The clean-up of viscous crude-oil spills is a global challenge. Hydrophobic and oleophilic oil sorbents have been demonstrated as promising candidates for oil-spill remediation. However, the sorption speeds of these oil sorbents for viscous crude oil are rather limited. Herein we report a Joule-heated graphene-wrapped sponge (GWS) to clean-up viscous crude oil at a high sorption speed. The Joule heat of the GWS reduced in situ the viscosity of the crude oil, which prominently increased the oil-diffusion coefficient in the pores of the GWS and thus speeded up the oil-sorption rate. The oil-sorption time was reduced by 94.6% compared with that of non-heated GWS. Besides, the oil-recovery speed was increased because of the viscosity decrease of crude oil. This in situ Joule self-heated sorbent design will promote the practical application of hydrophobic and oleophilic oil sorbents in the clean-up of viscous crude-oil spills.

Bioinspired polymeric woods with excellent overall performance can be fabricated by a self-assembly and curing process of resins.

Superelastic carbon aerogels have been widely explored by graphitic carbons and soft carbons. These soft aerogels usually have delicate microstructures with good fatigue resistance but ultralow strength. Hard carbon aerogels show great advantages in mechanical strength and structural stability due to the sp3‐C‐induced turbostratic “house‐of‐cards” structure. However, it is still a challenge to fabricate superelastic hard carbon‐based aerogels. Through rational nanofibrous structural design, the traditional rigid phenolic resin can be converted into superelastic hard carbon aerogels. The hard carbon nanofibers and abundant welded junctions endow the hard carbon aerogels with robust and stable mechanical performance, including superelasticity, high strength, extremely fast recovery speed (860 mm s−1), low energy‐loss coefficient (<0.16), long cycle lifespan, and heat/cold‐endurance. These emerging hard carbon nanofiber aerogels hold a great promise in the application of piezoresistive stress sensors with high stability and wide detection range (50 kPa), as well as stretchable or bendable conductors.

There is an urgent need for developing electromechanical sensor with both ultralow detection limits and ultrahigh sensitivity to promote the progress of intelligent technology. Here we propose a strategy for fabricating a soft polysiloxane crosslinked MXene aerogel with multilevel nanochannels inside its cellular walls for ultrasensitive pressure detection. The easily shrinkable nanochannels and optimized material synergism endow the piezoresistive aerogel with an ultralow Young’s modulus (140 Pa), numerous variable conductive pathways, and mechanical robustness. This aerogel can detect extremely subtle pressure signals of 0.0063 Pa, deliver a high pressure sensitivity over 1900 kPa−1, and exhibit extraordinarily sensing robustness. These sensing properties make the MXene aerogel feasible for monitoring ultra-weak force signals arising from a human’s deep-lying internal jugular venous pulses in a non-invasive manner, detecting the dynamic impacts associated with the landing and take-off of a mosquito, and performing static pressure mapping of a hair.

In the present study, we investigated the influence of diquat-induced oxidative stress on intestinal barrier, mitochondrial function, and the level of mitophagy in piglets. Twelve male Duroc × Landrace × Yorkshire 35-d-old pigs (weaned at 21 d of age), with an average body of 9.6 kg, were allotted to two treatments of six piglets each including the challenged group and the control group. The challenged pigs were injected with 100 mg/kg bodyweight diquat and control pigs injected with 0.9% (w/v) NaCl solution. The results showed that diquat injection decreased ADFI and ADG. Diquat decreased (P < 0.05) the activities of superoxide dismutase and glutathione peroxidase and increased (P < 0.05) the malondialdehyde concentrations. The lower (P < 0.05) transepithelial electrical resistance and higher (P < 0.05) paracellular permeability of fluorescein isothiocyanatedextran 4 kDa were found in diquat challenged piglets. Meanwhile, diquat decreased (P < 0.05) the protein abundance of claudin-1, occluding, and zonula occludens-1 in jejunum compared with the control group. Diquat-induced mitochondrial dysfunction, as demonstrated by increased (P < 0.05) reactive oxygen species production and decreased (P < 0.05) membrane potential of intestinal mitochondria. Diquat-injected pigs revealed a decrease (P < 0.05) of mRNA abundance of genes related to mitochondrial biogenesis and functions, PPARg coactivator-1α, mammalian-silencing information regulator-1, nuclear respiratory factor-1, mt transcription factor A, mt single-strand DNA-binding protein, mt polymerase r, glucokinase, citrate synthase, ATP synthase, and cytochrome coxidase subunit I and V in the jejunum. Diquat induced an increase (P < 0.05) in expression of mitophagy-related proteins, phosphatase and tensin homologue deleted on chromosome 10-induced putative kinase, and Parkin in the intestinal mitochondria, as well as an enhancement of the ratio of light chain 3-II (LC3-II) to LC3-I content in the jejunal mucosa. These results suggest that oxidative stress disrupted the intestinal barrier, caused mitochondrial dysfunction, and triggered mitophagy.

PHOSPHATE STARVATION RESPONSE1 (PHR1) is a key regulatory component of the response to phosphate (Pi) starvation. However, the regulation of in this response remains poorly understood. Here, we report that is a target of the transcription factors AUXIN RESPONSE FACTOR7 (ARF7) and ARF19 and is positively regulated by auxin signaling in Arabidopsis () roots. expression was induced by exogenous auxin and suppressed by auxin transport inhibitors in Arabidopsis roots. In the promoter, three auxin-response elements, which are bound directly by ARF7 and ARF19, were shown to be essential for expression. The, , and mutants showed down-regulated expression of and downstream Pi starvation-induced genes in roots; they also exhibited defective Pi uptake in roots and overaccumulation of anthocyanin in shoots. The induction of lateral root formation in response to low Pi and to exogenous auxin was decreased in the mutant, whereas the expression of () and was not changed significantly. PHR1 acted independently of LBD16 and LBD29 in the regulation of lateral root formation in response to low Pi. Under low-Pi conditions, lateral root impairment in the mutant was partially rescued by constitutive expression of , demonstrating that reduced expression contributed to the phenotype. In addition to, other genes encoding MYB-CC members also were targets of ARF7 and ARF19. Our work thus reveals a mechanism coordinating auxin signaling and the PHR1 regulon in Arabidopsis responses to Pi deficiency.

Hydrogel materials with high water content and good biocompatibility are drawing more and more attention now, especially for biomedical use. However, it still remains a challenge to construct hydrogel fibers with enough strength and toughness for practical applications. Herein, we report a bio-inspired lotus-fibermimetic spiral structure hydrogel bacterial cellulose fiber with high strength, high toughness, high stretchability, and energy dissipation, named biomimetic hydrogel fiber (BHF). The spiral-like structure endows BHF with excellent stretchability through plastic deformation and local failure, assisted by the breaking−reforming nature of the hydrogen bonding network among cellulose nanofibers. With the high strength, high stretchability, high energy dissipation, high hydrophilicity, porous structure, and excellent biocompatibility, BHF is a promising hydrogel fiber for biomedicine. The outstanding stretchability and energy dissipation of BHF allow it to absorb energy from the tissue deformation around a wound and effectively protect the wound from rupture, which makes BHF an ideal surgical suture.

In the present study, we investigated the influence of weaning on antioxidant status, intestinal integrity, mitochondrial function, and the mitophagy level in piglets (weaned at 21 d) during the 1 wk after weaning. The redox status was measured by antioxidant enzymes activities, related genes expression, and malondialdehyde (MDA) content in jejunum. The intestinal barrier function was assessed by the Ussing chamber and expression of tight junction proteins in the jejunum. The function of intestine mitochondria was measured by mitochondrial DNA (mtDNA) content and activities of mitochondria oxidative phosphorylation complexes. The levels of light chain 3-1 (LC3-I), light chain 3-II (LC3-II), PTEN-induced putative kinase 1 (PINK1), and Parkin were determined to investigate whether mitophagy is involved in the weaning process. The results showed that, as compared with the preweaning phase (d 0), weaning suppressed (P < 0.05) the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) on d 3 and d 7 postweaning, decreased (P < 0.05) the expression of copper and zinc superoxide dismutase (Cu/Zn-SOD), manganese-containing superoxide dismutase (Mn-SOD) on d 3 postweaning, declined (P < 0.05) the level of glutathione peroxidase 1 (GPX-1) and glutathione peroxidase 4 (GPX-4) on d 3 and d 7 postweaning, and increased (P < 0.05) MDA content in jejunum on d 3 and d 7 postweaning. The jejunal transepithelial electrical resistance and levels of occludin, claudin-1, and zonula occludens-1 on d 3 and d 7 postweaning were reduced (P < 0.05), and paracellular flux of fluorescein isothiocyanatedextran (4 kDa) on d 3 and d 7 postweaning was increased (P < 0.05). Weaning induced mitochondrial dysfunction, as demonstrated by decreased (P < 0.05) content of mtDNA on d 3 and d 7 postweaning and declined (P < 0.05) activities of mitochondria complexes (I, II, III, IV) in jejunum on d 1, d 3, and d 7 postweaning. Weaning led to an increased (P < 0.05) expression level of mitophagy-related proteins, PINK1 and Parkin, in the intestinal mitochondria, as well as an enhancement (P < 0.05) of the ratio of LC3-II to LC3-I content in the jejunal mucosa on d 1, d 3, and d 7 postweaning. These results suggest that weaning disrupted intestinal oxidative balance, and this imbalance may impair intestinal barrier and mitochondrial function and trigger mitophagy in piglets.