Numerical Simulation Analysis of Water Injection Seepage Law in Micro Porous Structure of Coal

In this paper, a nano Voxel X-ray 3D microscope is used to scan the long flame coal samples and to reconstruct the 3D pore structure by the use of microscopic computed tomography. With image segmentation technique, a model of micro-pore structure of coal is obtained from the reconstructed coal. With different planes selected as seepage inlets, a numerical simulation of low-pressure water seepage is conducted. Studies show that water pressure gradually decreases along the direction of water seepage and reaches the maximum at the pore-pipes with good connectivity near the inlet. Due to the difference between the structure and development direction of pores in the three dimensions, there is an optimal seepage outlet that is most appropriately corresponding to each seepage inlet. When different planes are selected as seepage inlets, the velocity of each seepage outlet is positively correlated with the seepage mass flow rate at the outlet

Natural plant polyphenols for alleviating oxidative damage in man: Current status and future perspectives

The balance between oxidation and reduction is important for maintaining a healthy biological system. Oxidative stress results from an imbalance between excessive formation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) and limited endogenous defense systems, and this imbalance can adversely alter lipids, proteins and DNA, causing a number of human diseases. Thus, exogenous antioxidants that can neutralize the effect of free radicals are needed to diminish the cumulative effects of oxidative damage over human life span. Current research reveals that phenolic compounds in plants possess high antioxidant activity and free radical scavenging capacity and can prevent the body from oxidative damage over human life span. This review focuses on the present understanding of free radicals and antioxidants and their importance in human health and disease. Information about the chemical features of free radicals as well as their deleterious effects on cell structures is reviewed. The chemical structure and anti-oxidative mechanisms of essential polyphenols and their potential health benefits are presented. In addition, the limitation of natural antioxidants and a perspective on likely future trends in this field are also discussed.Keywords: Free radicals, Oxidative stress, Natural antioxidants, Polyphenols, Health benefits, Reactive oxygen species, Reactive nitrogen specie

Autophagy protects against palmitate-induced apoptosis in hepatocytes

BACKGROUND: Non-alcoholic fatty liver disease, one of the most common liver diseases, has obtained increasing attention. Palmitate (PA)-induced liver injury is considered a risk factor for the development of non-alcoholic fatty liver disease. Autophagy, a cellular degradative pathway, is an important self-defense mechanism in response to various stresses. In this study, we investigated whether autophagy plays a protective role in the progression of PA-induced hepatocytes injury. RESULTS: Annexin V-FITC/PI staining by FCM analysis, TUNEL assay and the detection of PARP and cleaved caspase3 expression levels demonstrated that PA treatment prominently induced the apoptosis of hepatocytes. Meanwhile, treatment of PA strongly induced the formation of GFP-LC3 dots, the conversion from LC3I to LC3II, the decrease of p62 protein levels and the increase of autophagosomes. These results indicated that PA also induced autophagy activation. Autophagy inhibition through chloroquine pretreatment or Atg5shRNA infection led to the increase of cell apoptosis after PA treatment. Moreover, induction of autophagy by pretreatment with rapamycin resulted in distinct decrease of PA-induced apoptosis. Therefore, autophagy can prevent hepatocytes from PA-induced apoptosis. In the further study, we explored pathway of autophagy activation in PA-treated hepatocytes. We found that PA activated PKCα in hepatocytes, and had no influence on mammalian target of rapamycin and endoplasmic reticulum stress pathways. CONCLUSIONS: These results demonstrated that autophagy plays a protective role in PA-induced hepatocytes apoptosis. And PA might induce autophagy through activating PKCα pathway in hepatocytes

Birman-Wenzl-Murakami Algebra and the Topological Basis

In this paper, we use entangled states to construct 9x9-matrix representations of Temperley-Lieb algebra (TLA), then a family of 9x9-matrix representations of Birman-Wenzl-Murakami algebra (BWMA) have been presented. Based on which, three topological basis states have been found. And we apply topological basis states to recast nine-dimensional BWMA into its three-dimensional counterpart. Finally, we find the topological basis states are spin singlet states in special case.Comment: 11pages, 1 figur

Gallic acid ameliorates dextran sulfate sodium-induced ulcerative colitis in mice via inhibiting NLRP3 inflammasome

Background: Ulcerative colitis (UC) is a chronic recurrent inflammatory bowel disease (IBD). The conventional drugs for UC may induce severe side effects. Herbal medicine is considered as a complementary and alternative choice for UC.Purpose: This study aims to estimate the effect of natural polyphenol gallic acid (GA) on the NLRP3 inflammasome with dextran sulfate sodium (DSS)-induced colitis in mice.Study design: The body weights and symptoms of BALB/c mice were recorded. Histological evaluation, ELISA, q-PCR, immunohistochemistry, and western blotting were carried out to observe the morphology, cytokine contents, mRNA expressions, and protein expressions, respectively. Lipopolysaccharide (LPS)-induced RAW264.7 macrophage was used to probe GA’s effect on relative protein expression.Results: GA attenuated weight loss (p < 0.05), relieved symptoms, and ameliorated colonic morphological injury (p < 0.05) in mice with colitis induced by DSS. GA also lowered the contents of TNF-α, IL-1β, IL-18, IL-33, and IFN-γ in the serum and colon of mice, which were elevated by DSS, downregulated protein, and mRNA expressions of the NLRP3 pathway in the colon tissue. Furthermore, GA downregulated the expressions of NLRP3 (p < 0.05), iNOS (p < 0.01), COX2 (p < 0.01), and P-p65 (p < 0.05), and suppressed NO release (p < 0.001) in LPS-induced RAW264.7 cells.Conclusion: GA ameliorated DSS-induced UC in mice via inhibiting the NLRP3 inflammasome. These findings furnish evidence for the anti-inflammatory effect of herbal medicines containing GA on UC

Acaricidal Mechanism of Scopoletin Against Tetranychus cinnabarinus

Scopoletin is a promising acaricidal botanical natural compound against Tetranychus cinnabarinus, and its acaricidal mechanism maybe involve calcium overload according to our previous study. To seek potential candidate target genes of calcium overload induced by scopoletin in T. cinnabarinus, RNA-seq was utilized to detect changes in transcription levels. 24 and 48 h after treatment, 70 and 102 differentially expressed genes were obtained, respectively. Target genes included 3 signal transduction genes, 4 cell apoptosis genes, 4 energy metabolism genes, and 2 transcription factor genes. The role of 3 calcium signaling pathway-related genes, namely, G-protein-coupled neuropeptide receptor, Bcl-2 protein and guanylate kinase (designated TcGPCR, TcBAG, and TcGUK, respectively) in the calcium overload were investigated in this study. RT-qPCR detection showed that scopoletin treatment upregulated the expression level of TcGPCR and downregulated the expression level of TcBAG and TcGUK. The result of RNAi indicated that downregulation of TcGPCR decreased susceptibility to scopoletin, and downregulation of TcBAG and TcGUK enhanced susceptibility to scopoletin. Functional expression in Chinese hamster ovary cells showed that scopoletin induced a significant increase in intracellular free calcium [Ca2+]i levels by activating TcGPCR. These results demonstrated that the acaricidal mechanism of scopoletin was via disrupting intracellular Ca2+ homeostasis and calcium signaling pathway mediated by GPCR, BAG, and GUK

Graphene Quantum Dots Enhanced Electrochemical Performance of Polypyrrole as Supercapacitor Electrode

通过将吡咯单体在低温下与石墨烯量子点进行原位聚合，获得一种全新的聚吡咯/石墨烯量子点（PPY/GQD）复合材料. 实验中采用了扫描电子显微镜（SEM）、原子力显微镜（AFM）、X射线衍射(XRD)、红外（FT-IR）和热重（TGA）对复合物的表面形貌、结构进行表征. 结果表明，吡咯单体以石墨烯量子点为软模板，以化学键的方式在石墨烯量子点的表面聚合生长成片状聚吡咯. 通过机械冷压法将粉末状PPY/GQD复合物压成圆片电极，电极的电化学测试结果表明，PPY和GQD质量比为50:1所制得的复合物的电容量为485 F·g-1，同时在两千次循环之后电容量只降低了大约2%. 通过与同比例的PG（聚吡咯/石墨烯复合材料）以及纯PPY对比，发现聚吡咯/石墨烯量子点的高比容量及优异的循环稳定性将会使其在电化学超级电容器领域中具有的潜在的应用价值.With an objective to develop electrode materials with high specific capacitance and good stability, a completely new nanocomposite of Polypyrrole (PPY) and graphene quantum dots (GQD) was successfully obtained through in-situ polymerization of pyrrole in the presence of GQD suspension. The obtained composites with different mass ratios were characterized by X-Ray diffraction (XRD), Fourier transformed infrared spectroscopy (FT-IR) and scanning electron microscopy (SEM). GQD enhanced electrochemical performance of PPY and, as supercapacitor electrodes, the PPY/GQD composites with the mass ratio of PPY to GQD at 50:1 showed a competitive specific capacitance of 485 F·g-1 at a scan rate of 0.005 V·s-1. The attenuation of the specific capacitance is about 2% after 2000 cycles. The high specific capacitance and good stability of the PPY/GQD nanocomposites are promising for applications in electrochemical supercapacitors.This work was supported by the National Natural Science Foundation of China (No. 20906055), National “973 Program” (No. 2010CB933900), and the State Key Laboratory of Bioreactor Engineering (No. 2060204).This work was supported by the National Natural Science Foundation of China (No. 20906055), National “973 Program” (No. 2010CB933900), and the State Key Laboratory of Bioreactor Engineering (No. 2060204).作者联系地址：上海交通大学微纳科学技术研究院，上海 200240Author's Address: Key Laboratory for Thin Film and Microfabrication of the Ministry of Education, Research Institute of Micro/Nano Science and Technology, Shanghai Jiao Tong University, Shanghai 200240, China通讯作者E-mail：[email protected]

Dietary lipid and n-3 long-chain PUFA levels impact growth performance and lipid metabolism of juvenile mud crab, Scylla paramamosain

An 8 weeks feeding trial was conducted to evaluate the effects of dietary n-3 LC-PUFA levels on growth performance, tissue fatty acid profiles and relative expression of genes involved in lipid metabolism of mud crab (Scylla paramamosain). Ten isonitrogenous diets were formulated to contain five n-3 LC-PUFA levels at 7 % and 12 % dietary lipid levels. Highest weight gain and specific growth rate were observed in crabs fed the diets with 19.8 and 13.2 mg g-1 n-3 LC-PUFA at 7 % and 12 % lipid, respectively. Moisture and lipid contents in hepatopancreas and muscle were significantly influenced by dietary n-3 LC-PUFA at the two lipid levels. The DHA, EPA, n-3 LC-PUFA contents and n-3/n-6 PUFA ratio in hepatopancreas and muscle significantly increased as dietary n-3 LC-PUFA levels increased at both lipid levels. The expression levels of Δ6 FAD and ACO in hepatopancreas increased significantly, and expression levels of FAS, CPTⅠ and HSL were down-regulated, with increased dietary n-3 LC-PUFA regardless of lipid level. Based on weight gain, the n-3 LC-PUFA requirements of S. paramamosain were estimated to be 20.1 mg g-1 and 12.7 mg g-1 of diet at 7 % and 12 % dietary lipid, respectively. Over all, dietary lipid level influenced lipid metabolism, and purified, high-lipid diets rich in palmitic acid reduced the n-3 LC-PUFA requirement of juvenile mud crab

Compensatory guaiacyl lignin biosynthesis at the expense of syringyl lignin in 4CL1-knockout poplar

The lignin biosynthetic pathway is highly conserved in angiosperms, yet pathway manipulations give rise to a variety of taxon-specific outcomes. Knockout of lignin-associated 4-coumarate:CoA ligases (4CLs) in herbaceous species mainly reduces guaiacyl (G) lignin and enhances cell wall saccharification. Here we show that CRISPR-knockout of 4CL1 in poplar (Populus tremula x alba) preferentially reduced syringyl (S) lignin, with negligible effects on biomass recalcitrance. Concordant with reduced S-lignin was downregulation of ferulate 5-hydroxylases (F5Hs). Lignification was largely sustained by 4CL5, a low-affinity paralog of 4CL1 typically with only minor xylem expression or activity. Levels of caffeate, the preferred substrate of 4CL5, increased in line with significant upregulation of caffeoyl shikimate esterase1. Upregulation of caffeoyl-CoA O-methyltransferase1 and downregulation of F5Hs are consistent with preferential funneling of 4CL5 products toward G-lignin biosynthesis at the expense of S-lignin. Thus, transcriptional and metabolic adaptations to 4CL1-knockout appear to have enabled 4CL5 catalysis at a level sufficient to sustain lignification. Finally, genes involved in sulfur assimilation, the glutathione-ascorbate cycle, and various antioxidant systems were upregulated in the mutants, suggesting cascading responses to perturbed thioesterification in lignin biosynthesis