263 research outputs found

    Marine biogeochemical responses to the North Atlantic Oscillation in a coupled climate model

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    In this study a coupled ocean-atmosphere model containing interactive marine biogeochemistry is used to analyze interannual, lagged, and decadal marine biogeochemical responses to the North Atlantic Oscillation (NAO), the dominant mode of North Atlantic atmospheric variability. The coupled model adequately reproduces present-day climatologies and NAO atmospheric variability. It is shown that marine biogeochemical responses to the NAO are governed by different mechanisms according to the time scale considered. On interannual time scales, local changes in vertical mixing, caused by modifications in air-sea heat, freshwater, and momentum fluxes, are most relevant in influencing phytoplankton growth through light and nutrient limitation mechanisms. At subpolar latitudes, deeper mixing occurring during positive NAO winters causes a slight decrease in late winter chlorophyll concentration due to light limitation and a 10%–20% increase in spring chlorophyll concentration due to higher nutrient availability. The lagged response of physical and biogeochemical properties to a high NAO winter shows some memory in the following 2 years. In particular, subsurface nutrient anomalies generated by local changes in mixing near the American coast are advected along the North Atlantic Current, where they are suggested to affect downstream chlorophyll concentration with 1 year lag. On decadal time scales, local and remote mechanisms act contemporaneously in shaping the decadal biogeochemical response to the NAO. The slow circulation adjustment, in response to NAO wind stress curl anomalies, causes a basin redistribution of heat, freshwater, and biogeochemical properties which, in turn, modifies the spatial structure of the subpolar chlorophyll bloom

    CREB is a critical regulator of normal hematopoiesis and leukemogenesis

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    The cAMP-responsive element binding protein (CREB) is a 43-kDa nuclear transcription factor that regulates cell growth, memory, and glucose homeostasis. We showed previously that CREB is amplified in myeloid leukemia blasts and expressed at higher levels in leukemia stem cells from patients with myeloid leukemia. CREB transgenic mice develop myeloproliferative disease after 1 year, but not leukemia, suggesting that CREB contributes to but is not sufficient for leukemogenesis. Here, we show that CREB is most highly expressed in lineage negative hematopoietic stem cells (HSCs). To understand the role of CREB in hematopoietic progenitors and leukemia cells, we examined the effects of RNA interference (RNAi) to knock down CREB expression in vitro and in vivo. Transduction of primary HSCs or myeloid leukemia cells with lentiviral CREB shRNAs resulted in decreased proliferation of stem cells, cell- cycle abnormalities, and inhibition of CREB transcription. Mice that received transplants of bone marrow transduced with CREB shRNA had decreased committed progenitors compared with control mice. Mice injected with Ba/F3 cells expressing either Bcr-Abl wild-type or T315I mutation with CREB shRNA had delayed leukemic infiltration by bioluminescence imaging and prolonged median survival. Our results suggest that CREB is critical for normal myelopoiesis and leukemia cell proliferation
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