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.

This article presents a study that directly replicated the recently developed Balanced Time Perspective Scale (BTPS; J.D. Webster, 2011 ) and included middle-aged and older adults. Participants included 90 younger, 69 middle-aged, and 69 older adults who completed the BTPS and a measure of life satisfaction and happiness. A factor analysis replicated original findings with separate subscales for a past orientation and a future orientation obtaining simple structure (alphas = .94 and .95 respectively). A balanced time perspective predicted higher scores on both measures of well-being replicating the original J.D. Webster ( 2011 ) findings. A chi-square analysis indicated, as predicted, that the percentage of younger adults tended to be higher in the future-focused category, and the percentage of older adults tended to be higher in the past-focused category. Implications of a balanced time perspective on mental health over the life course are discussed.

Aldosterone, with pro-oxidation and pro-autophagy capabilities, plays a key role in liver fibrosis. However, the mechanisms underlying aldosterone-promoted liver sinusoidal endothelial cells (LSECs) defenestration remain unknown. Caveolin 1 (Cav1) displays close links with autophagy and fenestration. Hence, we aim to investigate the role of Cav1-related autophagy in LSECs defenestration. We found the increase of aldosterone/MR (mineralocorticoid receptor) level, oxidation, autophagy, and defenestration in LSECs in the human fibrotic liver, BDL or hyperaldosteronism models; while antagonizing aldosterone or inhibiting autophagy relieved LSECs defenestration in BDL-induced fibrosis or hyperaldosteronism models. In vitro, fenestrae of primary LSECs gradually shrank, along with the down-regulation of the NO-dependent pathway and the augment of the AMPK-dependent autophagy; these effects were aggravated by rapamycin (an autophagy activator) or aldosterone treatment. Additionally, aldosterone increased oxidation mediated by Cav1, reduced ATP generation, and subsequently induced the AMPK-dependent autophagy, leading to the down-regulation of the NO-dependent pathway and LSECs defenestration. These effects were reversed by MR antagonist spironolactone, antioxidants or autophagy inhibitors. Besides, aldosterone enhanced the co-immunoprecipitation of Cav1 with p62 and ubiquitin, and induced Cav1 co-immunofluorescence staining with LC3, ubiquitin, and F-actin in the perinuclear area of LSECs. Furthermore, aldosterone treatment increased the membrane protein level of Cav1, whereas decrease the cytoplasmic protein level of Cav1, indicating that aldosterone induced Cav1-related selective autophagy and F-actin remodeling to promote defenestration. Consequently, Cav1-related selective autophagy initiated by aldosterone-induced oxidation promotes LSECs defenestration via activating the AMPK-ULK1 pathway and inhibiting the NO-dependent pathway.

No abstract

No abstract

No abstract