Color-coded global topographic map of Mars

A Digital Terrain Model (DTM) was derived with both Mercator and Sinusoidal Equal-area projections from the global topographic map of Mars at a scale of 1:15 million and a contour interval of 1 km. Elevations on the map are referred to the Mars topographic datum that is defined by the gravity field at a 6.1-millibar pressure surface with respect to the center of mass of Mars. The DTM has a resolution at the equator of 1/59.226 degrees (exactly 1 km) per pixel. By using the DTM, color-coded global maps of Mars' topography were generated in both the Mercator projection and the Sinusoidal Equal-Area projection. On both maps, colors indicate 1 km increments of height. From the equal-are dataset, the positive and negative elevation distributions are calculated to be 67 and 33 percent, respectively

Mars elevation distribution

A Digital Terrain Model (DTM) of Mars was derived with both Mercator and Sinusoidal Equal-Area projections from the global topographic map of Mars (scale 1:15 million, contour interval 1 km). Elevations on the map are referred to Mars' topographic datum that is defined by the gravity field at a 6.1-millibar pressure surface with respect to the center of mass of Mars. The DTM has a resolution at the equator of 1/59.226 degrees (exactly 1 km) per pixel. By using the DTM, the volumetric distribution of Mars topography above and below the datum has previously been calculated. Three types of elevation distributions of Mars' topography were calculated from the same DTM: (1) the frequency distribution of elevations at the pixel resolution; (2) average elevations in increments of 6 degrees in both longitude and latitude; and (3) average elevations in 36 separate blocks, each covering 30 degrees of latitude and 60 degrees of longitude

Prostate transglutaminase (TGase-4) induces epithelial-to-mesenchymal transition in prostate cancer cells

More men die with prostate cancer (PCa) than from it. However, once PCa is no longer organ-confined, it is associated with significant mortality. Epithelial-to-mesenchymal transition (EMT) is one mechanism facilitating progression in cancer. Our studies of transglutaminase-4 TGase-4, a member of the TGase family, expressed in the prostate gland, have implicated it in the regulation of the invasive properties of PCa. The present study investigated the role of TGase-4 on EMT of PCa cells. Materials and Methods: A panel of PCa cell lines: CA-HPV-10, PZ-HPV-7, PC-3 and DU-145 were used. An anti- TGase-4 transgene was constructed to eliminate the expression of TGase-4 in CA-HPV-10 (positive for TGase-4). An expression construct for human TGase-4 was used to transfect PCa cells negative for TGase-4. The pattern of E-cadherin, N-cadherin and vimentin in these cells were evaluated using immunofluorescent staining. Cell motility was assessed using scratch wounding and ekectric cell-substrate impedance sensing (ECIS) assays. Results: Treatment of PZ-HPV-7 and CA-HPV- 10 cells with rhTGase-4 resulted in a significant increase in cell migration (1,407.9 Ω±6.4 Ω vs. 1,691.2 Ω±8.3 Ω in non-treated and rhTGase-4 treated cells, respectively, p<0.01). Cells strongly expressing E-cadherin showed substantial changes of E-cadherin staining in that, after treatment with TGase-4, the intercellular staining of E-cadherin was diminished. Concomitantly, there was acquisition of N-cadherin in TGase- 4-treated cells. Elimination of TGase-4 from CA-HPV-10 cells significantly decreased cell motility (128.1 Ω±107.4 Ω vs. 31.7 Ω±26.2 Ω, in CA-HPV-10 control and CA-HPV-10/TGase-4 knockout cells). Knocking- out TGase-4 from CA-HPV-10 cells also resulted in substantial loss of N-cadherin in the cells. Conclusion: TGase-4 resulted in loss of E-cadherin/acquisition of N-cadherin and cell migration indicating it is a keen regulator of EMT in prostate epithelia-derived cancer cells. In concert with its other properties involved in disease progression, the present observations suggest TGase-4 as a prospective marker of disease progression