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In a nutshell, I don’t use it very often. But I have most frequently used it for simple comparison of data sets, and updating same column with new data for several lists in many months. I have never seen it used for heavy calculations, like trends in every months.
In any case, it is supposed to be simple as possible, but still powerful.
Documentation I think is not very good. Yes, Excel is probably the most flexible program ever created, but it’s not without pitfalls.
In the case of Mac Office Excel 2007, there are “applets” called “assist” which does many of the more common tasks for you.
In addition, if you create a simple macro (only a few lines) it can be embedded into a “formula” which does the task you want. Macros can also be linked to make the data easier to see.
Finally, I’d like to mention “Excel Macros” which allow you to create macros in MS Word or MS Publisher. But the standard macros I’ve seen here are really basic, not what I’d call a developer.
04-14-2007, 06:33 AM
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We investigated the effect of a saponin, 3-O-beta-D-glucopyranosyl(1–>2)-alpha-L-arabinopyranosyl hederagenin-28-O-beta-D-glucopyranoside (1), isolated from the Korean ginseng root, on apoptosis in HepG2 cells. Compound 1 induced apoptosis in HepG2 cells in a dose-dependent manner; at a concentration of >10 microg/ml, the proapoptotic effect was mediated by caspases, and at concentrations of 1 and 10 microg/ml, it was enhanced by the mitochondrial pathway. These effects were accompanied by accumulation of Bax (a proapoptotic Bcl-2 family protein) in the cytoplasm. Compound 1 also induced DNA fragmentation in DNA ladder formation and caused a significant decrease in the mitochondrial membrane potential and release of cytochrome c. Compound 1 markedly induced apoptosis by disrupting mitochondrial membrane potential, inducing cytochrome c release and inhibiting the Bcl-2 protein. Furthermore, treatment with a caspase-8 inhibitor (Z-IETD-FMK) or a caspase-9 inhibitor (Z-LEHD-FMK) partly reduced compound 1-induced apoptosis; however, they only partially inhibited caspase-3 activity, suggesting that compound 1 triggered apoptosis through both the mitochondrial and death receptor pathways.JULY 2, 2018
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