The 2013 European Seismic Hazard Model: key components and results

The 2013 European Seismic Hazard Model (ESHM13) results from a community-based probabilistic seismic hazard assessment supported by the EU-FP7 project “Seismic Hazard Harmonization in Europe” (SHARE, 2009–2013). The ESHM13 is a consistent seismic hazard model for Europe and Turkey which overcomes the limitation of national borders and includes a through quantification of the uncertainties. It is the first completed regional effort contributing to the “Global Earthquake Model” initiative. It might serve as a reference model for various applications, from earthquake preparedness to earthquake risk mitigation strategies, including the update of the European seismic regulations for building design (Eurocode 8), and thus it is useful for future safety assessment and improvement of private and public buildings. Although its results constitute a reference for Europe, they do not replace the existing national design regulations that are in place for seismic design and construction of buildings. The ESHM13 represents a significant improvement compared to previous efforts as it is based on (1) the compilation of updated and harmonised versions of the databases required for probabilistic seismic hazard assessment, (2) the adoption of standard procedures and robust methods, especially for expert elicitation and consensus building among hundreds of European experts, (3) the multi-disciplinary input from all branches of earthquake science and engineering, (4) the direct involvement of the CEN/TC250/SC8 committee in defining output specifications relevant for Eurocode 8 and (5) the accounting for epistemic uncertainties of model components and hazard results. Furthermore, enormous effort was devoted to transparently document and ensure open availability of all data, results and methods through the European Facility for Earthquake Hazard and Risk (www.​efehr.​org)

miRNAs Expression Analysis in Paired Fresh/Frozen and Dissected Formalin Fixed and Paraffin Embedded Glioblastoma Using Real-Time PCR

miRNAs are small molecules involved in gene regulation. Each tissue shows a characteristic miRNAs epression profile that could be altered during neoplastic transformation. Glioblastoma is the most aggressive brain tumour of the adult with a high rate of mortality. Recognizing a specific pattern of miRNAs for GBM could provide further boost for target therapy. The availability of fresh tissue for brain specimens is often limited and for this reason the possibility of starting from formalin fixed and paraffin embedded tissue (FFPE) could very helpful even in miRNAs expression analysis. We analysed a panel of 19 miRNAs in 30 paired samples starting both from FFPE and Fresh/Frozen material. Our data revealed that there is a good correlation in results obtained from FFPE in comparison with those obtained analysing miRNAs extracted from Fresh/Frozen specimen. In the few cases with a not good correlation value we noticed that the discrepancy could be due to dissection performed in FFPE samples. To the best of our knowledge this is the first paper demonstrating that the results obtained in miRNAs analysis using Real-Time PCR starting from FFPE specimens of glioblastoma are comparable with those obtained in Fresh/Frozen samples

Pattern of care and effectiveness of treatment for glioblastoma patients in the real world: Results from a prospective population-based registry. Could survival differ in a high-volume center?

BACKGROUND: As yet, no population-based prospective studies have been conducted to investigate the incidence and clinical outcome of glioblastoma (GBM) or the diffusion and impact of the current standard therapeutic approach in newly diagnosed patients younger than aged 70 years. METHODS: Data on all new cases of primary brain tumors observed from January 1, 2009, to December 31, 2010, in adults residing within the Emilia-Romagna region were recorded in a prospective registry in the Project of Emilia Romagna on Neuro-Oncology (PERNO). Based on the data from this registry, a prospective evaluation was made of the treatment efficacy and outcome in GBM patients. RESULTS: Two hundred sixty-seven GBM patients (median age, 64 y; range, 29-84 y) were enrolled. The median overall survival (OS) was 10.7 months (95% CI, 9.2-12.4). The 139 patients 64aged 70 years who were given standard temozolomide treatment concomitant with and adjuvant to radiotherapy had a median OS of 16.4 months (95% CI, 14.0-18.5). With multivariate analysis, OS correlated significantly with KPS (HR = 0.458; 95% CI, 0.248-0.847; P = .0127), MGMT methylation status (HR = 0.612; 95% CI, 0.388-0.966; P = .0350), and treatment received in a high versus low-volume center (HR = 0.56; 95% CI, 0.328-0.986; P = .0446). CONCLUSIONS: The median OS following standard temozolomide treatment concurrent with and adjuvant to radiotherapy given to (72.8% of) patients aged 6470 years is consistent with findings reported from randomized phase III trials. The volume and expertise of the treatment center should be further investigated as a prognostic factor

Thermo-optical characteristics and concentration quenching effects in Nd(3+)doped yttrium calcium borate glasses

In this work we present a comprehensive study of the spectroscopic and thermo-optical properties of a set of samples with composition xNd(2)O(3)-(5-x)Y(2)O(3-)40CaO-55B(2)O(3) (0 <= x <= 1.0 mol%). Their fluorescence quantum efficiency (eta) values were determined using the thermal lens technique and the dependence on the ionic concentration was analyzed in terms of energy transfer processes, based on the Forster-Dexter model of multipolar ion-ion interactions. A maximum eta = 0.54 was found to be substantially higher than for yttrium aluminoborate crystals and glasses with comparable Nd(3+) content. As for the thermo-optical properties of yttrium calcium borate, they are comparable to other well-known laser glasses. The obtained energy transfer microparameters and the weak dependence of. on the Nd(3+) concentration with a high optimum Nd(3+) concentration put this system as a strong candidate for photonics applications. (C) 2011 American Institute of Physics. [doi:10.1063/1.3567091]Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)FAPESP[04/00093-0]CNPqFINEPFAPEALBrazil-France CAPES-COFECUB[455/04]PIBIC/CNPqCAPES/FAPEAL[PEB-2009-03-015 (04)

Epidemiological evidence against a role for C-reactive protein causing leptin resistance

&lt;p&gt;Objective: It has been suggested that elevated levels of C-reactive protein (CRP) might interfere with leptin signalling and contribute to leptin resistance. Our aim was to assess whether plasma levels of CRP influence leptin resistance in humans, and our hypothesis was that CRP levels would modify the cross-sectional relationships between leptin and measures of adiposity.&lt;/p&gt; &lt;p&gt;Design and methods: We assessed four measures of adiposity: BMI, waist circumference, fat mass and body fat (%) in 2113 British Regional Heart Study (BRHS) men (mean (S.D.) age 69 (5) years), with replication in 760 (age 69 (6) years) European Male Ageing Study (EMAS) subjects.&lt;/p&gt; &lt;p&gt;Results: In BRHS subjects, leptin correlated with CRP (Spearman's r=0.22, P&#60;0.0001). Leptin and CRP correlated with all four measures of adiposity (r value range: 0.22–0.57, all P&#60;0.0001). Age-adjusted mean levels for adiposity measures increased in relation to leptin levels, but CRP level did not consistently influence the β-coefficients of the regression lines in a CRP-stratified analysis. In BRHS subjects, the BMI vs leptin relationship demonstrated a weak statistical interaction with CRP (P=0.04). We observed no similar interaction in EMAS subjects and no significant interactions with other measures of adiposity in BRHS or EMAS cohorts.&lt;/p&gt; &lt;p&gt;Conclusion: We have shown that plasma CRP has little influence on the relationship between measures of adiposity and serum leptin levels in these middle-aged and elderly male European cohorts. This study provides epidemiological evidence against CRP having a significant role in causing leptin resistance.&lt;/p&gt