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Additional file 1: Methods. Table S1. Participant characteristics in the GNHS. Table S2. Participant characteristics of the CHNS. Table S3. Associations between α-diversity and cognitive impairment in the GNHS (n = 1430). Table S4. Associations between α-diversity and cognitive decline in the CHNS (n = 1300). Table S5. Weights for genus features contributing to the LASSO models. Table S6. Associations between bacterial taxonomy and cognitive performance in the CHNS (n = 1300). Table S7. Associations between Odoribacter and SCFAs in the GNHS. Table S8. Associations between serum acetic acid and brain structure in the GNHS. Table S9. Distribution of metagenomic features in the GNHS. Table S10. Associations between intra-individual alterations in gut microbial composition and cognitive impairment in the GNHS. Table S11. Metagenomic and metabolomic features associated with cognitive impairment in the GNHS. Table S12. Correlations of metagenomic and metabolic features with MMSE domains in the GNHS. Table S13. Correlations between metagenomic features and metabolites in the GNHS. Fig. S1 Overview of the multi-omics datasets of the GNHS. Fig. S2 Distribution of metagenomic and metabolomic features in the GNHS. Fig. S3 Correlation analyses on cognition-related metagenomic and metabolic traits in the GNHS. Fig. S4 Association of metagenomic pathways and serum metabolomics with cognitive function in the GNHS. Fig. S5 Networks of metagenomic pathways in the GNHS.

Objective: To quantify the expression of miR-195 and miR-497 in acute stroke and to evaluate their correlations with post-stroke cognitive impairment. Methods: A total of 108 patients with acute stroke admitted to our hospital from January, 2019 to June, 2020 were enrolled as a patient group, and 76 healthy volunteers were recruited as a normal group. Levels of serum miR-195 and miR-497 in the two groups were quantified. Neurological and cognitive functions were tested by National Institutes of Health Stroke Scale (NIHSS) and Montreal Cognitive Assessment (MoCA), respectively. Diagnostic value of serum miR-195 and miR-497 in acute stroke was evaluated by receiver operating characteristic (ROC) curve, and independent risk factors were determined by multivariate logistic regression. Results: Levels of serum miR-195 and miR-497 increased in acute stroke. The area under the curve (AUC) of serum miR-195 in the diagnosis of acute stroke was 0.901, while that of serum miR-497 was 0.922. Levels of miR-195 and miR-497 were positively correlated with NIHSS score and negatively correlated with MoCA score. Logistic regression analysis demonstrated that family history of stroke, diabetes, hypertension, NIHSS score, MoCA score, miR-195, and miR-497 were independent risk factors for acute stroke. Conclusion: Serum miR-195 and miR-497 are elevated in acute stroke and associated with the loss of neurologic and cognitive functions. They may be biomarkers for diagnosis and prognosis of acute stroke.

Yuanjue Sun,1,* Liguo Liu,2,* Yaling Wang,3 Aina He,3 Haiyan Hu,3 Jianjun Zhang,3 Mingyong Han,1 Yujing Huang3 1Cancer Therapy and Research Center, Shandong Provincial Hospital, Shandong University, 250021, Shandong, People’s Republic of China; 2Department of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, 200233 Shanghai, People’s Republic of China; 3Department of Medical Oncology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, 200233 Shanghai, People’s Republic of China *These authors contributed equally to this work Purpose: The aims of this study were to determine the effect of curcumin on osteosarcoma (OS) cells due to inactivation of the p-JAK2/p-STAT3 pathway and evaluate the prognostic value of this pathway in OS. Materials and methods: We exposed a human OS cell line (MG-63) to different concentrations of curcumin. Then, we characterized the effects on MG-63 cells using assays (cell viability, colony formation, cell cycle, wound healing, invasion), flow cytometry, Western blot, immunohistochemical analyses, and tumor xenograft. Results: The half-maximal inhibitory of curcumin for MG-63 cells at 24 hours was 27.6 µM. The number of colonies of MG-63 cells was decreased obviously upon curcumin (10 and 20 µM) treatment. We also found increased accumulation of MG-63 cells in the G2/M phase upon curcumin (10 and 20 µM) treatment. Apoptosis was increased in 10 and 20 µM curcumin-treated MG-63 cells. After incubation of physically wounded cells for 24 hours, the percentage wound width increased upon curcumin exposure. Curcumin obviously decreased the expression of pJAK-2 and pSTAT-3 in MG-63 cells in a dose-dependent manner. Curcumin dose-dependently inhibited the proliferation, migration, and invasion of MG-63 cells and induced arrest of the G0/G1 phase and apoptosis by inhibiting the p-JAK2/p-STAT3 pathway. The linear correlativity between expression of p-JAK2 and STAT3 was very prominent, and both were closely associated with lung metastasis. In vivo study suggested that curcumin suppressed tumor growth through JAK2/STAT3 signaling. Conclusion: Curcumin-mediated inhibition of the proliferation and migration of MG-63 cells was associated with inactivation of JAK/STAT signaling. Keywords: osteosarcoma, curcumin, multiplication, invasion