988 resultados para Zeno, Niccolò, d. ca. 1395.
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v. 1. Ab anno 1588. num. a. usque ad 20. novembris 1677. num. 2849.--v. 2. Ab anno 1678. num. 2850 usque ad diem 18. decembris 1779. num. 4395.--v. 3. Ab anno 1780. num. 4396. usque ad diem 27. maii 1826. num. 4620.a. Cui accedit appendix prima continuationis decretorum ab anno 1826. num. 4621. usque ad diem 11. martii 1837. num. 4810.--v. 4. Appendix II. continens continuationem decretorum ab anno 1837. num. 4811. usque ad diem 29. novembris 1856. num. 5230. Cum indice generali.--v. 5. Appendix III-IV continens continuationem decretorum a die 23 augusti 1856 n. 5231 ad diem 18 decembris 1877 n. 5715.
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Bibliographical footnotes.
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Vol. 3, pt. 2 has imprint: Monachii, Librariae J. J. Lentnerianae (E. Stahl) ; Neo-Eboraci, F. Pustet ; [etc., etc.]
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Resumen basado en el de la publicaci??n
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Resumen basado en el de la publicaci??n
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Pós-graduação em Medicina Veterinária - FMVZ
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The end of the last interglacial period, ~118 kyr ago, was characterized by substantial ocean circulation and climate perturbations resulting from instabilities of polar ice sheets. These perturbations are crucial for a better understanding of future climate change. The seasonal temperature changes of the tropical ocean, however, which play an important role in seasonal climate extremes such as hurricanes, floods and droughts at the present day, are not well known for this period that led into the last glacial. Here we present a monthly resolved snapshot of reconstructed sea surface temperature in the tropical North Atlantic Ocean for 117.7±0.8 kyr ago, using coral Sr/Ca and d18O records. We find that temperature seasonality was similar to today, which is consistent with the orbital insolation forcing. Our coral and climate model results suggest that temperature seasonality of the tropical surface ocean is controlled mainly by orbital insolation changes during interglacials.
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Imp. tomado del colofón
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Marca tip. en port. y colofón en h. [27]
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Regulation of ion channel function by intracellular processes is fundamental for controlling synaptic signaling and integration in the nervous system. Currents mediated by N-methyl-D-aspartate (NMDA) receptors decline during whole-cell recordings and this may be prevented by ATP. We show here that phosphorylation is necessary to maintain NMDA currents and that the decline is not dependent upon Ca2+. A protein tyrosine phosphatase or a peptide inhibitor of protein tyrosine kinase applied intracellularly caused a decrease in NMDA currents even when ATP was included. On the other hand, pretreating the neurons with a membrane-permeant tyrosine kinase inhibitor occluded the decline in NMDA currents when ATP was omitted. In inside-out patches, applying a protein tyrosine phosphatase to the cytoplasmic face of the patch caused a decrease in probability of opening of NMDA channels. Conversely, open probability was increased by a protein tyrosine phosphatase inhibitor. These results indicate that NMDA channel activity is reduced by a protein tyrosine phosphatase associated with the channel complex.
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When performed at increased external [Ca2+]/[Mg2+] ratio (2.5 mM/0.5 mM), temporary block of A1 adenosine receptors in hippocampus [by 8-cyclopentyltheophylline (CPT)] leads to a dramatic and irreversible change in the excitatory postsynaptic current (EPSC) evoked by Schaffer collateral/commissural (SCC) stimulation and recorded by in situ patch clamp in CA1 pyramidal neurons. The duration of the EPSC becomes stimulus dependent, increasing with increase in stimulus strength. The later occurring component of the EPSC is carried through N-methyl-D-aspartate (NMDA) receptor-operated channels but disappears under either the NMDA antagonist 2-amino-5-phosphonovaleric acid (APV) or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). These findings indicate that the late component of the SCC-evoked EPSC is polysynaptic: predominantly non-NMDA receptor-mediated SCC inputs excite CA1 neurons that recurrently excite each other by predominantly NDMA receptor-mediated synapses. These recurrent connections are normally silent but become active after CPT treatment, leading to enhancement of the late component of the EPSC. The activity of these connections is maintained for at least 2 hr after CPT removal. When all functional NMDA receptors are blocked by dizocilpine maleate (MK-801), subsequent application of CPT leads to a partial reappearance of NMDA receptor-mediated EPSCs evoked by SCC stimulation, indicating that latent NMDA receptors are recruited. Altogether, these findings indicate the existence of a powerful system of NMDA receptor-mediated synaptic contacts in SCC input to hippocampal CA1 pyramidal neurons and probably also in reciprocal connections between these neurons, which in the usual preparation are kept latent by activity of A1 receptors.
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This list appears to be the most comprehensive in this series. Although its contents are very similar to those of the list in Folder 2, there are some discrepancies. Entries are arranged by format (folio, quarto, octavo) and include the date the book was "delivered" (loaned), the name of the individual who borrowed it, and its author, title, and volume number. Many of the books had been out of the library for decades prior to the fire, with some loaned out since as early as 1742.