Agricultural HANPP Embodied in Consumption: Tracing Pressure on Ecosystems Based on an MRIO Analysis.

Agriculture is one of humankind's most significant sources of biomass; it also places tremendous pressure on ecosystems through its increasing demand for agricultural products. However, few studies have assessed human pressures on ecosystems from agricultural production and consumption based on a whole-supply-chain perspective. Based on the concept of human appropriation of net primary productivity (HANPP), we evaluate trends of agricultural HANPP embodied in consumption from a global perspective and trace the pressure from agriculture production that is exerted on the environment using an environmentally extended multiregional input-output (MRIO) model. The results show that agricultural HANPP embodied in consumption accounted for over two-thirds of total HANPP but brought about less than 7% of global value added. India, Brazil, and China were found to have the highest level of agricultural HANPP embodied in consumption. Agricultural net exporters were found to usually be low- and lower-income countries, while net importers are found to be high-income countries. According to the driving factor analysis, high-income and low-income countries should cooperate by adjusting consumption patterns and sharing agricultural technology to alleviate the pressure from agricultural production. Our study highlights the importance of agrarian expertise sharing and the need to develop sustainable and green agricultural production.

Protective effect of ginsenoside Rg1 on 661W cells exposed to oxygen-glucose deprivation/reperfusion via keap1/nrf2 pathway.

AIM: To construct an in vitro model of oxygen-glucose deprivation/reperfusion (OGD/R) induced injury to the optic nerve and to study the oxidative damage mechanism of ischemia-reperfusion (I/R) injury in 661W cells and the protective effect of ginsenoside Rg1. METHODS: The 661W cells were treated with different concentrations of Na2S2O4 to establish OGD/R model in vitro. Apoptosis, intracellular reactive oxygen species (ROS) levels and superoxide dismutase (SOD) levels were measured at different time points during the reperfusion injury process. The injury model was pretreated with graded concentrations of ginsenoside Rg1. Real-time polymerase chain reaction (PCR) was used to measure the expression levels of cytochrome C (cyt C)/B-cell lymphoma-2 (Bcl2)/Bcl2 associated protein X (Bax), heme oxygenase-1 (HO-1), caspase9, nuclear factor erythroid 2-related factor 2 (nrf2), kelch-like ECH-associated protein 1 (keap1) and other genes. Western blot was used to detect the expression of nrf2, phosphorylated nrf2 (pnrf2) and keap1 protein levels. RESULTS: Compared to the untreated group, the cell activity of 661W cells treated with Na2S2O4 for 6 and 8h decreased (P<0.01). Additionally, the ROS content increased and SOD levels decreased significantly (P<0.01). In contrast, treatment with ginsenoside Rg1 reversed the cell viability and SOD levels in comparison to the Na2S2O4 treated group (P<0.01). Moreover, Rg1 reduced the levels of caspase3, caspase9, and cytC, while increasing the Bcl2/Bax level. These differences were all statistically significant (P<0.05). Western blot analysis showed no significant difference in the protein expression levels of keap1 and nrf2 with Rg1 treatment, however, Rg1 significantly increased the ratio of pnrf2/nrf2 protein expression compared to the Na2S2O4 treated group (P<0.001). CONCLUSION: The OGD/R process is induced in 661W cells using Na2S2O4. Rg1 inhibits OGD/R-induced oxidative damage and alleviates the extent of apoptosis in 661W cells through the keap1/nrf2 pathway. These results suggest a potential protective effect of Rg1 against retinal I/R injury.

Studies on the interaction of five triazole fungicides with human renal transporters in cells.

The widespread use of triazole fungicides in agricultural production poses a potential risk to human health. This study investigates the interaction of five triazole fungicides, i.e., tebuconazole, triticonazole, hexaconazole, penconazole, and uniconazole with human renal transporters, including OAT1, OAT3, OCT2, OCTN1, OCTN2, MATE1, MATE2-K, MRP2, MDR1, and BCRP, using transgenic cell models. For uptake transporters, triticonazole was the substrate of OAT1 and OAT3 and the inhibitor of OCT2. Tebuconazole and penconazole inhibited OCTN2 (100 µM), while tebuconazole, triticonazole, hexaconazole, penconazole, and uniconazole inhibited MATE1 (100 µM). Tebuconazole and hexaconazole inhibited MATE2-K (100 µM). All five triazole fungicides were not substrates or strong inhibitors of MRP2, MDR1, and BCRP efflux transporters. Penconazole inhibited OCT2 with IC50 = 1.12 µM. Penconazole and uniconazole inhibited MATE1 with IC50 = 0.94 µM and 0.87 µM. Tebuconazole and hexaconazole inhibited MATE2-K with IC50 = 0.96 µM and 1.04 µM, indicating that triazole fungicides may inhibit renal drug transporter activity at low concentrations. Triticonazole was transported by OAT1 and OAT3, and the Km values of triticonazole were 5.81 ± 1.75 and 47.35 ± 14.27, respectively. Tebuconazole and uniconazole were transported by OAT3, and the Km values of tebuconazole and uniconazole were 30.28 ± 7.18 and 87.61 ± 31.70, respectively, which may induce nephrotoxicity.

Stepwise copolymerization of polybenzimidazole for a low dielectric constant and ultrahigh heat resistance.

Bio-based polymer materials having great potential due to the depletion of fossil-fuel resources have been applied as single-use and medicinal materials but their low thermomechanical resistance have limited wider applications. Here, ultrahigh thermoresistant bio-based terpolymers with a low dielectric constant, comprising polybenzimidazole and poly(benzoxazole-random-aramid), were prepared by a method involving stepwise polycondensation of three monomers, 3,4-diaminobenzoic acid for benzimidazoles, 3-amino-4-hydroxylbenzoic acid for benzoxazoles, and 4-aminobenzoic acid for aramids. For optimized monomer compositions, the obtained terpolymers exhibited dielectric constants lower than 3, and a 10% mass loss at approximately 760 °C which is a temperature higher than that for any other polymer material reported so far. The high thermal degradation temperatures of the prepared terpolymers were a result of the high interaction enthalpies of hydrogen bonding between imidazole rings in the polymer chains, which were obtained from density functional theory calculations using trimer models. Furthermore, the applicability of the prepared terpolymers as a wire-coating material for a simple motor insulation was demonstrated, indicating that it has significant potential to be used as a thermostable material with a low dielectric constant (k).

Self-supporting Atmosphere-Assisted Synthesis of 1D Mo2 C-based Catalyst for Efficient Hydrogen Evolution.

One-dimensional materials exhibit fascinating properties in electrocatalytic applications but their fabrication faces the challenge of tedious and complicated operations. We have developed a bottom-up strategy to construct a 1D metal carbide catalyst (Mo2 C@NC) consisting of ultrafine Mo2 C nanoparticles embedded within nitrogen-doped carbon layers by simply calcining a mixture of ammonium molybdate, urea and melamine. Experimental results and thermodynamic calculations demonstrate that the retainable pyrolysis-generated self-supporting atmosphere plays a crucial role in the crystalline phase and morphology of materials. When functioned as an electrocatalyst for the hydrogen evolution reaction (HER), the achieved Mo2 C@NC presents an excellent catalytic activity as well as outstanding stability. This work could shed fresh light onto the facile synthesis of effective HER catalysts with 1D nanostructure.

6-Dithio-2'-deoxyguanosine analogs induce reactive oxygen species-mediated tumor cell apoptosis via bi-targeting thioredoxin 1 and telomerase.

Thioredoxin 1 (Trx1) and telomerase play key roles in the development and progression process of most tumors, and they both are promising drug therapy targets. We have, for the first time, discovered that Trx1 and telomerase had a dual-target synergistic effect. Based on that results, we designed a series of 6-dithio-2'-deoxyguanosine analogs (named as YLS00X) and verified whether they can inhibit Trx1 and telomerase simultaneously. TrxR1/Trx1 system activity and telomerase expression were significantly inhibited by 6-dithio-2'-deoxyguanosine analogs, especially YLS004. YLS004 can also cause ROS accumulation, and induce tumor cell apoptosis. The vitro antitumor activity of 6-dithio-2'-deoxyguanosine analogs using MTT assay on 11 different human cancer cells and found that human colon cancer cells(HCT116) and melanoma cells (A375) were the most sensitive cells to 6-dithio-2'-deoxyguanosine analogs treatment and vivo xenografts models also confirmed that. The serum biochemical parameters and multiple organs HE staining results of subacute experiments indicated that YLS004 might be mildly toxic to immune organs, including the thymus, spleen, and hematopoietic system. Besides, YLS004 was rapidly metabolized in the rats' blood. Our study revealed that YLS004, a Trx1 and telomerase inhibitor, has strong anti-tumor effects to colon cancer and melanoma cells and is a promising new candidate drug.

The Drug-Resistance Mechanisms of Five Platinum-Based Antitumor Agents.

Platinum-based anticancer drugs, including cisplatin, carboplatin, oxaliplatin, nedaplatin, and lobaplatin, are heavily applied in chemotherapy regimens. However, the intrinsic or acquired resistance severely limit the clinical application of platinum-based treatment. The underlying mechanisms are incredibly complicated. Multiple transporters participate in the active transport of platinum-based antitumor agents, and the altered expression level, localization, or activity may severely decrease the cellular platinum accumulation. Detoxification components, which are commonly increasing in resistant tumor cells, can efficiently bind to platinum agents and prevent the formation of platinum-DNA adducts, but the adducts production is the determinant step for the cytotoxicity of platinum-based antitumor agents. Even if adequate adducts have formed, tumor cells still manage to survive through increased DNA repair processes or elevated apoptosis threshold. In addition, autophagy has a profound influence on platinum resistance. This review summarizes the critical participators of platinum resistance mechanisms mentioned above and highlights the most potential therapeutic targets or predicted markers. With a deeper understanding of the underlying resistance mechanisms, new solutions would be produced to extend the clinical application of platinum-based antitumor agents largely.