Experimental Study on Combined Microwave-Magnetic Separation-Flotation Coal Desulfurization.

In order to reduce the content of sulfur and ash in coal, improve the desulfurization and deashing rates, a combined experiment method of microwave magnetic separation-flotation was proposed for raw coal. The desulfurization and deashing rates of three experiment methods, namely, single magnetic separation, microwave magnetic separation, and microwave magnetic separation-flotation, were compared. Taking the microwave magnetic separation-flotation experiment method as the main line, the effects of the microwave irradiation time, microwave power, grinding time, magnetic field intensity, plate seam width, foaming agent dosage, collector dosage, and inhibitor dosage on desulfurization and deashing were discussed, and the mechanism of microwave irradiation on magnetic separation and flotation was revealed. The results show that under the conditions of a microwave irradiation time of 60 s, a microwave power of 80% of the rated power (800 W), a grinding time of 8 min, a plate seam width (the plate seam width of a magnetic separator sorting box) of 1 mm, a magnetic field intensity of 2.32 T, a foaming agent dosage of 90 g/t, a collector dosage of 2125 g/t, and an inhibitor dosage of 1500 g/t, the desulfurization and deashing effect is the best. The desulphurization rate is 76.51%, the sulfur removal rate of pyrite is 96.50%, and the deashing rate is 61.91%. Microwaves have the characteristic of selective heating, and the thermal conductivity of organic matter in coal is greater than that of mineral. Microwave irradiation can improve the reactivity of pyrite in coal, pyrolyze pyrite into high-magnetic pyrite, improve the magnetic properties, and improve the magnetic separation effect. Therefore, microwave irradiation plays a role in promoting magnetic separation. Through microwave irradiation, the positive and negative charges in coal molecules constantly vibrate and create friction under the action of an electric field force, and the thermal action generated by this vibration and friction process affects the structural changes in oxygen-containing functional groups in coal. With the increase in the irradiation time and power, the hydrophilic functional groups of -OH and -COOH decrease and the hydrophilicity decreases. Microwave heating evaporates the water in the pores of coal samples and weakens surface hydration. At the same time, microwave irradiation destroys the structure of coal and impurity minerals, produces cracks at the junction, increases the surface area of coal to a certain extent, enhances the hydrophobicity, and then improves the effect of flotation desulfurization and deashing. Therefore, after the microwave irradiation of raw coal, the magnetic separation effect is enhanced, and the flotation desulfurization effect is also enhanced.

Depletion of L-Methionine in Foods with an Engineered Thermophilic Methionine γ-lyase Efficiently Inhibits Tumor Growth.

Dietary restriction of l-methionine, an essential amino acid, exerts potent antitumor effects on l-methionine-dependent cancers. However, dietary restriction of l-methionine has not been practical for human therapy because of the problem with the administration of l-methionine concentration in foods. Here, a thermophilic methionine γ-lyase (MGL), that catalyzes the cleavage of the C-S bond in l-methionine to produce α-ketobutyric acid, methanethiol, and ammonia was engineered from human cystathionine γ-lyase and almost completely depleted l-methionine at 65 °C, a temperature that accelerates the volatilization of methanethiol and its oxidation products. The high efficiency of l-methionine lysis may be attributed to the cooperative fluctuation and moderate the structural rigidity of 4 monomers in the thermophilic MGL, which facilitates l-methionine access to the entrance of the active site. Experimental diets treated with thermophilic MGL markedly inhibited prostate tumor growth in mice, and in parallel, the in vivo concentrations of l-methionine, its transformation product l-cysteine, and the oxidative stress indicator malondialdehyde significantly decreased. These findings provide a technology for the depletion of l-methionine in foods with an engineered thermophilic MGL, which efficiently inhibits tumor growth in mice.

Formononetin ameliorates the LPS-induced inflammatory response and apoptosis of neuronal cells via NF-κB/NLRP3 signaling pathway.

The objective of this study was to investigate the impact of formononetin on cellular apoptosis and inflammatory responses following spinal cord injury (SCI), as well as the underlying mechanisms involved. In this study, PC12 cells were treated with lipopolysaccharide (LPS) and different concentrations of Formononetin (FT) (50 µM, 100 µM, 200 µM). To confirm the effect of nuclear factor-κB (NF-κB)/NLR family pyrin domain containing 3 (NLRP3) signaling pathways, the cells in the phorbol-12-myristate-13-acetate (PMA) group were treated with 0.1 µmol/L PMA (NF-κB/NLRP3 signaling pathway activators). The lactate dehydrogenase (LDH) concentration and cell viability, proliferating cell nuclear antigen (PCNA) fluorescence intensity, and cell apoptosis were determined using an LDH kit, Cell Counting Kit-8 (CCK-8), immunofluorescence, and flow cytometry assays, respectively. Tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-16 (IL-6) expression levels were detected by quantitative ELISA assay. The expression of proteins related to the NF-κB/NLRP3 signaling pathway was detected by western blotting. Our results showed that LPS increased LDH levels in PC12 cells, suggesting that inflammation caused PC12 cell damage. However, the PC12 cell damage was decreased by methylprednisolone. Formononetin promotes cell survival and proliferation, and prevents apoptosis in a concentration-dependent manner. Formononetin reduced the TNF-α, IL-1ß, and IL-6 levels in the LPS-treated model. Moreover, formononetin decreased the levels of p-p65 NF-κB and NLRP3 in PC12 cells. We conclude that formononetin ameliorated the inflammatory response and apoptosis in LPS-induced inflammatory injury in neuronal cells via the NF-κB/NLRP3 signaling pathway.

Hydroxysafflor Yellow A (HSYA) Protects Endplate Chondrocytes Against IL-1ß-Induced Injury Through Promoting Autophagy.

Background: Intervertebral disc degeneration (IDD) refers to intractable pain in patients' waist and legs, which is caused by internal structural disorder and degeneration of intervertebral. This disease severely affects the quality-of-life of people. It has been reported that hydroxysafflor yellow A (HSYA), the active ingredient in safflower extract, could inhibit IL-1ß-induced apoptosis of endplate chondrocytes. However, the mechanism by which HSYA regulates the occurrence and progression of IDD remains unclear. Methods: Rat endplate chondrocytes were isolated from the intervertebral disc. Next, toluidine blue staining and collagen II immunofluorescence staining were used to identify endplate chondrocytes. Then, MDC staining was used to detect the autophagy of endplate chondrocytes. In addition, Western blot was used to measure the expression of cleaved caspase 3, LC-3I/II and ATG7 in endplate chondrocytes. Results: IL-1ß obviously inhibited the viability and proliferation of endplate chondrocytes, while these phenomena were notably reversed by HSYA. Additionally, HSYA was able to inhibit IL-1ß-induced apoptosis of endplate chondrocytes. Moreover, HSYA protected endplate chondrocytes against IL-1ß-induced inflammation via inducing autophagy. Conclusion: HSYA protected rat endplate chondrocytes against IL-1ß-induced injury via promoting autophagy. Therefore, the present study might provide some theoretical basis for exploring novel and effective methods for patients with IDD.

Role of lncRNA PART1 in intervertebral disc degeneration and associated underlying mechanism.

Intervertebral disc degeneration (IDD) is a chronic skeletal muscle degeneration disease. Previous studies have demonstrated that long non-coding RNAs (lncRNAs) exert significant roles in serious illnesses. Prostate androgen-regulated transcript 1 (PART1) is an identified lncRNA that has been reported to be a regulator in a number of diseases. However, the potential effects of PART1 in IDD have yet to be fully elucidated. The present study aimed to investigate the roles of lncRNA PART1 in IDD and identify a possible underlying mechanism. Human nucleus pulposus (NP) cells were first exposed to lipopolysaccharide (LPS) to construct in vitro IDD models. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure lncRNA PART1 expression levels in 10 ng/ml LPS-stimulated NP cells and normal cells (untreated cells). Dual-luciferase reporter assays were conducted to verify the possible binding sites of microRNA (miR)-190a-3p on lncRNA PART1. In addition, NP cell viability and apoptosis were measured by performing MTT and flow cytometry, respectively. Expression and secretion of inflammatory factors (TNF-α, IL-1ß and IL-6) and extracellular matrix (ECM) degradation-related proteins (aggrecan and collagen type II) were measured using ELISA, RT-qPCR and western blotting. Expression levels of lncRNA PART1 in LPS-treated NP cells were found to be higher compared with those in the control groups. miR-190a-3p directly targeted lncRNA PART1. PART1 knockdown enhanced cell viability, reduced cell apoptosis, inhibited inflammatory factor secretion and promoted ECM degradation in LPS-stimulated NP cells. However, transfection with the miR-190a-3p inhibitor reversed the aforementioned PART1 knockdown-induced alterations in cell viability, apoptosis, inflammatory cytokine and ECM degradation. Collectively, these results suggest that PART1 accelerates the progression of IDD by directly targeting miR-190a-3p, which provides a novel target for IDD diagnosis and treatment.