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31.
Summary Cadmium and zinc uptake parameters were determined for intact corn (Zea mays L.) seedlings grown for 15 and 22 in nutrient solutions containing levels of Cd and Zn that were similar to those found in soil solutions. Uptake of both elements was assumed to follow Michaelis-Menten kinetics. Calculations were based on the concentrations of free ionic Cd (Cd2+) and Zn (Zn2+) rather than the total solution concentration. Rates of Zn uptake were measured by determining depletion of Zn for periods of up to 30 h from solutions containing initial concentrations of 1.5 and 10μmol Zn 1−1. Depletion curves suggested that Zn uptake characteristics were similar at both levels of Zn in solution. The Imax for Zn uptake decreased from 550 to 400 pmol m−2 root surface s−1 between 16 and 22 d of growth while Km decreased from 2.2 to 1.5 μmol Zn2+ 1−1. Cadmium uptake parameters were measured by controlling Cd2+ activities in nutrient solution betwen 6.3 to 164 nmol l−1 by continuous circulation of nutrient solution through a mixed-resin system. Imax for Cd uptake was 400 pmol m−2 root surface s−1 at 15 and 22 d of growth. The magnitude of Km increased from 30 to 100 nmol Cd2+ 1−1 during this time period. The Km value suggests that corn is efficient for Cd uptake. The results of these uptake studies are consistent with the observed uptake of Zn and Cd by corn seedlings in soils.  相似文献   
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Maintenance of substrate water potential in petri dishes is achieved by using vapor-pressure controlling, solute-amended agar gel discs attached to the inside of the top halves of the dishes.  相似文献   
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Background  

Cellular responses to death-promoting stimuli typically proceed through a differentiated multistage process, involving a lag phase, extensive death, and potential adaptation. Deregulation of this chain of events is at the root of many diseases. Improper adaptation is particularly important because it allows cell sub-populations to survive even in the continuous presence of death conditions, which results, among others, in the eventual failure of many targeted anticancer therapies.  相似文献   
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Series of aminopyridinecarboxamide-based inhibitors were synthesized and tested against human recombinant IKK-2 and in IL-1β stimulated synovial fibroblasts. The 2-amino-5-chloropyridine-4-carboxamides were identified as the most potent inhibitors with improved cellular activity.  相似文献   
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Loss of cell-cell adhesion in carcinoma cells may be an important step in the acquisition of an invasive, metastatic phenotype. We have examined the expression of the epithelial-specific cell adhesion molecule uvomorulin (E-cadherin, cell-CAM 120/80, L-CAM) in human breast cancer cell lines. We find that fibroblastoid, highly invasive, vimentin-expressing breast cancer cell lines do not express uvomorulin. Of the more epithelial-appearing, less invasive, keratin-expressing breast cancer cell lines, some express uvomorulin, and some do not. We examined the morphologies of the cell lines in the reconstituted basement membrane matrix Matrigel and measured the ability of the cells to traverse a Matrigel-coated filter as in vitro models for detachment of carcinoma cells from neighboring cells and invasion through basement membrane into surrounding tissue. Colonies of uvomorulin-positive cells have a characteristic fused appearance in Matrigel, whereas uvomorulin-negative cells appear detached. Cells which are uvomorulin negative and vimentin positive have a stellate morphology in Matrigel. We show that uvomorulin is responsible for the fused colony morphology in Matrigel since treatment of uvomorulin-positive MCF-7 cells with an antibody to uvomorulin caused the cells to detach from one another but did not induce invasiveness in these cells, as measured by their ability to cross a Matrigel-coated polycarbonate filter in a modified Boyden chamber assay. Two uvomorulin-negative, vimentin-negative cell lines are also not highly invasive as measured by this assay. We suggest that loss of uvomorulin-mediated cell-cell adhesion may be one of many changes involved in the progression of a carcinoma cell to an invasive phenotype.  相似文献   
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