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Void formation has been previously linked with native biofilm dispersion, the last stage of biofilm development in which sessile, surface-attached organisms liberate themselves from the biofilm to return to the planktonic state 14,17

Therefore, erastin treatment alone is insufficient to induce threshold levels of lipid peroxides, implying that DENV depends on ALOX12-dependent lipid peroxidation for efficient replication

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In CARE diabetic status compared to nondiabetic status per se was not associated with high concentrations of apoC-III-containing TG-rich lipoprotein particles, if their plasma TG levels were similar [123]

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