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The development of synthetic methodologies towards enhanced performance in biomass conversion is desirable due to the growing energy demand. Here we design two types of Ru impregnated MIL-100-Cr defect engineered metal-organic frameworks (Ru@DEMOFs) by incorporating defective ligands (DLs), aiming at highly efficient catalysts for biomass hydrogenation. Our results show that Ru@DEMOFs simultaneously exhibit boosted recyclability, selectivity and activity with the turnover frequency being about 10 times higher than the reported values of polymer supported Ru towards D-glucose hydrogenation. This work provides in-depth insights into (i) the evolution of various defects in the cationic framework upon DLs incorporation and Ru impregnation, (ii) the special effect of each type of defects on the electron density of Ru nanoparticles and activation of reactants, and (iii) the respective role of defects, confined Ru particles and metal single active sites in the catalytic performance of Ru@DEMOFs for D-glucose selective hydrogenation as well as their synergistic catalytic mechanism. The catalytic performance of metal‒organic frameworks can be tuned by introducing defects in their structure. Here, the authors introduce defects and impregnate ruthenium nanoparticles in cationic metal-organic frameworks, which enables enhanced recyclability and catalytic performance in D-glucose hydrogenation.

Glycine is a major amino acid in mammals and other animals. It is synthesized from serine, threonine, choline, and hydroxyproline via inter-organ metabolism involving primarily the liver and kidneys. Under normal feeding conditions, glycine is not adequately synthesized in birds or in other animals, particularly in a diseased state. Glycine degradation occurs through three pathways: the glycine cleavage system (GCS), serine hydroxymethyltransferase, and conversion to glyoxylate by peroxisomal d-amino acid oxidase. Among these pathways, GCS is the major enzyme to initiate glycine degradation to form ammonia and CO2 in animals. In addition, glycine is utilized for the biosynthesis of glutathione, heme, creatine, nucleic acids, and uric acid. Furthermore, glycine is a significant component of bile acids secreted into the lumen of the small intestine that is necessary for the digestion of dietary fat and the absorption of long-chain fatty acids. Glycine plays an important role in metabolic regulation, anti-oxidative reactions, and neurological function. Thus, this nutrient has been used to: (1) prevent tissue injury; (2) enhance anti-oxidative capacity; (3) promote protein synthesis and wound healing; (4) improve immunity; and (5) treat metabolic disorders in obesity, diabetes, cardiovascular disease, ischemia-reperfusion injuries, cancers, and various inflammatory diseases. These multiple beneficial effects of glycine, coupled with its insufficient de novo synthesis, support the notion that it is a conditionally essential and also a functional amino acid for mammals (including pigs and humans).

Background Alteration of the gut microbiota may contribute to the development of inflammatory bowel disease (IBD). Epigallocatechin-3-gallate (EGCG), a major bioactive constituent of green tea, is known to be beneficial in IBD alleviation. However, it is unclear whether the gut microbiota exerts an effect when EGCG attenuates IBD. Results We first explored the effect of oral or rectal EGCG delivery on the DSS-induced murine colitis. Our results revealed that anti-inflammatory effect and colonic barrier integrity were enhanced by oral, but not rectal, EGCG. We observed a distinct EGCG-mediated alteration in the gut microbiome by increasing Akkermansia abundance and butyrate production. Next, we demonstrated that the EGCG pre-supplementation induced similar beneficial outcomes to oral EGCG administration. Prophylactic EGCG attenuated colitis and significantly enriched short-chain fatty acids (SCFAs)-producing bacteria such as Akkermansia and SCFAs production in DSS-induced mice. To validate these discoveries, we performed fecal microbiota transplantation (FMT) and sterile fecal filtrate (SFF) to inoculate DSS-treated mice. Microbiota from EGCG-dosed mice alleviated the colitis over microbiota from control mice and SFF shown by superiorly anti-inflammatory effect and colonic barrier integrity, and also enriched bacteria such as Akkermansia and SCFAs. Collectively, the attenuation of colitis by oral EGCG suggests an intimate involvement of SCFAs-producing bacteria Akkermansia , and SCFAs, which was further demonstrated by prophylaxis and FMT. Conclusions This study provides the first data indicating that oral EGCG ameliorated the colonic inflammation in a gut microbiota-dependent manner. Our findings provide novel insights into EGCG-mediated remission of IBD and EGCG as a potential modulator for gut microbiota to prevent and treat IBD. 1weu4UfF6nDLmdPiHVjMmd Video Abstract

Background Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme in the metabolism of tryptophan into kynurenine. It is considered to be an immunosuppressive molecule that plays an important role in the development of tumors. However, the association between IDO and solid tumor prognosis remains unclear. Herein, we retrieved relevant published literature and analyzed the association between IDO expression and prognosis in solid tumors. Methods Studies related to IDO expression and tumor prognosis were retrieved using PMC, EMbase and web of science database. Overall survival (OS), time to tumor progression (TTP) and other data in each study were extracted. Hazard ratio (HR) was used for analysis and calculation, while heterogeneity and publication bias between studies were also analyzed. Results A total of 31 studies were included in this meta-analysis. Overall, high expression of IDO was significantly associated with poor OS (HR 1.92, 95% CI 1.52–2.43, P  < 0.001) and TTP (HR 2.25 95% CI 1.58–3.22, P  < 0.001). However, there was significant heterogeneity between studies on OS (I 2  = 81.1%, P  < 0.001) and TTP (I 2  = 54.8%, P  = 0.007). Subgroup analysis showed lower heterogeneity among prospective studies, studies of the same tumor type, and studies with follow-up periods longer than 45 months. Conclusions The high expression of IDO was significantly associated with the poor prognosis of solid tumors, suggesting that it can be used as a biomarker for tumor prognosis and as a potential target for tumor therapy.

Radiofrequency ablation (RFA) promotes tumor antigen-specific T cell responses and enhances the effect of immunotherapy in preclinical settings. Here we report that the existence of remnant tumor masses due to incomplete RFA (iRFA) is associated with earlier new metastases and poor survival in patients with colorectal cancer liver metastases (CRCLM). Using mouse models, we demonstrate that iRFA promotes tumor progression and hinders the efficacy of anti-PD-1 therapy. Immune analysis reveals that iRFA induces sustained local inflammation with predominant myeloid suppressor cells, which inhibit T cell function in tumors. Mechanistically, tumor cell-derived CCL2 is critical for the accumulation of monocytes and tumor-associated macrophages (TAMs). The crosstalk between TAMs and tumor cells enhances the CCL2 production by tumor cells. Furthermore, we find that administration of a CCR2 antagonist or the loss of CCL2 expression in tumor cells enhances the antitumor activity of PD-1 blockade, providing a salvage alternative for residual tumors after iRFA. Radiofrequency ablation is used to treat metastatic colorectal cancer. In this study, the authors show that incomplete ablation of tumours results in metastases and show in mouse models that the chemokine CCL2 recruits myeloid cells to the partially ablated tumours, which can block T cell function.

Dietary phenolic acids alleviate intestinal inflammation through altering gut microbiota composition and regulating macrophage activation. However, it is unclear how individual phenolic acids affect the interactions between intestinal microbiota and macrophages in the context of inflammatory bowel disease (IBD). Here, we aim to elucidate the mechanism by which phenolic acids alleviate gut inflammation. Mice with or without depletion of macrophages were administered with four individual phenolic acids including chlorogenic, ferulic, caffeic, and ellagic acids, following dextran sulfate sodium (DSS) treatment. Gut microbiota depletion and fecal microbiota transplantation were further performed in mice to investigate the role of the gut microbiota in phenolic acid-mediated protective effect. Colitis severity was evaluated using histological, serological, and immunological measurements. Absence of intestinal microbiota and macrophage deteriorate the epithelial injury in DSS colitis. Chlorogenic acid mitigated colitis by reducing M1 macrophage polarization through suppression of pyruvate kinase M 2 (Pkm2)-dependent glycolysis and inhibition of NOD-like receptor protein 3 (Nlrp3) activation. However, ferulic acid-mediated reduction of colitis was neutrophil-dependent through diminishing the formation of neutrophil extracellular traps. On the other hand, the beneficial effects of caffeic acid and ellagic acid were dependent upon the gut microbiota. In fact, urolithin A (UroA), a metabolite transformed from ellagic acid by the gut microbiota, was found to alleviate colitis and enhance gut barrier function in an IL22-dependent manner. Overall, our findings demonstrated that the mechanisms by which phenolic acid protected against colitis were resulted from the interaction between gut microbiota and macrophage-neutrophil.

Dysregulation of small non‐coding RNA (ncRNA) is associated with various human diseases including cancer. This study aimed to evaluate the circulating exosomal small RNAs including microRNAs (miRNAs) and P‑element‑induced wimpy testis (PIWI)‐interacting RNAs (piRNAs) as sensitive and specific non‐invasive biomarkers for gastric cancer (GC) diagnosis. Serum exosomal small RNA transcriptome was examined using unique molecular identifiers (UMI) small RNA sequencing. Dysregulated miRNAs and piRNAs were verified in 70 GC patients and 60 healthy controls (HC) by reverse transcription quantitative PCR. The expressions of miR‐1307‐3p, piR‐019308, piR‐004918 and piR‐018569 in serum exosomes were significantly increased in GC group as compared to those in HC group. Moreover, GC patients with metastasis had significantly higher expression levels of piR‐004918 and piR‐019308 than GC patients without metastasis. The area under the curve (AUC) for miR‐1307‐3p, piR‐019308, piR‐004918 and piR‐018569 in the GC group was 0.845, 0.820, 0.754 and 0.732, respectively. The combination of carcinoembryonic antigen (CEA) and carbohydrate antigen (CA) 199 can improve the AUC of miR‐1307‐3p to 0.902 and piR‐019308 to 0.914 for GC diagnosis. In conclusion, our findings indicate that serum exosomal piRNAs are promising non‐invasive diagnostic biomarkers for GC patients and potential markers for monitoring metastasis.

Sodium-ion batteries (SIBs) have been proposed as a potential substitute for commercial lithium-ion batteries due to their excellent storage performance and cost-effectiveness. However, due to the substantial radius of sodium ions, there is an urgent need to develop anode materials with exemplary electrochemical characteristics, thereby enabling the fabrication of sodium-ion batteries with high energy density and rapid dynamics. Carbon materials are highly valued in the energy-storage field due to their diverse structures, low cost, and high reliability. This review comprehensively summarizes the typical structure; energy-storage mechanisms; and current development status of various carbon-based anode materials for SIBs, such as hard carbon, soft carbon, graphite, graphene, carbon nanotubes (CNTs), and porous carbon materials. This review also provides an overview of the current status and future development of related companies for sodium-ion batteries. Furthermore, it offers a summary and outlook on the challenges and opportunities associated with the design principles and large-scale production of carbon materials with high-energy-density requirements. This review offers an avenue for exploring outstanding improvement strategies for carbon materials, which can provide guidance for future application and research.

Ulcerative colitis (UC) is a debilitating inflammatory bowel disease characterized by intestinal inflammation, barrier dysfunction, and dysbiosis, with limited treatment options available. This study systematically investigates the therapeutic potential of a synbiotic composed of galactooligosaccharides (GOS) and Limosilactobacillus reuteri in a murine model of colitis, revealing that GOS and L. reuteri synergistically protect against intestinal inflammation and barrier dysfunction by promoting the synthesis of pentadecanoic acid, an odd-chain fatty acid, from Bacteroides acidifaciens . Notably, the synbiotic, B. acidifaciens , and pentadecanoic acid are each capable of suppressing intestinal inflammation and enhancing tight junction by inhibiting NF-κB activation. Furthermore, similar reduction in B. acidifaciens and pentadecanoic acid levels are also observed in the feces from both human UC patients and lipopolysaccharide-induced intestinal inflammation in pigs. Our findings elucidate the protective mechanism of the synbiotic and highlight its therapeutic potential, along with B. acidifaciens and pentadecanoic acid, for UC and other intestinal inflammatory disorders. Here, Yujun Wu and colleagues report that a synbiotic composed of galactooligosaccharides and Limosilactobacillus reuteri alleviates gut inflammation in animals by enriching pentadecanoic acid synthesis from Bacteroides acidifaciens , showing potential for treating ulcerative colitis.

Background: Metabolic associated steatohepatitis (MASH) represents a severe subtype of metabolic associated fatty liver disease (MASLD), with an increased risk of progression to cirrhosis and hepatocellular carcinoma. The nomenclature shift from nonalcoholic steatohepatitis (NASH)/nonalcoholic fatty liver disease (NAFLD) to MASH/MASLD, underscores the pivotal role of metabolic factors in disease progression. Diagnosis of MASH currently hinges on liver biopsy, a procedure whose invasive nature limits its clinical utility. This study aims to identify and validate metabolism-related genes (MRGs) markers for the non-invasive diagnosis of MASH. Methods: This study extracted multiple datasets from the GEO database to identify metabolism-related differentially expressed genes (MRDEGs). Protein-Protein Interaction (PPI) network and machine learning algorithms, including Least Absolute Shrinkage and Selection Operator (LASSO) regression, Support Vector Machine-Recursive Feature Elimination (SVM-RFE), and Random Forest (RF), were applied to screen for signature MRDEGs. The diagnostic performance of these MRDEGs was evaluated using the Receiver Operating Characteristic (ROC) curve and further validated using independent external datasets. Additionally, enrichment analysis was performed to uncover key driver pathways in MASH. The infiltration levels of various immune cell types were assessed using single sample Gene Set Enrichment Analysis (ssGSEA). Finally, Spearman correlation analysis confirmed the association between signature genes and immune cells. Results: We successfully identified seven signature MRDEGs, including CYP7A1, GCK, AKR1B10, HPRT1, GPD1, FADS2, and ENO3, through PPI network analysis and machine learning algorithms. The gene model displayed exceptional diagnostic performance in the training and validation cohorts, as evidenced by the area under ROC curve (AUC) exceeding 0.9. Further enrichment analysis revealed that signature MEDEGs were primarily involved in multiple biological pathways related to glucose and lipid metabolism. Immune infiltration analysis indicated a significant increase in the infiltration levels of activated CD8 T cells, gamma-delta T cells, natural killer cells, and CD56bright NK cells in patients with MASH. Conclusion: This study successfully identified seven signature MRDEGs as significant diagnostic biomarkers for MASH. The findings not only offer novel strategies for non-invasive diagnosis of MASH but also highlight the substantial role of immune cell infiltration in the progression of MASH.