Triboelectric nanogenerators (TENGs) converting mechanical energy into electrical energy have received much attention because of their huge potential applications for supplying power to electronic devices. Improving the performance of TENGs has become a research hot point because of their output limited current. In this paper, we propose a flexible single-electrode triboelectric nanogenerator based on porous NaCO/polydimethylsiloxane (PDMS) structure to enhance the triboelectric performance for nanogenerators. To compare their output performance, NaCl and sugar are normally used as sacrificial template for triboelectric nanogenerator. As an experimental result, the nanogenerator based on porous NaCO/PDMS structure obtains the open-circuit voltage of 125 V and maximum output current of 100 μA, which are higher than that generated by NaCl/PDMS and sugar/PDMS TENGs. And the generated electric energy of NaCO/PDMS TENG could instantaneously power 42 commercial light-emitting diodes without any energy storage devices. This developed porous NaCO/PDMS TENG could open a new application field for self-powered personal electronics because of its flexibility, simple manufacturing process, and the ability to harvest mechanical energy from human motions.

Summary Vibrio parahaemolyticus is a Gram-negative marine bacterium that causes acute gastroenteritis in humans. The virulence of V. parahaemolyticus is dependent upon a type III secretion system (T3SS2). One effector for T3SS2, VopC, is a homolog of the catalytic domain of cytotoxic necrotizing factor (CNF), and was recently reported to be a Rho family GTPase activator and to be linked to internalization of V. parahaemolyticus by nonphagocytic cultured cells. Here, we provide direct evidence that VopC deamidates Rac1 and CDC42, but not RhoA, in vivo. Our results also suggest that VopC, through its activation of Rac1, contributes to formation of actin stress fibers in infected cells. Invasion of host cells, which occurs at a low frequency, does not seem linked to Rac1 activation, but instead appears to require CDC42. Finally, using an infant rabbit model of V. parahaemolyticus infection, we show that the virulence of V. parahaemolyticus is not dependent upon VopC-mediated invasion. Genetic inactivation of VopC did not impair intestinal colonization nor reduce signs of disease, including fluid accumulation, diarrhea, and tissue destruction. Thus, although VopC can promote host cell invasion, such internalization is not a critical step of the disease process, consistent with the traditional view of V. parahaemolyticus as an extracellular pathogen.

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