Jeannette M. Dypbukt

TL;DR: It is shown that glutamate can induce either early necrosis or delayed apoptosis in cultures of cerebellar granule cells, suggesting that mitochondrial function is a critical factor that determines the mode of neuronal death in excitotoxicity.

TL;DR: In this paper, the redox cycling quinone, 2,3-dimethoxy-1,4-naphthoquinone (DMNQ), was shown to stimulate growth, triggered apoptosis, or caused necrosis of pancreatic RINm5F cells, depending on the dose and duration of the exposure.

TL;DR: Low levels of oxidative stress can lead to activation of enzymes involved in cell signaling, in particular, the activity of protein kinase C is markedly increased by oxidation‐reduction–cycling quinones through a thiol/disulfide exchange mechanism, which may represent a mechanism by which prooxidants can modulate cell growth and differentiation.

TL;DR: In this paper, the role of mitochondria and calcineurin in the development of either type of cell death was examined, and cyclosporin A was added immediately after glutamate removal, which prevented delayed apoptosis of neurons that had survived the necrotic phase.

TL;DR: It is shown that IL-1 beta induces apoptosis in a pancreatic beta-cell line, RINm5F cells, and that the production of nitric oxide preceded the appearance of typical features of apoptosis.