Chacaltaya: towards a solution of the knee ....?

Cosmic rays physics is currently being studied with rather sophisticated detectors running in a variety of experimental conditions and atmospheric depths around the world. In this paper we describe the reasons why cosmic ray physics experiments at high altitudes like Chacaltaya are so important for resolving some of the open problems in cosmic physics. A discussion on the future prospects of the high altitude mountain laboratories such as Chacaltaya for cosmic ray physics is presented.Comment: 8 pages, 4 figures, to appear in Proceedings of the "Chacaltaya Meeting on Cosmic Ray Physics", Il Nuovo Ciment

Enhanced graphene nonlinear response through geometrical plasmon focusing

We propose a simple approach to couple light into graphene plasmons and focus these excitations at focal spots of a size determined by the plasmon wavelength, thus producing high optical field enhancement that boosts the nonlinear response of the material. More precisely, we consider a graphene structure in which incident light is coupled to its plasmons at the carbon edges and subsequently focused on a spot of size comparable to the plasmon wavelength. We observe large confinement of graphene plasmons, materializing in small, intense focal spots, in which the extraordinary nonlinear response of this material leads to relatively intense harmonic generation. This result shows the potential of plasmon focusing in suitably edged graphene structures to produce large field confinement and nonlinear response without involving elaborated nanostructuring.Peer ReviewedPostprint (published version

Measure of the size of CP violation in extended models

In this letter we introduce a possible measure of the size of CP violation in the Standard Model and its extensions, based on quantities invariant under the change of weak quark basis. We also introduce a measure of the ``average size'' of CP violation in a model, which can be used to compare the size of CP violation in models involving extra sequential or vector-like quarks, or left-right symmetry.Comment: LaTeX, 7 pages, no figure

Two minor determinants of myelin basic protein induce experimental allergic encephalomyelitis in SJL/J mice

Experimental allergic encephalomyelitis (EAE)' is an autoimmune inflammatory demyelinating disease in the central nervous system (CNS) of animals immunized with myelin basic protein (MBP). The disease is directly mediated by Thelper cells that recognize MBP in the context ofclass II antigens of the MHC (1-3). In nude mice, a single clone of adoptively transferred MBP-reactive T helper cells can cause EAE (4), suggesting that these are the only T cells required for disease induction. As a prototypic model of T helper cell-mediated autoimmune disease, observations in EAE could likely be applicable to other T helper cell-mediated diseases such as murine lupus (5), thyroiditis (6), collagen arthritis (7), and adjuvant arthritis (8), as well as human autoimmune diseases. The MBP epitope is determined in part by the MHC. Using proteolytic peptide fragments of MBP, SJL/J (H-2s) and BIO.T(6R) (H-2q) mice were found to develop EAE to the COOH-terminal peptide of MBP, whereas PL/J (H-2u) and A/J (H-2k) mice developed EAE to the NH2-terminal peptide of MBP (9). Recently, by using synthetic peptides that overcome the difficulties of obtaining pure uncontaminated proteolytic peptides, a single T cell encephalitogenic epitope for PL/J mice has been identified . This epitope consists of the first nine NH2-terminal amino acid residues of MBP which must be acetylated at the a amino group to induce disease (10). Similar fine mapping of the encephalitogenic T cell epitope(s) for SJL/J mice has not been done, in part because of the large size of the COOH-terminal peptic fragment of MBP (residues 89-169 of rat MBP, reference 9). MouseMBP consists offour major forms due to differential RNA splicing of exons II and VI (11), resulting in molecular masses of 21, 18.5, 17.5, and 14 kD, in the relative amounts of 1 :10:3.5:35 . Since EAE can also be induced with the small form of rat MBP (14 kD), which has exons II and VI of the MBP gene deleted (12), the COOH-terminal encephalitogenic determinant for SJL/J mice must be present within a segment ofonly 42 amino acid residues . Consistent withthis notion is the observation that this peptide sequence is identical among the MBPs of several mammalian species, including mouse, rat, bovine, guinea pig, and porcine, all of which can induce EAE in SJL/mice (13, 14). To identify the SJL/J encephalitogenic T cell epitope(s), overlapping peptides to the COOH-terminal region ofthe small form of mouse MBP were synthesized. Two overlapping peptides encompassing an 18-amino acid region were found to elicit EAE in SJL/J mice. The finding of a single peptide region of MBP that is responsible for encephalitogenic T cell epitopes in SJL/J mice is analogous to that of the PL/J mice and has implications for the development of specific therapy for T cell-mediated autoimmune diseases