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)

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.

Ablation of P/Q-type Ca2+ channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the α1A-subunit

The Ca2+ channel α1A-subunit is a voltage-gated, pore-forming membrane protein positioned at the intersection of two important lines of research: one exploring the diversity of Ca2+ channels and their physiological roles, and the other pursuing mechanisms of ataxia, dystonia, epilepsy, and migraine. α1A-Subunits are thought to support both P- and Q-type Ca2+ channel currents, but the most direct test, a null mutant, has not been described, nor is it known which changes in neurotransmission might arise from elimination of the predominant Ca2+ delivery system at excitatory nerve terminals. We generated α1A-deficient mice (α1A−/−) and found that they developed a rapidly progressive neurological deficit with specific characteristics of ataxia and dystonia before dying ≈3–4 weeks after birth. P-type currents in Purkinje neurons and P- and Q-type currents in cerebellar granule cells were eliminated completely whereas other Ca2+ channel types, including those involved in triggering transmitter release, also underwent concomitant changes in density. Synaptic transmission in α1A−/− hippocampal slices persisted despite the lack of P/Q-type channels but showed enhanced reliance on N-type and R-type Ca2+ entry. The α1A−/− mice provide a starting point for unraveling neuropathological mechanisms of human diseases generated by mutations in α1A.

The AMPA receptor subunit GluR-B in its Q/R site-unedited form is not essential for brain development and function

Calcium permeability of l-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) in excitatory neurons of the mammalian brain is prevented by coassembly of the GluR-B subunit, which carries an arginine (R) residue at a critical site of the channel pore. The codon for this arginine is created by site-selective adenosine deamination of an exonic glutamine (Q) codon at the pre-mRNA level. Thus, central neurons can potentially control the calcium permeability of AMPARs by the level of GluR-B gene expression as well as by the extent of Q/R-site editing, which in postnatal brain, positions the R codon into >99% of GluR-B mRNA. To study whether the small amount of unedited GluR-B is of functional relevance, we have generated mice carrying GluR-B alleles with an exonic arginine codon. We report that these mutants manifest no obvious deficiencies, indicating that AMPAR-mediated calcium influx into central neurons can be solely regulated by the levels of Q/R site-edited GluR-B relative to other AMPAR subunits. Notably, a targeted GluR-B gene mutant with 30% reduced GluR-B levels had 2-fold higher AMPAR-mediated calcium permeability in hippocampal pyramidal cells with no sign of cytotoxicity. This constitutes proof in vivo that elevated calcium influx through AMPARs need not generate pathophysiological consequences.

Transient cardiac expression of constitutively active Gαq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways

Cardiac hypertrophy and dilatation can result from stimulation of signal transduction pathways mediated by heterotrimeric G proteins, especially Gq, whose α subunit activates phospholipase Cβ (PLCβ). We now report that transient, modest expression of a hemagglutinin (HA) epitope-tagged, constitutively active mutant of the Gq α subunit (HAα*q) in hearts of transgenic mice is sufficient to induce cardiac hypertrophy and dilatation that continue to progress after the initiating stimulus becomes undetectable. At 2 weeks, HAα*q protein is expressed at less than 50% of endogenous αq/11, and the transgenic hearts are essentially normal morphologically. Although HAα*q protein declines at 4 weeks and is undetectable by 10 weeks, the animals develop cardiac hypertrophy and dilatation and die between 8 and 30 weeks in heart failure. As the pathology develops, endogenous αq/11 rises (2.9-fold in atria; 1.8-fold in ventricles). At 2 weeks, basal PLC activity is increased 9- to 10-fold in atria but not ventricles. By 10 weeks, it is elevated in both, presumably because of the rise in endogenous αq/11. We conclude that the pathological changes initiated by early, transient HAα*q expression are maintained in part by compensatory changes in signal transduction and other pathways. Cyclosporin A (CsA) prevents hypertrophy caused by activation of calcineurin [Molkentin, J. D., Lu, J.-R., Antos, C. L., Markham, B., Richardson, J., Robbins, J., Grant, S. R. & Olson, E. N. (1998) Cell 93, 215–228]. Because HAα*q acts upstream of calcineurin, we hypothesized that HAα*q might initiate additional pathways leading to hypertrophy and dilatation. Treating HAα*q mice with CsA diminished some, but not all, aspects of the hypertrophic phenotype, suggesting that multiple pathways are involved.

Desensitization of the Neurokinin-1 Receptor (NK1-R) in Neurons: Effects of Substance P on the Distribution of NK1-R, Gαq/11, G-Protein Receptor Kinase-2/3, and β-Arrestin-1/2

Observations in reconstituted systems and transfected cells indicate that G-protein receptor kinases (GRKs) and β-arrestins mediate desensitization and endocytosis of G-protein–coupled receptors. Little is known about receptor regulation in neurons. Therefore, we examined the effects of the neurotransmitter substance P (SP) on desensitization of the neurokinin-1 receptor (NK1-R) and on the subcellular distribution of NK1-R, Gαq/11, GRK-2 and -3, and β-arrestin-1 and -2 in cultured myenteric neurons. NK1-R was coexpressed with immunoreactive Gαq/11, GRK-2 and -3, and β-arrestin-1 and -2 in a subpopulation of neurons. SP caused 1) rapid NK1-R–mediated increase in [Ca2+]i, which was transient and desensitized to repeated stimulation; 2) internalization of the NK1-R into early endosomes containing SP; and 3) rapid and transient redistribution of β-arrestin-1 and -2 from the cytosol to the plasma membrane, followed by a striking redistribution of β-arrestin-1 and -2 to endosomes containing the NK1-R and SP. In SP-treated neurons Gαq/11 remained at the plasma membrane, and GRK-2 and -3 remained in centrally located and superficial vesicles. Thus, SP induces desensitization and endocytosis of the NK1-R in neurons that may be mediated by GRK-2 and -3 and β-arrestin-1 and -2. This regulation will determine whether NK1-R–expressing neurons participate in functionally important reflexes.

Low- and high-level transgenic expression of β2-adrenergic receptors differentially affect cardiac hypertrophy and function in Gαq-overexpressing mice

Transgenic overexpression of Gαq in the heart triggers events leading to a phenotype of eccentric hypertrophy, depressed ventricular function, marked expression of hypertrophy-associated genes, and depressed β-adrenergic receptor (βAR) function. The role of βAR dysfunction in the development of this failure phenotype was delineated by transgenic coexpression of the carboxyl terminus of the βAR kinase (βARK), which acts to inhibit the kinase, or concomitant overexpression of the β2AR at low (≈30-fold, Gαq/β2ARL), moderate (≈140-fold, Gαq/β2ARM), and high (≈1,000-fold, Gαq/β2ARH) levels above background βAR density. Expression of the βARK inhibitor had no effect on the phenotype, consistent with the lack of increased βARK levels in Gαq mice. In marked contrast, Gαq/β2ARL mice displayed rescue of hypertrophy and resting ventricular function and decreased cardiac expression of atrial natriuretic factor and α-skeletal actin mRNA. These effects occurred in the absence of any improvement in basal or agonist-stimulated adenylyl cyclase (AC) activities in crude cardiac membranes, although restoration of a compartmentalized β2AR/AC signal cannot be excluded. Higher expression of receptors in Gαq/β2ARM mice resulted in salvage of AC activity, but hypertrophy, ventricular function, and expression of fetal genes were unaffected or worsened. With ≈1,000-fold overexpression, the majority of Gαq/β2ARH mice died with cardiomegaly at 5 weeks. Thus, although it appears that excessive, uncontrolled, or generalized augmentation of βAR signaling is deleterious in heart failure, selective enhancement by overexpressing the β2AR subtype to limited levels restores not only ventricular function but also reverses cardiac hypertrophy.

Conserved structural features of the synaptic fusion complex: SNARE proteins reclassified as Q- and R-SNAREs

SNARE [soluble NSF (N-ethylmaleimide-sensitive fusion protein) attachment protein receptor] proteins are essential for membrane fusion and are conserved from yeast to humans. Sequence alignments of the most conserved regions were mapped onto the recently solved crystal structure of the heterotrimeric synaptic fusion complex. The association of the four α-helices in the synaptic fusion complex structure produces highly conserved layers of interacting amino acid side chains in the center of the four-helix bundle. Mutations in these layers reduce complex stability and cause defects in membrane traffic even in distantly related SNAREs. When syntaxin-4 is modeled into the synaptic fusion complex as a replacement of syntaxin-1A, no major steric clashes arise and the most variable amino acids localize to the outer surface of the complex. We conclude that the main structural features of the neuronal complex are highly conserved during evolution. On the basis of these features we have reclassified SNARE proteins into Q-SNAREs and R-SNAREs, and we propose that fusion-competent SNARE complexes generally consist of four-helix bundles composed of three Q-SNAREs and one R-SNARE.