Inland extent of the Weddell Sea Rift imaged by new aerogeophysical data

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Antarctic ice sheet fertilises the Southern Ocean

Southern Ocean (SO) marine primary productivity (PP) is strongly influenced by the availability of iron in surface waters, which is thought to exert a significant control upon atmospheric CO2 concentrations on glacial/interglacial timescales. The zone bordering the Antarctic Ice Sheet exhibits high PP and seasonal plankton blooms in response to light and variations in iron availability. The sources of iron stimulating elevated SO PP are in debate. Established contributors include dust, coastal sediments/upwelling, icebergs and sea ice. Subglacial meltwater exported at the ice margin is a more recent suggestion, arising from intense iron cycling beneath the ice sheet. Icebergs and subglacial meltwater may supply a large amount of bioavailable iron to the SO, estimated in this study at 0.07–0.2 Tg yr−1. Here we apply the MIT global ocean model (Follows et al., 2007) to determine the potential impact of this level of iron export from the ice sheet upon SO PP. The export of iron from the ice sheet raises modelled SO PP by up to 40%, and provides one plausible explanation for seasonally very high in situ measurements of PP in the near-coastal zone. The impact on SO PP is greatest in coastal regions, which are also areas of high measured marine PP. These results suggest that the export of Antarctic runoff and icebergs may have an important impact on SO PP and should be included in future biogeochemical modelling.Leverhulme Trust (Philip Leverhulme Prize)Leverhulme Trust (Leverhulme Research Fellowship)Leverhulme Trust (PDRA grant F/00182/BY)Royal Society (Great Britain) (Fellowship)European Commission (Marie-Curie Intra-European Fellowship)Natural Environment Research Council (Great Britain) (NERC Fellowship NE/J019062/1

Antarctic ice sheet fertilises the Southern Ocean

Open access journalSouthern Ocean (SO) marine primary productivity (PP) is strongly influenced by the availability of iron in surface waters, which is thought to exert a significant control upon atmospheric CO2 concentrations on glacial/interglacial timescales. The zone bordering the Antarctic Ice Sheet exhibits high PP and seasonal plankton blooms in response to light and variations in iron availability. The sources of iron stimulating elevated SO PP are in debate. Established contributors include dust, coastal sediments/upwelling, icebergs and sea ice. Subglacial meltwater exported at the ice margin is a more recent suggestion, arising from intense iron cycling beneath the ice sheet. Icebergs and subglacial meltwater may supply a large amount of bioavailable iron to the SO, estimated in this study at 0.07-0.2 Tg yr-1. Here we apply the MIT global ocean model (Follows et al., 2007) to determine the potential impact of this level of iron export from the ice sheet upon SO PP. The export of iron from the ice sheet raises modelled SO PP by up to 40%, and provides one plausible explanation for seasonally very high in situ measurements of PP in the near-coastal zone. The impact on SO PP is greatest in coastal regions, which are also areas of high measured marine PP. These results suggest that the export of Antarctic runoff and icebergs may have an important impact on SO PP and should be included in future biogeochemical modelling.Philip Leverhulme PrizeLeverhulme Research FellowshipLeverhulme TrustRoyal Society Fellowship7th European Community Framework Programme - Marie Curie Intra European FellowshipNatural Environment Research Council (NERC

A temperate former West Antarctic ice sheet suggested by an extensive zone of bed channels

Several recent studies predict that the West Antarctic Ice Sheet will become increasingly unstable under warmer conditions. Insights on such change can be assisted through investigations of the subglacial landscape, which contains imprints of former ice-sheet behavior. Here, we present radio-echo sounding data and satellite imagery revealing a series of ancient large sub-parallel subglacial bed channels preserved in the region between the Möller and Foundation Ice Streams, West Antarctica. We suggest that these newly recognized channels were formed by significant meltwater routed along the icesheet bed. The volume of water required is likely substantial and can most easily be explained by water generated at the ice surface. The Greenland Ice Sheet today exemplifies how significant seasonal surface melt can be transferred to the bed via englacial routing. For West Antarctica, the Pliocene (2.6–5.3 Ma) represents the most recent sustained period when temperatures could have been high enough to generate surface melt comparable to that of present-day Greenland. We propose, therefore, that a temperate ice sheet covered this location during Pliocene warm periods

Century-scale simulations of the response of the West Antarctic Ice Sheet to a warming climate

We use the BISICLES adaptive mesh ice sheet model to carry out one, two, and three century simulations of the fast-flowing ice streams of the West Antarctic Ice Sheet, deploying sub-kilometer resolution around the grounding line since coarser resolution results in substantial underestimation of the response. Each of the simulations begins with a geometry and velocity close to present-day observations, and evolves according to variation in meteoric ice accumulation rates and oceanic ice shelf melt rates. Future changes in accumulation and melt rates range from no change, through anomalies computed by atmosphere and ocean models driven by the E1 and A1B emissions scenarios, to spatially uniform melt rate anomalies that remove most of the ice shelves over a few centuries. We find that variation in the resulting ice dynamics is dominated by the choice of initial conditions and ice shelf melt rate and mesh resolution, although ice accumulation affects the net change in volume above flotation to a similar degree. Given sufficient melt rates, we compute grounding line retreat over hundreds of kilometers in every major ice stream, but the ocean models do not predict such melt rates outside of the Amundsen Sea Embayment until after 2100. Within the Amundsen Sea Embayment the largest single source of variability is the onset of sustained retreat in Thwaites Glacier, which can triple the rate of eustatic sea level rise

The GATA1s isoform is normally down-regulated during terminal haematopoietic differentiation and over-expression leads to failure to repress MYB, CCND2 and SKI during erythroid differentiation of K562 cells

Background: Although GATA1 is one of the most extensively studied haematopoietic transcription factors little is currently known about the physiological functions of its naturally occurring isoforms GATA1s and GATA1FL in humans—particularly whether the isoforms have distinct roles in different lineages and whether they have non-redundant roles in haematopoietic differentiation. As well as being of general interest to understanding of haematopoiesis, GATA1 isoform biology is important for children with Down syndrome associated acute megakaryoblastic leukaemia (DS-AMKL) where GATA1FL mutations are an essential driver for disease pathogenesis. <p/>Methods: Human primary cells and cell lines were analyzed using GATA1 isoform specific PCR. K562 cells expressing GATA1s or GATA1FL transgenes were used to model the effects of the two isoforms on in vitro haematopoietic differentiation. <p/>Results: We found no evidence for lineage specific use of GATA1 isoforms; however GATA1s transcripts, but not GATA1FL transcripts, are down-regulated during in vitro induction of terminal megakaryocytic and erythroid differentiation in the cell line K562. In addition, transgenic K562-GATA1s and K562-GATA1FL cells have distinct gene expression profiles both in steady state and during terminal erythroid differentiation, with GATA1s expression characterised by lack of repression of MYB, CCND2 and SKI. <p/>Conclusions: These findings support the theory that the GATA1s isoform plays a role in the maintenance of proliferative multipotent megakaryocyte-erythroid precursor cells and must be down-regulated prior to terminal differentiation. In addition our data suggest that SKI may be a potential therapeutic target for the treatment of children with DS-AMKL

The implications of defining obesity as a disease: a report from the Association for the Study of Obesity 2021 annual conference

Unlike various countries and organisations, including the World Health Organisation and the European Parliament, the United Kingdom does not formally recognise obesity as a disease. This report presents the discussion on the potential impact of defining obesity as a disease on the patient, the healthcare system, the economy, and the wider society. A group of speakers from a wide range of disciplines came together to debate the topic bringing their knowledge and expertise from backgrounds in medicine, psychology, economics, and politics as well as the experience of people living with obesity. The aim of their debate was not to decide whether obesity should be classified as a disease but rather to explore what the implications of doing so would be, what the gaps in the available data are, as well as to provide up-to-date information on the topic from experts in the field. There were four topics where speakers presented their viewpoints, each one including a question-and-answer section for debate. The first one focused on the impact that the recognition of obesity could have on people living with obesity regarding the change in their behaviour, either positive and empowering or more stigmatising. During the second one, the impact of defining obesity as a disease on the National Health Service and the wider economy was discussed. The primary outcome was the need for more robust data as the one available does not represent the actual cost of obesity. The third topic was related to the policy implications regarding treatment provision, focusing on the public's power to influence policy. Finally, the last issue discussed, included the implications of public health actions, highlighting the importance of the government's actions and private stakeholders. The speakers agreed that no matter where they stand on this debate, the goal is common: to provide a healthcare system that supports and protects the patients, strategies that protect the economy and broader society, and policies that reduce stigma and promote health equity. Many questions are left to be answered regarding how these goals can be achieved. However, this discussion has set a good foundation providing evidence that can be used by the public, clinicians, and policymakers to make that happen

Meltwater produced by wind–albedo interaction stored in an East Antarctic ice shelf

Surface melt and subsequent firn air depletion can ultimately lead to disintegration of Antarctic ice shelves1,2 causing grounded glaciers to accelerate3 and sea level to rise. In the Antarctic Peninsula, foehn winds enhance melting near the grounding line4, which in the recent past has led to the disintegration of the most northerly ice shelves5,6. Here, we provide observational and model evidence that this process also occurs over an East Antarctic ice shelf, where meltwaterinduced firn air depletion is found in the grounding zone. Unlike the Antarctic Peninsula, where foehn events originate from episodic interaction of the circumpolar westerlies with the topography, in coastal East Antarctica high temperatures are caused by persistent katabatic winds originating from the ice sheet’s interior. Katabatic winds warm and mix the air as it flows downward and cause widespread snow erosion, explaining >3 K higher near-surface temperatures in summer and surface melt doubling in the grounding zone compared with its surroundings. Additionally, these winds expose blue ice and firn with lower surface albedo, further enhancing melt. The in situ observation of supraglacial flow and englacial storage of meltwater suggests that ice-shelf grounding zones in East Antarctica, like their Antarctic Peninsula counterparts, are vulnerable to hydrofracturing7

Acute ingestion of a novel whey-derived peptide improves vascular endothelial responses in healthy individuals: a randomized, placebo controlled trial

<p>Abstract</p> <p>Background</p> <p>Whey protein is a potential source of bioactive peptides. Based on findings from <it>in vitro </it>experiments indicating a novel whey derived peptide (NOP-47) increased endothelial nitric oxide synthesis, we tested its effects on vascular function in humans.</p> <p>Methods</p> <p>A randomized, placebo-controlled, crossover study design was used. Healthy men (n = 10) and women (n = 10) (25 ± 5 y, BMI = 24.3 ± 2.3 kg/m²) participated in two vascular testing days each preceded by 2 wk of supplementation with a single dose of 5 g/day of a novel whey-derived peptide (NOP-47) or placebo. There was a 2 wk washout period between trials. After 2 wk of supplementation, vascular function in the forearm and circulating oxidative stress and inflammatory related biomarkers were measured serially for 2 h after ingestion of 5 g of NOP-47 or placebo. Macrovascular and microvascular function were assessed using brachial artery flow mediated dilation (FMD) and venous occlusion strain gauge plethysmography.</p> <p>Results</p> <p>Baseline peak FMD was not different for Placebo (7.7%) and NOP-47 (7.8%). Placebo had no effect on FMD at 30, 60, and 90 min post-ingestion (7.5%, 7.2%, and 7.6%, respectively) whereas NOP-47 significantly improved FMD responses at these respective postprandial time points compared to baseline (8.9%, 9.9%, and 9.0%; <it>P </it>< 0.0001 for time × trial interaction). Baseline reactive hyperemia forearm blood flow was not different for placebo (27.2 ± 7.2%/min) and NOP-47 (27.3 ± 7.6%/min). Hyperemia blood flow measured 120 min post-ingestion (27.2 ± 7.8%/min) was unaffected by placebo whereas NOP-47 significantly increased hyperemia compared to baseline (29.9 ± 7.8%/min; <it>P </it>= 0.008 for time × trial interaction). Plasma myeloperoxidase was increased transiently by both NOP-47 and placebo, but there were no changes in markers inflammation. Plasma total nitrites/nitrates significantly decreased over the 2 hr post-ingestion period and were lower at 120 min after placebo (-25%) compared to NOP-47 (-18%).</p> <p>Conclusion</p> <p>These findings indicate that supplementation with a novel whey-derived peptide in healthy individuals improves vascular function.</p

N-Acetylcysteine inhibits platelet-monocyte conjugation in patients with type 2 diabetes with depleted intraplatelet glutathione: a randomised controlled trial

AIMS/HYPOTHESIS: The aim of this study was to determine whether oral dosing with N-acetylcysteine (NAC) increases intraplatelet levels of the antioxidant, glutathione (GSH), and reduces platelet–monocyte conjugation in blood from patients with type 2 diabetes. METHODS: In this placebo-controlled randomised crossover study, the effect of oral NAC dosing on platelet–monocyte conjugation and intraplatelet GSH was investigated in patients with type 2 diabetes (eligibility criteria: men or post-menopausal women with well-controlled diabetes (HbA(1c) < 10%), not on aspirin or statins). Patients (n = 14; age range 43–79 years, HbA(1c) = 6.9 ± 0.9% [52.3 ± 10.3 mmol/mol]) visited the Highland Clinical Research Facility, Inverness, UK on day 0 and day 7 for each arm of the study. Blood was sampled before and 2 h after oral administration of placebo or NAC (1,200 mg) on day 0 and day 7. Patients received placebo or NAC capsules for once-daily dosing on the intervening days. The order of administration of NAC and placebo was allocated by a central office and all patients and research staff involved in the study were blinded to the allocation until after the study was complete and the data fully analysed. The primary outcome for the study was platelet–monocyte conjugation. RESULTS: Oral NAC reduced platelet–monocyte conjugation (from 53.1 ± 4.5% to 42.5 ± 3.9%) at 2 h after administration and the effect was maintained after 7 days of dosing. Intraplatelet GSH was raised in individuals with depleted GSH and there was a negative correlation between baseline intraplatelet GSH and platelet–monocyte conjugation. There were no adverse events. CONCLUSIONS/INTERPRETATION: The NAC-induced normalisation of intraplatelet GSH, coupled with a reduction in platelet–monocyte conjugation, suggests that NAC might help to reduce atherothrombotic risk in type 2 diabetes. FUNDING: Chief Scientist Office (CZB/4/622), Scottish Funding Council, Highlands & Islands Enterprise and European Regional Development Fund. TRIAL REGISTRATION: isrctn.org ISRCTN89304265 ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00125-012-2685-z) contains peer-reviewed but unedited supplementary material, which is available to authorised users