Intrinsically Stretchable Floating Gate Memory Transistors for Data Storage of Electronic Skin Devices.

To propel electronic skin (e-skin) to the next level by integrating artificial intelligence features with advanced sensory capabilities, it is imperative to develop stretchable memory device technology. A stretchable memory device for e-skin must offer, in particular, long-term data storage while ensuring the security of personal information under any type of deformation. However, despite the significance of these needs, technology related to stretchable memory devices remains in its infancy. Here, we report an intrinsically stretchable floating gate (FG) polymer memory transistor. The device features a dual-stimuli (optical and electrical) writing system to prevent easy erasure of recorded data. An FG comprising an intermixture of Ag nanoparticles and elastomer and with proper energy-band alignment between the semiconductor and dielectric facilitated sustainable memory performance, while achieving a high memory on/off ratio (>105) and a long retention time (106 s) with the ability to withstand 50% uniaxial or 30% biaxial strain. In addition, our memory transistor exhibited high mechanical durability over multiple stretching cycles (1000 times), along with excellent environmental stability with respect to factors such as temperature, moisture, air, and delamination. Finally, we fabricated a 7 × 7 active-matrix memory transistor array for personalized storage of e-skin data and successfully demonstrated its functionality.

Autonomous self-healing supramolecular polymer transistors for skin electronics.

Skin-like field-effect transistors are key elements of bio-integrated devices for future user-interactive electronic-skin applications. Despite recent rapid developments in skin-like stretchable transistors, imparting self-healing ability while maintaining necessary electrical performance to these transistors remains a challenge. Herein, we describe a stretchable polymer transistor capable of autonomous self-healing. The active material consists of a blend of an electrically insulating supramolecular polymer with either semiconducting polymers or vapor-deposited metal nanoclusters. A key feature is to employ the same supramolecular self-healing polymer matrix for all active layers, i.e., conductor/semiconductor/dielectric layers, in the skin-like transistor. This provides adhesion and intimate contact between layers, which facilitates effective charge injection and transport under strain after self-healing. Finally, we fabricate skin-like self-healing circuits, including NAND and NOR gates and inverters, both of which are critical components of arithmetic logic units. This work greatly advances practical self-healing skin electronics.

Attenuated mitochondrial NADP+-dependent isocitrate dehydrogenase activity enhances EGCG-induced apoptosis.

(-)-Epigallocatechin-3-gallate (EGCG), a well-known chemopreventive factor, induces cancer cells undergoing apoptosis. Over the last several years, we have shown that the mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) functions as an antioxidant and anti-apoptotic protein by supplying NADPH to antioxidant systems. Here, we show that EGCG induced the inactivation of IDPm as a purified enzyme and in cultured cancer cells in a dose- and time-dependent manner. Loss of enzyme activity was associated with the depletion of the thiol groups in protein. In addition, transfection of HeLa cells with an IDPm small interfering RNA (siRNA) markedly attenuated the activity of IDPm and substantially enhanced EGCG-induced apoptosis as indicated by the morphological evidence of apoptosis, DNA fragmentation, and the modulation of mitochondrial function and apoptotic marker proteins. Taken together, our results suggest that the suppression of IDPm activity resulted in the disruption of cellular redox balance and subsequently exacerbates EGCG-induced apoptotic cell death in HeLa cells. These results might have implications for developing an effective combination modality in cancer treatment.

Suppression of mitochondrial NADP(+)-dependent isocitrate dehydrogenase activity enhances curcumin-induced apoptosis in HCT116 cells.

Curcumin is a polyphenol derived from the plant Curcuma longa that induces apoptotic cell death in malignant cancer cell lines. It has been shown previously that mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) plays an essential role in defense against oxidative stress by supplying NADPH for antioxidant systems. This study demonstrates that curcumin decreased the activity of IDPm, both as a purified enzyme and in cultured cells. It also shows that curcumin-induced apoptosis in the colon cancer cell line HCT116 is significantly enhanced by suppression of IDPm activity. Transfection of HCT116 cells with an IDPm small interfering RNA (siRNA) markedly decreased activity of IDPm, enhancing cellular susceptibility to curcumin-induced apoptosis, as reflected by DNA fragmentation, cellular redox status, mitochondria dysfunction and modulation of apoptotic marker proteins. Together, these results suggest that application of curcumin together with IDPm siRNA may be an effective combination modality in the treatment of cancer.