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The Scandinavian topography and bathymetry have been shaped by ice through numerous glacial cycles in the Quaternary. In this study, we investigate how the changing morphology has influenced the Scandinavian ice sheet (SIS) in return. We use a higher-order ice-sheet model to simulate the SIS through a glacial period on three different topographies, representing different stages of glacial landscape evolution in the Quaternary. By forcing the three experiments with the same climate conditions, we isolate the effects of a changing landscape morphology on the evolution and dynamics of the ice sheet. We find that early Quaternary glaciations in Scandinavia were limited in extent and volume by the pre-glacial bathymetry until glacial deposits filled depressions in the North Sea and built out the Norwegian shelf. From middle-late Quaternary (â¼0.5 Ma) the bathymetry was sufficiently filled to allow for a faster southward expansion of the ice sheet causing a relative increase in ice-sheet volume and extent. Furthermore, we show that the formation of The Norwegian Channel during recent glacial periods restricted southward ice-sheet expansion, only allowing for the ice sheet to advance into the southern North Sea close to glacial maxima. Finally, our experiments indicate that different stretches of The Norwegian Channel may have formed in distinct stages during glacial periods since â¼0.5 Ma. These results highlight the importance of accounting for changes in landscape morphology through time when inferring ice-sheet history from ice-volume proxies and when interpreting climate variability from past ice-sheet extents.

Rock slope failures in the Lake District, UK, have been associated with deglacial processes after the Last Glacial Maximum, but the controls and timing of the failures remain poorly known. A cirque headwall failure was investigated to determine failure mechanisms and timing. The translated wedge of rock is thin and lies on a steep failure plane, yet the friable strata were not disrupted by downslope movement. Fault lines and a failure surface, defining the wedge, were used as input to a numerical model of rock wedge stability. Various failure scenarios indicated that the slope was unstable and would have failed catastrophically if not supported by glacial ice in the base of the cirque. The amount of ice required to buttress the slope is insubstantial, indicating likely failure during the thinning of the cirque glacier. We propose that, as the ice thinned, the wedge was lowered slowly down the cirque headwall, gradually exposing the failure plane. A cosmogenic 10Be surface exposure age of 18.0±1.2 ka from the outer surface of the wedge indicates Late Devensian de-icing of the backwall of the cirque, with a second exposure age from the upper portion of the failure plane yielding 12.0±0.8 ka. The 18.0±1.2 ka date is consistent with a small buttressing ice mass being present in the cirque at the time of regional deglaciation. The exposure age of 12.0±0.8 ka represents a minimum age, as the highly fractured surface of the failure plane has experienced post-failure mass-wasting. Considering the chronology, it appears unlikely that the cirque was reoccupied by a substantial ice mass during the Younger Dryas stadial.

Abstract Ice streams regulate most ice mass loss in Antarctica. Determining ice stream response to warmer conditions during the Pliocene could provide insights into their future behaviour, but this is hindered by a poor representation of subglacial topography in ice-sheet models. We address this limitation using a high-resolution model for Dronning Maud Land (East Antarctica). We show that contrary to dynamic thinning of the region’s ice streams following ice-shelf collapse, the largest ice stream, Jutulstraumen, thickens by 700 m despite lying on a retrograde bed slope. We attribute this counterintuitive thickening to a shallower Pliocene subglacial topography and inherent high lateral stresses at its flux gate. These conditions constrict ice drainage and, combined with increased snowfall, allow ice accumulation upstream. Similar stress balances and increased precipitation projections occur across 27% of present-day East Antarctica, and understanding how lateral stresses regulate ice-stream discharge is necessary for accurately assessing Antarctica’s future sea-level rise contribution.

Abstract The East Antarctic Ice Sheet stores a vast amount of freshwater, which makes it the single largest potential contributor to future sea-level rise. However, the lack of well-constrained geological records of past ice sheet changes impedes model validation, hampers mass balance estimates, and inhibits examination of ice loss mechanisms. Here we identify rapid ice-sheet thinning in coastal Dronning Maud Land from Early to Middle Holocene (9000–5000 years ago) using a deglacial chronology based on in situ cosmogenic nuclide surface exposure dates from central Dronning Maud Land, in concert with numerical simulations of regional and continental ice-sheet evolution. Regional sea-level changes reproduced from our refined ice-load history show a highstand at 9000–8000 years ago. We propose that sea-level rise and a concomitant influx of warmer Circumpolar Deep Water triggered ice shelf breakup via the marine ice sheet instability mechanism, which led to rapid thinning of upstream coastal ice sheet sectors.

Abstract The impact of late Cenozoic climate on the East Antarctic Ice Sheet is uncertain. Poorly constrained patterns of relative ice thinning and thickening impair the reconstruction of past ice-sheet dynamics and global sea-level budgets. Here we quantify long-term ice cover of mountains protruding the ice-sheet surface in western Dronning Maud Land, using cosmogenic Chlorine-36, Aluminium-26, Beryllium-10, and Neon-21 from bedrock in an inverse modeling approach. We find that near-coastal sites experienced ice burial up to 75–97% of time since 1 Ma, while interior sites only experienced brief periods of ice burial, generally <20% of time since 1 Ma. Based on these results, we suggest that the escarpment in Dronning Maud Land acts as a hinge-zone, where ice-dynamic changes driven by grounding-line migration are attenuated inland from the coastal portions of the East Antarctic Ice Sheet, and where precipitation-controlled ice-thickness variations on the polar plateau taper off towards the coast.

The aim of DANARREST is to collect data on processes of care and outcomes for patients with in-hospital cardiac arrest in Denmark, and thereby facilitate and monitor quality and quality improvement initiatives. In-hospital cardiac arrest patients with a clinical indication for cardiopulmonary resuscitation in Denmark. DANARREST includes a number of descriptive variables as well as seven quality of care indicators; four related to processes of care and three related to clinical outcomes. The four process measures are related to whether the cardiac arrest was witnessed, whether the cardiac arrest was ECG-monitored, the timing of cardiopulmonary resuscitation, and the timing of the first rhythm analysis. The three outcomes measures include return of spontaneous circulation, 30-day survival, and 1-year survival. DANARREST started in 2013, and the coverage has increased steadily since. As of 2017, 95% of relevant hospitals are reporting data with an estimated coverage rate of approximately 80%. DANARREST is a relatively new national registry of in-hospital cardiac arrests in Denmark, with a high coverage rate. The registry provides an opportunity to monitor and improve quality of care for patients with in-hospital cardiac arrest.

Diagnostic assays currently used to monitor the efficacy of COVID-19 vaccines measure levels of antibodies to the receptor-binding domain of ancestral SARS-CoV-2 (RBDwt). However, the predictive value for protection against new variants of concern (VOCs) has not been firmly established. Here, we used bead-based arrays and flow cytometry to measure binding of antibodies to spike proteins and receptor-binding domains (RBDs) from VOCs in 12,000 serum samples. Effects of sera on RBD-ACE2 interactions were measured as a proxy for neutralizing antibodies. The samples were obtained from healthy individuals or patients on immunosuppressive therapy who had received two to four doses of COVID-19 vaccines and from COVID-19 convalescents. The results show that anti-RBDwt titers correlate with the levels of binding- and neutralizing antibodies against the Alpha, Beta, Gamma, Delta, Epsilon and Omicron variants. The benefit of multiplexed analysis lies in the ability to measure a wide range of anti-RBD titers using a single dilution of serum for each assay. The reactivity patterns also yield an internal reference for neutralizing activity and binding antibody units per milliliter (BAU/ml). Results obtained with sera from vaccinated healthy individuals and patients confirmed and extended results from previous studies on time-dependent waning of antibody levels and effects of immunosuppressive agents. We conclude that anti-RBDwt titers correlate with levels of neutralizing antibodies against VOCs and propose that our method may be implemented to enhance the precision and throughput of immunomonitoring.

The Danish multidisciplinary renal cancer group (DaRenCa) established the nationwide database DaRenCaData in 2010. The Danish Cancer Registry (DCR) has been considered the golden standard. In contrast to DCR, DaRenCaData required the diagnosis to be histologically or cytologically verified. DaRenCaData and DCR have not previously been compared. We included patients with renal cell carcinoma registered in DaRenCaData and/or DCR from August 1st 2010 to December 31st 2015. We computed completeness and positive predictive value (PPV) of a diagnosis in DaRenCaData compared with DCR, 1-year, 3-year and 5-year mortality rate ratios, and relative survival. We identified 4890 patients in the two registries. Of these, 4326 were registered in DaRenCaData and 4714 in DCR. Completeness of DaRenCaData was 88% [95% CI, 87-89%] and increased during the period from 82% to 94%. The PPV was 96% [95% CI, 95-97%]. A total of 4150 patients (85%) were found in both registries, 4% (176 patients) in DaRenCaData only, and 12% (564 patients) in DCR only. The relative survival was higher for patients in DaRenCaData vs DCR; the 1-year and 5-year relative survival was 85% vs 81% and 65% vs 59%, respectively. Compared with patients registered in both registries, the mortality rates were higher in patients registered in DaRenCaData only (1-year hazard ratio (HR)=2.84 [95% CI, 2.20-3.68]) or DCR only (1-year HR=4.29 [95% CI, 3.72-4.93]). Observed in both registries, survival improved over time with a 7% yearly reduction in death based on estimations of 1-year mortality rate ratios. DaRenCaData had high and increasing completeness and high PPV, establishing it as a high-quality research database. Observed in both registries, renal cell carcinoma mortality declined over time; patients only registered in DCR or DaRenCaData had poorer outcomes. This study points to the importance of assessing the inclusion criteria when interpreting registry-based studies.

Spinal cord injury (SCI) is a devastating condition consisting of an instant primary mechanical injury followed by a secondary injury that progresses for weeks to months. The cytokine tumor necrosis factor (TNF) plays an important role in the pathophysiology of SCI. We investigated the effect of myeloid TNF ablation (peripheral myeloid cells (macrophages and neutrophils) and microglia) versus central myeloid TNF ablation (microglia) in a SCI contusion model. We show that TNF ablation in macrophages and neutrophils leads to reduced lesion volume and improved functional outcome after SCI. In contrast, TNF ablation in microglia only or TNF deficiency in all cells had no effect. TNF levels tended to be decreased 3 h post-SCI in mice with peripheral myeloid TNF ablation and was significantly decreased 3 days after SCI. Leukocyte and microglia populations and all other cytokines (IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, and IFNγ) and chemokines (CCL2, CCL5, and CXCL1) investigated, in addition to TNFR1 and TNFR2, were comparable between genotypes. Analysis of post-SCI signaling cascades demonstrated that the MAPK kinase SAPK/JNK decreased and neuronal Bcl-XL levels increased post-SCI in mice with ablation of TNF in peripheral myeloid cells. These findings demonstrate that peripheral myeloid cell-derived TNF is pathogenic in SCI.

Diagnostic assays currently used to monitor the efficacy of COVID-19 vaccines measure levels of antibodies to the receptor-binding domain of ancestral SARS-CoV-2 (RBDwt). However, the predictive value for protection against new variants of concern (VOCs) has not been firmly established. Here, we used bead-based arrays and flow cytometry to measure binding of antibodies to spike proteins and receptor-binding domains (RBDs) from VOCs in 12,000 sera. Effects of sera on RBD-ACE2 interactions were measured as a proxy for neutralizing antibodies. The samples were obtained from healthy individuals or patients on immunosuppressive therapy who had received two to four doses of COVID-19 vaccines and from COVID-19 convalescents. The results show that anti-RBDwt titers correlate with the levels of binding- and neutralizing antibodies against the Alpha, Beta, Gamma, Delta, Epsilon and Omicron variants. The benefit of multiplexed analysis lies in the ability to measure a wide range of anti-RBD titers using a single dilution of serum for each assay. The reactivity patterns also yield an internal reference for neutralizing activity and binding antibody units per milliliter (BAU/ml). Results obtained with sera from vaccinated healthy individuals and patients confirmed and extended results from previous studies on time-dependent waning of antibody levels and effects of immunosuppressive agents. We conclude that anti-RBDwt titers correlate with levels of neutralizing antibodies against VOCs and propose that our method may be implemented to enhance the precision and throughput of immunomonitoring. Competing Interest Statement 1. Trung The Tran has nothing to disclose. 2. Eline Bonne Vaage has nothing to disclose. 3. Adi Mehta has nothing to disclose. 4. Adity Chopra has nothing to disclose. 5. Anette Kolderup has received support from South-Eastern Norway Regional Health Authority (Grant no 10357 and 2021069. The payments were made to the institution, Oslo University Hospital, and covered salary and consumables) and from Juni Andrell, Stockholm University, Sweden (cDNA encoding 8xHis-tagged HexaPro spike protein and 6xHis-tagged receptor binding domain (RBD) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Wuhan, in the expression plasmids pαH and pCAGGS, respectively. 6. Aina Karen Anthi has received support from South-Eastern Norway Regional Health Authority (Grant no 2019084. The payments were made to the institution, Oslo University Hospital, and covered salary and consumables). She has also received support from Juni Andrell, Stockholm University, Sweden (cDNA encoding 8xHis-tagged HexaPro spike protein and 6xHis-tagged receptor binding domain (RBD) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Wuhan, in the expression plasmids pαH and pCAGGS, respectively. 7. M. Konig has received speaker honoraria from Novartis, Biogen, Sanofi, and Merck and support from Coalition for Epidemic Preparedness Innovations (CEPI) through Oslo University Hospital. 8. Gro Nygard has received support from Coalition for Epidemic Preparedness Innovations (CEPI) through Oslo University Hospital. 9. Andreas Lind has nothing to disclose. 10. Fredrik Muller has nothing to disclose. 11. Lise Sofie Haug Nissen-Meyer has nothing to disclose. 12. Per Magnus has received support from Norwegian Institute of Public Health for collection of blood samples in NorFlu and MoBa since 2020. 13. Lill-Iren Schou Trogstad has received support from Norwegian Institute of Public Health for collection of blood samples in NorFlu and MoBa since 2020. 14. Siri Mjaaland has nothing to disclose. 15. Arne Soraas has received support from Norwegian Cancer Association, Norwegian research Council, and Southeastern Norway Health Authority. 16. Karsten Midtvedt has nothing to disclose. 17. Anders Asberg has received payment to the institution from Sandos and Orifarm 18. Andreas Barratt-Due has nothing to disclose. 19. Asle Wilhelm Medhus has received a grant from Takeda (Grant to a research-initiated project, payment to institution). 20. Marte Lie Hoivik has received research grants to the institution from Pfizer, Janssen, Takeda, Ferring, Tillotts and has participated on a Data Safety Monitoring Board or Advisory Board at Takeda with personal fees. 21. Knut Lundin has nothing to disclose. 22. Randi Fuglaas Karlsen has nothing to disclose. 23. Reidun Dahle has nothing to disclose. 24. Karin Danielsson has nothing to disclose. 25. Kristine Stien Thomassen has nothing to disclose. 26. Grete Birkeland Kro has nothing to disclose. 27. Rebecca Jane Cox has nothing to disclose. 28. Fan Zhou has nothing to disclose. 29. Nina Langeland has nothing to disclose. 30. Pal Aukrust has received support from Klinbeforsk. grants for COVID-19 research 2020. 31. Espen Melum has nothing to disclose. 32. Tone Lise Avitsland has nothing to disclose. 33. Kristine Wiencke has nothing to disclose. 34. Jan Cato Holter has received support from Oslo University hospital, Research Council of Norway (Grant no 312780), and Philantropic donation from Vivaldi Invest A/A owned by Jon Steohenson von Tetzchner. 35. Ludvig Andre Munthe has received support from CEPI (Oslo University Hospital, University of Oslo), funding from University of Oslo, RCN, Norwegian Cancer Society, Health South East Health Research Funds (Stiftelsen KG Jebsen Grant 19), consulting fees in 20201: Astrazeneca for a panel discussing options for Long-Acting anti-SARS-CoV-2 Biologic AZD 7442, 4-time slots, < 1000USD, and payment for expert testimony in 20201 (Part of the expert panel for Norwegian Medicines Agency on vaccinology and associated topics, salary 1500USD and part of the expert panel for Norwegian Institute of Public Health for Norwegian Corona Vaccination Program. 8 meetings. Pro Bono). 36. Gunnveig Grodeland has received support from South-Eastern Norway Regional Health Authority, grants from the Research Council of Norway and EU-Horizon 2020, consulting fees from the Norwegian System of Compensation to Patients, honoraria from Bayer, ThermoFisher, and Saofi. She has also participated on the Data Safety Monitoring Board or Advisory Board with AstraZeneca. 37. Jan Terje Andersen has received support from South-Eastern Norway Regional Health Authority (Grant no 10357 and 2021069. The payments were made to the institution, Oslo University Hospital, and covered salary and consumables) and from Juni Andrell, Stockholm University, Sweden (cDNA encoding 8xHis-tagged HexaPro spike protein and 6xHis-tagged receptor-binding domain (RBD) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Wuhan, in the expression plasmids pαH and pCAGGS, respectively. He has collaborated with Roche, Tillotts Pharma, SJJ Solutions, Argenx, and Nordic Nanovector. Not directly related to the work of this manuscript. 38. John Torgils Vaage has nothing to disclose. 39. Fridtjof Lund-Johansen has received support from the South-Eastern Norway Regional Health Authority grant for developing COVID-19 serology. He has also received support from The Coalition for Epidemic Preparedness and Innovation (CEPI), a grant to monitor vaccine responses in patients on immunosuppressive therapy. Footnotes * Updating the title of the manuscript