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tuberculosis infection inside human monocytes ( M

4.2 Acute inflammatory amplification phase: neutrophil recruitment, NETosis, and programmed cell death The recruitment and activation of IL-1 , TNF - , complement fragment C5a, and chemical factors produced by macrophages and synoviocytes lead to a rapid influx of neutrophils into the articular cavity, marking the peak of the local inflammatory response, shows more significant performance under high crystal load conditions

As previously mentioned, the brain is enriched in two major PUFAs

The Ca 2+ imbalance and the malfunctioning of mitochondria form a vicious cyclemake the brain organization of ATP production insufficient, the release of mPTP leads to fine cytosolic edema, and results in intracellular Ca 2+ overload of the nerve cells, which eventually causes nerve cell death