Cu(hfa)2)2(4-tpt)]n (1), with a 2:1 Cu:4-tpt ratio, could be precipitated in either 1,1,2-trichloroethane or supercritical CO2. In (1), 4-tpt shows a tritopic coordination mode, but only half of the Cu(hfa)2 subunits act as a node, thus connecting two 4-tpt and giving a 1D network. The other half of Cu(hfa)2 subunits are connected only to one pyridine and thus protrude along the chains. The later Cu(hfa)2 fragments show a labile character and can be dissolved in diethyl ether to give the second MOF [Cu(hfa)2(4-tpt)]n (2), with a 1:1 Cu:4-tpt ratio. The compound (2) has also a 1D structure, with all the incorporated copper atoms acting as nodes. In this case, the packing of the chains defines accessible channels, which are perpendicular to the chain axis. After activation, N2 adsorption/desorption measurements at 77 K confirm the microporous character of (2) with an apparent surface area of 190 m2 g−1. Besides, at 273 K this material clearly shows a significant adsorption of CO2 prompted by noncoordinated nitrogen in the triazine linker

Venetoclax causes metabolic reprogramming independent of BCL-2 inhibition

BH3-mimetics are a new class of anti-cancer drugs that inhibit anti-apoptotic Bcl-2 proteins. In doing so, BH3-mimetics sensitise to cell death. Venetoclax is a potent, BCL-2 selective BH3-mimetic that is clinically approved for use in chronic lymphocytic leukaemia. Venetoclax has also been shown to inhibit mitochondrial metabolism, this is consistent with a proposed role for BCL-2 in metabolic regulation. We used venetoclax to understand BCL-2 metabolic function. Similar to others, we found that venetoclax inhibited mitochondrial respiration. In addition, we also found that venetoclax impairs TCA cycle activity leading to activation of reductive carboxylation. Importantly, the metabolic effects of venetoclax were independent of cell death because they were also observed in apoptosis-resistant BAX/BAK-deficient cells. However, unlike venetoclax treatment, inhibiting BCL-2 expression had no effect on mitochondrial respiration. Unexpectedly, we found that venetoclax also inhibited mitochondrial respiration and the TCA cycle in BCL-2 deficient cells and in cells lacking all anti-apoptotic BCL-2 family members. Investigating the basis of this off-target effect, we found that venetoclax-induced metabolic reprogramming was dependent upon the integrated stress response and ATF4 transcription factor. These data demonstrate that venetoclax affects cellular metabolism independent of BCL-2 inhibition. This off-target metabolic effect has potential to modulate venetoclax cytotoxicity