11 research outputs found

    A Novel Hyperspectral Method to Detect Moldy Core in Apple Fruits

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    An innovative low-cost device based on hyperspectral spectroscopy in the near infrared (NIR) spectral region is proposed for the non-invasive detection of moldy core (MC) in apples. The system, based on light collection by an integrating sphere, was tested on 70 apples cultivar (cv) Golden Delicious infected by Alternaria alternata, one of the main pathogens responsible for MC disease. Apples were sampled in vertical and horizontal positions during five measurement rounds in 13 days’ time, and 700 spectral signatures were collected. Spectral correlation together with transmittance temporal patterns and ANOVA showed that the spectral region from 863.38 to 877.69 nm was most linked to MC presence. Then, two binary classification models based on Artificial Neural Network Pattern Recognition (ANN-AP) and Bagging Classifier (BC) with decision trees were developed, revealing a better detection capability by ANN-AP, especially in the early stage of infection, where the predictive accuracy was 100% at round 1 and 97.15% at round 2. In subsequent rounds, the classification results were similar in ANN-AP and BC models. The system proposed surpassed previous MC detection methods, needing only one measurement per fruit, while further research is needed to extend it to different cultivars or fruits

    Oxazoline-containing phosphazene derivatives, part III:Synthesis and characterization of novel cyclophosphazenes functionalized with chiral 2-oxazoline groups

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    In this paper we describe the synthesis and the characterization of a series of cyclophosphazenes substituted with 2-oxazoline-containing moieties, with and without optical activity. These products could be obtained by reacting cyclophosphazenes containing six (hexachlorocyclophosphazene, C-6-Cl), two (2,2-dichloro-4,4,6,6-bis[spiro(2′,2″-dioxy-1′, 1″-biphenyl)]cyclophosphazene, C-2-Cl) and one (pentakis(phenoxy) monochlorocyclophosphazene, C-1-Cl) chlorine atoms, respectively, with a series of 4-hydroxyphenyl-2-oxazolines, as obtained by condensation reaction of methyl-4-hydroxybenzoate with 2-aminoethanol and with chiral and racemic 1-amino-2-propanol, and successive cyclization reactions of the resulting hydroxyamides to 2-oxazoline compounds

    Expanding the clinical-pathological and genetic spectrum of RYR1-related congenital myopathies with cores and minicores: an Italian population study

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    Mutations in the RYR1 gene, encoding ryanodine receptor 1 (RyR1), are a well-known cause of Central Core Disease (CCD) and Multi-minicore Disease (MmD). We screened a cohort of 153 patients carrying an histopathological diagnosis of core myopathy (cores and minicores) for RYR1 mutation. At least one RYR1 mutation was identified in 69 of them and these patients were further studied. Clinical and histopathological features were collected. Clinical phenotype was highly heterogeneous ranging from asymptomatic or paucisymptomatic hyperCKemia to severe muscle weakness and skeletal deformity with loss of ambulation. Sixty-eight RYR1 mutations, generally missense, were identified, of which 16 were novel. The combined analysis of the clinical presentation, disease progression and the structural bioinformatic analyses of RYR1 allowed to associate some phenotypes to mutations in specific domains. In addition, this study highlighted the structural bioinformatics potential in the prediction of the pathogenicity of RYR1 mutations. Further improvement in the comprehension of genotype-phenotype relationship of core myopathies can be expected in the next future: the actual lack of the human RyR1 crystal structure paired with the presence of large intrinsically disordered regions in RyR1, and the frequent presence of more than one RYR1 mutation in core myopathy patients, require designing novel investigation strategies to completely address RyR1 mutation effect

    The actin-binding protein EPS8 binds VE-cadherin and modulates YAP localization and signaling

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    Vascular endothelial (VE)-cadherin transfers intracellular signals contributing to vascular hemostasis. Signaling through VE-cadherin requires association and activity of different intracellular partners. Yes-associated protein (YAP)/TAZ transcriptional cofactors are important regulators of cell growth and organ size. We show that EPS8, a signaling adapter regulating actin dynamics, is a novel partner of VE-cadherin and is able to modulate YAP activity. By biochemical and imaging approaches, we demonstrate that EPS8 associates with the VE-cadherin complex of remodeling junctions promoting YAP translocation to the nucleus and transcriptional activation. Conversely, in stabilized junctions, 14-3-3-YAP associates with the VE-cadherin complex, whereas Eps8 is excluded. Junctional association of YAP inhibits nuclear translocation and inactivates its transcriptional activity both in vitro and in vivo in Eps8-null mice. The absence of Eps8 also increases vascular permeability in vivo, but did not induce other major vascular defects. Collectively, we identified novel components of the adherens junction complex, and we introduce a novel molecular mechanism through which the VE-cadherin complex controls YAP transcriptional activity
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