On Invariant Structures of Black Hole Charges

We study "minimal degree" complete bases of duality- and "horizontal"- invariant homogeneous polynomials in the flux representation of two-centered black hole solutions in two classes of D=4 Einstein supergravity models with symmetric vector multiplets' scalar manifolds. Both classes exhibit an SL(2,R) "horizontal" symmetry. The first class encompasses N=2 and N=4 matter-coupled theories, with semi-simple U-duality given by SL(2,R) x SO(m,n); the analysis is carried out in the so-called Calabi-Vesentini symplectic frame (exhibiting maximal manifest covariance) and until order six in the fluxes included. The second class, exhibiting a non-trivial "horizontal" stabilizer SO(2), includes N=2 minimally coupled and N=3 matter coupled theories, with U-duality given by the pseudo-unitary group U(r,s) (related to complex flux representations). Finally, we comment on the formulation of special Kaehler geometry in terms of "generalized" groups of type E7.Comment: 1+24 pages; 1 Table. v2 : Eqs. (1.2) and (1.3) added; Eq. (2.87) change

Evidence for the decay BS0→K‾∗0μ+μ− {B}_S^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}

International audienceA search for the decay ${B}_S^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}$ is presented using data sets corresponding to 1.0, 2.0 and 1.6 fb$^{−1}$ of integrated luminosity collected during pp collisions with the LHCb experiment at centre-of-mass energies of 7, 8 and 13 TeV, respectively. An excess is found over the background-only hypothesis with a significance of 3.4 standard deviations. The branching fraction of the ${B}_S^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}$ decay is determined to be $\mathrm{\mathcal{B}}\left({B}_s^0\to {\overline{K}}^{\ast 0}{\mu}^{+}{\mu}^{-}\right)=\left[2.9\pm 1.0\left(\mathrm{stat}\right)\pm 0.2\left(\mathrm{syst}\right)\pm 0.3\left(\mathrm{norm}\right)\right]\times {10}^{-8}$ , where the first and second uncertainties are statistical and systematic, respectively. The third uncertainty is due to limited knowledge of external parameters used to normalise the branching fraction measurement

Fasting potentiates the anticancer activity of tyrosin kinase inhibitors by strenghtening MAPK signalling inhibition.

Tyrosine kinase inhibitors (TKIs) are now the mainstay of treatment in many types of cancer. However, their benefit is frequently short-lived, mandating the search for safe potentiation strategies. Cycles of fasting enhance the activity of chemo-radiotherapy in preclinical cancer models and dietary approaches based on fasting are currently explored in clinical trials. Whether combining fasting with TKIs is going to be potentially beneficial remains unknown. Here we report that starvation conditions increase the ability of commonly administered TKIs, including erlotinib, gefitinib, lapatinib, crizotinib and regorafenib, to block cancer cell growth, to inhibit the mitogen-activated protein kinase (MAPK) signaling pathway and to strengthen E2F-dependent transcription inhibition. In cancer xenografts models, both TKIs and cycles of fasting slowed tumor growth, but, when combined, these interventions were significantly more effective than either type of treatment alone. In conclusion, cycles of fasting or of specifically designed fasting-mimicking diets should be evaluated in clinical studies as a means to potentiate the activity of TKIs in clinical use

Realities and expectations of pharmacogenomics and personalized medicine: Impact of translating genetic knowledge into clinical practice

The implementation of genetic data for a better prediction of response to medications and adverse drug reactions is becoming a reality in some clinical fields. However, to be successful, personalized medicine should take advantage of an informational structured framework of genetic, phenotypic and environmental factors in order to provide the healthcare system with useful tools that can optimize the effectiveness of specific treatment. The impact of personalized medicine is potentially enormous, but the results that have so far been gathered are often difficult to translate into clinical practice. In this article we have summarized the most relevant applications of pharmacogenomics on diseases to which they have already been applied and fields in which they are currently emerging. The article provides an overview of the opportunities and shortcomings of the implementation of genetic information into personalized medicine and its full adoption in the clinic. In the second instance, it provides readers from different fields of expertise with an accessible interpretation to the barriers and opportunities in the use/adoption of pharmacogenomic testing between the different clinical areas