548 research outputs found

    Velos antiguos i modernos en los rostros de las mugeres sus con ueniençias, i daños : ilustración de la Real Premática de las Tapadas...a la señora doña María de Auellaneda...

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    Contiene: "Discurso geneálogico de la ilustre Casa y descendencia de Avellaneda"Sign.: [parágrafo-7parágrafo]4, 8[parágrafo]2, A-Z4, 2A-2L4, 2MHojas impresas por ambas carasPortada calcográficaDigitalización. Vitoria-Gasteiz : Fundación Sancho el Sabio, 2008Digitalización. Vitoria-Gasteiz : Archivos y Bibliotecas, Junio 1995Carton

    [Bando, 1831-02-10.]

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    Título tomado del principio de texto.Bando firmado por Martín León de Jáuregui, Romualdo de Landecho y Miguel de Artiñano, Secretario.Bando fechado en Bilbao, a 10 de febrero de 1831

    Cationic Amino Acid Uptake Constitutes a Metabolic Regulation Mechanism and Occurs in the Flagellar Pocket of Trypanosoma cruzi

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    Trypanosomatids' amino acid permeases are key proteins in parasite metabolism since they participate in the adaptation of parasites to different environments. Here, we report that TcAAP3, a member of a Trypanosoma cruzi multigene family of permeases, is a bona fide arginine transporter. Most higher eukaryotic cells incorporate cationic amino acids through a single transporter. In contrast, T. cruzi can recognize and transport cationic amino acids by mono-specific permeases since a 100-fold molar excess of lysine could not affect the arginine transport in parasites that over-express the arginine permease (TcAAP3 epimastigotes). In order to test if the permease activity regulates downstream processes of the arginine metabolism, the expression of the single T. cruzi enzyme that uses arginine as substrate, arginine kinase, was evaluated in TcAAP3 epimastigotes. In this parasite model, intracellular arginine concentration increases 4-folds and ATP level remains constant until cultures reach the stationary phase of growth, with decreases of about 6-folds in respect to the controls. Interestingly, Western Blot analysis demonstrated that arginine kinase is significantly down-regulated during the stationary phase of growth in TcAAP3 epimastigotes. This decrease could represent a compensatory mechanism for the increase in ATP consumption as a consequence of the displacement of the reaction equilibrium of arginine kinase, when the intracellular arginine concentration augments and the glucose from the medium is exhausted. Using immunofluorescence techniques we also determined that TcAAP3 and the specific lysine transporter TcAAP7 co-localize in a specialized region of the plasma membrane named flagellar pocket, staining a single locus close to the flagellar pocket collar. Taken together these data suggest that arginine transport is closely related to arginine metabolism and cell energy balance. The clinical relevance of studying trypanosomatids' permeases relies on the possibility of using these molecules as a route of entry of therapeutic drugs

    Epítome de la crónica del Rey Don Iván el Segundo de Castilla

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    Sign. : [calderón]\p6\s, A-Z\p6\s, Aa-Hh\p6\s.Desde p.308 a 342 "Libro quinto. Claros varones que florecieron en España... reducido a un breve catálogo por el noble caballero Fernán Pérez de Guzmán, corregido y adicionado por el Doctor Lorenço Galindez de Carvajal..."Esc. del editor Gabriel de LeónAntep.Texto a dos col.Port. a dos tintas.Copia digital. Valladolid : Junta de Castilla y León. Consejería de Cultura y Turismo, 2009-201

    Characterization of the Role of NKA in the Control of Puberty Onset and Gonadotropin Release in the Female Mouse.

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    The tachykinin neurokinin B (NKB, Tac2) is critical for proper GnRH release in mammals, however, the role of the other tachykinins, such as substance P (SP) and neurokinin A (NKA) in reproduction, is still not well understood. In this study, we demonstrate that NKA controls the timing of puberty onset (similar to NKB and SP) and stimulates LH release in adulthood through NKB-independent (but kisspeptin-dependent) mechanisms in the presence of sex steroids. Furthermore, this is achieved, at least in part, through the autosynaptic activation of Tac1 neurons, which express NK2R (Tacr2), the receptor for NKA. Conversely, in the absence of sex steroids, as observed in ovariectomy, NKA inhibits LH through a mechanism that requires the presence of functional receptors for NKB and dynorphin (NK3R and KOR, respectively). Moreover, the ability of NKA to modulate LH secretion is absent in Kiss1KO mice, suggesting that its action occurs upstream of Kiss1 neurons. Overall, we demonstrate that NKA signaling is a critical component in the central control of reproduction, by contributing to the indirect regulation of kisspeptin release

    Tachykinin signaling is required for the induction of the preovulatory LH surge and normal LH pulses.

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    Tachykinins (NKA, NKB and Substance P) are important components of the neuroendocrine control of reproduction by directly stimulating Kiss1 neurons to control GnRH pulsatility, essential for reproduction. Despite this role of tachykinins for successful reproduction, knockout mice for Tac1 (NKA/SP) and Tac2 (NKB) genes are fertile, resembling the phenotype of human patients bearing NKB signaling mutations, who often reverse their hypogonadal phenotype. This suggests the existence of compensatory mechanisms among the different tachykinin ligand-receptor systems, to maintain reproduction in the absence of one of them. In order to test this hypothesis, we generated complete tachykinin deficient mice (Tac1/Tac2KO). Male mice displayed delayed puberty onset and decreased LH pulsatility (frequency and amplitude of LH pulses) but preserved fertility. However, females did not show signs of puberty onset (first estrus) within 45 days after vaginal opening, displayed low frequency (but normal amplitude) of LH pulses and 80% of them remained infertile. Further evaluation identified a complete absence of the preovulatory LH surge in Tac1/Tac2KO females as well as in WT females treated with NKB or SP receptor antagonists. These data confirmed a fundamental role for tachykinins in the timing of puberty onset and LH pulsatility and uncovered a role of tachykinin signaling in the facilitation of the preovulatory LH surge. Overall, these findings indicate that tachykinin signaling plays a dominant role in the control of ovulation, with potential implications as pathogenic mechanism and therapeutic target to improve reproductive outcomes in women with ovulation impairments
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