Isotopic Characterization of Mercury Atmosphere-Foliage and Atmosphere-Soil Exchange in a Swiss Subalpine Coniferous Forest.

To understand the role of vegetation and soil in regulating atmospheric Hg0, exchange fluxes and isotope signatures of Hg were characterized using a dynamic flux bag/chamber at the atmosphere-foliage/soil interfaces at the Davos-Seehornwald forest, Switzerland. The foliage was a net Hg0 sink and took up preferentially the light Hg isotopes, consequently resulting in large shifts (-3.27‰) in δ202Hg values. The soil served mostly as net sources of atmospheric Hg0 with higher Hg0 emission from the moss-covered soils than from bare soils. The negative shift of δ202Hg and Δ199Hg values of the efflux air relative to ambient air and the Δ199Hg/Δ201Hg ratio among ambient air, efflux air, and soil pore gas highlight that Hg0 re-emission was strongly constrained by soil pore gas evasion together with microbial reduction. The isotopic mass balance model indicates 8.4 times higher Hg0 emission caused by pore gas evasion than surface soil photoreduction. Deposition of atmospheric Hg0 to soil was noticeably 3.2 times higher than that to foliage, reflecting the high significance of the soil to influence atmospheric Hg0 isotope signatures. This study improves our understanding of Hg atmosphere-foliage/soil exchange in subalpine coniferous forests, which is indispensable in the model assessment of forest Hg biogeochemical cycling.

The soil-air exchange of OCPs and PCBs in the Tibetan Plateau: Emphasis on episodic transport of unintentionally produced PCBs.

Organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) in paired ambient and surface air fugacity samples were measured in the Tibetan Plateau (TP) from 2019 to 2022. The air concentrations of previously intentionally produced chemicals like dichlorodiphenyltrichloroethane (DDT) and hexachlorocyclohexane (HCH) declined. Their soil-air exchange direction ranged from equilibrium to volatilization, suggesting that the TP is acting as a secondary source of most OCPs and PCBs with the pollution alleviation. However, considerably high atmospheric levels of PCB-11, an indicator of unintentionally produced PCBs (UP-PCBs), were recorded in the southern TP. Strong episodic long-range atmospheric transport (LRAT) and deposition of PCB-11 events took place mostly in summer. Those events associated with winds from potential sources and less rainfall interception along the air mass transport routes accounted for a significant fraction of overall atmospheric deposition in the TP. Meanwhile, cryoturbation and plowing are suspected to be important factors contributing to the reemission of PCB-11 from surface soil. The high abundance of PCB-11 and strong deposition/evaporation events highlights potential environmental and health risks of UP-POPs in the TP.

Occurrence and distribution of organophosphate flame retardants in the typical soil profiles of the Tibetan Plateau, China.

The urbanization and development of Tibetan Plateau (TP) probably results in a significant contamination of organic pollutants, such as organophosphate flame retardants (OPFRs). However, there is a lack of monitoring and evaluation of their occurrence and risks in the soil of TP. We investigated the concentrations, vertical distributions, potential sources, and ecological risks of OPFRs in soil profiles from four regions of TP, China. The total concentrations of OPFRs in all soil samples ranged from 1.35 to 126 ng/g with a median of 12.6 ng/g. Relatively high concentrations were discovered in the top soils from Lhasa, suggesting a rising contamination around cities of TP due to anthropogenic disturbance. Tri-n-butyl phosphate (TNBP) was the dominant OPFRs followed by tris(2-chloroethyl) phosphate (TCEP). Vertical distribution of ΣOPFRs was discovered, especially at site Lhasa. Source apportionment based on principle component analysis and correlation analysis suggests that OPFRs in the TP soil mainly originate from atmospheric transport, while some OPFRs in the top soil may be also influenced by nearby sources. The vertical distributions of OPFRs in soil may be influenced by both soil and chemical properties, as well as their use. The ecological risk quotients (RQs) of 6 OPFRs in the TP soil were calculated, and most of their ecological risks were relatively low or negligible. However, for the worst-case scenario calculated by the 95th percentile concentrations, TNBP and tris(2-chloro-isopropyl) phosphate (TCIPP) at site Lhasa and cresyl diphenyl phosphate (CDP) at site Nagri had moderate risks. More attentions should be paid to the Tibetan Plateau in the future due to the rising ecological risks of OPFRs, especially to the areas around cities.

Status and risks of selenium deficiency in a traditional selenium-deficient area in Northeast China.

In agricultural lands with selenium (Se) deficiency, bioavailability of Se in plants is low. Residents from large-scale agricultural production areas with Se deficiency often suffer from endemic diseases because of consumption of agricultural products lacking in Se. One such area in Northeast China where Keshan disease and Kashin-Beck disease originated, was selected for investigating the geochemistry, influencing factors, and risks of Se in the agroecosystems. Analysis of field samples indicates that the Se deficiency in soil is significantly reduced compared with that of several decades ago, and 62.6% of soils are now Se-sufficient in the southern Songnen Plain. However, Se in crop products remains low due to weak soil-plant transfer, resulting in high risks of Se deficiency related diseases in the rural population of this area. Structural equation modeling, principal component analysis, and other statistical analyses revealed that climate conditions and soil physical and chemical properties are the key factors influencing the spatial distribution of soil Se. Extensive use of agricultural fertilizers may indirectly inhibit the migration of Se from soil to plants. Ensuring sufficient Se contents in agricultural products to meet the minimum daily requirements of residents remains a challenge in Se-deficient areas, especially in the increased agricultural production environment in China.

Splicing factor SF3b6 promotes proliferation and migration of gastric cancer cells through MAPK signaling pathway / 中国肿瘤生物治疗杂志

@#[Abstract] Objective: To explore the effect and mechanism of splicing factor 3b subunit 6 (SF3b6) on the proliferation, apoptosis, invasion and migration of gastric cancer cells. Methods: Tissue microarrays were used to detect the expression of SF3b6 in gastric cancer tissues and adjacent tissues. WB and qPCR were used to detect the expression of SF3b6 in normal immortalized gastric epithelial cells (GES-1) and gastric cancer cell lines (HGC27, AGS, BGC823, MGC803, SGC7901, MKN45). AGS and MGC803 cells were transfected with SF3b6 siRNA, and BGC823 and SGC7901 cells were transfected with SF3b6 over-expression plasmid for functional experiments. CCK-8 assay was used to detect the regulation of SF3b6 on the proliferation of gastric cancer cells; Transwell migration and invasion experiments were used to detect the effect of SF3b6 on the migration and invasion of gastric cancer cells; Flow cytometry was used to detect cell apoptosis; and WB was adopted to detect expressions of apoptosis and migration-related molecules and MAPK signaling pathway associated proteins. Results: The expression level of SF3b6 in gastric cancer MGC803 and AGS cells was significantly higher while in BGC823 and SGC7901 cells was significantly lower than that in normal gastric epithelial GES-1 cells (P<0.05 or P<0.01). SF3b6 knockdown inhibited the proliferation, migration and invasion, but promoted cell apoptosis of gastric cancer cell lines AGS and MGC803 (P<0.05 or P<0.01); However, over-expression of SF3b6 promoted the proliferation, migration and invasion of gastric cancer cell lines BGC823 and SGC7901 (P<0.05 or P<0.01). Mechanism study showed that SF3b6 knockdown promoted the activation of JNK and p38 and expression of apoptosis-related protein cleaved caspase-9, cleaved PARP and Bax (P<0.05 or P<0.01), and meanwhile inhibited the process of epithelial to mesenchymal transition (EMT) in gastric cancer cells. Conclusion: The splicing factor SF3b6 enhances cell proliferation and migration via MAPK signaling pathway, thereby promoting tumor progression.

LncRNA SNHG5 regulates SOX4 expression through competitive binding to miR-489-3p in acute myeloid leukemia.

OBJECTIVES: Currently, lncRNA plays an important role in the occurrence and development of acute myeloid leukemia (AML), including SNHG5. However, the role and mechanism of SNHG5 in AML remains unclear. In this study, we explored the regulatory mechanism of SNHG5 in the development of AML. METHODS AND RESULTS: QRT-PCR was used to investigate the expression of SNHG5, miR-489-3p, and SOX. The proliferation and apoptosis of AML cells were analyzed by cell transfection, cell counting kit-8 (CCK8), and flow cytometric analysis. Moreover, the expression analysis of marker proteins was detected by western blot. Through luciferase activity assay, RNA pull-down, and RNA-binding protein immunoprecipitation (RIP), we proved that SNHG5 could bind miR-489-3p and SOX4 which might be the target gene of miR-489-3p. RESULTS: We first found that SNHG5 was up-regulated in both AML patient bone marrow samples and various AML cell lines. Second, we found that knockdown of SNHG5 inhibited proliferation of AML cells and promoted apoptosis. It was found that SNHG5 could bind miR-489-3p, and the relative expression of SNHG5 was negatively correlated with miR-489-3p. Further results suggested that SOX4 might be the target gene of miR-489-3p. Finally, our experimental data indicated that knockdown of SNHG5 could reduce the tumor volume and down-regulated SOX4 levels in vivo. CONCLUSIONS: Our results demonstrated that SNHG5 affected the expression of SOX4 through binding miR-489-3p to regulate proliferation and apoptosis of AML, which might act as a prospective prognostic biological marker and a promising therapeutic target for AML.

Levels, sources, isotope signatures, and health risks of mercury in street dust across China.

Spatial distribution and isotope signature of mercury (Hg) in street dusts across China were investigated by collecting dust samples from 14 cities and reviewing previously published data from an additional 46 cities. Potential sources of street dust and the associated health risks to humans were also assessed. The total Hg (THg) concentrations in street dust ranged from 0.020-39.1 mg kg-1 with an average of 0.433 ±â€¯0.185 mg kg-1 in the 60 cities. Street dust samples collected from 14 cities were characterized by slightly negative δ202Hg (-0.61 ±â€¯0.92‰) and near-zero Δ199Hg (-0.03 ±â€¯0.08‰) values, and coal combustion and industrial activities were estimated to be the major sources of Hg in street dust. The estimated average probable daily intake (PDI) of THg from street dust exposure for adults and children (1.36E-03 and 1.27E-02 µg d-1 kg-1, respectively) were comparable to their respective exposures via rice consumption in China. Children being exposed to THg in dust is a major concern in mercury mining areas (e.g., Wangshan and Xunyang), and may also be a concern in cities with major coal-based industries and nonferrous metal smelting. Results from this study suggest that exposure to street dust is not a primary MeHg exposure pathway in China.

Polyphyllin I induces apoptosis and autophagy via modulating JNK and mTOR pathways in human acute myeloid leukemia cells.

Polyphyllin I (PPI), a bioactive component extracted from Paris polyphylla, was reported to have potent anticancer activities in previous studies. However, there were few reports on the effects and underlying mechanism of PPI in human acute myeloid leukemia cells. The present study demonstrated that PPI had an inhibitory effect through inducing apoptosis and autophagy in THP-1 and NB4 cells. PPI induced apoptosis via activating JNK pathway, as evidenced by the decreased Bcl-2 levels and increased Bax, cleaved-caspase-3 and phosphorylated-JNK expressions. In addition, PPI promoted autophagy as evidenced with increased expressions of LC3-II and Beclin-1 in western blot and autophagic vacuoles in MDC staining, which was associated with the inhibition of AKT-mTOR pathway. Furthermore, JNK inhibitor SP600125 and autophagy inhibitor 3-MA were employed to evaluate the role of apoptosis and autophagy in PPI-induced cell death. We found that autophagy and apoptosis were both causes of cell death induced by PPI. These data suggested that PPI could be a potent therapeutic agent for the treatment of human acute myeloid leukemia.