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As a trial for the complete establishment of mussel watch program, it was shown that the ciliary stroke of Mytilus edulis can be used as an indicator of its bioaccumulation of pollutants from sea water whenit was measured by use of a high function OES endoscope. This is reasonable because the ciliary strokes result in the intake of phytoplankton by raising the constant water current along the cilia from an inhalant siphon transported to the mouth. The ciliary strokes showed anevident diel fluctuation with the maximal activity during the night.The contribution of mucus excretion was evident for efficient filter-feeding. The ciliary stroke and the mucus excretion were activated almost simultaneously showing similar diel fluctuation while filter-feeding. The maximal ciliary stroke was observed at 20 deg. C in salt solution from 3.0 to 4.0% salinities. The stroke follows the Arrheniusequation in the temperature range from 5 to 30 deg. C with a break at around 20 deg. C when the experiment was performed with salt solution between 1.0 to 3.3% salinities. [ABSTRACT FROM AUTHOR]

Squamous cell carcinomas (SCC) are often preceded by potentially malignant precursor lesions, most of which remain benign. The terminal exhaustion phenotypes of effector T-cells and the accumulation of myeloid-derived suppressor cells (MDSC) have been thoroughly characterized in established SCC. However, it is unclear what precancerous lesions harbor a bona fide high risk for malignant transformation and how precancerous epithelial dysplasia drives the immune system to the point of no return. Here we show that expression of SRY-box transcription factor 2 (SOX2) in precancerous lesions imparts an irreversible risk that recruits suppressive myeloid cells by promoting the release of CCL2. We developed a unique genetically engineered mouse model (GEMM) to recapitulate the malignant transformation of epithelial dysplasia to SCC in the oral mucosa with high histologic and phenotypic fidelity. Using a combination of longitudinal human specimens and the Sox2-GEMM, we found that the myeloid cells in precancerous epithelial dysplasia exhibit a distinctive dichotomous profile featuring high levels of IL-1α-SLC2A1 and low levels of type-I interferon (IFN-I) signatures, which occurs before SCC emerges histologically. Brief priming of myeloid cells with IL-1α desensitizes them to IFN-I agonists and makes myeloid-derived suppressor cells (MDSC) even more suppressive of T-cell activation. Mechanistically, IL-1 activation represses the expression of DHHC3/7 enzymes, which are responsible for the palmitoylation of stimulator of interferon genes (STING). Early blockade of IL1 signaling using pharmacologic and genetic approaches similarly reduces MDSC and SLC2A1 high myeloid cells, suppresses epithelial dysplasia transformation, and extends survival. This work establishes a previously unrecognized SOX2-CCL2-IL1 pathway that leads to irreversible immune escape when precancerous epithelial lesions transform., Competing Interests: Conflict of Interest: Y.L.L. has filed U.S. Prov. Patent Appl. No.: 63/527,223. Y.L.L. and J.J.M. are co-founders of Saros Therapeutics and serve on its scientific advisory board. Other authors do not have conflicts of interest relevant to this manuscript. Declaration of Interest: J.J.M. and Y.L.L. is a co-founder of Saros Therapeutics and serves on its scientific advisory board. Y.L.L. has licensed the NOOC1 cell line to Kerafast Inc. Y.L.L. received U.S. patent US-11701433-B2. YLL has filed a U.S. Prov. Patent Appl. No.: 63/527,223.