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Herein, three supported catalysts, CuO/Al2O3, CeO2/Al2O3, and CuO-CeO2/Al2O3, were synthesized by the convenient impregnation method to reveal the effect of CeO2 addition on catalytic performance and reaction mechanism for toluene oxidation. Compared with CuO/Al2O3, the T50 and T90 (the temperatures at 50% and 90% toluene conversion, respectively) of CuO-CeO2/Al2O3 were reduced by 33 and 39 °C, respectively. N2 adsorption-desorption experiment, XRD, SEM, EDS mapping, Raman, EPR, H2-TPR, O2-TPD, XPS, NH3-TPD, Toluene-TPD, and in-situ DRIFTS were conducted to characterize these catalysts. The excellent catalytic performance of CuO-CeO2/Al2O3 could be attributed to its strong copper-cerium interaction and high oxygen vacancies concentration. Moreover, in-situ DRIFTS proved that CuO-CeO2/Al2O3 promoted the conversion of toluene to benzoate and accelerated the deep degradation path of toluene. This work provided valuable insights into the development of efficient and economical catalysts for volatile organic compounds.

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Despite widespread deployment and investigation of ultrafiltration (UF) for secondary effluent purification, the challenge of membrane fouling due to effluent organic matter (EfOM) remains formidable. This study introduced a novel pretreatment method utilizing Co nanoparticles-encapsulated carbon nanotubes activated peroxymonosulfate (Co@CNT/PMS) to degrade EfOM and mitigate membrane fouling. Characterization of Co@CNT revealed the efficient encapsulation of Co nanoparticles within nanotubes, which notably enhanced the catalytic degradation of bisphenol A and typical organics. The tube-encapsulated structure increased the concentration of reactive species within the confined nanoscopic space, thereby improving the probability of collisions with pollutants and promoting their degradation. The Co@CNT/PMS pretreatment led to substantial reductions in aromatic compounds, fluorescent components, and both high and middle molecular weight substances. These changes proved crucial in diminishing the fouling potential in subsequent UF processes, where reversible and irreversible fouling resistances decreased by 97.1 % and 72.8 %, respectively. The transition volume from pore blocking to cake filtration markedly increased, prolonging the formation of a dense fouling layer. Surface properties analysis indicated a significant reduction of pollutants on membrane surfaces after the Co@CNT/PMS pretreatment. This study underscored the efficacy of confinement-based advanced oxidization pretreatment in enhancing UF performance, presenting a viable resolution to membrane fouling.

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Multiple myeloma (MM) is a malignancy of plasma cells accompanied by immune dysfunction. This study aimed to provide a comprehensive and dynamic characterization of the peripheral immune environment in MM patients and find its diagnostic and prognostic values for therapy. The peripheral immune profiles of MM inpatients and healthy controls were assessed by flow cytometry. A longitudinal study of immune subsets was observed during cycles of chemotherapy. The diagnostic and prognostic models were established based on immune subsets by the absolute shrinkage and selection operator (LASSO) and multivariate regression. MM patients possessed an impeded immune landscape, including reduced activation of B cells, increased effective T cells and regulatory T cells (Tregs), augmented CD16 expression on monocytes and dendritic cell percentages, decreased CD56dimCD16+ natural killer cells (NKs), and amplified CD56bright and HLA-DR+ natural killer T cells (NKTs). Chemotherapy has different dynamic effects on specific cells, of which 2 cycles is the key turning point. NKT, dendritic cells, naïve Tc and Th cells, HLA-DR+ Tc cells, CD56dim NKTs, CD16++ monocytes, and CD25+ B cells could have the diagnostic value, and a prognostic model including neutrophils, naïve Tc cells, CD56brightCD16dim NKs, and CD16+ dendritic cells was established with acceptable accuracy. Our data showed dynamic and abnormal peripheral immune profiles in MM patients, which had prognostic values and could provide the basis for clinical therapy.

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Proton exchange membrane (PEM) electrolysis holds great promise for green hydrogen production, but suffering from high loading of platinum-group metals (PGM) for large-scale deployment. Anchoring PGM-based materials on supports can not only improve the atomic utilization of active sites but also enhance the intrinsic activity. However, in practical PEM electrolysis, it is still challenging to mediate hydrogen adsorption/desorption pathways with high coverage of hydrogen intermediates over catalyst surface. Here, operando generated stable palladium (Pd) hydride nanoclusters anchored on tungsten carbide (WCx) supports were constructed for hydrogen evolution in PEM electrolysis. Under PEM operando conditions, hydrogen intercalation induces formation of Pd hydrides (PdHx) featuring weakened hydrogen binding energy (HBE), thus triggering reverse hydrogen spillover from WCx (strong HBE) supports to PdHx sites, which have been evidenced by operando characterizations, electrochemical results and theoretical studies. This PdHx-WCx material can be directly utilized as cathode electrocatalysts in PEM electrolysis with ultralow Pd loading of 0.022 mg cm-2, delivering the current density of 1 A cm-2 at the cell voltage of ~1.66 V and continuously running for 200 hours without obvious degradation. This innovative strategy via tuning the operando characteristics to mediate reverse hydrogen spillover provide new insights for designing high-performance supported PGM-based electrocatalysts.

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Ferroptosis is implicated in several diseases, including iron overload-induced osteoarthritis (IOOA), which is marked by oxidative stress, iron imbalance, and lipid peroxidation. Given rosiglitazone's (RSG) ability to inhibit lipid peroxidation and ferroptosis, this study aims to assess its therapeutic potential for treating IOOA. Our in vitro results show that RSG targets acyl-CoA synthetase long-chain family member 4 to mitigate impairments induced by interleukin-1 beta and ferric ammonium citrate, including cell apoptosis, senescence, inflammatory responses, extracellular matrix degradation, and ferroptosis. RSG reduced intracellular iron content, alleviated oxidative stress and lipid peroxidation, mitigated damage to membrane-bound organelles, and enhanced glucose transport. Additionally, pre-treatment with RSG imparted anti-ferroptotic properties to chondrocytes. In vivo, RSG alleviated cartilage degradation, inflammatory responses, and ferroptosis in mice with IOOA. In conclusion, RSG exhibits chondroprotective and anti-ferroptotic effects by suppressing lipid peroxidation and restoring iron homeostasis, highlighting its potential for treating IOOA.

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In recent decades, global aquaculture has expanded rapidly, raising concerns about coastal environmental degradation due to unregulated or poorly regulated discharge of aquaculture tailwater. Despite the crucial role of dissolved organic matter (DOM) in biogeochemical processes and aquatic biodiversity, the influence of aquaculture type on the molecular characteristics of DOM remains largely unexplored. Herein, this study investigated the variations in chemical and spectroscopic properties as well as molecular characteristics and composition of DOM across different aquaculture types including crustacean, fish and shellfish. Our findings revealed notable differences in DOM quantities among different aquaculture types, with crustacean and fish aquaculture water containing higher DOM amount compared to shellfish aquaculture water. This disparity can be attributed to the more frequent formulated feeds of crustacean and fish in contrast to shellfish aquaculture. Furthermore, distinct differences were also observed in the characteristics and composition of DOM among the different aquaculture waters. Specifically, DOM in shellfish aquaculture water exhibited a higher abundance of unsaturated and reduced molecules as well as increased aromaticity compared to the other two aquaculture waters. Conversely, DOM from fish aquaculture water showed a greater contribution from terrestrial origin characterized by elevated levels of plant-based components such as lignin-like and tannin-like compounds. Interestingly, DOM from shellfish aquaculture water contained lower levels of microbial-derived components such as lipid-like and protein-like compounds, likely due to reduced microorganism populations resulting from lower nutrients availability and higher salinity. Overall, these significant variations in characteristics and composition of DOM underscore the potential impacts of aquaculture type on the DOM biogeochemical cycle and the environmental quality in aquatic ecosystems.

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The binding mechanism of molecular interaction between bicalutamide and human serum albumin (HSA) in a pH 7.4 phosphate buffer was studied using various spectroscopic techniques in combination with molecular modeling. Fluorescence data revealed that the fluorescence quenching of HSA by bicalutamide was a static quenching procedure. The binding constants and number of binding sites were evaluated at different temperatures. The thermodynamic parameters, ΔH and ΔS, were calculated to be 4.30 × 104 J·mol-1 and 245 J·mol-1·K-1, respectively, suggesting that the binding of bicalutamide to HSA was driven mainly by hydrophobic interactions and hydrogen bonds. The displacement studies indicated neither Sudlow's site I nor II but subdomain IB as the main binding site for bicalutamide on HSA. The binding distance between bicalutamide and HSA was determined to be 3.54 nm based on the Förster theory. Analysis of circular dichroism, synchronous, and 3D fluorescence spectra demonstrated that HSA conformation was slightly altered in the presence of bicalutamide.

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Non-alcoholic fatty liver disease (NAFLD) and myocardial infarction (MI) are two major health burdens with significant prevalence and mortality. This study aimed to explore the co-expressed genes to understand the relationship between NAFLD and MI and identify potential crucial biomarkers of NAFLD-related MI using bioinformatics and machine learning. Functional enrichment analysis was conducted, a co-protein-protein interaction (PPI) network diagram was constructed, and support vector machine-recursive feature elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) techniques were employed to identify one differentially expressed gene (DEG), Thrombospondin 1 (THBS1). THBS1 demonstrated strong performance in distinguishing NAFLD patients (AUC = 0.981) and MI patients (AUC = 0.900). Immuno-infiltration analysis revealed significantly lower CD8+ T cells and higher neutrophil levels in patients with NAFLD and MI. CD8+ T cells and neutrophils were effective in distinguishing NAFLD/MI from healthy controls. Correlation analysis showed that THBS1 was positively correlated with CCR (chemokine receptor), MHC class (major histocompatibility complex class), neutrophils, parainflammation, and Tfh (follicular helper T cells), and negatively correlated with CD8+ T cells, cytolytic activity, and TIL (tumor-infiltrating lymphocytes) in NAFLD and MI patients. THBS1 emerged as a novel biomarker for diagnosing NAFLD/MI in comparison to healthy controls. The results indicate that CD8+ T cells and neutrophils could serve as inflammatory immune features for differentiating patients with NAFLD/MI from healthy individuals.

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INTRODUCTION: Tinnitus is a prevalent and disabling condition characterized by the perception of sound in the absence of external acoustic stimuli. The hyperactivity of the auditory pathway is a crucial factor in the development of tinnitus. This study aims to examine genetic expression variations in the dorsal cochlear nucleus (DCN) and inferior colliculus (IC) following the onset of tinnitus using transcriptomic analysis. The goal is to investigate the relationship between hyperactivity in the DCN and IC. METHODS: To confirm the presence of tinnitus behavior, we utilized the gap pre-pulse inhibition of the acoustic startle (GPIAS) response paradigm. In addition, we conducted auditory brainstem response (ABR) tests to determine the baseline hearing thresholds, and repeated the test one week after subjecting the rats to noise exposure (8-16 kHz, 126 dBHL, 2 h). Samples of tissue were collected from the DCN and IC in both the tinnitus and non-tinnitus groups of rats. We employed RNA sequencing and quantitative PCR techniques to analyze the changes in gene expression between these two groups. This allowed us to identify any specific genes or gene pathways that may be associated with the development or maintenance of tinnitus in the DCN and IC. RESULTS: Our results demonstrated tinnitus-like behavior in rats exposed to noise, as evidenced by GPIAS measurements. We identified 61 upregulated genes and 189 downregulated genes in the DCN, along with 396 upregulated genes and 195 downregulated genes in the IC. Enrichment analysis of the DCN revealed the involvement of ion transmembrane transport regulation, synaptic transmission, and negative regulation of neuron apoptotic processes in the development of tinnitus. In the IC, the enrichment analysis indicated that glutamatergic synapses and neuroactive ligand-receptor interaction pathways may significantly contribute to the process of tinnitus development. Additionally, protein-protein interaction (PPI) networks were constructed, and 9 hub genes were selected based on their betweenness centrality rank in the DCN and IC, respectively. CONCLUSIONS: Our findings reveal enrichment of differential expressed genes (DEGs) associated with pathways linked to alterations in neuronal excitability within the DCN and IC when comparing the tinnitus group to the non-tinnitus group. This indicates an increased trend in neuronal excitability within both the DCN and IC in the tinnitus model rats. Additionally, the enriched signaling pathways within the DCN related to changes in synaptic plasticity suggest that the excitability changes may propagate to IC. NEW AND NOTEWORTHY: Our findings reveal gene expression alterations in neuronal excitability within the DCN and IC when comparing the tinnitus group to the non-tinnitus group at the transcriptome level. Additionally, the enriched signaling pathways related to changes in synaptic plasticity in the differentially expressed genes within the DCN suggest that the excitability changes may propagate to IC.

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Background: The intricate relationship among gut microbiota, serum metabolites, and immunophenotypes may significantly impact myocarditis. However, direct causal links between these domains and myocarditis are not well understood. Methods: The study performed Mendelian randomization (MR) analysis using genetic data from public sources. Exposure data included 211 gut microbiota, 486 serum metabolites, and 731 immunophenotypes from Mibiogen, the Metabolomics GWAS server, and GWAS catalog databases. Single nucleotide polymorphisms (SNPs) were selected as instrumental variables based on established criteria. Myocarditis data from GWAS (427,911 participants, 24, 180, 570 SNPs) were used as the outcome variable. MR analysis was conducted using Inverse Variance Weighting (IVW), with Cochran's Q test for heterogeneity and Egger's intercept to assess horizontal pleiotropy. Results: 9 gut microbiota, 10 serum metabolites, and 2 immunophenotypes were negatively associated with myocarditis risk. In contrast, 5 gut microbiota, 12 serum metabolites, and 7 immunophenotypes were positively associated with myocarditis risk (all, P < 0.05). Sensitivity analyses confirmed the stability of these results. Conclusion: This MR study suggests that gut microbiota, serum metabolites, and immunophenotypes may causally influence myocarditis risk. These findings provide genetic evidence for myocarditis etiology and could inform future precision prevention and treatment strategies.

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Objective: This study aims to analyze the relationship between papillary thyroid carcinoma (PTC) and various factors. Methods: The study involved two groups-PTC patients and non-PTC controls. We utilized binary logistic regression and Least Absolute Shrinkage and Selection Operator (Lasso) regression for variable selection and risk factor analysis. Correlation analysis was performed using Spearman's rank correlation. The diagnostic value of thyroid stimulating hormone (TSH) levels for PTC was assessed using Receiver Operating Characteristic (ROC) curves. Results: PTC patients exhibited higher body mass index (BMI) (23.71 vs. 22.66, p<0.05) and TSH levels (3.38 vs. 1.59, p<0.05). Urinary iodine concentration (UIC) was an independent predictor of PTC (OR=1.005, p<0.05). The optimal TSH threshold for PTC diagnosis was 2.4 mIU/L [The Area Under the Curve (AUC)=67.3%, specificity=71.4%, sensitivity=70.1%]. TSH levels positively correlated with BMI (r=0.593, p<0.05) and UIC (r=0.737, p<0.05). Conclusions: UIC may be an independent predictor of PTC, and TSH levels have some diagnostic value for identifying PTC.

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Background and objective: The rupture risk of intracranial aneurysms (IAs) is related to their arterial origin, but whether the different segments of the artery have different risks and act as independent risk factors is still unknown. Our study aimed to investigate the rupture risk of IAs in different arterial segments in a large Chinese cohort. Methods: Imaging and clinical data of consecutive patients with IAs diagnosed by Computed Tomography angiography (CTA) from January 2013 to December 2022 were collected. Two neuroradiologists independently identified ruptured and unruptured IAs based on imaging and medical records. The internal carotid artery (ICA), middle cerebral artery (MCA), anterior cerebral artery (ACA), vertebral artery (VA), and posterior cerebral artery (PCA) were segmented according to the Bouthillier and Fischer segmentation methods. Stenoses of the proximal parent vessel were evaluated and documented. The Institutional Review Board (IRB) at Beijing Tiantan Hospital approved this retrospective study. Results: A total of 3,837 aneurysms {median size 3.5 mm [interquartile range (IQR) 2.6-5.1 mm]; 532 ruptured} were included in this study from 2,968 patients [mean age: 57 years (IQR 50-64); male patients: 1,153]. Ruptured aneurysms were most commonly located in the posterior inferior cerebellar artery (PICA) (52.9%), anterior communicating artery (ACoA) (33.8%), other locations (33.3%), ACA (22.4%), and basilar artery (BA) (21.4%). The locations with the highest likelihood of rupture were the C7 ICA (21.3%), M2 MCA (24.0%), distal MCA (25.0%), and A2 ACA (28.1%). IAs originating from the C7 (p < 0.001), dM1 (p = 0.022), and dA1 (p = 0.021) segments were independent risk factors for rupture. IAs without stenosis of the proximal parent vessel were associated with a higher risk of rupture (p = 0.023). Conclusion: There are unique associations between the origins of aneurysms from various arterial segments. Aneurysms originating from the anterior communicating artery (ACoA), BA, PICA, A2, dA, C7, and M2 indicate a higher risk of rupture. Aneurysms originating from C4, C5, and C6 indicate a lower risk of rupture. C7 IAs, ACoA IAs, and PICA IAs seem to be independent risk factors.

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The interplay between immune components and the epithelium plays a crucial role in the development and progression of head and neck squamous cell carcinoma (HNSCC). Natural killer (NK) cells, one of the main tumor-killing immune cell populations, have received increasing attention in HNSCC immunotherapy. In this review, we explore the mechanism underlying the interplay between NK cells and HNSCC. A series of immune evasion strategies utilized by cancer cells restrict HNSCC infiltration of NK cells. Overcoming these limitations can fully exploit the antineoplastic potential of NK cells. We also investigated the tumor-killing efficacy of NK cell-based immunotherapies, immunotherapeutic strategies, and new results from clinical trials. Notably, cetuximab, the most essential component of NK cell-based immunotherapy, inhibits the epidermal growth factor receptor (EGFR) signaling pathway and activates the immune system in conjunction with NK cells, inducing innate effector functions and improving patient prognosis. In addition, we compiled information on other areas for the improvement of patient prognosis using anti-EGFR receptor-based monoclonal antibody drugs and the underlying mechanisms and prognoses of new immunotherapeutic strategies for the treatment of HNSCC.

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Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), cholesteryl ester transfer protein (CETP) and apolipoprotein C3 (APOC3) are pivotal regulators of lipid metabolism, with licensed drugs targeting these genes. The use of lipid-lowering therapy via the inhibition of these genes has demonstrated a reduction in the risk of cardiovascular disease. However, concerns persist regarding their potential long-term impact on aortic diseases and calcific aortic valve disease (CAVS). This study aims to investigate causal relationships between genetic variants resembling these genes and aortic disease, as well as calcific aortic valve disease using Mendelian randomization (MR). Methods: We conducted drug-target Mendelian randomization employing summary-level statistics of low-density lipoprotein cholesterol (LDL-C) to proxy the loss-of-function of PCSK9, HMGCR, CETP and APOC3. Subsequently, we investigated the association between drug-target genetic variants and calcific aortic valve stenosis and aortic diseases, including thoracic aortic aneurysm (TAA), abdominal aortic aneurysm (AAA), and aortic dissection (AD). Results: The genetically constructed variants mimicking lower LDL-C levels were associated with a decreased risk of coronary artery disease, validating their reliability. Notably, HMGCR inhibition exhibited a robust protective effect against TAA (odds ratio (OR): 0.556, 95% CI: 0.372-0.831, p = 0.004), AAA (OR: 0.202, 95% CI: 0.107-0.315, p = 4.84 × 10-15), and AD (OR: 0.217, 95% CI: 0.098-0.480, p = 0.0002). Similarly, PCSK9, CETP and APOC3 inhibition proxies reduced the risk of AAA (OR: 0.595, 95% CI: 0.485-0.730, p = 6.75 × 10-7, OR: 0.127, 95% CI: 0.066-0.243, p = 4.42 × 10-10, and OR: 0.387, 95% CI: 0.182-0.824, p = 0.014, respectively) while showing a neutral impact on TAA and AD. Inhibition of HMGCR, PCSK9, and APOC3 showed promising potential in preventing CAVS with odds ratios of 0.554 (OR: 0.554, 95% CI: 0.433-0.707, p = 2.27 × 10-6), 0.717 (95% CI: 0.635-0.810, p = 9.28 × 10-8), and 0.540 (95% CI: 0.351-0.829, p = 0.005), respectively. However, CETP inhibition did not demonstrate any significant benefits in preventing CAVS (95% CI: 0.704-1.544, p = 0.836). The consistency of these findings across various Mendelian randomization methods, accounting for different assumptions concerning genetic pleiotropy, enhances the causal inference. Conclusions: Our MR analysis reveals that genetic variants resembling statin administration are associated with a reduced risk of AAA, TAA, AD and CAVS. HMGCR, PCSK9 and APOC3 inhibitors but not CETP inhibitors have positive benefits of reduced CAVS. Notably, PCSK9, CETP and APOC3 inhibitors exhibit a protective impact, primarily against AAA, with no discernible benefits extending to TAA or AD.

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This paper studies the adverse effect of air pollution on corporate research and development (R&D) and how sustainable development moderates this negative impact in emerging market economies (EMEs). Using a sample of 18 EMEs' firm-level data, the empirical results show that firms substantially reduce R&D expenses in the face of increasing air pollution, and this adverse effect becomes less pronounced with higher levels of sustainable development. Our analyses suggest that air pollution negatively affects R&D by increasing firms' difficulties in hiring highly skilled people or raising operation and production costs. Furthermore, we divide our sample firms into two groups according to some institutional quality factors related to sustainable development. The negative impact of air pollution on R&D is lower in countries with higher levels of institutional quality. Based on our research, to attract more R&D investment, EMEs should not only make an effort to manage air pollution but also invest more in human capital and improve their institutional quality to amplify the impact of their efforts.

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Plants are frequently exposed to herbivory and mechanical damage that results in wounding. Two fundamental strategies, regeneration and healing, are employed by plants upon wounding. It is not fully understood how plants make different decisions, and how wound healing is sustained until the damaged tissues recover. In this study, we find that the local auxin accumulation patterns, determined by wounding modes, may activate different recovery programs in wounded tissues. Wounding triggers a transient jasmonic acid (JA) signaling that promotes lignin deposition in the first few hours after wounding occurs. This early response is subsequently relayed to ABA signaling via MYC2. The induced JA signaling promotes ABA biosynthesis to maintain the expression of RAP2.6, a key factor for sustained lignin biosynthesis and the later wound healing process. Our findings provide mechanistic insights into how plants heal from wounding and elucidate the molecular mechanisms underlying the prolonged healing process following wounding.

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Soybean (Glycine max (L.) Merr) is one of the most important crops worldwide, but its yield is vulnerable to abiotic stresses. In Arabidopsis, the AlkB homologue (ALKBH) family genes plays a crucial role in plant development and stress response. However, the identification and functions of its homologous genes in soybean remain obscured. Here, we identified a total of 22 ALKBH genes in soybean and classified them into seven subfamilies according to phylogenetic analysis. Gene duplication events among the family members and gene structure, conserved domains, and motifs of all candidate genes were analyzed. By comparing the changes in the m6A levels on mRNA from hair roots between soybean seedlings harboring the empty vector and those harboring the GmALKBH10B protein, we demonstrated that all four GmALKBH10B proteins are bona fide m6A RNA demethylases in vivo. Subcellular localization and expression patterns of the GmALKBH10B revealed that they might be functionally redundant. Furthermore, an analysis of cis-elements coupled with gene expression data demonstrated that GmALKBH10B subfamily genes, including GmALKBH10B1, GmALKBH10B2, GmALKBH10B3, and GmALKBH10B4, are likely involved in the cis-elements' response to various environmental stimuli. In summary, our study is the first to report the genome-wide identification of GmALKBH family genes in soybean and to determine the function of GmALKBH10B proteins as m6A RNA demethylases, providing insights into GmALKBH10B genes in response to abiotic stresses.

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Mobility and bioavailability of hexavalent chromium (Cr(VI)) in agricultural soils are affected by interactions between Cr(VI) and returned crop straws. However, the effect of straw decomposition on Cr(VI) removal and underlying mechanisms remain unclear. In this study, Cr(VI) removal by pristine and decomposed rice/rape straws was investigated by batch experiments and a series of spectroscopies. The results showed that straw decomposition inhibited Cr(VI) removal, regardless of straw types. However, the potential mechanisms of the inhibition were distinct for the two straws. For the rice straw, a lower zeta potential after decomposition suppressed Cr(VI) sorption and subsequent reduction. In addition, less Cr(VI) was reduced by the decomposed rice straw-derived dissolved organic matter (DOM) than the pristine one. In contrast, for the rape straw, due to the increased zeta potential after decomposition, the decreased Cr(VI) removal was mainly ascribed to less Cr(VI) reduction by the rape straw-derived DOM. These results emphasized the significant roles of straw surface potential and DOM in Cr(VI) removal, depending on straw types and decomposition, which facilitate the fundamental understanding of Cr(VI) removal by straws and are helpful for predicting the environmental risk of Cr and rational straw return in Cr(VI)-contaminated fields.

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BACKGROUND: Acinetobacter baumannii (A. baumannii) has become a significant nosocomial pathogen globally over the past decade due to the increasing prevalence of antibiotic-resistant isolates. The formation of the mucoid phenotype is a crucial adaptive defense response to external pressure, but the phenotypic and genotypic characteristics and their relationship with sequence types (ST) and K locus (KL) types remain unclear. METHODS: In this study, we screened a total of 736 A. baumannii isolates, from which we identified and characterized 13 mucoid isolates. The study explored the clinical characteristics of patients with mucoid isolates, investigated the mucoid phenotype, performed capsule observation, quantified capsule production, and assessed antimicrobial susceptibility. Subsequently, whole-genome sequencing (WGS) was used to analyze the sequence types (ST), loci for capsular polysaccharide (KL), antibiotic resistance genes, virulence genes, and core-genome single-nucleotide polymorphisms (SNPs). Additionally, the virulence of all mucoid strains was evaluated through serum resistance assay, biofilm-forming assay, and Galleria mellonella survival assay. RESULTS: All mucoid A. baumannii isolates were found to be encapsulated and extremely drug-resistant. Among patients infected with these isolates, 92.3% had pulmonary infections, and the 30-day mortality rate was 61.5%. The analysis revealed that not all strains are highly virulent. Whole-genome sequencing (WGS) identified the sequence types as ST136, ST208, ST381, ST195, and ST281, and the capsular types as KL77, KL7, KL33, KL2, and KL3. The ST208 and KL7 isolates exhibited higher virulence and greater biofilm formation, with KL7 isolates also showing higher capsule production. Despite these differences, no significant variations in virulence genes were observed among the mucoid isolates, except for biofilm-associated and quorum-sensing genes. The highly virulent ST208/KL7 strains (AB276, AB313, and AB552) lacked biofilm-associated genes (csuA/BABCDE), indicating these genes do not directly cause differences in biofilm formation. CONCLUSION: The mucoid A. baumannii isolates were extensively drug-resistant, and infections caused by these isolates could lead to higher mortality. However, not all strains had high virulence, with variations likely related to specific sequence types (ST) and K locus (KL) types.