The impact of agricultural insurance on consumer food safety: empirical evidence from provincial-level data in China.

In the exploration of the efficacy of agricultural subsidy policies, agricultural insurance, as a key element of this policy system, has garnered widespread attention for its potential impact on consumer food safety. This paper delves into the influence of agricultural insurance on the safety of food consumed by individuals, based on provincial panel data in China from 2011 to 2021. The findings indicate that agricultural insurance significantly reduces the incidence of foodborne disease and enhances food safety. Mediating effect tests reveal that agricultural insurance effectively boosts food safety through two key pathways: promoting innovation in agricultural technology and reducing environmental pollution. Moreover, the analysis of moderating effects highlights that increased consumer confidence positively enhances the impact of agricultural insurance. Heterogeneity tests further show that in the provinces with higher levels of agricultural development and stronger government support for agriculture, the role of agricultural insurance in improving food safety is more pronounced. This research not only empirically verifies the effectiveness of agricultural insurance in enhancing food safety but also provides robust theoretical support and practical guidance for the precise formulation and effective implementation of agricultural subsidy policies, particularly agricultural insurance policies, offering significant reference value for policy-makers.

Characteristics of number concentration, size distribution and components of particulate matter emitted from a typical large civil airport.

Civil airports are recognized as significant contributors to fine particulate matter, especially ultra-fine particulate matter (UFP). The pollutants from airport activities have a notable adverse impact on global climate, urban air quality, and public health. However, there is a lack of practical observational studies on the characterization of integrated pollutant emissions from large civil airports. This study aims to focus on the combined emission characteristics of particulate number concentration (PNC), size distribution, and components at a large civil airport, especially UFP. The findings reveal that airport activities significantly contribute to elevated PNC levels during aircraft activity in downwind conditions (four times higher than background levels) and upwind conditions (7.5 times higher). UFP dominates the PNC around the airport. The particle size distribution shows two peaks occurring around 10-30 nm and 60-80 nm. Notably, particles within the ranges of 17-29 nm and 57-101 nm account for 65.9 % and 12.0 % of the total PNC respectively. Aircraft landing has the greatest impact on particles sized between 6 and 17 nm while takeoff affects particles sized between 29 and 57 nm resulting in a respective increase in PNC by factors of approximately 3.27 and 35.4-fold increase compared to background levels. Different aircraft types exhibit varying effects on PNC with A320 and A321 showing more pronounced effects during takeoff and landing.The presence of airports leads to roughly five-fold rise in elemental component concentrations with Si being highest followed by OC, Ca, Al, Fe, Ca2+, EC, and Mg2+. The OC/EC ratio under high aircraft activity in downwind conditions falls within range of approximately 2.5-3.5. These characteristic components and ratio can be considered as identifying species for civil airports. PMF model show about 75 % of the particulate emissions at the airport boundary were related to airport activities.

Amygdalin promotes the activity of T cells to suppress the progression of HBV-related hepatocellular carcinoma via the JAK2/STAT3 signaling pathway.

BACKGROUND: Hepatitis B virus (HBV) infection is a high-risk factor of hepatocellular carcinoma (HCC). Cellular immune responses are essential for HCC development, and the CD4+ and CD8+ T subtypes are identified as the primary anti-tumor immune cells. In the study, we investigated the effect and mechanism of amygdalin in the cellular immune response in HBV-related HCC and HCC progression. METHODS: The cell proliferation was examined by MTT analysis. Cells metastasis ability was detected by Invasion and migration assays. Quantification of apoptotic cells was performed with Flow cytometer assay. The protein levels of p-STAT3, STAT3, p-JAK2, JAK2, caspase-3, cleaved caspase-3 were detected by performing immunoblotting assays. RESULTS: We demonstrate that amygdalin treatment could rescue the HBV-T cell viability and IFN-γ and TNF-αproduction. In HBV-T cells, the MFI levels of CD8+ are lower than that in NC-T cells. Moreover, the phosphorylation levels of STAT3 and JAK2 are higher in HBV-T cells, compared to those in NC-T cells, and then reduced by amygdalin treatment. Co-culture with HBV-T cells could reduce IFN-γ and TNF-α, production while increase IL-6 and IL-10 production in HepG2.2.15 cells; these alterations could be partially reversed by amygdalin pretreatment. Finally, co-culture with HBV-T cells significantly promoted the cell viability, inhibited the apoptosis, and promoted the migration of HepG2.2.15 cells, and these alterations could be partially reversed by amygdalin treatment. CONCLUSION: Our findings provide a rationale for further studies on the functions and mechanism of amygdalin inhibiting HBV-related HCC cell proliferation, invasion, and migration via T cell-mediated tumor immunity.

Amygdalin inhibits TGFß1-induced activation of hepatic stellate cells (HSCs) in vitro and CCl4-induced hepatic fibrosis in rats in vivo.

The activation of hepatic stellate cells (HSCs) has been considered one of the major events in hepatic fibrosis. Amygdalin has been used to treat cancers and alleviate pain; however, its role and mechanism in HSC activation and hepatic fibrosis remain unclear. In the present study, transforming growth factor-beta 1 (TGF-ß1) stimulated the activation of HSCs, as indicated by significantly increased alpha-smooth muscle actin (α-SMA), desmin, collagen I, and tissue inhibitor of metalloproteinase-1 (TIMP-1) protein levels. Amygdalin treatment dramatically suppressed TGF-ß1-induced HSC proliferation and activation. Moreover, amygdalin treatment also reduced the TGF-ß1-induced secretion of cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), platelet-derived growth factor (PDGF), and chemokine (C-C motif) ligand 2 (CCL2), as well as the phosphorylation of Smad2, Smad3, and p65. In the CCl4-stimulated liver fibrosis rat model, amygdalin treatment improved liver fibrosis and liver damage by reducing focal necrosis, collagen fiber accumulation, and the protein levels of α-SMA, desmin, collagen I, and TIMP-1 in hepatic tissue samples and reducing serum alanine transaminase (ALT) and aspartate transaminase (AST) levels. In conclusion, we demonstrated the suppressive effects of amygdalin in TGF-ß1-induced HSC activation through modulating proliferation, fibrogenesis, and inflammation signaling in vitro and the antifibrotic effects of amygdalin in CCl4-stimulated hepatic fibrosis in rats in vivo.