Exploring the diversity of dissolved organic matter (DOM) properties and sources in different functional areas of a typical macrophyte - derived lake combined with optical spectroscopy and FT-ICR MS analysis.

Lake Baiyangdian is one of China's largest macrophyte - derived lakes, facing severe challenges related to water quality maintenance and eutrophication prevention. Dissolved organic matter (DOM) was a huge carbon pool and its abundance, property, and transformation played important roles in the biogeochemical cycle and energy flow in lake ecosystems. In this study, Lake Baiyangdian was divided into four distinct areas: Unartificial Area (UA), Village Area (VA), Tourism Area (TA), and Breeding Area (BA). We examined the diversity of DOM properties and sources across these functional areas. Our findings reveal that DOM in this lake is predominantly composed of protein - like substances, as determined by excitation - emission matrix and parallel factor analysis (EEM - PARAFAC). Notably, the exogenous tyrosine-like component C1 showed a stronger presence in VA and BA compared to UA and TA. Ultrahigh - resolution mass spectrometry (FT - ICR MS) unveiled a similar DOM molecular composition pattern across different functional areas due to the high relative abundances of lignan compounds, suggesting that macrophytes significantly influence the material structure of DOM. DOM properties exhibited specific associations with water quality indicators in various functional areas, as indicated by the Mantel test. The connections between DOM properties and NO3N and NH3N were more pronounced in VA and BA than in UA and TA. Our results underscore the viability of using DOM as an indicator for more precise and scientific water quality management.

Selenium deficiency exacerbates ROS/ER stress mediated pyroptosis and ferroptosis induced by bisphenol A in chickens thymus.

Bisphenol A (BPA) is an industrial pollutant that can cause immune impairment. Selenium acts as an antioxidant, as selenium deficiency often accompanies oxidative stress, resulting in organ damage. This study is the first to demonstrate that BPA and/or selenium deficiency induce pyroptosis and ferroptosis-mediated thymic injury in chicken and chicken lymphoma cell (MDCC-MSB-1) via oxidative stress-induced endoplasmic reticulum (ER) stress. We established a broiler chicken model of BPA and/or selenium deficiency exposure and collected thymus samples as research subjects after 42 days. The results demonstrated that BPA or selenium deficiency led to a decrease in antioxidant enzyme activities (T-AOC, CAT, and GSH-Px), accumulation of peroxides (H2O2 and MDA), significant upregulation of ER stress-related markers (GRP78, IER 1, PERK, EIF-2α, ATF4, and CHOP), a significant increase in iron ion levels, significant upregulation of pyroptosis-related gene (NLRP3, ASC, Caspase1, GSDMD, IL-18 and IL-1ß), significantly increase ferroptosis-related genes (TFRC, COX2) and downregulate GPX4, HO-1, FTH, NADPH. In vitro experiments conducted in MDCC-MSB-1 cells confirmed the results, demonstrating that the addition of antioxidant (NAC), ER stress inhibitor (TUDCA) and pyroptosis inhibitor (Vx765) alleviated oxidative stress, endoplasmic reticulum stress, pyroptosis, and ferroptosis. Overall, this study concludes that the combined effects of oxidative stress and ER stress mediate pyroptosis and ferroptosis in chicken thymus induced by BPA exposure and selenium deficiency.

Biosynthesis of a Functional Fragment of Human Collagen II in Pichia pastoris.

Collagen II (COL2) is the major component of cartilage tissue and is widely applied in pharmaceuticals, food, and cosmetics. In this study, COL fragments were extracted from human COL2 for secretory expression in Pichia pastoris. Three variants were successfully secreted by shake flask cultivation with a yield of 73.3-100.7 mg/L. The three COL2 variants were shown to self-assemble into triple-helix at 4 °C and capable of forming higher order assembly of nanofiber and hydrogel. The bioactivities of the COL2 variants were validated, showing that sample 205 exhibited the best performance for inducing fibroblast differentiation and cell migration. Meanwhile, sample 205 and 209 exhibited higher capacity for inducing in vitro blood clotting than commercial mouse COL1. To overexpress sample 205, the expression cassettes were constructed with different promoters and signal peptides, and the fermentation condition was optimized, obtaining a yield of 172 mg/L for sample 205. Fed-batch fermentation was carried out using a 5 L bioreactor, and the secretory protease Pep4 was knocked out to avoid sample degradation, finally obtaining a yield of 3.04 g/L. Here, a bioactive COL2 fragment was successfully identified and can be overexpressed in P. pastoris; the variant may become a potential biomaterial for skin care.

Enhancing interfacial electron transfer through PANI electron bridge for tailoring dynamic reconstruction and achieving high-performance water oxidation.

Tailoring the dynamic reconstruction of transition metal compounds into highly active oxyhydroxides through surface electron state modification is crucial for advancing water oxidation, yet remains a formidable challenge. In this study, a unique polyaniline (PANI) electron bridge was integrated into the metal-organic frameworks (MOFs)/layer double hydroxides (LDHs) heterojunction to expedite electron transfer from MOFs to LDHs, facilitating electron accumulation at the metal sites within MOF and electron-deficient LDHs. This configuration promotes the surface dynamic reconstruction of LDHs into highly active oxyhydroxides while safeguarding the MOF from corrosion in harsh environments over extended periods. The optimized electronic structure modification of both MOFs and LDHs enhances reaction kinetics. The superior MIL-88B(Fe)@PANI@NiCo LDH catalyst achieved 10 mA∙cm-2 at an overpotential of 202 mV and demonstrated stable operation for 120 h at this current density. This research introduces an innovative approach for guiding electron transfer and dynamic catalyst reconstruction by constructing a PANI electron bridge, potentially paving the way for more efficient catalytic systems.

Management of oblique root fracture in the middle third of two maxillary immature central incisors with severe caries in mixed dentitions: a case report.

Mid-root fractures are rare injuries in young permanent teeth and tend to have poor prognoses. This study presents a case of oblique root fracture of both maxillary immature central incisors in the middle third accompanied by delayed dental visit and severe caries of all primary teeth. After restoring all the primary and permanent teeth that needed stabilization, the coronal fragments were repositioned and stabilized with a flexible splint consisting of orthodontic wire and composite resin. A comprehensive and sequential dental treatment for other oral diseases and oral hygiene instructions were provided. A 16-month follow-up revealed that the two injured young permanent incisors were healed, surrounded by hard tissues and continued to grow both in length of the root and thickness of the root canal wall, with significant improvement in oral hygiene. Based on the outcome of this case, initial stabilization without endodontic therapy could be considered a successful treatment modality for young permanent teeth with oblique root fracture due to the growth of fractured teeth with vital pulp and the maintenance of natural dentition.

Analysis of surgical complexity and short-term prognostic indicators in NSCLC patients: neoadjuvant targeted therapy versus neoadjuvant chemoimmunotherapy.

Background: Neoadjuvant therapy improves survival benefits in patients with locally advanced non-small cell lung cancer but increases tissue density, presenting challenges for surgeons. Objectives: To compare the differences in surgical complexity and short-term prognostic outcomes between neoadjuvant targeted therapy (NTT) and neoadjuvant chemoimmunotherapy (NCI). Design/methods: This study enrolled 106 patients underwent curative surgery after neoadjuvant therapy between January 2020 and December 2023 at the National Cancer Center of China. Differences in surgical complexity and short-term prognostic outcomes between the two neoadjuvant therapy cohorts were evaluated. The pathological indicators such as pathological response rate and lymph node upstaging/downstaging were then analyzed. Results: In total, 33 patients underwent NTT and 73 underwent NCI preoperatively. Patients who received NTT showed a higher minimally invasive surgery rate (84.8% versus 53.4%, p < 0.01), shorter operative time (144 versus 184 min, p < 0.01), lower conversion rate (3.3% versus 17.8%, p = 0.03), less postoperative drainage (day 3: 140 versus 200 mL, p = 0.03), and lower incidence of postoperative complications including arrhythmias (6.1% versus 26%, p = 0.02). The pathological response rate in the NTT and NCI groups was 70% and 75%, respectively, with the latter group showing a higher complete pathological response rate. The two groups had no significant differences in major pathological response and lymph node pathological response rate. Conclusion: Patients who received NTT presented fewer surgical challenges for surgeons and had better surgical outcomes than those who received NCI therapy, with comparable pathological response rates between the two cohorts. Accordingly, NTT is the preferred induction regimen for patients harboring mutation status.

CPT1A-IL-10-mediated macrophage metabolic and phenotypic alterations ameliorate acute lung injury.

BACKGROUND: Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common acute respiratory failure due to diffuse pulmonary inflammation and oedema. Elaborate regulation of macrophage activation is essential for managing this inflammatory process and maintaining tissue homeostasis. In the past decades, metabolic reprogramming of macrophages has emerged as a predominant role in modulating their biology and function. Here, we observed reduced expression of carnitine palmitoyltransferase 1A (CPT1A), a key rate-limiting enzyme of fatty acid oxidation (FAO), in macrophages of lipopolysaccharide (LPS)-induced ALI mouse model. We assume that CPT1A and its regulated FAO is involved in the regulation of macrophage polarization, which could be positive regulated by interleukin-10 (IL-10). METHODS: After nasal inhalation rIL-10 and/or LPS, wild type (WT), IL-10-/-, Cre-CPT1Afl/fl and Cre+CPT1Afl/fl mice were sacrificed to harvest bronchoalveolar lavage fluid, blood serum and lungs to examine cell infiltration, cytokine production, lung injury severity and IHC. Bone marrow-derived macrophages (BMDMs) were extracted from mice and stimulated by exogenous rIL-10 and/or LPS. The qRT-PCR, Seahorse XFe96 and FAO metabolite related kits were used to test the glycolysis and FAO level in BMDMs. Immunoblotting assay, confocal microscopy and fluorescence microplate were used to test macrophage polarization as well as mitochondrial structure and function damage. RESULTS: In in vivo experiments, we found that mice lacking CPT1A or IL-10 produced an aggravate inflammatory response to LPS stimulation. However, the addition of rIL-10 could alleviate the pulmonary inflammation in mice effectively. IHC results showed that IL-10 expression in lung macrophage decreased dramatically in Cre+CPT1Afl/fl mice. The in vitro experiments showed Cre+CPT1Afl/fl and IL-10-/- BMDMs became more "glycolytic", but less "FAO" when subjected to external attacks. However, the supplementation of rIL-10 into macrophages showed reverse effect. CPT1A and IL-10 can drive the polarization of BMDM from M1 phenotype to M2 phenotype, and CPT1A-IL-10 axis is also involved in the process of maintaining mitochondrial homeostasis. CONCLUSIONS: CPT1A modulated metabolic reprogramming and polarisation of macrophage under LPS stimulation. The protective effects of CPT1A may be partly attributed to the induction of IL-10/IL-10 receptor expression.

Diagnostic efficacy of SEPT9 and PAX5 gene methylation in gastrointestinal cancer and precancerous lesions.

To assess the diagnostic efficacy of SEPT9 along with PAX5 gene methylation detection in gastrointestinal cancer and precancerous lesions, the peripheral blood of 62 patients with gastric cancer (GC) and 60 patients with no evidence of disease (as the control group) were retrospectively collected. The methylation rates of PAX5 and SEPT9 gene promoters in blood samples of GC group were detected by PCR. At the same time, the differences in methylation rates of genes in the two groups were compared, and the predictive value of plasma methylation PAX5 and SEPT9 in GC was evaluated by receiver operating characteristic (ROC) curve. We found that there were 41 cases of methylated PAX5 gene promoter region and 39 cases of methylated SEPT9 gene promoter region in GC group. The control group contained 14 cases of PAX5 gene promoter methylation and 12 cases of RNF¹80 gene promoter methylation. The occurrence of PAX5 promoter methylation was correlated with age of GC patients. There were statistically significant differences in mSEPT9 gene in patients with different TNM stages. Kaplan-Meier survival curve analysis revealed that the three-year overall survival rate of GC patients with PAX5 methylation was lower than that of GC patients without PAX5 methylation. No significant difference was discovered in 3-year overall survival rate between GC patients with SEPT9 methylation and those without SEPT9 methylation. Combined detection could not improve the diagnostic value of GC, but could promote diagnosis sensitivity. In summary, the risk of PAX5 and SEPT9 gene methylation in GC patients presents higher when compared with healthy people. PAX5 gene methylation is closely related to age, while SEPT9 is closely related to tumor TNM stage, and PAX5 gene methylation can decrease the survival rate of GC patients. Detection of PAX5 gene methylation level can assist in evaluating the prognosis of GC patients.

Loss of tumor suppressors promotes inflammatory tumor microenvironment and enhances LAG3+T cell mediated immune suppression.

Low response rate, treatment relapse, and resistance remain key challenges for cancer treatment with immune checkpoint blockade (ICB). Here we report that loss of specific tumor suppressors (TS) induces an inflammatory response and promotes an immune suppressive tumor microenvironment. Importantly, low expression of these TSs is associated with a higher expression of immune checkpoint inhibitory mediators. Here we identify, by using in vivo CRISPR/Cas9 based loss-of-function screening, that NF1, TSC1, and TGF-ß RII as TSs regulating immune composition. Loss of each of these three TSs leads to alterations in chromatin accessibility and enhances IL6-JAK3-STAT3/6 inflammatory pathways. This results in an immune suppressive landscape, characterized by increased numbers of LAG3+ CD8 and CD4 T cells. ICB targeting LAG3 and PD-L1 simultaneously inhibits metastatic progression in preclinical triple negative breast cancer (TNBC) mouse models of NF1-, TSC1- or TGF-ß RII- deficient tumors. Our study thus reveals a role of TSs in regulating metastasis via non-cell-autonomous modulation of the immune compartment and provides proof-of-principle for ICB targeting LAG3 for patients with NF1-, TSC1- or TGF-ß RII-inactivated cancers.

Ferroptosis-Related Gene Signatures in Epilepsy: Diagnostic and Immune Insights.

Epilepsy is characterized by a multifaceted aetiology. Ferroptosis has recently been implicated in seizure pathophysiology, although its mechanistic role in epilepsy remains obscure. We examined the roles of ferroptosis-related genes (FRGs) in epilepsy cohorts from the GSE143272 dataset. We investigated the associations between gene expression and the immune response by performing CIBERSORT and MCP-counter analyses. By employing unsupervised consensus clustering and weighted gene coexpression network analysis (WGCNA), we delineated robust gene clusters across cohorts. Single-cell RNA sequencing data from the GSE201048 dataset provided insights into the interactions between pivotal ferroptosis-related genes and immune cells. Additionally, we employed qRT‒PCR technology to measure the levels of these central genes in the tissues of epileptic patients and mice. Our findings revealed seven pivotal genes (TFRC, POR, PTGS2, RELA, PGD, TRIM21, and QSOX1) at the forefront in epilepsy specimens. A diagnostic model harnessing these genes exhibited substantial efficacy (AUC = 0.913). Similarly, the qRT‒PCR analysis of samples from epileptic patients and mouse epileptic brain tissues substantiated these findings. Stratification of 91 patients with epilepsy via WGCNA, based on gene expression, revealed distinct immunological profiles. The scRNA-seq data further indicated increased expression of central genes in macrophages and microglia. Notably, these cells and those with elevated ferroptosis scores were significantly enriched in inflammation-related pathways. These findings support the strong involvement of FRGs in the pathogenesis of epilepsy, particularly neuroinflammation. These central genes hold promise as novel diagnostic biomarkers for epilepsy.

A study on the impact of acute exercise on cognitive function in Alzheimer's disease or mild cognitive impairment patients: A narrative review.

This narrative review follows the JBI approach and comprehensively explores the effects and mechanisms of acute exercise on cognitive function in Alzheimer's disease (AD) and Mild cognitive impairment (MCI) patients. The results showed that the combination of acute exercise and cognitive training improved the cognitive function of AD patients better than aerobic exercise or resistance training alone. For patients with MCI, moderate intensity acute aerobic exercise and resistance exercise were beneficial to enhance Inhibitory control (IC), but high-intensity acute exercise was adverse to improve IC; Brain-derived neurotrophic factor (BDNF) and Insulin-like growth factor 1 (IGF-1) may assume the potential mediating mechanism of acute exercise on cognitive function in AD and MCI patients, but more research is needed to further confirm this mechanism.

Unveiling Atomic-Scaled Local Chemical Order of High-Entropy Intermetallic Catalyst for Alkyl-Substitution-Dependent Alkyne Semihydrogenation.

High-entropy intermetallic (HEI) nanocrystals, composed of multiple elements with an ordered structure, are of immense interest in heterogeneous catalysis due to their unique geometric and electronic structures and the cocktail effect. Despite tremendous efforts dedicated to regulating the metal composition and structures with advanced synthetic methodologies to improve the performance, the surface structure, and local chemical order of HEI and their correlation with activity at the atomic level remain obscure yet challenging. Herein, by determining the three-dimensional (3D) atomic structure of quinary PdFeCoNiCu (PdM) HEI using atomic-resolution electron tomography, we reveal that the local chemical order of HEI regulates the surface electronic structures, which further mediates the alkyl-substitution-dependent alkyne semihydrogenation. The 3D structures of HEI PdM nanocrystals feature an ordered (intermetallic) core enclosed by a disordered (solid-solution) shell rather than an ordered surface. The lattice mismatch between the core and shell results in apparent near-surface distortion. The chemical order of the intermetallic core increases with annealing temperature, driving the electron redistribution between Pd and M at the surface, but the surface geometrical (chemically disordered) configurations and compositions are essentially unchanged. We investigate the catalytic performance of HEI PdM with different local chemical orders toward semihydrogenation across a broad range of alkynes, finding that the electron density of surface Pd and the hindrance effect of alkyl substitutions on alkynes are two key factors regulating selective semihydrogenation. We anticipate that these findings on surface atomic structure will clarify the controversy regarding the geometric and/or electronic effects of HEI catalysts and inspire future studies on tuning local chemical order and surface engineering toward enhanced catalysts.

Based on network pharmacology and molecular docking to explore the potential mechanism of shikonin in periodontitis.

OBJECTIVES: To investigate the potential mechanisms of shikonin in preventing and treating periodontitis using network pharmacology and molecular docking methods. MATERIALS AND METHODS: The targets of shikonin were obtained in TCMSP and SEA databases, and targets of periodontitis were gathered from the OMIM, GeneCards and Drugbank Databases. The intersecting targets were entered into the DAVID database to obtain the relevant biological functions and pathways by GO and KEGG enrichment analysis. The obtained targets were analysed the protein-protein interaction (PPI) in STRING platform. In Cytoscape 3.8.0, the network analysis function with the MCODE plug-in were used to obtain the key targets, of shikonin and periodontitis. Molecular docking and molecular dynamics simulation (MD) were used to assess the affinity between the shikonin and the key targets. RESULTS: Shikonin was screened for 22 targets and periodontitis was screened for 944 targets, the intersecting targets were considered as potential therapeutic targets. The targets played important roles in cellular response to hypoxia, response to xenobiotic stimulus and positive regulates of apoptotic process by GO enrichment analysis. 10 significant pathways were analyzed by KEGG, such as human cytomegalovirus infection and PI3K-Akt signaling pathway, etc. Cytoscape software screened the key genes including AKT1, CCL5, CXCR4, PPARG, PTEN, PTGS2 and TP53. Molecular docking and MD results showed that shikonin could bind stably to the targets. CONCLUSIONS: The present study enriched the molecular mechanisms in periodontitis with shikonin, providing potential therapeutic targets for periodontitis.

BUB1 potentiates gastric cancer proliferation and metastasis by activating TRAF6/NF-κB/FGF18 through m6A modification.

AIMS: Gastric cancer (GC) is one of the most common malignant tumors of the digestive system. High expression of the mitotic kinase BUB1 has been shown to be associated with the development of many cancers, but the role of BUB1 in GC is still unclear. The current study aimed to investigate the role of BUB1 in GC. MATERIALS AND METHODS: BUB1 inhibitor, siRNA or BUB1 overexpression plasmid-mediated functional studies were performed in vitro and in vivo to explore the oncogenic role of BUB1 in GC. The expression of BUB1 and FGF18 in GC tumor samples was determined by IHC staining. RNA-seq, Western blot, MeRIP-qPCR and Co-IP assays were used to investigate the molecular mechanisms by which BUB1 regulates GC progression. KEY FINDINGS: Knockdown of BUB1 significantly inhibited the proliferation and metastasis of GC cells in vitro and in vivo. Moreover, overexpression of BUB1 significantly promoted the proliferation, migration and invasion of GC cells. High expression of BUB1 and FGF18 in GC tissues predicted poor prognosis in GC patients. Mechanistically, BUB1 interacted with METTL3 and induced m6A modification of TRAF6 mRNA, further activating the NF-κB/FGF18 axis in GC cells. SIGNIFICANCE: Our results confirmed that BUB1 acts as a positive regulator of GC cell proliferation and metastasis by activating the TRAF6/NF-κB/FGF18 pathway through METTL3-mediated m6A methylation. Targeting the BUB1/METTL3/TRAF6/NF-κB/FGF18 axis might be a novel diagnostic and therapeutic strategy in GC.

Interfacial delivery of carbon monoxide via smart titanium implant coating for enhanced soft tissue integration with switchable antibacterial and immunomodulatory properties.

Soft tissue integration around titanium (Ti) implants is weaker than that around natural teeth, compromising long-term success of Ti implants. Carbon monoxide (CO) possesses distinctive therapeutic properties, rendering it as a highly promising candidate for enhancing STI. However, achieving controlled CO generation at the STI interface remains challenging. Herein, a controlled CO-releasing dual-function coating was constructed on Ti surfaces. Under near-infrared (NIR) irradiation, the designed surface could actively accelerate CO generation for antibiosis against both aerobic and anaerobic bacteria. More importantly, in the absence of NIR, the slow release of CO induces macrophage polarization from pro-inflammatory phenotype towards pro-regenerative phenotype. In a rat implantation model with induced infection, the designed surface effectively controlled the bacterial infection, alleviates accompanying inflammation and modulated immune microenvironment, leading to enhanced STI. Single-cell sequencing revealed that the coating alters the cytokine profile within the soft tissue, thereby influencing cellular functions. Differentially expressed genes in macrophages are highly enriched in the PIK3-Akt pathway. Furthermore, the cellular communication between fibroblasts and macrophages was significantly enhanced through the CXCL12/CXCL14/CXCR4 and CSF1-CSF1R ligand-receptor pair. These findings indicate that our coating showed an appealing prospect for enhancing STI around Ti implants, which would ultimately contribute to the improved long-term success of Ti implants.

Modulating the Bader Charge Transfer in Single p-Block Atoms Doped Pd Metallene for Enhanced Oxygen Reduction Electrocatalysis.

Metallene is considered as an emerging family of electrocatalysts due to its atomically layered structure and unique surface stress. Here we propose a strategy to modulate the Bader charge transfer (BCT) between Pd surface and oxygenated intermediates via p-d electronic interaction by introducing single-atomp-block metal (M = In, Sn, Pb, Bi) into Pd metallene nanosheets towards efficient oxygen reduction reaction (ORR). X-ray absorption and photoelectron spectroscopy suggests that doping p-block metals could facilitate electron transfer to Pd sites and thus downshift the d-band center of Pd and weaken the adsorption energy of O intermediates. Among them, the developed Bi-Pd metallene shows extraordinarily high ORR mass activity of 11.34 A mgPd-1 and 0.86 A mgPd-1 at 0.9 V and 0.95 V in alkaline solution, respectively, representing the best Pd-based ORR electrocatalysts ever reported. In the cathode of a Zinc-air battery, Bi-Pd metallene could achieve an open-circuit voltage of 1.546 V and keep stable for 760 h at 10 mA cm-2. Theoretical calculations suggest that the BCT between Pd surface and *OO intermediates greatly affects the bond length between them (dPd-*OO) and Bi doping could appropriately reduce the amount of BCT and stretch the dPd-*OO, thus enhancing the ORR activity.

Intestinal epithelial Cldn-7 regulates intestinal inflammation by altering the gut microbiota.

BACKGROUND AND AIM: Tight junctions maintain gut homeostasis by forming a physical barrier that protects the gut from invasion by microbiota. Cldn-7 is an important component involved in this protection, but the relationship between Cldn-7, intestinal inflammation, and gut microbiota has not been clarified. Here, we hypothesize that Cldn-7 depletion affects intestinal inflammation by altering the gut microbiota. METHODS: Based on the induced intestinal condition of Cldn-7 knockout mice (Cldn7fl/fl;villin-CreaERT2), we established the intestinal flora depletion model and colitis model by antibiotic drinking and feeding with dextran sodium sulfate (DSS). The environment of Cldn-7 gene deletion mice was changed by co-housing experiment. AB-PAS staining and Muc2 were used to detect the effect of co-housing and Cldn-7 deficiency on the mucus layer after flora depletion. qRT-PCR was used to detect the expression of intestinal inflammatory factors and AMPs in mice. Feces were collected and proportions of microbiota were analyzed by 16 S rRNA amplicon sequencing. RESULTS: Mice in the co-housing experiment had altered intestinal microbiota, including diversity, composition, and functional prediction, compared to controls. Intestinal inflammation was restored to some extent following altered intestinal microbiota. The intestinal inflammation caused by Cldn-7 deficiency and susceptibility to DSS could be reduced after antibiotic administration compared to controls, in terms of phenotype, pathological changes, inflammatory factors, mucus barrier, and expression of AMPs. CONCLUSIONS: In analyses of intestinal tissues, colitis induction, and gut microbiota in mice with intestinal disruption of Cldn-7, we found this protein to prevent intestinal inflammation by regulating the gut microbiota. Cldn-7might therefore be an important mediator of host-microbiome interactions. Our research has revealed that Cldn-7 plays an indispensable role in maintaining intestinal homeostasis by regulating the gut microbiota and impacting intestinal inflammation. These findings provide new insights into the pathogenesis of ulcerative colitis.

A Piezoelectric Nanogenerator-Driven Dual-Mode Platform for Visualization and Impedance Sensing.

Traditional visual biosensing platforms rely on color to display detection results, which can be influenced by individual visual abilities, equipment, parameters, and lighting conditions during photo capture. This limitation significantly impedes the advancement of next-generation portable electrochemical biosensors. Therefore, we propose a visual biosensing device that utilizes distance as an indicator, enabling the facile determination of the length of discoloration, which is inversely proportional to the concentration of the target analyte. The separation of the Signal Generation (SG) and Signal Output (SO) regions effectively mitigates potential interference from the sample color. Additionally, the SG region can be disassembled to facilitate electrochemical impedance spectroscopy (EIS) detection in laboratory settings, enabling dual-mode detection. Meanwhile, the utilization of piezoelectric nanogenerators (PENG) empowers the entire point-of-care testing (POCT) sensing device, effectively addressing the issue of a limited battery life. The biosensing device exhibited a satisfactory linear range (EIS mode, 5 pg/L to 5 mg/L; visual mode, 0.5 ng/L to 5 mg/L) and a low limit of detection (EIS mode, 2.3 pg/L; visual mode, 0.14 ng/L) with S/N = 3 for ochratoxin A (OTA) under optimized conditions. The self-powered and cost-effective dual-mode biosensing platform developed for OTA detection offers clear and easily interpretable results, demonstrating a high accuracy in laboratory settings.

RNA-Seq Reveals Pathways Responsible for Meat Quality Characteristic Differences between Two Yunnan Indigenous Chicken Breeds and Commercial Broilers.

Poultry is a source of meat that is in great demand in the world. The quality of meat is an imperative point for shoppers. To explore the genes controlling meat quality characteristics, the growth and meat quality traits and muscle transcriptome of two indigenous Yunnan chicken breeds, Wuding chickens (WDs) and Daweishan mini chickens (MCs), were compared with Cobb broilers (CBs). The growth and meat quality characteristics of these two indigenous breeds were found to differ from CB. In particular, the crude fat (CF), inosine monophosphate content, amino acid (AA), and total fatty acid (TFA) content of WDs were significantly higher than those of CBs and MCs. In addition, it was found that MC pectoralis had 420 differentially expressed genes (DEGs) relative to CBs, and WDs had 217 DEGs relative to CBs. Among them, 105 DEGs were shared. The results of 10 selected genes were also confirmed by qPCR. The differentially expressed genes were six enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathways including lysosomes, phagosomes, PPAR signaling pathways, cell adhesion molecules, cytokine-cytokine receptor interaction, and phagosome sphingolipid metabolism. Interestingly, four genes (LPL, GK, SCD, and FABP7) in the PPAR signal pathway related to fatty acid (FA) metabolism were elevated in WD muscles, which may account for higher CF, inosine monophosphate content, and AA and FA contents, key factors affecting meat quality. This work laid the foundation for improving the meat quality of Yunnan indigenous chickens, especially WD. In future molecular breeding, the genes in this study can be used as molecular screening markers and applied to the molecular breeding of chicken quality characteristics.

Mechanism of N2O formation in catalytic after-treatment systems of ammonia/hydrogen-fuelled engines.

The combustion processes and catalytic after-treatment of ammonia/hydrogen-fueled engines, including NOx storage and reduction (NSR) and noble-metal selective catalytic reduction (SCR), can produce the byproduct N2O, a potent greenhouse gas that weakens the zero-carbon attribute of these fuels. Currently, the mechanism of N2O formation on DeNOx catalysts remains unclear due to limited research on catalytic after-treatment for such engines and the complexity of surface catalytic reactions. To elucidate the formation of N2O on the DeNOx catalysts of ammonia/hydrogen fuel engines, the impact factors on N2O formation on platinum catalysts (typical catalysts in NSR and noble-metal SCR) were investigated using first-principles molecular dynamics (FPMD). By employing the blue-moon ensemble enhanced sampling method and the slow-growth approach for free energy surface exploration, together with density functional theory (DFT) for electronic structure analysis, a linear relationship between the spin splitting of the d states of Pt clusters and N2O formation energy barriers was revealed, along with the increased structural sensitivity of Pt clusters with fewer atoms. It is highlighted that the energy barrier for N2O formation is determined by the matching degree of energy levels between molecules and surfaces. These findings provide atomic-scale insights into N2O formation on DeNOx catalysts for ammonia/hydrogen-fueled engines, facilitating N2O emission control for carbon-free engines.