Surfaces can be fit to thickness maps in either Cartesian or polar coordinates. For Cartesian coordinates the surfaces were fit to data in the original 512 128 scan grid. For polar coordinates, data were converted by nearest-neighbor interpolation to a dense polar grid with its origin at the foveal center (point of maximum outer segment length; see Fig. 1) and the discontinuity at 180 oriented horizontally (i.e., along the fast B-scan direction) on the temporal side. Barring large tilts of the subject's head during acquisition, the discontinuity will approximately follow the temporal meridian and temporal raphe.20 The fits in Cartesian coordinates used 25 order-four (cubic) B-splines in each direction with both directions penalized by λ = 0.6. The fits in polar coordinates used 16 order-five (quartic) B-splines in the radial direction with λ = 0.2 and 39 order-four (cubic) B-splines in the angular direction with λ = 3.0. Higher-order B-splines were used radially to provide more accurate radial derivatives.21,22 The number of basis functions was chosen to give a reasonable representation of the data. Computational time was quite fast (
The factory-correct Blue Mist paint is one of those that look particularly nice in the sunshine. It contrasts with everything from a blacktop driveway to a green lawn, and so it makes for an instantly noticeable car wherever it's parked. That's why you love to have in on a coupe that's been properly upgraded to the Super Sport look. The louver-style hood, blacked-out grille, full SS396 badging, ribbed rocker panels, and the Rally wheel package make this distinctive hardtop quite imposing. Plus, the flying buttress C-pillar, front & rear sheetmetal overhangs, and wraparound chrome bumpers were all part of a package that made the '66 Chevelle one of the most sophisticated cars of the era. So this is beauty and brawn all in the first impression.
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In most cases, it is quite advantageous to interconnect a small turbine with the customer's utility service, thereby using the utility for backup power to cover the variability of the turbine's energy production as well as storage of excess energy. Such interconnection typically requires utility permission, which is usually in the form of an interconnection agreement. This agreement will address metering and billing arrangements with the utility and may include requirements for additional safety equipment or procedures, protection devices, and inspections.[38]
Some utilities require small wind turbine owners to maintain liability insurance in amounts of $1 million or more to protect them from liability for facilities they do not own and have no control over. Other utilities consider the insurance requirements excessive and unduly burdensome, making wind energy uneconomic. In seven states (California, Georgia, Maryland, Nevada, Oklahoma, Oregon, and Washington), laws or regulatory authorities prohibit utilities from imposing any insurance requirements on small wind systems that qualify for net metering. In at least two other states (Idaho, Virginia), regulatory authorities have allowed utilities to impose insurance requirements but have reduced the required coverage amounts to levels consistent with conventional residential or commercial insurance policies (e.g., $100,000 to $300,000). If your insurance amounts seem excessive, you can ask for a reconsideration from regulatory authorities (in the case of private investor-owned utilities) or the utility's governing board (in the case of publicly owned utilities).
Human colon carcinoma cell lines SW480, SW620, and DLD1 were tested for their susceptibility to β-lapachone-mediated growth inhibition. As assessed by colony formation assays, SW480, SW620, and DLD1 cells were quite sensitive to β-lapachone, with an IC50 of 2 to 3 µM (Fig. 1), which is similar to that found for prostate cancer cells (7).
We further analyzed apoptosis by flow-cytometric analysis of DNA content and DNA laddering assays. Unlike annexin V staining, which detects apoptotic cells at significantly earlier stages, both these methods only detect late apoptotic cells with the appearance of DNA fragmentation. Since more cell death was observed in SW620 cells after β-lapachone treatment, and a higher percentage of early apoptotic cells was detected by annexin V staining, we focused on SW620 cells for late apoptotic analysis by using these two methods. As shown in Figure 4B, at 24 hr post-treatment, β-lapachone induced 6.9% of SW620 cells in sub-G1 population, which represents late-stage apoptotic cells, as compared to 0.22% in untreated cells. The percentage of late apoptotic cells was quite low as compared to early apoptotic cells detected by annexin V staining (36%; Fig. 4A), suggesting that apoptosis occurred quite slowly in colon cancer cells after treatment. This is consistent with the observation by others that colon cancer cells do not undergo apoptosis rapidly (32). The slowly occurring apoptosis was further demonstrated by DNA laddering analysis, which showed that DNA ladders were not detected until 48 hr post-treatment (Fig. 4C), and by flow cytometric analysis of DNA content, which showed that the percentages of sub-G1 population representing late apoptotic cells increased at later time points (Fig. 3A).
We next examined the effects of β-lapachone on the expression of other cell cycle regulatory and apoptosis-related proteins. The p53 tumor suppressor is involved in the control of cell cycle checkpoints and apoptosis (34). As expected, p53 was quite abundant in mutant p53-expressing SW480 and SW620 cells, whereas it was not detectable in p53-deficient DLD1 cells (Fig. 5). After exposure to β-lapachone, mutant p53 in SW480 cells was drastically down-regulated to an almost undetectable level. However, in SW620 and DLD1 cells, p53 was not significantly affected by β-lapachone.
In this study, we demonstrated that human colon cancer cells SW480, SW620, and DLD1 were quite sensitive to β-lapachone-mediated cytotoxicity. These colon cancer cells were arrested in different stages of S phase, following β-lapachone treatment. The cell cycle alterations were congruous with changes in cell cycle regulatory proteins. In SW480 cells, consistent with the induced S-phase arrest, β-lapachone up-regulated the S phase-specific cyclin A, but down-regulated the G2/M phase-specific cyclin B1 and its associated kinase cdc2. In SW620 cells, consistent with the induced late S/G2-phase arrest, β-lapachone up-regulated both cyclin A and B1. In DLD1 cells, consistent with the induced early S-phase arrest, β-lapachone did not affect cyclin A, but down-regulated cyclin B1 and cdc2.
β-Lapachone-induced cell death of these colon cancer cells is by apoptosis, as demonstrated by annexin V staining, flow-cytometrie analysis of DNA content, and DNA laddering analysis. The apoptosis occurred quite slowly, over many hours, as in camptothecin-induced apoptosis in colon cancer cells (32).
At some time, some person decided to install this plug-in (to many systems). The reason to install it was to read one or more PDF files. The PDF files may have been downloaded, sent in email, produced by a system, included in the manual for a product, used in official info, anything. If your company's record keeping does not tell you when or why this decision was made, you can only follow the notes in my previous post. 2ff7e9595c
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