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For improving charge density and sensitivity at the large strain , a high-performance elastic-material-based triboelectric nanogenerators with the large-strain was developed based on a novel gradient nano-doping strategy, which via gradient electrical field caused by the inhomogeneous concentration field of PTFE nanoparticles in sponge materials, that enabled for self-powered pressure sensing in smart boxing equipment and athletic big data analytics. [Display omitted] Elastic-material-based triboelectric nanogenerators (EMB-TENGs) are most effective to harvest random (low frequency, low amplitude) and distributed mechanical energy. However, the low output of EMB-TENGs caused by drastic charge attenuation and low sensitivity limits its applications. Here, we propose a gradient nano-doping strategy to boost the charge density and sensitivity of triboelectric sponge materials via the gradient electrical field caused by the inhomogeneous concentration field of polytetrafluoroethylene nanoparticles. The triboelectric charge density (537 μC·m−3) and the peak power density (732.6 mW·m−3) is increased by 1.2 times and 1.8 times. A sensitivity of 1.851 kPa−1 is successfully realized at 50% compressive strain. From this, a self-powered smart boxing bag with functions of both the force analysis and real-time counting statistic was developed at the large strain. This work presents a new method for design and development of triboelectric materials, as well as expanding the functionalities and applications of self-powered system combining with the EMB-TENGs. [ABSTRACT FROM AUTHOR]

Owing to the simplicity, scalability, and cost-efficiency, solution-processable two-dimensional (2D) semiconductors have attracted great interest in electronic applications, especially as the channel material for field-effect transistors (FETs). Inkjet printing is a lithography-free technique to achieve drop-on-demand patterning of solution-processable 2D ink. However, thus far, inkjet-printed 2D FETs exhibit limited performance due to the coffee-ring effect and consequent discontinuity of the printed 2D material films. Here, we report high-performance and flexible inkjet-printed MoS2 FETs with high mobilities and high on/off ratios and their gas sensing applications. By preparing high-quality MoS2 ink comprised of MoS2 nanoplates using electrochemical exfoliation and then applying a binary solvent comprised of 2-butanol and isopropanol, the obtained ink was printed to form a continuous and relatively uniform MoS2 film, and high-performance printed MoS2 FETs were demonstrated, with mobilities of 11 cm2 V–1 s–1 and on/off ratios of 106. Furthermore, low-voltage gate modulation was achieved by applying an ion gel gate, and robust electrical performance under tensile strain was observed for the ion gel-gated MoS2 FETs printed on flexible substrates. As the printed MoS2 film is abundant in edge sites and sulfur vacancies, we further demonstrated our MoS2 FETs as high-performance gas sensors with a limit of detection of 10 ppb for NO2 and 0.5 ppm for NH3, together with a fast recovery rate. [ABSTRACT FROM AUTHOR]

The nephron cortical collecting duct (CCD) is composed of principal cells, which mediate Na, K, and water transport, and intercalated cells (ICs), which are specialized for acid-base transport. There are two canonical IC forms: acid-secreting α-ICs and HC[O.sub.3]-secreting β-ICs. Chronic acidosis increases α-ICs at the expense of β-ICs, thereby increasing net acid secretion by the CCD. We found by growth factor quantitative PCR array that acidosis increases expression of mRNA encoding SDF1 (or CXCL12) in kidney cortex and isolated CCDs from mouse and rabbit kidney cortex. Exogenous SDF1 or pH 6.8 media increased [H.sup.+] secretion and decreased HC[O.sub.3] secretion in isolated perfused rabbit CCDs. Acid-dependent changes in [H.sup.+] and HC[O.sub.3] secretion were largely blunted by AMD3100, which selectively blocks the SDF1 receptor CXCR4. In mice, diet-induced chronic acidosis increased α-ICs and decreased β-ICs. Additionally, IC-specific Cxcr4 deletion prevented IC subtype alterations and magnified metabolic acidosis. SDF1 was transcriptionally regulated and a target of the hypoxia-sensing transcription factor HIF1α. IC-specific deletion of Hif1α produced no effect on mice fed an acid diet, as α-ICs increased and β- ICs decreased similarly to that observed in WT littermates. However, Hif1α deletion in all CCD cells prevented acidosis-induced IC subtype distribution, resulting in more severe acidosis. Cultured principal cells exhibited an HIF1α-dependent increase of Sdf1 transcription in response to media acidification. Thus, our results indicate that principal cells respond to acid by producing SDF1, which then acts on adjacent ICs., Introduction The kidney responds to an acid load by increasing the rate of net [H.sup.+] secretion in the proximal and collecting tubules as well as by increasing the capacity to [...]