Integration of a permanent OBS offshore NE Iberian Peninsula to the CAtalan Seismic Network

We summarize the results of more than 3 years of operation of a permanent Ocean Bottom Seismometer (OBS)deployed 40 km offshore Catalonia in terms of the site ambient noise conditions and quality of the data acquired. As observed on most of the ocean-floor observatories, the noise level at the OBS site is quite large on all components. However, the integration of the OBS station into the Catalan seismic network has allowed to improve hypocenter locations.Peer Reviewe

Ionotropic and metabotropic glutamate receptor mediation of glucocorticoid-induced apoptosis in hippocampal cells and the neuroprotective role of synaptic N-methyl-D-aspartate receptors

Glutamate receptors have been proposed to mediate the apoptotic actions of glucocorticoids in hippocampal cells. To further analyze the role of glutamate receptors in this process, we pretreated primary hippocampal cells from neonatal (postnatal day 4) rats with antagonists of ionotropic glutamate receptor (iGluR) and metabotropic glutamate receptor (mGluR) antagonists before exposure to the specific glucocorticoid receptor agonist dexamethasone (DEX) at a dose of 1 μM. Dizocilpine (MK801; a general N-methyl-Daspartic acid [NMDA] receptor antagonist, NMDAR antagonist) and ifenprodil (a specific ligand of the NMDAR 2B subunit, NR2B), were used to block iGluR; (RS)-α-ethyl-4-carboxyphenylglycine (E4CPG) and (RS)-α-cyclopropyl-4- phosphonophenyl-glycine (CPPG) were employed as I/II (E4CPG) and II/III (CPPG) mGluR antagonists. Blockade of iGluR resulted in a significant attenuation of DEX-induced cell death; the finding that ifenprodil exerted a similar potency to MK801 demonstrates the involvement of NR2B receptors in glucocorticoid-induced cell death. Apoptosis accounted for a significant amount of the cell loss observed, as detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling histochemistry for the in situ labeling of DNA breaks; apoptotic cells were distinguished from necrosis on the basis of morphological criteria, including chromatin condensation, membrane blebbing and presence of apoptotic bodies. Treatment with E4CPG and CPPG completely abolished the apoptotic response to DEX, thus showing the additional contribution of mGluR to the phenomenon. Further, dose-response studies with NMDA revealed that whereas high (10 μM) doses of NMDA themselves elicit cytotoxic responses, low (1–5 μM) concentrations of NMDA can effectively oppose DEX-induced cell death. Interestingly, the neuroprotective actions of low dose NMDA stimulation were abolished when either synaptic or extrasynaptic NMDA receptors were blocked with MK801 in combination with the GABA receptor antagonist bicuculline (synaptic) or ifenprodil (extrasynaptic). In summary, the present data show that both iGluR and mGluR mediate the neurotoxic effects of glucocorticoids on hippocampal cells and that pre-treatment with low doses of NMDA, by acting on synaptic and extrasynaptic receptors, render hippocampal cells less vulnerable to glucocorticoid insults.German Academic Exchange Service - Personnel Exchange Acções Integradas Luso-Alemãs The Portuguese Rectors’ Conference Portuguese Institute for International Co-operation in Science and Technolog

Ground-Shaking Scenarios and Urban Risk Evaluation of Barcelona using the Risk-UE Capacity Spectrum Based Method

The Capacity Spectrum Based Method (CSBM) developed in the framework of the European project Risk-UE has been applied to evaluate the seismic risk for the city of Barcelona, Spain. Accordingly, four damage states are defined for the buildings, the action is expressed in terms of spectral values and the seismic quality of the buildings, that is, their vulnerability, is evaluated by means of capacity spectra. The probabilities of the damage states are obtained considering a lognormal probability distribution. The most relevant seismic risk evaluation results obtained for Barcelona, Spain, are given in the article as scenarios of expected losses

Seismic hazard and risk scenarios for Barcelona, Spain, using the Risk-UE vulnerability index method

The vulnerability index method, in its version developed in the framework of the European project Risk-UE, has been adapted and applied in this article, to evaluate the seismic risk for the city of Barcelona (Spain) through a GIS based tool. According to this method, which defines five damage states, the action is expressed in terms of the macroseismic intensity and the seismic quality of the buildings by means of a vulnerability index. The probabilities of damage states are obtained considering a binomial or beta-equivalent probability distribution. The most relevant seismic risk evaluation results obtained, for current buildings and monuments of Barcelona, are given in the article as scenarios of expected losses

MSH3 polymorphisms and protein levels affect CAG repeat instability in huntington's disease mice

Expansions of trinucleotide CAG/CTG repeats in somatic tissues are thought to contribute to ongoing disease progression through an affected individual's life with Huntington's disease or myotonic dystrophy. Broad ranges of repeat instability arise between individuals with expanded repeats, suggesting the existence of modifiers of repeat instability. Mice with expanded CAG/CTG repeats show variable levels of instability depending upon mouse strain. However, to date the genetic modifiers underlying these differences have not been identified. We show that in liver and striatum the R6/1 Huntington's disease (HD) (CAG)~100 transgene, when present in a congenic C57BL/6J (B6) background, incurred expansion-biased repeat mutations, whereas the repeat was stable in a congenic BALB/cByJ (CBy) background. Reciprocal congenic mice revealed the Msh3 gene as the determinant for the differences in repeat instability. Expansion bias was observed in congenic mice homozygous for the B6 Msh3 gene on a CBy background, while the CAG tract was stabilized in congenics homozygous for the CBy Msh3 gene on a B6 background. The CAG stabilization was as dramatic as genetic deficiency of Msh2. The B6 and CBy Msh3 genes had identical promoters but differed in coding regions and showed strikingly different protein levels. B6 MSH3 variant protein is highly expressed and associated with CAG expansions, while the CBy MSH3 variant protein is expressed at barely detectable levels, associating with CAG stability. The DHFR protein, which is divergently transcribed from a promoter shared by the Msh3 gene, did not show varied levels between mouse strains. Thus, naturally occurring MSH3 protein polymorphisms are modifiers of CAG repeat instability, likely through variable MSH3 protein stability. Since evidence supports that somatic CAG instability is a modifier and predictor of disease, our data are consistent with the hypothesis that variable levels of CAG instability associated with polymorphisms of DNA repair genes may have prognostic implications for various repeat-associated diseases

The ALERT-ES Project for earthquakes in Cape San Vicente region

The main goal of the ALERT-ES project ("Sistema de Alerta Sismica Temprana: Aplicacion al Sur de España" ) is to study the feasibility of an Earthquake Early Warning System (EEWS) for the potentially damaging earthquakes that occur in the zone Cape S. Vicente-Gulf of Cadiz (S. Spain). This area is characterized by the occurrence of large and damaging earthquakes such as the 1755 Lisbon (Imax=X) or 1969 S. Vicente Cape (Ms=8,1) events. Most earthquakes in this area have their epicenters offshore at epicentral distances between 150 and 250 kms off the coast line, so a feasibility study is needed before an EEWS system implementation. The project has two different parts: the development of algorithms for the rapid estimation of the magnitude for South Spain earthquakes from the very beginning of P-waves and the development of the corresponding new software modules and their implementation in the EarthWorm and SeisComP systems. A pilot experience will be carried out during the project, using observations from coastal stations and OBS. Broadband records from a selection of 19 earthquakes (M≥4.0) occurred in the period 2006 to 2010 in Cape S. Vicente and Gulf of Cadiz have been used for an off line testing of PRESTO methodology developed at Naples University (Italy). Preliminary results show that for a Mw 6.1 shock with epicenter 200 km SW of Cape of S. Vicente the blind area has a radius of 227 km, providing with a lead-time of 28s in Huelva, 36s in Cadiz and 47s in Seville

Characterization of the behavior of carotenoids from pitanga (Eugenia uniflora) and buriti (Mauritia flexuosa) during microemulsion production and in a dynamic gastrointestinal system

Uncommon tropical fruits are emerging as raw-material for new food products with health benefits. This work aimed at formulating and processing microemulsions from pitanga (Eugenia uniflora) and buriti (Mauritia flexuosa) fruits, since they are very rich in carotenoids (particularly lycopene and -carotene), in order to encapsulate and increase carotenoids bioaccessibility. Pitanga and buriti microemulsions were produced by applying a direct processing (high-speed homogenization at 15,000 rpm and ultrasound with 20 kHz probe at 40% amplitude) of the whole pulp together with surfactant (Tween 80 or Whey Protein Isolate at 2%) and corn oil (5%). All treatments (HSHUS for 04, 40, 44, 48 minmin) applied were able to increase the amount of carotenoid released. However, the processing also decreased the total amount of carotenoids in the whole pulp of studied fruits. The impact of processing during microemulsion production was not severe. The overall data suggest that the presence of surfactant and oil during processing may protect the carotenoids in fruits and microemulsions. Final recovery of total carotenoids, after passing the samples through a dynamic gastrointestinal system that simulates the human digestion, was higher for microemulsions than for whole pulps. High losses of total carotenoids in buriti and -carotene and lycopene in pitanga occurred during jejunum and ileum phases. The present work confirms that it is possible to increase -carotene and lycopene bioaccessibility from fruits by directly processing microemulsions (p<0.01).This work was supported by the São Paulo Research Foundation—FAPESP through research funding [Grant #2015/15507-9] and Ph.D. scholarship for Paulo Berni [Grant #2014/15119-6] and a Research Internships Abroad (BEPE) support [Grant #2016/13355-0]. The author Ana C. Pinheiro is recipient of a fellowship from the Portuguese Foundation for Science and Technology (FCT) [Grant SFRH/BPD/101181/2014]info:eu-repo/semantics/publishedVersio

Methods for assessing DNA repair and repeat expansion in Huntington's Disease

Huntington’s disease (HD) is caused by a CAG repeat expansion in the HTT gene. Repeat length can change over time, both in individual cells and between generations, and longer repeats may drive pathology. Cellular DNA repair systems have long been implicated in CAG repeat instability but recent genetic evidence from humans linking DNA repair variants to HD onset and progression has reignited interest in this area. The DNA damage response plays an essential role in maintaining genome stability, but may also license repeat expansions in the context of HD. In this chapter we summarize the methods developed to assay CAG repeat expansion/contraction in vitro and in cells, and review the DNA repair genes tested in mouse models of HD. While none of these systems is currently ideal, new technologies, such as long-read DNA sequencing, should improve the sensitivity of assays to assess the effects of DNA repair pathways in HD. Improved assays will be essential precursors to high-throughput testing of small molecules that can alter specific steps in DNA repair pathways and perhaps ameliorate expansion or enhance contraction of the HTT CAG repeat