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In this work, a new method of near-infrared curing 3D printing sodium silicate sands (NIRC3DPSSS) driven by photovoltaic cells was proposed, and the Span-80 moisture resistance modifier was studied. NIRC3DPSSS had the advantages of high strength, rapid curing and low residual strength. However, the 24h storage strength would reduce because Na+ in the bonding bridges could absorb moisture. The experimental results showed that the strength of Span-80 modified sands molds reached 0.95MPa after 4 hours in a humidistat with 99%RH (relative humidity) containing 2.2% sodium silicate, an increase of 97.9% comparing to common sands molds. In air(80%RH), the strength reached 1.25MPa, an increase of 40.4%. The optimal effect of modification was achieved when Span-80 was 0.066% of the raw sands. Additionally, the bonding film and bridges in sodium silicate sands modified with Span-80 were more stable, smoother and free of cracks when observed using scanning electron microscopy (SEM) and energy dispersive spectroscopy(EDS).

Abstract Aryl hydrocarbon receptor (AhR) plays an important role in inflammation and immunity as a new therapeutic target for infectious disease and sepsis. Punicalagin (PUN) is a Chinese herbal monomer extract of pomegranate peel that has beneficial anti-inflammatory, antioxidant and anti-infective effects. However, whether PUN is a ligand of AhR, its effect on AhR expression, and its signaling pathway remain poorly understood. In this study, we found that PUN was a unique polyphenolic compound that upregulated AhR expression at the transcriptional level, and regulated the AhR nongenomic pathway. AhR expression in lipopolysaccharide-induced macrophages was upregulated by PUN in vitro and in vivo in a time- and dose-dependent manner. Using specific inhibitors and siRNA, induction of AhR by PUN depended on sequential phosphorylation of 90-kDa ribosomal S6 kinase (p90RSK), which was activated by the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphoinositide-dependent protein kinase (PDK)1 pathways. PUN promoted p90RSK-mediated activator protein-1 (AP-1) activation. AhR knockout or inhibitors reversed suppression of interleukin (IL)-6 and IL-1β expression by PUN. PUN decreased Listeria load and increased macrophage survival via AhR upregulation. In conclusion, we identified PUN as a novel selective AhR modulator involved in AhR expression via the MEK/ERK and PDK1 pathways targeting p90RSK/AP-1 in inflammatory macrophages, which inhibited macrophage inflammation and promoted bactericidal activity.

PurposeTo evaluate the predictive value of the Controlling Nutritional Status (CONUT) score and Injury Severity Score (ISS) in assessing physiological abnormalities and outcomes in trauma patients.MethodsA retrospective analysis was conducted on 354 trauma patients. Physiological parameters were assessed, including cardiovascular function, inflammatory response, liver and kidney function, and nutritional status. The CONUT score and ISS were calculated for each patient. Binary logistic regression was used to identify independent predictors of trauma severity. Receiver operating characteristic (ROC) curve analysis evaluated the predictive accuracy of the CONUT and ISS scores for adverse outcomes.ResultsSeverely injured patients exhibited more significant abnormalities in cardiovascular function, inflammatory response, liver and kidney function, and nutritional status compared to those with minor injuries. These patients had significantly higher CONUT scores. Logistic regression analysis identified white blood cell count, hemoglobin, and CONUT score as independent predictors of trauma severity. ROC analysis showed that both CONUT and ISS scores effectively predicted adverse outcomes, with ISS demonstrating better specificity.ConclusionThe CONUT and ISS scores are effective tools for predicting physiological abnormalities and adverse outcomes in trauma patients. Incorporating these scores into clinical practice may enhance prognostic assessments and improve management strategies for trauma patients.

Soybean fermentation has a balancing effect on the regulation of intestinal flora. Relative research between fermented soybeans and intestinal microbiota is limited. Our aim was to explore the effects of soybean fermented fowder on lipopolysaccharide (LPS) induced intestinal microflora and corresponding functions in loach. 16S rDNA high-throughout sequencing was applied to estimate differences in the intestinal microbiota and predict genes function. Analysis of the overall of sequencing data showed that the ratio of Effective Tags in both the control group and the treatment group was greater than 80 %. Based on six major classifications involved in the phylum, class, order, family, genus, and species, we acquired the changes in the composition of intestinal microorganisms after the supplement of soybean fermented powder. These results showed that the dominant bacteria in the two groups were basically distinct at different levels. Alpha diversity analysis indicated that the microbial richness and uniformity of soybean fermented powder decreased compared to the control group. PICRUSt and Taxfun tools analysis of intestinal flora illustrated the functional genes of the six groups were mainly involved in metabolism, genetic information processing, cellular processes, environmental information processing, and human diseases at the level 1. These data clearly demonstrated the effect of soybean fermented powder on the gut microbiome. Not only that, it provides new ideas and insights for achieving high-quality utilization of soybean fermented powder. The potential mechanisms of soybean fermented powder to alter gut flora and intestinal microbiome function can further be explored.

BackgroundHost-microbiota crosstalk has been implicated in multiple host metabolic pathway axes that regulate intestinal barrier function. Although constitutive cytochrome P4501A1 (CYP1A1) expression perturbs the microbiome-derived autoregulatory loop following enteric infection, little is known about the role of host CYP1A1 in modulating gut microbiome-mediated signaling during methicillin-resistant Staphylococcus aureus (MRSA)-induced abdominal sepsis and its effects on intestinal barrier integrity.MethodsAbdominal sepsis was induced by the intraperitoneal injection of MRSA in mice. The effect of CYP1A1 deficiency on gut barrier integrity was investigated using RNA sequencing, microbiome analyses, and targeted metabolomics. The microbiota-produced metabolites were validated in patients with sepsis and persistent MRSA infection.ResultsMice lacking CYP1A1 exhibited an altered gut microbiome, a reduced metabolic shift from lysine to cadaverine in the caecal contents and antimicrobial molecule production (Retnlb, Gbp7, and Gbp3), and they were protected against gut barrier disruption when subjected to MRSA challenge. These beneficial effects were validated in aryl hydrocarbon receptor (AHR) knockout (KO) mice by cohousing with CYP1A1 KO mice and abrogated after supplementation with cadaverine or Enterococcus faecalis, the primary microbiota genus for cadaverine synthesis. Antibiotic-driven gut dysbacteriosis impaired the survival benefit and disrupted the intestinal barrier integrity in CYP1A1 KO mice after MRSA infection. Furthermore, increased cadaverine levels in feces and serum were detected in critically ill patients with gut leakiness during persistent MRSA infection, whereas cadaverine was not detected in healthy controls. Additionally, microbiota-derived cadaverine induced enterocyte junction disruption by activating the histamine H4 receptor/nuclear factor-κB/myosin light-chain kinase signaling pathway.ConclusionThis study revealed the unexpected function of host CYP1A1 in microbiota-mediated cadaverine metabolism, with crucial consequences for dysbacteriosis following MRSA-induced abdominal sepsis, indicating that inhibiting CYP1A1 or blocking cadaverine-histamine H4 receptor signaling could be a potential therapeutic target against abdominal sepsis.Clinical Trial Registration[http://www.chictr.org.cn/index.aspx], identifier [ChiCTR1800018646].