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As an alternative to Li‐ion batteries, aqueous Zn batteries have gained attention due to the abundance of Zn metal, low reduction potential (–0.76 V vs. standard hydrogen electrode), and high theoretical capacity (820 mAh g–1) of multivalent Zn2+ ion. However, the growth of Zn dendrites and the formation of irreversible surface reaction byproducts pose challenges for ensuring a long battery lifespan and commercialization. Herein, the Cu foil coated with a single‐walled carbon nanotube (SWCNT) layer using a facile doctor blade casting method is utilized. The SWCNT‐coated Cu foil demonstrates a significantly longer battery lifespan compared to the bare Cu in the half‐cell tests. Through operando optical microscopy imaging, we are able to provide intuitive evidence that Zn deposition occurs between the carbon nanotube (CNT) coating and Cu substrate, in agreement with the computational results. Also, with various imaging techniques, the flat morphology and homogeneous distribution of Zn beneath the SWCNT layer are demonstrated. In addition, the full‐cell using CNT‐coated Cu exhibits a long cycle life compared to the control group, thereby demonstrating improved electrochemical performance with limited Zn for the cycling process. [ABSTRACT FROM AUTHOR]

The rechargeable aqueous zinc metal battery is considered one of the most promising next-generation batteries for energy storage systems, owing to its low negative standard reduction potential (−0.76 vs. the standard hydrogen electrode (SHE)), low cost of zinc and water, and no fire-risk. However, the formation of zinc dendrites and hydrogen evolution hinder the commercialization of rechargeable aqueous zinc metal batteries. In this study, we investigate the use of 6-aminohexanoic acid (6-AA), a type of amino acid, as an electrolyte in a 1 M ZnSO4 solution. The 6-AA molecules become zwitterions, reducing side reactions by adsorbing onto the zinc metal surface and blocking water molecules and other ions, except for zinc ions. Additionally, the adsorbed 6-AA molecules hinder the two-dimensional diffusion of zinc ions on the zinc metal surface and thereby reduce the formation of zinc dendrites. The 6-AA additive enables reduced corrosion, and uniform zinc deposition is observed. Moreover, both the Zn‖Zn symmetric cell and Zn‖Cu cell with the 6-AA added electrolyte exhibit a long cycle life, and the α-MnO2‖Zn full cell shows improved cycle performance by using the 6-AA additive. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2008.04.009 Byline: Yongjun Yin (a), Andrew C. White (a), Sung-Ho Huh (a), Matthew J. Hilton (b), Hidemi Kanazawa (a), Fanxin Long (a)(b), David M. Ornitz (a) Keywords: Fibroblast growth factor 9 (FGF9); Fibroblast growth factor receptor (FGFR); Wnt2a; Wnt7b; [beta]-Catenin; Lung development; Mesenchyme Abstract: Lung mesenchyme is a critical determinant of the shape and size of the lung, the extent and patterning of epithelial branching, and the formation of the pulmonary vasculature and interstitial mesenchymal components of the adult lung. Fibroblast growth factor 9 (FGF9) is a critical regulator of lung mesenchymal growth; however, upstream mechanisms that modulate the FGF mesenchymal signal and the downstream targets of mesenchymal FGF signaling are poorly understood. Here we have identified a robust regulatory network in which mesenchymal FGF signaling regulates [beta]-Catenin mediated WNT signaling in lung mesenchyme. By conditionally inactivating [beta]-Catenin in lung mesenchyme, we show that mesenchymal WNT-[beta]-Catenin signaling is essential for lung development and acts to regulate the cell cycle G1 to S transition and the FGF responsiveness of mesenchyme. Together, both FGF and WNT signaling pathways function to sustain mesenchymal growth and coordinate epithelial morphogenesis during the pseudoglandular stage of lung development. Author Affiliation: (a) Department of Developmental Biology, Washington University School of Medicine, Campus Box 8103, 660 S. Euclid Avenue, St. Louis, MO 63110, USA (b) Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA Article History: Received 10 March 2008; Revised 3 April 2008; Accepted 7 April 2008

NO, produced from L-arginine in a reaction catalyzed by NO synthase, is an endogenous free radical with multiple functions in mammalian cells. Here, we demonstrate that endogenously produced NO can suppress c-Jun N-terminal kinase (JNK) activation in intact cells. Treatment of BV-2 murine microglial cells with IFN-[Gamma] induced endogenous NO production, concomitantly suppressing JNK1 activation. Similarly, IFN-[Gamma] induced suppression of JNK1 activation in RAW264.7 murine macrophage cells and rat alveolar macrophages. The IFN-[Gamma]-induced suppression of JNK1 activation in BV-2, RAW264.7, or rat alveolar macrophage cells was completely prevented by [N.sup.G]-nitro-L-arginine, a NO synthase inhibitor. Interestingly, the IFN-[Gamma]-induced suppression of JNK1 activation was not affected by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, an inhibitor of guanylyl cyclase. 8-Bromo-cGMP, a membrane-permeant analogue of cGMP, did not change JNK1 activation in intact cells either. In contrast, S-nitro-N-acetyI-DL-penicillamine (SNAP), a NO donor, inhibited JNK1 activity in vitro. Furthermore, a thiol reducing agent, DTT, reversed not only the in vitro inhibition of JNK1 activity by SNAP but also the in vivo suppression of JNK1 activity by IFN-[Gamma]. Substitution of serine for cysteine-116 in JNK1 abolished the inhibitory effect of IFN-[Gamma] or SNAP on JNK1 activity in vivo or in vitro, respectively. Moreover, IFN-[Gamma] enhanced endogenous S-nitrosylation of JNK1 in RAW264.7 cells. Collectively, our data suggest that endogenous NO mediates the IFN-[Gamma]-induced suppression of JNK1 activation in macrophage cells by means of a thiolredox mechanism.