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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

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[12] At even higher pH, the other carboxylic acid group loses its proton and the acid exists almost entirely as the glutamate anion OOCCH(NH + 3 )(CH 2 ) 2 COO , with a single negative charge overall

Thinner fluids can be transmitted through narrow-diameter, high-gauge needles