Instanton Induced Neutrino Majorana Masses in CFT Orientifolds with MSSM-like spectra

Recently it has been shown that string instanton effects may give rise to neutrino Majorana masses in certain classes of semi-realistic string compactifications. In this paper we make a systematic search for supersymmetric MSSM-like Type II Gepner orientifold constructions admitting boundary states associated with instantons giving rise to neutrino Majorana masses and other L- and/or B-violating operators. We analyze the zero mode structure of D-brane instantons on general type II orientifold compactifications, and show that only instantons with O(1) symmetry can have just the two zero modes required to contribute to the 4d superpotential. We however discuss how the addition of fluxes and/or possible non-perturbative extensions of the orientifold compactifications would allow also instantons with $Sp(2)$ and U(1) symmetries to generate such superpotentials. In the context of Gepner orientifolds with MSSM-like spectra, we find no models with O(1) instantons with just the required zero modes to generate a neutrino mass superpotential. On the other hand we find a number of models in one particular orientifold of the Gepner model $(2,4,22,22)$ with $Sp(2)$ instantons with a few extra uncharged non-chiral zero modes which could be easily lifted by the mentioned effects. A few more orientifold examples are also found under less stringent constraints on the zero modes. This class of $Sp(2)$ instantons have the interesting property that R-parity conservation is automatic and the flavour structure of the neutrino Majorana mass matrices has a simple factorized form.Comment: 68 pages, 2 figures; v2. typos corrected, refs adde

Gauge thresholds in the presence of oblique magnetic fluxes

We compute the one-loop partition function and analyze the conditions for tadpole cancellation in type I theories compactified on tori in the presence of internal oblique magnetic fields. We check open - closed string channel duality and discuss the effect of T-duality. We address the issue of the quantum consistency of the toroidal model with stabilized moduli recently proposed by Antoniadis and Maillard (AM). We then pass to describe the computation of one-loop threshold corrections to the gauge couplings in models of this kind. Finally we briefly comment on coupling unification and dilaton stabilization in phenomenologically more viable modelsComment: 34 pages, 2 figures; references added, major changes to the discussion of the model proposed by Antoniadis and Maillar

G. DWORKIN, Harmless Wrongdoing in A. Cadoppi (a cura di), Laicità, Valori e Diritto penale, The Moral Limits of the Criminal Law, Giuffrè, Milano, 2010

Traduzione dall'inglese all'italian

Intracerebroventricular interleukin-1 alpha increases immunocyte beta-endorphin concentrations in the rat:involvement of corticotropin releasing hormone and neurotransmitters

The opioid peptide \u3b2-endorphin (BE) is synthesized and secreted by the cells of the immune system and has been shown to participate in the modulation of immune responses, e.g. during stress. Interleukin-1 (IL-1) is a potent activator of the corticotropin-releasing hormone (CRH) system in the hypothalamus, and it has been shown to be involved in many stress responses, including immunosuppression. We studied the effect of centrally injected IL- 1\u3b1 on immunocyte BE concentrations in the rat. IL-1\u3b1 (1 ng/rat, intracerebroventricularly) significantly (P < 0.01) increased the concentrations of the peptide in splenocytes, lymph node cells, and peripheral blood mononuclear cells 2 and 24 h after treatment. Intracerebroventricular, but not iv, administration of 2 \u3bcg IL-1 receptor antagonist blocked the IL-1\u3b1-induced increase. These effects were also prevented by the intracerebroventricular administration of the CRH receptor antagonist \u3b1-helical CRH-(9-41). Treatment with 6-hydroxydopamine and 5,7- dihydroxytryptamine, which deplete the catecholaminergic or the serotoninergic systems, respectively, blocked the increase in BE induced by the cytokine. In contrast, hypophysectomy and treatment with indomethacin did not modify the effect of IL. The increase in immunocyte BE, therefore, seems to depend on the activation of CRH, catecholamines, and serotonin, but to be independent of activation of the hypothalamus-pituitary-adrenal-axis and prostaglandins. The immunocyte BE increase could be involved in the immunosuppression induced by central IL-1\u3b1

Central effects of tumor factor alfa and interleukin-1a on nociceptive thresholds and spontaneous locomotor activity

To extend the knowledge on the central effects of cytokines, we studied the effects of tumor necrosis factor \u3b1 and interleukin-1\u3b1 on nociceptive thresholds and spontaneous locomotor activity in rats. After central administration, both tumor necrosis factor \u3b1 and interleukin-1\u3b1 significantly (P<0.001) increase the nociceptive thresholds as measured by the hot-plate test. Tumor necrosis factor \u3b1, but not interleukin-1\u3b1 decreases spontaneous locomotor activity evaluated by the Animex test. The increase in nociceptive thresholds induced by tumor necrosis factor \u3b1 or interleukin-1\u3b1 is not affected by the opiate receptor antagonist naloxone, or antisera against the endogenous opioids \u3b2-endorphin, met-enkephalin or dynorphin. The analgesic effect of tumor necrosis factor \u3b1 is completely antagonized by anti-IL-1 antibodies. Moreover, the cyclooxygenase inhibitor indomethacin does not antagonize the increase of nociceptive thresholds induced by either cytokine