Phototransformation of tetrabromobisphenol A bis (allyl ether) in an aqueous solution: Role of environmentally persistent free radicals.

Tetrabromobisphenol A bis (allyl ether) (TBBPA-BAE) represents an extensively used brominated flame retardant (BFRs) in the production of many fields and their phototransformation in natural water is still unclear. The environmentally persistent free radicals (EPFRs) with preserved activities could exist in the environment for a long time and involve in the phototransformation of many organic pollutants. Here, the photodegradation of TBBPA-BAE with the degradation rate constant (k = 0.060 h-1) under simulate sunlight and the promoting effect of EPFRs on TBBPA-BAE photodegradation (k = 0.135 h-1) were investigated. According to the detected photogenerated electrons (e-) and singlet oxygen (1O2) rather than hydroxyl radicals (•OH) by the electron paramagnetic resonance (EPR), the effect mechanism may not be related to the typical •OH induced by EPFRs. The possible transformation pathways of the ether cleavage, hydrolysis and hydroxylation of propenyl bond and the debromination were proposed by the primary byproducts identified by UPLC-Q-Exactive Orbitrap MS. EPFRs caused a further debromination and ether cleavage and probably be due to EPFRs directly providing electrons to TBBPA-BAE which promoted the photodegradation of TBBPA-BAE, and their reaction mechanism needed further attention. Overall, this study provided useful information to understand the role of EPFRs on phototransformation of TBBPA-BAE in water.

DNA damage-induced proteasome phosphorylation controls substrate recognition and facilitates DNA repair.

Upon DNA damage, numerous proteins are targeted for ubiquitin-dependent proteasomal degradation, which is an integral part of the DNA repair program. Although details of the ubiquitination processes have been intensively studied, little is known about whether and how the 26S proteasome is regulated in the DNA damage response (DDR). Here, we show that human Rpn10/PSMD4, one of the three ubiquitin receptors of the 26S proteasome, is rapidly phosphorylated in response to different types of DNA damage. The phosphorylation occurs at Rpn10-Ser266 within a conserved SQ motif recognized by ATM/ATR/DNA-PK. Blockade of S266 phosphorylation attenuates homologous recombination-mediated DNA repair and sensitizes cells to genotoxic insults. In vitro and in cellulo experiments indicate that phosphorylation of S266, located in the flexible linker between the two ubiquitin-interacting motifs (UIMs) of Rpn10, alters the configuration of UIMs, and actually reduces ubiquitin chain (substrate) binding. As a result, essential DDR proteins such as BRCA1 are spared from premature degradation and allowed sufficient time to engage in DNA repair, a scenario supported by proximity labeling and quantitative proteomic studies. These findings reveal an inherent self-limiting mechanism of the proteasome that, by controlling substrate recognition through Rpn10 phosphorylation, fine-tunes protein degradation for optimal responses under stress.

Host specificity and cophylogeny in the "animal-gut bacteria-phage" tripartite system.

Cophylogeny has been identified between gut bacteria and their animal host and is highly relevant to host health, but little research has extended to gut bacteriophages. Here we use bee model to investigate host specificity and cophylogeny in the "animal-gut bacteria-phage" tripartite system. Through metagenomic sequencing upon different bee species, the gut phageome revealed a more variable composition than the gut bacteriome. Nevertheless, the bacteriome and the phageome showed a significant association of their dissimilarity matrices, indicating a reciprocal interaction between the two kinds of communities. Most of the gut phages were host generalist at the viral cluster level but host specialist at the viral OTU level. While the dominant gut bacteria Gilliamella and Snodgrassella exhibited matched phylogeny with bee hosts, most of their phages showed a diminished level of cophylogeny. The evolutionary rates of the bee, the gut bacteria and the gut phages showed a remarkably increasing trend, including synonymous and non-synonymous substitution and gene content variation. For all of the three codiversified tripartite members, however, their genes under positive selection and genes involving gain/loss during evolution simultaneously enriched the functions into metabolism of nutrients, therefore highlighting the tripartite coevolution that results in an enhanced ecological fitness for the whole holobiont.

Three odorant-binding proteins of small hive beetles, Aethina tumida, participate in the response of bee colony volatiles.

Aethina tumida (small hive beetle, SHB) is a rapidly spreading invasive parasite of bee colonies. The olfactory system plays a key role in insect behavior, and odorant-binding proteins (OBPs) are involved in the first step of the olfactory signal transduction pathway and the detection of host volatiles. However, the olfactory mechanism of OBPs in SHB-localized bee colonies is unclear. In this study, electroantennogram (EAG) and behavioral bioassay showed that only three compounds (2-heptanone, ocimene, and ethyl palmitate) from bee colonies triggered high electrophysiological and behavioral responses. Three antenna-specific OBP genes (OBP6, OBP11, and OBP19) were identified, and they were significantly expressed on adult days 6-7. Furthermore, by combining RNA interference (RNAi) with EAG, olfactometer bioassay, competitive fluorescence binding assays, and molecular docking, we found that these three OBP genes were involved in the recognition of 2-heptanone and ethyl palmitate, and AtumOBP6 is also involved in the recognition of ocimene. These data indicate that AtumOBP6, AtumOBP11, and AtumOBP19 play an important role in the olfactory response to bee colony volatiles. Our results provide new insights into the functions of the OBP families in A. tumida and help to explore more potential target genes for environmentally friendly pest control strategies.

ß-Cyclodextrin enhanced bioavailability of petroleum hydrocarbons in industrially contaminated soil: A phytoremediation field study.

Low remediation efficiency due to low bioavailability is a primary restrictive factor for phytoremediation applications. Specifically, this investigation examines whether Suaeda heteroptera Kitagawa (S. heteroptera) can be used in combination with ß-cyclodextrin (ß-CD) to remediate contaminated site. The study was conducted on the growth response of S. heteroptera, bioavailability and dissipation of petroleum hydrocarbons (PHs) in soil under the influence of ß-CD Our preliminary studies confirmed that ß-CD is effective in increasing the biomass and height of plants. The presence of ß-CD could dramatically elevate polycyclic aromatic hydrocarbons (PAHs) and n-alkanes in S. heteroptera. Moreover, a remarkable positive correlation between PHs levels in roots with the dosage of ß-CD and a negative correlation between the PHs levels in roots with KOW of PHs have been observed. The dissipation of n-alkanes was estimated to be 38.73-62.27%, and the dissipation of PAHs was 36.59-60.10%. In addition, the dissipation behavior of n-alkanes and PAHs was well agreement with the first-order kinetic model. These results display that applying ß-CD accelerated the desorption process of PHs from soil and promoted the absorption process of PHs onto the root epidermis. The enhancement of phytoremediation was achieved by increasing the bioavailability of PHs.

There has been an increasing concern regarding soil contamination by petroleum hydrocarbons (PHs) released by industrial activities. The study attempted to investigate how ß-CD affects the phytoremediation of PHs-contaminated sites. The findings of this study offer an environmentally friendly and cost-effective method of phytoremediating industrially contaminated sites using ß-CD enhanced-phytoremediation.

Membrane remodeling by FAM92A1 during brain development regulates neuronal morphology, synaptic function, and cognition.

The Bin/Amphiphysin/Rvs (BAR) domain protein FAM92A1 is a multifunctional protein engaged in regulating mitochondrial ultrastructure and ciliogenesis, but its physiological role in the brain remains unclear. Here, we show that FAM92A1 is expressed in neurons starting from embryonic development. FAM92A1 knockout in mice results in altered brain morphology and age-associated cognitive deficits, potentially due to neuronal degeneration and disrupted synaptic plasticity. Specifically, FAM92A1 deficiency impairs diverse neuronal membrane morphology, including the mitochondrial inner membrane, myelin sheath, and synapses, indicating its roles in membrane remodeling and maintenance. By determining the crystal structure of the FAM92A1 BAR domain, combined with atomistic molecular dynamics simulations, we uncover that FAM92A1 interacts with phosphoinositide- and cardiolipin-containing membranes to induce lipid-clustering and membrane curvature. Altogether, these findings reveal the physiological role of FAM92A1 in the brain, highlighting its impact on synaptic plasticity and neural function through the regulation of membrane remodeling and endocytic processes.

Gut microbiome and metabolism alterations in schizophrenia with metabolic syndrome severity.

BACKGROUND: Schizophrenia (SCZ) patients undergoing antipsychotic treatment demonstrated a high prevalence and harmful effects of metabolic syndrome (MetS), which acted as the major cause of cardiovascular disease. The major clinical challenge is the lack of biomarkers to identify MetS episodes and prevent further damage, while the mechanisms underlying these drug-induced MetS remain unknown. METHODS: This study divided 173 participants with SCZ into 3 groups (None, High risk, and MetS, consisting of 22, 88, and 63 participants, respectively). The potential biomarkers were searched based on 16S rRNA gene sequence together with metabolism analysis. Logistic regression was used to test the effects of the genus-metabolites panel on early MetS diagnoses. RESULTS: A genus-metabolites panel, consisting of Senegalimassilia, sphinganine, dihomo-gamma-linolenoylcholine, isodeoxycholic acid, and MG (0:0/22:5/0:0), which involved in sphigolipid metabolism, fatty acid metabolism, secondary bile acid biosynthesis and glycerolipid metabolism, has a great discrimination efficiency to MetS with an area under the curve (AUC) value of 0.911 compared to the None MetS group (P = 1.08E-8). Besides, Senegalimassilia, 3-Hydroxytetradecanoyl carnitine, isodeoxycholic acid, and DG(TXB2/0:0/2:0) distinguished between subgroups robustly and exhibited a potential correlation with the severity of MetS in patients with SCZ, and may act as the biomarkers for early MetS diagnosis. CONCLUSIONS: Our multi-omics study showed that one bacterial genus-five lipid metabolites panel is the potential risk factor for MetS in SCZ. Furthermore, Senegalimassilia, 3-Hydroxytetradecanoyl carnitine, isodeoxycholic acid, and DG(TXB2/0:0/2:0) could serve as novel diagnostic markers in the early stage. So, it is obvious that the combination of bacterial genus and metabolites yields excellent discriminatory power, and the lipid metabolism provide new understanding to the pathogenesis, prevention, and therapy for MetS in SCZ.

Loss of ß2-integrin function results in metabolic reprogramming of dendritic cells, leading to increased dendritic cell functionality and anti-tumor responses.

Dendritic cells (DCs) are the main antigen presenting cells of the immune system and are essential for anti-tumor responses. DC-based immunotherapies are used in cancer treatment, but their functionality is not optimized and their clinical efficacy is currently limited. Approaches to improve DC functionality in anti-tumor immunity are therefore required. We have previously shown that the loss of ß2-integrin-mediated adhesion leads to epigenetic reprogramming of bone marrow-derived DCs (BM-DCs), resulting in an increased expression of costimulatory markers (CD86, CD80, and CD40), cytokines (IL-12) and the chemokine receptor CCR7. We now show that the loss of ß2-integrin-mediated adhesion of BM-DCs also leads to a generally suppressed metabolic profile, with reduced metabolic rate, decreased ROS production, and lowered glucose uptake in cells. The mRNA levels of glycolytic enzymes and glucose transporters were reduced, indicating transcriptional regulation of the metabolic phenotype. Surprisingly, although signaling through a central regulator of immune cell metabolisms, the mechanistic target of rapamycin (mTOR), was increased in BM-DCs with dysfunctional integrins, rapamycin treatment revealed that mTOR signaling was not involved in suppressing DC metabolism. Instead, bioinformatics and functional analyses showed that the Ikaros transcription factor may be involved in regulating the metabolic profile of non-adhesive DCs. Inversely, we found that induction of metabolic stress through treatment of cells with low levels of an inhibitor of glycolysis, 2-deoxyglucose (2DG), led to increased BM-DC activation. Specifically, 2DG treatment led to increased levels of Il-12 and Ccr7 mRNA, increased production of IL-12, increased levels of cell surface CCR7 and increased in vitro migration and T cell activation potential. Furthermore, 2DG treatment led to increased histone methylation in cells (H3K4me3, H3K27me3), indicating metabolic reprogramming. Finally, metabolic stress induced by 2DG treatment led to improved BM-DC-mediated anti-tumor responses in vivo in a melanoma cancer model, B16-OVA. In conclusion, our results indicate a role for ß2-integrin-mediated adhesion in regulating a novel type of metabolic reprogramming of DCs and DC-mediated anti-tumor responses, which may be targeted to enhance DC-mediated anti-tumor responses in cancer immunotherapy.

Vaginal microbial profile of cervical cancer patients receiving chemoradiotherapy: the potential involvement of Lactobacillus iners in recurrence.

The vaginal microbiome is an immune defense against reproductive diseases and can serve as an important biomarker for cervical cancer. However, the intrinsic relationship between the recurrence and the vaginal microbiome in patients with cervical cancer before and after concurrent chemoradiotherapy is poorly understood. Here, we analyzed 125 vaginal microbial profiles from a patient cohort of stage IB-IVB cervical cancer using 16S metagenomic sequencing and deciphered the microbial composition and functional characteristics of the recurrent and non-recurrent both before and after chemoradiotherapy. We demonstrated that the abundance of beneficial bacteria and stability of the microbial community in the vagina decreased in the recurrence group, implying the unique characteristics of the vaginal microbiome for recurrent cervical cancer. Moreover, using machine learning, we identified Lactobacillus iners as the most important biomarker, combined with age and other biomarkers (such as Ndongobacter massiliensis, Corynebacterium pyruviciproducens ATCC BAA-1742, and Prevotella buccalis), and could predict cancer recurrence phenotype before chemoradiotherapy. This study prospectively employed rigorous bioinformatics analysis and highlights the critical role of vaginal microbiota in post-treatment cervical cancer recurrence, identifying promising biomarkers with prognostic significance in the context of concurrent chemoradiotherapy for cervical cancer. The role of L. iners in determining chemoradiation resistance in cervical cancer warrants further detailed investigation. Our results expand our understanding of cervical cancer recurrence and help develop better strategies for prognosis prediction and personalized therapy.

Rare codon recoding for efficient noncanonical amino acid incorporation in mammalian cells.

The ability to genetically encode noncanonical amino acids (ncAAs) has empowered proteins with improved or previously unknown properties. However, existing strategies in mammalian cells rely on the introduction of a blank codon to incorporate ncAAs, which is inefficient and limits their widespread applications. In this study, we developed a rare codon recoding strategy that takes advantage of the relative rarity of the TCG codon to achieve highly selective and efficient ncAA incorporation through systematic engineering and big data-model predictions. We highlight the broad utility of this strategy for the incorporation of dozens of ncAAs into various functional proteins at the wild-type protein expression levels, as well as the synthesis of proteins with up to six-site ncAAs or four distinct ncAAs in mammalian cells for downstream applications.

LUZP1 regulates the maturation of contractile actomyosin bundles.

Contractile actomyosin bundles play crucial roles in various physiological processes, including cell migration, morphogenesis, and muscle contraction. The intricate assembly of actomyosin bundles involves the precise alignment and fusion of myosin II filaments, yet the underlying mechanisms and factors involved in these processes remain elusive. Our study reveals that LUZP1 plays a central role in orchestrating the maturation of thick actomyosin bundles. Loss of LUZP1 caused abnormal cell morphogenesis, migration, and the ability to exert forces on the environment. Importantly, knockout of LUZP1 results in significant defects in the concatenation and persistent association of myosin II filaments, severely impairing the assembly of myosin II stacks. The disruption of these processes in LUZP1 knockout cells provides mechanistic insights into the defective assembly of thick ventral stress fibers and the associated cellular contractility abnormalities. Overall, these results significantly contribute to our understanding of the molecular mechanism involved in actomyosin bundle formation and highlight the essential role of LUZP1 in this process.

pH-responsive drug-loaded peptides enhance drug accumulation and promote apoptosis in tumor cells.

The efficacy of chemotherapeutic drugs in tumor treatment is limited by their toxicity and side effects due to their inability to selectively accumulate in tumor tissue. In addition, chemotherapeutic agents are easily pumped out of tumor cells, resulting in their inadequate accumulation. To overcome these challenges, a drug delivery system utilizing the amphiphilic peptide Pep1 was designed. Pep1 can self-assemble into spherical nanoparticles (PL/Pep1) and encapsulate paclitaxel (PTX) and lapatinib (LAP). PL/Pep1 transformed into nanofibers in an acidic environment, resulting in longer drug retention and higher drug concentrations within tumor cells. Ultimately, PL/Pep1 inhibited tumor angiogenesis and enhanced tumor cell apoptosis. The use of shape-changing peptides as drug carriers to enhance cancer cell apoptosis is promising.

NIR-II light powered hydrogel nanomotor for intravesical instillation with enhanced bladder cancer therapy.

Intravesical instillation is the common therapeutic strategy for bladder cancer. Besides chemo drugs, nanoparticles are used as intravesical instillation reagents, offering appealing therapeutic approaches for bladder cancer treatment. Metal oxide nanoparticle based chemodynamic therapy (CDT) converts tumor intracellular hydrogen peroxide to ROS with cancer cell-specific toxicity, which makes it a promising approach for the intravesical instillation of bladder cancer. However, the limited penetration of nanoparticle based therapeutic agents into the mucosa layer of the bladder wall poses a great challenge for the clinical application of CDT in intravesical instillation. Herein, we developed a 1064 nm NIR-II light driven hydrogel nanomotor for the CDT for bladder cancer via intravesical instillation. The hydrogel nanomotor was synthesized via microfluidics, wrapped with a lipid bilayer, and encapsulates CuO2 nanoparticles as a CDT reagent and core-shell structured Fe3O4@Cu9S8 nanoparticles as a fuel reagent with asymmetric distribution in the nanomotor (LipGel-NM). An NIR-II light irradiation of 1064 nm drives the active motion of LipGel-NMs, thus facilitating their distribution in the bladder and deep penetration into the mucosa layer of the bladder wall. After FA-mediated endocytosis in bladder cancer cells, CuO2 is released from LipGel-NMs due to the acidic intracellular environment for CDT. The NIR-II light powered active motion of LipGel-NMs effectively enhances CDT, providing a promising strategy for bladder cancer therapy.

Research on consumers' purchase intention of cultural and creative products-Metaphor design based on traditional cultural symbols.

Chinese traditional cultural symbols possess great aesthetic and cultural value, and are widely utilized in product design. In this study, we explore the relationship between metaphor design based on traditional cultural symbols, customer experience and cultural identity, and further estimate how these three variables stimulate consumers' perceived value to generate consumers' purchase intention. Based on existing traditional cultural literature and Stimulus-organism-response theory (SOR), we proposed a theoretical research model to characterize the relationship among metaphor design based on traditional cultural symbols, customer experience, cultural identity, perceived value and consumers' purchase intention. A research survey was conducted and 262 questionnaires were collected in total with 241 valid. We used Smart PLS graph version 3.0 for data analysis. Results indicate that the cognition of metaphor design based on traditional cultural symbols and customer experience has a direct and significant impact on the emotional value thereby, eliciting consumers' purchase intention, metaphor design based on traditional cultural symbols is directly and indirectly (i.e., through customer experience or perceived value) positively associated with consumers' purchase intention, also customer experience is directly and indirectly (i.e., through perceived value) associated with consumer purchase intention, cultural identity mediates the indirect effect of customer experience and perceived value on purchase intention, the moderating role of cultural identity between customer experience and perceived value is not significant. Our findings help to expand the existing literature on consumer purchase intentions by rationally using traditional cultural symbols in the product metaphor design.

Uptake, biotransformation and physiological response of TBBPA derivatives in Helianthus annus.

Tetrabromobisphenol A (TBBPA) and its derivatives are widely used as brominated flame retardants. Because of their high production and wide environment distribution, TBBPA derivatives have increased considerable concern. Previous studies have primarily focused on TBBPA, with limited information available on its derivative. In this study, we investigated the uptake, biotransformation and physiological response of two derivatives, Tetrabromobisphenol A bis(allyl ether) (TBBPA BAE) and Tetrabromobisphenol A bis(2,3-dibromopropylether) (TBBPA BDBPE), in Helianthus annus (H. annus) through a short-term hydroponic assay. The results revealed that H. annus could absorb TBBPA BAE and TBBPA BDBPE from solution, with removal efficiencies of 98.33 ± 0.5% and 98.49 ± 1.56% after 10 days, respectively, which followed first-order kinetics. TBBPA BAE was absorbed, translocated and accumulated while TBBPA BDBPE couldn't be translocated upward due to its high hydrophobicity and low solubility. The concentrations of TBBPA derivatives in plants peaked within 72 h, and then decreased. We identified twelve metabolites resulting from ether bond breakage, debromination, and hydroxylation in H. annus. The high-level TBBPA BAE suppressed the growth and increased malondialdehyde (MDA) content of H. annus, while TBBPA BDBPE didn't pose a negative effect on H. annus. TBBPA BAE and TBBPA BDBPE increased the activity of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), with higher levels of these enzymes activity found in high concentration treatments. Contrastingly, TBBPA BAE exhibited higher toxicity than TBBPA BDBPE, as indicated by greater antioxidant enzyme activity. The findings of this study develop better understanding of biotransformation mechanisms of TBBPA derivatives in plants, contributing to the assessment of the environmental and human health impacts of these contaminants.

BMSC-derived exosomes regulate the Treg/Th17 balance through the miR-21-5p/TLR4/MyD88/NF-κB pathway to alleviate dry eye symptoms in mice.

Bone marrow mesenchymal stem cell (BMSC)-derived exosomes (BMSC-Exos) have a variety of biological functions and are extensively involved in the regulation of inflammatory diseases, as well as tissue repair and regeneration. However, the mechanism of action of these compounds in dry eye disease (DED) in mice is still unclear. This study demonstrated that the Treg/Th17 ratio was strongly imbalanced in DED clinical samples. BMSC-Exos can modulate the Treg/Th17 balance, improve the integrity of the corneal epithelial layer, and ameliorate DED progression in mice. Mechanistically, BMSC-Exos dramatically decreased the levels of IL-17 and IL-22; increased the levels of IL-4, IL-10, and TGF-ß1; and increased tear secretion and the number of goblet cells in the conjunctiva in mice, thus alleviating the progression of DED. This effect is achieved by BMSC-Exos through the delivery of miR-21-5p to target and restrain TLR4, thereby restraining the MyD88/NF-κB pathway. Our study showed that the upregulation of miR-21-5p in BMSC-Exos may be a therapeutic target for DED. These findings support new ideas and a basis for treating DED, as well as for further study of the application value of exosomes in alleviating DED.

GTPBP8 modulates mitochondrial fission through a Drp1-dependent process.

Mitochondrial fission is a tightly regulated process involving multiple proteins and cell signaling. Despite extensive studies on mitochondrial fission factors, our understanding of the regulatory mechanisms remains limited. This study shows the critical role of a mitochondrial GTPase, GTPBP8, in orchestrating mitochondrial fission in mammalian cells. Depletion of GTPBP8 resulted in drastic elongation and interconnectedness of mitochondria. Conversely, overexpression of GTPBP8 shifted mitochondrial morphology from tubular to fragmented. Notably, the induced mitochondrial fragmentation from GTPBP8 overexpression was inhibited in cells either depleted of the mitochondrial fission protein Drp1 (also known as DNM1L) or carrying mutated forms of Drp1. Importantly, downregulation of GTPBP8 caused an increase in oxidative stress, modulating cell signaling involved in the increased phosphorylation of Drp1 at Ser637. This phosphorylation hindered the recruitment of Drp1 to mitochondria, leading to mitochondrial fission defects. By contrast, GTPBP8 overexpression triggered enhanced recruitment and assembly of Drp1 at mitochondria. In summary, our study illuminates the cellular function of GTPBP8 as a pivotal modulator of the mitochondrial division apparatus, inherently reliant on its influence on Drp1.

Mechanism of tartaric acid mediated dissipation and biotransformation of tetrabromobisphenol A and its derivatives in soil.

Biotransformation is a major dissipation process of tetrabromobisphenol A and its derivatives (TBBPAs) in soil. The biotransformation and ultimate environmental fate of TBBPAs have been widely studied, yet the effect of root exudates (especially low-molecular weight organic acids (LMWOAs)) on the fate of TBBPAs is poorly documented. Herein, the biotransformation behavior and mechanism of TBBPAs in bacteriome driven by LMWOAs were comprehensively investigated. Tartaric acid (TTA) was found to be the main component of LMWOAs in root exudates of Helianthus annus in the presence of TBBPAs, and was identified to play a key role in driving shaping bacteriome. TTA promoted shift of the dominant genus in soil bacteriome from Saccharibacteria_genera_incertae_sedis to Gemmatimonas, with a noteworthy increase of 24.90-34.65% in relative abundance of Gemmatimonas. A total of 28 conversion products were successfully identified, and ß-scission was the principal biotransformation pathway for TBBPAs. TTA facilitated the emergence of novel conversion products, including 2,4-dibromophenol, 3,5-dibromo-4-hydroxyacetophenone, para-hydroxyacetophenone, and tribromobisphenol A. These products were formed via oxidative skeletal cleavage and debromination pathways. Additionally, bisphenol A was observed during the conversion of derivatives. This study provides a comprehensive understanding about biotransformation of TBBPAs driven by TTA in soil bacteriome, offering new insights into LMWOAs-driven biotransformation mechanisms.

The dissipation of organophosphate esters mediated by ryegrass root exudate oxalic acid in soil: Analysis of enzymes activities, microorganism.

Complex rhizoremediation is the main mechanism of phytoremediation in organic-contaminated soil. Low molecular weight organic acids (LMWOAs) in root exudates have been shown to increase the bioavailability of contaminants and are essential for promoting the dissipation of contaminants. The effects of root exudates on the dissipation of organophosphate esters (OPEs) in soil are unclear. Consequently, we studied the combined effects of root exudates, soil enzymes and microorganisms on OPEs (tri (1-chloro-2-propyl) phosphate (TCPP) and triphenyl phosphate (TPP)) dissipation through pot experiments. Oxalic acid (OA) was confirmed to be the main component of LMWOAs in root exudates of ryegrass. The existence of OA increased the dissipation rate of OPEs by 6.04%-25.50%. Catalase and dehydrogenase activities were firstly activated and then inhibited in soil. While, urease activity was activated and alkaline phosphatase activity was inhibited during the exposure period. More bacteria enrichment (e.g., Sphingomonas, Pseudomonas, Flavisolibacter, Pontibacter, Methylophilus and Massilia) improved the biodegradation of OPEs. In addition, the transformation paths of OPEs hydrolysis and methylation under the action of root exudates were observed. This study provided theoretical insights into reducing the pollution risk of OPEs in the soil.

BMSC Alleviates Dry Eye by Inhibiting the ROS-NLRP3-IL-1ß Signaling Axis by Reducing Inflammation Levels.

PURPOSE: Bone marrow mesenchymal stem cells (BMSC) have multiple biological functions and are widely involved in regulating inflammatory diseases, tissue repair and regeneration. However, the mechanism of their action in dry eye disease (DED) is currently unclear. The purpose of this study was to investigate the effect of BMSCs in the treatment of dry eye mice and to explore its specific therapeutic mechanism. METHODS: Mouse corneal epithelial cells (MCECs) were treated with 500 mOsM sodium chloride hypertonic solution to induce a DED cell model. The dry eye animal model was constructed by adding 5 µL 0.2% benzalkonium chloride solution to mouse eyes. Western blotting was used to detect the expression of related proteins, and flow cytometry, enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining, hematoxylin-eosin (HE) staining, and periodic acid schiff (PAS) staining were used to detect cell and eye tissue damage. RESULTS: The experimental results showed that BMSCs can reduce the levels of reactive oxygen species (ROS) and inflammatory factors in MCECs, promote cell proliferation, inhibit cell apoptosis, improve the integrity of the corneal epithelial layer in vivo, promote an increase in the number of goblet cells, and alleviate DED. Further exploration of the molecular mechanism of BMSCs treatment revealed that BMSCs alleviate the progression of DED by inhibiting the ROS-NLRP3-IL-1ß signaling pathway. CONCLUSION: BMSCs inhibit ROS-NLRP3-IL-1ß signaling axis, reducing inflammation levels and alleviating dry eye symptoms. These findings provide new ideas and a basis for the treatment of DED and provide an experimental basis for further research on the application value of BMSCs in alleviating DED.