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In order to overcome the shortage of ^3\mathrm He detectors for subcritical experiments in the IPEN/MB-01 reactor, some experiments were performed employing less sensitive detectors, such as BF3, and a logic input module, which sums the counts from different detectors. Through microscopic and macroscopic neutron noise technique, it was possible to obtain, respectively, Rossi- $\alpha $ distribution and Auto Power Spectral Densities (APSD) for each detector configuration and various subcritical levels, and the prompt neutron decay constant ( $\alpha $ ) was extracted through a least squares procedure. In addition, Cross Power Spectral Densities (CPSD) were acquired for different types of detectors and the correlation among those detectors was confirmed. It was also observed that there was no loss of correlation among the neutron pulses, and therefore, the CPSD curves demonstrated the presence of correlated events. The $\alpha $ parameter was used as an indicator for the comparison of the results and for the quality of the experimental data. The obtained values demonstrate that the sum of counts technique does not present loss of information (correlated neutrons) even for different models and types of detectors, suggesting that the technique may be employed in neutron noise measurements for subcritical reactivity. [ABSTRACT FROM PUBLISHER]

To allow celiac patients to have meals out, a growing number of restaurants and pizzas houses that simultaneously provide gluten-free (GF) pizzas and wheat-based (WB) pizzas have recently been opened in Italy. In these restaurants, GF pizzas are prepared with GF raw materials, following procedures that minimize the risk of gluten cross-contact. Here, we evaluate the risk of gluten cross-contact of GF pizzas in relation to the preparation procedures, thus aiming at identifying a safe procedure for cooking GF pizzas. Our results show that, when specific requirements are complied with, the simultaneous cooking of GF and WB pizzas is a procedure as safe as having an oven dedicated to GF pizzas or the alternate cooking of GF and WB pizzas in the same oven.

The downstream cascade of the inflammatory response to gliadin in celiac intestinal mucosa encompasses the early activation of the innate immunity that triggers the adaptive response. Therefore, the in vitro study of the pathogenic mechanism of celiac disease (CD) on enterocytes alone or mucosal T lymphocytes alone does not fully consider all the aspects of gliadin-dependent inflammation. Although the in vitro culture of specimens of intestinal mucosa obtained from celiac patients is the gold standard for the study of CD, this technique presents several technical challenges and the bioptic specimens are not easily available. So, in this paper, we described the gliadin-dependent cytokine production in a bidimensional cellular system, which is able to mimic both the innate and the adaptive steps of the mucosal immune response of CD. In the upper compartment, the intestinal epithelial cells are grown on a filter, and in the lower compartment, the mononuclear cells isolated from peripheral blood of celiac patients are cultured. Cells were apically exposed to the toxic gliadin peptide p31-43 for 3 h and then with the immunodominant gliadin fragment pα-9 for 21 h. The incubation with gliadin peptides resulted in increased levels of IL-15, INF-γ, IL-6, tumor necrosis factor (TNF)-α, IL-1β, and CCL 2, 3 and 4 in the basal supernatants, with respect to cells exposed to medium alone. The p31-43-driven epithelial priming of mucosal response consists of transglutaminase (TG2)-mediated deamidation of the immunostimulatory gliadin peptides, as demonstrated by the inhibition of pα-9 activity, when the system is exposed to blocking anti-TG2 antibody.

The aim of this study was to determine the incidence of HBV markers in patients with alcoholic liver disease and to compare the results with those of patients with non-alcoholic liver disease and control subjects. We tried to determine whether the association between alcohol intake and HBV infection increases the risk of developing severe liver disease. The results showed an increased incidence of HBsAg in alcoholic patients when compared with controls as well as an increased incidence of severe chronic liver disease in HBV-positive groups when compared with HBV-negative groups. We conclude that HBV infection is an important additional risk factor for the development of severe liver disease in alcoholic patients.