Direct observation of the oceanic CO2 increase revisited

We show, from recent data obtained at specimen North Pacific stations, that the fossil fuel CO2 signal is strongly present in the upper 400 m, and that we may consider areal extrapolations from geochemical surveys to determine the magnitude of ocean fossil fuel CO2 uptake. The debate surrounding this topic is illustrated by contrasting reports which suggest, based upon atmospheric observations and models, that the oceanic CO2 sink is small at these latitudes; or that the oceanic CO2 sink, based upon oceanic data and models, is large. The difference between these two estimates is at least a factor of two. There are contradictions arising from estimates based on surface partial pressures of CO2 alone, where the signal sought is small compared with regional and seasonal variability; and estimates of the accumulated subsurface burden, which correlates well other oceanic tracers. Ocean surface waters today contain about 45 μmol⋅kg−1 excess CO2 compared with those of the preindustrial era, and the signal is rising rapidly. What limits should we place on such calculations? The answer lies in the scientific questions to be asked. Recovery of the fossil fuel CO2 contamination signal from analysis of ocean water masses is robust enough to permit reasonable budget estimates. However, because we do not have sufficient data from the preindustrial ocean, the estimation of the required Redfield oxidation ratio in the upper several hundred meters is already blurred by the very fossil fuel CO2 signal we seek to resolve.

Muscarinic acetylcholine receptor down-regulation limits the extent of inhibition of cell cycle progression in Chinese hamster ovary cells.

Cellular desensitization is believed to be important for growth control but direct evidence is lacking. In the current study we compared effects of wild-type and down-regulation-resistant mutant m3 muscarinic receptors on Chinese hamster ovary (CHO-K1) cell desensitization, proliferation, and transformation. We found that down-regulation of m3 muscarinic acetylcholine receptors was the principal mechanism of desensitization of receptor-activated inositol phosphate phospholipid hydrolysis in these cells. Activation of wild-type and mutant receptors inhibited anchorage-independent growth as assayed by colony formation in agar. However, the potency for inhibition of anchorage-independent growth was greater for cells expressing the mutant receptor. Activation of either receptor also initially inhibited anchorage-dependent cell proliferation in randomly growing populations. Rates of DNA synthesis and cell division were profoundly reduced by carbachol in cells expressing either receptor at early time points. Analysis of cell cycle parameters indicated that cell cycle progression was inhibited at transitions from G1 to S and G2/M to G1 phases. However, mutant receptor effects on anchorage-dependent growth were sustained, whereas wild-type receptor effects were transient. Thus, receptor down-regulation restored cell cycle progression. In contrast, activation of either receptor blocked entry into the cell cycle from quiescence, and this response was not reduced by receptor down-regulation. Therefore, activation of m3 muscarinic acetylcholine receptors inhibited CHO cell anchorage-dependent and -independent growth. In anchored cells carbachol inhibited the cell cycle at three distinct points. Inhibitions at two of these points were eliminated by wild-type receptor down-regulation while the other was not. These results directly demonstrate that desensitization mechanisms can act as principal determinants of cellular growth responses.