Biblioteques i biblioteconomia a l'Estat espanyol

Panorámica divulgativa del món bibliotecari espanyol en el marc de la celebració del 59é Congrés de l'IFLA a Barcelona, l'agost d'enguany. Se n'apunten els precedents historics i se'n descriu l'organitzacio actual. S'ofereixen algunes dades básiques sobre la lectura pública, les biblioteques escolars, universitàries, especialitzades i de recerca, així con sobre la Biblioteca Nacional. En cada cas s'analitzen el marc legal, l'estructura, els desenvolupaments tecnològics i els programes de cooperació en curs. Finalment, s'esbossen les línies generals d'evolució del mercat de la informació i es descriuen breument la formació dels professionals i les seves associacions.

CDS/ISIS: un bon producte a un preu regalat

Presentació de la base de dades que conté la col·lecció del Laboratori de l'Escola Universitaria Jordi Rubió i Balaguer de Biblioteconomia i Documentació amb el gestor CDS/ISIS -desenvolupat per la Unesco-. Després d'una explicació general sobre CDS/ISIS, s'exposa amb detall el procés del disseny de la base de dades: definició dels camps del registre seguint una adaptació del Format Comú de Comunicació (CCF); definició de les pantalles d'entrada de dades; selecció dels camps a indexar i métodes d'indexacióemprats, i definició del format de sortida. Finalment, es fa una avaluació del producte.

L'avaluació de webs d'ajuntament: presentació d'una eina d'anàlisi i estat de la qüestió a les comarques de Girona

Anàlisi dels continguts i de la gestió dels lloc web dels ajuntaments de les comarques de Girona. Els ajuntaments catalans s'estan fent visibles a Internet, amb l'oferta de serveis que els són propis. L'estudi té una doble vessant. D'una banda, s'ha confeccionatuna taula d'avaluació per a llocs web d'ajuntament, extrapolable a d'altres anàlisis, que es basa en les possibilitats de gestió de la web i l'interès que té per als ciutadans. De l'altra, es presenta l'estat de la qüestió a la província de Girona a 1 de gener de 2001. L'estudi destaca greus deficiències, com la falta de interactivitat amb els ciutadans, la manca d'un bon sistema de recuperació i difusió de les pàgines web i la gairebé inexistència d'ús dels llenguatges d'autodescripció estàndards. Finalment, l'article conclou amb un seguit de propostes que poden tenir presents els responsables dels ajuntaments electrònics per millorar-los.

Cinquanta idees per sorprendre des de la biblioteca pública

The offer of new products and services is the main way to enhance the image of public libraries in public opinion and to attract the media attention that they deserve. Presented here for professional consideration and comment are fifty surprising, simple and realistic ideas that can be carried out by public libraries, with the aim of reaching unknown user groups and of maintaining the fidelity of current users.

Cincuenta ideas para sorprender desde la biblioteca pública

The offer of new products and services is the main way to enhance the image of public libraries in public opinion and to attract the media attention that they deserve. Presented here for professional consideration and comment are fifty surprising, simple and realistic ideas that can be carried out by public libraries, with the aim of reaching unknown user groups and of maintaining the fidelity of current users.

Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding

Cellular prion protein (PrPC) is a glycosyl-phosphatidylinositol¿anchored glycoprotein. When mutated or misfolded, the pathogenic form (PrPSC) induces transmissible spongiform encephalopathies. In contrast, PrPC has a number of physiological functions in several neural processes. Several lines of evidence implicate PrPC in synaptic transmission and neuroprotection since its absence results in an increase in neuronal excitability and enhanced excitotoxicity in vitro and in vivo. Furthermore, PrPC has been implicated in the inhibition of N-methyl-D-aspartic acid (NMDA)¿mediated neurotransmission, and prion protein gene (Prnp) knockout mice show enhanced neuronal death in response to NMDA and kainate (KA). In this study, we demonstrate that neurotoxicity induced by KA in Prnp knockout mice depends on the c-Jun N-terminal kinase 3 (JNK3) pathway since Prnpo/oJnk3o/o mice were not affected by KA. Pharmacological blockage of JNK3 activity impaired PrPC-dependent neurotoxicity. Furthermore, our results indicate that JNK3 activation depends on the interaction of PrPC with postsynaptic density 95 protein (PSD-95) and glutamate receptor 6/7 (GluR6/7). Indeed, GluR6¿PSD-95 interaction after KA injections was favored by the absence of PrPC. Finally, neurotoxicity in Prnp knockout mice was reversed by an AMPA/KA inhibitor (6,7-dinitroquinoxaline-2,3-dione) and the GluR6 antagonist NS-102. We conclude that the protection afforded by PrPC against KA is due to its ability to modulate GluR6/7-mediated neurotransmission and hence JNK3 activation.

Pro-inflammatory gene expression and neurotoxic effects of activated microglia are attenuated by absence of CCAAT/enhancer binding protein beta

Background. Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein ß (C/EBPß) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPß in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPß-null glial cultures. Methods. Due to fertility and mortality problems associated with the C/EBPß-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPß-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPß DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. Results. C/EBPß mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon ¿ (IFN¿). Quantitative chromatin immunoprecipitation showed binding of C/EBPß to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFN¿ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1ß and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPß. In addition, neurotoxicity elicited by LPS+IFN¿-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPß in microglia.

p38/MKP-1-regulated AKT coordinates macrophage transitions and resolution of inflammation during tissue repair

Repair of damaged tissue requires the coordinated action of inflammatory and tissue-specific cells to restore homeostasis, but the underlying regulatory mechanisms are poorly understood. In this paper, we report new roles for MKP-1 (mitogen-activated protein kinase [MAPK] phosphatase-1) in controlling macrophage phenotypic transitions necessary for appropriate muscle stem cell¿dependent tissue repair. By restricting p38 MAPK activation, MKP-1 allows the early pro- to antiinflammatory macrophage transition and the later progression into a macrophage exhaustion-like state characterized by cytokine silencing, thereby permitting resolution of inflammation as tissue fully recovers. p38 hyperactivation in macrophages lacking MKP-1 induced the expression of microRNA-21 (miR-21), which in turn reduced PTEN (phosphatase and tensin homologue) levels, thereby extending AKT activation. In the absence of MKP-1, p38-induced AKT activity anticipated the acquisition of the antiinflammatory gene program and final cytokine silencing in macrophages, resulting in impaired tissue healing. Such defects were reversed by temporally controlled p38 inhibition. Conversely, miR-21¿AKT interference altered homeostasis during tissue repair. This novel regulatory mechanism involving the appropriate balance of p38, MKP-1, miR-21, and AKT activities may have implications in chronic inflammatory degenerative diseases.

Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding

Cellular prion protein (PrPC) is a glycosyl-phosphatidylinositol¿anchored glycoprotein. When mutated or misfolded, the pathogenic form (PrPSC) induces transmissible spongiform encephalopathies. In contrast, PrPC has a number of physiological functions in several neural processes. Several lines of evidence implicate PrPC in synaptic transmission and neuroprotection since its absence results in an increase in neuronal excitability and enhanced excitotoxicity in vitro and in vivo. Furthermore, PrPC has been implicated in the inhibition of N-methyl-D-aspartic acid (NMDA)¿mediated neurotransmission, and prion protein gene (Prnp) knockout mice show enhanced neuronal death in response to NMDA and kainate (KA). In this study, we demonstrate that neurotoxicity induced by KA in Prnp knockout mice depends on the c-Jun N-terminal kinase 3 (JNK3) pathway since Prnpo/oJnk3o/o mice were not affected by KA. Pharmacological blockage of JNK3 activity impaired PrPC-dependent neurotoxicity. Furthermore, our results indicate that JNK3 activation depends on the interaction of PrPC with postsynaptic density 95 protein (PSD-95) and glutamate receptor 6/7 (GluR6/7). Indeed, GluR6¿PSD-95 interaction after KA injections was favored by the absence of PrPC. Finally, neurotoxicity in Prnp knockout mice was reversed by an AMPA/KA inhibitor (6,7-dinitroquinoxaline-2,3-dione) and the GluR6 antagonist NS-102. We conclude that the protection afforded by PrPC against KA is due to its ability to modulate GluR6/7-mediated neurotransmission and hence JNK3 activation.