19 research outputs found

    Association between daily screen time and risk of stroke among middle-aged and elderly people: research based on China health and nutrition survey

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    BackgroundWe aimed to explore the independent associations between screen time and the risk of stroke among Chinese adults based on the China Health and Nutrition Survey (CHNS).MethodsData on Chinese adults aged older than 40 years from the CHNS in during 2004–2009 were selected. A total of 4,587 individuals were included in 2009, including screen time and the risk of stroke. Simultaneously, we traced the previous screen time to 2004 for those with outcome measures in 2009 (n = 2,100). Basic information, lifestyle, and screen behavior were obtained through face-to-face interviews and self-completed questionnaires. Anthropometric data collected included blood pressure, body weight, height, hip circumference, and waist circumference. Fasting blood was obtained for measurements of lipid and glucose levels. Cross-sectional analysis and cohort analysis were both performed using multivariate logistic regression.ResultsOf all participants, 3,004 (65.49%) participants spent more than 2 h per day on screen time. Taking the men who spent less than 2 h on screen per day as reference, the crude odds ratio (OR) of the high risk of stroke was 1.53 [95% confidence interval (CI), 1.20–1.95] for the men who spent 2–3 h per day on screen and 2.37 (95% CI, 1.78–3.16) for the men who spent more than 3 h per day on screen. This difference remained significant after adjusting for confounding factors. No association was observed among women. However, in the cohort analysis with screen time in 2006 as the independent variable, the association between screen time and stroke risk was found both in men [OR, 1.83 (95% CI, 1.19–2.82)] and women [OR, 1.48 (95% CI, 1.10–1.99)]).ConclusionWe found that the high screen time was associated with an increased stroke risk, which was pronounced in men, warranting a universal need to limit screen time in order to improve health

    Genome and transcriptome of Selaginella kraussiana reveal evolution of root apical meristems in vascular plants

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    The evolution of roots allowed vascular plants to adapt to land environments. Fossil evidence indicates that roots evolved independently in euphyllophytes (ferns and seed plants) and lycophytes, the two lineages of extant vascular plants. Based on a high-quality genome assembly, mRNA sequencing (mRNA-seq) data, and single-cell RNA-seq data for the lycophyte Selaginella kraussiana, we show that the two root origin events in lycophytes and euphyllophytes adopted partially similar molecular modules in the regulation of root apical meristem (RAM) development. In S. kraussiana, the RAM initiates from the rhizophore primordium guided by auxin and duplicates itself by dichotomous branching. The auxin signaling pathway directly upregulates euAINTEGUMENTAb (SkeuANTb), and then SkeuANTb directly promotes the expression of SkeuANTa and the WUSCHEL-RELATED HOMEOBOX13b (SkWOX13b) for RAM maintenance, partially similar to the molecular pathway involving the euANT-branch PLETHORA (AtPLT) genes and AtWOX5 in root initiation in the seed plant Arabidopsis thaliana. Other molecular modules, e.g., SHORT-ROOT and SCARECROW, also have partially similar expression patterns in the RAMs of S. kraussiana and A. thaliana. Overall, our study not only provides genome and transcriptome tools of S. kraussiana but also indicates the employment of some common molecular modules in RAMs during root origins in lycophytes and euphyllophytes

    New Quantitative Structure–Activity Relationship Model for Angiotensin-Converting Enzyme Inhibitory Dipeptides Based on Integrated Descriptors

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    Angiotensin-converting enzyme (ACE) inhibitory peptides derived from food proteins have been widely reported for hypertension treatment. In this paper, a benchmark data set containing 141 unique ACE inhibitory dipeptides was constructed through database mining, and a quantitative structure–activity relationships (QSAR) study was carried out to predict half-inhibitory concentration (IC<sub>50</sub>) of ACE activity. Sixteen descriptors were tested and the model generated by G-scale descriptor showed the best predictive performance with the coefficient of determination (<i>R</i><sup>2</sup>) and cross-validated <i>R</i><sup>2</sup> (<i>Q</i><sup>2</sup>) of 0.6692 and 0.6220, respectively. For most other descriptors, <i>R</i><sup>2</sup> were ranging from 0.52 to 0.68 and <i>Q</i><sup>2</sup> were ranging from 0.48 to 0.61. A complex model combining all 16 descriptors was carried out and variable selection was performed in order to further improve the prediction performance. The quality of model using integrated descriptors (<i>R</i><sup>2</sup> 0.7340 ± 0.0038, <i>Q</i><sup>2</sup> 0.7151 ± 0.0019) was better than that of G-scale. An in-depth study of variable importance showed that the most correlated properties to ACE inhibitory activity were hydrophobicity, steric, and electronic properties and C-terminal amino acids contribute more than N-terminal amino acids. Five novel predicted ACE-inhibitory peptides were synthesized, and their IC<sub>50</sub> values were validated through in vitro experiments. The results indicated that the constructed model could give a reliable prediction of ACE-inhibitory activity of peptides, and it may be useful in the design of novel ACE-inhibitory peptides

    Artesunate treats obesity in male mice and non-human primates through GDF15/GFRAL signalling axis

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    Abstract Obesity, a global health challenge, is a major risk factor for multiple life-threatening diseases, including diabetes, fatty liver, and cancer. There is an ongoing need to identify safe and tolerable therapeutics for obesity management. Herein, we show that treatment with artesunate, an artemisinin derivative approved by the FDA for the treatment of severe malaria, effectively reduces body weight and improves metabolic profiles in preclinical models of obesity, including male mice with overnutrition-induced obesity and male cynomolgus macaques with spontaneous obesity, without inducing nausea and malaise. Artesunate promotes weight loss and reduces food intake in obese mice and cynomolgus macaques by increasing circulating levels of Growth Differentiation Factor 15 (GDF15), an appetite-regulating hormone with a brainstem-restricted receptor, the GDNF family receptor α-like (GFRAL). Mechanistically, artesunate induces the expression of GDF15 in multiple organs, especially the liver, in mice through a C/EBP homologous protein (CHOP)-directed integrated stress response. Inhibition of GDF15/GFRAL signalling by genetic ablation of GFRAL or tissue-specific knockdown of GDF15 abrogates the anti-obesity effect of artesunate in mice with diet-induced obesity, suggesting that artesunate controls bodyweight and appetite in a GDF15/GFRAL signalling-dependent manner. These data highlight the therapeutic benefits of artesunate in the treatment of obesity and related comorbidities

    Gut microbiota-derived tryptamine and phenethylamine impair insulin sensitivity in metabolic syndrome and irritable bowel syndrome

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    Abstract The incidence of metabolic syndrome is significantly higher in patients with irritable bowel syndrome (IBS), but the mechanisms involved remain unclear. Gut microbiota is causatively linked with the development of both metabolic dysfunctions and gastrointestinal disorders, thus gut dysbiosis in IBS may contribute to the development of metabolic syndrome. Here, we show that human gut bacterium Ruminococcus gnavus-derived tryptamine and phenethylamine play a pathogenic role in gut dysbiosis-induced insulin resistance in type 2 diabetes (T2D) and IBS. We show levels of R. gnavus, tryptamine, and phenethylamine are positively associated with insulin resistance in T2D patients and IBS patients. Monoassociation of R. gnavus impairs insulin sensitivity and glucose control in germ-free mice. Mechanistically, treatment of R. gnavus-derived metabolites tryptamine and phenethylamine directly impair insulin signaling in major metabolic tissues of healthy mice and monkeys and this effect is mediated by the trace amine-associated receptor 1 (TAAR1)-extracellular signal-regulated kinase (ERK) signaling axis. Our findings suggest a causal role for tryptamine/phenethylamine-producers in the development of insulin resistance, provide molecular mechanisms for the increased prevalence of metabolic syndrome in IBS, and highlight the TAAR1 signaling axis as a potential therapeutic target for the management of metabolic syndrome induced by gut dysbiosis
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