24 research outputs found

    The internal structure of poly(methyl methacrylate) latexes in nonpolar solvents

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    Hypothesis: Poly(methyl methacrylate) (PMMA) latexes in nonpolar solvents are an excellent model system to understand phenomena in low dielectric media, and understanding their internal structure is critical to characterizing their performance in both fundamental studies of colloidal interactions and in potential industrial applications. Both the PMMA cores and the poly(12-hydroxystearic acid) (PHSA) shells of the latexes are known to be penetrable by solvent and small molecules, but the relevance of this for the properties of these particles is unknown. Experiments: These particles can be prepared in a broad range of sizes, and two PMMA latexes dispersed in n-dodecane (76 and 685 nm in diameter) were studied using techniques appropriate to their size. Small-angle scattering (using both neutrons and X-rays) was used to study the small latexes, and analytical centrifugation was used to study the large latexes. These studies enabled the calculation of the core densities and the amount of solvent in the stabilizer shells for both latexes. Both have consequences on interpreting measurements using these latexes. Findings: The PHSA shells are highly solvated (∼85% solvent by volume), as expected for effective steric stabilizers. However, the PHSA chains do contribute to the intensity of neutron scattering measurements on concentrated dispersions and cannot be ignored. The PMMA cores have a slightly lower density than PMMA homopolymer, which shows that only a small free volume is required to allow small molecules to penetrate into the cores. Interestingly, the observations are essentially the same, regardless of the size of the particle; these are general features of these polymer latexes. Despite the latexes being used as a model physical system, the internal chemical structure is complex and must be fully considered when characterizing them

    Erik H. Monkkonen, Murder in New York City

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    Contribution of Interleukin-12 (IL-12) and the CD28/B7 and CD40/CD40 Ligand Pathways to the Development of a Pathological T-Cell Response in IL-10-Deficient Mice

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    The ability of interleukin-10 (IL-10) to suppress accessory cell functions required for optimal T-cell activation makes it an important inhibitor of cell-mediated immunity. Thus, after infection with the protozoan parasite Toxoplasma gondii, IL-10 knockout (KO) mice develop a CD4(+)-T-cell-dependent shock-like reaction with high levels of IL-12 and gamma interferon (IFN-γ) in serum, leading to death of mice during the acute phase of infection. Previous studies from this laboratory have shown that simultaneous blockade of CD28 and CD40 can prevent this lethal reaction by inhibiting the production of IFN-γ. However, the blockade of costimulation did not affect systemic levels of IL-12. To better understand the relationship between IL-12 and the CD28 and CD40 pathways in mediating immune hyperactivity, antagonists of these factors were used to determine their effects on the development of a pathological T-cell response in IL-10 KO mice. Blockade of IL-12 or the CD28/B7 interaction alone did not affect survival; however, the combined blockade of both pathways resulted in decreased production of IFN-γ and the survival of IL-10 KO mice. To assess the role of the two ligands for CD28, B7.1 and B7.2, IL-10 KO mice were treated with αIL-12 plus αB7.1 or αB7.2 or the combination of all three antibodies. These studies revealed that blockade of both B7 molecules is required for decreased production of IFN-γ and survival of infected IL-10 KO mice, suggesting that B7.1 and B7.2 can contribute to the lethal shock-like reaction in IL-10 KO mice. In contrast, neutralization of IL-12 and blockade of the CD40/CD40 ligand (CD40L) interaction in vivo did not alter the production of IFN-γ and only resulted in a small delay in time to death of mice. Together, these data suggest that the CD28/B7 interaction has a central role in the development of a pathological T-cell response in IL-10 KO mice, which is distinct from the role of the CD40/CD40L and IL-12 pathways
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