WO3-Doped Indium Oxide Thick Films for Ozone Detection at Low Temperature

Ozone, a strong oxidizing gas, has dramatically increased its concentration in the troposphere during the last decades. Since high O3 concentrations are hazardous to human health, the development of effective methods and economic devices to detect this gas is an urgent need. In this frame, In2O3 is well known as an n-type ozone sensitive and selective material, generally displaying its optimal sensing capability in the temperature range 200–350 °C. To enhance the sensing capability of In2O3 and to decrease its operative temperature, in this work, commercial In2O3 powders were doped with 2.5 wt. % WO3. Pure and doped-In2O3 materials were used to develop sensing devices by screen-printing technology. Resistance measurements were performed in the temperature range 25 °C–150 °C under 200–500 ppb O3. Best results were obtained at 75 °C with sensor’s responses as high as 40 under 200 ppb of ozone

Molecules as building blocks for a CFD-PBE model to describe the effect of fluid dynamics on nanoparticle formation

Recently research efforts have focused on the effect of fluid dynamics on particle formation processes, by using special mixing devices, that allow to perform controlled experiments, and complex models, that allow to quantify its influence on the final particle size. The standard modelling approach consists in considering three different steps: nucleation, molecular growth and aggregation. This is usually done by simulating the process with a population balance equation (PBE) coupled with computational fluid dynamics (CFD), in which these three different steps are considered separately. The PBE is often written using as internal coordinate the actual particle size or volume; here, we propose a new modelling strategy that overcomes the concepts of nucleation and molecular growth, by using as internal coordinate the number of molecules which aggregate, or self-assemble, together forming a nanoparticle. The novel modelling approach is therefore defined as a purely-aggregative model

Step-by-step iconographic description of a prolonged but still favourable course of orbital cellulitis in a child with acute rhinosinusitis: an iconographic case study

Orbital cellulitis is an infrequent complication of acute ethmoiditis possibly leading to life- or visual-threatening complications. Despite its natural history is well known, its clinical evolution may widely vary among patients, and even in the most favourable cases long-term sequelae may persist. We here provide a step-by-step iconographic description of a periorbital and orbital cellulitis occurring in a child with ipsilateral acute rhinosinusitis. Our report shows that an unusual long-term evolution of periorbital and orbital cellulitis is possible also in apparently favourable cases

Identification of the zinc finger 216 (ZNF216) in human carcinoma cells. A potential regulator of EGFR activity

Epidermal Growth Factor Receptor (EGFR), a member of the ErbB family of receptor tyrosine kinase (RTK) proteins, is aberrantly expressed or deregulated in tumors and plays pivotal roles in cancer onset and metastatic progression. ZNF216 gene has been identified as one of Immediate Early Genes (IEGs) induced by RTKs. Overexpression of ZNF216 protein sensitizes 293 cell line to TNF-α induced apoptosis. However, ZNF216 overexpression has been reported in medulloblastomas and metastatic nasopharyngeal carcinomas. Thus, the role of this protein is still not clearly understood. In this study, the inverse correlation between EGFR and ZNF216 expression was confirmed in various human cancer cell lines differently expressing EGFR. EGF treatment of NIH3T3 cells overexpressing both EGFR and ZNF216 (NIH3T3-EGFR/ZNF216), induced a long lasting activation of EGFR in the cytosolic fraction and an accumulation of phosphorylated EGFR (pEGFR) more in the nuclear than in the cytosolic fraction compared to NIH3T3-EGFR cells. Moreover, EGF was able to stimulate an increased expression of ZNF216 in the cytosolic compartment and its nuclear translocation in a time-dependent manner in NIH3T3-EGFR/ZNF216. A similar trend was observed in A431 cells endogenously expressing the EGFR and transfected with Znf216. The increased levels of pEGFR and ZNF216 in the nuclear fraction of NIH3T3-EGFR/ZNF216 cells were paralleled by increased levels of phospho-MAPK and phospho-Akt. Surprisingly, EGF treatment of NIH3T3-EGFR/ZNF216 cells induced a significant increase of apoptosis thus indicating that ZNF216 could sensitize cells to EGF-induced apoptosis and suggesting that it may be involved in the regulation and effects of EGFR signaling

Mechanisms of endothelial cell dysfunction in cystic fibrosis

Although cystic fibrosis (CF) patients exhibit signs of endothelial perturbation, the functions of the cystic fibrosis conductance regulator (CFTR) in vascular endothelial cells (EC) are poorly defined. We sought to uncover biological activities of endothelial CFTR, relevant for vascular homeostasis and inflammation. We examined cells from human umbilical cords (HUVEC) and pulmonary artery isolated from non-cystic fibrosis (PAEC) and CF human lungs (CF-PAEC), under static conditions or physiological shear. CFTR activity, clearly detected in HUVEC and PAEC, was markedly reduced in CF-PAEC. CFTR blockade increased endothelial permeability to macromolecules and reduced trans‑endothelial electrical resistance (TEER). Consistent with this, CF-PAEC displayed lower TEER compared to PAEC. Under shear, CFTR blockade reduced VE-cadherin and p120 catenin membrane expression and triggered the formation of paxillin- and vinculin-enriched membrane blebs that evolved in shrinking of the cell body and disruption of cell-cell contacts. These changes were accompanied by enhanced release of microvesicles, which displayed reduced capability to stimulate proliferation in recipient EC. CFTR blockade also suppressed insulin-induced NO generation by EC, likely by inhibiting eNOS and AKT phosphorylation, whereas it enhanced IL-8 release. Remarkably, phosphodiesterase inhibitors in combination with a β2 adrenergic receptor agonist corrected functional and morphological changes triggered by CFTR dysfunction in EC. Our results uncover regulatory functions of CFTR in EC, suggesting a physiological role of CFTR in the maintenance EC homeostasis and its involvement in pathogenetic aspects of CF. Moreover, our findings open avenues for novel pharmacology to control endothelial dysfunction and its consequences in CF

Pneumococcal conjugate vaccines and otitis media.

Peer Reviewe

Phenotype Profiling and Allergy in Otitis-Prone Children

Background: Otitis-prone children can present some distinctive clinical patterns and although a number of known risk factors for recurrent acute otitis media (RAOM) are known, no dedicated epidemiological models have been developed to explain clinical heterogeneity.Methods: A preliminary retrospective pilot study was planned to evaluate the possible effect of allergic disease in the development of different disease phenotypes in otitis-prone children aged 3–10 years, particularly the absence (simple RAOM), or presence of episodes of otitis media with effusion between acute infections (RAOM with OME).Results: Analysis was based on the data contained in 153 charts (55.6% males, mean age of 59.4 ± 16.4 months). 75.8% of children had a simple RAOM and 24.2% a RAOM with OME. Atopy or allergy were documented in respectively 47.7 and 41.3% of children considered as a whole. The prevalence of atopy or allergy was significantly higher in the children with a RAOM with OME (atopy: 73.0 vs. 39.5%, p < 0.001; allergy: 60.0 vs. 36.1%, p = 0.049), who also more frequently showed adenoidal hypertrophy (p = 0.016), chronic adenoiditis (p = 0.007), conductive hearing loss (p = 0.004), and impaired tympanometry (p < 0.001).Conclusions: These data suggest that children with a RAOM with OME are clinically different from children with simple RAOM, as they have a more complex clinical presentation that includes not only adenoidal disease and audiological impairment, but also an underlying allergy or atopy. The possibility that the factors mentioned above may be differently involved in the heterogeneous clinical manifestations occurring in otitis-prone children needs to be further investigated in ad hoc epidemiological studies