Implementation of social technologies in community networks: From digital curation perspective

This article gives a brief introduction to the digital curation (DC) concept emphasizing on its role to the Knowledge Management (KM) and Library community users

Mapping the hierarchy of EAD to VRA Core 4.0 through CIDOC CRM

Metadata interoperability requires the development of mappings and crosswalks between different schemas. Crosswalks development is a laborious and complex task especially when metadata of compound objects include hierarchical structures. A typical case of such a complexity is finding aids that describe archives that include hierarchies of subordinate components. This paper makes a step forward to obtaining interoperability between two well-known metadata schemas, the EAD standard for the encoding of archival descriptions and the VRA Core 4.0 standard for describing compound visual resources. The paper presents an algorithm for mapping archival hierarchical structures expressed in the EAD standard to the VRA Core 4.0 standard. The input of the algorithm can be any EAD document as well as the crosswalk from EAD to VRA Core that has already been defined, by exploiting the mappings of both EAD and VRA Core 4.0 to the CIDOC Conceptual Reference Model. The output of the proposed process is a VRA Core 4.0 document that includes the information of the EAD document and represents its archival structure. © Springer International Publishing AG 2016

Event-based Archival Information Organization

Event-based information organization methods from other communities provide insights for rethinking archival information organization and redesigning archival description metadata. Differences between event and function are analyzed, and the possibility of using events as a kind of provenance to organize and describe archival information is discussed. Two approaches to redesigning archival description metadata are discussed: making the current narrative descriptions of archives management events more structured and replacing encoded archival description with a metadata framework based on recordkeeping and archives management events in records life cycle

Hepatitis C virus modulates lipid regulatory factor Angiopoietin-like 3 gene expression by repressing HNF-1 alpha activity

Background & Aims: HCV relies on host lipid metabolism to complete its life cycle and HCV core is crucial to this interaction. Liver secreted ANGPTL-3 is an LXR-and HNF-1 alpha-regulated protein, which plays a key role in lipid metabolism by increasing plasma lipids via inhibition of lipase enzymes. Here we aimed to investigate the modulation of ANGPTL-3 by HCV core and identify the molecular mechanisms involved. Methods: qRT-PCR and ELISA were used to assess ANGPTL-3 mRNA and protein levels in HCV patients, the JFH-1 infectious system and liver cell lines. Transfections, chromatin immunoprecipitation and immunofluorescence delineated parts of the molecular mechanisms implicated in the core-mediated regulation of ANGPTL-3 gene expression. Results: ANGPTL-3 gene expression was decreased in HCV-infected patients and the JFH-1 infectious system. mRNA and promoter activity levels were down-regulated by core. The response was lost when an HNF-1 alpha element in ANGPTL-3 promoter was mutated, while loss of HNF-1 alpha DNA binding to this site was recorded in the presence of HCV core. HNF-1 alpha mRNA and protein levels were not altered by core. However, trafficking between nucleus and cytoplasm was observed and then blocked by an inhibitor of the HNF-1 alpha-specific kinase Mirk/Dyrk1B. Transactivation of LXR/RXR signalling could not restore coremediated down-regulation of ANGPTL-3 promoter activity. Conclusions: ANGPTL-3 is negatively regulated by HCV in vivo and in vitro. HCV core represses ANGPTL-3 expression through loss of HNF-1 alpha binding activity and blockage of LXR/RXR transactivation. The putative ensuing increase in serum lipid clearance and uptake by the liver may sustain HCV virus replication and persistence. (C) 2013 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved

BM88/CEND1 coordinates cell cycle exit and differentiation of neuronal precursors

During development, coordinate regulation of cell cycle exit and differentiation of neuronal precursors is essential for generation of appropriate number of neurons and proper wiring of neuronal circuits. BM88 is a neuronal protein associated in vivo with terminal neuron-generating divisions, marking the exit of proliferative cells from the cell cycle. Here, we provide functional evidence that BM88 is sufficient to initiate the differentiation of spinal cord neural precursors toward acquisition of generic neuronal and subtype-specific traits. Gain-of-function approaches show that BM88 negatively regulates proliferation of neuronal precursors, driving them to prematurely exit the cell cycle, down-regulate Notch1, and commit to a neuronal differentiation pathway. The combined effect on proliferation and differentiation results in precocious induction of neurogenesis and generation of postmitotic neurons within the ventricular zone. The dual action of BM88 is not recapitulated by the cell cycle inhibitor p27Kip1, suggesting that cell cycle exit does not induce differentiation by default. Mechanistically, induction of endogenous BM88 by forced expression of the proneural gene Mash1 indicates that BM88 is part of the differentiation program activated by proneural genes. Furthermore, BM88 gene silencing conferred by small interfering RNA in spinal cord neural progenitor cells enhances cell cycle progression and impairs neuronal differentiation. Our results implicate BM88 in the synchronization of cell cycle exit and differentiation of neuronal precursors in the developing nervous system