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Metal exposure is associated with vascular endothelial inflammation, an early pathological phenotype of atherosclerotic cardiovascular events. However, the underlying mechanism linking exposure, metabolic changes, and outcomes remains unclear. We aimed to investigate the metabolic changes underlying the associations of chronic exposure to metal mixtures with vascular endothelial inflammation. We recruited 960 adults aged 20-75 years from residential areas surrounding rivers near abandoned lead-zinc mine and classified them into river area and non-river area exposure groups. Urine levels of 25 metals, Framingham risk score (FRS), and serum concentrations of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), as biomarkers of vascular endothelial inflammation, were assessed. A "meet-in-the-middle" approach was applied to identify causal intermediate metabolites and metabolic pathways linking metal exposure to vascular endothelial inflammation in representative metabolic samples from 64 participants. Compared to the non-river area exposure group, the river area exposure group had significantly greater urine concentrations of chromium, copper, cadmium, and lead; lower urine concentrations of selenium; elevated FRS; and increased concentrations of ICAM-1 and VCAM-1. In total, 38 differentially abundant metabolites were identified between the river area and non-river area exposure groups. Among them, 25 metabolites were significantly associated with FRS, 8 metabolites with ICAM-1 expression, and 10 metabolites with VCAM-1 expression. Furthermore, fructose, ornithine, alpha-ketoglutaric acid, urea, and cytidine monophosphate, are potential mediators of the relationship between metal exposure and vascular endothelial inflammation. Additionally, the metabolic changes underlying these effects included changes in arginine and proline metabolism, pyrimidine metabolism, starch and sucrose metabolism, galactose metabolism, arginine biosynthesis, and alanine, aspartate, and glutamate metabolism, suggesting the disturbance of amino acid metabolism, the tricarboxylic acid cycle, nucleotide metabolism, and glycolysis. Overall, our results reveal biomechanisms that may link chronic exposure to multiple metals with vascular endothelial inflammation and elevated cardiovascular risk.

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Severe acute malnutrition (SAM) is a major public health concern in Yemen, particularly in areas affected by ongoing conflict war. SAM is defined as a very low weight for height, by visible severe wasting, or by the presence of nutritional edema. The prevalence of SAM in Yemen has increased dramatically since the onset of the conflict. Prior studies have focused on evaluating prevalence, but this novel study aimed to assess the risk factors associated with SAM prevalence. Five thousand two hundred and seventeen patients of SAM admitted at 12 sentinel hospitals were enrolled, and data were collected and analyzed. Marasmus was the most common form. Numerous risk factors contribute to the high prevalence of SAM in Yemen, including food insecurity. The current conflict has hampered food production, distribution, and access. Awareness of risk factors can prevent SAM in the general population.

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BACKGROUND: Ideal cardiovascular health (CVH) is related to the future risk of cardiovascular disease. Sleep duration is an important factor influencing health outcomes. The association between sleep duration and CVH is unclear. OBJECTIVES: We aimed to explore the associations between sleep duration and CVH among Chinese adults. METHODS: This cross-sectional study was based on nationally representative samples from 2009 China Health and Nutrition Survey (CHNS). Sleep duration was categorized as ≤6, 7, 8, and ≥9 h. The CVH scores were evaluated. Generalized linear regressions and restricted cubic splines were used to determine the association between sleep duration and CVH. RESULTS: A total of 8,103 Chinese adults with a mean age of 50.29 (14.97) years were included. The mean (SD) CVH score was 3.96 (1.43). Only 36.7% of the participants had ideal CVH. Sleep duration was positively associated with ideal CVH (P-trend < 0.05). When comparing the long sleep duration with the short sleep duration, short sleep duration significantly decreased the mean CVH score, ß = -0.24 (95% CI: -0.36, -0.13) and increased the risk of nonideal CVH, OR = 1.38 (95% CI: 1.15, 1.67) by generalized linear regressions. The restricted cubic splines showed CVH did not have a significant nonlinear relationship with sleep duration. The P-value for nonlinear was 0.161. The association of sleep duration with CVH had no obvious threshold. CONCLUSION: Short sleep duration was associated with decreased odds of ideal CVH and lower mean CVH score. Confirmation through longitudinal studies is needed.

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Maladapted vascular endothelial metabolism in the context of endothelial function differing in phenotype remains unknown, which limits our understanding of the heterogeneous pathogenesis of atherosclerotic cardiovascular disease (CVD). This study aimed to profile serum metabolic alterations of different vascular endothelial function phenotypes in asymptomatic adults at extreme cardiovascular risk. In addition to 12 CVD patients, 103 individuals free of CVD were categorized as having normal endothelial function (NEF) (n = 30), cardiovascular risk-promoting endothelial function (PEF) (n = 18), cardiovascular risk-resistant endothelial function (REF) (n = 25), and vulnerable endothelial function (VEF) (n = 30). Serum metabolic profiles were detected using gas chromatography time-of-flight/mass spectrometry and multivariate statistics. Compared to the NEF group, a total of 17, 17, 22, and 13 differential metabolites were identified in the PEF, REF, VEF, and CVD groups, respectively. Of the altered metabolic pathways, multiple pathways were consistent between the PEF and CVD groups, including pyrimidine metabolism, starch and sucrose metabolism, aminoacyl-tRNA biosynthesis, arginine and proline metabolism, and d-glutamine and d-glutamate metabolism. Notably, a relative increase in low-calorie sugar in galactose metabolism was exclusively found in the REF group, and a relative increase in the ratio of acetyl-CoA to CoA was suggested in the VEF group based on elevated butanoate metabolism and reduced pantothenate and CoA biosynthesis. Our findings clearly indicate distinct metabolic patterns across groups with heterogeneous vascular endothelial function in the context of extreme cardiovascular risk, and improve our understanding of the pathogenic heterogeneity of early CVD in asymptomatic populations.

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Impaired vascular endothelial function has attracted attention as a prognostic indicator of cardiovascular prevention. The association between impaired endothelial function and cardiovascular risk in the asymptomatic population, however, has been poorly explored. We evaluated the association of brachial artery flow-mediated dilation (FMD) with Framingham-estimated 10-year cardiovascular disease (CVD) risk in subjects free of CVD, especially by cardiovascular risk profiles. In total, 680 adults aged 30-74 years were enrolled from Rongan and Rongshui of Liuzhou, Guangxi, China, through a cross-sectional study in 2015. In the full-adjusted model, the odds ratio for the estimated 10-year CVD risk comparing the low FMD (<6%) with the high FMD (≥10%) was 2.81 (95% confidence interval [CI]: 1.21, 6.53; P for trend = 0.03). In subgroup analyses, inverse associations between FMD and the estimated 10-year CVD risk were found in participants with specific characteristics. The adjusted odds ratios, comparing the 25th and the 75th percentiles of FMD, were 2.77 (95% CI: 1.54, 5.00) for aged ≥60 years, 1.77 (95% CI: 1.16, 2.70) for female, 1.59 (95% CI: 1.08, 2.35) for nonsmokers, 1.74 (95% CI: 1.02, 2.97) for hypertension, 1.59 (95% CI: 1.04, 2.44) for normal glycaemia, 2.03 (95% CI: 1.19, 3.48) for C-reactive protein ≥10 mg/L, and 1.85 (95% CI: 1.12, 3.06) for eGFR <106 mL/minute per 1.73 m2. Therefore, impaired endothelial function is associated with increased CVD risk in asymptomatic adults. This inverse association is more likely to exist in subjects with higher cardiovascular risk.

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Requirements for selenium and other antioxidant nutrients are increased in pro-oxidant and pro-inflammatory conditions such as excess adiposity. Data concerning the association of excess general and central adiposity with circulating selenium concentrations, however, are limited. We examined the cross-sectional associations of body mass index (BMI), percent body fat (%BF), and waist circumference (WC) with serum selenium concentrations in 6440 men and 6849 women aged ≥20 years who participated in the U.S. Third National Health and Nutrition Examination Survey. In multivariable analyses, the average difference (95% confidence interval (CI)) in serum selenium comparing the highest with the lowest quartiles of BMI was -4.0 (-5.5, -1.6) ng/mL in both men and women. These inverse associations were evident after further adjustment for WC. For %BF, the average differences (95% CI) in serum selenium between the highest and the lowest quartiles of %BF were -1.7 (-4.2, 0.7) ng/mL in men and -4.5 (-7.0, -1.9) ng/mL in women. The inverse association in women persisted after adjusting for WC. For WC, the average differences (95% CI) in serum selenium between the highest and the lowest quartiles were -1.9 (-3.8, -0.1) ng/mL in men and -3.9 (-5.8, -2.0) ng/mL in women. After further adjustment for BMI, the inverse association became positive in men and null in women. Our findings suggest that general and central adiposity have different associations with serum selenium levels and that these associations may depend on gender.

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This study aimed to determine the metabolic profile of non-toxic cadmium (Cd)-induced dysfunctional endothelial cells using human umbilical vein endothelial cells (HUVECs). HUVECs (n = 6 per group) were treated with 0, 1, 5, or 10 µM cadmium chloride (CdCl2) for 48 h. Cell phenotypes, including nitric oxide (NO) production, the inflammatory response, and oxidative stress, were evaluated in Cd-exposed and control HUVECs. Cd-exposed and control HUVECs were analysed using gas chromatography time-of-flight/mass spectrometry. Compared to control HUVECs, Cd-exposed HUVECs were dysfunctional, exhibiting decreased NO production, a proinflammatory state, and non-significant oxidative stress. Further metabolic profiling revealed 24 significantly-altered metabolites in the dysfunctional endothelial cells. The significantly-altered metabolites were involved in the impaired tricarboxylic acid (TCA) cycle, activated pyruvate metabolism, up-regulated glucogenic amino acid metabolism, and increased pyrimidine metabolism. The current metabolic findings further suggest that the metabolic changes linked to TCA cycle dysfunction, glycosylation of the hexosamine biosynthesis pathway (HBP), and compensatory responses to genomic instability and energy deficiency may be generally associated with dysfunctional phenotypes, characterized by decreased NO production, a proinflammatory state, and non-significant oxidative stress, in endothelial cells following non-toxic Cd exposure.

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This study was to evaluate the association of urine arsenic with predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk in U.S. adults with hypertension. Cross-sectional analysis was conducted in 1570 hypertensive adults aged 40-79 years in the 2003-2012 National Health and Nutrition Examination Survey (NHANES) with determinations of urine arsenic. Predicted 10-year ASCVD risk was estimated by the Pooled Cohort Equations, developed by the American College of Cardiology/American Heart Association in 2013. For men, after adjustment for sociodemographic factors, urine dilution, ASCVD risk factors and organic arsenic intake from seafood, participants in the highest quartiles of urine arsenic had higher 10-year predicted ASCVD risk than in the lowest quartiles; the increases were 24% (95% confidence interval (CI): 2%, 53%) for total arsenic, 13% (95% CI: 2%, 25%) for dimethylarsinate and 22% (95% CI: 5%, 40%) for total arsenic minus arsenobetaine separately. For women, the corresponding increases were 5% (95% CI: -15%, 29%), 10% (95% CI: -8%, 30%) and 0% (95% CI: -15%, 19%), respectively. Arsenic exposure, even at low levels, may contribute to increased ASCVD risk in men with hypertension. Furthermore, our findings suggest that particular circumstances need urgently to be considered while elucidating cardiovascular effects of low inorganic arsenic levels.

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BACKGROUND: Body mass index (BMI) and hemoglobin (Hb) are positively associated with hypertensive disorders among pregnant women. The aim of this study was to estimate a potential interaction between high BMI and high Hb concentrations on systolic blood pressure (SBP) and diastolic blood pressure (DBP) in pregnancy. METHODS: We recruited 4497 single-birth women aged 18-43 years who received routine antenatal care at three hospitals of Guigang, Guangxi, China, from December 2007 to January 2011. Of 4497 participants, 3472 women were in the first trimester, with following up, 2986 women and 2261 women were left in the second and third trimester, respectively. Clinical data were derived from medical records of each woman. We used multivariable linear regression, by trimesters of pregnancy, to evaluate the associations of high BMI and high Hb concentrations with SBP and DBP according to cross-sectional design. RESULTS: In multivariable analyses, BMI was positively associated with SBP throughout all trimesters, but the corresponding association for Hb concentrations only in the first trimester, whereas both BMI and Hb concentrations were positively associated with DBP in the first and third trimesters. After full adjustment for confounding, the average differences in SBP and DBP comparing women with high BMI and high Hb to those with non-high BMI and non-high Hb were 2.9 mmHg (95% CI: 0.8 to 5.0 mmHg) and 3.9 mmHg (95% CI: 1.5 to 6.3 mmHg) in the first trimester, 2.6 mmHg (95% CI: 0.4 to 4.8 mmHg) and 1.5 mmHg (95% CI: -1.3 to 4.3 mmHg) in the second trimester, and 4.8 mmHg (95% CI: 2.3 to 7.4 mmHg) and 5.7 mmHg (95% CI: 3.2 to 8.3 mmHg) in the third trimester, respectively. With respect to the interaction, significant combined effects between high BMI and high Hb were confirmed on SBP (P = 0.02) and DBP (P = 0.004) in the third trimester, and the amount of interaction on SBP and DBP were 2.0 mmHg (95% CI: 0.1 to 3.9 mmHg) and 2.3 mmHg (95% CI: 0.4 to 4.3 mmHg), respectively. CONCLUSION: Our findings suggest that high BMI and high Hb concentrations may have a synergistic effect on blood pressure in late stage of pregnancy.

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OBJECTIVE: To investigate the association between single nucleotide polymorphisms (SNPs) in cytokine IL-6, IL-10 genes and HBV-related hepatocellular carcinoma (HCC). METHODS: A hospital-based case-control study was conducted in 381 cases with HBV-related HCC, 340 HBsAg carriers and 359 non-tumor controls. Genotypes of -572 site of IL-6 gene and -819, -592 sites of IL-10 gene were determined by real-time polymorphism chain reaction. Unconditional logistic regression was used to estimate the odds ratios (ORs) and 95 confidence intervals (CIs). RESULTS: For the G/C alleles of -572 loci on IL-6 gene, there were significant differences between the three groups (P < 0.05). Compared with CC genotype, GG genotype increased the risk of HBV infection (OR = 2.171, 95%CI: 1.068 - 4.415), but did not seem to be associated with HCC. For the alleles of -819 and -592 site of IL-10 gene, there were significant differences between the three groups (P < 0.05). Compared with CC genotype, TT genotype increased the risks of both HCC (OR = 2.791, 95%CI: 1.326 - 5.874), and HCC in HBsAg carriers (OR = 3.522, 95%CI: 1.707 - 7.266). When compared with CC genotype on -592 site, the AA genotype reduced the risk of both HCC (OR = 0.389, 95%CI: 0.173 - 0.875), and HCC in HBsAg carriers (OR = 0.336, 95%CI: 0.154 - 0.734). CONCLUSION: The SNPs in -572 site of IL-6 gene might be associated with the risk of HBV infection. The SNPs in -819 site of IL-10 gene increased the risk of HCC, but -592 site of IL-10 gene decreased the risk of HCC.

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OBJECTIVE: To explore congenital heart diseases (CHD) in their offsprings in association with parental methylenetetrahydrofolate reductase (MTHFR) gene C677T, cystathionine beta-synthase (CBS) gene T833C, and environmental factors. METHODS: A 1:1 case-control study was carried out to investigate 115 pairs of case and controlled children and their parents, and the parents' MTHFR gene 677 C-->T mutation and CBS gene 833 T-->C mutation were also identified. The possible risk factors were analysed by simple and multiple factors logistic regression methods. RESULTS: Results revealed that 5 factors were related to the occurrence of CHD in the offsprings: maternal exposures to pesticides in the early stage of pregnancy (OR = 8.62), suffering from diseases during pregnancy (OR = 2.069), catching cold in the early stage of pregnancy (OR = 4.125), under depressed or nervous condition during pregnancy (OR = 4.653), maternal MTHFR 677TT genotype (OR = 3.872). CONCLUSION: These results suggested that maternal MTHFR 677TT genotype was one of the risks to the occurrence of CHD in offspring but parents' CBS gene 833 T-->C mutation did not get involved in CHD. In addition, the occurrence of CHD was related to maternal exposures to pesticides, catching a cold, suffering from diseases, depressed or under nervous condition in the early stage of pregnancy or during pregnancy.

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