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Polyvinyl alcohol (PVA) nanofibers containing Ag nanoparticles were prepared by electrospinning PVA/silver nitrate (AgNO3) aqueous solutions, followed by short heat treatment, and their antimicrobial activity was investigated for wound dressing applications. Since PVA is a water soluble and biocompatible polymer, it is one of the best materials for the preparation of wound dressing nanofibers. After heat treatment at 155 °C for 3 min, the PVA/AgNO3 nanofibers became insoluble, while the Ag+ ions therein were reduced so as to produce a large number of Ag nanoparticles situated preferentially on their surface. The residual Ag+ ions were reduced by subsequent UV irradiation for 3 h. The average diameter of the Ag nanoparticles after the heat treatment was 5.9 nm and this value increased slightly to 6.3 nm after UV irradiation. It was found that most of the Ag+ ions were reduced by the simple heat treatment. The PVA nanofibers containing Ag nanoparticles showed very strong antimicrobial activity. © 2006 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 44: 2468–2474, 2006

Anti-protective antigen antibody was reported to enhance macrophage killing of ingested Bacillus anthracis spores, but it was unclear whether the antibody-mediated macrophage killing mechanism was directed against the spore itself or the vegetative form emerging from the ingested and germinating spore. To address this question, we compared the killing of germination-proficient (gp) and germination-deficient (⌬gerH) Sterne 34F2 strain spores by murine peritoneal macrophages. While macrophages similarly ingested both spores, only gp Sterne was killed at 5 h (0.37 log kill). Pretreatment of macrophages with gamma interferon (IFN-␥) or opsonization with immunoglobulin G (IgG) isolated from a subject immunized with an anthrax vaccine enhanced the killing of Sterne to 0.49 and 0.73 log, respectively, but the combination of IFN-␥ and IgG was no better than either treatment alone. Under no condition was there killing of ⌬gerH spores. To examine the ability of the exosporium to protect spores from macrophages, we compared the macrophage-mediated killing of nonsonicated (exosporium ؉ ) and sonicated (exosporium ؊ ) Sterne 34F2 spores. More sonicated spores than nonsonicated spores were killed at 5 h (0.98 versus 0.37 log kill, respectively). Pretreatment with IFN-␥ increased the sonicated spore killing to 1.39 log. However, the opsonization with IgG was no better than no treatment or pretreatment with IFN-␥. We conclude that macrophages appear unable to kill the spore form of B. anthracis and that the exosporium may play a role in the protection of spores from macrophages.

The growth of the electronic industry and the widespread use of electronic equipment in communications, computations, automations, bio-medicine, space, and other purposes have led to many electromagnetic interference (EMI) problems as systems operate in close proximity. It is likely to become more severe in the future, unless proper EMI control methodology and techniques are used to meet the electromagnetic compatibility requirements. This article presents a comprehensive review of EMI shielding theory and materials. Furthermore, a method for fabricating a multifunctional metal composite fabric with electromagnetic (EM) shielding characteristics was successfully developed. The parameters influencing EM shielding properties of the metal composite fabrics were investigated. It was shown that the EM shielding effectiveness of the metal composite fabrics could be tailored by modifying the metal grid size and geometry.

The macrophage proinflammatory response to Francisella tularensis (Ft) live vaccine strain (LVS) was shown previously to be TLR2 dependent. The observation that intracellular Ft LVS colocalizes with TLR2 and MyD88 inside macrophages suggested that Ft LVS might signal from within the phagosome. Macrophages infected with LVSΔiglC, a Ft LVS mutant that fails to escape from the phagosome, displayed greatly increased expression of a subset of TLR2-dependent, proinflammatory genes (e.g., Tnf) but decreased expression of others (e.g., Ifnb1). This latter subset was similarly mitigated in IFN-β−/− macrophages indicating that while Ft LVS-induced TLR2 signaling is necessary, cytosolic sensing of Ft to induce IFN-β is required for full induction of the macrophage proinflammatory response. Although LVSΔiglC greatly increased IL-1β mRNA in wild-type macrophages, protein secretion was not observed. IL-1β secretion was also diminished in Ft LVS-infected IFN-β−/− macrophages. rIFN-β failed to restore IL-1β secretion in LVSΔiglC-infected macrophages, suggesting that signals in addition to IFN-β are required for assembly of the inflammasome and activation of caspase-1. IFN-β plays a central role in controlling the macrophage bacterial burden: bacterial recovery was greater in IFN-β−/− than in wild-type macrophages and treatment of Ft LVS-infected macrophages with rIFN-β or 5,6-dimethylxanthenone-4-acetic acid, a potent IFN-β inducer, greatly decreased the intracellular Ft LVS burden. In toto, these observations support the hypothesis that the host inflammatory response to Ft LVS is complex and requires engagement of multiple signaling pathways downstream of TLR2 including production of IFN-β via an unknown cytosolic sensor and activation of the inflammasome.

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