Giving new life to out-of-print books: when publishers’ and libraries’ interests meet

The Library of the Université Libre de Bruxelles and Editions de l’Université de Bruxelles (EUB), the University’s publishing imprint, have recently agreed to collaborate to provide free online access to recent out-of-print books published by EUB. The e-books are available on the Digithèque website, a collection of digital copies of printed books created by the Library. This initiative is valuable for the scientific community and the general public who can freely access the books online, for the authors whose books have been digitized and widely disseminated, and for the publisher whose collections become more visible on the Internet, thereby generating more traffic on its website and potentially increasing sales of its other books. Around 20 books have been made available online so far. This article describes the context of the agreement, how the collaboration operates, the options of file conversion vs. book scanning, issues relating to copyright and users’ rights, how access is provided to the digital copies, and future collaborative projects of the Library and EUB

Study on the economic and technical evolution of the scientific publication markets in Europe

Intervention au 34e congrès LIBER qui s\u27est tenu à Groningue aux Pays-Pas du 6 au 9 juillet 2005. Présentation des résultats de l\u27étude menée au nom de la Commission européenne par l\u27Université libre de Bruxelles et celle de Toulouse 1 sur le marché de l\u27édition scientifique en Europe

In situ UHVEM study of {113}-defect formation in Si nanowires

Results are presented of a study of {113}-defect formation in vertical Si nanowire n-type tunnel field effect transistors with nanowire diameters ranging from 40 to 500 nm. The nanowires are etched into an epitaxial moderately As doped n-type layer grown on a heavily As doped n(+) Si substrate. p(+) contacts on the nanowire are created by epitaxial growth of a heavily B doped layer. Using focused ion beam cutting, samples for irradiation are prepared with different thicknesses so that the nanowires are fully or partially embedded in the sample thickness. {113}-defects are created in situ by 2 MeV e-irradiation in an ultra-high voltage electron microscope between room temperature and 375 degrees C. The observations are discussed in the frame of intrinsic point defect properties, taking into account the role of dopants and capping layers. The important impact of the specimen thickness is elucidated

Natural marine and terrestrial compounds as modulators of matrix metalloproteinases-2 (MMP-2) and MMP-9 in alzheimer’s disease

Several studies have reported neuroprotective effects by natural products. A wide range of natural compounds have been investigated, and some of these may play a beneficial role in Alzheimer’s disease (AD) progression. Matrix metalloproteinases (MMPs), a family of zinc-dependent endopeptidases, have been implicated in AD. In particular, MMP-2 and MMP-9 are able to trigger several neuroinflammatory and neurodegenerative pathways. In this review, we summarize and discuss existing literature on natural marine and terrestrial compounds, as well as their ability to modulate MMP-2 and MMP-9, and we evaluate their potential as therapeutic compounds for neurodegenerative and neuroinflammatory diseases, with a focus on Alzheimer’s disease

Systemic levels of IL-23 are strongly associated with disease activity in rheumatoid arthritis but not spondyloarthritis

Objectives Th17 cells are an effector T-cell population that plays a role in chronic inflammatory conditions and is dependent on IL-23 for their survival and expansion. More recently, a genetic association was discovered between polymorphisms in the gene coding for the IL-23 receptor and spondyloarthritis. This study aimed to evaluate the role of Th17-associated cytokines in spondyloarthritis pathogenesis by measuring their levels in the joints and circulation as well as correlating them with disease activity parameters. Methods Paired synovial fluid (SF), serum and synovial biopsies were obtained from 30 non-PsA (psoriatic arthritis) spondyloarthritis, 22 PsA and 22 rheumatoid arthritis (RA) patients. IL-17, IL-23 and CCL20 were measured by ELISA in the SF and serum of patients and correlated with systemic and local parameters of disease activity. Results Concentrations of CCL20, a major Th17-attracting chemokine, tended to be higher in the joints of RA than in spondyloarthritis patients. Interestingly, levels of CCL20 were markedly higher in SF as opposed to serum. In addition, there was a remarkable association between the expression of the Th17 cytokine system and the presence of intimal lining layer hyperplasia in RA. Also in the serum, there was a tendency for higher IL-23 levels in RA, which correlated strongly with disease activity parameters. Conclusions Th17-related cytokines are expressed in joints of spondyloarthritis as well as RA patients. IL-23 levels, however, correlate with disease activity parameters in RA only. These results point towards a differential regulation of the Th17 cytokine system in spondyloarthritis compared with RA

Inhibition of MMP-9-dependent degradation of gelatin, but not other MMP-9 substrates, by the MMP-9 hemopexin domain blades 1 and 4

11 p.-5 fig.-1 tab.Degradation and remodeling of the extracellular matrix by matrix metalloproteinases (MMPs) plays important roles in normal development, inflammation, and cancer. MMP-9 efficiently degrades the extracellular matrix component gelatin, and the hemopexin domain of MMP-9 (PEX9) inhibits this degradation. To study the molecular basis of this inhibition, we generated GST fusion proteins containing PEX9 or truncated forms corresponding to specific structural blades (B1-B4) of PEX9. GST-PEX9 inhibited MMP-9-driven gelatin proteolysis, measured by gelatin zymography, FITC-gelatin conversion, and DQ-gelatin degradation assays. However, GST-PEX9 did not prevent the degradation of other MMP-9 substrates, such as a fluorogenic peptide, αB crystalline, or nonmuscular actin. Therefore, PEX9 may inhibit gelatin degradation by shielding gelatin and specifically preventing its binding to MMP-9. Accordingly, GST-PEX9 also abolished the degradation of gelatin by MMP-2, confirming that PEX9 is not an MMP-9 antagonist. Moreover, GST-B4 and, to a lesser extent, GST-B1 also inhibited gelatin degradation by MMP-9, indicating that these regions are responsible for the inhibitory activity of PEX9. Accordingly, ELISAs demonstrated that GST-B4 and GST-B1 specifically bound to gelatin. Our results establish new functions of PEX9 attributed to blades B4 and B1 and should help in designing specific inhibitors of gelatin degradation.This work was supported by Grant SAF2012-31613 and Red Temática de Investigación Cooperativa en Cáncer Grant RD12/0036/0061 from the Ministry of Economy and Competitivity (Spain) (to A. G.-P.); by Grant S2010/ BMD-2314 (to A. G.-P.) from the Comunidad de Madrid/European Union;and by the Concerted Research Actions Grant GOA 2013–2015 and the fund for Scientific Research of Flanders (to G. O.).Peer reviewe

Differential inhibition of activity, activation and gene expression of MMP-9 in THP-1 cells by azithromycin and minocycline versus bortezomib : a comparative study

Gelatinase B or matrix metalloproteinase-9 (MMP-9) (EC 3.4.24.35) is increased in inflammatory processes and cancer, and is associated with disease progression. In part, this is due to MMP-9-mediated degradation of extracellular matrix, facilitating influx of leukocytes into inflamed tissues and invasion or metastasis of cancer cells. MMP-9 is produced as proMMP-9 and its propeptide is subsequently removed by other proteases to generate proteolytically active MMP-9. The significance of MMP-9 in pathologies triggered the development of specific inhibitors of this protease. However, clinical trials with synthetic inhibitors of MMPs in the fight against cancer were disappointing. Reports on active compounds which inhibit MMP-9 should be carefully examined in this regard. In a considerable set of recent publications, two antibiotics (minocycline and azythromycin) and the proteasome inhibitor bortezomib, used in cancers, were reported to inhibit MMP-9 at different stages of its expression, activation or activity. The current study was undertaken to compare and to verify the impact of these compounds on MMP-9. With exception of minocycline at high concentrations (>100 μM), the compounds did not affect processing of proMMP-9 into MMP-9, nor did they affect direct MMP-9 gelatinolytic activity. In contrast, azithromycin specifically reduced MMP-9 mRNA and protein levels without affecting NF-κB in endotoxin-challenged monocytic THP-1 cells. Bortezomib, although being highly toxic, had no MMP-9-specific effects but significantly upregulated cyclooxygenase-2 (COX-2) activity and PGE2 levels. Overall, our study clarified that azithromycin decreased the levels of MMP-9 by reduction of gene and protein expression while minocycline inhibits proteolytic activity at high concentrations