Sabén ya de veritat q'eixos moros volen guerra, ... [Texto impreso]

Octavilla

Apología libri de reditibus ecclesiasticis... Super c. ultimo XVI. q. I. Sermone primùm Hispano compositi, [et] ab eodem postea latinitate donati [Texto impreso] : adversus N. in nonnulis ei contradicentem

Contiene: Propvgnacvlvm apologiae libri de reditibvs ecclesiasticis Doct. Martini Azpilcveta ...

Cuaderno de las Leyes y nueuas decisiones hechas y ordenadas en la ciudad de Toro sobre las dudas de derecho q continuamente solían y suele ocurrir en estos reynos ... Con la glosa de Miguel de Cifuentes. 1546 [Texto impreso]

Datos de imp. tomados del colofón

Experimento de propagación en banda Q con Alphasat: Técnicas para la compensación del desapuntamiento

El grupo de investigación GTIC-Radiocomunicaciones de la Universidad Politécnica de Madrid (UPM) participa en uno de los experimentos de propagación de APEX (Alphasat Propagation Experiment), denominado Alphasat propagation experiment by measuring the copolar level of the Q-Band beacon at 39.4 GHz. El experimento comenzó en abril de 2014, midiendo la señal de 39,4 GHz. Durante los primeros meses hasta septiembre de 2014, se hicieron medidas con apuntamiento fijo. El satélite no es geoestacionario sino que tiene una cierta inclinación, por lo que su posición aparente no es fija, describiendo una pequeña elipse en el cielo. Como consecuencia de esto se produce una variación sistemática en el nivel de la señal recibida que hay que eliminar. El presente Trabajo fin de Grado recoge técnicas útiles para llevar a cabo la compensación del desapuntamiento producido por el apuntamiento fijo configurado en el receptor diseñado por el grupo de investigación GTIC-Radiocomunicaciones de la UPM. El conjunto de datos utilizado, ha sido preprocesado con anterioridad llevándose a cabo un proceso de marcado y sincronización de los datos obtenidos a través de la baliza a 39,4 GHz enviada desde el Alphasat. A lo largo del documento se interpretarán y compararán los resultados obtenidos mediante gráficas elaboradas tras la aplicación de las técnicas que se describen en el desarrollo del mismo.

Arnaldi de Villanova Medici acutissimi opera nuperrime reuisa: vna cum ipsius vita recenter hic apposita. Cu[m]q[ue] tractatu de philosophoru[m] lapide. Additionibus marginalibus tabulaq[ue] librorum et capitulorum in hac novissima impressionne diligenter additis [Texto impreso]

Fecha de 1532 y segundo impresor tomados del colofón

Historia del misterio divino del... sacramento del altar q. esta en los corporales de Daroca... en la còquista que el... rey... Jayme el primero hizo a los moros del reyno de Valencia... [Texto impreso]

Autor consta en prelim

Opressão econômica e violência social: retratos do cotidiano em três parábolas da Fonte Q (Q 12,39-40; 42-46; 19,12-27)

Num ambiente como o da Galiléia do século I, onde o ensino era realizado nas comunidades religiosas, vilarejos e núcleos familiares de forma oral, o método de fixação de ensinos mediante a assimilação de símbolos do cotidiano era fundamental. Por conta disso, acreditamos que, dentre as fontes orais ou escritas preservadas e organizadas pelos Evangelhos Sinóticos, as parábolas de Jesus compõem o gênero literário mais original por terem sido preservadas na memória, com maior precisão pelos primeiros seguidores de Jesus. Muitos estudiosos empreenderam importantes trabalhos para pesquisar o lugar social das parábolas de Jesus, a maioria deles partindo dos próprios textos dispostos como estão nos Evangelhos. Neste trabalho, nos propomos trabalhar as parábolas de Jesus como ditos bem preservados pela oralidade a partir da teoria da Fonte Q, que é tratada como um dos estratos mais primitivos da tradição formativa dos Evangelhos Sinóticos e do movimento de Jesus. As parábolas do Ladrão (Q 12,39-40), Servo Infiel (Q 12,42-46) e do Dinheiro Confiado (Q 19,12-27) sempre foram vistas pela tradição eclesial como parábolas que tratam da necessária vigilância do cristão por conta da repentina parusia de Jesus. No entanto, nesse trabalho vamos além, pois acreditamos que essas parábolas tratam do contexto social da Galiléia do século I, onde são retratadas a opressão econômica e a violência social imposta aos pequenos proprietários e camponeses empobrecidos.(AU)

Opressão econômica e violência social: retratos do cotidiano em três parábolas da Fonte Q (Q 12,39-40; 42-46; 19,12-27)

Num ambiente como o da Galiléia do século I, onde o ensino era realizado nas comunidades religiosas, vilarejos e núcleos familiares de forma oral, o método de fixação de ensinos mediante a assimilação de símbolos do cotidiano era fundamental. Por conta disso, acreditamos que, dentre as fontes orais ou escritas preservadas e organizadas pelos Evangelhos Sinóticos, as parábolas de Jesus compõem o gênero literário mais original por terem sido preservadas na memória, com maior precisão pelos primeiros seguidores de Jesus. Muitos estudiosos empreenderam importantes trabalhos para pesquisar o lugar social das parábolas de Jesus, a maioria deles partindo dos próprios textos dispostos como estão nos Evangelhos. Neste trabalho, nos propomos trabalhar as parábolas de Jesus como ditos bem preservados pela oralidade a partir da teoria da Fonte Q, que é tratada como um dos estratos mais primitivos da tradição formativa dos Evangelhos Sinóticos e do movimento de Jesus. As parábolas do Ladrão (Q 12,39-40), Servo Infiel (Q 12,42-46) e do Dinheiro Confiado (Q 19,12-27) sempre foram vistas pela tradição eclesial como parábolas que tratam da necessária vigilância do cristão por conta da repentina parusia de Jesus. No entanto, nesse trabalho vamos além, pois acreditamos que essas parábolas tratam do contexto social da Galiléia do século I, onde são retratadas a opressão econômica e a violência social imposta aos pequenos proprietários e camponeses empobrecidos.(AU)

Copresentation of natural HIV-1 agonist and antagonist ligands fails to induce the T cell receptor signaling cascade

It is not known how human immunodeficiency virus type 1 (HIV-1)-derived antagonist peptides interfere with intracellular activation of cytotoxic T lymphocytes (CTL). We identified Gag epitope variants in HIV-1-infected patients that act as antagonists of CTL responses to unmutated epitopes. We then investigated the effect that presentation of each variant has on the early events of T cell receptor (TCR) signal transduction. We found that altered peptide ligands (APL) failed to induce phosphorylation of pp36, a crucial adaptor protein involved in TCR signal transduction. We further investigated the effect that simultaneous presentation of APL and native antigen at low, physiological, peptide concentrations (1 nM) has on TCR signal transduction, and we found that the presence of APL can completely inhibit induction of the protein tyrosine phosphorylation events of the TCR signal transduction cascade.

Platelet signal transduction defect with Gα subunit dysfunction and diminished Gαq in a patient with abnormal platelet responses

G proteins play a major role in signal transduction upon platelet activation. We have previously reported a patient with impaired agonist-induced aggregation, secretion, arachidonate release, and Ca2+ mobilization. Present studies demonstrated that platelet phospholipase A2 (cytosolic and membrane) activity in the patient was normal. Receptor-mediated activation of glycoprotein (GP) IIb-IIIa complex measured by flow cytometry using antibody PAC-1 was diminished despite normal amounts of GPIIb-IIIa on platelets. Ca2+ release induced by guanosine 5′-[γ-thio]triphosphate (GTP[γS]) was diminished in the patient’s platelets, suggesting a defect distal to agonist receptors. GTPase activity (a function of α-subunit) in platelet membranes was normal in resting state but was diminished compared with normal subjects on stimulation with thrombin, platelet-activating factor, or the thromboxane A2 analog U46619. Binding of 35S-labeled GTP[γS] to platelet membranes was decreased under both basal and thrombin-stimulated states. Iloprost (a stable prostaglandin I2 analog) -induced rise in cAMP (mediated by Gαs) and its inhibition (mediated by Gαi) by thrombin in the patient’s platelet membranes were normal. Immunoblot analysis of Gα subunits in the patient’s platelet membranes showed a decrease in Gαq (<50%) but not Gαi, Gαz, Gα12, and Gα13. These studies provide evidence for a hitherto undescribed defect in human platelet G-protein α-subunit function leading to impaired platelet responses, and they provide further evidence for a major role of Gαq in thrombin-induced responses.

Altered 3′-terminal RNA structure in phage Qβ adapted to host factor-less Escherichia coli

The RNA phage Qβ requires for the replication of its genome an RNA binding protein called Qβ host factor or Hfq protein. Our previous results suggested that this protein mediates the access of replicase to the 3′-end of the Qβ plus strand RNA. Here we report the results of an evolutionary experiment in which phage Qβ was adapted to an Escherichia coli Q13 host strain with an inactivated host factor (hfq) gene. This strain initially produced phage at a titer ≈10,000-fold lower than the wild-type strain and with minute plaque morphology, but after 12 growth cycles, phage titer and plaque size had evolved to levels near those of the wild-type host. RNAs isolated from adapted Qβ mutants were efficient templates for replicase without host factor in vitro. Electron microscopy showed that mutant RNAs, in contrast to wild-type RNA, efficiently interacted with replicase at the 3′-end in the absence of host factor. The same set of four mutations in the 3′-terminal third of the genome was found in several independently evolved phage clones. One mutation disrupts the base pairing of the 3′-terminal CCCoh sequence, suggesting that the host factor stimulates activity of the wild-type RNA template by melting out its 3′-end.

Inhibition of RNA polymerase II transcription in human cells by synthetic DNA-binding ligands

Sequence-specific DNA-binding small molecules that can permeate human cells potentially could regulate transcription of specific genes. Multiple cellular DNA-binding transcription factors are required by HIV type 1 for RNA synthesis. Two pyrrole–imidazole polyamides were designed to bind DNA sequences immediately adjacent to binding sites for the transcription factors Ets-1, lymphoid-enhancer binding factor 1, and TATA-box binding protein. These synthetic ligands specifically inhibit DNA-binding of each transcription factor and HIV type 1 transcription in cell-free assays. When used in combination, the polyamides inhibit virus replication by >99% in isolated human peripheral blood lymphocytes, with no detectable cell toxicity. The ability of small molecules to target predetermined DNA sequences located within RNA polymerase II promoters suggests a general approach for regulation of gene expression, as well as a mechanism for the inhibition of viral replication.

Homeostatic expansion and phenotypic conversion of naïve T cells in response to self peptide/MHC ligands

Recent data suggest that survival of resting, naïve T cells requires an interaction with self MHC molecules. From analysis of the class I MHC-restricted T cell receptor transgenic strain OT-I, we report a different response. Rather than merely surviving, these T cells proliferated slowly after transfer into T-depleted syngeneic hosts. This expansion required both T cell “space” and expression of normal levels of self class I MHC molecules. Furthermore, we demonstrate that during homeostatic expansion in a suitable environment, naïve phenotype (CD44low) OT-I T cells converted to memory phenotype (CD44med/high), despite the absence of foreign antigenic stimulation. On the other hand, cells undergoing homeostatic expansion did not acquire cytolytic effector function. The significance of these data for reactivity of T cells with self peptide/MHC ligands and the implications for normal and abnormal T cell homeostasis are discussed.

Altered peptide ligands act as partial agonists by inhibiting phospholipase C activity induced by myasthenogenic T cell epitopes

Myasthenia gravis (MG) is a T cell-regulated, antibody-mediated autoimmune disease. Two peptides representing sequences of the human acetylcholine receptor α-subunit, p195–212 and p259–271, previously were shown to stimulate the proliferation of peripheral blood lymphocytes of patients with MG and were found to be immunodominant T cell epitopes in SJL and BALB/c mice, respectively. Single amino acid-substituted analogs of p195–212 and p259–271, as well as a dual analog composed of the tandemly arranged two single analogs, were shown to inhibit, in vitro and in vivo, MG-associated autoimmune responses. Stimulation of T cells through the antigen-specific T cell receptor activates tyrosine kinases and phospholipase C (PLC). Therefore, in attempts to understand the mechanism of action of the analogs, we first examined whether the myasthenogenic peptides trigger tyrosine phosphorylation and activation of phospholipase C. For that purpose, we measured generation of inositol phosphates and tyrosine phosphorylation of PLC after stimulation of the p195–212- and p259–271-specific T cell lines with these myasthenogenic peptides. Both myasthenogenic peptides stimulated generation of inositol phosphates as well as tyrosine phosphorylation of PLC. However, the single and dual analogs, although inducing tyrosine phosphorylation of PLC, could not induce PLC activity. Furthermore, the single and dual analogs inhibited the induced PLC activity whereas they could not inhibit tyrosine phosphorylation of PLC that was caused by the myasthenogenic peptides. Thus, the altered peptides and the dual analog act as partial agonists. The down-regulation of PLC activity by the analogs may account for their capacity to inhibit in vitro MG-associated T cell responses.

Cannabinoid CB1 receptors and ligands in vertebrate retina: Localization and function of an endogenous signaling system

CB1, a cannabinoid receptor enriched in neuronal tissue, was found in high concentration in retinas of rhesus monkey, mouse, rat, chick, goldfish, and tiger salamander by using a subtype-specific polyclonal antibody. Immunolabeling was detected in the two synaptic layers of the retina, the inner and outer plexiform layers, of all six species examined. In the outer plexiform layer, CB1 was located in and/or on cone pedicles and rod spherules. Labeling was detected in some amacrine cells of all species and in the ganglion cells and ganglion cell axons of all species except fish. In addition, sparse labeling was found in the inner and/or outer segments of the photoreceptors of monkey, mouse, rat, and chick. Using GC/MS to detect possible endogenous cannabinoids, we found 3 nmol of 2-arachidonylglycerol per g of tissue, but no anandamide was detectable. Cannabinoid receptor agonists induced a dramatic reduction in the amplitude of voltage-gated L-type calcium channel currents in identified retinal bipolar cells. The presence and distribution of the CB1 receptor, the large amounts of 2-arachidonylglycerol found, and the effects of cannabinoids on calcium channel activity in bipolar cells suggest a substantive role for an endogenous cannabinoid signaling system in retinal physiology, and perhaps vision in general.