Associations of urine metals and metal mixtures during pregnancy with cord serum vitamin D Levels: A prospective cohort study with repeated measurements of maternal urinary metal concentrations.

BACKGROUND: Vitamin D deficiency has been associated with the increased risk of many diseases, especially during early life. Exposure to some toxic metals may decrease vitamin D levels in adults and children in previous studies. However, less is known about the associations of maternal metals exposure during pregnancy with newborns' vitamin D status. OBJECTIVE: We conducted a prospective cohort study to investigate the relationships between urine metals and metal mixtures during pregnancy and newborns' vitamin D status. METHODS: Urine samples of 598 pregnant women were collected in each trimester and cord blood samples of newborns were collected at delivery. The concentrations of 20 metals in urine and 25-hydroxyvitamin D [25(OH)D] in cord serum were quantified. Generalized linear models were used to estimate the associations between individual metals and cord serum total 25(OH)D. We applied Bayesian Kernel Machine Regression (BKMR) to evaluate the mixture and interaction effects of urine metals. RESULTS: In individual metals analyses, we reported that a double increase in urine vanadium (V), cobalt (Co), and thallium (Tl) throughout pregnancy was associated with a 9.91% [95% confidence interval (CI): -18.58%, -0.30%], 11.42% (95% CI: -17.73%, -4.63%), and 12.64% (95% CI: -21.44%, -2.86%) decrease in cord serum total 25(OH)D, respectively. Exposures to the three metals during the whole pregnancy were also correlated to increased odds for newborns' vitamin D deficiency (<20 ng/mL) [odds ratio (95% CI): 1.80 (1.05, 3.10) for V, 1.88 (1.25, 2.82) for Co, and 1.90 (1.07, 3.38) for Tl]. BKMR analyses revealed a negative influence of metal mixtures (V+Co+Tl) on neonatal vitamin D status, as well as potential synergism between V and Co and between V and Tl. CONCLUSIONS: Our study provides evidence of negative impacts of maternal exposure to V, Co, and Tl during pregnancy on cord serum vitamin D levels at delivery. Potential synergism between V and Co and between V and Tl existed in their associations with cord serum total 25(OH)D.

Fine particulate matter exposure and perturbation of serum metabolome: A longitudinal study in Baoding, China.

Metabolomics represents a powerful tool for measuring environmental exposures and biological responses to unveil potential mechanisms. Few studies have investigated the effects of exposure to fine particulate matter (PM2.5) longitudinally on serum metabolomics in regions with high-level PM2.5. Therefore, we examined the changes of serum metabolomics corresponding to individual PM2.5 exposure levels in spring and autumn among 63 healthy college students in Baoding city, Hebei, China. The metabolic profiling was determined by ultra-performance liquid chromatography coupled to quadrupole time-of-flight mass spectrometry. The average level of individual PM2.5 in the spring was 1.82-fold higher than in the autumn (240 µg/m3 vs 132 µg/m3). Males were exposed to a higher level of PM2.5 than females in the spring. Metabolic profiling was clearly separated by orthogonal partial least square-discriminant analysis in males but not in females. In the analysis of the associations between the metabolome and PM2.5 of the two seasons, the changes of 14 serum metabolites were significantly associated with PM2.5 in males. The metabolites related to heme metabolism (bilirubin, biliverdin), energy metabolism and oxidative stress (2-Octenoylcarnitine, N-Heptanoylglycine, and acetylcysteine), phospholipid metabolism (lysophosphatidic acid, phospholipid acid, and lysophosphatidylethanolamine), and tryptophan metabolism (N-Acetylserotonin, indolepyruvate, and melatonin) were decreased in the range of 2.16%-6.80% for each 10 µg/m3 increase of PM2.5, while thyrotropin-releasing hormone, glutathione, and phosphatidylethanolamine related to energy metabolism and oxidative stress, and phospholipid metabolism were increased in the range of 2.95%-4.90% for each 10 µg/m3 increase of PM2.5. This longitudinal study suggests that higher PM2.5 exposure may induce perturbations in serum metabolic signaling related to oxidative stress and inflammation, and males may be more prone to these metabolic perturbations.

Relevance of serum interleukin-33 and ST2 levels and the natural course of chronic hepatitis B virus infection.

BACKGROUND: Interleukin-33 (IL-33) and ST2 have been demonstrated to be associated with liver damage. However, their potential value in hepatitis B virus (HBV) infection remains unknown. This study was designed to investigate the change of serum IL-33 and ST2 levels in the natural course of chronic HBV infection. METHODS: A total of 120 patients with chronic hepatitis B (CHB), 20 chronic hepatitis B virus carriers in immunotolerant phase and 28 healthy controls were enrolled in this study. All patients with CHB were divided into four groups according to their serum ALT levels. The serum levels of IL-33 and ST2 of all participants were determined by enzyme-linked immunosorbent assay, and compared between each two out of those six groups. RESULTS: No significant differences were found in serum levels of IL-33 and ST2 between the group of CHB with ALT 1-2 upper limit of normal and the healthy controls (P = 0.354 for IL-33 and P = 0.815 for ST2). Other than that, there were significant differences when serum levels of IL-33 and ST2 were compared between any other two out of those six groups (P < 0.05, respectively). The overall correlation analysis indicated that changes of serum IL-33 and ST2 levels were positively associated with ALT levels in patients with chronic HBV infection (rs = 0.879, P < 0.001 for IL-33 and rs = 0.923, P < 0.001 for ST2). No significant differences were found when the serum levels of ALT, IL-33 and ST2 were compared between patients with HBeAg-positive CHB and HBeAg-negative CHB. CONCLUSIONS: Our study revealed that the serum levels of IL-33 and ST2 varied in different courses of chronic hepatitis B virus infection. The serum levels of IL-33 and ST2 elevated as serum ALT levels increased in patients with CHB. They might indicate liver damage for patients with CHB, just like ALT.

Demethylation of tumor necrosis factor-α converting enzyme predicts poor prognosis in acute-on-chronic hepatitis B liver failure.

BACKGROUND AND OBJECTIVE: Tumor necrosis factor-α converting enzyme (TACE) has been demonstrated to be involved in liver inflammation. However, the significance of TACE methylation in acute-on-chronic hepatitis B liver failure (ACHBLF) has not been demonstrated. This study aims to evaluate TACE methylation status in ACHBLF and determine its predictive value for prognosis. METHODS: Forty-five patients with ACHBLF, 80 with chronic hepatitis B (CHB) and 54 healthy controls (HCs) were enrolled. The methylation status of TACE promoter was determined by methylation-specific polymerase chain reaction. The TACE mRNA expression was determined by quantitative real-time polymerase chain reaction. The plasma levels of TACE, TNF-α, sTNFRI, sTNFRII were measured by enzyme-linked immunosorbent assay. RESULTS: TACE methylation was significantly lower in patients with ACHBLF than those with CHB (χ(2)=24.69, P<0.01) and HCs (χ(2)=35.93, P<0.01). Meanwhile, TACE methylation was significantly lower in CHB patients than HCs (χ(2)=4.03, P<0.05). TACE methylation was significantly inversely associated with its mRNA expression (r=-0.68; P<0.01). The plasma levels of TACE, TNF-α, sTNFRI, sTNFRII were significantly higher in patients with ACHBLF than those with CHB (P<0.05, respectively) and HCs (P<0.05, respectively). In patients with ACHBLF, significantly higher prothrombin activity, lower total bilirubin and MELD score were found in TACE methylated group than unmethylated group (P<0.05). ACHBLF patients with methylated TACE showed significantly better survival than those without (P<0.01). CONCLUSION: This study showed that demethylation of TACE promoter occurred in ACHBLF and might serve as a potential prognostic marker.

Overexpression of serum sST2 is associated with poor prognosis in acute-on-chronic hepatitis B liver failure.

BACKGROUND AND OBJECTIVE: Interleukin-33 (IL-33) and soluble ST2 (sST2) have been demonstrated to be involved in liver injury. The present study aims to evaluate serum IL-33 and sST2 level in acute-on-chronic hepatitis B liver failure (ACHBLF) and determine their predictive value for prognosis. METHODS: Serum IL-33 and sST2 level in patients with ACHBLF, chronic hepatitis B (CHB) and healthy controls (HCs) were determined by enzyme-linked immunosorbent assay (ELISA). Clinical and laboratory parameters were obtained. RESULTS: Serum IL-33 was significantly higher in patients with ACHBLF (313.10±419.97pg/ml) than those with CHB (97.25±174.67pg/ml, P<0.01) and HCs (28.39±6.53pg/ml, P<0.01). Serum sST2 was significantly higher in patients with ACHBLF (1545.87±1135.70pg/ml) than those with CHB (152.55±93.28pg/ml, P<0.01) and HCs (149.27±104.90pg/ml, P<0.01). In all participants, serum IL-33 was significantly correlated with sST2 (r=0.43, P<0.01). In patients with ACHBLF, serum IL-33 was significantly correlated with alanine aminotransferase (ALT; r=0.26, P=0.04). Serum sST2 was significantly correlated with total bilirubin (TBIL; r=0.59, P<0.01), Log10 [HBV DNA] (r=-0.47, P<0.01) and model for end-stage liver diseases (MELD; r=0.28, P=0.03). Serum sST2 had an area under the receiver operating characteristic curve (AUC) of 0.81 in predicting 3-month mortality of ACHBLF. Patients with ACHBLF who had sST2 >1507pg/ml showed significantly poorer survival than those who had sST2 ≤1507pg/ml (P<0.01). Moreover, measurement of sST2 and MELD together significantly improved the diagnostic value of MELD alone (P<0.05). CONCLUSIONS: Our study showed that serum IL-33 and sST2 were overexpressed in ACHBLF and sST2 might potentially serve as a prognostic marker for it.

THE PRELIMINARY RESEARCH ABOUT THE REASONS OF BUSTING BAGS OCCASIONALLY DURING SOY STORAGE / 微生物学通报

Shan Qi soy has busting bags, bacteria sum overproof, continue acidification and other problems occasionally during the storage. It's probably caused by the Lactobacillus continue growth in the soy. We tried expounding the relationship between growth and producing acid when Lactobacillus growing in the thin fermented material.