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- De Boer, Agatha M., et al.
(författare)
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Control of the glacial carbon budget by topographically induced mixing
- 2014
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Ingår i: Geophysical Research Letters. - 0094-8276 .- 1944-8007. ; 41:12, s. 4277-4284
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Tidskriftsartikel (refereegranskat)abstract
- Evidence for the oceanic uptake of atmospheric CO2 during glaciations suggests that there was less production of southern origin deep water but, paradoxically, a larger volume of southern origin water than today. Here we demonstrate, using a theoretical box model, that the inverse relationship between volume and production rate of this water mass can be explained by invoking mixing rates in the deep ocean that are proportional to topographic outcropping area scaled with ocean floor slope. Furthermore, we show that the resulting profile, of a near-linear decrease in mixing intensity away from the bottom, generates a positive feedback on CO2 uptake that can initiate a glacial cycle. The results point to the importance of using topography-dependent mixing when studying the large-scale ocean circulation, especially in the paleo-intercomparison models that have failed to produce the weaker and more voluminous bottom water of the Last Glacial Maximum.
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| 3. |
- Sachweh, MCC, et al.
(författare)
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Incompatible effects of p53 and HDAC inhibition on p21 expression and cell cycle progression
- 2013
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Ingår i: Cell death & disease. - : Springer Science and Business Media LLC. - 2041-4889. ; 4, s. e533-
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Tidskriftsartikel (refereegranskat)abstract
- Nutlin-3 selectively activates p53 by inhibiting the interaction of this tumor suppressor with its negative regulator murine double minute 2 (mdm2), while trichostatin A (TSA) is one of the most potent histone deacetylase (HDAC) inhibitors currently available. As both Nutlin-3 and TSA increase the levels of the cell cycle inhibitor p21(cip1/waf1) in cells, we investigated whether a combination of these compounds would further augment p21 levels. Contrary to expectations, we found that short-term exposure to Nutlin-3 and TSA in combination did not have an additive effect on p21 expression. Instead, we observed that activation of p53 prevented the ability of TSA to increase p21 levels. Furthermore, TSA inhibited Nutlin-3-induced expression of p53-dependent mRNAs including P21. This negative effect of TSA on Nutlin-3 was significantly less pronounced in the case of hdm2, another p53 downstream target. Aside from suggesting a model to explain these incompatible effects of Nutlin-3 and TSA, we discuss the implications of our findings in cancer therapy and cell reprogramming.
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