We report advances on a novel membrane-based iron-chloride redox flow rechargeable battery that is based on inexpensive, earthabundant, and eco-friendly materials. The development and large-scale commercialization of such an iron-chloride flow battery technology has been hindered hitherto by low charging efficiency resulting from parasitic hydrogen evolution at the negative electrode and high overpotential losses. We have demonstrated a high charging efficiency of 97% by maintaining the negative electrolyte at a pH value of 2 and by using indium chloride as an electrolyte additive. The high charging efficiency of the negative electrode was found to be stable over at least 50 cycles. Further, we have demonstrated that with a graphite felt electrode, the overpotential losses were substantially mitigated at the positive and negative electrodes allowing the electrodes to be operated at current densities as high as 100 mA/cm 2 . With these technical advancements, the iron-chloride redox flow battery has an increased prospect of being a sustainable and efficient solution for large-scale energy storage. Large-scale energy storage systems that are inexpensive, robust, and highly efficient are essential for the integration of renewable energy sources like solar and wind into the electrical power grid. Rechargeable batteries are particularly promising for such grid-scale applications because of their efficiency, modularity, and flexibility to siting.1-4 Several battery systems including lithium-ion, lead-acid, sodium-sulfur, and the all-vanadium redox flow battery have been deployed at the mega-watthour scale.4-8 However, the levelized cost of energy delivered (LCOE) for these state-of-art battery systems is about ten to fifty times higher than the target values identified by the U.S. Department of Energy (DoE). [9][10][11] In addition, the aforementioned battery systems pose challenges from the standpoint of sustainability and environmental friendliness because of the relatively expensive and toxic materials used. Therefore, the development of high-performance and long-life batteries that use inexpensive, eco-friendly, and abundantlyavailable materials is an important topic of current research.Redox flow batteries for large-scale energy storage.-Redox flow batteries are particularly well-suited for large-scale energy storage applications. 3,4,[12][13][14][15][16] Unlike conventional battery systems, in a redox flow battery, the positive and negative electroactive species are stored in tanks external to the cell stack. Therefore, the energy storage capability and power output of a flow battery can be varied independently to suit the desired application. For example, if an application requires a battery with high energy content, the amount of electroactive species in the tanks can be increased without significant modification to the cell stack. As the electroactive material is held in the external tanks, an increase in the amount of electroactive species does not require an increase in the volume of the cell stack. Thus, m...

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Guanine nucleotide-binding α-subunit 12 (Gα) is upregulated in activated hepatic stellate cells (HSCs) as a consequence of the dysregulation of a specific microRNA that is abundant in HSCs, facilitating the progression of liver fibrosis. This event is mediated by c-Jun N-terminal kinase-dependent ATG12-5 formation and the promotion of autophagy. We suggest that Gα and its associated regulators could serve as new targets in HSCs for the treatment of liver fibrosis.

The Sestrin2 (Sesn2) is an evolutionary conserved enzyme that scavenges reactive oxygen species and regulates autophagy through the AMPK-mTOR pathway. The present study was aimed at determining whether Toll-like receptor (TLR) signaling regulates Sesn2 expression and identifying the underlying molecular mechanism. Lipopolysaccharide (LPS), a representative TLR4 ligand, significantly increased the levels of Sesn2 protein in macrophages. LPS also increased Sesn2 mRNA levels and luciferase reporter activity; however, the mRNA levels of Sesn1 were not affected by LPS. Moreover, treatment of macrophages with other TLR ligands (eg, polyI:C or peptidoglycan) also induced Sesn2 expression. We found that LPS-mediated Sesn2 induction was transcriptionally regulated by AP-1 and Nrf2, and that overexpression of c-Jun or Nrf2 increased Sesn2 protein levels and Sesn2 promoter-driven luciferase reporter activity. Moreover, deletion of the antioxidant response element (ARE) in the Sesn2 promoter or Nrf2 knockout abolished LPS-mediated induction of Sesn2. LPS induced Sesn2 gene expression through p38 and PI3K activation. Surprisingly, treatment with the proteasome inhibitor MG132, but not the lysosomal inhibitor chloroquine, caused Sesn2 to accumulate in the cells. In the presence of MG132, we observed that Sesn2 was ubiquitinated. However, LPS treatment attenuated Sesn2 ubiquitination induced by MG132, which resulted in Sesn2 accumulation. Mice treated with D-galactosamine (Gal)/LPS exhibited enhanced Sesn2 expression in the liver. Moreover, infection with a recombinant adenovirus encoding Sens2 markedly reduced the number of Gal/LPS-induced TUNEL-positive cells. Our results suggest that TLR-mediated Sesn2 induction is dependent on AP-1, Nrf2, and the inhibition of ubiquitin-mediated degradation of Sesn2 and might protect cells against endotoxin toxicity.