The Sabatier principle for Battery Anodes: Chemical Kinetics and Reversible Electrodeposition at Heterointerfaces

How surface chemistry influences reactions occurring thereupon has been a long-standing question of broad scientific and technological interest for centuries. Recently, it has re-emerged as a critical question in a subdiscipline of chemistry - electrochemistry at heterointerphases, where the answers have implications for both how, and in what forms, humanity stores the rising quantities of renewable electric power generated from solar and wind installations world-wide. Here we consider the relation between the surface chemistry at such interphases and the reversibility of electrochemical transformations at a rechargeable battery electrode. Conventional wisdom holds that stronger chemical interaction between the metal deposits and electrode promotes reversibility. We report instead that a moderate strength of chemical interaction between the deposit and the substrate, neither too weak nor too strong, enables highest reversibility and stability of the plating/stripping redox processes at a battery anode. Analogous to the empirical Sabatier principle for chemical heterogeneous catalysis, our finding arises from the confluence of competing processes - one driven by electrochemistry and the other by chemical alloying. Based on experimental evaluation of metal plating/stripping systems in battery anodes of contemporary interest, we show that such knowledge provides a powerful tool for designing key materials in highly reversible electrochemical energy storage technologies based on earth-abundant, low-cost metals.Comment: 64 pages. Initially submitted on March 16th, 2021; revised version submitted on November 14th, 2021 to the same Journa

Synthesis and Photocatalytic Activity of Single-Crystalline Hollow rh-In₂O₃ Nanocrystals

We report here for the first time the hollow, metastable, single-crystal, rhombohedral In₂O₃ (rh-In₂O₃) nanocrystals synthesized by annealing solvothermally prepared InOOH solid nanocrystals under ambient pressure at 400 °C, through a mechanism of the Kirkendall effect, in which pore formation is attributed to the difference in diffusion rates of anions (OH^– and O^2–) in a diffusion couple. The InOOH solid nanocrystals were prepared via a controlled hydrolysis solvothermal route by using In­(NO₃)₃·4.5H₂O as a starting material and glycerol–ethanol as a mixed solvent. The glycerol–ethanol mixed solvent plays a key role on the formation of the intermediate InOOH, thus the final product of rh-In₂O₃. The as-synthesized In₂O₃ nanocrystals present excellent photocatalytic degradation of rhodamine B (RhB) and methylene blue (MB) dyes, which present ∼92% degradation of RhB or MB after 4 or 3 h reaction in the presence of the as-synthesized In₂O₃ nanocrystals, respectively

HMGB1-activatied NLRP3 inflammasome induces thrombocytopenia in heatstroke rat

Background Thrombocytopenia, an early common complication in heatstroke (HS), has been widely considered as a mortality predictor of HS. The mechanism underlying thrombocytopenia in HS remains unknown. It is not known whether NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is activated in HS platelet, which, in turn, induces platelet activation and thrombocytopenia. This study tried to clarify the activation of the NOD-like receptor signaling pathway under HS conditions and investigate its roles in mediating HS-induced thrombocytopenia. Methods Rat HS models were established in a certain ambient temperature and humidity. Platelets, isolated from blood, were counted and CD62P, an index of platelet activation, was measured by flow cytometry in all rats. The colocalization of NLRP3 inflammasome in platelet was detected by confocal fluorescence microscopy. Mitochondrial-derived reactive oxygen species (ROS) was detected using the molecular probes. Plasma HMGB1 and IL-1β levels were measured by ELISA. Results Platelet activation, showed by upregulated CD62P, and thrombocytopenia were observed in HS rats. HS activated the NLRP3 inflammasome, which was induced by elevated levels of ROS, while the upregulated CD62P and thrombocytopenia triggered by NLRP3 inflammasome were attributed to the high mobility group box protein 1 (HMGB1) inplasma. Moreover, inhibition of the NOD-like receptor signaling pathway in rats with HS suppressed platelet activation and the decline of platelet count. Similar results were obtained when the receptor toll-like receptor 4 (TLR4)/advanced glycation end product (RAGE) was blocked. Conclusions The NOD-like receptor signaling pathway induces platelet activation and thrombocytopenia in HS rats. These findings suggested that the NLRP3 inflammasome might be the potential target for HS treatment

Synthesis and Applications of γ‑Tungsten Oxide Hierarchical Nanostructures

γ-WO₃ hierarchical nanostructures were synthesized by using a biomolecule-assisted hydrothermal approach between Na₂WO₄·2H₂O and glycine acid (HOOC–CH₂–NH₂) in HCl solution. The phase, structure, and morphology of the as-synthesized products were characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM), high resolution TEM (HRTEM), Fourier transform infrared (FT-IR) spectroscopy, ultraviolet–visible (UV–vis) spectroscopy, and photoluminescence (PL) spectroscopy. The as-synthesized γ-WO₃ nanostructures exhibit super-hydrophobicity, photocatalytic activity, and enhanced anode performance for lithium ion batteries with three times the capacity of commercial graphite per unit volume, which may open up a wide range of potential applications in environmental protection and energy storage

The negative feedback loop of NF-κB/miR-376b/NFKBIZ in septic acute kidney injury

Sepsis is the leading cause of acute kidney injury (AKI). However, the pathogenesis of septic AKI remains largely unclear. Here, we demonstrate a significant decrease of microRNA-376b (miR-376b) in renal tubular cells in mice with septic AKI. Urinary miR-376b in these mice was also dramatically decreased. Patients with sepsis with AKI also had significantly lower urinary miR-376b than patients with sepsis without AKI, supporting its diagnostic value for septic AKI. LPS treatment of renal tubular cells led to the activation of NF-κB, and inhibition of NF-κB prevented a decrease of miR-376b. ChIP assay further verified NF-κB binding to the miR-376b gene promoter upon LPS treatment. Functionally, miR-376b mimics exaggerated tubular cell death, kidney injury, and intrarenal production of inflammatory cytokines, while inhibiting miR-376b afforded protective effects in septic mice. Interestingly, miR-376b suppressed the expression of NF-κB inhibitor ζ (NFKBIZ) in both in vitro and in vivo models of septic AKI. Luciferase microRNA target reporter assay further verified NFKBIZ as a direct target of miR-376b. Collectively, these results illustrate the NF-κB/miR-376b/NFKBIZ negative feedback loop that regulates intrarenal inflammation and tubular damage in septic AKI. Moreover, urinary miR-376b is a potential biomarker for the diagnosis of AKI in patients with sepsis