Neuro-fuzzy application for concrete strength prediction using combined non-destructive tests

The application of the neuro-fuzzy inference system to predict the compressive strength of concrete is presented in this study. The adaptive neuro-fuzzy inference system (ANFIS) is introduced for training and testing the data sets consisting of various parameters. To investigate the influence of various parameters which affect the compressive strength, 1551 data pairs are collected from the technical literature. These data sets cover early and late compressive strengths from 3 to 365 days and low and high strength in the range 6·3–107·7 MPa. To reflect the effects of other uncertain parameters and in situ conditions, the results of non-destructive tests (NDTs) such as ultrasonic pulse velocity (UPV) and rebound hammer test are also included as input parameters, in addition to mix proportion and curing histories. For the testing of trained ANFIS models, 20 cube specimens and 210 cylinders are prepared, and compressive test and NDTs are conducted. For the comparative study of the applicability of ANFIS models combined with NDT results, four ANFIS models are developed. Depending on whether the input parameters of ANFIS models include NDT results or not, these are distinguished from each other. Among the four models, the ‘ANFIS-UR' model having the parameters for both UPV and rebound hammer test results shows the best accuracy in the prediction of compressive strength

Ozone effects on blood biomarkers of systemic inflammation, oxidative stress, endothelial function, and thrombosis: The Multicenter Ozone Study in oldEr Subjects (MOSES).

The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55-70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p<0.01. There were no effects of ozone on the three primary markers of systemic inflammation and a prothrombotic state: C-reactive protein, monocyte-platelet conjugates, and microparticle-associated tissue factor activity. However, among the secondary endpoints, endothelin-1, a potent vasoconstrictor, increased from pre- to post-exposure with ozone concentration (120 vs 0 ppb: 0.07 pg/mL, 95% confidence interval [CI] 0.01, 0.14; 70 vs 0 ppb: -0.03 pg/mL, CI -0.09, 0.04; p = 0.008). Nitrotyrosine, a marker of oxidative and nitrosative stress, decreased with increasing ozone concentrations, with marginal significance (120 vs 0 ppb: -41.5, CI -70.1, -12.8; 70 vs 0 ppb: -14.2, CI -42.7, 14.2; p = 0.017). GSTM1 status did not modify the effect of ozone exposure on any of the outcomes. These findings from healthy older adults fail to identify any mechanistic basis for the epidemiologically described cardiovascular effects of exposure to ozone. The findings, however, may not be applicable to adults with cardiovascular disease

Transcriptome-pathology correlation identifies interplay between TDP-43 and the expression of its kinase CK1E in sporadic ALS.

Sporadic amyotrophic lateral sclerosis (sALS) is the most common form of ALS, however, the molecular mechanisms underlying cellular damage and motor neuron degeneration remain elusive. To identify molecular signatures of sALS we performed genome-wide expression profiling in laser capture microdissection-enriched surviving motor neurons (MNs) from lumbar spinal cords of sALS patients with rostral onset and caudal progression. After correcting for immunological background, we discover a highly specific gene expression signature for sALS that is associated with phosphorylated TDP-43 (pTDP-43) pathology. Transcriptome-pathology correlation identified casein kinase 1ε (CSNK1E) mRNA as tightly correlated to levels of pTDP-43 in sALS patients. Enhanced crosslinking and immunoprecipitation in human sALS patient- and healthy control-derived frontal cortex, revealed that TDP-43 binds directly to and regulates the expression of CSNK1E mRNA. Additionally, we were able to show that pTDP-43 itself binds RNA. CK1E, the protein product of CSNK1E, in turn interacts with TDP-43 and promotes cytoplasmic accumulation of pTDP-43 in human stem-cell-derived MNs. Pathological TDP-43 phosphorylation is therefore, reciprocally regulated by CK1E activity and TDP-43 RNA binding. Our framework of transcriptome-pathology correlations identifies candidate genes with relevance to novel mechanisms of neurodegeneration

Reflections on the Implementation of Tidal Energy in Ecuador

Renewable energy is a topic frequently discussed due to the need to change the forms of generation, from the centralized to the distributed form and take advantage of the potentials that are scattered in the territory and use local resources and thereby diversify the schemes of distributed generation that allows the man in his daily work to pass from consumption of energy to generator, in this way the environmental impacts are reduced that today accelerate the change of temperature in the planet, noticing in recent years the oil and its derivatives are responsible for this phenomenon. The objective of the research is to reflect on tidal energy, knowing that the province of Manabí, is the one that has the largest coastal area and where there is a potential that can be studied for future use

Diversity of vertebrate splicing factor U2AF35 : identification of alternatively spliced U2AF1 mRNAS

© 2004 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. This is an Open Access article under the CC BY license.U2 small nuclear ribonucleoprotein auxiliary factor small subunit (U2AF(35)) is encoded by a conserved gene designated U2AF1. Here we provide evidence for the existence of alternative vertebrate transcripts encoding different U2AF(35) isoforms. Three mRNA isoforms (termed U2AF(35)a-c) were produced by alternative splicing of the human U2AF1 gene. U2AF(35)c contains a premature stop codon that targets the resulting mRNA to nonsense-mediated mRNA decay. U2AF(35)b differs from the previously described U2AF(35)a isoform in 7 amino acids located at the atypical RNA Recognition Motif involved in dimerization with U2AF(65). Biochemical experiments indicate that isoform U2AF(35)b, which has been highly conserved from fish to man, maintains the ability to interact with U2AF(65), stimulates U2AF(65) binding to a pre-mRNA, and promotes U2AF splicing activity in vitro. Real time, quantitative PCR analysis indicates that U2AF(35)a is the most abundant isoform expressed in murine tissues, although the ratio between U2AF(35)a and U2AF(35)b varies from 10-fold in the brain to 20-fold in skeletal muscle. We propose that post-transcriptional regulation of U2AF1 gene expression may provide a mechanism by which the relative cellular concentration and availability of U2AF(35) protein isoforms are modulated, thus contributing to the finely tuned control of splicing events in different tissues.This work was supported in part by Grant POCTI/MGI/36547/2000 from Fundação para a Ciência e Tecnologia, Portugal, and by Grant RG0300/2000-M from the Human Frontier Science Program Organization. Supported by Fundação para a Ciência e Tecnologia Fellowship PRAXIS XXI/BD/18044/98. Supported by Fundação para a Ciência e Tecnologia Fellowship POCTI SFRH/BPD/9388/2002. Supported by Fundação para a Ciência e Tecnologia Fellowship PRAXIS XXI SFRH/BD/2914/2000.info:eu-repo/semantics/publishedVersio

FUS (fused in sarcoma) is a component of the cellular response to topoisomerase I–induced DNA breakage and transcriptional stress

FUS (fused in sarcoma) plays a key role in several steps of RNA metabolism, and dominant mutations in this protein are associated with neurodegenerative diseases. Here, we show that FUS is a component of the cellular response to topoisomerase I (TOP1)–induced DNA breakage; relocalising to the nucleolus in response to RNA polymerase II (Pol II) stalling at sites of TOP1-induced DNA breaks. This relocalisation is rapid and dynamic, reversing following the removal of TOP1-induced breaks and coinciding with the recovery of global transcription. Importantly, FUS relocalisation following TOP1-induced DNA breakage is associated with increased FUS binding at sites of RNA polymerase I transcription in ribosomal DNA and reduced FUS binding at sites of RNA Pol II transcription, suggesting that FUS relocates from sites of stalled RNA Pol II either to regulate pre-mRNA processing during transcriptional stress or to modulate ribosomal RNA biogenesis. Importantly, FUS-mutant patient fibroblasts are hypersensitive to TOP1-induced DNA breakage, highlighting the possible relevance of these findings to neurodegeneration

Magnetic order in orbital models of the iron pnictides

We examine the appearance of the experimentally-observed stripe spin-density-wave magnetic order in five different orbital models of the iron pnictide parent compounds. A restricted mean-field ansatz is used to determine the magnetic phase diagram of each model. Using the random phase approximation, we then check this phase diagram by evaluating the static spin susceptibility in the paramagnetic state close to the mean-field phase boundaries. The momenta for which the susceptibility is peaked indicate in an unbiased way the actual ordering vector of the nearby mean-field state. The dominant orbitally resolved contributions to the spin susceptibility are also examined to determine the origin of the magnetic instability. We find that the observed stripe magnetic order is possible in four of the models, but it is extremely sensitive to the degree of the nesting between the electron and hole Fermi pockets. In the more realistic five-orbital models, this order competes with a strong-coupling incommensurate state which appears to be controlled by details of the electronic structure below the Fermi energy. We conclude by discussing the implications of our work for the origin of the magnetic order in the pnictides.Comment: 19 pages, 19 figures; published version, typos corrected, references adde