Nanoparticle Flotation Collectors III: The Role of Nanoparticle Diameter

The ability of polystyrene nanoparticles to promote glass bead flotation was measured as a function of nanoparticle diameter. In all cases, smaller nanoparticles were more effective flotation collectors, even when compared at constant nanoparticle number concentration. The superior performance of smaller particles was explained by two mechanisms, acting in parallel. First, smaller particles deposit more quickly giving more effective flotation in those cases where nanoparticle deposition kinetics is rate determining; the sensitivity of nanoparticle deposition rates to particle size was illustrated by kinetic measurements on a quartz crystal microbalance silica surface. Second, for a given coverage of nanoparticles on the glass beads, the mean distance between neighboring nanoparticle surfaces decreases with particle diameter. We propose that the expansion of the three phase contact line, after initial bead/bubble attachment, is favored with decreasing the distance between neighboring hydrophobic particles

Nanoparticle Flotation CollectorsThe Influence of Particle Softness

The ability of polymeric nanoparticles to promote glass bead and pentlandite (Pn, nickel sulfide mineral) attachment to air bubbles in flotation was measured as a function of the nanoparticle glass transition temperature using six types of nanoparticles based on styrene/N-butylacrylate copolymers. Nanoparticle size, surface charge density, and hydrophobicity were approximately constant over the series. The ability of the nanoparticles to promote air bubble attachment and perform as flotation collectors was significantly greater for softer nanoparticles. We propose that softer nanoparticles were more firmly attached to the glass beads or mineral surface because the softer particles had a greater glass/polymer contact areas and thus stronger overall adhesion. The diameters of the contact areas between polymeric nanoparticles and glass surfaces were estimated with the Young–Laplace equation for soft, liquidlike particles, whereas JKR adhesion theory was applied to the harder polystyrene particles. The diameters of the contact areas were estimated to be more than an order of magnitude greater for the soft particles compared to harder polystyrene particles

A Colloidal Stability Assay Suitable for High-Throughput Screening

A library of 32 polystyrene copolymer latexes, with diameters ranging between 53 and 387 nm, was used to develop and demonstrate a high-throughput assay using a 96-well microplate platform to measure critical coagulation concentrations, a measure of colloidal stability. The most robust assay involved an automated centrifugation–decantation step to remove latex aggregates before absorbance measurements, eliminating aggregate interference with optical measurements made through the base of the multiwell plates. For smaller nanoparticles (diameter <150 nm), the centrifugation–decantation step was not required as the interference was less than with larger particles. Parallel measurements with a ChemiDoc MP plate scanner gave indications of aggregation; however, the results were less sensitive than the absorbance measurements

Recruitment/activation of DCs in the lymph node and periphery blood of mice treated with LBNSE-GM-CSF.

<p>BALB/c mice were infected with 10 IMLD₅₀ DRV and treated at 0 (A) or 4 (B) dpi with medium, 10⁷ FFU live or inactivated LBNSE-GM-CSF. At days 3, 6, and 9 post treatment, single cell suspensions were prepared from inguinal lymph node or peripheral blood and stained with antibodies against surface markers of DCs (CD11c+). The stained cells were analyzed by flow cytometry. All data are from n = 3 mice in each group and presented as mean values ± standard errors (SE). Asterisk indicates significant differences between the indicated experimental groups as calculated by one-way ANOVA: <i>*, p<0.05; **, p<0.01.</i></p

Protective efficacy of recombinant RABVs administrated after infection i.m. with DRV.

<p>ICR mice (group of 10) at age of 4–6 weeks were infected i.m. with 10 IMLD₅₀ DRV, and treated with 10⁷ FFU LBNSE-GM-CSF by intracerebral (A), intramuscular (B), intradermal (C) or intranasal (D) route at different time point post infection, or treated with live or UV-inactivated LBNSE-GM-CSF at day 4 post infection (E). Infected and treated mice were observed daily for 20 days and survivorship was recorded and analyzed. Asterisk indicates significant differences between the indicated experimental groups as calculated by Log-rank test: <i>*, p<0.05;</i> **, <i>p<0.01;</i> ***, <i>p<0.001.</i></p

Virus titers in the brain of mice infected im with DRV (10 IMLD₅₀) and treated with rRABVs at 4 dpi.

<p>*rRABV (GM-CSF), recombinant RABV expressing GM-CSF.</p>†<p>Virus titer in the brain (FFU/g tissue).</p><p>- No virus was detected.</p

Differentiation of inflammatory cells infiltrated into CNS by flow cytomeric analyses.

<p>BALB/c mice were infected i.m. with 10 IMLD₅₀ DRV and were treated at either 0 or 4 dpi with medium, 10⁷ FFU live or inactivated LBNSE-GM-CSF. Leukocytes from CNS were recovered by Percoll centrifugation and stained with cell surface markers CD11b (Microglia/macrophage), Ly6G (Neutrophils) and CD3 (T cells). The stained cells were analyzed by flow cytometry. Representative flow cytometric plots of infiltrated cells in mouse brain at day 6 post treatment for each of the treatment groups (A). The absolute numbers of indicated inflammatory cells in the brain were presented for mice treated at day 0 (B) or 4 (C) dpi, respectively. All data are from n = 3 mice per group. Asterisk indicates significant differences between the indicated experimental groups as calculated by one-way ANOVA: <i>*, p<0.05; **, p<0.01.</i></p

Induction of BBB permeability after treatment with LBNSE-GM-CSF.

<p>Mice were treated with medium or 10⁷ FFU LBNSE-GM-CSF at 0 (A) or 4 (B) dpi. BBB permeability was determined by uptake of sodium fluorescein at day 6 post treatment. Data are given as mean values + SEM. Asterisks indicate significant differences between the indicated experimental groups: <i>*, p<0.05; **, p<0.01.</i></p

Enhancement of BBB permeability induced by MCP-1 improves protection in mice treated with UV-inactivated rRABV.

<p>Mice were treated with medium or MCP-1 (25 µg) by ic, BBB permeability was determined by uptake of sodium fluorescein at day 2 post treatment (A). ICR mice (group of 10) at age of 4–6 weeks were infected i.m. with 10 IMLD₅₀ DRV, and then treated with medium, MCP-1 (25 µg), 10⁷ FFU LBNSE-GM-CSF, UV-inactivated LBNSE-GM-CSF (equivalent to 10⁷ FFU) or a mixture of MCP-1 (25 µg) and UV-inactivated LBNSE-GM-CSF (equivalent to 10⁷ FFU) by ic at day 4 post infection. The mice were observed for 20 days post infection, and survivorship was recorded and analyzed. Asterisk indicates significant differences between the indicated experimental groups as calculated by one-way ANOVA or Log-rank test: <i>*, p<0.05; **, p<0.01.</i></p

Concentration of chemokines and cytokines in the brain of mice treated with LBNSE-GM-CSF.

<p>BALB/c mice were infected with 10 IMLD₅₀ DRV and treated at either 0 (A) or 4 (B) dpi with medium, 10⁷ FFU live or UV-inactivated LBNSE-GM-CSF, brain samples were collected at days 3, 6, and 9 post treatment. Total RNA was extracted from the brain tissue and mRNA of chemokines and cytokines was analyzed by qRT-PCR. The mRNA copy number was normalized to the housekeeping gene GAPDH. Levels of gene expression in a test sample are presented as the fold change over that detected in sham-infected controls. Data represent the average from three independent experiments. Asterisk indicates significant differences between the indicated experimental groups as calculated by one-way ANOVA: <i>*, p<0.05;</i> **, <i>p<0.01.</i></p