539 research outputs found

    Young Galaxy Candidates in the Hubble Frontier Fields. IV. MACS J1149.5+2223

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    We search for high-redshift dropout galaxies behind the Hubble Frontier Fields (HFF) galaxy cluster MACS J1149.5+2223, a powerful cosmic lens that has revealed a number of unique objects in its field. Using the deep images from the Hubble and Spitzer space telescopes, we find 11 galaxies at z > 7 in the MACS J1149.5+2223 cluster field, and 11 in its parallel field. The high-redshift nature of the bright z sime 9.6 galaxy MACS1149-JD, previously reported by Zheng et al., is further supported by non-detection in the extremely deep optical images from the HFF campaign. With the new photometry, the best photometric redshift solution for MACS1149-JD reduces slightly to z = 9.44 ± 0.12. The young galaxy has an estimated stellar mass of (7\pm 2)\times {10}^{8}\,{M}_{\odot }, and was formed at $z={13.2}_{-1.6}^{+1.9} when the universe was ≈300 Myr old. Data available for the first four HFF clusters have already enabled us to find faint galaxies to an intrinsic magnitude of {M}_{{UV}}\simeq -15.5, approximately a factor of 10 deeper than the parallel fields

    Compressive properties of min-mod-type limiters in modelling shockwave-containing flows

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    The long-ignored compressive properties of Min-mod-type limiter is investigated in this manuscript by demonstrating its potential in numerically modelling shockwave-containing flows, especially in shock wave/boundary layer interaction (SWBLI) problems. Theoretical studies were firstly performed based on Sweby’s total variation diminishing (TVD) limiter region and Spekreijse’s monotonicity-preserving limiter region to indicate Min-mod-type limiters’ compressive properties. The influence of limiters on the solution accuracy was evaluated using a hybrid-order analysis method based on the grid-independent study in three typical shockwave-containing flows. The conclusions are that, Min-mod-type limiter can be utilized as a dissipative and/or compressive limiter, but depending on the reasonable value of the compression parameter. The compressive Min-mod limiter tends to be more attractive in modelling shockwave-containing flows as compared to other commonly preferred limiters because of its stable computational process and its high-resolution predictions. However, the compressive Min-mod limiter may suffer from its slightly poor convergence, as that observed in other commonly accepted smooth limiters in modelling SWBLI problems. © 2020, The Author(s)

    Grp78 promotes the invasion of hepatocellular carcinoma

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    <p>Abstract</p> <p>Background</p> <p>Glucose regulated protein 78 (Grp78) is involved in the invasion and metastasis in many human cancers including gastric cancer, breast cancer, prostate cancer. But the role of Grp78 in the invasion of human hepatocellular carcinoma has not been reported. In this article, we examined if Grp78 was associated with the invasion of hepatocellular carcinoma and explored the possible underlying mechanism.</p> <p>Methods</p> <p>The Grp78 and FAK expression levels in 44 patients with hepatocellular carcinoma were examined using immunohistochemistry. Grp78 overexpressing SMMC7721 cells were established by pcDNA3.1 (+)-Grp78 transfection and screened by G418. Grp78 and FAK levels in Grp78 overexpressing cells were down-regulated by siRNA transfection. The invasion status of tumor cells was evaluated by transwell assay in vitro, and chick embryo metastasis model in vivo. Cell spreading was determined by cell spreading assay, and quantitatively measured by Orisis software HUG. Grp78, pY397 FAK, pY576/577 FAK and FAK levels were detected by western blot. RhoA activity was detected by GST pulldown assay. The distribution of actin cytoskeleton was observed by fluorescent staining.</p> <p>Results</p> <p>Grp78 expression levels in 44 patients with hepatocellular carcinoma were negatively correlated with tumor grading, and positively correlated with portal invasion and intra-hepatic invasion. Overexpression of Grp78 in SMMC7721 cells promoted the invasion of cancer cells in vitro and in vivo, and this increase in tumor cell invasion was blocked by Grp78 siRNA knockdown. Our results also revealed that overexpression of Grp78 in SMMC7721 cells accelerated the process of cell spreading and promoted lamellipodia formation. Further analysis showed that overexpression of Grp78 in SMMC7721 cells increased pY397 and pY576/577 levels of FAK. Grp78 siRNA knockdown decreased FAK activation and activity. Our results also revealed that Grp78 overexpression in SMMC7721 cells decreased RhoA-GTP level, and Grp78 siRNA knockdown rescued RhoA-GTP level in Grp78 overexpressing cells, indicating Grp78 inhibited RhoA activity in hepatocellular carcinoma cells. Furthermore, overexpression of Grp78 in SMMC7721 cells increased phospho-p190RhoGAP level. FAK siRNA knockdown in Grp78 overexpressing cells reversed phospho-p190RhoGAP level. These data suggested that Grp78 inhibited RhoA activity by up-regulated phospho-p190RhoGAP level and Grp78 mediated p190RhoGAP phosphorylation is FAK dependent.</p> <p>Conclusion</p> <p>Grp78 promoted the invasion of hepatocellular carcinoma both in vitro and in vivo. Overexpression of Grp78 in hepatocellular carcinoma cells enhanced the activation and activity of FAK which negatively regulated Rock kinase activity by promoting the phosphorylation of p190RhoGAP.</p
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