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Ralstonia solanacearum (Rs), a soilborne phytopathogen, causes bacterial wilt disease in a broad range of hosts. Common approaches, for example, the direct reduction of the pathogen using classic single broad-spectrum probiotics, suffer from poor colonization efficiency, interference by resident microbiota, and nonnative-microorganism invasion. The soil microbiota plays an important role in plant health. Revealing the intrinsic linkage between the microbiome and the occurrence of disease and then applying it to agroecosystems for the precise control of soilborne diseases should be an effective strategy. Here, we surveyed the differences in the microbiome between healthy and diseased soils used for tomato planting across six climatic regions in China by using 16S rRNA amplicon and metagenomic sequencing. The roles of species associated with disease symptoms were further validated. Healthy soil possessed more diverse bacterial communities and more potential plant probiotics than diseased soil. Healthy soil simultaneously presented multiple strategies, including specifically antagonizing Rs, decreasing the gene expression of the type III secretion system of Rs, and competing for nutrition with Rs. Bacteria enriched in diseased samples promoted the progression of tomato bacterial wilt by strengthening the chemotaxis of pathogens. Therefore, Rs and its collaborators should be jointly combatted for disease suppression. Our research provides integrated insights into a multifaceted strategy for the biocontrol of tomato bacterial wilt based on the individual network of local microbiota. IMPORTANCE In the current work, the relationship between the soil microbiota and tomato bacterial wilt on a large scale offered us a comprehensive understanding of the disease. The delicate strategy of the microbiota in soil used for growing tomatoes to conquer the strong competitor, Rs, was revealed by microbiome research. The collaborators of Rs that coexist in a common niche with Rs strengthened our understanding of the pathogenesis of bacterial wilt. Bacteria enriched in healthy soil that antagonized pathogens with high specificity provide a novel view for ecofriendly probiotics mining. Our study offers new perspectives on soilborne-pathogen biocontrol in agroecosystems by decoding the rule of the natural ecosystem.

Objective: To examine whether maternal hair or cord blood selenium levels are associated with infant congenital heart defects (CHDs)., Method: A hospital-based case-control study was performed with samples collected from 2010 to 2014. Selenium levels in maternal hair and fetal cord serum were measured using Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). Data from medical records of infants with CHDs were collected. Logistic regression analysis was employed to examine the independent association between maternal selenium exposure and fetal CHD., Results: In total, 888 pregnant women were included in this study. Median (interquartile range) selenium levels in of maternal hair was similar in the control and CHD group. A significant association was detected between increased maternal hair selenium concentration and CHDs in offspring (adjusted odds ratio [aOR] 3.57, 95 %CI, 1.90-6.70). The association was present in all CHD groups, including septal defects, conotruncal defects, left ventricular outflow tract obstruction, right ventricular outflow tract obstruction, and anomalous pulmonary venous return., Conclusion: High maternal selenium level is significantly associated with the occurrence of fetal CHD., (© 2019 John Wiley & Sons, Ltd.)

Objectives: This study aimed to analyze the association between fetal lead or aluminum exposure and congenital heart disease (CHD) occurrence as well as to explore the mechanism of oxidative stress in heart development., Methods: Lead and aluminum concentrations were measured by ICP-MS in umbilical serum. The oxidative stress statuses were analyzed by measuring SOD, GPx and MDA with colorimetric assays., Results: Higher concentrations of Al were seen in the CHD groups compared to the controls. The risk of CHD occurrence increased markedly in the highly elevated Al group (aOR 2.08, 95%CI 1.11-3.88). With increasing Al and Pb levels, the activity of SOD decreased, and the level of MDA increased. Significantly decreased activity of SOD and GPx were found in the CHD groups (P < 0.05)., Conclusion: Fetal aluminum exposure may contribute to CHD occurrence. Oxidative stress was related to the concentration of Pb and Al, which may be involved in the occurrence of CHD., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background The overall incidence of hyperphenylalaninemia (HPA) in China is 1:11,763, with tetrahydrobiopterin (BH4) deficiency accounting for 8.55% of patients with HPA in the mainland. Much progress has been made in the diagnosis and treatment of BH4 deficiency with the introduction of neonatal screening in China. However, the screening rate is still low and screening is not universally available. Methods A total of 44 BH4-deficient patients were enrolled in this study, of which 39 were diagnosed with BH4 deficiency, while the remaining five showed typical characteristics of BH4 deficiency at a later period. The entire coding regions and adjacent intronic regions of GCH1, PTS, PCBD1 and QDPR genes were analyzed using target sequencing. Results Nineteen (n=19) different mutations in the PTS gene including four novel mutations and one mutation in QDPR were identified. p.P87S, p.D96N, IVS1-291A>G, p.N52S, p.K91R, p.V56M, p.T106M and p.F40GfsX53 in PTS were the prevalent mutations with ≥3% relative frequency. The mutation p.R221X in the QDPR gene was found with relatively lower frequencies (2.27%). The remaining 12 mutations in PTS were found at relative frequencies of 1.14%. Conclusions The results could be of value for genetic counseling and prenatal diagnosis in the patients' families and for the molecular diagnosis of BH4 deficiencies. Furthermore, four novel mutations expand and improve the PTS mutation database.

Mutations in the gene encoding phenylalanine hydroxylase (PAH) are associated with various degrees of phenylketonuria (PKU). The aim of our study was to define the genotype-phenotype correlations of mutations in the PAH gene that cause phenylketonuria (PKU) among the Chinese mainland population. Mutations in the PAH gene were analysed by next-generation sequencing, and a genotype-phenotype correlation analysis was performed in 1079 patients. Fifteen "null + null" genotypes, including four homoallelic and eleven heteroallelic genotypes, were clearly associated with classic PKU. Five functionally hemizygous (p.E280K, p.R252Q, p.E56D, p.S310F and p.T372R) and four compound heterozygous (p.T278I/p.S359L, p.R408W/p.R243Q, p.F161S/p.R243Q and p.F161S/p.R413P) genotypes were clearly associated with classic PKU. Ten functionally hemizygous genotypes, p.G257V, p.R158W, p.L255S, p.G247V, p.F161S, p.R158Q, p.V388M, p.I65T, p.I324N and p.R400K, were frequently associated with classic PKU. Three functionally hemizygous genotypes, p.P147L, p.I95del and p.F331S, and four compound heterozygous genotypes, p.G257V/p.R408Q, p.A434D/p.R413P, p.R243Q/p.A47E and p.R241C/p.G239D, were consistently correlated with mild PKU. Three functionally hemizygous genotypes, p.H107R, p.Q419R and p.F392I, and nine compound heterozygous genotypes (p.G312V/p.R241C, p.R243Q/p.V230I, p.R243Q/p.A403V, p.R243Q/p.Q419R, p.R243Q/p.R53H, p.R243Q/p.H107R, p.R241C/p.R408Q, p.R241C/p.H220P and p.R53H/p.R400K) were consistent with mild hyperphenylalaninaemia (MHP). Our study provides further support for the hypothesis that the PAH genotype is the main factor that determines the phenotype of PKU.

The major causes of congenital heart diseases (CHDs) are the interactions of genetic and environmental factors. We conducted a case-control study in 357 mothers of CHDs fetuses and 270 control mothers to investigate the association of maternal PAHs exposure, AHR, CYP1A1, CYP1A2, CYP1B1 and CYP2E polymorphisms, the interaction between PAHs exposure and genetic variants with the risk of CHDs. The higher level PAHs exposure was associated with the risk of CHDs (aOR = 2.029, 95% CI: 1.266, 3.251) or subtypes. The haplotypes of AHR or CYP1A2 were associated with the risk of CHDs: AHR: C-G-A-C: aOR = 0.765; T-A-G-A: aOR = 1.33; CYP1A2: A-T:aOR = 1.75; C-C: aOR = 0.706. When exposed to higher level PAHs, the risk of CHDs among the mothers carrying rs2158041 "C/T or T/T" genotype or rs7811989 "G/A or A/A" genotype in AHR was 1.724 (χ 2  = 7.209, P = 0.007) or 1.735 (χ 2  = 7.364, P = 0.007) times greater than the aOR in the mothers carrying wild genotype. The multiplicative-scale interactions between PAHs exposure and polymorphisms of CYP1A2 rs4646425 (P = 0.03) or CYP2E1 rs915908 (P = 0.0238) on the risk of CHDs were observed. Our study suggests that maternal AHR polymorphisms may modify the association of PAHs exposure with CHDs, CYP1A2 or CYP2E1 polymorphisms significantly interact with PAHs exposure on CHDs.

Context: Several studies have investigated the association between heavy metal exposure and congenital heart defects (CHDs). However, there are limited data regarding the relationship between barium exposure and the occurrence of CHDs. The objective of this study was to analyze the association between barium exposure in mothers and the risk of CHD in offspring., Materials and Methods: We developed a case-control study with 399 cases and 490 controls with normal live births in China. The concentrations of barium in hair of pregnant woman and fetal placenta were measured. We used a logistic regression analysis to explore the association between barium exposure and the risk of CHD., Results: Logistic regression analysis indicated that the median concentration of barium in maternal hair in the CHD group was 4.180 ng/mg (adjusted odds ratio [aOR], 1.230; 95% confidence interval [CI], 1.146-1.321; p < .001), which was significantly higher than that in the control group (2.740 ng/mg). Furthermore, the median concentration of barium in fetal placental tissue in the CHD group was 0.617 ng/mg, while that in the control group was 0.447 ng/mg (aOR, 1.392; 95% CI, 1.074-1.659; p = .003). Significant differences in the concentration of barium in hair were also found between the different CHD subtypes and the controls. These differences were found in cases with septal defects (p < .001), conotruncal defects (p < .001), right ventricular outflow track obstruction (p < .001), left ventricular outflow track obstruction (p < .001), and anomalous pulmonary venous return (p = .010). Significantly different barium concentrations in fetal tissue were only found in cases with septal defects (p = .010)., Conclusions: Maternal barium exposure was dose-dependently related to the risk of CHD in the offspring. Our findings suggest that the occurrence of some subtypes of CHD is associated with barium exposure.