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- Soltwedel, T., et al.
(författare)
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Natural variability or anthropogenically-induced variation? Insights from 15 years of multidisciplinary observations at the arctic marine LTER site HAUSGARTEN
- 2016
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Ingår i: Ecological Indicators. - : Elsevier BV. - 1470-160X. ; 65, s. 89-102
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Tidskriftsartikel (refereegranskat)abstract
- Time-series studies of arctic marine ecosystems are rare. This is not surprising since polar regions are largely only accessible by means of expensive modern infrastructure and instrumentation. In 1999, the Alfred Wegener Institute, Helmholtz-Centre for Polar and Marine Research (AWI) established the LTER (Long-Term Ecological Research) observatory HAUSGARTEN crossing the Fram Strait at about 79°N. Multidisciplinary investigations covering all parts of the open-ocean ecosystem are carried out at a total of 21 permanent sampling sites in water depths ranging between 250 and 5500 m. From the outset, repeated sampling in the water column and at the deep seafloor during regular expeditions in summer months was complemented by continuous year-round sampling and sensing using autonomous instruments in anchored devices (i.e., moorings and free-falling systems). The central HAUSGARTEN station at 2500 m water depth in the eastern Fram Strait serves as an experimental area for unique biological in situ experiments at the seafloor, simulating various scenarios in changing environmental settings. Long-term ecological research at the HAUSGARTEN observatory revealed a number of interesting temporal trends in numerous biological variables from the pelagic system to the deep seafloor. Contrary to common intuition, the entire ecosystem responded exceptionally fast to environmental changes in the upper water column. Major variations were associated with a Warm-Water-Anomaly evident in surface waters in eastern parts of the Fram Strait between 2005 and 2008. However, even after 15 years of intense time-series work at HAUSGARTEN, we cannot yet predict with complete certainty whether these trends indicate lasting alterations due to anthropologically-induced global environmental changes of the system, or whether they reflect natural variability on multiyear time-scales, for example, in relation to decadal oscillatory atmospheric processes. © 2015 The Authors. Published by Elsevier Ltd.
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| 2. |
- Porse, BT, et al.
(författare)
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Loss of C/EBP alpha cell cycle control increases myeloid progenitor proliferation and transforms the neutrophil granulocyte lineage
- 2005
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Ingår i: Journal of Experimental Medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 202:1, s. 85-96
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Tidskriftsartikel (refereegranskat)abstract
- CCAAT/enhancer binding protein (C/EBP)alpha is a myeloid-specific transcription factor that couples lineage commitment to terminal differentiation and cell cycle arrest, and is found mutated in 9% of patients who have acute myeloid leukemia (AML). We previously showed that mutations which dissociate the ability of C/EBP alpha to block cell cycle progression through E2F inhibition from its function as a transcriptional activator impair the in vivo development of the neutrophil granulocyte and adipose lineages. We now show that such mutations increase the capacity of bone marrow ( BM) myeloid progenitors to proliferate, and predispose mice to a granulocytic myeloproliferative disorder and transformation of the myeloid compartment of the BM. Both of these phenotypes were transplantable into lethally irradiated recipients. BM transformation was characterized by a block in granulocyte differentiation, accumulation of myeloblasts and promyelocytes, and expansion of myeloid progenitor populations - all characteristics of AML. Circulating myeloblasts and hepatic leukocyte infiltration were observed, but thrombocytopenia, anemia, and elevated leukocyte count - normally associated with AML - were absent. These results show that disrupting the cell cycle regulatory function of C/EBP alpha is sufficient to initiate AML-like transformation of the granulocytic lineage, but only partially the peripheral pathology of AML.
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