Decaying into the Hidden Sector

The existence of light hidden sectors is an exciting possibility that may be tested in the near future. If DM is allowed to decay into such a hidden sector through GUT suppressed operators, it can accommodate the recent cosmic ray observations without over-producing antiprotons or interfering with the attractive features of the thermal WIMP. Models of this kind are simple to construct, generic and evade all astrophysical bounds. We provide tools for constructing such models and present several distinct examples. The light hidden spectrum and DM couplings can be probed in the near future, by measuring astrophysical photon and neutrino fluxes. These indirect signatures are complimentary to the direct production signals, such as lepton jets, predicted by these models.Comment: 40 pages, 5 figure

Search for a vector gauge boson in phi meson decays with the KLOE detector

The existence of a light dark force mediator has been tested with the KLOE detector at DAPHNE. This particle, called U, is searched for using the decay chain phi-->etaU, eta-->pi+pi-pi0, U-->e+e-. No evidence is found in 1.5 fb-1 of data. The resulting exclusion plot covers the mass range 5<M_U<470 MeV, setting an upper limit on the ratio between the U boson coupling constant and the fine structure constant, alpha'/alpha, of <= 2x10^-5 at 90% C.L. for 50<M_U<420 MeV.Comment: 13 pages, 8 figure

Roquin suppresses the PI3K-mTOR signaling pathway to inhibit T helper cell differentiation and conversion of treg to Tfr cells.

Roquin proteins preclude spontaneous T cell activation and aberrant differentiation of T follicular helper (Tfh) or T helper 17 (Th17) cells. Here we showed that deletion of Roquin-encoding alleles specifically in regulatory T (Treg) cells also caused the activation of conventional T cells. Roquin-deficient Treg cells downregulated CD25, acquired a follicular Treg (Tfr) cell phenotype, and suppressed germinal center reactions but could not protect from colitis. Roquin inhibited the PI3K-mTOR signaling pathway by upregulation of Pten through interfering with miR-17 92 binding to an overlapping cis-element in the Pten 3&#39; UTR, and downregulated the Foxo1-specific E3 ubiquitin ligase Itch. Loss of Roquin enhan ced Akt-mTOR signaling and protein synthesis, whereas inhibition of PI3K or mTOR in Roquin-deficient T cells corrected enhanced Tfh and Th17 or reduced iTreg cell differentiation. Thereby, Roquin-mediated control of PI3K-mTOR signaling prevents autoimmunity by restraining activation and differentiation of conventional T cells and specialization of Treg cells. Essig et al. show that spontaneous activation and aberrant differentiation of Roquin-deficient T cells involves cell-intrinsic causes in not only conventional T cells but also impaired Treg cell function. In both cell types, Roquin inhibits the PI3K-mTOR signaling pathway at several levels, thereby controlling protein biosynthesis and limiting differentiation toward Th17 and Tfh cells as well as preventing the conversion and functional specialization of Treg into Tfr cells

Capillary haemangioma of the testis

A case of testicular capillary haemangioma is reported and the importance of intraoperative examination of this very rare lesion emphasised. Capillary haemangioma of the testis can be similar to malignant testicular tumours on clinical presentation, as well as on ultrasonography and magnetic resonance imaging, and therefore should be included in the intraoperative differential diagnosis. Because of the benign nature of this lesion, conservative surgical treatment by means of tumour enucleation with preservation of the testis is possible, if intraoperative examination of frozen sections of representative tissue can be performed. Key Words: testis • haemangiom