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Thus, the transition from crystal deposition to acute inflammation can be conceptualized as a two-hit process: First hit: MSU crystal deposition on cartilage surfaces activates synovial fibroblasts to release CCL2/MCP-1, recruiting monocytes and establishing subclinical inflammation

An increase in tonus of 0.5 mN was used as threshold for vasoconstriction because this difference is larger than the variation observed in the basal tonus of aorta rings