A droplet impacting hydrophobic surfaces is explored via lattice Boltzmann method (LBM) simulations. Dynamics of the spreading and retraction processes of the impacting droplet with different surface wettability ( θ=106{degree sign}~145{degree sign}) at various Weber numbers ( We=15~35) and Reynolds numbers ( Re=235~359) are investigated. It indicates that the spreading time, the time interval from a droplet just touching the surface to reaching the maximum spreading diameter, is a fixed value that is not related to the above factors. The retraction time, the time interval from a droplet reaching the maximum spreading diameter to rebounding the surface, is just closely dependent on the surface wettability. Therefore, the contact time, the sum of the spreading time and the retraction time, is mainly related to the retraction process and dependent on the surface wettability. The time is commonly normalized as the non-dimensional time, τ= t/( ρR03/ s)1/2, where R0 is the initial droplet radius and s is the surface tension. The emphasis of this work is placed on establishing a relationship of the contact time with the surface wettability. Based on simulation research and theoretical modeling, the surface wettability is incorporated into the scaling law of contact time and a modified scaling law, tc~( R0/ V0) We1/2(1-cos θ)-1/2, where V0 denotes the initial impact velocity, is established for a droplet impacting hydrophobic surfaces of θ=106{degree sign}~145{degree sign}and We=15~35. It is demonstrated that the scale relationship can be well applied to calculate the contact time of a droplet impacting hydrophobic surfaces for moderate Weber numbers.
The mechanical reason for rock and concrete failure is trans-scale fracture, which can be divided into three phases: (1) microcrack evolution, (2) macrocrack nucleation, (3) macrocrack growth and run-through. Using the idea that a microcrack could be regarded as a well-organized aggregation of nucleated microdefects, the size growth model of the largest microcrack based on the accumulated number of microdefect nucleation is established. In order to test the validity of the model, trans-scale fracture of a plate made of heterogeneous material is numerically simulated to display the microcrack's evolution. Statistical analysis of the number and sizes of the microcracks indicates that the predicted size of the largest microcrack according to the model is in close agreement with the measured crack size prior to peak stress, but not at all close to the measured values after the peak. At the end of the paper, some remaining problems are proposed for the further work.
More accurate tree models, such as branch skeleton, are needed to acquire forest inventory data. Currently available algorithms for constructing a branch skeleton from a LiDAR point cloud have low accuracy with problems such as irrational connection near trunk bifurcation, excessive central deviation and topological errors. Using the C++ and PCL library, a novel algorithm of the incomplete simulation of tree transmitting water and nutrients (ISTTWN), based on geometric characteristics for tree branch skeleton extraction, was developed in this research. The algorithm is an incomplete simulation of tree transmitting water and nutrients. Improvements were made to improve the time and memory consumption. The result show that the ISTTWN algorithm without any improvements is quite time consuming but has consecutive output. After improvement with iteration, the process is faster and has more detailed output. Breakpoint connection is added to recover continuity. The ISTTWN algorithm with improvements can produce a more accurate skeleton and cost less time than a previous algorithm. The superiority and effectiveness of the method are demonstrated, which provides a reference for the subsequent study of tree modeling and a prospect of application in other fields, such as virtual reality, computer games and movie scenes.
Background: Colorectal cancer (CRC) is one of the most common tumors globally and a leading cause of cancer-related death. In China, CRC is the third most common cancer type. Sauchinone is known to exhibit anti-tumor and anti-inflammatory activity, but its effects on CRC have not been investigated to-date background: Colorectal cancer (CRC) is among the common types of cancer and is the leading cause of mortality due to cancer. It is the third most common type of cancer in China. Sauchinone is known to exhibit anti-tumor and anti-inflammatory activities. However, the cellular role of Sauchinone in hepatocyte cells remains unknown. Objective: To investigate the effects of Sauchinone on CRC development and metastasis and its underlying mechanism(s) of action. Methods: SW480 and HCT116 cells were treated with a range of concentrations of Sauchinone. Cell proliferation was measured using EDU assays and flow cytometry. Results: Treatment with 50 µM Sauchinone decreased the expression of MMP2 and MMP9 and downregulated PD-L1 expression (PD-1/PD-L1) leading to checkpoint inhibition. Sauchinone treatment also enhanced the cytotoxicity of SW840 and HCT116 cells co-cultured with CD8+ T cells. The overexpression of PD-L1 rescued the anti-proliferative and cytotoxic effects of Sauchinone in both types. result: We showed that protein levels of matrix metalloproteinase (MMP2 and MMP9) significantly decreased in the presence of 50 µM concentrations of Sauchinone. We also showed that Sauchinone inhibited the immune checkpoint pathway (PD-1/PD-L1) of colorectal cancer cells by down regulating the protein levels of PD-L1 in both cells. LDH assay shows that sauchinone treated cells cytotoxicity level rose after cells were co-cultured with CD8+ T cells. Finally we showed that PD-L1 overexpression rescued the anti-proliferative effect of Sauchinone in both cells. Conclusions: We show that Sauchinone suppresses CRC cell growth through the downregulation of MMP2 and MM9 expression and PD-1/PD-L1 mediated checkpoint inhibition. Collectively, these data highlight the promise of Sauchinone as a future anti-CRC therapeutic. conclusion: This study showed the cellular mechanism of Sauchinone in colorectal cancer cells via targeting PD-1/PD-L1 checkpoint pathway and matrix metalloproteinase proteins, and it may act as a therapeutic candidate in future for CRC cancer.
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