Homocysteine concentration in coronary artery disease and severity of coronary lesions.

Our previous study reckons that the impact of the rs1801133 variant of 5,10-methylenetetrahydrofolate reductase (MTHFR) on coronary artery disease (CAD) is possibly mediated by cardiometabolic disorder. This study is performed to verify this hypothesis. Four hundred and thirty CAD patients and 216 CAD-free individuals were enrolled in this case-control study. The rs1801133 variant was genotyped by PCR-RFLP. Severity of coronary lesions was evaluated by number of stenotic coronary vessels and extent of coronary stenosis. The rs1801133 T allele significantly increased homocysteine levels in patients with CAD and CAD-free individuals. Individuals with the T allele of rs1801133 had an increased risk of developing CAD. In contrast, individuals with the TT genotype of rs1801133 were at high risk of multiple vessel lesions. The carriers of CT genotype had higher levels of systolic blood pressure (SBP), low-density lipoprotein cholesterol (LDL-C), and high-sensitivity C-reactive protein (hs-CRP), and lower levels of apolipoprotein A1 (APOA1) than those with CC genotype in male patients with CAD. The receiver operating characteristic (ROC) curve and precision-recall (PR) curve indicated that hyperhomocysteinemia was sensitive to predict the severity of CAD. Multivariate logistic regression revealed that homocysteine, rs1801133, age, smoking, weight, body mass index (BMI), lipoprotein(a) [Lp(a)], and hs-CRP were independent risk factors for CAD. The increased risk of CAD and severity of coronary lesions associated with rs1801133 in the Chinese Han population were attributed, at least partly, to high homocysteine levels. Hyperhomocysteinemia had a high predictive value for severe CAD or multiple vessel lesions.

Comparative analysis of the hypothalamus transcriptome of laying ducks with different residual feeding intake.

Feed costs account for approximately 60 to 70% of the cost of poultry farming, and feed utilization is closely related to the profitability of the poultry industry. To understand the causes of the differences in feeding in Shan Partridge ducks, we compared the hypothalamus transcriptome profiles of 2 groups of ducks using RNA-seq. The 2 groups were: 1) low-residual feed intake (LRFI) group with low feed intake but high feed efficiency, and 2) high-residual feed intake (HRFI) group with high feed intake but low feed efficiency. We found 78 DEGs were enriched in 9 differential Kyoto Encyclopedia of Genes and Genome (KEGG) pathways, including neuroactive ligand-receptor interaction, GABAergic synapse, nitrogen metabolism, cAMP signaling pathway, calcium signaling pathway, nitrogen metabolism, tyrosine metabolism, ovarian steroidogenesis, and gluconeogenesis. To further identify core genes among the 78 DEGs, we performed protein-protein interaction and coexpression network analyses. After comprehensive analysis and experimental validation, 4 core genes, namely, glucagon (GCG), cholecystokinin (CCK), gamma-aminobutyric acid type A receptor subunit delta (GABRD), and gamma-aminobutyric acid type A receptor subunit beta1 (GABRB1), were identified as potential core genes responsible for the difference in residual feeding intake between the 2 breeds. We also investigated the level of cholecystokinin (CCK), neuropeptide Y (NPY), peptide YY (PYY), ghrelin, and glucagon-like peptide1 (GLP-1) hormones in the sera of Shan Partridge ducks at different feeding levels and found that there was a difference between the 2 groups with respect to GLP-1 and NPY levels. The findings will serve as a reference for future research on the feeding efficiency of Shan Partridge ducks and assist in promoting their genetic breeding.

Prognostic value of serum uric acid in patients with acute heart failure: A meta-analysis.

BACKGROUND: Conflicting results have been reported on the prognostic significance of serum uric acid (SUA) in patients with acute heart failure (AHF). This meta-analysis aimed to determine the prognostic significance of SUA level in patients with AHF. METHODS: We made a comprehensive literature search in Pubmed and Embase databases from inception to April 6, 2018. All available observational studies or post hoc analysis of randomized controlled trial that evaluated the prognostic value of SUA level in patients with AHF were eligible. Outcome of interests were all-cause mortality and the combined endpoint of death or readmission. Prognostic values of SUA level were summarized as higher vs lower SUA category or per 1 mg/ml SUA rise. RESULTS: Ten studies involving 12,854 AHF patients were identified and analyzed. AHF patients with the highest SUA level had an increased risk of all-cause mortality (risk ratio [RR] 1.43; 95% confidence intervals [CI] 1.31-1.56) and combined endpoint of death or readmission (RR 1.68; 95% CI 1.33-2.13) after adjusting potential variables. In addition, per 1 mg/ml SUA rise significantly increased by 11% and 12% higher risk all-cause mortality and combined endpoint of death or readmission, respectively. A leave out 1 study sensitivity analysis confirmed the reliability of the pooling effect sizes. CONCLUSION: This meta-analysis indicates that elevated SUA level independently predicts all-cause mortality and the combined endpoint of death or readmission in AHF patients. Measurement of SUA level may improve risk stratification of adverse outcomes in these patients.