We conducted an extensive suite of true triaxial experiments in two porous sandstones, Bentheim (porosity ≈ 24%) and Coconino (17.5%). Our experiments demonstrate that failure of both sandstones is not only a function of σ3 but also of σ2. For a given σ3, σ1 at failure (σ1,peak) increases as σ2 is raised above σ3 between tests. The σ1,peak reaches a peak as σ2 is about halfway between σ3 and σ1 and then gradually decreases such that when σ2 ≈ σ1,peak, it approaches its initial magnitude when σ2 = σ3. For a constant σ3, failure‐plane angle increases with σ2 by a maximum of less than 10° as σ2 rises from σ2 = σ3 to σ2 = σ1,peak. The effect of σ2 on both failure level and failure‐plane angle is stronger in the lower‐porosity Coconino sandstone than in the Bentheim sandstone. The σ2 dependence of failure mode in the Bentheim is different than Coconino over the same σ3 range. Both sandstones failed dilatantly at low σ3 magnitudes. However, at high σ3 (100–120 MPa), Bentheim sandstone developed shear‐enhanced compaction bands, followed by pure compaction bands at σ3 = 150 MPa. Compaction bands were not observed in the Coconino. Microscopic observations via SEM reveal that tensile microcracking is dominant when shear banding occurs (under low σ3), while pervasive grain crushing and pore collapse inside compaction bands are observed at high σ3.

Aims: Angiotensin II (AngII), a vasoconstrictive peptide of the renin–angiotensin system (RAS), promotes hepatic fibrogenesis and induces microRNA-21(mir-21) expression. Angiotensin-(1–7) [Ang-(1–7)] is a peptide of the RAS, which attenuates liver fibrosis. Recently, it was reported that the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome participated in liver fibrosis. However, it remains unclear how mir-21 mediates AngII-induced NLRP3 inflammasome activation. We investigate the role of AngII-induced mir-21 in the regulation of NLRP3 inflammasome/IL-1β axis in liver fibrosis.Results: In vivo, circulating mir-21 was upregulated in patients with liver fibrosis and was positively correlated with liver fibrosis and oxidation. Treatment with Ang-(1–7) inhibited mir-21, NLRP3 inflammasome, and liver fibrosis after bile duct ligation (BDL) or AngII infusion. Inhibition of mir-21 suppressed the Smad7/Smad2/3/NOX4, Spry1/ERK/NF-κB pathway, NLRP3 inflammasome, and liver fibrosis induced by AngII infusion. In vitro, AngII upregulated mir-21 expression via targeting Smad7 and Spry1 in primary hepatic stellate cells (HSCs). In contrast, Ang-(1–7) suppressed mir-21 expression and oxidation induced by AngII. Overexpression of mir-21 promoted oxidation, and collagen production enhanced the effect of AngII on NLRP3 inflammasome activation via the Spry1/ERK/NF-κB, Smad7/Smad2/3/NOX4 pathways. However, downregulation of mir-21 exerted the opposite effects.Innovation and Conclusions: Mir-21 mediates AngII-activated NLRP3 inflammasome and resultant HSC activation via targeting Spry1 and Smad7. Ang-(1–7) protected against BDL or AngII infusion-induced hepatic fibrosis and inhibited mir-21 expression. Antioxid. Redox Signal. 27, 1–20.

The electrode–electrolyte interface stability is a critical factor influencing cycle performance of All-solid-state lithium batteries (ASSLBs). Here, we propose a LiF- and Li3N-enriched artificial solid state electrolyte interphase (SEI) protective layer on metallic lithium (Li). The SEI layer can stabilize metallic Li anode and improve the interface compatibility at the Li anode side in ASSLBs. We also developed a Li1.5Al0.5Ge1.5(PO4)3–poly­(ethylene oxide) (LAGP-PEO) concrete structured composite solid electrolyte. The symmetric Li/LAGP-PEO/Li cells with SEI-protected Li anodes have been stably cycled with small polarization at a current density of 0.05 mA cm–2 at 50 °C for nearly 400 h. ASSLB-based on SEI-protected Li anode, LAGP-PEO electrolyte, and LiFePO4 (LFP) cathode exhibits excellent cyclic stability with an initial discharge capacity of 147.2 mA h g–1 and a retention of 96% after 200 cycles.