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Although previous studies have discussed the association between mobile phone use addiction (MPUA) and depressive symptoms in adolescents, studies on Chinese adolescents are limited, with no studies being reported on adolescents from ethnic minority areas within Yunnan. This study aimed to explore the mediating mechanism of insomnia in the association between MPUA and depressive symptoms among Yunnan college students.A sample survey was conducted among 10,121 college students from four colleges in Yunnan province, China, from November to December 2021 via cluster sampling. Insomnia was assessed using the Insomnia Severity Index Scale, MPUA was assessed using the Self-Rating Questionnaire for Adolescent Problematic Mobile Phone Use, and depressive symptoms were assessed using the Patient Health Questionnaire-9 items. A generalized linear model was used to analyze the association between MPUA, insomnia, and depressive symptoms. The structural equation model was used to analyze the mediating effect of insomnia.The positive rates of depressive symptoms, MPUA, and insomnia were 39.2 %, 30.8 %, and 22.3 %, respectively. After adjusting for the demographic and confounding variables, MPUA (β = 0.14, 95 % CI: 0.13-0.15, P 0.01) and insomnia (β = 0.44, 95 % CI: 0.43-0.46, P 0.01) were associated with depressive symptoms (P 0.05). The mediating effect of insomnia accounted for 34.7 % of the total effect in the mediating model of MPUA associated with depressive symptoms.Our findings suggest that insomnia partially mediates the association between MPUA and depressive symptoms among Yunnan college students.

Peanut (Arachis hypogaea L.) is one of the most important economic and oil crops in the world. At present, peanut varieties with rich anthocyanin in testa are rare in the market, but the selection and breeding of varieties with the related traits has always attracted the attention of breeders. In this study, two peanut varieties with the pink and purple testa, G110 (G) and Z18-40 (Z) were used to conduct interaction joint analysis of multi-omics and miRNA-target gene. The anthocyanin content of Z18-40 was 7.49–8.62-folds higher than G110 on 30 DAF (days after flowering) and 45 DAF via Ultraviolet-visible Spectrophotometer (UV-5800, Shanghai, China). And then, a total of 14 candidate genes related with the anthocyanin biosynthesis were identified for correlation in different comparison groups (R2 ≥ 0.80), among of a novel gene Ah21440 related with hydroxycinnamoyl transferase (HCT) biosynthesis was identified. In addition, Cyanidin 3-O-glucoside (Kuromanin, pmb0550) was the only common differentially accumulated metabolite (DAM) identified using multi-omics joint analysis in G1_vs_G2, Z1_vs_Z2, G1_vs_Z1, and G2_vs_Z2, respectively. Correlation analysis of miRNA-target genes and DEGs in the transcriptome shows that, AhmiR2950, AhmiR398, AhmiR50, and AhmiR51 regulated to HCT and chalcone biosynthesis related candidate genes (Ah21440, AhCHS, AhCHI). Lastly, all of 14 candidate genes and 4 differentially expressed miRNAs were validated using quantitative real-time PCR (qRT-PCR), which trends were consistent with that of the former transcriptome data. The results provide important reference for in-depth research on the anthocyanin metabolism mechanism in peanut testa.

Mengdie Hu, Xiuting Huang, Xueyao Han, Linong Ji Department of Endocrinology and Metabolism, Peking University People’s Hospital, Peking University Diabetes Center, Beijing 100044, People’s Republic of ChinaCorrespondence: Linong Ji; Xueyao HanDepartment of Endocrinology and Metabolism, Peking University People’s Hospital, Peking University Diabetes Center, Beijing 100044, People’s Republic of ChinaTel +86 10-8832 5578Fax +86 10-8832 4371Email prof_jilinong@aliyun.com; xueyaohan@sina.comPurpose: Mutations in hepatocyte nuclear factor 1α (HNF1α) are the cause of maturity-onset diabetes of the young type 3 (MODY3) and involved in the development of hepatocellular adenoma and abnormal lipid metabolism. Previously, we have found that the serum microRNA (miR)-122 levels in MODY3 patients were lower than those in type 2 diabetes mellitus and healthy controls. This study aimed to investigate the mechanism of decreased miR-122 levels in patients with MODY3 and whether low levels of miR-122 mediate tumorigenesis and abnormal lipid metabolism associated with HNF1α deficiency in human hepatocytes.Methods: The expression of miR-122 was examined by real-time PCR. Dual-luciferase reporter assay was performed to confirm the transcriptional regulation of miR-122 by HNF1α. HepG2 cells were transfected with siRNA or miRNA mimic to downregulate or upregulate the expression of HNF1α or miR-122, respectively. CCK-8 and colony formation assay were used to determine cell proliferation. Lipid accumulation was examined by Oil Red O staining and intracellular triglyceride and cholesterol quantification assays.Results: HNF1α regulated the expression of miR-122 by directly binding to its promoter. Knockdown of HNF1α in HepG2 cells reduced the expression of miR-122, increased proliferation and promoted intracellular cholesterol accumulation. Overexpression of miR-122 partially rescued the phenotypes associated with HNF1α deficiency in human hepatocytes. Mechanistically, HNF1α modulated cholesterol homeostasis via miR-122-dependent activation of sterol regulatory element-binding protein-2 (SREBP-2) and regulation of proprotein convertase subtilisin/kexin type 9 (PCSK9). Moreover, circulating miR-122 levels were associated with serum cholesterol levels.Conclusion: Loss of HNF1α function led to hepatocyte proliferation and abnormal cholesterol metabolism by downregulating miR-122. Our findings revealed a novel mechanism that low levels of miR-122 mediate tumorigenesis and abnormal lipid metabolism associated with MODY3. MiR-122 may be a potential therapeutic target for the treatment of MODY3.Keywords: MODY3, HNF1α, miR-122, cholesterol metabolism, hepatocellular adenoma