3D-printed Magnetic Resonance (MR)-based gynecological phantom for image-guided brachytherapy training.

PURPOSE/OBJECTIVES: There is a clinical need to develop anatomic phantoms for simulation-based learning in gynecological brachytherapy. Here, we provide a step-by-step approach to build a life-sized gynecological training phantom based on magnetic resonance imaging (MRI) of an individual patient. Our hypothesis is that this phantom can generate convincing ultrasound (US) images that are similar to patient scans. METHODS: Organs-at-risk were manually segmented using patient scans (MRI). The gynecological phantom was constructed using positive molds from 3D printing and polyvinyl chloride (PVC) plastisol. Tissue texture/acoustic properties were simulated using different plastic softener/hardener ratios and microbead densities. Nine readers (residents) were asked to evaluate 10 cases (1 ultrasound image per case) and categorize each as a "patient" or "phantom" image. To evaluate whether the phantom and patient images were equivalent, we used a multireader, multicase equivalence study design with two composite null hypotheses with proportion (pr) at H01: pr ≤ 0.35 and H02: pr ≥ 0.65. Readers were also asked to review US videos and identify the insertion of an interstitial needle into the pelvic phantom. Computed Tomography (CT) and magnetic resonance (MR) images of the phantom were acquired for a feasibility study. RESULTS: Readers correctly classified "patient" and "phantom" scans at pr = 53.3% ± 6.2% (p values 0.013 for H01 and 0.054 for H02, df = 5.96). Readers reviewed US videos and identified the interstitial needle 100% of the time in transabdominal view, and 78% in transrectal view. The phantom was CT and MR safe. CONCLUSIONS: We have outlined a manufacturing process to create a life-sized, gynecological phantom that is compatible with multi-modality imaging and can be used to simulate clinical scenarios in image-guided brachytherapy procedures.

Staphylococcus aureus Epicutaneous Exposure Drives Skin Inflammation via IL-36-Mediated T Cell Responses.

Staphylococcus aureus colonization contributes to skin inflammation in diseases such as atopic dermatitis, but the signaling pathways involved are unclear. Herein, epicutaneous S. aureus exposure to mouse skin promoted MyD88-dependent skin inflammation initiated by IL-36, but not IL-1α/ß, IL-18, or IL-33. By contrast, an intradermal S. aureus challenge promoted MyD88-dependent host defense initiated by IL-1ß rather than IL-36, suggesting that different IL-1 cytokines trigger MyD88 signaling depending on the anatomical depth of S. aureus cutaneous exposure. The bacterial virulence factor PSMα, but not α-toxin or δ-toxin, contributed to the skin inflammation, which was driven by IL-17-producing γδ and CD4+ T cells via direct IL-36R signaling in the T cells. Finally, adoptive transfer of IL-36R-expressing T cells to IL-36R-deficient mice was sufficient for mediating S. aureus-induced skin inflammation. Together, this study defines a previously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation involving IL-36R/MyD88-dependent IL-17 T cell responses.