Investigations on Caesium Dispersion and Molybdenum Coating on SPIDER Components

SPIDER is the 100 keV full-size Negative Ion Source prototype of the ITER Neutral Beam Injector, operating at Consorzio RFX in Padova, Italy. The largest Negative Ion Source in the world, SPIDER generates an RF driven plasma from which Deuterium or Hydrogen negative ions are produced and extracted. At the end of 2021, a scheduled long-term shutdown started to introduce major modifications and improvements aiming to solve issues and drawbacks identified during the first three years of SPIDER operations. The first action of the shutdown period was the disassembly and characterization of the SPIDER beam source after removal from the vacuum vessel and its placement inside the clean room. Each component was carefully assessed and catalogued, following a documented procedure. Some source components, i.e., the Plasma Grid, Extraction Grid and Bias Plate, revealed the presence of different and non-uniform red, white and green coatings that might be correlated to back-streaming positive ions impinging on grid surfaces, electrical discharges and caesium evaporation. Thus, several analyses have been carried out to understand the nature of such coatings, with the study still ongoing. The evidence of caesium evaporation and deposition on molybdenum-coated SPIDER components, such as the formation of oxides and hydroxides, is demonstrated through surface characterization analyses with the use of the Scanning Electron Microscope (SEM), X-ray Diffraction (XRD) and X-ray Photoelectron Spectroscopy (XPS).     

Automated quantification of uveitic keratic precipitates by use of anterior segment optical coherence tomography

Background

Evaluation of ocular inflammation via common imaging modalities like optical coherence tomography (OCT) has emphasised cell visualisation, but automated detection of uveitic keratic precipitates (KPs) remains unexplored.

Methods

Anterior segment (AS)-OCT dense volumes of the corneas of patients with uveitic KPs were collected at three timepoints: with active (T0), clinically improving (T1), and resolved (T2) inflammation. At each visit, visual acuity and clinical grading of the anterior chamber cells were assessed. A bespoke algorithm was used to create an en face rendering of the KPs and to calculate their volume and a ratio of the volume of precipitates over the analysed area. The variation of AS-OCT-derived measurements over time was assessed, and compared with clinical grading.

Results

Twenty eyes from 20 patients (13 females, mean age 39 years) were studied. At T0, the mean volume of the corneal KPs was 0.1727 mm³, and it significantly reduced to 0.1111 mm³ (p = 0.03) only at T2. The ratio between the volume of the KPs and the corneal area decreased from T0 (0.007) to T1 (0.006; p = 0.2) and T2 (0.004; p = 0.009). There was a statistically significant correlation between the AC cell count and the AS-OCT volume measurements of the KPs at the three time points.

Conclusions

AS-OCT can image uveitic KPs and through a bespoke algorithm we were able to create an en face rendering allowing us to extrapolate their volume. We found that objective quantification of KPs correlated with inflammatory cell counts in the anterior chamber.     

Celiac disease prevalence and predisposing-HLA in a cohort of 93 Williams-Beuren syndrome patients

Williams-Beuren syndrome is considered to be at increased risk for celiac disease, as for recent literature data and celiac disease guidelines, despite pathogenic mechanisms are still unclear. Our study analyzed the prevalence of autoimmune disorders, HLA DQ2 and/or DQ8 haplotypes, of transglutaminase antibodies and of diagnosis of celiac disease in a cohort of 93 Williams-Beuren syndrome's patients (mean age 21.26 years). Our study showed an increased prevalence of celiac disease equal to 10.8% (10/93 patients). We did not find a significant different frequency of predisposing HLA in subjects with Williams-Beuren syndrome compared to literature data in the general population (49.5% vs. 42.9%, with p > .1), nor a susceptibility to autoimmunity. This suggests that the increased prevalence of celiac disease in Williams-Beuren syndrome cannot be ascribed to HLA haplotype and may be related to other factors that still need to be identified in these patients.