The ability to monitor the inflammatory state of the middle ear mucosa would provide clinical utility. To enable spectral measurements on the mucosa whilst rejecting background signal from the eardrum an anti-confocal system is investigated. In contrast to the central pinhole in a confocal system the anti-confocal system uses a central stop to reject light from the in-focus plane, the eardrum, with all other light detected. Monte Carlo simulations of this system show an increase in detected signal and improved signal-to-background ratio compared to a conventional confocal set-up used to image the middle ear mucosa. System parameters are varied in the simulation and their influence on the level of background rejection are presented.
To improve the diagnostic prediction of recurrence of otitis media with effusion after surgery, an anti-confocal system combined with spectroscopic measurements is proposed to reject unwanted signals from the eardrum and assess the blood content. The anti-confocal system was experimentally evaluated on both optical middle ear phantom and human skin. Results showed effective rejection of signals from the eardrum using a central stop replacing the confocal pinhole, while still detecting signals from the middle ear mucosa. The system is sensitive to changes in blood content, but scattering and absorption characteristics of the eardrum can distort the measurement. Confocal detection of eardrum properties was shown to be a promising approach to correct measurements.
Monocyte chemoattractant protein 1 (MCP‐1) is thought to be the most important chemokine for the recruitment of macrophages (MΦs) to the tumor microenvironment. We examined the role of MCP‐1 on tumor associated MΦs, inflammation, and intestinal tumorigenesis in a genetic mouse model of colon cancer. Male ApcMin/+, ApcMin/+/MCP‐1−/− or wild type mice (n=10/group) were sacrificed at 18 wks of age and intestines were analyzed for polyp burden, apoptosis, β‐catenin expression, MΦ number & phenotype, and inflammation. MCP‐1−/− decreased overall polyp number by 25% and large polyp number by 45% (P<0.05). This was consistent with an increase in apoptotic cells (P<0.05). Similarly, the number of β‐catenin positive polyps was reduced in ApcMin/+/MCP‐1−/− mice (P<0.05). MCP‐1 deficient mice showed decreased F4/80 positive cells in the polyp tissue (P=0.06) and surrounding intestinal tissue (P<0.05), and there was a decrease in CD206 mRNA expression (P<0.05). Further, MCP‐1−/− offset the increased mRNA expression of IL‐1β & IL‐6 in intestinal tissue and IL‐1β & TNF‐α in polyp tissue (P<0.05) and prevented the decrease in SOCS1 expression (P<0.05). Circulating IL‐6 levels were also decreased in MCP‐1−/− mice (P<0.05). We demonstrate that MCP‐1 is an important mediator of tumor growth and cancer‐induced inflammation and may serve as an important biomarker and/or therapeutic target in colon cancer.
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