228 research outputs found

    The need for municipal action planning against flood risk: the risk-informed journey of the municipality of Oliva (Spain)

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    [EN] Society demands higher safety levels, including those actions related to urban planning and protection against natural hazards and manmade threats. Therefore, authorities respond to these demands through new regulatory and operational frameworks to cope with existing and future risks. The Spanish regulatory framework regarding flood risk management, based on the European context, defines the required procedures for emergency management, involving all authorities responsable for civil protection and urban planning. This framework requires all municipalities at medium or high flood risk to develop and implement local action plans against flood risk (PAMRI, by its acronym in Spanish), which must include a risk estimation, analysis and evaluation, along with the description of actions for a risk-informed urban planning and emergency management. The City Council of Oliva developed the corresponding plan, approved by the regional government in June 2016, including new aspects such as the figure of the Technical Director, and a comprehensive and quantitative flood risk analysis to support decisionmaking on emergency management and planning.Research activities related to the work described in this article are part of the INICIA project, “Metodología de evaluación de INversiones en Infraestructuras del Ciclo Integral del Agua basada en indicadores de riesgo y de eficiencia energética”, within the framework of the National Programme for Research Aimed at the Challenges of Society “Retos 2013”, with reference BIA2013-48157-C2-1-R-AR.Porta-Sancho, JR.; Castillo Rodríguez, JT.; Escuder Bueno, I.; Perales-Momparler, S. (2016). The need for municipal action planning against flood risk: the risk-informed journey of the municipality of Oliva (Spain). VITRUVIO - International Journal of Architectural Technology and Sustainability. 1(2):67-78. https://doi.org/10.4995/vitruvio-ijats.2016.684967781

    Prediction of Evapotranspiration in a Mediterranean Region Using Basic Meteorological Variables

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    A critical need for farmers, particularly those in arid and semiarid areas is to have a reliable, accurate and reasonably accessible means of estimating the evapotranspiration rates of their crops to optimize their irrigation requirements. Evapotranspiration is a crucial process because of its influence on the precipitation that is returned to the atmosphere. The calculation of this variable often starts from the estimation of reference evapotranspiration, for which a variety of methods have been developed. However, these methods are very complex either theoretically and/or because of the large amount of parameters on which they are based, which makes the development of a simple and reliable methodology for the prediction of this variable important. This research combined three concepts such as cluster analysis, multiple linear regression (MLR), and Voronoi diagrams to achieve that end. Cluster analysis divided the study area into groups based on its weather characteristics, whose locations were then delimited by drawing the Voronoi regions associated with them. Regression equations were built to predict daily reference evapotranspiration in each cluster using basic climate variables produced in forecasts made by meteorological agencies. Finally, the Voronoi diagrams were used again to regionalize the crop coefficients and calculate evapotranspiration from the values of reference evapotranspiration derived from the regression models. These operations were applied to the Valencian region (Spain), a Mediterranean area which is partly semiarid and for which evapotranspiration is a critical issue. The results demonstrated the usefulness and accuracy of the methodology to predict the water demands of crops and hence enable farmers to plan their irrigation needs.This paper was possible thanks to the research project RHIVU (Ref. BIA2012-32463), financed by the Spanish Ministry of Economy and Competitiveness with funds from the State General Budget (PGE) and the European Regional Development Fund (ERDF). The authors also wish to express their gratitude to the Spanish Ministry of Agriculture, Food and Environment (MAGRAMA) for providing the data necessary to develop this study

    Promoter methylation regulates cyclooxygenase expression in breast cancer

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    INTRODUCTION: Overexpression of cyclooxygenase (COX-2) is commonly observed in human cancers. In a murine model of metastatic breast cancer, we observed that COX-2 expression and enzyme activity were associated with enhanced tumorigenic and metastatic potential. In contrast to the high COX-2 expression in metastatic tumors, transplantation of poorly tumorigenic tumor cell lines to syngeneic mice results in less COX-2 expression and less COX-2 activity in vivo. Aberrant CpG island methylation, and subsequent silencing of the COX-2 promoter, has been observed in human cancer cell lines and in some human tumors of the gastrointestinal tract. METHODS: Using bisulfite modification and a methylation-specific PCR, we examined the methylation status of the COX-2 promoter in a series of four closely-related murine mammary tumors differing in COX-2 expression and metastatic potential. RESULTS: We showed that line 410, which does not express COX-2 in vivo, exhibited evidence of promoter methylation. Interestingly, the metastatic counterpart of this cell (line 410.4) displayed only the unmethylated COX-2 promoter, as did two additional cell lines (lines 66.1 and 67). The methylation patterns observed in vitro were maintained when these murine mammary tumor lines were transplanted to syngeneic mice. Treatment with the DNA demethylating agent 5-aza-deoxycytidine increased COX-2 mRNA, increased protein and increased enzyme activity (prostaglandin synthesis). CONCLUSIONS: These results indicate that COX-2 promoter methylation may be one mechanism by which tumor cells regulate COX-2 expression. Upregulation of COX-2 expression in closely related metastatic lesions versus nonmetastatic lesions may represent a shift towards the unmethylated phenotype

    Global gene disruption in human cells to assign genes to phenotypes

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    Insertional mutagenesis in a haploid background can disrupt gene function[superscript 1]. We extend our earlier work by using a retroviral gene-trap vector to generate insertions in >98% of the genes expressed in a human cancer cell line that is haploid for all but one of its chromosomes. We apply phenotypic interrogation via tag sequencing (PhITSeq) to examine millions of mutant alleles through selection and parallel sequencing. Analysis of pools of cells, rather than individual clones[superscript 1] enables rapid assessment of the spectrum of genes involved in the phenotypes under study. This facilitates comparative screens as illustrated here for the family of cytolethal distending toxins (CDTs). CDTs are virulence factors secreted by a variety of pathogenic Gram-negative bacteria responsible for tissue damage at distinct anatomical sites[superscript 2]. We identify 743 mutations distributed over 12 human genes important for intoxication by four different CDTs. Although related CDTs may share host factors, they also exploit unique host factors to yield a profile characteristic for each CDT

    CpG methylation potentiates pixantrone and doxorubicin-induced DNA damage and is a marker of drug sensitivity

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    DNA methylation is an epigenetic modification of the mammalian genome that occurs predominantly at cytosine residues of the CpG dinucleotide. Following formaldehyde activation, pixantrone alkylates DNA and particularly favours the CpG motif. Aberrations in CpG methylation patterns are a feature of most cancer types, a characteristic that may determine their susceptibility to specific drug treatments. Given their common target, DNA methylation may modulate the DNA damage induced by formaldehyde-activated pixantrone. In vitro transcription, mass spectrometry and oligonucleotide band shift assays were utilized to establish that pixantrone–DNA adduct formation was consistently enhanced 2–5-fold at discrete methylated CpG doublets. The methylation-mediated enhancement was exquisitely sensitive to the position of the methyl substituent since methylation at neighboring cytosine residues failed to confer an increase in pixantrone–DNA alkylation. Covalent modification of DNA by formaldehyde-activated doxorubicin, but not cisplatin, was augmented by neighbouring CpG methylation, indicating that modulation of binding by CpG methylation is not a general feature of all alkylators. HCT116 colon cancer cells vastly deficient in CpG methylation were 12- and 10-fold more resistant to pixantrone and doxorubicin relative to the wild-type line, suggesting that these drugs may selectively recognize the aberrant CpG methylation profiles characteristic of most tumour types

    The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia

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    Cytarabine (ara-C) is the most effective agent for the treatment of acute myeloid leukaemia (AML). Aberrant expression of enzymes involved in the transport/metabolism of ara-C could explain drug resistance. We determined mRNA expression of these factors using quantitative-real-time-PCR in leukemic blasts from children diagnosed with de novo AML. Expression of the inactivating enzyme pyrimidine nucleotidase-I (PN-I) was 1.8-fold lower in FAB-M5 as compared to FAB-M1/2 (P=0.007). In vitro sensitivity to deoxynucleoside analogues was determined using the MTT-assay. Human equilibrative nucleoside transporter-1 (hENT1) mRNA expression and ara-C sensitivity were significantly correlated (rp=−0.46; P=0.001), with three-fold lower hENT1 mRNA levels in resistant patients (P=0.003). hENT1 mRNA expression also seemed to correlate inversely with the LC50 values of cladribine (rp=−0.30; P=0.04), decitabine (rp=−0.29; P=0.04) and gemcitabine (rp=−0.33; P=0.02). Deoxycytidine kinase (dCK) and cytidine deaminase (CDA) mRNA expression seemed to correlate with in vitro sensitivity to gemcitabine (rp=−0.31; P=0.03) and decitabine (rp=0.33; P=0.03), respectively. The dCK/PN-I ratio correlated inversely with LC50 values for gemcitabine (rp=−0.45, P=0.001) and the dCK/CDA ratio seemed to correlate with LC50 values for decitabine (rp=−0.29; 0.04). In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML

    Analysis of DNA Methylation in Various Swine Tissues

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    DNA methylation is known to play an important role in regulating gene expression during biological development and tissue differentiation in eukaryotes. In this study, we used the fluorescence-labeled methylation-sensitive amplified polymorphism (F-MSAP) method to assess the extent and pattern of cytosine methylation in muscle, heart, liver, spleen, lung, kidney and stomach from the swine strain Laiwu, and we also examined specific methylation patterns in the seven tissues. In total, 96,371 fragments, each representing a recognition site cleaved by either or both EcoRI + HpaII and EcoRI + MspI, the HpaII and MspI are isoschizomeric enzymes, were amplified using 16 pairs of selective primers. A total of 50,094 sites were found to be methylated at cytosines in seven tissues. The incidence of DNA methylation was approximately 53.99% in muscle, 51.24% in the heart, 50.18% in the liver, 53.31% in the spleen, 51.97% in the lung, 51.15% in the kidney and 53.39% in the stomach, as revealed by the incidence of differential digestion. Additionally, differences in DNA methylation levels imply that such variations may be related to specific gene expression during tissue differentiation, growth and development. Three types of bands were generated in the F-MSAP profile, the total numbers of these three types of bands in the seven tissues were 46,277, 24,801 and 25,293, respectively
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