Shuang Qiu

TL;DR: Shikonin, a naturally occurring naphthoquinone, induced a cell death in MCF-7 and HEK293 distinct from apoptosis and characterized with (a) a morphology of necrotic cell death, (b) loss of plasma membrane integrity, loss of mitochondrial membrane potentials, activation of autophagy, but not a contributing factor; (e) elevation of reactive oxygen species with no critical roles contributing to cell death; and (f) the cell death was prevented by a small molecule, necrostatin-1, that specifically

TL;DR: It is found that in a mouse model in which peripheral nerve injury leads to the development of neuropathic pain, the insular cortex showed changes in synaptic plasticity, which were associated with a long-term increase in the amount of synaptic N-methyl-d-aspartate receptors, but not that of extrasynaptic NMDARs.

TL;DR: It is shown that honokiol can induce a cell death distinct from apoptosis in HL60, MCF-7, and HEK293 cell lines, and this is the first report to document an induction of mitochondrial permeability transition pore-associated cell death by Honokiol.

TL;DR: It is reported that pyramidal cells in the deep layers of the ACC send direct descending projecting terminals to the dorsal horn of the spinal cord after peripheral nerve injury, and postsynaptic excitatory responses of these descending projecting neurons were significantly enhanced.

TL;DR: The results suggest that the expression of AMPARs is enhanced in the insular cortex after nerve injury by a pathway involving AC1, AKAP79/150, and PKA, and such enhancement may at least in part contribute to behavioral sensitization together with other cortical regions, such as the anterior cingulate and the prefrontal cortices.