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Liver inflammation could be elicited by swainsonine in livestock, affecting the development of agriculture and animal husbandry. Our previous study showed an important role of bile acids (BAs) in swainsonine-induced hepatic inflammation. However, its pathogenesis, particularly the roles of a comprehensive profile of liver and serum metabolites and microbial-derived indole metabolites, has not been clarified. This study aimed to demonstrate the mechanisms linking the indole-producing bacteria and indole metabolites to swainsonine-induced hepatic inflammation by combining Targeted 500 metabolomics and quantitative analysis of indole metabolites. Swainsonine significantly disturbed the liver and serum metabolomes in mice. Genus Akkermansiaalleviating inflammation and genus Lactobacillusproducing indole metabolites were significantly declined. Indole acetic acid (IAA) was the only reduced aryl hydrocarbon receptor (AHR) ligand in this study. Analogously, some bacteria causing liver damage markedly increased. These findings suggested that indole-producing bacteria and indole metabolites may be potential triggers of swainsonine-induced hepatic inflammation.

Objective: The incidence of pulmonary nodules has been increasing over the past 30 years. Different types of nodules are associated with varying degrees of malignancy, and they engender inconsistent treatment approaches. Therefore, correct distinction is essential for the optimal treatment and recovery of the patients. The commonly-used medical imaging methods have limitations in distinguishing lung nodules to date. A new approach to this problem may be provided by electrical properties of lung nodules. Nevertheless, difference identification is the basis of correct distinction. So, this paper aims to investigate the differences in electrical properties between various lung nodules. Methods: At variance with existing studies, benign samples were included for analysis. A total of 252 specimens were collected, including 126 normal tissues, 15 benign nodules, 76 adenocarcinomas, and 35 squamous cell carcinomas. The dispersion properties of each tissue were measured over a frequency range of 100 Hz to 100 MHz. And the relaxation mechanism was analyzed by fitting the Cole-Cole plot. The corresponding equivalent circuit was estimated accordingly. Results: Results validated the significant differences between malignant and normal tissue. Significant differences between benign and malignant lesions were observed in conductivity and relative permittivity. Adenocarcinomas and squamous cell carcinomas are significantly different in conductivity, first-order, second-order differences of conductivity, $\alpha$-band Cole-Cole plot parameters and capacitance of equivalent circuit. The combination of the different features increased the tissue groups' differences measured by Euclidean distance up to 94.7%. Conclusion and significance: In conclusion, the four tissue groups reveal dissimilarity in electrical properties. This characteristic potentially lends itself to future diagnosis of non-invasive lung cancer.

The controversy surrounding the impact of acesulfame potassium (Ace-K) on metabolic health has been growing. Here, male C57BL/6 mice were given Ace-K for 11 weeks (sterile water as the control group, 40 mg/kg body weight as the low dose group, 120 mg/kg as the high dose group), subsequently gut microbiome and targeted metabolomics were conducted to evaluate the effect of Ace-K on host health. Gut microbiota was perturbed by Ace-K, as evidenced by the down-regulation of beneficial bacteria and the increased abundance of Collinsellaassociated with inflammation. Fatty acids metabolism was altered by Ace-K, as evidenced by elevated long chain fatty acids (LCFAs) in liver and serum. Notably, the reduction of related genes and proteins correlated to carnitine metabolism and hepatic carnitine metabolites by Ace-K led to a reduction in the β-oxidation of LCFAs, ultimately causing the accumulation of LCFAs. These findings uncovered new perspectives on Ace-K-induced hepatic inflammation and fatty acids accumulation.

Endophytic fungi can benefit the host plant and increase the plant resistance. Now, there is no in-depth study of how Alternaria oxytropis(A. oxytropis) is enhancing the ability of inhibiting pathogenic fungi in Oxytropis ochrocephala(O. ochrocephala). In this study, the fungal community and metabolites associated with endophyte-infected (EI) and endophyte-free (EF) O. ochrocephalawere compared by multiomics. The fungal community indicated that there was more A. oxytropis, less phylum Ascomycota, and less genera Leptosphaeria, Colletotrichum, and Comoclathrisin the EI group. As metabolic biomarkers, the levels of swainsonine and apigenin-7-O-glucoside-4-O-rutinoside were significantly increased in the EI group. Through in vitro validation experiments, swainsonine and apigenin-7-O-glucoside-4-O-rutinoside can dramatically suppress the growth of pathogenic fungi Leptosphaeria sclerotioidesand Colletotrichum americae-borealisby increasing the level of oxidative stress. This work suggested that O. ochrocephalacontaining A. oxytropiscould increase the resistance to fungal diseases by markedly enhancing the content of metabolites inhibiting pathogenic fungi.

Swainsonine induced liver inflammation in livestock; however, the underlying mechanisms, especially the role of bile acids (BAs), in the pathogenesis remained elusive. Here, our results showed that swainsonine induced hepatic inflammation via changing BA metabolism and gut microbiota in mice. Swainsonine significantly upregulated the levels of deoxycholic acid (DCA) and taurine-β-muricholic acid (T-β-MCA) in the serum and liver of mice due to the markedly increased genus Clostridiumand the decreased genus Lactobacillusin the gut. As antagonists of the farnesoid X receptor (FXR), elevated DCA and T-β-MCA inhibited hepatic Fxrgene expression and thus suppressed FXR-SHP signaling and activated hepatic Cyp7a1gene expression, which induced a significant upregulation of the total BA level in serum, contributing to liver inflammation. These findings offer new insights into the underlying mechanisms in which swainsonine induced liver inflammation in mice via the gut–liver axis and suggest that gut microbiota and its metabolite BAs may be underlying triggering factors.