Electrodeposition of a Au-Dy 2 O 3 Composite Solid Oxide Fuel Cell Catalyst from Eutectic Urea/Choline Chloride Ionic Liquid

In this research we have fabricated and tested Au/Dy2O3 composites for applications as Solid Oxide Fuel Cell (SOFC) electrocatalysts. The material was obtained by a process involving electrodeposition of a Au-Dy alloy from a urea/choline chloride ionic liquid electrolyte, followed by selective oxidation of Dy to Dy2O3 in air at high temperature. The electrochemical kinetics of the electrodeposition bath were studied by cyclic voltammetry, whence optimal electrodeposition conditions were identified. The heat-treated material was characterised from the morphological (scanning electron microscopy), compositional (X-ray fluorescence spectroscopy) and structural (X-ray diffractometry) points of view. The electrocatalytic activity towards H2 oxidation and O2 reduction was tested at 650 °C by electrochemical impedance spectrometry. Our composite electrodes exhibit an anodic activity that compares favourably with the only literature result available at the time of this writing for Dy2O3 and an even better cathodic performance

Convolutors on Sω(RN)\mathcal{S}_\omega(\mathbb{R}^N)

In this paper we continue the study of the spaces $\mathcal{O}_{M,\omega}(\mathbb{R}^N)$ and $\mathcal{O}_{C,\omega}(\mathbb{R}^N)$ undertaken in [1]. We determine new representations of such spaces and we give some structure theorems for their dual spaces. Furthermore, we show that $\mathcal{O}'_{C,\omega}(\mathbb{R}^N)$ is the space of convolutors of the space $\mathcal{S}_\omega(\mathbb{R}^N)$ of the $\omega$-ultradifferentiable rapidly decreasing functions of Beurling type (in the sense of Braun, Meise and Taylor) and of its dual space $\mathcal{S}'_\omega(\mathbb{R}^N)$. We also establish that the Fourier transform is an isomorphism from $\mathcal{O}'_{C,\omega}(\mathbb{R}^N)$ onto $\mathcal{O}_{M,\omega}(\mathbb{R}^N)$. In particular, we prove that this isomorphism is topological when the former space is endowed with the strong operator lc-topology induced by $\mathcal{L}_b(\mathcal{S}_\omega(\mathbb{R}^N))$ and the last space is endowed with its natural lc-topology.Comment: arXiv admin note: text overlap with arXiv:2011.0396

Topological Properties of Weighted Composition Operators in Sequence Spaces

For fixed sequences u=(ui)i∈N,φ=(φi)i∈N , we consider the weighted composition operator Wu,φ with symbols u, φ defined by x=(xi)i∈N↦u(x∘φ)=(uixφi)i∈N . We characterize the continuity and the compactness of the operator Wu,φ when it acts on the weighted Banach spaces lp(v) , 1 ≤ p≤ ∞ , and c(v) , with v=(vi)i∈N a weight sequence on N . We extend these results to the case in which the operator Wu,φ acts on sequence (LF)-spaces of type lp(V) and on sequence (PLB)-spaces of type ap(V) , with p∈ [1 , ∞] ∪ { 0 } and V a system of weights on N . We also characterize other topological properties of Wu,φ acting on lp(V) and on ap(V) , such as boundedness, reflexivity and to being Montel.

Multiphysics Finite-Element Modeling of the Neuron/Electrode Electrodiffusive Interaction

Understanding the biological-electrical transduction mechanisms is essential for reliable neural signal recording and feature extraction. As an alternative to state-of-the-art lumped-element circuit models, here we adopt a multiscale-multiphysics finite-element modeling framework. The model couples ion transport with the Hodgkin-Huxley model and the readout circuit, and is used to investigate a few relevant case studies. This approach is amenable to explore ion transport in the extracellular medium otherwise invisible to circuit model analysis

Clinical, epidemiological and virological features of acute hepatitis B in Italy

Purpose To evaluate the association of hepatitis B virus (HBV) genotypes, basal core promoter (BCP)/precore (PC) and S gene mutations with the clinical-epidemiological characteristics of acute hepatitis B (AHB) in Italy. Methods During July 2005–January 2007, 103 symptomatic AHB patients were enrolled and prospectively followed up at 15 national hospitals. HBV genotypes, BCP/ PC and S gene variants were determined by nested-PCR and direct sequence analysis. Results Genotype D, A and F were detected in 49, 45 and 6 % of patients, respectively. BCP, PC, and BCP plus PC variants were found in 3.1, 11.3 and 7.2 % of patients, respectively. At enrollment, 68.3 % of patients were hepatitis B e antigen (HBeAg)-positive and 31.7 % HBeAg-negative. BCP/PC mutations were more common in HBeAg-negative than in HBeAg-positive patients (p < 0.0001). Compared to genotype D patients, those harboring non-D genotypes were more frequently males (p = 0.023), HBeAg-positive (p < 0.001), had higher bilirubin (p = 0.014) and viremia (p = 0.034) levels and less frequently carried BCP/PC mutations (p < 0.001). Non-D genotype patients more often were from Central Italy (p = 0.001) and reported risky sexual exposure (p = 0.021). Two patients had received vaccination before AHB: one harbored genotype F; the other showed a S gene mutation. Four patients developed fulminant AHB; mutations were found in 2 of 3 patients who underwent BCP/ PC sequencing. After a 6-month follow-up, only 2 (2.8 %) patients developed persistent infection. Conclusion AHB by non-D genotypes is increasing in Italy and is associated with risky sexual exposure. The ability of some genotypes to cause persistent and/or severe infection in Italy warrants larger studies for clarificatio

Cardiac Fibroblasts Contribute to Myocardial Dysfunction in Mice with Sepsis: The Role of NLRP3 Inflammasome Activation

Myocardial contractile dysfunction in sepsis is associated with the increased morbidity and mortality. Although the underlying mechanisms of the cardiac depression have not been fully elucidated, an exaggerated inflammatory response is believed to be responsible. Nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome is an intracellular platform that is involved in the maturation and release of interleukin (IL)-1 beta. The aim of the present study is to evaluate whether sepsis activates NLRP3 inflammasome/caspase-1/IL-1 beta pathway in cardiac fibroblasts (CFs) and whether this cytokine can subsequently impact the function of cardiomyocytes (cardiac fibroblast-myocyte crosstalk). We show that treatment of CFs with lipopolysaccharide (LPS) induces upregulation of NLRP3, activation of caspase-1, as well as the maturation (activation) and release of IL-1 beta. In addition, the genetic (small interfering ribonucleic acid [siRNA]) and pharmacological (glyburide) inhibition of the NLRP3 inflammasome in CFs can block this signaling pathway. Furthermore, the inhibition of the NLRP3 inflammasome in cardiac fibroblasts ameliorated the ability of LPS-chalenged CFs to impact cardiomyocyte function as assessed by intracellular cyclic adenosine monophosphate (cAMP) responses in cardiomyocytes. Salient features of this the NLP3 inflammasome/ caspase-1 pathway were confirmed in in vivo models of endotoxemia/sepsis. We found that inhibition of the NLRP3 inflammasome attenuated myocardial dysfunction in mice with LPS and increased the survival rate in mice with feces-induced peritonitis. Our results indicate that the activation of the NLRP3 inflammasome in cardiac fibroblasts is pivotal in the induction of myocardial dysfunction in sepsis

Autofluorescence of Model Polyethylene Terephthalate Nanoplastics for Cell Interaction Studies

This work contributes to fill one of the gaps regarding nanoplastic interactions with biological systems by producing polyethylene terephthalate (PET) model nanoplastics, similar to those found in the marine environment, by means of a fast top-down approach based on mechanical fragmentation. Their size distribution and morphology were characterized by laser diffraction and atomic force microscopy (AFM). Their autofluorescence was studied by spectrofluorimetry and fluorescence imaging, being a key property for the evaluation of their interaction with biota. The emission spectra of label-free nanoplastics were comparable with those of PET nanoplastics labeled with Nile red. Finally, the suitability of label-free nanoplastics for biological studies was assessed by in vitro exposure with Mytilus galloprovincialis hemolymphatic cells in a time interval up to 6 h. The nanoplastic internalization into these cells, known to be provided with phagocytic activity, was assessed by fluorescence microscopy. The obtained results underlined that the autofluorescence of the model PET nanoplastics produced in the laboratory was adequate for biological studies having the potential to overcome the disadvantages commonly associated with several fluorescent dyes, such as the tendency to also stain other organic materials different from plastics, to form aggregates due to intermolecular interactions at high concentrations with a consequent decrease in fluorescence intensity, and to dye desorption from nanoparticles. The results of the autofluorescence study provide an innovative approach for plastic risk assessment

Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1

Background: Hemorrhagic shock and resuscitation (HS/R) can induce multiple organ failure which is associated with high mortality. The lung is an organ commonly affected by the HS/R. Acute lung injury is a major cause of dysfunction in other organ systems. The objective of this study is to test the hypothesis that HS/R causes increased gut permeability which results in induction of high mobility group box1 protein (HMGB1) and further leads to the development of acute lung inflammation. Materials and methods: A mouse model of HS/R was employed in this study. Gut permeability and bacterial translocation were assessed with circulating FD4 and lipopolysaccharide (LPS). Circulating HMGB1 was determined with ELISA. Acute lung inflammation (ALI) was determined with lung myeloperoxidase (MPO) activity and pulmonary protein leakage. Results: HS/R induced intestinal barrier dysfunction as evidenced by increased circulating FD4 and LPS at 30 min and 2 hrs after resuscitation, respectively. In addition, circulating HMGB1 levels were increased in mice with HS/R as compared with sham animals (p \u3c 0.05). HS/R resulted in ALI (increased lung MPO activity and pulmonary protein leakage in mice with HS/R compared with sham mice, p \u3c 0.05). Inhibition of HMGB1 (A-box and TLR4(-/-)) attenuated the ALI in mice with HS/R. However, inhibition of HMGB1 did not show protective effect on gut injury in early phase of HS/R in mice. Conclusions: Our results suggest that induction of HMGB1 is important in hemorrhagic shock and resuscitation-induced acute lung inflammation