The mixing on a single-particle level of chemically incompatible nanoparticles is an outstanding challenge for many applications. Burgeoning research activity suggests that entropic templating is a potential strategy to address this issue. Herein, using systematic computer simulations of model nanoparticle systems, we show that the entropy-templated interfacial organization of nanoparticles significantly depends on the stiffness of tethered chains. Unexpectedly, the optimal chain stiffness can be identified wherein a system exhibits the most perfect mixing for a certain compression ratio. Our simulations demonstrate that entropic templating regulated by chain stiffness precisely reflects various entropic repulsion states that arise from typical conformation regimes of semiflexible chains. The physical mechanism of the chain stiffness effect is revealed by analyzing the entropic repulsion states of tethered chains and quantitatively estimating the resulting entropy penalties, which provides direct evidence that supports the key role of entropic transition in the entropic templating strategy, as suggested in experiments. Moreover, the model nanoparticle systems are found to evolve into binary nanoparticle superlattices by remixing at extremely high stiffness. The findings facilitate the wide application of the entropic templating strategy in creating interfacially reactive nanomaterials with ordered structures on the single-nanoparticle level as well as mechanomutable responses.
Objective: To describe the prevalence of metabolic syndrome (MetS) in adolescents and its association with several MetS-related biochemical markers. Methods: A cross-sectional analysis was carried out and data were extracted from the Nutrition and Health Surveillance in Primary and Secondary school students of Beijing (NHSPSB) 2017. Participants were aged 10–15 years old. MetS was diagnosed using the recommended criteria for Chinese adolescents. The associations among MetS, biochemical biomarkers, and socioeconomic status were estimated by multivariable linear regression. Results: The prevalence of MetS in adolescents in Beijing was 3% in the total sample, 4% in boys, and 2% in girls. Moreover, the prevalence of MetS in the overweight and obesity populations were 5% and 12% respectively. The prevalence of MetS remained higher in boys than in girls. The concentrations of alanine aminotransferase (ALT), serum uric acid (SUA), low density lipoprotein (LDL), and C-reactive protein (CRP) were higher in the MetS children in comparison with non-MetS children (All p < 0.05), while the high-density lipoprotein (HDL) concentration was lower in MetS children. After adjusting for socioeconomic parameters in the multivariable regression model, MetS was strongly associated with ALT, SUA, HDL, and LDL. The five components of MetS indicated that abdominal obesity and a high serum triglyceride (TG) concentration were tightly linked with ALT, SUA, LDL, and CRP; while a low HDL concentration and elevated blood pressure were related to enhanced ALT, UA, and CRP. Additionally, impaired fasting glucose was only related to increased ALT. Conclusion: The epidemiological issues of MetS in Beijing adolescents should be known across socioeconomic classes. Early intervention strategies, such as dietary pattern interventions and physical excise, should be designed for that population to reduce the disease burdens of cardiovascular disease (CVD), Type 2 diabetes (T2D), and steatohepatitis in adulthood.
Background: China and the United States (US) ranked first and third in terms of new liver cancer cases and deaths globally in 2020. Therefore, a comprehensive assessment of trends in the incidence of primary liver cancer with four major etiological factors between China and the US during the past 30 years with age-period-cohort (APC) analyses is warranted. Methods: Data were obtained from the Global Burden of Disease 2019, and period/cohort relative risks were estimated by APC modeling from 1990 to 2019. Results: In 2019, there were 211,000 new liver cancer cases in China and 28,000 in the US, accounting for 39.4% and 5.2% of global liver cancer cases, respectively. For China, the age-standardized incidence rate (ASIR) consecutively decreased before 2005 but increased slightly since then, whereas the ASIR continuously increased in the US. Among the four etiological factors of liver cancer, the fastest reduction in incidence was observed in hepatitis B virus-related liver cancer among Chinese women, and the fastest increase was in nonalcoholic steatosis hepatitis (NASH)-related liver cancer among American men. The greatest reduction in the incidence of liver cancer was observed at the age of 53 years in Chinese men (À5.2%/year) and 33 years in Chinese women (À6.6%/year), while it peaked at 58 years old in both American men and women (4.5%/year vs. 2.8%/year). Furthermore, the period risks of alcohol-and NASH-related liver cancer among Chinese men have been elevated since 2013. Simultaneously, leveledoff period risks were observed in hepatitis C viral-related liver cancer in both American men and women. Conclusions: Currently, both viral and lifestyle factors have been and will continue to play an important role in the time trends of liver cancer in both countries. More tailored and efficient preventive strategies should be designed to target both viral and lifestyle factors to prevent and control liver cancer.
To the Editor: Previous studies paid less attention on the reasons of anemia in schoolchildren, particularly in a relatively well-off area, which might hamper policy design for anemia control. Thus, the present study would explore the reasons for anemia in schoolchildren aged 5 to 11 years in Beijing based on personal data including dietary intake and serum biomarkers of nutrients.
Background: Genome-wide association studies (GWASs) have consistently identified MAP2K5 as an obesity susceptibility gene. To deepen our understanding of the potential causal genetic variants of this region, a fine-mapping study of MAP2K5 was conducted.Methods and Results: SNPs rs7175517 (G > A) and rs4776970 (T > A) were identified as the leading SNPs associated with BMI in both Chinese and the United Kingdom populations. Second, colocalization of GWAS and expression quantitative trait loci (eQTL) analyses and bioinformatic analyses indicated that rs7175517 is the functionally leading variant in the MAP2K5 gene region. Dual-luciferase assays indicated that the G allele of rs7175517 reduced the mRNA expression of MAP2K5 in HEK293T cells. The possible mechanism was that the G allele interacted with more RNA repressors from nuclei extracts, which was evidenced by electrophoretic mobility shift assays (EMSAs). Furthermore, the pathway enrichment analyses of the products from DNA pull-down and protein mass spectrometry demonstrated that the G allele of rs7175517 might interact with RNA catabolic or splicing transcription factors, which consequentially increased adiposity deposition.Conclusion: SNP rs7175517 of the MAP2K5 gene was the putative causal variant associated with BMI. More precisely designed in vitro or animal experiments are warranted to further delineate the function of MAP2K5 in adipogenesis.
Background: Genome-wide association studies (GWASs) have consistently identified MAP2K5 as the obesity susceptible gene. To deepen our understanding of the potential causal genetic variants of this region, a fine-mapping study of MAP2K5 was conducted. Results: First, a target single nucleotide polymorphisms (SNPs) sequencing of MAP2K5 was carried out in 2030 Chinese children and followed by a fine mapping with the UK biobank GWAS data in 264,838 adults to identify the leading SNPs within the MAP2K5 gene region. SNP rs7175517 (G>A) and rs4776970(T>A) were identified as the leading SNPs associated with BMI in both Chinese and the UK population. Second, colocalization of GWAS and expression quantitative trait loci (eQTL) analyses and bioinformatic functional annotations indicated that rs7175517 is the leading variants in MAP2K5 gene region functionally. Additionally, dual luciferase assay indicated that the G allele of rs7175517 reduced the mRNA expression of MAP2K5 in HEK293T cells. The possible mechanism was that the G allele of rs7175517 interacted with more RNA repressors from nuclei extracts, which was evidenced by electrophoretic mobility shift assays (EMSAs). Furthermore, the pathway enrichment analyses of the products from DNA pull-down and protein mass spectrometry demonstrated that the G allele of rs7175517 might interact with RNA catabolic or splicing transcription factors, which consequentially increased the adiposity deposition. Conclusions: SNP rs7175517 of MAP2K5 gene was the putative causal variant associated with BMI. More precisely designed in vitro or animal experiments are warranted to further delineate the function of MAP2K5 in the adipogenesis.
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