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The biomass‐based chemicals from renewable resources are countermeasures to ease the problem of fossil fuel shortage. This work is to develop a biobased functional reactive modifier for thermosetting epoxy resins appropriate for excellent overall performance. The novel maleimide‐cardanol modifiers (CA‐HPM) is synthesized from natural extract cardanol (CA) and N‐(4‐hydroxyphenyl) maleimide (HPM), which is then mixed with phenolic epoxy resin and linear phenolic novolac resin systems. CA‐HPM plays a versatile role in tuning the comprehensive properties of epoxy such as thermal property, adhesive property, and thermo‐mechanical property. Systems with CA‐HPM show slightly lower curing activity and distinct decreased single glass transition temperature (Tg). Besides, the crosslinking density of the cured resin increases, meanwhile the thermal stability keeps at high level, which is due to the rigid five‐membered ring structure of maleimide. Metal lap shear test results manifest that the adhesion between epoxy resin and metal interface augments. With 10% CA‐1HPM, the cured resin exhibits lower equilibrium water sorption (1.88%) and diffusion coefficient (2.94 × 10−8 s−1 cm2). This biobased functional reactive modifier has provided balanced overall performance and would pave the way to a wide range of possible "eco‐friendly" applications. [ABSTRACT FROM AUTHOR]

A mineral's morphology is usually related to its growth process and environment. This study reported crystal growth of OsO2 through hydrolysis experiments of K2OsCl6 at 150–550 °C and 100 MPa to investigate the growth mechanism of OsO2 and the transport and enrichment of Os in chlorine-bearing hydrothermal fluids. Time-series experimental results showed that the OsO2 crystals grow from 40–150 nm irregular nanoparticles to 150–450 nm nanospheres with time. As the temperature and initial solution concentrations increase, OsO2 can form more uniform and larger OsO2 nanosphere crystals, suggesting a positive effect of temperature and initial solution concentration on the crystal growth of OsO2. The results indicate that the nucleation and aggregate growth driven by the hydrolysis of Os–chloride complex controls the early growth of OsO2 crystals for a short duration; however, after the hydrolysis reaches equilibrium, the growth process of OsO2 nanosphere crystals is dominated mostly by the Ostwald ripening, where the diffusion of Os ions along the fluid–nanocrystal boundary facilitates the coarsening. Given that the transport and cycle of Os from the lithosphere to the hydrosphere is controlled mainly by the stability of the Os–chloride complex, OsO2 nanosphere crystals could occur in seafloor hydrothermal vent systems. [ABSTRACT FROM AUTHOR]

Formononetin (FOR), a natural flavonoid derived from Radix Astragali , has been reported to have anti-inflammatory and anti-oxidative effects. However, its protective mechanism against mastitis is still unknown. Nuclear factor kappa-B (NF-κB) signaling pathway plays an important role in inflammation, especially mastitis. Aryl hydrocarbon receptor (AhR) is involved in inflammatory regulation and defense against diseases. We investigated the protective effect of FOR on LPS-induced mastitis in mice and the effect of Ahr and NF-κB signaling pathways on the development of mastitis. In this study, mastitis model was induced by LPS injection through the nipple duct. Protective effect of FOR on LPS-induced mastitis was assessed by FOR pretreatment. The protective mechanism of FOR against mastitis was further investigated using LPS stimulation on mouse mammary epithelial cells EpH4-Ev. The results showed that LPS-induced mammary histological injury was inhibited by FOR. FOR significantly inhibited LPS-induced MPO activity. FOR administration enhanced the integrity of blood-milk barrier. In vitro and in vivo experiments showed that FOR inhibited LPS-induced NF-κB signaling pathway activation and the production of inflammatory factors TNF-α and IL-1ß. Moreover, FOR increased the expression of tight junction protein and enhanced blood-milk barrier integrity. LPS activated AhR and Src expression. But FOR induced significant increase in AhR inhibited Src phosphorylation to exert anti-inflammatory effects. In addition, AhR antagonist CH223191 reversed the inhibition of FOR on Src expression. And the inhibition of FOR on NF-κB activation and inflammatory cytokine production were reversed by AhR antagonist CH223191. In conclusion, FOR had protective effects against LPS-induced mastitis via suppressing inflammation and enhancing blood-milk barrier integrity via AhR-induced Src inactivation. [ABSTRACT FROM AUTHOR]

Cycloaliphatic epoxy resin was modified by phenyl methyl silicone resin to investigate the influence of silicone content on the performance and reliability of epoxy packaged light-emitting diode. The silicone modification of epoxy encapsulants was characterized by transform infrared (FT-IR) spectrophotometer. Rotational rheometer was used to study rheology behavior. Differential scanning calorimetry, thermogravimetric analyses, dynamic mechanical analysis, thermomechanical analyzer were introduced to measure the thermal and mechanical properties. Ultraviolet visible spectrophotometer was utilized to study heat and ultraviolet resistance. In reliability test, scanning acoustic microscope and scanning electron microscope were applied to observe interfacial delamination. Water sorption process was monitored using gravimetric measurement. FT-IR study shows a chemical bonding between hydroxyl group of silicone resin and epoxy resin. With the incorporation of silicone resin, favorable properties were obtained such as higher thermal decomposition temperature, lower equilibrium water sorption, and better heat and UV resistance. Among these systems, 10% silicone modified epoxy resin exhibits the best performance in reliability test. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a type of high-risk heavy metal that can damage organs such as the liver, but its mechanism is not yet clear. Ferroptosis is a newly discovered mode of regulatory cell death. We explored whether ferroptosis is involved in Cd-induced liver damage and the underlying mechanism. Our research showed that Cd induced liver damage by inducing ferroptosis, and the use of ferroptosis inhibitors reduced the degree of liver damage. Moreover, the occurrence of ferroptosis was accompanied by the activation of the PERK-eIF2α-ATF4-CHOP signaling pathway, and inhibiting endoplasmic reticulum (ER) stress reduced ferroptosis demonstrating that ferroptosis induced by Cd is dependent on ER stress. In addition, chloroquine, a common autophagy inhibitor, mitigated ferroptosis caused by Cd exposure. Then, the iron chelator deferoxamine reduced Cd-induced lipid peroxidation and cell death, demonstrating that the iron regulation disorder caused by ferritin phagocytosis contributes to the Cd-induced ferroptosis. In conclusion, our results show that Cd-induced liver toxicity is accompanied by ferroptosis, which contributes to Cd inducing oxidative stress to trigger autophagy and ER stress to promote the process of ferroptosis. • Cd induces ferroptosis of hepatocytes. • ER stress and autophagy as triggers of ferroptosis caused by Cd exposure. • Autophagy of ferritin leads to ferroptosis through the degradation of ferritin under Cd exposure. [ABSTRACT FROM AUTHOR]

Endometritis is a serious reproductive disease in mammals that commonly results in reproductive loss and even permanent infertility. Kynurenic acid (KYNA) is the main bioactive metabolite of tryptophan degradation and exhibits neuroprotective and anticonvulsant properties. However, little is known about the role of KYNA in achieving endometritis remission. This study investigated the protective effects and mechanisms of KYNA using a mouse model of against lipopolysaccharide (LPS)-induced endometritis. The endometritis model was induced by an intrauterine injection of LPS, and KYNA was intraperitoneally injected before and two hours after LPS treatment. Twenty-four hours after LPS administration, pathological changes in uterine tissues were observed by hematoxylin- and eosin (H&E) staining. The levels of the inflammatory factors, TNF-α and IL-1β, were measured by ELISA. The myeloperoxidase (MPO) activity in uterine tissues was detected using MPO kits and immunohistochemistry. Furthermore, the expression of signaling pathway proteins and tight junction proteins occludin and ZO-1 in uterine tissues was detected by western blot. KYNA prominently inhibited uterine pathological injury and neutrophil infiltration and restricted the secretion of TNF-α and IL-1β in the uteri of subjects with endometritis. Furthermore, KYNA upregulated the levels of the tight junction proteins (TJPs)occludin and ZO-1 in the uterus. In vitro, KYNA inhibited LPS-induced TNF-α and IL-1β production, and NF-κB activation in mouse endometrial epithelial cells (mEECs). In addition, KYNA increased the expression of G protein-coupled receptor 35 (GPR35) and inhibition of GPR35 reversed the anti-inflammatory effects of KYNA. In conclusion, KYNA protected against LPS-induced endometritis by maintaining epithelial barrier permeability and suppressing proinflammatory responses via the GRP35/NF-κB signaling pathway. • Kynurenic acid inhibited the uterus pathological injury and inflammatory cytokines production induced by LPS. • Kynurenic acid up-regulated the levels of the tight junctions proteins occludin and ZO-1. • Kynurenic acid inhibited LPS-induced TNF-α and IL-1β production, NF-κB activation in mouse endothelial cells. • Inhibition of GPR35 reversed the anti-inflammatory effects of kynurenic acid. [ABSTRACT FROM AUTHOR]

This study reports a novel preparation method of zirconia micro-nanoflakes with high (001) facets that is generated through a hydrolysis reaction of the fluozirconic acid (H2ZrF6). Zirconia micro-nanoflakes synthesized at varied conditions were analyzed by the SEM, EDS, μ-XRD, and Raman spectroscopy to characterize the morphology and probe into the crystal growth mechanism. The synthesized zirconia crystals in the form of elliptical micro-nanoflakes or irregular nanoflakes generally display the highly exposed (001) facets with a thickness of 1–100 nm and a length of 0.1–2.0 μm. As the temperature and initial solution concentration increased, the particle sizes of the synthesized zirconia micro-nanoflakes became more uniform and the thicknesses of the (001) facets became larger, suggesting that the synthesized zirconia crystals grow along the (001) facets and mostly along the c-axis direction. This is confirmed by the data from the μ-XRD patterns. The results also demonstrate that an oriented attachment-based growth occurring in a fluorine-rich solution environment was involved in the aggregation and coarsening of zirconia micro-nanoflakes. Meanwhile, synthesized zirconia micro-nanoflakes also evolved from a mixture of monoclinic and tetragonal systems to a pure monoclinic system (i.e., baddeleyite) with the temperature increasing, suggesting a key role of temperature regarding zirconia's growth. [ABSTRACT FROM AUTHOR]

In this paper, we report a novel and simple method for synthesizing the microspheres self-assembled from ultrathin anatase TiO2 nanosheets with a high percentage of (001) facets via the hydrolysis process of the single-reagent (potassium fluorotitanate). We then used optical microscopy, scanning electron microscopy, and high-resolution confocal laser Raman spectroscopy to characterize the microspheres generated under different conditions. The study found that the size of the anatase TiO2 microspheres synthesized was 0.5–3 μm. As the synthesis time increased, the corroded surface of the microspheres gradually increased, resulting in the gradual disappearance of the edges and corners of the anatase nanosheets. The exposure percentage of the (001) facets of ultrathin anatase nanosheets synthesized for 2 h at 180–200 °C are close to 100%. The microsphere whose surface is completely covered by these anatase nanosheets also has nearly 100% exposed (001) facets. This new anatase nanosheet-based self-assembled microsphere will have great application potential in pollution prevention, environmental protection, and energy fields. [ABSTRACT FROM AUTHOR]

Acute cadmium (Cd) exposure is a significant risk factor for renal injury and lacks effective treatment strategies. Ferroptosis is a recently identified iron-dependent form of nonapoptotic cell death mediated by membrane damage resulting from lipid peroxidation, and it is implicated in many diseases. However, whether ferroptosis is involved in Cd-induced renal injury and, if so, how it operates. Here, we show that Cd can induce ferroptosis in kidney and renal tubular epithelial cells, as demonstrated by elevation of intracellular iron levels and lipid peroxidation, as well as impaired antioxidant production. Treatment with a ferroptosis inhibitor alleviated Cd-induced cell death. Intriguingly, we established that Cd-induced ferroptosis depended on endoplasmic reticulum (ER) stress, by demonstrating that Cd activated the PERK-eIF2α-ATF4-CHOP pathway and that inhibition of ER stress reduced ferroptosis caused by Cd. We further found that autophagy was required for Cd-induced ferroptosis because the inhibition of autophagy by chloroquine mitigated Cd-induced ferroptosis. Furthermore, we showed that iron dysregulation by ferritinophagy contributed to Cd-induced ferroptosis, by showing that the iron chelator desferrioxamine alleviated Cd-induced cell death and lipid peroxidation. In addition, ER stress is likely activated by MitoROS which trigger autophagy and ferroptosis. Collectively, our results indicate that ferroptosis is involved in Cd-induced renal toxicity and regulated by the MitoROS-ER stress-ferritinophagy axis. [Display omitted] • Cadmium (Cd) exposure induces ferroptosis in mice and renal tubular epithelial cells. • ER stress is required for Cd-induced ferroptosis in renal tubular epithelial cells. • ER stress-mediated ferritinophagy promotes ferroptosis by the degradation of ferritin. • Mitochondrial ROS manipulates the ER stress-autophagy triggered ferroptosis caused by Cd. [ABSTRACT FROM AUTHOR]

Tannic acid and Fe3+ were used in this study to create a polyphenol-metal network-based composite film for the preservation of Melaleuca bracteata essential oils. The inhibition rate of ABTS and DPPH free radicals reached more than 90% at an essential oil concentration of 20 mg/mL. Additive quantities of 2.0% essential oil nano-emulsion, 0.8% tannic acid/Fe3+ solution, 0.4% microcrystalline cellulose, and 1% chitosan were used to maximize the characteristics of the composite films. When combined with FTIR analysis, X-ray diffraction and scanning electron microscopy revealed that the composite film containing the essential oil emulsion had a more reticulated structure. The essential oil composite layer on mangoes increased the fruit shelf time to 12 days, decreased weight loss by 10.81±4.70%, increased the amount of soluble solids by 2.03±0.31%, and increased the amount of vitamin C by 2.18±0.09%. A trustworthy technical method for the storage and transportation of agricultural goods is offered by this study., (© 2024 Wiley‐VCH GmbH.)

The major enzyme encoded by the glucosinolate biosynthetic gene AOP2 is involved in catalyzing the conversion of glucoiberin (GIB) into sinigrin (SIN) in Brassicaceae crops. The AOP2 proteins have previously been identified in several Brassicaceae species, but not in Tumorous stem mustard. As per this research, the five identified members of the AOP2 family from the whole genome of Brassica juncea named BjuAOP2.1 - BjuAOP2.5 were found to be evenly distributed on five chromosomes. The subcellular localization results implied that BjuAOP2 proteins were mainly concentrated in the cytoplasm. Phylogenetic analysis of the AOP2 proteins from the sequenced Brassicaceae species in BRAD showed that BjuAOP2 genes were more closely linked to Brassica carinata and Brassica rapa than Arabidopsis . In comparison with other Brassicaceae plants, the BjuAOP2 members were conserved in terms of gene structures, protein sequences, and motifs. The light response and hormone response elements were included in the BjuAOP2 genes' cis-regulatory elements. The expression pattern of BjuAOP2 genes was influenced by the different stages of development and the type of tissue being examined. The BjuAOP2 proteins were used to perform the heterologous expression experiment. The results showed that all the five BjuAOP2 proteins can catalyze the conversion of GIB to SIN with different catalytic activity. These results provide the basis for further investigation of the functional study of BjuAOP2 in Tumorous stem mustard glucosinolate biosynthesis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Chen, Liu, Xiang, Zhang, Liu, Liu and Chen.)

Intestinal microbiota-mediated aryl hydrocarbon receptor (AhR) activation plays an important role in host-microbiota interactions and disease development. However, whether AhR activation mediates infection-induced inflammation in remote organs is not clear. The purpose of this study is to assess the effects and underlying mechanism of AhR activation and gut microbiota-mediated dietary tryptophan (Trp) metabolism on infection-induced inflammation using an Escherichia coli (E. coli)-induced endometritis model in mice. We found that AhR activation by 6-formylindolo (3,2-b) carbazole (Ficz), which is an AhR agonist derived from the photooxidation of Trp, alleviated E. coli-induced endometritis by repairing barrier function and inhibiting inflammatory responses, while inhibition of AhR by CH223191, which is a synthetic AhR antagonist, aggravated E. coli-induced endometritis. Gut dysbiosis damaged AhR activation and exacerbated E. coli-induced endometritis in mice, which responded to the reduced abundance of AhR ligand producers, such as Lactobacillus spp. Supplementation with dietary Trp ameliorated E. coli-induced endometritis in a microbiota-dependent manner, which was associated with the production of AhR ligands. Administration of AhR ligands, including indole and indole aldehyde, but not indole-3-propionic acid, rescued the protective effect of Trp on E. coli-induced endometritis in dysbiotic mice. Moreover, consumption of Lactobacillus reuteri (L. reuteri) containing AhR ligand-producing capability also alleviated E. coli-induced endometritis in mice in an AhR-dependent manner. Our results demonstrate that microbiota-mediated AhR activation is a key factor in fighting pathogen-caused inflammation, which leads to a potential strategy to regulate the gut microbiota and metabolism by dietary Trp or probiotics for the intervention of infectious diseases and reproductive health. IMPORTANCE Infection-induced endometritis is a common and frequently occurring disease in humans and animals. Accumulating evidence suggests an important role of the gut microbiota in the development of infection-induced inflammation. Whether and how gut microbiota-mediated AhR activation regulates the pathogenesis of pathogen-induced endometritis remains unknown. The current study found that AhR activation ameliorated E. coli-induced endometritis, and inhibition of AhR produced negative results. Gut dysbiosis reduced the abundance of AhR ligand producers including Lactobacillus spp., damaged AhR activation, and exacerbated E. coli-induced endometritis. Supplementation with dietary Trp, AhR ligands, and L. reuteri containing AhR ligand-producing capability alleviated E. coli-induced endometritis in mice. Our results suggest an important role of microbiota-mediated AhR activation in the pathogenesis of endometritis and provide potential strategies for the intervention of infectious diseases and reproductive health by regulating the gut microbiota and metabolism.