Antifungal peptide-loaded alginate microfiber wound dressing evaluated against Candida albicans in vitro and ex vivo.

Invasive fungal infections have high mortality rates, and many current antimycotics are limited by host toxicity and drug resistance. Recent experiments in our laboratory have demonstrated the antifungal activity of dKn2-7, a synthetic peptide, against Candida albicans. The purpose of the current study was to develop a wound dressing capable of dKn2-7 release for extended periods to help combat fungal infection in wounds.

Optimized peptide extraction method for analysis of antimicrobial peptide Kn2-7/dKn2-7 stability in human serum by LC-MS.

Aim: To develop an extraction protocol and determine stability for antimicrobial peptide (AMP) Kn2-7 and its d-enantiomer dKn2-7 in human serum.

Materials & Methods: We compared use of ethanol, acetonitrile, RapiGest SF Surfactant and 1% formic acid in ethanol for AMP recovery from serum prior to liquid chromatography-mass spectrometry quantification.

Results: Precipitation of samples with 1% formic acid in ethanol caused the least amount of AMP loss during extraction from serum.

Targeted laser therapy synergistically enhances efficacy of antibiotics against multi-drug resistant Staphylococcus aureus and Pseudomonas aeruginosa biofilms.

The growing prevalence of biofilm-associated multi-drug resistant (MDR) bacteria necessitates the innovation of non-traditional approaches to improve the effectiveness of mainstay antibiotics. Here, we evaluated the use of gold nanoparticle (GNP)-targeted pulsed laser therapy to enhance antibiotic efficacy against in vitro methicillin-resistant Staphylococcus aureus (MRSA) and MDR Pseudomonas aeruginosa biofilms. Treatment with antibody-conjugated GNPs followed by nanosecond-pulsed laser irradiation at 532 nm (~1.

Enzymatic degradation of in vitro Staphylococcus aureus biofilms supplemented with human plasma.

Enzymatic debridement is a therapeutic strategy used clinically to remove necrotic tissue from wounds. Some of the enzymes utilized for debridement have been tested against bacterial pathogens, but the effectiveness of these agents in dispersing clinically relevant biofilms has not been fully characterized. Here, we developed an in vitro Staphylococcus aureus biofilm model that mimics wound-like conditions and employed this model to investigate the antibiofilm activity of four enzymatic compounds.

Photothermal killing of Staphylococcus aureus using antibody-targeted gold nanoparticles.

Purpose: The continued emergence of multidrug resistant bacterial infections and the decline in discovery of new antibiotics are major challenges for health care throughout the world. This situation has heightened the need for novel antimicrobial therapies as alternatives to traditional antibiotics. The combination of metallic nanoparticles and laser exposure has been proposed as a strategy to induce physical damage to bacteria, regardless of antibiotic sensitivity.

DNA aptamers as a novel approach to neutralize Staphylococcus aureus α-toxin.

Staphylococcus aureus is a versatile pathogen capable of causing a broad spectrum of diseases ranging from superficial skin infections to life threatening conditions such as endocarditis, septicemia, pneumonia and toxic shock syndrome. In vitro and in vivo studies identified an exotoxin, α-toxin, as a major cause of S. aureus toxicity.

Protein changes in macrophages induced by plasma from rats exposed to 35 GHz millimeter waves.

A macrophage assay and proteomic screening were used to investigate the biological activity of soluble factors in the plasma of millimeter wave-exposed rats. NR8383 rat macrophages were incubated for 24 h with 10% plasma from male Sprague-Dawley rats that had been exposed to sham conditions, or exposed to 42 °C environmental heat or 35 GHz millimeter waves at 75 mW/cm² until core temperature reached 41.0 °C.

Gene expression changes in the skin of rats induced by prolonged 35 GHz millimeter-wave exposure.

To better understand the cellular and molecular responses to overexposure to millimeter waves, alterations in the gene expression profile and histology of skin after exposure to 35 GHz radiofrequency radiation were investigated. Rats were subjected to sham exposure, to 42 degrees C environmental heat, or to 35 GHz millimeter waves at 75 mW/cm(2). Skin samples were collected at 6 and 24 h after exposure for Affymetrix GeneChip analysis.

Comparison of blood pressure and thermal responses in rats exposed to millimeter wave energy or environmental heat.

Electromagnetic fields at millimeter wave lengths are being developed for commercial and military use at power levels that can cause temperature increases in the skin. Previous work suggests that sustained exposure to millimeter waves causes greater heating of skin, leading to faster induction of circulatory failure than exposure to environmental heat (EH). We tested this hypothesis in three separate experiments by comparing temperature changes in skin, subcutis, and colon, and the time to reach circulatory collapse (mean arterial blood pressure, 20 mmHg) in male Sprague-Dawley rats exposed to the following conditions that produced similar rates of body core heating within each experiment: (1) EH at 42 degrees C, 35 GHz at 75 mW/cm, or 94 GHz at 75 mW/cm under ketamine and xylazine anesthesia; (2) EH at 43 degrees C, 35 GHz at 90 mW/cm, or 94 GHz at 90 mW/cm under ketamine and xylazine anesthesia; and (3) EH at 42 degrees C, 35 GHz at 90 mW/cm, or 94 GHz at 75 mW/cm under isoflurane anesthesia.

TNF receptor 1, IL-1 receptor, and iNOS genetic knockout mice are not protected from anthrax infection.

Anthrax produces at least two toxins that cause an intense systemic inflammatory response, edema, shock, and eventually death. The relative contributions of various elements of the immune response to mortality and course of disease progression are poorly understood. We hypothesized that knockout mice missing components of the immune system will have an altered response to infection.