6 research outputs found
Modeling the underlying mechanisms for organic memory devices: Tunneling, electron emission and oxygen adsorbing
We present a combined experimental and theoretical study to get insight into
both memory and negative differential resistance (NDR) effect in organic memory
devices. The theoretical model we propose is simply a one-dimensional metallic
island array embedding within two electrodes. We use scattering operator method
to evaluate the tunneling current among the electrode and islands to establish
the basic bistable I-V curves for several devices. The theoretical results
match the experiments very well, and both memory and NDR effect could be
understood comprehensively. The experimental correspondence, say, the
experiment of changing the pressure of oxygen, is addressed as well.Comment: 5 pages, 3 figure
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PD-L1-mediated gasdermin C expression switches apoptosis to pyroptosis in cancer cells and facilitates tumour necrosis.
Although pyroptosis is critical for macrophages against pathogen infection, its role and mechanism in cancer cells remains unclear. PD-L1 has been detected in the nucleus, with unknown function. Here we show that PD-L1 switches TNFα-induced apoptosis to pyroptosis in cancer cells, resulting in tumour necrosis. Under hypoxia, p-Stat3 physically interacts with PD-L1 and facilitates its nuclear translocation, enhancing the transcription of the gasdermin C (GSDMC) gene. GSDMC is specifically cleaved by caspase-8 with TNFα treatment, generating a GSDMC N-terminal domain that forms pores on the cell membrane and induces pyroptosis. Nuclear PD-L1, caspase-8 and GSDMC are required for macrophage-derived TNFα-induced tumour necrosis in vivo. Moreover, high expression of GSDMC correlates with poor survival. Antibiotic chemotherapy drugs induce pyroptosis in breast cancer. These findings identify a non-immune checkpoint function of PD-L1 and provide an unexpected concept that GSDMC/caspase-8 mediates a non-canonical pyroptosis pathway in cancer cells, causing tumour necrosis