390 research outputs found
Ablation observations for 2008–2011 from the Programme for Monitoring of the Greenland Ice Sheet (PROMICE)
Recent estimates from the glaciological community agree that the Greenland ice sheet is losing mass at an accelerated pace due to climate change (Velicogna 2009; Khan et al. 2010; Rignot et al. 2011). This has caught the attention of the public and policy makers due to the potential impact on sea-level rise (Dahl-Jensen et al. 2009). The mass loss can be attributed approximately equally to increases in meltwater runoff from surface melt and iceberg production (van den Broeke et al. 2009)
Programme for Monitoring of the Greenland Ice Sheet (PROMICE): first temperature and ablation records
The Greenland ice sheet is reacting to climate change. Yet, mass-budget estimates differ considerably, partly due to climatic variability and partly to uncertainties in the techniques of assessing mass change (IPCC 2007). Nevertheless, all recent estimates agree that the ice sheet is losing mass (e.g. 286 Gt/yr; Velicogna 2009) at an accelerating rate (Rignot et al. 2011). On top of this, the area with a negative mass budget is expanding rapidly (Khan et al. 2010). The mass loss is attributed equally to increases in both iceberg production and melting of the ice sheet (Van den Broeke et al. 2009). The increasing mass loss in recent years has caught public attention and given rise to concern worldwide due to its potential impact on sea level. In the light of this, the Programme for Monitoring of the Greenland Ice Sheet (PROMICE) was initiated in 2007 (Ahlstrøm & PROMICE project team 2008), lead by the Geological Survey of Denmark and Greenland (GEUS). PROMICE undertakes surface mass-budget measurements using automatic weather stations, quantifies the mass loss by iceberg calving using remotely sensed data from satellites and airborne surveys and tracks changes in the extent of glaciers. In this paper, we focus on weather station measurements, which are crucial in calculating the energy exchange between the atmosphere and the ice sheet, and in validating model calculations of the surface mass budget. In particular, we present the observed temperatures and investigate how their high 2010 values affected ablation in southern Greenlan
Katabatic winds and piteraq storms: observations from the Greenland ice sheet
In 2007 the Programme for Monitoring the Greenland Ice Sheet (PROMICE) was initiated to observe and gain insight into the mass budget of Greenland ice masses. By means of in situ observations and remote sensing, PROMICE assesses how much mass is gained as snow accumulation on the surface versus how much is lost by iceberg calving and surface ablation (Ahlstrøm et al. 2008). A key element of PROMICE is a network of automatic weather stations (AWSs) designed to quantify components of the surface mass balance, including the energy exchanges contributing to surface ablation (Van As et al. 2013)
Liquid Water Flow and Retention on the Greenland Ice Sheet in the Regional Climate Model HIRHAM5: Local and Large-Scale Impacts
Regional climate-model performance in Greenland firn derived from in situ observations
Recent record-warm summers in Greenland (Khan et al. 2015) have started affecting the higher regions of the ice sheet (i.e. the accumulation area), where increased melt has altered the properties of firn (i.e. multi-year snow). At high altitudes, meltwater percolates in the porous snow and firn, where it refreezes. The result is mass conservation, as the refrozen meltwater is essentially stored (Harper et al. 2012). However, in some regions increased meltwater refreezing in shallow firn has created thick ice layers. These ice layers act as a lid, and can inhibit meltwater percolation to greater depths, causing it to run off instead (Machguth et al. 2016). Meltwater at the surface also results in more absorbed sunlight, and hence increased melt in the accumulation area (Charalampidis et al. 2015). These relatively poorly understood processes are important for ice-sheet mass-budget projections
The implication of nonradiative energy fluxes dominating Greenland ice sheet exceptional ablation area surface melt in 2012
Quantifying the Surface Energy Fluxes in South Greenland during the 2012 High Melt Episodes Using In-situ Observations
Two high melt episodes occurred on the Greenland ice sheet in July 2012, during which nearly the entire ice sheet surface experienced melting. Observations from an automatic weather station (AWS) in the lower ablation area in South Greenland reveal the largest daily melt rates (up to 28 cm d-1 ice equivalent) ever recorded on the ice sheet. The two melt episodes lasted 6 days, equivalent to 6% of the June-August melt period, but contributed 14 % to the total annual ablation of 8.5 m ice equivalent. We employ a surface energy balance model driven by AWS data to quantify the relative importance of the energy budget components contributing to melt through the melt season. During the days with largest daily melt rates, surface turbulent heat input peaked at 552 Wm-2, 77 % of the surface melt energy, which is otherwise typically dominated by absorbed solar radiation. We find that rain contributed ca. 7 % to melt during these episodes
Phase I/II Study of Bortezomib-BEAM and Autologous Hematopoietic Stem Cell Transplantation for Relapsed Indolent Non-Hodgkin Lymphoma, Transformed, or Mantle Cell Lymphoma
AbstractA phase I/II trial was designed to evaluate the safety and efficacy of adding bortezomib to standard BEAM (BCNU, etoposide, cytarabine, melphalan) and autologous hematopoietic stem cell transplantation (ASCT). Eligible patients had relapsed/refractory indolent or transformed non-Hodgkin lymphoma or mantle cell lymphoma (MCL) that was relapsed/refractory or in first partial (PR) or complete remission (CR). Patients received bortezomib on days −11, −8, −5, and −2 before ASCT. Phase I had 4 dose cohorts (.8, 1, 1.3, and 1.5 mg/m2) and 3 patients were accrued to each. Any nonhematological ASCT-related toxicity >2 on the Bearman scale occurring between day −11 and engraftment defined the maximum tolerated dose (MTD). After the MTD has been reached, another 20 patients were enrolled at this dose to determine a preliminary overall response rate (ORR). Patients who were in CR or PR at day +100 were considered responders. The study enrolled 42 patients through August 14, 2009. The median age was 58 (range, 34 to 73) years, with 33 males and 9 females. The most common diagnoses were MCL (23 patients) and follicular lymphoma (7 patients). The median number of prior therapies was 1 (range, 0 to 6). The median follow-up was 4.88 (range, 1.07 to 6.98) years. Thirteen patients were treated in phase I and 29 patients were treated in phase II. The MTD was initially determined to be 1.5 mg/m2 but it was later decreased to 1 mg/m2 because of excessive gastrointestinal toxicity and peripheral neuropathy. The ORR was 95% at 100 days and 87% at 1 year. For all 38 evaluable patients at 1 year, responses were CR 84%, PR 1%, and progressive disease 13%. Progression-free survival (PFS) was 83% (95% CI, 68% to 92%) at 1 year, and 32% (15% to 51%) at 5 years. Overall survival (OS) was 91% (95% CI, 79% to 96%) at 1 year and 67% (50% to 79%) at 5 years. The most common National Cancer Institute grade 3 toxicities were neutropenic fever (59%), anorexia (21%), peripheral neuropathy (19%), orthostatic hypotension/vasovagal syncope (16%), and 1 patient failed to engraft. Compared with 26 MCL in CR1 historic controls treated with BEAM and ASCT, PFS was 85% and 43% for the BEAM group versus 87% and 57% for those who received bortezomib in addition to standard BEAM (V-BEAM) at 1 and 5 years, respectively (log-rank P = .37). OS was 88% and 50% for the BEAM group versus 96% and 72% for V-BEAM at 1 and 5 years, respectively (log-rank P = .78). In conclusion, V-BEAM and ASCT is feasible. The toxicities were manageable and we did not observe any treatment-related mortalities; however, we did observe an excess of autonomic dysfunction and ileus, which is concerning for overlapping toxicity with BEAM conditioning. Determining relative efficacy of V-BEAM compared to BEAM would require a randomized trial
Magnetic-field generation in helical turbulence
We investigate analytically the amplification of a weak magnetic field in a
homogeneous and isotropic turbulent flow lacking reflectional symmetry (helical
turbulence). We propose that the spectral distributions of magnetic energy and
magnetic helicity can be found as eigenmodes of a self-adjoint,
Schr\"odinger-type system of evolution equations. We argue that large-scale and
small-scale magnetic fluctuations cannot be effectively separated, and that the
conventional alpha-model is, in general, not an adequate description of the
large-scale dynamo mechanism. As a consequence, the correct numerical modeling
of such processes should resolve magnetic fluctuations down to the very small,
resistive scales.Comment: 4 page
Short Communication Bcl-2 Expression Inhibits Liver Carcinogenesis and Delays the Development of Proliferating Foci
Tumor development is thought to require both increased proliferation and inhibition of apoptosis. However , the relationship between cell replication and cell death in liver tumorigenesis is complex because both proliferation and apoptosis increase during hepatocarcinogenesis. To investigate the effect of the anti-apoptotic gene Bcl-2 in liver carcinogenesis, we established a line of double transgenic mice that express transforming growth factor-␣ (TGF-␣) , a liver mitogen , and Bcl-2. Double transgenic mice , TGF-␣ and Bcl-2 single transgenics , and wild type received an injection of diethylnitrosamine at 15 days of age. This alkylating agent induces liver carcinogenesis and its effect is greatly enhanced by TGF-␣. We report that Bcl-2 expression inhibited diethylnitrosamine-induced liver carcinogenesis and counteracted the enhancing effect of TGF-␣. Bcl-2 delayed the growth of proliferative foci at the early stages of carcinogenesis and inhibited cell proliferation in these foci. The effect of Bcl-2 on liver carcinogenesis is consistent with its reported ability to interfere with cell replication. The data demonstrate that the expression of an antiapoptotic gene during liver carcinogenesis causes a delay rather than an increase in tumorigenesis. The discovery that overexpression of Bcl-2 in follicular lymphomas, caused by a chromosomal translocation, inhibits apoptosis without increasing cell proliferation established a new mode of action for oncogenes
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