Spatial Effects of Air Pollution on the Siting of Enterprises: Evidence from China.

The siting of enterprises is important for enterprises to formulate business objectives and business strategies, both of which are crucial to the development of enterprises in the future. Although there exists an irrefutable fact that the increasingly serious environmental problems are affecting the behaviors of enterprises, how air pollution affects the siting of enterprises has received little academic attention. Therefore, using the dataset of Chinese prefecture-level cities from 2014 to 2020, this paper employs the Spatial Durbin Model to investigate the direct and spatial spillover effects of air pollution on the site selection of enterprises. In addition, this paper also establishes a mediation effect model to explore the impact mechanism of air pollution on the site selection of enterprises. The empirical results show that air pollution exerts a negative impact on both the local and spatially related regions' enterprises' site selection, and the above conclusion is reinforced through a series of robustness checks. The heterogeneity analysis demonstrates that air pollution has a greater inhibitory effect on the siting of low-cleaning enterprises and small-scale enterprises for the local and adjacent regions. The mechanism analysis results indicate that air pollution inhibits the siting of enterprises by reducing the local labor endowment and market scale. Our study enriches the relevant theory of air pollution and enterprises' location nexus, and it also provides an empirical basis for the Chinese government to formulate policies related to air governance and the siting of enterprises.

Peptides from Extruded Lupin (Lupinus albus L.) Regulate Inflammatory Activity via the p38 MAPK Signal Transduction Pathway in RAW 264.7 Cells.

In this study, protein was extracted from extruded lupin and submitted to gastroduodenal digests to obtain lupin peptides, which were characterized using ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). After this, IQDKEGIPPDQQR (IQD), the lupine peptide monomer characterized after UPLC-MS/MS, was screened out by macrophage inflammatory cytokine production assay. RNA-sequencing analysis was performed to explore the mechanisms underlying the anti-inflammatory activity associated with this peptide. The results indicated that lupin peptides effectively inhibited the lipopolysaccharide-induced overproduction of proinflammatory mediators. IQD inhibited the production of tumor necrosis factor-α, interleukin (IL)-6, IL-1ß, and monocyte chemoattractant protein-1 by 51.20, 38.52, 44.70, and 40.43%, respectively. RNA-sequencing results showed that IQD inhibited the inflammatory response by regulating the gene expression of the p38 mitogen-activated protein kinase pathway and inhibiting downstream inflammatory cytokines. These bioactive peptides may be used to develop new ingredients for anti-inflammatory nutritional supplements.

Genetic variations of VEGF gene were associated with tetralogy of fallot risk in a Chinese Han population.

OBJECTIVES: Tetralogy of Fallot (TOF) is one of the most common forms of congenital heart disease. In this study, we aimed at investigating the associations between genetic variations of vascular endothelial growth factor (VEGF) gene and the risk of TOF in a Chinese Han population. Our findings may contribute to a deeper understanding of TOF pathogenesis and better diagnostic and therapeutic suggestions. METHODS: A total of 165 TOF patients and 240 controls from a Chinese Han population in Shenyang and Harbin were recruited in the current study. Nine single-nucleotide polymorphisms (SNPs) (-2578C/A, -460T/C, -1154G/A, -634G/C, 534C/T, +398G/A, +963C/T, 752C/T, 913G/A) were genotyped by the MALDI-TOF MassARRAY system. Individual SNPs as well as their haplotypes were analyzed for their associations with TOF risk, using odds ratios and the 95% confidence interval under codominant and dominant models. RESULTS: In the single SNP analyses, the mutant homozygous genotypes of -2578C/A (rs699947) and +963C/T (rs3025039) were related with an increased risk of TOF. In addition, carriers with the mutant A allele of -1154G/A (rs1570360) were supposed to have a significantly elevated TOF risk. Similarly, compared with the wild homozygote GG carriers, the GC carrier of -634G/C (rs2010963) revealed a significant relationship with susceptibility of TOF, but not for the mutant homozygote CC carriers. However, no significant association was found for the other five SNPs. Meanwhile, haplotype analysis revealed that CCA and ATA in block 1 (-2578C/A, -460T/C, and -1154G/A) and TTG and TCA in block 3 (+963C/T, 752C/T, and 913G/A) were significantly related with an increased TOF risk compared with the most common haplotypes. CONCLUSION: In summary, our results suggested that VEGF variants (-2578C/A, -1154G/A, -634G/C, +963G/A) were involved in the susceptibility of TOF. However, validation of our study needs further study in various ethnics to reveal the functional relationship between VEGF polymorphisms and TOF risk, which may contribute to diagnosis and therapy of TOF.