951 resultados para Library Company of Philadelphia.
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Supplements accompany some issues.
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Mode of access: Internet.
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[V.1.] Proceedings on Master's sale -- [v.2.] Decree of forclosure and sale -- [v.3.] Ancillary decree of foreclosure and sale.
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Mode of access: Internet.
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Mode of access: Internet.
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On spine: G.B.C.
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"Reprinted from News Notes of California libraries, v.4 no. 2."
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The evolution of the pianoforte, by T.L. Southgate.- Our English songs, by W.H. Cummings.- The early English viols and their music, by H. Watson.- Madrigals, rounds, catches, glees, and part-songs, by E.M. Lee.- The recorder, flute, fife, and piccolo, by J. Finn.- Music in England in the year 1604, by Sir F. Bridge.- Our dances of bygone days, by A.S. Rose.- Masques and early operas, by A.H.D. Prendergast.- English opera after Purcell, by F.J. Sawyer.- Our cathedral composers and their works, by G.F. Huntley.- The single and double reed instruments, by D.J. Blaikley.- The water-organ of the ancients and the organ of to-day, by F.W. Galpin.- The regal and its successors: the harmonica, by T.L. Southgate.- The violin family and its music, by W.W. Cobbett.- The brass wind instruments, by J.E. Borland.- Some notes on early printed music, by A.H. Littleton.- Music of the country-side, by Sir E. Clarke.
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Binders title: Library edition of the British poets.
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The present thesis encompasses the two researches projects I conducted during my PhD program in Molecular Biology and Pathology. The common thread is represented by the analysis of the signaling pathways implicated in the pathophysiology of the two most aggressive Philadelphia-negative myeloproliferative neoplasms, namely, atypical chronic myeloid leukemia (aCML) and primary myelofibrosis (PMF). In the last decade, since the description of the JAK2V617F mutation in 2005, the field of the molecular characterization of Philadelphia-negative myeloproliferative neoplasms has experienced an astonishing implementation that led to the discovery of 16 new mutations involving signal transduction, epigenetic modifiers, cell cycle regulators. Nevertheless, their pathogenetic relevance and whether they could represent good “druggable” candidates have to be proved yet. In the first section I provide the first report of the signaling cascade down-stream the rare cytogenetic lesion t(8;9)(p22;p24)/PCM1-JAK2 associated with aCML, finding that it selectively activates the ERK1/2 signaling without affecting JAK/STAT phosphorylation. In the second part, I investigated the implication of the ε isoform of novel Protein kinase Cs (PKCs) in the pathophysiology of the aberrant megakaryocytopoiesis in PMF, concluding that the over-expression of PKCε detains a crucial relevance in the aberrant behavior of PMF megakaryocytes and its inhibition is capable to restore their normal differentiation and abrogate the anti-apoptotic signaling. Both results are discussed in the view of their therapeutic implications. In case PCM1/JAK2-related hematologic neoplasms, ERK-inhibitors rather than JAK-inhibitors (i.e. ruxolitinib) should be considered as a “tailored” drugs. In case of PMF, PKCε-inhibitors (i.e. εV1-2 peptide) configure as an appealing strategy to re-direct the megakaryocytic neoplastic clone.
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A petition from the Company of Stationers to Parliament to introduce some form of legislative regulation of the press. The petition is significant in revealing the extent to which the Stationers depended upon the state to support the regulation of the book trade, as well as the nature of the various public and private interest arguments upon which they sought to base their claim. The commentary articulates the various arguments presented by the Stationers within their petition. The benefits of the legal regulation they suggested concerned not only the censorship and suppression of seditious and heretical texts, but also facilitated the advancement of learning and knowledge and the flourishing of the printing industry itself. In addition, the petition presents the figure of the ‘author' as reliant upon the benefit of his work, and that the ‘production of the Brain' was to be regarded as equivalent to any other commodity or chattel.
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This project is a diagnosis of update needs and training for professionals in bibliotecology and its results will be used for the design of a Program of Permanent training in bibliotecology, which will be implemented in Bibliotecology School, Documentation and Information of the National University.The studied population is composed by all the teachers of Bibliotecology School, Documentation and Information of the National University, in October, 2007, and all the graduated students of licentiate of the EBDI from 2000 to 2007.The results of this investigation were obtained by means of a questionnaire that was filled by each one of the members of these two populations, who corresponded to 25 teachers of the EBDI and 18 graduates of licentiate. This one also presents the information that was obtained in interviews realized to the managers of the principal institutions who are professionals contracted in bibliotecology.The results obtained of this diagnosis will allow the elaboration of the Program of Permanent training in bibliotecology, considering the formative needs of the professionals in bibliotecology of the EBDI. This project includes the following products:a) Description of the social and demographic characteristics of teachers and of graduated of licentiate of the EBDI.b) Diagnosis of needs to update and training of bibliotecology professional teachers and of graduated of licentiate of the EBDI.c) Determination of the knowledge and skills that the needs to satisfy what big employers ask for.d) Recommendations for the program. Implementation.
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This handbook is the original papers on experiences, innovations, reviews, technical advances and trends in theory and practice of professionals in information science (LIS, documentation, information, communication, etc..).Its purpose is to serve as a dissemination tool, discussion forum, a means of supporting the professional development and continuing education, experience-sharing tool, and a window to understanding the changes that occur in the professional environment.
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This document describes each step of the research conducted to understand the factors that may be influencing the low enrollment of freshmen who have experienced the “Escuela de Bibliotecologia, Documentacion e Informacion de la Universidad Nacional” in recent years. It also raises a didactic - multimedia, in response to identified needs, to help improve the problems encountered by making use of technological tools with an educational foundation that fosters reflection of the population to be targeted by the product. Finally, it presents the conclusions and recommendations drawn from the research.
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The BCR gene is involved in the pathogenesis of Philadelphia chromosome-positive (Ph$\sp1$) leukemias. Typically, the 5$\sp\prime$ portion of BCR on chromosome 22 becomes fused to a 5$\sp\prime$ truncated ABL gene from chromosome 9 resulting in a chimeric BCR-ABL gene. To investigate the role of the BCR gene product, a number of BCR peptide sequences were used to generate anti-BCR antibodies for detection of BCR and BCR-ABL proteins. Since both BCR and ABL proteins have kinase activity, the anti-BCR antibodies were tested for their ability to immunoprecipitate BCR and BCR-ABL proteins from cellular lysates by use of an immunokinase assay. Antisera directed towards the C-terminal portions of P160 BCR, sequences not present in BCR-ABL proteins, were capable of co-immunoprecipitating P210 BCR-ABL from the Ph$\sp1$- positive cell line K562. Re-immunoprecipitation studies following complete denaturation showed that C-terminal BCR antisera specifically recognized P160 BCR but not P210 BCR-ABL. These and other results indicated the presence of a P160 BCR/P210 BCR-ABL protein complex in K562 cells. Experiments performed with Ph$\sp1$-positive ALL cells and uncultured Ph$\sp1$-positive patient white blood cells established the general presence of BCR/BCR-ABL protein complexes in BCR-ABL expressing cells. However, two cell lines derived from Ph$\sp1$-positive patients lacked P160 BCR/P210 BCR-ABL complexes. Lysates from one of these cell lines mixed with lysates from a cell line that expresses only P160 BCR failed to generate BCR/BCR-ABL protein complexes in vitro indicating that P160 BCR and P210 BCR-ABL do not simply oligomerize.^ Two-dimensional tryptic maps were performed on both BCR and BCR-ABL proteins labeled in vitro with $\sp{32}$P. These maps indicate that the autophosphorylation sites in BCR-ABL proteins are primarily located within BCR exon 1 sequences in both P210 and P185 BCR-ABL, and that P160 BCR is phosphorylated in trans in similar sites by the activated ABL kinase of both BCR-ABL proteins. These results provide strong evidence that P160 BCR serves as a target for the BCR-ABL oncoprotein.^ K562 cells, induced to terminally differentiate with the tumor promoter TPA, show a loss of P210 BCR-ABL kinase activity 12-18 hours after addition of TPA. This loss coincides with the loss of activity in P160 BCR/P210 BCR-ABL complexes but not with the loss of the P210 BCR-ABL, suggesting the existence of an inactive form of P210 BCR-ABL. However, a degraded BCR-ABL protein served as the kinase active form preferentially sequestered within the remaining BCR/BCR-ABL protein complex.^ The results described in this thesis form the basis for a model for BCR-ABL induced leukemias which is presented and discussed. ^