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Träfflista för sökning "WFRF:(Marchetti B) srt2:(2015-2019)"

Sökning: WFRF:(Marchetti B) > (2015-2019)

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1.
  • Walker, Anthony P, et al. (författare)
  • Horizon 2020 EuPRAXIA design study
  • 2017
  • Ingår i: Journal of Physics: Conference Series. - : IOP Publishing. - 1742-6588 .- 1742-6596. ; 874:1
  • Tidskriftsartikel (refereegranskat)abstract
    • The Horizon 2020 Project EuPRAXIA ("European Plasma Research Accelerator with eXcellence In Applications") is preparing a conceptual design report of a highly compact and cost-effective European facility with multi-GeV electron beams using plasma as the acceleration medium. The accelerator facility will be based on a laser and/or a beam driven plasma acceleration approach and will be used for photon science, high-energy physics (HEP) detector tests, and other applications such as compact X-ray sources for medical imaging or material processing. EuPRAXIA started in November 2015 and will deliver the design report in October 2019. EuPRAXIA aims to be included on the ESFRI roadmap in 2020.
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2.
  • Tschandl, P., et al. (författare)
  • Comparison of the accuracy of human readers versus machine-learning algorithms for pigmented skin lesion classification: an open, web-based, international, diagnostic study
  • 2019
  • Ingår i: The Lancet Oncology. - 1470-2045 .- 1474-5488. ; 20:7, s. 938-947
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Whether machine-learning algorithms can diagnose all pigmented skin lesions as accurately as human experts is unclear. The aim of this study was to compare the diagnostic accuracy of state-of-the-art machine-learning algorithms with human readers for all clinically relevant types of benign and malignant pigmented skin lesions. Methods: For this open, web-based, international, diagnostic study, human readers were asked to diagnose dermatoscopic images selected randomly in 30-image batches from a test set of 1511 images. The diagnoses from human readers were compared with those of 139 algorithms created by 77 machine-learning labs, who participated in the International Skin Imaging Collaboration 2018 challenge and received a training set of 10 015 images in advance. The ground truth of each lesion fell into one of seven predefined disease categories: intraepithelial carcinoma including actinic keratoses and Bowen's disease; basal cell carcinoma; benign keratinocytic lesions including solar lentigo, seborrheic keratosis and lichen planus-like keratosis; dermatofibroma; melanoma; melanocytic nevus; and vascular lesions. The two main outcomes were the differences in the number of correct specific diagnoses per batch between all human readers and the top three algorithms, and between human experts and the top three algorithms. Findings: Between Aug 4, 2018, and Sept 30, 2018, 511 human readers from 63 countries had at least one attempt in the reader study. 283 (55·4%) of 511 human readers were board-certified dermatologists, 118 (23·1%) were dermatology residents, and 83 (16·2%) were general practitioners. When comparing all human readers with all machine-learning algorithms, the algorithms achieved a mean of 2·01 (95% CI 1·97 to 2·04; p<0·0001) more correct diagnoses (17·91 [SD 3·42] vs 19·92 [4·27]). 27 human experts with more than 10 years of experience achieved a mean of 18·78 (SD 3·15) correct answers, compared with 25·43 (1·95) correct answers for the top three machine algorithms (mean difference 6·65, 95% CI 6·06–7·25; p<0·0001). The difference between human experts and the top three algorithms was significantly lower for images in the test set that were collected from sources not included in the training set (human underperformance of 11·4%, 95% CI 9·9–12·9 vs 3·6%, 0·8–6·3; p<0·0001). Interpretation: State-of-the-art machine-learning classifiers outperformed human experts in the diagnosis of pigmented skin lesions and should have a more important role in clinical practice. However, a possible limitation of these algorithms is their decreased performance for out-of-distribution images, which should be addressed in future research. Funding: None. © 2019 Elsevier Ltd
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3.
  • Botticella, M. T., et al. (författare)
  • Supernova rates from the SUDARE VST-omegacam search II. Rates in a galaxy sample
  • 2017
  • Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 598
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims. This is the second paper of a series in which we present measurements of the supernova (SN) rates from the SUDARE survey. The aim of this survey is to constrain the core collapse (CC) and Type Ia SN progenitors by analysing the dependence of their explosion rate on the properties of the parent stellar population averaging over a population of galaxies with different ages in a cosmic volume and in a galaxy sample. In this paper, we study the trend of the SN rates with the intrinsic colours, the star formation activity and the masses of the parent galaxies. To constrain the SN progenitors we compare the observed rates with model predictions assuming four progenitor models for SNe Ia with different distribution functions of the time intervals between the formation of the progenitor and the explosion, and a mass range of 8-40 M for CC SN progenitors. Methods. We considered a galaxy sample of approximately 130 000 galaxies and a SN sample of approximately 50 events. The wealth of photometric information for our galaxy sample allows us to apply the spectral energy distribution (SED) fitting technique to estimate the intrinsic rest frame colours, the stellar mass and star formation rate (SFR) for each galaxy in the sample. The galaxies have been separated into star-forming and quiescent galaxies, exploiting both the rest frame U-V vs. V-J colour-colour diagram and the best fit values of the specific star formation rate (sSFR) from the SED fitting. Results. We found that the SN Ia rate per unit mass is higher by a factor of six in the star-forming galaxies with respect to the passive galaxies, identified as such both on the U-V vs. V-J colour-colour diagram and for their sSFR. The SN Ia rate per unit mass is also higher in the less massive galaxies that are also younger. These results suggest a distribution of the delay times (DTD) less populated at long delay times than at short delays. The CC SN rate per unit mass is proportional to both the sSFR and the galaxy mass, confirming that the CC SN progenitors explode soon after the end of the star formation activity. The trends of the Type Ia and CC SN rates as a function of the sSFR and the galaxy mass that we observed from SUDARE data are in agreement with literature results at different redshifts suggesting that the ability of the stellar populations to produce SN events does not vary with cosmic time. The expected number of SNe Ia is in agreement with that observed for all four DTD models considered both in passive and star-forming galaxies so we can not discriminate between different progenitor scenarios. The expected number of CC SNe is higher than that observed, suggesting a higher limit for the minimum progenitor mass. However, at least part of this discrepancy between expected and observed number of CC SNe may reflect a fluctuation due to the relatively poor statistics. We also compare the expected and observed trends of the SN Ia rate with the intrinsic U-J colour of the parent galaxy, assumed to be a tracer of the age distribution. While the slope of the relation between the SN Ia rate and the U-J colour in star-forming galaxies can be well-reproduced by all four DTD models considered, only the steepest of them is able to account for the rates and colour in star-forming and passive galaxies with the same value of the SN Ia production efficiency. The agreement between model predictions and data could be found for the other DTD models, but with a productivity of SN Ia higher in passive galaxies compared to star-forming galaxies.
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6.
  • L'Episcopo, F, et al. (författare)
  • GSK-3β-induced Tau pathology drives hippocampal neuronal cell death in Huntington's disease : involvement of astrocyte-neuron interactions
  • 2016
  • Ingår i: Cell Death and Disease. - : Springer Science and Business Media LLC. - 2041-4889. ; 7, s. 1-14
  • Tidskriftsartikel (refereegranskat)abstract
    • Glycogen synthase kinase-3β (GSK-3β) has emerged as a critical factor in several pathways involved in hippocampal neuronal maintenance and function. In Huntington's disease (HD), there are early hippocampal deficits both in patients and transgenic mouse models, which prompted us to investigate whether disease-specific changes in GSK-3β expression may underlie these abnormalities. Thirty-three postmortem hippocampal samples from HD patients (neuropathological grades 2-4) and age- and sex-matched normal control cases were analyzed using real-time quantitative reverse transcription PCRs (qPCRs) and immunohistochemistry. In vitro and in vivo studies looking at hippocampal pathology and GSK-3β were also undertaken in transgenic R6/2 and wild-type mice. We identified a disease and stage-dependent upregulation of GSK-3β mRNA and protein levels in the HD hippocampus, with the active isoform pGSK-3β-Tyr(216) being strongly expressed in dentate gyrus (DG) neurons and astrocytes at a time when phosphorylation of Tau at the AT8 epitope was also present in these same neurons. This upregulation of pGSK-3β-Tyr(216) was also found in the R6/2 hippocampus in vivo and linked to the increased vulnerability of primary hippocampal neurons in vitro. In addition, the increased expression of GSK-3β in the astrocytes of R6/2 mice appeared to be the main driver of Tau phosphorylation and caspase3 activation-induced neuronal death, at least in part via an exacerbated production of major proinflammatory mediators. This stage-dependent overactivation of GSK-3β in HD-affected hippocampal neurons and astrocytes therefore points to GSK-3β as being a critical factor in the pathological development of this condition. As such, therapeutic targeting of this pathway may help ameliorate neuronal dysfunction in HD.
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7.
  • Malapelle, Francesco, et al. (författare)
  • Automatic 3DS Conversion of Historical Aerial Photographs
  • 2015
  • Ingår i: IC3D 2015, International Conference on 3D Imaging. - 9781509012657
  • Konferensbidrag (refereegranskat)abstract
    • In this paper we present a method for the generation of 3D stereo (3DS) pairs from sequences of historical aerial photographs. The goal of our work is to provide a stereoscopic display when the existing exposures are in a monocular sequence. Each input image is processed using its neighbours and a synthetic image is rendered, which, together with the original one, form a stereo pair. Promising results on real images taken from a historical photo archive are shown, that corroborate the viability of generating 3DS data from monocular footage.
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8.
  • Trabelsi, M. S., et al. (författare)
  • Farnesoid X receptor inhibits glucagon-like peptide-1 production by enteroendocrine L cells
  • 2015
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 6
  • Tidskriftsartikel (refereegranskat)abstract
    • Bile acids are signalling molecules, which activate the transmembrane receptor TGR5 and the nuclear receptor FXR. BA sequestrants (BAS) complex bile acids in the intestinal lumen and decrease intestinal FXR activity. The BAS-BA complex also induces glucagon-like peptide-1 (GLP-1) production by L cells which potentiates beta-cell glucose-induced insulin secretion. Whether FXR is expressed in L cells and controls GLP-1 production is unknown. Here, we show that FXR activation in L cells decreases proglucagon expression by interfering with the glucose-responsive factor Carbohydrate-Responsive Element Binding Protein (ChREBP) and GLP-1 secretion by inhibiting glycolysis. In vivo, FXR deficiency increases GLP-1 gene expression and secretion in response to glucose hence improving glucose metabolism. Moreover, treatment of ob/ob mice with the BAS colesevelam increases intestinal proglucagon gene expression and improves glycaemia in a FXR-dependent manner. These findings identify the FXR/GLP-1 pathway as a new mechanism of BA control of glucose metabolism and a pharmacological target for type 2 diabetes.
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