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Herein, the modification of indium oxide thermoelectric materials was carried out to investigate the effect of Si doping on the thermoelectric properties of In2O3. By precisely controlling the doping concentration of Si, a series of Si-doped In2O3 have been successfully prepared, and the thermoelectric properties have been systematically studied. The experimental results indicate that appropriate Si doping content can optimize the band structure and carrier concentration, significantly increase the electrical conductivity and power factor of In2O3, and effectively reduce the thermal conductivity, increase the thermoelectric value (ZT value) of the material with the highest value of ∼0.316 (973 K). In addition, Si doping could enhance the Vickers hardness of the material and improve the mechanical properties of the material. This study not only provides a new idea for optimizing the performances of indium oxide thermoelectric materials, but also provides a valuable reference for the development and application of thermoelectric materials.

BackgroundThe 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.MethodsThe 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.Results9 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.ConclusionThis 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.

In2O3 based materials are one of the most promising high-temperature thermoelectric materials for application. Herein, Sm doped In2O3 samples were prepared by mechanical alloying, high-temperature calcination, and discharge plasma sintering, and the influence mechanism of rare earth element doping on the thermoelectric properties of In2O3 based semiconductors was studied. The results indicate that the electrical conductivity increased significantly. Due to the introduction of Sm impurity levels, the density of states near the Fermi level significantly increases. The bandgap widens, and the mobility first decreases and then increases. Due to the increase in carrier concentration, the absolute value of the Seebeck coefficient decreases, but the gain effect caused by the increase in conductivity is greater than the debuff caused by the decrease in the absolute value of the Seebeck coefficient. The power factor increases after Sm doping.The thermal conductivity decreases due to the decrease in Young's modulus, enhanced heterogeneous scattering, and enhanced heavy element scattering. The ZT value was raised to ∼0.327 at 973 K, obtained by Sm doped In2O3 sample with x = 0.060, which is ∼6 times as that of the pristine In2O3 sample.

ABSTRACTCurrent evidence indicates that the next-generation probiotic Akkermansia muciniphila (A. muciniphila) has therapeutic potential for nonalcoholic fatty liver disease (NAFLD), especially its inflammatory stage known as nonalcoholic steatohepatitis (NASH). However, the mechanisms of A. muciniphila in NASH prevention remain unknown. Here, A. muciniphila supplementation prevented hepatic inflammation in high-fat diet-induced NASH mice, characterized by reduced hepatic proinflammatory macrophages (M1) and γδT and γδT17 cells. Consistently, hepatic M1 and γδT cells were enriched in biopsy-proven NASH patients and high-fat/high-carbohydrate diet-induced NASH mice. Antibiotics reduced hepatic M1, γδT and γδT17 cells in NASH mice. Furthermore, A. muciniphila inhibited intestinal barrier disruption and accordingly downregulated hepatic Toll-like receptor 2 (TLR2) expression in NASH mice. The activation of TLR2 by lipoteichoic acid enriched hepatic γδT17 cells (not M1) in normal diet-fed mice and neutralized the γδT cell-lowering and liver inflammation-protecting effects of A. muciniphila in NASH mice. Additionally, activated γδT cells could promote macrophage polarization via IL−17. Our study first supported that A. muciniphila prevented NASH by modulating TLR2-activated γδT17 cells and further macrophage polarization, facilitating clinical therapeutic applications.

Abstract Background Atherosclerosis is the main pathological change in atherosclerotic cardiovascular disease, and its underlying mechanisms are not well understood. The aim of this study was to explore the hub genes involved in atherosclerosis and their potential mechanisms through bioinformatics analysis. Methods Three microarray datasets from Gene Expression Omnibus (GEO) identified robust differentially expressed genes (DEGs) by robust rank aggregation (RRA). We performed connectivity map (CMap) analysis and functional enrichment analysis on robust DEGs and constructed a protein‒protein interaction (PPI) network using the STRING database to identify the hub gene using 12 algorithms of cytoHubba in Cytoscape. Receiver operating characteristic (ROC) analysis was used to assess the diagnostic potency of the hub genes.The CIBERSORT algorithm was used to perform immunocyte infiltration analysis and explore the association between the identified biomarkers and infiltrating immunocytes using Spearman’s rank correlation analysis in R software. Finally, we evaluated the expression of the hub gene in foam cells. Results A total of 155 robust DEGs were screened by RRA and were revealed to be mainly associated with cytokines and chemokines by functional enrichment analysis. CD52 and IL1RN were identified as hub genes and were validated in the GSE40231 dataset. Immunocyte infiltration analysis showed that CD52 was positively correlated with gamma delta T cells, M1 macrophages and CD4 memory resting T cells, while IL1RN was positively correlated with monocytes and activated mast cells. RT-qPCR results indicate that CD52 and IL1RN were highly expressed in foam cells, in agreement with bioinformatics analysis. Conclusions ​This study has established that CD52 and IL1RN may play a key role in the occurrence and development of atherosclerosis, which opens new lines of thought for further research on the pathogenesis of atherosclerosis.

The structural characteristics and anti-inflammatory activity of Tremella fuciformis polysaccharides (TFPs) were investigated. The study showed that TFPs were mainly composed of mannose, rhamnose, glucuronic acid, glucose, galactose, xylose, and fucose. TFPs significantly inhibited monosodium urate (MSU)-induced inflammation of RAW264.7 cells, as well as the secretion levels of TNF-α, IL-1β, and IL-18 cytokines. The concentrations of malondialdehyde and reactive oxygen species in RAW264.7 macrophages were reduced, but superoxide dismutase activity was increased. RNA-Seq technology was applied to explore the mechanisms of TFPs ameliorating MSU-induced inflammation of RAW264.7 macrophages. Results revealed that TFPs significantly reduce MSU-stimulated inflammatory damage in RAW 264.7 cells by inhibiting signaling pathways like the hypoxia inducible factor-1 (HIF-1) signaling pathway and erythroblastic oncogene B (ErbB) signaling pathway. This study provides a foundation for TFPs to be developed as novel anti-inflammatory drugs.

Acute liver failure (ALF) has an abrupt onset with a frequently fatal outcome. Previous studies have found that oral antibiotics prevent drug-induced liver injury in animal experiments, indicating that the gut microbiota plays a critical role in the pathophysiological process. However, the underlying mechanism has not been fully understood. This study explored the comprehensive role of the gut microbiota in ALF using multi-omics. A cocktail of broad-spectrum antibiotics (Abx) pretreatment by gavage for four weeks improved the survival of D-(+)-galactosamine hydrochloride (D-Gal)/lipopolysaccharide (LPS)-induced ALF in C57BL/6 mice. RNA sequencing showed that inflammatory responses were inhibited and metabolic pathways were upregulated in the liver of Abx-treated ALF mice. The 16S rRNA gene sequencing revealed that Abx reshaped the composition and function of the gut microbiota, with an increased proportion of tryptophan (Trp) metabolism. In addition, global metabolic profiling by ultra-performance liquid chromatography–mass spectrometry (UPLC–MS) indicated that the gut microbiota post-Abx intervention reduced Trp excretion, liberated more Trp to the host, and enhanced the kynurenine (Kyn) pathway with increased production of Kyn. As an endogenous aryl hydrocarbon receptor (AhR) ligand, Kyn has anti-inflammatory and immunosuppressive effects. Furthermore, AhR-targeted treatments affected the outcome of ALF mice with or without Abx pretreatment, indicating that AhR directly regulated susceptibility to ALF, at least in part. This study demonstrates that the gut microbiota-dependent control of the Trp metabolism could regulate host susceptibility to ALF by modulating the activity of AhR, and thus provides a promising target for better management of ALF.

An experiment was conducted on the polyphenol content, flavonoid content, anthocyanin content, and antioxidant capacity of Furong plum (Prunus salicina Lindl. cv. “furong”) at different maturity stages to determine the most suitable maturity stage. The inhibition of plum polyphenols on xanthine oxidase (XOD) was measured, and its kinetics were studied to reveal the inhibitory mechanism. The experimental results showed that the polyphenol, flavonoid and anthocyanin contents of plums at the ripe stage were the highest, reaching 320.46 mg GAE/100 g FW, 204.21 mg/100 g FW, and 66.24 mg/100 g FW, respectively, in comparison those of the plums at the immature and mid-ripe stages. The antioxidant capacity of the ripe plums was stronger than it was during the other stages of the plums growth. Among them, the total polyphenols of the ripe plums exhibited the strongest antioxidant capacity (IC50 values against DPPH and hydroxyl radicals were 28.19 ± 0.67 μg/mL and 198.16 ± 7.55 μg/mL, respectively), which was between the antioxidant capacity of the free polyphenols and bound polyphenols. The major phenolic monomer compounds of plum polyphenols were flavan-3-ols (epicatechin, catechin, proanthocyanidin, and procyanidin B2), flavonols (myricetin), and phenolic acids (chlorogenic acid, ferulic acid, and protocatechuic acid). Additionally, plum polyphenols exhibited a strong inhibitory effect on XOD, with an IC50 value of 77.64 μg/mL. The inhibition kinetics showed that plum polyphenols are mixed-type inhibitors that inhibit XOD activity and that the inhibition process is reversible. The calculated values of Ki and α were 16.53 mmol/L and 0.26, respectively.

Recovery from gastrointestinal (GI) surgery is often interrupted by the unpredictable occurrence of postoperative complications, including infections, anastomotic leak, GI dysmotility, malabsorption, cancer development, and cancer recurrence, in which the implication of gut microbiota is beginning to emerge. Gut microbiota can be imbalanced before surgery due to the underlying disease and its treatment. The immediate preparations for GI surgery, including fasting, mechanical bowel cleaning, and antibiotic intervention, disrupt gut microbiota. Surgical removal of GI segments also perturbs gut microbiota due to GI tract reconstruction and epithelial barrier destruction. In return, the altered gut microbiota contributes to the occurrence of postoperative complications. Therefore, understanding how to balance the gut microbiota during the perioperative period is important for surgeons. We aim to overview the current knowledge to investigate the role of gut microbiota in recovery from GI surgery, focusing on the crosstalk between gut microbiota and host in the pathogenesis of postoperative complications. A comprehensive understanding of the postoperative response of the GI tract to the altered gut microbiota provides valuable cues for surgeons to preserve the beneficial functions and suppress the adverse effects of gut microbiota, which will help to enhance recovery from GI surgery.

Objective. To analyze the influencing factors of tumor volume, body immunity, and poor prognosis after 125I particle therapy for differentiated thyroid cancer. Methods. A total of 104 patients with differentiated TC who were treated with 125I particles during January 2020 to January 2021 was picked. These subjects were graded as low-dose group (80Gy-110Gy) and high-dose group (110Gy-140Gy) according to the minimum dose received by 90% of the target volume (D90) after surgery. The tumor volume before and after treatment was compared, and fasting venous blood was collected before and after treatment. The content of thyroglobulin (Tg) was detected by electrochemiluminescence immunoassay. The levels of absolute lymphocyte count (ALC), lymphocytes, neutrophils, and monocytes were detected on automatic blood cell analyzer. The lymphocyte to monocyte ratio (LMR), neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ration (PLR) were calculated. The changes in the condition of patients were closely observed, and the occurrence of adverse reactions in the two groups were compared. The risk factors influencing the efficacy of 125I particle therapy for differentiated TC were analyzed through multivariate logistic regression analysis. Results. The total effective rate of patients in the low- and high-dose groups was 78.85% and 82.69%, respectively (P>0.05). Compared with the pretreatment period, the tumor volume and Tg level in both groups were much lower (P0.05). At 1 week of the treatment, the total incidence of adverse reactions such as nausea, radiation gastritis, radiation parotitis, and neck discomfort was obviously higher in the high-dose group than in the low-dose group (P

The gastrointestinal (GI) tract harbors trillions of commensal microbes, called the gut microbiota, which plays a significant role in the regulation of GI physiology, particularly GI motility. The GI tract expresses an array of receptors, such as toll-like receptors (TLRs), G-protein coupled receptors, aryl hydrocarbon receptor (AhR), and ligand-gated ion channels, that sense different gut microbiota-derived bioactive substances. Specifically, microbial cell wall components and metabolites, including lipopeptides, peptidoglycan, lipopolysaccharides (LPS), bile acids (BAs), short-chain fatty acids (SCFAs), and tryptophan metabolites, mediate the effect of gut microbiota on GI motility through their close interactions with the enteroendocrine system, enteric nervous system, intestinal smooth muscle, and immune system. In turn, GI motility affects the colonization within the gut microbiota. However, the mechanisms by which gut microbiota interacts with GI motility remain to be elucidated. Deciphering the underlying mechanisms is greatly important for the prevention or treatment of GI dysmotility, which is a complication associated with many GI diseases, such as irritable bowel syndrome (IBS) and constipation. In this perspective, we overview the current knowledge on the role of gut microbiota and its metabolites in the regulation of GI motility, highlighting the potential mechanisms, in an attempt to provide valuable clues for the development of gut microbiota-dependent therapy to improve GI motility.

Blanching is a critical step in the processing of Tremella fuciformis (T. fuciformis). The effects of different blanching methods (boiling water blanching (BWB), ultrasonic-low temperature blanching (ULTB), and high-temperature steam (HTS)) on the quality and moisture migration characteristics of T. fuciformis were investigated. The results showed that the T. fuciformis blanched by ULTB (70 °C, 2 min, 40 kHz, 300 W) had the best quality, including a brighter appearance, superior texture, and good sensory features, with a polysaccharide content of 3.90 ± 0.02%. The moisture migration characteristics of T. fuciformis after blanching exhibited four peaks, displayed strong and weak chemically bound water, immobilized water, and free water, whereas ULTB had a weak effect on the freedom of water in T. fuciformis. The study will provide the foundation for the factory processing of T. fuciformis.

Acute gouty arthritis is an acute inflammatory reaction caused by the deposition of monosodium urate (MSU) crystals in joints and surrounding soft tissues. Controlling inflammation is the key to preventing acute gouty arthritis. Anti-inflammatory activities and the possible molecular mechanisms of plum (Prunus salicina Lindl cv. “furong”) polyphenols (PSLP) on RAW264.7 macrophage cells induced by monosodium urate were investigated. PPSF significantly inhibited the activity of inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-18 (IL-18). In addition, PPSF exhibited excellent activation of superoxide dismutase (SOD) activity and reduction of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels in RAW264.7 macrophages. The results of global screening of all transcripts by RNA-seq revealed 8585 differentially expressed genes between the PSLP-treated group and the MUS group. From GO analysis, PSLP could affect the occurrence and development of RAW264.7 macrophage inflammation through biological processes, such as organic substance metabolism, intracellular organelles, and binding function. The regulation mechanism of PSLP on MSU-induced RAW264.7 macrophage inflammation may be achieved through the HIF-1 signaling pathway, renal cell carcinoma, the ErbB signaling pathway, and the FoxO signaling pathway. Therefore, PSLP has great prospects in the prevention of gout and similar inflammatory diseases.

Diverse liver diseases undergo a similar pathophysiological process in which liver regeneration follows a liver injury. Given the important role of the gut-liver axis in health and diseases, the role of gut microbiota-derived signals in liver injury and regeneration has attracted much attention. It has been observed that the composition of gut microbiota dynamically changes in the process of liver regeneration after partial hepatectomy, and gut microbiota modulation by antibiotics or probiotics affects both liver injury and regeneration. Mechanically, through the portal vein, the liver is constantly exposed to gut microbial components and metabolites, which have immense effects on the immunity and metabolism of the host. Emerging data demonstrate that gut-derived lipopolysaccharide, gut microbiota-associated bile acids, and other bacterial metabolites, such as short-chain fatty acids and tryptophan metabolites, may play multifaceted roles in liver injury and regeneration. In this perspective, we provide an overview of the possible molecular mechanisms by which gut microbiota-derived signals modulate liver injury and regeneration, highlighting the potential roles of gut microbiota in the development of gut microbiota-based therapies to alleviate liver injury and promote liver regeneration.

Traumatic brain injury (TBI) is a common cause of disability and mortality, affecting millions of people every year. The neuroinflammation and immune response post-TBI initially have neuroprotective and reparative effects, but prolonged neuroinflammation leads to secondary injury and increases the risk of chronic neurodegenerative diseases. Persistent microglial activation plays a critical role in chronic neuroinflammation post-TBI. Given the bidirectional communication along the brain–gut axis, it is plausible to suppose that gut microbiota dysbiosis post-TBI influences microglial activation. In the present study, hippocampal microglial activation was observed at 7 days and 28 days post-TBI. However, in TBI mice with a depletion of gut microbiota, microglia were activated at 7 days post-TBI, but not at 28 days post-TBI, indicating that gut microbiota contributes to the long-term activation of microglia post-TBI. In addition, in conventional mice colonized by the gut microbiota of TBI mice using fecal microbiota transplant (FMT), microglial activation was observed at 28 days post-TBI, but not at 7 days post-TBI, supporting the role of gut microbiota dysbiosis in persistent microglial activation post-TBI. The RNA sequencing of the hippocampus identified a microglial activation gene, Lyz2, which kept upregulation post-TBI. This persistent upregulation was inhibited by oral antibiotics and partly induced by FMT. 16s rRNA gene sequencing showed that the composition and function of gut microbiota shifted over time post-TBI with progressive dysbiosis, and untargeted metabolomics profiling revealed that the tryptophan metabolic phenotype was differently reshaped at 7 days and 28 days post-TBI, which may play a role in the persistent upregulation of Lyz2 and the activation of microglia. This study implicates that gut microbiota and Lyz2 are potential targets for the development of novel strategies to address persistent microglial activation and chronic neuroinflammation post-TBI, and further investigations are warranted to elucidate the specific mechanism.