35 research outputs found

    Hydrocode modeling of the spallation process during hypervelocity impacts: Implications for the ejection of Martian meteorites

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    Hypervelocity ejection of material by impact spallation is considered a plausible mechanism for material exchange between two planetary bodies. We have modeled the spallation process during vertical impacts over a range of impact velocities from 6 to 21 km/s using both grid- and particle-based hydrocode models. The Tillotson equations of state, which are able to treat the nonlinear dependence of density on pressure and thermal pressure in the strongly shocked matter, were used to study the hydrodynamic and thermodynamic response after impacts. The effects of material strength and gravitational acceleration were not considered. A two-dimensional time-dependent pressure field within a 1.5-fold projectile radius from the impact point was investigated in cylindrical coordinates to address the generation of spalled material. A resolution test was also performed to reject ejected materials with peak pressures that were too low due to artificial viscosity. The relationship between ejection velocity veject and peak pressure Ppeak was also derived. Our approach shows that late stage acceleration in an ejecta curtain occurs due to the compressible nature of the ejecta, resulting in an ejection velocity that can be higher than the ideal maximum of the resultant particle velocity after passage of a shock wave. We also calculate the ejecta mass that can escape from a planet like Mars (i.e., veject higher than 5 km/s) that matches the petrographic constraints from Martian meteorites, and which occurs when Ppeak from 30-50 GPa. Although the mass of such ejecta is limited to from 0.1-1 percent of the projectile mass in vertical impacts, this is sufficient for spallation to have been a plausible mechanism for the ejection of Martian meteorites. Finally, we propose that impact spallation is a plausible mechanism for the generation of tektites.Comment: 67 pages, 28 figures, accepted for publication in Icaru

    DOX/ICG Coencapsulated Liposome-Coated Thermosensitive Nanogels for NIR-Triggered Simultaneous Drug Release and Photothermal Effect

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    Chemo-photothermal therapy has shown enormous potential in treating cancer. To achieve the chemo-photothermal synergistic effect, an efficient nanoparticulate system with the ability for simultaneous codelivery of chemotherapeutic drug and photothermal agent as well as photothermal-triggered drug release is highly desirable. Herein, an in situ polymerization within liposome template was designed to prepare liposome-coated poly­(<i>N</i>-isopropylacrylamide-<i>co</i>-acrylamide) (P­(NIPAM-<i>co</i>-AAM)) nanogels, which can efficiently coencapsulate a NIR dye indocyanine green (ICG) and high amount of doxorubicin hydrochloride (DOX). The DOX/ICG coloaded hybrid nanogels, denoted as DI-NGs@lipo, integrated the desirable functions of PEGylated liposomes and thermosensitive nanogels. The PEGylated liposome shell provided excellent storage stability, hemodynamic stability, and fluorescence stability. Meanwhile, the thermosensitive P­(NIPAM-<i>co</i>-AAM) nanogels core endowed DI-NGs@lipo with volume phase transition temperature (VPTT) at about 40 °C, allowing for thermo-controlled transformation and drug release. The significant photothermal effect of DI-NGs@lipo and the simultaneous hyperthermia-triggered DOX release were observed under NIR light irradiation. The DI-NGs@lipo was demonstrated to be uptaken by 4T1 murine breast cancer cells via endocytosis, enhancing the distribution of DOX in the cell nucleus. Compared with chemo or photothermal treatment alone, the combination treatment of DI-NGs@lipo with NIR light irradiation induced significantly higher cytotoxicity to 4T1 cells, demonstrating the chemo-photothermal synergistic therapeutic effects on tumor cells. In a word, the strategy provided here offers a facile approach to develop a multifunctional nanoplatform for codelivery of DOX and ICG, which can synergistically improve the cancer-cell-killing efficiency, demonstrating great potential in chemo-photothermal therapy

    Effects of UA and radiation on ROS formation.

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    <p>The concentrations of intracellular ROS were detected using the membrane-permeable fluorescent probes 20, 70-dichlorofluorescin diacetate (DCFH-DA) by flow cytometry. The mean fluorescent intensity (MFI) represented intracellular ROS level. The MFIs difference between combination group and RT group was significant (P < 0.01) (ns: not significant; **:P < 0.01).</p

    Effects of UA and radiation on cell-cycle progressing and apoptotic cell death of BGC-823 cells.

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    <p>DNA content of fixed and PI-stained cells was measured by flow cytometry, and cell-cycle was analyzed. Percentages of cells in each phase of the cell cycle were provided in each diagram (Fig 3A). Compared with IR group, the addition of UA induced cell cycle arrest at the G<sub>1</sub> phase and G<sub>2</sub>/M phase and a significantly decline of S phase, demonstrating resistance to radiation therapy. Fig 3B showed the proportion of apoptotic cells (annexin V<sup>+</sup>, PI<sup>+/-</sup>). The combination group induced more apoptosis of BGC-823 cells compared with the other three groups.</p

    Cytotoxic effects of UA in BGC-823 cells.

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    <p>After 48h incubation with UA at the indicated concentrations, cytotoxicity was determined by the MTT assay. UA caused cytotoxicity in a dose-dependent manner, the IC<sub>50</sub> of UA for BGC-823 was 17.5ug/ml, and we defined 10ug/ml as a slight cytotoxicity (sub-cytotoxicity) (<15%) concentration.</p

    Effects of UA and radiation on the percentage of Ki-67 positive cells.

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    <p>Fig 5A showed the images of the results of Ki-67 immunohistochemical staining of BGC-823 cell line (magnification: 10 x 40). Percentage of Ki-67 positive cells of the combined group decreased significantly compared with the control group, as well as the radiation therapy group. Fig 5B showed that the difference between the control group and the UA group was non-significant; However, there was a significant decline between the combination group and the RT group (** P < 0.01).</p

    The mRNA expression levels of ERCC1,TS,TOPO1 and APTX, and their correlation with drug sensitivity.

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    <p>A, The mRNA expression levels of ERCC1,TS,TOPO1 and APTX. The lines in the middle stood for mean with SEM; n = 40. B, correlation between ERCC1 mRNA expression levels and Pt sensitivity (rho = −0.645, <i>P</i><0.001, n = 40). C, correlation between TS mRNA expression levels and 5-FU sensitivity (rho = −0.803, <i>P</i><0.001, n = 40). D, correlation between APTX mRNA expression levels and EVO sensitivity (rho = −0.322, <i>P = </i>0.036, n = 40).</p