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The finite element method (FEM) has been widely used to model interaction of tillage tool and soil, because it is capable to provide an accurate prediction of tillage resistance. However, there is little research on modeling soil-root interaction in soil tillage practice. The object of this paper is to advance a well adaptable numerical assistance to simulate the root-soil interaction and predict the resistance force on a stubble cutting tool. A 3D dynamic simulation model using the FEM was established to predict the resistance acting on the stubble-cutting blade in the present work. Soil was modeled as elastic-plastic material, corn stubble was simplified as an assembly of lines with various diameters, and soil and stubble were tied together as a complex. Two stubble-cutting blades with different cutting edges and two forward velocities were examined using a FE computation model and verified experimentally by field tests. Comparison result of simulation and experiment showed that the prediction from the FE model agreed well with the measurements in a field test. It can be concluded from these results that the FE model designed in this work is capable of being used as a convenient and dependable prediction tool in analysis and development of the working capacity of tillage tool.

International audience; {112-2} twinning commonly takes place in α-titanium (α-Ti). High-resolution transmission electron microscopies (HRTEM) explored various steps along {112-2} coherent twin boundary. Topological model of {112-2} twin revealed twinning disconnections (TDs) that are represented by (bi, ) corresponding to a step height and a shear vector bi. Atomistic simulations were conducted to study the energies and kinetics of TDs. Combining microscopies and atomistic simulations, we concluded that (b3, ) is the elementary TD and (b1, ) is the reassembly TD. Steps observed in HRTEM thus can be treated as a reassembly of (b3, ) TDs and (b1, ) TDs. In addition, Electron Backscatter Diffraction (EBSD) maps revealed {112-2} → {112-1} double twins in α-Ti. Using two-dimensional and three-dimensional atomistic simulations, we demonstrated the nucleation of (b1, ) TD and → double twin through the interaction between basal dislocation and {112-2} twin. Our results enrich the understanding of {112-2} twinning including TDs, steps, and {112-1} secondary twins in hexagonal metals.

Long noncoding RNAs (lncRNAs) have emerged as critical regulators for gene expression in multiple levels, and thus are involved in various physiological and pathological processes. Sirtuin 1 (SIRT1) has been established to exert key roles in diverse biological process through deacetylation of substrates, including DNA damage repair. Nevertheless, the regulatory relationship between SIRT1 and lncRNAs, and the effect of lncRNA on SIRT1-mediated functions were still far to be elucidated. We herein uncovered that lncRNA miR17HG was notably down-regulated in SIRT1 deficient cells, and significantly up-regulated after ectopic expression of SIRT1. Subsequently, the results of dual luciferase reporter (DLR) showed that SIRT1 dramatically enhanced the promoter activity of miR-17-92 cluster. Furthermore, we specifically knocked down the previous demonstrated transcription factor for miR-17-92 cluster, C-Myc, which was the validated substrate of SIRT1. As expected, miR17HG and miR-17-92 miRNAs were evidently down-regulated after silencing of C-Myc; and silencing of C-Myc significantly reversed the effect of SIRT1 on miR17HG expression, suggesting that SIRT1 endowed cells with elevated miR17HG expression through stabilization of C-Myc. What’s more, silencing of miR17HG significantly inhibited the repair of DNA DSBs, while enforced expression of miR17HG promoted DSBs repair. Fascinatingly, overexpression of miR17HG evidently enhanced the deacetylation activity of SIRT1, while silencing of miR17HG conferred diminished deacetylation activity. In addition, the results of RIP unraveled the physical interaction between miR17HG and SIRT1. Taken together, we presented evidences that miR17HG and SIRT1 probably formed a positive feedback loop, which exerted crucial effect on DSBs repair.

Lattice quantum chromodynamics (lattice QCD) is a theory based on quantum chromodynamics, which is widely used in strong interaction related calculations. As a research method that can give accurate and reliable theoretical results, with the improvement of computer ability, Lattice QCD is playing an increasingly important role in recent years. Distillation method is an important numerical method to calculate hadron correlation function in lattice QCD, and can improve the signal-to-noise ratio of calculated physical quantities. Distillation is a method to approximately compute full propagator via replace the laplacian operator with it's outerproduct of laplace eigenvectors. In this way, the construction of operators is independent of the inversion of propagator which is costful. The eigenvector system and perambulator can be used in different physical projects and we don't need to compute these data repeatedly. It's also convinent for computing disconnected part of correlation function. However, it also faces to the problem of large amount of data in constructing correlation function because the difficulty of compuation is proportional to the cubic of the number of eigenvectors, so it is necessary to further improve its computational efficiency. A program is developed in this work to construct correlation function of quark bilinear with distillation method, and solved the bottleneck of computing performance by using MPI(Message Passing Interface, https://www.open-mpi.org), OpenMP(Open Multi-Processing) and SIMD(Single Instruction Multiple Data) multi-level optimization technology. And this program distribute timeslices to different MPI processes because the computation of each timeslice is independent. In order to show the efficiency of our program some tests result are presented. After various tests of the program, it shows that our design can support large-scale computation. Under the strong scalability test, the parallel computing efficiency of 512 processes can still achieve about 70%. The ability of calculating correlation function is greatly improved. The correction of results also has been checked via compute pseudo-scalar correlators of charmonium. Three different \begin{document}$ 0^{-+}$\end{document} operators were adopted for variational analysis and there effecitive mass plateau were compared with the effective mass obtained from the tradional method with point source. The results of distillation method are consistent with traditional method. After variational analysis, three state is obtained, which means the variational analysis take effects and the correlation functions obtained from distillation method is reasonable.

Lipid accumulation in podocytes can lead to the destruction of cellular morphology, in addition to cell dysfunction and apoptosis, which is a key factor in the progression of chronic kidney disease (CKD). Berberine (BBR) is an isoquinoline alkaloid extracted from medicinal plants such asemCoptis chinensis/em, which has been reported to have a lipid‑lowering effect and prevent CKD progression. Therefore, the present study aimed to investigate the effect of BBR on palmitic acid (PA)‑induced podocyte apoptosis and its specific mechanism using anemin vitro/emmodel. Cell death was measured using the Cell Counting Kit‑8 colorimetric assay. Cell apoptotic rate was assessed by flow cytometry. The expression of endoplasmic reticulum (ER) stress‑ and apoptosis‑related proteins was detected by western blotting or immunofluorescence. Reactive oxygen species (ROS) were evaluated by 2',7'‑dichlorofluorescein diacetate fluorescence staining. The results of the present study revealed that BBR treatment decreased PA‑induced podocyte apoptosis. In addition, 4‑phenylbutyric acid significantly reduced PA‑induced cell apoptosis and the expression of ER stress‑related proteins, which indicated that ER stress was involved in PA‑induced podocyte apoptosis. In addition, N‑acetylcysteine inhibited PA‑induced excessive ROS production, ER stress and cell apoptosis of podocytes. BBR also significantly reduced PA‑induced ROS production and ER stress in podocytes. These results suggested that PA mediated podocyte apoptosis through enhancing ER stress and the production of ROS. In conclusion, BBR may protect against PA‑induced podocyte apoptosis, and suppression of ROS‑dependent ER stress may be the key mechanism underlying the protective effects of BBR.

Aims Although autophagy impairment is a well-established cause of muscle atrophy and P300 has recently been identified as an important regulator of autophagy, the effects of P300 on autophagy and muscle atrophy in type 2 diabetes (T2D) remain unexplored. We aimed at characterizing the role of P300 in diabetic muscle and its underlying mechanism. Main methods Protein levels of phosphorylated P300, total P300, acetylated histone H3, LC3, p62 and myosin heavy chain, and mRNA levels of Atrogin-1 and MuRF1 were analyzed in palmitic acid (PA)-treated myotubes and db/db mice. Autophagic flux was assessed using transmission electron microscopy, immunofluorescence and mRFP-GFP-LC3 lentivirus transfection in cells. Muscle weight, blood glucose and grip strength were measured in mice. Hematoxylin and eosin (H&E) staining was performed to determine changes in muscle fiber size. To investigate the effects of P300 on autophagy and myofiber remodeling, a P300 specific inhibitor, c646, was utilized. 3-Methyladenine (3-MA) was utilized to inhibit autophagosomes formation, and chloroquine (CQ) was used to block autophagic flux. Key findings Phosphorylation of P300 in response to PA enhanced its activity and subsequently suppressed autophagic flux, leading to atrophy-related morphological and molecular changes in myotubes. Inhibition of P300 reestablished autophagic flux and ameliorated PA-induced myotubes atrophy. However, this effect was largely abolished by co-treatment with the autophagy inhibitor CQ. In vivo results demonstrated that inhibition of P300 partially rescued muscle wasting in db/db mice, accompanied with autophagy reactivation. Significance The findings revealed that T2D-induced overactivation of P300 contributes to muscle atrophy by blocking autophagic flux.

To explore the effects of different dosages of 4-nonylphenol (4-NP) on the fatty acid synthesis and estrogen receptor α (ERα) expression in the livers of F1 and F2 rats.

CD73 deficiency increased marrow edema and enhancement. Representative micro-MRI images of spinal cord at 3Â days post-injury. (PDF 459Â kb)

The sequences of the primers and probes used to genotype the rs895819 polymorphism. (DOCX 89Â kb)

Analysis of circulating mature miR-27a levels in three genotypes of 51 healthy controls. (DOCX 89Â kb)