Fabrication of phospholipid–xanthan microcapsules by combining microfluidics with self-assembly

We report the synthesis of an amphiphilic polysaccharide, a phospholipid (1,2-dioleoyl-sn-glycero-phosphoetilamine, DOPE) conjugated with the anionic xanthan gum, and its ability to spontaneously self-assemble under mild aqueous conditions. This work also aimed to apply a microfluidic platform that can precisely fabricate microsized and monodispersed capsules for cell encapsulation. Stable hollow capsular structures were obtained by the generation of homogeneous spherical droplets of the self-assembled polymer in the microfluidic device through the formation of a water-in-oil emulsion, followed by the stabilization of the polymer aggregates in a separate collection vessel containing phosphate-buffered saline (physiological ionic strength and pH). The properties (size, morphology, permeability) and performance (stability) of the obtained microcapsules were studied, as well their ability to support the viability, function and proliferation of encapsulated cells. ATDC5 cells were encapsulated within the capsules and shown to remain viable, evidencing increased cellular metabolic activity over 21 days of in vitro culture. By combining microfluidic droplet generation and self-assembly of xanthan–DOPE, we were able to fabricate microcapsules that provided an adequate environment for cells to survive and proliferate.     

Tooth sensitivity and efficacy of in-office bleaching in restored teeth

ObjectivesThe aim of this clinical trial was to evaluate efficacy (BE) and tooth sensitivity (TS) of in-office bleaching with a 35% hydrogen peroxide (HP) in patients with aesthetic restorations.MethodsHydrogen peroxide 35% was applied in two sessions, of three 15 min applications, in 15 patients with upper anterior sound teeth (S) and 15 with aesthetic restorations (R). The colour was recorded at baseline, one week and 6 months after treatment completion. Patients recorded TS on a 0–4 scale. The BE was evaluated by two-way ANOVA and Tukey's tests (α = 0.05). The percentage of patients with TS was evaluated by Fisher's exact test and TS intensity of treatments was compared with Mann–Whitney U-test (α = 0.05).ResultsAll participants experienced TS at least once during treatment. Higher TS intensity was observed in R (1.5 [1/1.75]) compared to S (0.5 [0/1.25]) during the bleaching (p < 0.05). S and R demonstrated similar tooth colour enhancement compared to baseline (p < 0.05) and both presented colour stability after 6 months of evaluation (p > 0.05).ConclusionsThe in-office bleaching with 35% HP was effective in patients with aesthetic restorations, however, a higher intensity of TS was observed during the bleaching protocol.Clinical relevanceIn-office dental bleaching can be performed in patients with adhesive restorations promoting satisfactory results; however, it can promote higher intensity of sensitivity compared to patients with sound teeth.     

Characterization of a Factor H Mutation That Perturbs the Alternative Pathway of Complement in a Family with Membranoproliferative GN

Complement C3 activation is a characteristic finding in membranoproliferative GN (MPGN). This activation can be caused by immune complex deposition or an acquired or inherited defect in complement regulation. Deficiency of complement factor H has long been associated with MPGN. More recently, heterozygous genetic variants have been reported in sporadic cases of MPGN, although their functional significance has not been assessed. We describe a family with MPGN and acquired partial lipodystrophy. Although C3 nephritic factor was shown in family members with acquired partial lipodystrophy, it did not segregate with the renal phenotype. Genetic analysis revealed a novel heterozygous mutation in complement factor H (R83S) in addition to known risk polymorphisms carried by individuals with MPGN. Patients with MPGN had normal levels of factor H, and structural analysis of the mutant revealed only subtle alterations. However, functional analysis revealed profoundly reduced C3b binding, cofactor activity, and decay accelerating activity leading to loss of regulation of the alternative pathway. In summary, this family showed a confluence of common and rare functionally significant genetic risk factors causing disease. Data from our analysis of these factors highlight the role of the alternative pathway of complement in MPGN.