Long-rod penetration: the transition zone between rigid and hydrodynamic penetration modes

AbstractLong-rod penetration in a wide range of velocity means that the initial impact velocity varies in a range from tens of meters per second to several kilometers per second. The long rods maintain rigid state when the impact velocity is low, the nose of rod deforms and even is blunted when the velocity gets higher, and the nose erodes and fails to lead to the consumption of long projectile when the velocity is very high due to instantaneous high pressure. That is, from low velocity to high velocity, the projectile undergoes rigid rods, deforming non-erosive rods, and erosive rods. Because of the complicated changes of the projectile, no well-established theoretical model and numerical simulation have been used to study the transition zone. Based on the analysis of penetration behavior in the transition zone, a phenomenological model to describe target resistance and a formula to calculate penetration depth in transition zone are proposed, and a method to obtain the boundary velocity of transition zone is determined. A combined theoretical analysis model for three response regions is built by analyzing the characteristics in these regions. The penetration depth predicted by this combined model is in good agreement with experimental result

An novel role of sphingosine kinase-1 (SPHK1) in the invasion and metastasis of esophageal carcinoma

<p>Abstract</p> <p>Background</p> <p>Treatment failure for esophageal carcinoma is frequently due to lymph node metastasis and invasion to neighboring organs. The aim of the present study was to investigate invasion- and metastasis-related genes in esophageal carcinoma cells <it>in vitro </it>and <it>in vivo</it>.</p> <p>Methods</p> <p>A metastasis model using a Matrigel invasion clonal selection approach was employed to establish a highly invasive subline EC9706-P4 from the esophageal carcinoma cell (ESCC) line EC9706. The differentially expressed genes of the subline and the parental cells determined by gene microarrays were further analyzed by RT-PCR and Western blotting.</p> <p>Results</p> <p>We identified <it>sphingosine kinase 1 (SPHK1) </it>as an invasion and metastasis-related gene of esophageal cancer. <it>SPHK1 </it>was overexpressed in the EC9706-P4 subline with high invasive capacity. Among six ESCC lines tested, KYSE2 and KYSE30 cells showed the highest <it>SPHK1 </it>mRNA and protein expressions as well as the most invasive phenotype. By Western blotting, in 7/12 cases (58%), SPHK1 expression was higher in esophageal carcinomas than in the companion normal tissue. In 23/30 cases (76%), SPHK1 protein expression was upregulated in the tumors compared to matched normal tissue by immunohistochemistry (IHC). Esophageal carcinoma tissue microarray analysis indicated that SPHK1 expression correlated with the depth of tumor invasion (<it>P </it>< 0.0001) and lymph node metastasis (<it>P </it>= 0.016). By Kaplan-Meier analysis, strong SPHK1 expression was significantly associated with clinical failure (<it>P </it>< 0.01), suggesting the involvement of SPHK1 in aggressiveness of human esophageal carcinoma. <it>SPHK1 </it>overexpression significantly increased the invasiveness of EC9706 cells <it>in vitro </it>and also increased EC9706 cell growth and spontaneous metastasis <it>in vivo</it>, promoting significant increases in tumor growth, tumor burden and spontaneous lung metastasis in nude mice. <it>SPHK1 </it>expression significantly correlated with the expression of many EGFR pathway genes associated with invasion of cancer cells. SPHK1 protein expression also significantly correlated with the phosphorylation of EGFR.</p> <p>Conclusion</p> <p>In summary, our data implicate <it>SPHK1 </it>in the metastasis of esophageal cancer. Our study also identified downstream mediators of SPHK1 in esophageal cancer cells that may mediate enhanced malignant behavior, and several of these mediators may be useful as therapeutic targets.</p

A heavy metal P-type ATPase OsHMA4 prevents copper accumulation in rice grain

Rice is a major source of calories and mineral nutrients for over half the world’s human population. However, little is known in rice about the genetic basis of variation in accumulation of copper (Cu), an essential but potentially toxic nutrient. Here we identify OsHMA4 as the likely causal gene of a quantitative trait locus controlling Cu accumulation in rice grain. We provide evidence that OsHMA4 functions to sequester Cu into root vacuoles, limiting Cu accumulation in the grain. The difference in grain Cu accumulation is most likely attributed to a single amino acid substitution that leads to different OsHMA4 transport activity. The allele associated with low grain Cu was found in 67 of the 1,367 rice accessions investigated. Identification of natural allelic variation in OsHMA4 may facilitate the development of rice varieties with grain Cu concentrations tuned to both the concentration of Cu in the soil and dietary needs