Nowadays, most products for dental restoration are produced from acrylic resins based on heat-cured Poly(Methyl MethAcrylate) (PMMA). The addition of metal nanoparticles to organic materials is known to increase the surface hydrophobicity and to reduce adherence to biomolecules. This paper describes the use of nanostructured materials, TiO₂and Fe₂O₃, for simultaneously coloring and/or improving the antimicrobial properties of PMMA resins. Nanoparticles of metal oxides were included during suspension polymerization to produce hybrid metal oxides-alginate-containing PMMA. Metal oxide nanoparticles were characterized by dynamic light scattering, and X-ray diffraction. Physicochemical characterization of synthesized resins was assessed by a combination of spectroscopy, scanning electron microscopy, viscometry, porosity, and mechanical tests. Adherence ofCandida albicanscells and cellular compatibility assays were performed to explore biocompatibility and microbial adhesion of standard and novel materials. Our results show that introduction of biocompatible metal nanoparticles is a suitable means for the improvement of conventional acrylic dental resins.

The degradation of a mixture of phenol, 4-chlorophenol (4CP), 2,4-dichlorophenol (24DCP) and 2,4,6-trichlorophenol (246TCP) by acclimated activated sludge and by isolated bacteria was studied. Activated sludge was acclimated for 70 days to 40 mg phenols/l then the microorganisms responsible for the CP degradation were isolated and identified. Four types of Gram-negative bacteria (Aeromonas sp., Pseudomonas sp. Flavomonas oryzihabitans, and Chryseomonas luteola) were identified. Also, two acid-fast bacilli with distinct glycolipid patterns were isolated. From their chemical composition and their growth characteristics, both isolates appeared to be mycobacteria closely related to Mycobacterium peregrinum. The degradation kinetics of each phenol by Aeromonas sp., Pseudomonas sp. Flavomonas oryzihabitans, Chryseomonas luteola and activated sludge were determined. The acclimated activated sludge degradation rates were from one to two orders of magnitude higher than those of pure strains when uptake rates were calculated in terms of the viable biomass (CFU). The specific substrate uptake rate for acclimated activated sludge varied between 8.2 and 15.8 × 10⁻⁷ mg/CFU·d (407-784 mg/gVSS·d). Aeromonas sp. had the highest specific substrate uptake rate of the pure strains, based on a VSS basis (33-57 mg/gVSS·d) but, in terms of viable biomass (5.0-15.6 × 10⁻⁸ mg/CFU·d), the Pseudomonas sp. rate was the highest. Specific substrate uptake rates were 1.8 mg chlorinated phenols/g VSS·d for unacclimated activated sludge.

2,3-Di-O-acyl-trehalose (DAT) is a glycolipid located on the outer layer of theMycobacterium tuberculosiscell envelope. Due to its noncovalent linkage to the mycobacterial peptidoglycan, DAT could easily interact with host cells located in the focus of infection. The aim of the present work was to study the effects of DAT on the proliferation of murine spleen cells. DAT was purified from reference strains ofM. tuberculosis,orM. fortuitumas a surrogate source of the compound, by various chromatography and solvent extraction procedures and then chemically identified. Incubation of mouse spleen cells with DAT inhibited in a dose-dependent manner concanavalin A-stimulated proliferation of the cells. Experiments, including the propidium iodide exclusion test, showed that these effects were not due to death of the cells. Tracking of cell division by labeling with 5,6-carboxyfluorescein diacetate succinimidyl ester revealed that DAT reduces the rounds of cell division. Immunofluorescence with an anti-CD3 monoclonal antibody indicated that T lymphocytes were the population affected in our model. Our experiments also suggest that the extent of the suppressive activity is strongly dependent on the structural composition of the acyl moieties in DATs. Finally, the inhibitory effect was also observed on antigen-induced proliferation of mouse spleen cells specific forToxoplasma gondii. All of these data suggest that DAT could have a role in the T-cell hyporesponsiveness observed in chronic tuberculosis.