[Children's dietary patterns and dietary networks in five regions in China].

OBJECTIVE: To analyze the dietary patterns and dietary networks of children in China, explore regional differences in dietary habits in each region. METHODS: The subjects of the study were children aged 3-17(n=5824) in North Coast Economic Zone, Northeast, Central China, East Coast Economic Zone and Southwest Economic Zone who participated in the China Health and Nutrition Survey. The dietary pattern was obtained by factor analysis. Using mutual information, a measure to detect both linear and non-linear correlations between food groups constructed the dietary networks. RESULTS: Factor analysis resulted in five dietary patterns. Pattern 1 was related to high intakes of wheat and other cereals, pattern 2 was related to high intakes of fruits, milk, eggs and fast foods, pattern 3 was associated with high intakes of tubers, snacks, cakes, beverages and fast foods. The Northeast, Central China and North Coast Economic Zone regions had higher pattern 1 score. Pattern 2 scored higher for North Coast Economic Zone and East Coast Economic Zone regions. Pattern 3 scores in the Northeast region were higher than North Coast Economic Zone and East Coast Economic Zone regions. North Coast Economic Zone, Central China and Southwest Economic Zone regions had focused networks. The network of Northeast and East Coast Economic Zone regions were multiple. All regions were characterized by vegetables, or cereals as the hub. CONCLUSION: The dietary patterns and networks of children in the five regions of China exhibit regional differences.

Long-term exposure to ambient PM2.5 and its components on menarche timing among Chinese adolescents: evidence from a representative nationwide cohort.

BACKGROUND: Ambient air pollutants have been suggested to affect pubertal development. Nevertheless, current studies indicate inconsistent effects of these pollutants, causing precocious or delayed puberty onset. This study aimed to explore the associations between long-term exposure to particulate matter with aerodynamic diameters ≤ 2.5 µm (PM2.5) along with its components and menarche timing among Chinese girls. METHOD: Self-reported age at menarche was collected among 855 girls from China Health and Nutrition Survey 2004 to 2015. The pre-menarche annual average concentrations of PM2.5 and its components were calculated on the basis of a long-term (2000-2014) high-resolution PM2.5 components dataset. Generalized linear models (GLM) and logistic regression models were used to analyze the associations of exposure to a single pollutant (PM2.5, sulfate, nitrate, ammonium, black carbon and organic matter) with age at menarche and early menarche (< 12 years), respectively. Weighted quantile sum methods were applied to examine the impacts of joint exposure on menarche timing. RESULTS: In the adjusted GLM, per 1 µg/m3 increase of annual average concentrations of nitrate and ammonium decreased age at menarche by 0.098 years and 0.127 years, respectively (all P < 0.05). Every 1 µg/m3 increase of annual average concentrations of PM2.5 (OR: 1.04, 95% CI: 1.00-1.08), sulfate (OR: 1.23, 95% CI: 1.01-1.50), nitrate (OR: 1.23, 95% CI: 1.06-1.43) and ammonium (OR: 1.32, 95% CI: 1.06-1.66) were significantly positively associated with early menarche. Higher level of joint exposure to PM2.5 and its components was associated with 11% higher odds of early menarche (P = 0.04). Additionally, the estimated weight of sulfate was the largest among the mixed pollutants. CONCLUSIONS: Long-term exposure to PM2.5 and its components could increase the risk of early menarche among Chinese girls. Moreover, sulfate might be the most critical components responsible for this relationship. Our study provides foundation for targeted prevention of PM2.5 components.

Sex- and time-specific associations of obesity with glycaemic traits: A two-step multivariate Mendelian randomization study.

AIM: To assess the sex- and time-specific causal effects of obesity-related anthropometric traits on glycaemic traits. MATERIALS AND METHODS: We used univariate and multivariate Mendelian randomization to assess the causal associations of anthropometric traits (gestational variables, birth weight, childhood body mass index [BMI], BMI, waist-to-hip ratio [WHR], BMI-adjusted WHR [WHRadj BMI]) with fasting glucose and insulin in Europeans from the Early Growth Genetics Consortium (n ≤ 298 142), the UK Biobank, the Genetic Investigation of Anthropometric Traits Consortium (n ≤ 697 734; females: n ≤ 434 794; males: n ≤ 374 754) and the Meta-Analyses of Glucose and Insulin-related traits Consortium (n ≤ 151 188; females: n ≤ 73 089; males: n ≤ 67 506), adjusting for maternal genetic effects, smoking, alcohol consumption, and age at menarche. RESULTS: We observed a null association for gestational variables, a negative association for birth weight, and positive associations for childhood BMI and adult traits (BMI, WHR, and WHRadj BMI). In female participants, increased birth weight causally decreased fasting insulin (betaIVW , -0.07, 95% confidence interval [CI] -0.11 to -0.03; p = 1.92 × 10-3 ), but not glucose levels, which was annulled by adjusting for age at menarche. In male participants, increased birth weight causally decreased fasting glucose (betainverse-variance-weighted (IVW) , -0.07, 95% CI -0.11 to -0.03; p = 3.22 × 10-4 ), but not insulin levels. In time-specific analyses, independent effects of birth weight were absent in female participants, and were more pronounced in male participants. Independent effects of childhood BMI were attenuated in both sexes; independent effects of adult traits differed by sex. CONCLUSIONS: Our findings provide evidence for causal and independent effects of sex- and time-specific anthropometric traits on glycaemic variables, and highlight the importance of considering multiple obesity exposures at different time points in the life course.

Systemic inflammation mediates the association between environmental tobacco smoke and depressive symptoms: A cross-sectional study of NHANES 2009-2018.

BACKGROUND: Depression is associated with both environmental tobacco smoke (ETS) and inflammation. However, whether systemic inflammation mediates the ETS-depression relationship is unclear. METHODS: We analyzed 19,612 participants from the 2009-2018 National Health and Nutrition Examination Survey (representing approximately 206,284,711 USA individuals), utilizing data of depressive symptoms (assessed by Patient Health Questionnaire-9), blood cotinine level (an ETS biomarker), dietary inflammatory index (DII, assessed by 24-h dietary recall) and inflammation, represented by immune-inflammation index (SII) and systemic inflammation response index (SIRI). RESULTS: Weighted multivariable logistic regression showed that a higher blood cotinine level is significantly associated with a higher depressive symptoms risk (OR = 1.79, 1.35-2.38). After adjusting for covariates, the effect in smokers (OR = 1.220, 95 % CI: 1.140-1.309) is larger than that in non-smokers (OR = 1.150, 95 % CI: 1.009-1.318). Compared to the lowest level, depressive symptoms risks in participants with the highest level of SII, SIRI and DII are 19 % (OR = 1.19, 1.05-1.35), 15 % (OR = 1.15, 1.01-1.31) and 88 % (OR = 1.88, 1.48-2.39) higher, respectively. Weighted linear regression demonstrated positive correlations of SII (ß = 0.004, 0.001-0.006), SIRI (ß = 0.009, 0.005-0.012) and DII (ß = 0.213, 0.187-0.240) with blood cotinine level. Restricted cubic splines model showed a linear dose-response relationship between blood cotinine and depressive symptoms (Pnon-linear = 0.410), with decreasing risk for lower DII. And SII and SIRI respectively mediate 0.21 % and 0.1 % of the association between blood cotinine and depressive symptoms. LIMITATION: Cross-sectional design, and lack of medication data for depression. CONCLUSIONS: Positive association of ETS (blood cotinine) with depressive symptoms risk is partly mediated by systemic inflammation, and anti-inflammatory diet could be beneficial.

Shared Genetics and Comorbid Genes of Amyotrophic Lateral Sclerosis and Parkinson's Disease.

BACKGROUND: Comorbidity exists between amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), but the role of genetic factors is unclear. OBJECTIVE: We aim to investigate genetic correlation, causal relationship, and comorbid genes between ALS and PD. METHODS: Leveraging the largest genome-wide association study data (ALS: 27,205 cases, 110,881 controls; PDG: 33,674 cases, 449,056 controls), we used linkage disequilibrium score regression and Mendelian randomization analysis for genetic correlation and causal inference. We performed genome-wide cross-trait analysis via Multi-Trait Analysis of Genome-Wide Association Studies and Cross-Phenotype Association to identify specific single-nucleotide polymorphisms, followed by functional mapping and annotation. Integrating expression quantitative trait loci data from 13 brain regions, we conducted a transcriptome-wide association study via functional summary-based imputation and joint-tissue imputation to explore comorbid genes, followed by pathway enrichment analysis. RESULTS: We found that PD positively correlates with ALS (rg = 0.144, P = 0.026) and confers a causal effect (odds ratio = 1.09, 95% confidence interval: 1.03-1.15, P = 3.00 × 10-3 ). We identified nine single-nucleotide polymorphisms (eight new), associating with three risk loci (chromosomes 4, 10, and 17) and seven genes (TMEM175, MAPT, NSF, LRRC37A2, ARHGAP27, GAK, and FGFRL1). In transcriptome-wide association study analysis, we showed six previously unreported pleiotropic genes (KANSL1, ARL17B, EFNA1, WNT3, ERCC8, and ADAM15), and we found these candidate genes are mainly enriched in negative regulation of neuron projection development (GO:0010977). CONCLUSIONS: Our work demonstrates shared genetic architecture between ALS and PD, reports new pleiotropic genes, and sheds light on the comorbid mechanism. © 2023 International Parkinson and Movement Disorder Society.

Microbiota and mycobiota in bronchoalveolar lavage fluid of silicosis patients.

BACKGROUND: The contribution of bronchoalveolar lavage fluid (BALF) microbiota and mycobiota to silicosis has recently been noticed. However, many confounding factors can influence the accuracy of BALF microbiota and mycobiota studies, resulting in inconsistencies in the published results. In this cross-sectional study, we systematically investigated the effects of "sampling in different rounds of BALF" on its microbiota and mycobiota. We further explored the relationship between silicosis fatigue and the microbiota and mycobiota. METHODS: After obtaining approval from the ethics board, we collected 100 BALF samples from 10 patients with silicosis. Demographic data, clinical information, and blood test results were also collected from each patient. The characteristics of the microbiota and mycobiota were defined using next-generation sequencing. However, no non-silicosis referent group was examined, which was a major limitation of this study. RESULTS: Our analysis indicated that subsampling from different rounds of BALF did not affect the alpha- and beta-diversities of microbial and fungal communities when the centrifuged BALF sediment was sufficient for DNA extraction. In contrast, fatigue status significantly influenced the beta-diversity of microbes and fungi (Principal Coordinates Analysis, P = 0.001; P = 0.002). The abundance of Vibrio alone could distinguish silicosis patients with fatigue from those without fatigue (area under the curve = 0.938, 95% confidence interval [CI] 0.870-1.000). Significant correlations were found between Vibrio and haemoglobin levels (P < 0.001, ρ = -0.64). CONCLUSIONS: Sampling in different rounds of BALF showed minimal effect on BALF microbial and fungal diversities; the first round of BALF collection was recommended for microbial and fungal analyses for convenience. In addition, Vibrio may be a potential biomarker for silicosis fatigue screening.

Investigating the shared genetic architecture of post-traumatic stress disorder and gastrointestinal tract disorders: a genome-wide cross-trait analysis.

BACKGROUND: Observational studies suggest a correlation between post-traumatic stress disorder (PTSD) and gastrointestinal tract (GIT) disorders. However, the genetic overlap, causal relationships, and underlining mechanisms between PTSD and GIT disorders were absent. METHODS: We obtained genome-wide association study statistics for PTSD (23 212 cases, 151 447 controls), peptic ulcer disease (PUD; 16 666 cases, 439 661 controls), gastroesophageal reflux disease (GORD; 54 854 cases, 401 473 controls), PUD and/or GORD and/or medications (PGM; 90 175 cases, 366 152 controls), irritable bowel syndrome (IBS; 28 518 cases, 426 803 controls), and inflammatory bowel disease (IBD; 7045 cases, 449 282 controls). We quantified genetic correlations, identified pleiotropic loci, and performed multi-marker analysis of genomic annotation, fast gene-based association analysis, transcriptome-wide association study analysis, and bidirectional Mendelian randomization analysis. RESULTS: PTSD globally correlates with PUD (rg = 0.526, p = 9.355 × 10-7), GORD (rg = 0.398, p = 5.223 × 10-9), PGM (rg = 0.524, p = 1.251 × 10-15), and IBS (rg = 0.419, p = 8.825 × 10-6). Cross-trait meta-analyses identify seven genome-wide significant loci between PTSD and PGM (rs13107325, rs1632855, rs1800628, rs2188100, rs3129953, rs6973700, and rs73154693); three between PTSD and GORD (rs13107325, rs1632855, and rs3132450); one between PTSD and IBS/IBD (rs4937872 and rs114969413, respectively). Proximal pleiotropic genes are mainly enriched in immune response regulatory pathways, and in brain, digestive, and immune systems. Gene-level analyses identify five candidates: ABT1, BTN3A2, HIST1H3J, ZKSCAN4, and ZKSCAN8. We found significant causal effects of GORD, PGM, IBS, and IBD on PTSD. We observed no reverse causality of PTSD with GIT disorders, except for GORD. CONCLUSIONS: PTSD and GIT disorders share common genetic architectures. Our work offers insights into the biological mechanisms, and provides genetic basis for translational research studies.

Age-Dependent and Body Composition-Dependent Association of Child Gut Microbial Enterotype With Puberty Timing: A Chinese Cohort.

CONTEXT: Puberty timing, which is vital for adult well-being, has recently been suggested to be linked to specific gut taxa. However, the impact of comprehensive gut microbiome structure assessed by enterotype on puberty timing remains unknown. OBJECTIVE: Investigate the prospective association of gut microbial enterotype with puberty timing and the potential interaction of age and body composition. METHODS: This study included 1826 children from the Chinese Adolescent Cohort Study, a cohort that has collected information on sociodemographics, dietary intake, physical activity, anthropometry, and pubertal development of children aged 6-8 years since 2013 and follows them up annually until the age of 15 years. Fecal samples have been collected annually since 2019 and analyzed for 16S rRNA sequencing and targeted fecal metabolomics. Cox proportional hazard regression models were used to investigate the prospective association of enterotype with puberty timing and the impact of age and body mass index (BMI) sex- and age-independent standard deviation score (SDS). RESULTS: 592 (32.4%) and 1234 (67.6%) children belonged to the Prevotella-rich enterotype and the Bacteroides-rich enterotype, respectively. Children with the Bacteroides-rich enterotype experienced their menarche/voice break later than those with the Prevotella enterotype (hazard ratio 0.53, 95% CI 0.28-0.98), P = .02). Moreover, this association was more pronounced among younger children with higher BMI SDS (P for interaction = .006). CONCLUSION: Our findings supported a role for gut microbial communities in pubertal development, in which younger children with higher body mass seems more sensitive.

Benzo[b]fluoranthene induced oxidative stress and apoptosis in human airway epithelial cells via mitochondrial disruption.

Benzo[b]fluoranthene (BbF) is a common constituent of polycyclic aromatic hydrocarbons (PAHs). While numerous studies revealed adverse effects of PAHs on human health, the health effects of individual PAHs differ, and few investigations were performed on BbF. Therefore, the present study established cytotoxicity models of human lung epithelial cells (BEAS-2B cells) and bronchial epithelial cells (16HBE cells) exposed to BbF (10, 20, and 40 µM) for 24 h to reveal the mechanisms. Results from cytotoxicity and proliferation studies demonstrated that BbF inhibited cell growth in a dose-dependent manner. Flow cytometric analysis showed that BbF induced the appearance of a sub G1 peak, S-phased arrest, and apoptosis in both cells. Mechanistic investigations illustrated that BbF promoted reactive oxygen species (ROS) production, altered the expression of oxidative stress indicators, and decreased mitochondrial membrane potential. BbF also interfered with the expression of regulators associated with mitochondria disruption pathway. Taken together, these results strongly suggested that BbF inhibited cell growth and induced apoptosis in human airway epithelial cells via ROS-mediated mitochondria disruption.

A prospective analysis of optimal total weight gain ranges and trimester-specific weight gain rates for Chinese pregnant women.

BACKGROUND: Gestational weight gain (GWG) criteria recommended by the Institute of Medicine may not be appropriate for Asians. Our aims are to investigate the association between GWG and adverse pregnancy outcomes, and to propose optimal total GWG and rates of GWG for Chinese women. METHODS: Prospective data of 51,125 mother-child pairs from 27 hospitals and community health care centers from Guizhou, Yunnan and Sichuan provinces in China between 2014 and 2018 were analyzed. Generalized Additive Models were performed to determine the associations of GWG with the risk of aggregated adverse outcomes (gestational diabetes mellitus, preeclampsia, cesarean delivery, stillbirth, preterm birth, macrosomia, large for gestational age, and small for gestational age). The range that did not exceed a 2.5% increase from the lowest risk of aggregated adverse outcomes was defined as the optimal GWG range. RESULTS: Among all participants, U-shaped prospective association was found between GWG and the risk of aggregated adverse pregnancy outcomes. The optimal GWG range of 8.2-13.0 kg was proposed for underweight, 7.3-12.5 kg for normal weight, and 2.0-9.4 kg for overweight/obese women. Meanwhile, a higher GWG rate in the first two trimesters than that in the last trimester was suggested, except for overweight/obese women. After stratified by maternal age, mothers ≥35 years were suggested to gain less weight compared to younger mothers. CONCLUSIONS: To keep a balance between maternal health and neonatal growth, optimal GWG ranges based on Asia-specific BMI categories was suggested for Chinese women with different pre-gravid BMIs and maternal ages.

Brain Proteome-Wide and Transcriptome-Wide Asso-ciation Studies, Bayesian Colocalization, and Mendelian Randomization Analyses Reveal Causal Genes of Parkinson's Disease.

How genome-wide associated loci confer risk for Parkinson's disease is unclear. We aim to reveal causal genes through effects on brain proteins to provide new pathogenesis insights for Parkinson's disease. Proteome-wide and transcriptome-wide associations were determined by functional summary-based imputation leveraging data from genome-wide association summary (56 306 Europeans, 1.4 million controls), brain proteomes (528 cases from 2 separate data sets), and transcriptome (452 cases), followed by Mendelian randomization, Bayesian colocalization, cell-type-specific and brain regional expression, and drug-gene interaction analyses. As a result, genetically regulated protein abundances of 11 genes were associated with Parkinson's disease. Five genes (CD38, GPNMB, TMEM175, RAB7L1, and HIP1R) were colocalized. Four genes (GPNMB, SEC23IP, CD38, and DGKQ) demonstrated Mendelian randomized correlations (p < 8.10 × 10-5). Higher GPNMB level (1.47, 1.28-1.68) and lower CD38 level (0.319, 0.24-0.43) were causally associated with higher risk of Parkinson's disease, consistent with transcriptomic evaluations. CD38 and GPNMB were preferentially enriched in astrocytes and oligodendrocyte precursor cells, respectively. And CD38 and GPNMB were suggested to be the targets of many oncological drugs from Drug-Gene Interaction database. In conclusion, utilizing multidimensional data, GPNMB and CD38 were prioritized as the causal genes of Parkinson's disease, crucial for mechanistic and therapeutic investigations.

Benzo[b]fluoranthene (B[b]F) affects apoptosis, oxidative stress, mitochondrial membrane potential and expressions of blood-brain barrier markers in microvascular endothelial cells.

Exposure to polycyclic aromatic hydrocarbons (PAHs) contributes to the damage of blood-brain barrier. While a number of studies were focused on benzo[a]pyrene, direct effects and mechanisms of benzo[b]fluoranthene (B[b]F), another main component of PAHs, on blood-brain barrier (BBB) are not documented. Here, we investigated if B[b]F at concentrations of environmental relevance could affect apoptosis, oxidative stress, mitochondrial membrane potential (MMP) and BBB marker expression in mouse brain microvascular endothelial (bEnd.3) cells, an in vitro model typically used to study BBB toxicology. Cells were treated with varying concentrations of B[b]F (0, 10, 20 and 40 µM) for 48 h. Cell proliferation, cell cycle, apoptosis, oxidative stress, MMP and BBB marker expressions were evaluated by label-free real-time cell analysis, flow cytometry, immunofluorescence and Western-blot. The proliferation of bEnd.3 cells was inhibited by B[b]F in a concentration dependent manner. B[b]F treatment significantly affected cell cycle, induced apoptosis, increased levels of reactive oxygen species (ROS) and disputed MMP. Expressions of BBB marker Occludin and Claudin-5 were decreased in the presence of 40 µM B[b]F. In conclusion, B[b]F might damage BBB by affecting proliferation, apoptosis, ROS level and Occludin and Claudin-5 expressions in microvascular endothelial cells.

Prospective association of family members' sugar-sweetened beverages intake with children's sugar-sweetened beverages consumption in China.

PURPOSE: We aimed to investigate whether parental and siblings' sugar-sweetened beverage (SSB) intake had prospective impact on children's SSB consumption, and the potential sex difference in these associations. METHODS: This study included a total of 904 children and their parents enrolled from 2004 to 2011 China Health and Nutrition Survey (CHNS) cohort study. SSB consumption information was estimated using a short dietary questionnaire and total energy intake was assessed with three-day 24-h dietary assessments at recruitment and follow-up surveys. Multivariate logistic or linear regression analyses were used to assess the association for SSB consumption between parents, siblings and children after adjusting for age, body mass index (BMI) z-score, household income and parental educational level. RESULTS: In this study, a majority (87.6%) of children consumed SSB. Among them, the median consumption of SSB was 70.3 ml/day per capita and 205.4 ml/day per consumer. Parental SSB consumption was relevant to children's SSB consumption, and this association was more pronounced in boys than in girls. Meanwhile, fathers seemed to have a stronger impact on whether children consume SSB than mothers which was reflected by lower P and higher OR. Additionally, children's SSB intake was prospectively associated with their older siblings' SSB consumption (P for trend < 0.03). CONCLUSIONS: Parental and older siblings' SSB consumption was relevant to children's SSB intake. Particularly, boys were more susceptible to parental impact than girls, and fathers seemed to have a greater influence on children than mothers.

Identification of 5 Potential Predictive Biomarkers for Alzheimer's Disease by Integrating the Unified Test for Molecular Signatures and Weighted Gene Coexpression Network Analysis.

BACKGROUND: Previous transcriptome-wide association study (TWAS) has documented 21 genes associated with Alzheimer's disease (AD) risk, but the predictive biomarkers remain unexplored. METHODS: TWAS leveraging the unified test for molecular signatures (UTMOST) was performed in 75,000 cases and 420,000 controls with 10 brain tissue gene expression references. Weighted gene coexpression network analysis (WGCNA) was conducted in GSE5281 and GSE48350 data sets containing 167 AD samples and 247 controls. Random forest (RF) analysis was applied to screen the potential predictive biomarkers based on overlapping genes identified by TWAS and WGCNA, followed by comprehensive bioinformatic analyses with differential gene expression, functional enrichment, and correlation with immune cells. A nomogram was established to verify the predictive power of the identified biomarkers. RESULTS: TWAS revealed 78 candidate genes (p < 2.89 × 10-6). In WGCNA turquoise module, 3 718 AD-related genes were screened. RF identified 5 predictive biomarkers (FAM71E1, DDB2, AP4M1, GPR4, DOC2A), which are enriched in the global genome nucleotide excision repair pathway and associated with immune cell designations "Natural.killer.T.cell," "Memory.B.cell," "T.follicular.helper.cell," "Neutrophil," and "MDSC." The nomogram based on the 5 markers showed a high predictive power. CONCLUSION: Five potential predictive biomarkers for AD were identified, providing new insights into the pathogenesis and etiology of AD.

Targeted nanomedicines remodeling immunosuppressive tumor microenvironment for enhanced cancer immunotherapy.

Cancer immunotherapy has significantly flourished and revolutionized the limited conventional tumor therapies, on account of its good safety and long-term memory ability. Discouragingly, low patient response rates and potential immune-related side effects make it rather challenging to literally bring immunotherapy from bench to bedside. However, it has become evident that, although the immunosuppressive tumor microenvironment (TME) plays a pivotal role in facilitating tumor progression and metastasis, it also provides various potential targets for remodeling the immunosuppressive TME, which can consequently bolster the effectiveness of antitumor response and tumor suppression. Additionally, the particular characteristics of TME, in turn, can be exploited as avenues for designing diverse precise targeting nanomedicines. In general, it is of urgent necessity to deliver nanomedicines for remodeling the immunosuppressive TME, thus improving the therapeutic outcomes and clinical translation prospects of immunotherapy. Herein, we will illustrate several formation mechanisms of immunosuppressive TME. More importantly, a variety of strategies concerning remodeling immunosuppressive TME and strengthening patients' immune systems, will be reviewed. Ultimately, we will discuss the existing obstacles and future perspectives in the development of antitumor immunotherapy. Hopefully, the thriving bloom of immunotherapy will bring vibrancy to further exploration of comprehensive cancer treatment.

Development of the Chinese preschooler dietary index: a tool to assess overall diet quality.

BACKGROUND: Diet quality in early childhood has a long-term impact on health outcomes. However, there are scarce dietary indexes for Chinese preschool children, and the existing indexes had limited validity and reliability. This study thus aimed to develop a dietary index for preschool children based on the Chinese Dietary Guideline and Chinese Dietary Reference Intakes and to assess their overall diet quality using the China Health and Nutrition Survey (CHNS). METHODS: The Chinese Preschooler Dietary Index (CPDI) included 11 components, covering 9 food group components and two nutrient components. The total scores of CPDI ranged from 0 to 90, with a higher score indicating greater diet quality. This study assessed the diet quality of 1742 preschoolers aged two to five years old from CHNS using the CPDI. Dietary intake data were obtained using three-day 24-h diet recalls, and sociodemographic information was also collected. Cochran-Mantel-Haensel (CMH) test was used to explore the association between demographic and CPDI total scores. The principal component analysis, correlation analysis and Cronbach's alpha were used to evaluate the relative reliability and validity of the CPDI. Finally, a stepwise multiple regression analysis was performed to explore potential influencing factors of CPDI. RESULTS: Among the 1742 CHNS preschool children, more than 70% resided in rural areas and 41.2% of the sample were raised in a low-income family. The mean CPDI score of the preschoolers was 38.8 ± 12.9. Higher diet scores were correlated with higher energy and nutrient intake. Children with higher age (ß = 0.93, SE = 0.26, P = 0.0003), raised in a home with higher household income (ß = 3.11, SE = 0.27, P < 0.0001) or living in urban areas (ß = -4.44, SE = 0.66, P < 0.0001) were associated with higher CPDI scores. CONCLUSIONS: The CPDI is useful in evaluating the diet quality of preschool children. Based on the CPDI, the diet quality of Chinese preschoolers needs to be improved, especially in rural areas.

Human antigen R affects the migration and invasion of human lung cancer A549 cells via regulating E-cadherin suppressor Snail.

Recent studies demonstrated that the progression and metastasis of lung cancer were associated with human antigen R (HuR), a post-transcriptional RNA-binding protein that stabilize and regulate the expression of many tumor-related genes. Although HuR was shown to affect the expressions of epithelial cadherin (E-cadherin), a tumor migration suppressor, in airway epithelial cells, esophageal squamous and colon cancer cells, direct evaluation for the effect and mechanism of HuR on the migration and invasion of lung cancer cells is not documented. In this study, HuR was knocked down via RNA interference and overexpressed using recombinant plasmid in adenocarcinomic human alveolar basal epithelial A549 cells. No apparent inhibition of cell viability was observed. HuR knocked down significantly suppressed A549 migration and invasion in scratch wound healing and transwell assays, with an increase in E-cadherin expression, while the overexpression of HuR notably facilitated A549 migration and invasion, with a decrease in E-cadherin level. In addition, immunoprecipitation study showed that HuR directly interacted with Snail, a repressor of E-cadherin, and upregulated the expression of Snail in A549 cells. These combined results suggested that the effect of HuR on A549 migration and invasion was realized by stabilizing and increasing the expression of Snail, which in-turn interfered with the expression of E-cadherin. The finding of this study revealed direct evidence that HuR affected the migration and invasion of lung cancer cells via regulating E-cadherin and Snail, providing an additional reference and mechanistic clue for further researches and therapeutic strategies in treating lung cancer.