Statement Of Problem: Studies on the assessment of the marginal fit of interim crowns with optical coherence tomography (OCT) are lacking.
Purpose: The purpose of this in vitro study was to apply OCT to evaluate and to compare the impact of conventional and computer-aided design and computer-aided manufacturing (CAD-CAM) fabrication methods and different materials, including bis-acryl, conventional polymethyl-methacrylate (PMMA), and CAD-CAM PMMA, on the marginal fit of interim crowns.
Material And Methods: Thirty crown specimens were fabricated, with 20 PMMA crowns divided into 2 groups based on the fabrication method: the conventional method (Group Jet, n=10) and the CAD-CAM method (Group CAD-CAM PMMA, n=10).
Macrophages express pattern recognition and cytokine receptors that mediate proinflammatory signal transduction pathways to combat microbial infection. To retaliate against such responses, pathogenic microorganisms have evolved multiple strategies to impede innate immune signaling. Recent studies demonstrated that YopJ suppression of TAK1 signaling during Yersinia pseudotuberculosis infection promotes the assembly of a RIPK1-dependent death-inducing complex that enables caspase-8 to directly cleave and activate gasdermin D (GSDMD).
View Article and Find Full Text PDFBACKGROUND Primary cutaneous lymphomas (PCL) are a multifaceted spectrum of cutaneous T cell lymphoma (CTCL) and cutaneous B cell lymphomas (CBCL). Mycosis fungoides (MF) is a rare subset of CTCL that primarily affects adults, and its occurrence in children is exceedingly rare. Most pediatric MF manifests as hypopigmented patches resembling other benign dermatoses, causing diagnostic challenges.
View Article and Find Full Text PDFTLR4 and TNFR1 signalling promotes potent proinflammatory signal transduction events, thus, are often hijacked by pathogenic microorganisms. We recently reported that myeloid cells retaliate Yersinia blockade of TAK1/IKK signalling by triggering RIPK1-dependent caspase-8 activation that promotes downstream GSDMD and GSDME-mediated pyroptosis in macrophages and neutrophils respectively. However, the upstream signalling events for RIPK1 activation in these cells are not well defined.
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