PubMed · 10509211
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A Joynes. 1999. Technique is not enough.. https://pubmed.ncbi.nlm.nih.gov/10509211/
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BACKGROUND: Burn injuries trigger complex immune responses and gene expression changes, impacting wound healing and systemic inflammation. Understanding these changes is crucial for identifying biomarkers and therapeutic targets. METHODS: We analyzed two gene expression omnibus datasets (wound tissue [GSE8056] and blood [GSE37069]) to identify differentially expressed genes (DEGs) in burn injury samples versus controls. Immune cell proportions were assessed using CIBERSORT. Functional enrichment analyses (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) and protein-protein interaction networks were constructed to identify key genes and pathways. RESULTS: We identified 1170 upregulated and 1227 downregulated DEGs. Gene Ontology analysis revealed enrichment in neutrophil activation, inflammatory response, and extracellular matrix organization. Kyoto Encyclopedia of Genes and Genomes analysis highlighted cytokine-cytokine receptor interaction, TNF, and IL-17 signaling pathways. Immune infiltration analysis showed significant changes in neutrophils, macrophages (M1/M2), and T-cell subsets. Protein-protein interaction network analysis identified five hub genes: JUN, STAT1, Bcl2, MMP9, and TLR2. CONCLUSIONS: This study provides a comprehensive bioinformatic analysis of gene expression and immune responses in burn injuries. The identified DEGs, hub genes, and pathways offer insights into the immune response mechanisms and suggest potential targets for diagnostic and therapeutic interventions in burn injury management.
Numerous reported burn injuries have been sustained during clinical MRI procedures. The aim of this study was to investigate the possible factors that may be responsible for such burns. Experiments were performed to investigate three possible mechanisms for causing heating in copper wire during MRI: direct electromagnetic induction in a conductive loop, induction in a resonant conducting loop, and electric field resonant coupling with a wire (the antenna effect). Maximum recorded temperature rises were 0.6 degrees C for the loop, 61.1 degrees C for the resonant loop, and 63.5 degrees C for the resonant antenna. These experimental findings suggest that, contrary to common belief, it is unlikely that direct induction in a conductive loop will result in thermal injury. Burn incidents are more likely to occur due to the formation of resonant conducting loops and from extended wires forming resonant antenna. The characteristics of resonance should be considered when formulating safety guidelines.
BACKGROUND AND OBJECTIVE: To analyze the effects of laser pulse duration and cryogen spray cooling (CSC) on epidermal damage and depth of collagen coagulation in skin resurfacing with repetitive Er:YAG laser irradiation. STUDY DESIGN/MATERIALS AND METHODS: Evolution of temperature field in skin is calculated using a simple one-dimensional model of sub-ablative pulsed laser exposure and CSC. The model is solved numerically for laser pulse durations of 150 and 600 microsec, and 6 msec cryogen spurts delivered just prior to ("pre-cooling"), or during and after ("post-cooling") the 600 microsec laser pulse. RESULTS: The model indicates a minimal influence of pulse duration on the extent of thermal effect in dermis, but less epidermal damage with 600 microsec pulses as compared to 150 microsec at the same pulse fluence. Application of pre- or post-cooling reduces the peak surface temperature after laser exposure and accelerates its relaxation toward the base temperature to a different degree. However, the temperature profile in skin after 50 msec is in either example very similar to that after a lower-energy laser pulse without CSC. CONCLUSIONS: When applied in combination with repetitive Er:YAG laser exposure, CSC strongly affects the amount of heat available for dermal coagulation. As a result, CSC may not provide spatially selective epidermal protection in Er:YAG laser skin resurfacing.