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DesignThere is a strong correlation between dietary intake and allergic diseases. Ultra-processed foods (UPFs) are gradually becoming dominant worldwide and causing health problems for children and adults. We hope to determine whether links exist between UPFs and allergic symptoms.MethodsWe investigated data from 2,736 children (16–19 years) and 4,256 adults (≥20 years) from the National Health and Nutritional Examination Survey (NHANES) 2005–2006. The associations between the mean UPFs contribution to total energy intake and all allergic symptoms (IgE, current asthma, allergy, rash, sneeze, wheeze, eczema, and hay fever) were estimated by weighted multivariate logistic regression.ResultsLogistic regression analysis showed UFPs were negatively associated with IgE levels in children. Those with higher quartiles had a reduced risk from 16% (OR, 0.84, 95%CI, 0.55 to 1.28) to 34% (OR, 0.66, 95%CI, 0.49 to 0.89), p for trend = 0.006. UPFs were also positively related to current asthma in children with an increased risk of 11% (OR, 1.11, 95%CI, 0.79 to 1.56) to 76% (OR, 1.76, 95%CI, 1.10 to 2.82), p for trend = 0.0393. UPFs were also associated with eczema in girls. But there was no association observed between UPFs and allergic symptoms in adults.ConclusionOur results suggested that UPFs assessed by the NOVA system were associated with IgE, current asthma in children, and eczema in girls. These results further support the need to test the association of modern dietary patterns with allergic symptoms.

ObjectiveNon-invasive disease indicators are currently limited and need further research due to the increased non-alcoholic fatty liver disease (NAFLD) prevalence worldwide. The serum uric acid-to-high-density lipoprotein cholesterol ratio (UHR) has been recognized as a novel inflammatory and metabolic marker. Herein, we explored the correlation between UHR and the risk of NAFLD in-depth.MethodsA total of 3,766 participants were included in our survey, and the National Health and Nutrition Examination Survey (NHANES) 2017–2018 cycle provided the cross-sectional study population. Weighted multivariable logistic regression and multivariate linear regression analyses were performed to assess the association between the UHR and the odds of NAFLD and liver steatosis and fibrosis severity, respectively. Moreover, we explored the non-linear relationship between the UHR and NAFLD by the generalized additive model.ResultsNAFLD probabilities were statistically demonstrated to be positively correlated with the UHR (OR = 1.331 per SD increase, 95% CI: 1.100, 1.611). The positive connection of the UHR with NAFLD risk persisted significantly in female subjects but not in male subjects in subgroup analyses stratified by gender. The non-linear relationship analysis demonstrated that a UHR between ~20 and 30% suggested a saturation effect of NAFLD risk. Furthermore, a dramatically positive correlation was found between the UHR and hepatic steatosis severity but not fibrosis. Finally, the receiver operating characteristic analysis suggested that UHR had a better predictive value for NAFLD than either serum uric acid (sUA) or high-density lipoprotein cholesterol (HDL) alone [UHR (area under curve): 0.6910; 95% CI: 0.6737–0.7083; P < 0.0001].ConclusionOur investigation revealed that the elevated UHR level was independently related to an increased NAFLD risk and the severity of liver steatosis in American individuals. The correlation differed according to sex. This non-invasive indicator may enhance the capacity to predict the onset of NAFLD and may uncover alternative therapeutic interventional targets.

Background: Multiple studies showed that long-chain noncoding RNA H19 (LncRNA H19) is high-expressed in human and mouse abdominal aortic aneurysms (AAAs). We speculated that it plays an important role in arterial disease, and therefore studied the role and mechanism of H19 in aortic dissection (AD). Methods: The expressions of related genes in human aortic smooth muscle cells (HASMCs) induced by platelet-derived growth factor BB (PDGF-BB) or in the aortic tissue of AD patients/mice were identified by Western blot and quantitative real-time polymerase chain reaction. The targeting relationship between H19 and miR-193b-3p was predicted and verified by bioinformatics analysis, dual luciferase assay, RNA pull-down assay, RNA immunoprecipitation (RIP), and Pearson correlation coefficient. The H19 and miR-193b-3p effects on the biological functions of tissues and cells were examined by MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, thiazolyl blue tetrazolium bromide) assay, wound-healing assay, and Hematoxylin–Eosin (HE) staining. Results: LncRNA H19 was abnormally high-expressed in thoracic aorta tissues of AD patients, and it could competitively bind to and inhibit miR-193b-3p. In the PDGF-BB group, the expressions of H19, matrix metallopeptidase (MMP) 2 (MMP-2) and MMP-9 were up-regulated and the expressions of miR-193b-3p, α-SMA, and SM22α were down-regulated; moreover, the proliferation and migration rate of HASMCs were increased. However, H19 silencing reversed the regulation of PDGF-BB on HASMCs. More interestingly, miR-193b-3p inhibitor could partially reverse the effect of H19 silencing. In addition, the above results were verified by animal experiments, showing that shH19 and up-regulated miR-193b-3p could significantly reduce the thoracic aorta pathological damage in AD mice. Conclusion: LncRNA H19 regulated smooth muscle cell function by sponging miR-193b-3p and it participated in the development of AD.

Background Type 2 diabetes mellitus (T2DM) is a well-known independent risk factor for non-alcoholic fatty liver disease (NAFLD). However, research exploring the association between blood glucose management and the risk of NAFLD status in subjects without diabetes was insufficient. This study aimed to explore the association of glycated hemoglobin (HbA1c) with NAFLD status and the severity of liver steatosis and fibrosis in non-diabetic people. Methods A cross-sectional analysis was conducted on 2998 non-diabetic American adults using data from the National Health and Nutrition Examination Survey (NHANES) 2017–2018 cycle. We used multivariable logistic regression models to evaluate the association between HbA1c and NAFLD status and the severity of liver steatosis and fibrosis. Interaction and stratified analyses were additionally performed. Results The multivariate regression analyses showed that HbA1c was associated independently with NAFLD status in all the models (model1: OR = 2.834, 95%CI: 2.321, 3.461; model 2: OR = 2.900, 95%CI: 2.312, 3.637 and model 3: OR = 1.664, 95%CI: 1.284, 2.156). We further performed the interaction and stratified analyses and discovered a significant interaction between HbA1c and BMI (Pinteraction < 0.05). Finally, a robust link was shown between HbA1c level and the severity of liver steatosis, which was mainly significant in the prediabetes group, while the correlation was not significant in HbA1c level and severity of liver fibrosis after controlling for all the potential confounders. Conclusions We concluded that HbA1c level was positively correlated to the risk of developing NAFLD in a large non-diabetic American population. Moreover, HbA1c level was associated with the severity of liver steatosis in subjects with prediabetes, suggesting that routine screening for HbA1c among individuals with prediabetes is necessary.