Objective To characterise the oral microbiome, gut microbiome and serum lipid profiles in patients with active COVID-19 and recovered patients; evaluate the potential of the microbiome as a non-invasive biomarker for COVID-19; and explore correlations between the microbiome and lipid profile. Design We collected and sequenced 392 tongue-coating samples, 172 faecal samples and 155 serum samples from Central China and East China. We characterised microbiome and lipid molecules, constructed microbial classifiers in discovery cohort and verified their diagnostic potential in 74 confirmed patients (CPs) from East China and 37 suspected patients (SPs) with IgG positivity. Results Oral and faecal microbial diversity was significantly decreased in CPs versus healthy controls (HCs). Compared with HCs, butyric acid-producing bacteria were decreased and lipopolysaccharide-producing bacteria were increased in CPs in oral cavity. The classifiers based on 8 optimal oral microbial markers (7 faecal microbial markers) achieved good diagnostic efficiency in different cohorts. Importantly, diagnostic efficacy reached 87.24% in the cross-regional cohort. Moreover, the classifiers successfully diagnosed SPs with IgG antibody positivity as CPs, and diagnostic efficacy reached 92.11% (98.01% of faecal microbiome). Compared with CPs, 47 lipid molecules, including sphingomyelin (SM)(d40:4), SM(d38:5) and monoglyceride(33:5), were depleted, and 122 lipid molecules, including phosphatidylcholine(36:4p), phosphatidylethanolamine (PE)(16:0p/20:5) and diglyceride(20:1/18:2), were enriched in confirmed patients recovery. Conclusion This study is the first to characterise the oral microbiome in COVID-19, and oral microbiomes and lipid alterations in recovered patients, to explore their correlations and to report the successful establishment and validation of a diagnostic model for COVID-19.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide, leading to a large global cancer burden. Hepatocyte growth factor (HGF) and its high-affinity receptor, mesenchymal epithelial transition factor (c-Met), are closely related to the onset, progression, and metastasis of multiple tumors. The HGF/c-Met axis is involved in cell proliferation, movement, differentiation, invasion, angiogenesis, and apoptosis by activating multiple downstream signaling pathways. In this review, we focus on the function of the HGF/c-Met axis in HCC. The HGF/c-Met axis promotes the onset, proliferation, invasion, and metastasis of HCC. Moreover, it can serve as a biomarker for diagnosis and prognosis, as well as a therapeutic target for HCC. In addition, it is closely related to drug resistance during HCC treatment.

Coronavirus disease 2019 (COVID‐19) has spread worldwide. To date, no specific drug for COVID‐19 has been developed. Thus, this randomized, open‐label, controlled clinical trial (ChiCTR2000029853) was performed in China. A total of 20 mild and common COVID‐19 patients were enrolled and randomly assigned to receive azvudine and symptomatic treatment (FNC group), or standard antiviral and symptomatic treatment (control group). The mean times of the first nucleic acid negative conversion (NANC) of ten patients in the FNC group and ten patients in the control group are 2.60 (SD 0.97; range 1–4) d and 5.60 (SD 3.06; range 2–13) d, respectively (p = 0.008). The mean times of the first NANC of four newly diagnosed subjects in the FNC group and ten subjects in the control group are 2.50 (SD 1.00; range 2–4) d and 9.80 (SD 4.73; range 3–19) d, respectively (starting from the initial treatment) (p = 0.01). No adverse events occur in the FNC group, while three adverse events occur in the control group (p = 0.06). The preliminary results show that FNC treatment in the mild and common COVID‐19 may shorten the NANC time versus standard antiviral treatment. Therefore, clinical trials of FNC treating COVID‐19 with larger sample size are warranted.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer‐related death worldwide. The prognosis of HCC remains very poor; thus, an effective treatment remains urgent. Herein, a type of nanomedicine is developed by conjugating Fe@Fe₃O₄ nanoparticles with ginsenoside Rg3 (NpRg3), which achieves an excellent coupling effect. In the dimethylnitrosamine‐induced HCC model, NpRg3 application significantly prolongs the survival of HCC mice. Further research indicates that NpRg3 application significantly inhibits HCC development and eliminates HCC metastasis to the lung. Notably, NpRg3 application delays HCC‐induced ileocecal morphology and gut microbial alterations more than 12 weeks during HCC progression. NpRg3 administration elevates the abundance of Bacteroidetes and Verrucomicrobia, but decreases Firmicutes. Twenty‐nine predicted microbial gene functions are enriched, while seven gene functions are reduced after NpRg3 administration. Moreover, the metabolomics profile presents a significant progression during HCC development, but NpRg3 administration corrects tumor‐dominant metabolomics. NpRg3 administration decreases 3‐indolepropionic acid and urea, but elevates free fatty acids. Importantly, NpRg3 application remodels the unbalanced correlation networks between gut microbiota and metabolism during HCC therapy. In conclusion, nanoparticle conjugation of ginsenoside Rg3 inhibits HCC development and metastasis via the remodeling of unbalanced gut microbiota and metabolism in vivo, providing an antitumor therapy strategy.

Gut microbiota is key to human health and disease. Convincing studies have demonstrated that dysbiosis in the commensal gut microbiota is associated with intestinal and extra-intestinal diseases. Recent explorations have significantly contributed to the understanding of the relationship between gut microbiota and bone diseases (osteoporosis, osteoarthritis, rheumatoid arthritis, and bone cancer). Gut microbiota and its metabolites may become associated with the development and progression of bone disorders owing to their critical role in nutrient absorption, immunomodulation, and the gut–brain–bone axis (regulation hormones). In this work, we review the recent developments addressing the effect of gut microbiota modulation on skeletal diseases and explore a feasible preventive approach and therapy for bone diseases.

Objective: The intestinal microbiome is associated with various autoimmune diseases. Regional difference is the main influencing factor of intestinal microbial difference. This study aimed to identify the differences in fecal microbiome between autoimmune hepatitis (AIH) patients and healthy controls (HCs) in Central China, and to validate the efficacy of fecal microbiome as a diagnostic tool for AIH. Design: We collected 115 fecal samples from AIH patients (N = 37) and HCs (N = 78) in Central China and performed gene sequencing. Fecal microbiomes were characterized and microbial markers for AIH were identified. Results: Fecal microbial diversity showed a downward trend in AIH compared with HCs. Fecal microbial communities significantly differed between both groups. At the phylum level, Verrucomicrobia abundance was significantly increased, while Lentisphaerae and Synergistetes were significantly decreased in the AIH patients vs. the HCs. Compared to the HCs, 15 genera, including Veillonella, Faecalibacterium, and Akkermansia, were enriched, while 19 genera, such as Pseudobutyrivibrio, Lachnospira, and Ruminococcaceae, were decreased in the AIH patients. Ten genera, including Veillonella, Faecalibacterium, and Akkermansia, predominated in the AIH patients. Five microbial biomarkers were deemed optimal diagnostic tools for AIH. The probability of disease was significantly increased in AIH group vs. HCs, achieving 83.25% value of area under the curve. Conclusion: We present the characteristics of AIH patients in Central China for the first time. Five microbial biomarkers, including Lachnospiraceae, Veillonella, Bacteroides, Roseburia, and Ruminococcaceae, achieved a high potential distinguishing AIH patients from HCs.