Hardness and structure characterization of Ti(6)Al(4)V films produced by reactive magnetron sputtering on a conventional austenitic stainless steel

Ti(6)Al(4)V thin films were grown by magnetron sputtering on a conventional austenitic stainless steel. Five deposition conditions varying both the deposition chamber pressure and the plasma power were studied. Highly textured thin films were obtained, their crystallite size (C) 2008 Elsevier Ltd. All rights reserved.

Different epitopes of the LACK protein are recognized by V beta 4 V alpha 8 CD4+ T cells in H-2b and H-2d mice susceptible to Leishmania major.

After inoculation of Leishmania major, a rapid production of IL-4 by LACK-specific CD4+ T cells has been shown to drive Th2 cell development in susceptible mice i.e. BALB/c and C57BL/6 mice rendered susceptible by neutralization of IFN-gamma at the onset of infection. Here, we showed that peptide AA 156-173 induced an early IL-4 mRNA expression not only in BALB/c mice but also in resistant B10.D2 mice when IFN-gamma is neutralized. Epitope mapping of LACK protein demonstrated that peptide containing AA 293-305 induced early IL-4 mRNA transcripts in susceptible H-2b mice i.e. BALB/b and resistant C57BL/6 mice when IFN-gamma is neutralized. Stringently, the early IL-4 response to the H-2d (AA 156-173) or the H-2b (AA 293-305) epitopes occurred in V beta 4 V alpha 8 CD4+ T cells from either H-2d or H-2b susceptible mice, respectively.

IL-4 rapidly produced by V beta 4 V alpha 8 CD4+ T cells instructs Th2 development and susceptibility to Leishmania major in BALB/c mice.

BALB/c mice develop aberrant T helper 2 (Th2) responses and suffer progressive disease after infection with Leishmania major. These outcomes depend on the production of interleukin-4 (IL-4) early after infection. Here we demonstrate that the burst of IL-4 mRNA, peaking in draining lymph nodes of BALB/c mice 16 hr after infection, occurs within CD4+ T cells that express V beta 4 V alpha 8 T cell receptors. In contrast to control and V beta 6-deficient BALB/c mice, V beta 4-deficient BALB/c mice were resistant to infection, demonstrating the role of these cells in Th2 development. The early IL-4 response was absent in these mice, and T helper 1 responses occurred following infection. Recombinant LACK antigen from L. major induced comparable IL-4 production in V beta 4 V alpha 8 CD4+ cells. Thus, the IL-4 required for Th2 development and susceptibility to L. major is produced by a restricted population of V beta 4 V alpha 8 CD4+ T cells after cognate interaction with a single antigen from this complex organism.

Rapid IL-4 production by Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells in resistant mice treated once with anti-IL-12 or -IFN-gamma antibodies at the onset of infection with Leishmania major instructs Th2 cell development, resulting in nonhealing lesions.

Rapid production of IL-4 by Leishmania homolog of mammalian RACK1 (LACK)-reactive CD4(+) T cells expressing the V beta 4-V alpha 8 TCR chains has been shown to drive aberrant Th2 cell development and susceptibility to Leishmania major in BALB/c mice. In contrast, mice from resistant strains fail to express this early IL-4 response. However, administration of either anti-IL-12 or -IFN-gamma at the initiation of infection allows the expression of this early IL-4 response in resistant mice. In this work we show that Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells also expressing the V beta 4-V alpha 8 TCR chains are the source of the early IL-4 response to L. major in resistant mice given anti-IL-12 or -IFN-gamma Abs only at the onset of infection. Strikingly, these cells were found to be required for the reversal of the natural resistance of C57BL/6 mice following a single administration of anti-IL-12 or -IFN-gamma Abs. Together these results suggest that a deficiency in mechanisms capable of down-regulating the early IL-4 response to L. major contributes to the exquisite susceptibility of BALB/c mice to L. major.

T cell receptor V beta repertoire in mice lacking endogenous mouse mammary tumor provirus.

When endogenous mouse mammary tumor virus (MMTV) superantigens (SAg) are expressed in the first weeks of life an efficient thymic deletion of T cells expressing MMTV SAg-reactive T cell receptor (TcR) V beta segments is observed. As most inbred mouse strains and wild mice contain integrated MMTV DNA, knowing the precise extent of MMTV influence on T cell development is required in order to study T cell immunobiology in the mouse. In this report, backcross breeding between BALB.D2 (Mtv-6, -7, -8 and -9) and 38CH (Mtv-) mice was carried out to obtain animals either lacking endogenous MMTV or containing a single MMTV locus, i.e. Mtv-6, -7, -8 or -9. The TcR V beta chain (TcR V beta) usage in these mice was analyzed using monoclonal antibodies specific for TcR V beta 2, V beta 3, V beta 4, V beta 5, V beta 6, V beta 7, V beta 8, V beta 11, V beta 12 and V beta 14 segments. Both Mtv-8+ mice and Mtv-9+ mice deleted TcR V beta 5+ and V beta 11+ T cells. Moreover, we also observed the deletion of TcR V beta 12+ cells by Mtv-8 and Mtv-9 products. Mtv-6+ and Mtv-7+ animals deleted TcR V beta 3+ and V beta 5+ cells, and TcR V beta 6+, V beta 7+ and V beta 8.1+ cells, respectively. Unexpectedly, TcR V beta 8.2+ cells were also deleted in some backcross mice expressing Mtv-7. TcR V beta 8.2 reactivity to Mtv-7 was shown to be brought by the 38CH strain and to result from an amino acid substitution (Asn-->Asp) in position 19 on the TcR V beta 8.2 fragment. Reactivities of BALB.D2 TcR V beta 8.2 and 38CH TcR V beta 8.2 to the exogenous infectious viruses, MMTV(SW) and MMTV(SHN), were compared. Finally, the observation of increased frequencies of TcR V beta 2+, V beta 4+ and V beta 8+ CD4+ T cell subsets in Mtv-8+ and Mtv-9+ mice, and TcR V beta 4+ CD4+ T cells in Mtv-6+ and Mtv-7+ mice, when compared with the T cell repertoire of Mtv- mice, is consistent with the possibility that MMTV products contribute to positive selection of T cells.

RECUEIL DES ŒUVRES POÉTIQUES de Jehan Molinet. Ms. in-fol. sur papier de 201 f., demi-rel. v. f, tr. r. (Rel. du XVIIIe siècle.)

Complainte (La) de Grece

COMPENDIVM // MVSICES DESCRIPTVM // AB ADRIANO PETIT COCLICO, // DISCIPVLO IOSQVINI DE PRES. // In quo praeter caetera tractantur haec : // De Modo ornate canendi. // De Regula Contrapuncti. // De compositione. // [4 vers latins adressés :] AD LECTOREM. // Impressum Norimbergae in officina Ioan- // nis Montani, & Vlrici Neuberi. // Cum priuilegio ad quinquennium. // M.D.LII.

Comprend : Fol. Diijr° - Sit nomen Domini benedictum in seculum (Fuga, à 4 v.) - Fol. Ej r° - Morior ego, si non habuero (Fuga, à 5 v.) - Fol. Ej r° - Fuga à 5 v. - Fol. Ej v° - Fuga à 2 v. - Fol. Ej v° - Fuga à 5 v. - Fol. Eij r° - Fuga à 5 v. - Fol. Eij v° - Fuga à 2 v. - Fol. Eiij v° - Fuga à 2 v. - Fol. Eiv r° - Fuga à 5 v. - Fol. Eiv v° - Fuga à 2 v. - Fol. F j r° - Canon à 3 v. - Fol. I j v° - Elegantia super Languir me fault (à 2 v.) - Fol. I ij v° - C'est à grant tort (Aliud exemplum, à 2 v.) - Fol. iiij v° - Fuga à 4 v. - Fol. Kiij r° - In omnibus requiem (à 1 v.) - Fol. Kiij v° - Salve sancta parens (à 1 v. (le début d'une autre voix sur la même portée en ms.)) - Fol. Liij r° - Vanitas vanitatum (à 4 v.) - Fol. Liij v° - Dixit Dominus (à 4 v.) - Fol. Liiij r° - Dixit Dominus (à 5 v. et faux-bourdon) - Fol. Liiij v° - O vos omnes (à 4 v.) - Fol. N j r° - Omnis arbor (à 2 v.) - Fol. N j v° - Pleni sunt coeli (à 2 v.) - Fol. Nij v° - Pleni sunt coeli (à 2 v.) - Fol. Niij r° - Christus spes mea (à 3 v.) - Fol. Niij r° - Et expecto resurectionem mortuorum (à 3 v.) - Fol. Niij v° - Pleni sunt coeli (à 3 v.) - Fol. Niiij v° - A solis ortu cardine ([Hymne], à 4 v.) - Fol. O j v° - [Canon] à 4 v. - Fol. O j v° - Revertere (à 4 v.) - Fol. O j v° - Adolescens graditur (à 5 v.) - Fol. Oij r° - Dominus mihi adiutor (Fuga, à 5 v.) - Fol. Oij v° - Surrexit Christus hodie (à 5 v.) - Fol. Oiij v° - Christus pro nobis passus est (à 5 v.) - Fol. Oiiij v° - Agnus Dei (à 6 v.) - Fol. Pj v° - [Pièce sans texte] (à 6 v.) - Fol. Pij v° - Sumite psalmum (Fuga, à 6 v.) - Fol. Pij v° - Nobilis est (Fuga, à 6 v.) - Fol. Piij r° - Ambulate dum lucem habetis (Fuga, à 7 v.) - Fol. Piij r° - Sancta Trinitas (Fuga, à 7 v.) - Fol. Piij v° - Omnis consummationis vidi finem (Canon, à 8 v. dont 4 notées)

El V. P. Antonio de Vieyra de la Compañia de Jesus : todos sus sermones y obras diferentes que de su original portugués se han traducidoen castellano : reducidos esta primera vez a orden e impresos en quatro tomos.

UANL