Objective: We aimed to determine the clinical prognostic factors of chronic rhinosinusitis after endoscopic sinus surgery (ESS) in order to better guide the management of patients. Methods: A total of 254 patients with chronic rhinosinusitis after ESS with a follow-up of 24 months were evaluated retrospectively. Clinical grouping, hyperplasia of the ethmoid bone, anatomic variations, allergy, polyps, previous sinonasal surgery and recurrent polyps were analyzed. Results: The success rates were 64.4 and 91.9% with and without hyperplasia of the ethmoid bone, 87.6 and 86.4% with and without anatomic variations, 67.9 and 92.0% with and without allergy, 81.0 and 94.0% with and without polyps, 72.8 and 93.6% with and without history of surgery and 52.3 and 94.3% with and without recurrent polyps. In logistic multiple regression analysis, allergy (p = 0.0002; estimate, –4.2094), nasal polyps (p = 0.0007; estimate, –3.6393) and history of surgery (p < 0.0001; estimate, –5.0938) were found to reach a statistically significant level. Conclusions: We propose that allergy, polyps and history of surgery might be significant indicators of poor prognosis after ESS.

It is well known that gut microbial imbalance is a potential factor for the occurrence and development of diabetes mellitus (DM) and its complications. Moreover, the heart and gut microbiota can regulate each other through the gut–metabolite–heart axis. In this study, metagenomics, metabolomics, and transcriptomics were chosen to sequence the changes in gut microbiota, serum metabolite levels, and differentially expressed genes (DEGs) in leptin receptor-deficient db/db mice and analyze the correlation between serum metabolites and gut microbiota or DEGs. According to the results, there were significant differences in the 1,029 cardiac genes and 353 serum metabolites in diabetic mice of the db/db group, including DEGs enriched in the PPAR signaling pathway and increased short-chain carboxylic acids (CAs), when compared with the normal db/m group. According to metagenomics, the gut microbiota of mice in the db/db group were disrupted, and particularly Lachnospiraceae bacteria and Oscillospiraceae bacteria significantly decreased. Also, according to the Pearson correlation analysis, a significant positive correlation was found between CAs and PPAR signaling pathway-related DEGs, and a negative correlation was found between CAs and the abundance of the above-mentioned species. To sum up, type 2 diabetes mellitus (T2DM) can upregulate the expression of partial cardiac genes through the levels of serum short-chain CAs affected by gut microbiota, thus playing a role in the occurrence and development of diabetic cardiomyopathy (DCM). IMPORTANCE: Our research results clearly link the changes in heart genes of T2DM and normal mice with changes in serum metabolites and gut microbiota, indicating that some genes in biological processes are closely related to the reduction of protective microbiota in the gut microbiota. This study provides a theoretical basis for investigating the mechanism of DCM and may provide preliminary evidence for the future use of gut microbiota therapy for DCM.

As a commonly known aggressive liver-related manifestation within the spectrum of metabolic syndrome with a significant risk of progressing to cirrhosis and hepatocellular carcinoma, metabolic dysfunction-associated steatohepatitis (MASH) is closely intertwined with obesity, insulin resistance, and dyslipidemia. Although the gut microbiota is implicated in MASH progression, the underlying mechanisms require further investigation. In this study, we sought to combine the analysis of the liver transcriptome, circulating metabolome, and gut microbiota to investigate the potential molecular mechanisms underlying the reciprocal regulation between gut microbiota and liver immune signaling. We utilized a high-fat and methionine/choline-deficient diet (HFMCD)-induced MASH model in a db/db mouse. Following annotation analysis using KEGG and Metorigin, a comprehensive correlation analysis was conducted among these genes and specific metabolites (such as L-glutamine, isocitric acid, putrescine, pyroglutamic acid, rhamnose) and gut microbiota genera ( Enteroccus and Romboutsia ). The results revealed intricate interactions among the liver’s immune microenvironment, the metabolome, and the gut microbiota. These interactions suggest a potential regulatory mechanism for metabolic disorders and immune responses. IMPORTANCE: Our multi-omics analysis showed that the interactions between gut microbiota and liver immune responses mediated by the disorders in lipid, amino acid, and glucose metabolism are associated with activation of the JAK-STAT and NF-κB signaling pathway in MASH. The multi-omics analysis provides valuable insights into the interactions among microbiota, circulating metabolites, and immune signaling. These insights can be harnessed to enhance the management of MASH.