MRI compatibility of silver based wound dressings.

As silver dressings gain more widespread use, it is more likely that patients with silver-based dressings will also undergo magnetic resonance imaging (MRI). In current practice, these dressings are removed prior to imaging due to concerns over heating and image distortion. As dressing changes can be painful, the need to remove dressings simply for MRI may increase pain and contribute to opioid dependency. To examine the need for dressing removal, American Society for Testing and Materials International standards for assessing device deflection and torque were performed on 5 silver containing and 3 non-silver control dressings. Magnetically induced heating and image distortion were examined in a porcine hind limb wound dressed with control and test dressings. The limb was scanned in a clinical high field 3T MRI scanner using a series of standard MRI sequences (Survey, T1-weighted SE, T1-weighted IR TSE, T2-weighted TSE, DUAL TSE, and FLAIR). Deflection and torsion were not detected in control or silver-based dressings. For all combinations of dressings and MRI scans, average heating was between 0-0.2°C. Additionally, dressings, in dry and hydrated forms, caused no image distortion in any MRI scan performed. Evaluation of MRI safety and compatibility revealed no concerns for safety or image distortion in any of the silver-containing wound dressings tested thus it would be acceptable to leave these dressings intact during MRI. The ability to leave dressings in place during imaging will provide a significant benefit to patient care by reducing pain associated with dressing removal.

Functional expression of system x(c)- is upregulated by asbestos but not crystalline silica in murine macrophages.

CONTEXT: Inhalation of asbestos or silica is associated with chronic and progressive diseases, including fibrosis, cancer, and increased risk of systemic autoimmunity. Because there is a need for treatment options for these diseases, a better understanding of their mechanistic etiologies is essential. While oxidative stress in macrophages is an early consequence of these exposures, it may also serve as a signaling mechanism involved in downstream immune dysregulation. The system x(c)(-) exchange protein is induced by oxidative stress, and exchanges equimolor levels of extracellular cystine for intracellular glutamate. Cystine is subsequently reduced to cysteine, the rate-limiting precursor for glutathione synthesis. OBJECTIVE: As the primary transporter responsible for cystine/glutamate exchange on macrophages, system x(c)- was hypothesized to be inducible in response to asbestos and silica, and to increase viability through protection from oxidative stress. RESULTS: When challenged with amphibole asbestos, but not crystalline silica, RAW 264.7 macrophages increased expression of xCT and the rate of cystine/glutamate exchange in sodium-free conditions. This upregulation was prevented with N-acetylcysteine, implicating oxidative stress. Cystine protected the macrophages from asbestos-induced oxidative stress and cell death, supporting the hypothesis that imported cystine was used for synthesis of cellular antioxidants. System x(c)(-) inhibitors, glutamate and S-4-carboxyphenylglycine ((S)-4-CPG), significantly increased oxidative stress and cell death of asbestos-treated macrophages. CONCLUSION: System x(c)(-) plays a critical role in survival of macrophages exposed to asbestos, but not silica. These data demonstrate a very early difference in the cellular response to these silicates that may have important downstream implications in the pathologic outcome of exposure.

Cytokine Production Modified by System X(c)- After PM10 and Asbestos Exposure.

It has been shown that inhaled particulate matter such as air pollution and asbestos are linked to a number of immune diseases such as asthma, and Systemic Lupus Erythematosus (SLE), respectively. This research may contribute to understanding the mechanisms of how asbestos and air pollution particulate (PM10) produce oxidative stress on macrophages, as well as how the macrophages will respond to the oxidative stressors. Using Flow Cytometry, DCFDA Fluorescence, Glutamate Transport, and Cytokine Bead Array assays, we have shown that exposure to asbestos and PM10 up-regulates system x(c)- in macrophages, which reduces oxidative stress for the macrophage by providing substrates for antioxidants. The results demonstrate that asbestos, but not PM10, induces both expression and activity of system x(c)-. This led to differential cytokine production with a significantly increased expression of TNF alpha and MCP-1 for PM10 treatment but not for asbestos treatment. Inhibition of system x(c)- affected cytokine production only following asbestos exposure, further demonstrating a role for this antioxidant system in regulating immune outcomes for asbestos but not PM10. Understanding the mechanisms in which oxidative stress helps regulate macrophage responses may contribute to a better understanding of why certain diseases are brought on by asbestos and air pollution exposure.