57 research outputs found
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The Dorsa Argentea, Mars: New Comparisons to a Large Sample of Terrestrial Eskers and Quantitative Tests for Esker-Like Topographic Relationships
Get PDFThe Dorsa Argentea (DA) are an assemblage of ridges in Mars’ southern high latitudes (70°-80°S, 56°W-6°E). Glacial eskers and inverted channels remain as active hypotheses for their formation. The esker interpretation is widely used as a basis for reconstructions of meltwater production beneath a putative former ice sheet in the region of the DA during Mars’ Hesperian period, despite a lack of rigorous quantitative testing of the esker hypothesis. We undertake the first large-scale quantitative analysis of the plan view geometries of the DA in a comparison to >5900 terrestrial esker systems in Canada. Statistical tests for esker-like topographic relationships are also completed. Our results support the esker hypothesis and highlight that future studies of the DA and its parent ice sheet should more closely consider the ongoing debate over the spatio-temporal nature of terrestrial esker formation, and its implications for reconstructions of ice sheet meltwater production
Highly erosive glaciers on Mars - the role of water
Get PDFInternational audiencePolewards of 30 • in each hemisphere, the surface of Mars hosts a suite of landforms reminiscent of glacial landscapes on Earth. Amongst these landforms are: 1) Viscous Flow Features (VFF), which resemble glaciers on Earth and are thought to contain large volumes of water ice, 2) martian gullies which are km-scale features resembling water-eroded gullies on Earth and 3) arcuate ridges thought to be moraines from previous glaciations. Gullies have been long-associated with a surface unit originally called "pasted-on terrain" and now often called the "latitude dependant mantle". Arcuate ridges are often found at the base of hillslopes with gullies, but are also found on hillslopes with pasted-on terrain and no gullies. We have found a systematic lowering of the slope of the bedrock exposure located topographically above the pasted-on terrain whether that same slope hosts gullies or not. The lowered bedrock exposures display a different surface texture from bedrock exposed on other parts of the crater wall and from fresh crater walls-it appears fragmented and has reduced relief. Using 1-m-digital elevation models from the High Resolution Imaging Science Experiment (HiRISE) we compared the slopes of eight "eroded" craters and seven unmodified craters. We estimated their age using the crater size-frequency distribution of small craters on their ejecta blankets. From this information we calculated bedrock retreat rates for the eroded craters and found they were up to ∼103 m Myr-1-equivalent to erosion rates of wet-based glaciers on Earth. This is several orders of magnitude higher than previous estimates of erosion by VFF (10-2-101 m Myr-1), which themselves are roughly equivalent to cold-based glaciers on Earth. Such erosion rates are sufficient to erase previously existing landforms, such as martian gullies. We hypothesise, therefore, that the pasted-on terrain is a glacial deposit, overturning its previous interpretation as an airfall deposit of ice nucleated on dust. We maintain the interpretation of the arcuate ridges as moraines, but further conclude that they are likely the result of glaciotectonic deformation of sub-marginal and proglacial sediment in the presence of sediment pore-water. We do not support the generation of large quantities of glacial meltwater because it would have broken-up and degraded the arcuate ridges and pasted-on terrain an produced a suite of landforms (e.g., hummocky moraine, lacustrine forms, outwash plains, eskers) which are not observed
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Glacier-Linked Eskers on Mars: Environments of Recent Wet-Based Glaciation From Numerical Models
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Evidence for Recent Wet-Based Crater Glaciation in Tempe Terra, Mars.
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Mars’ mid-latitudes host abundant putative debris-covered water-ice glaciers (viscous flow features; VFF). Eskers emerging from 110-150 Myr-old VFF in Phlegra Montes and Tempe Terra provide evidence for rare occurences of past, localized basal melting of their parent VFF, despite the cold climates of the late Amazonian (see this conf.). Eskers are sinuous ridges comprising glaciofluvial sediment deposited by meltwater flowing through tunnels within glacial ice.
Here, we describe a population of sinuous ridges emerging from VFF in an unnamed ~45 km-diameter crater (38.47 N, 72.43 W) in Tempe Terra, ~600 km from the VFF-linked esker identified by Butcher et al. We consider two working hypotheses for the formation of the sinuous ridges; that they are either (1) eskers formed by melting of the glaciers from which they emerge, or (2) topographically inverted fluvial channels which formed prior to glaciation of the crater. We present observations from preliminary geomorphic mapping of the crater to start to test those hypotheses
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Morphometric Characterisation of Eskers Associated with an Extant Mid-Latitude Glacier on Mars
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Eskers associated with Extant Glaciers in Mid-Latitude Graben on Mars: Evidence for Geothermal Controls upon Recent Basal Melting
Get PDFOn the mechanisms governing gas penetration into a tokamak plasma during a massive gas injection
Get PDFA new 1D radial fluid code, IMAGINE, is used to simulate the penetration of gas into a tokamak plasma during a massive gas injection (MGI). The main result is that the gas is in general strongly braked as it reaches the plasma, due to mechanisms related to charge exchange and (to a smaller extent) recombination. As a result, only a fraction of the gas penetrates into the plasma. Also, a shock wave is created in the gas which propagates away from the plasma, braking and compressing the incoming gas. Simulation results are quantitatively consistent, at least in terms of orders of magnitude, with experimental data for a D 2 MGI into a JET Ohmic plasma. Simulations of MGI into the background plasma surrounding a runaway electron beam show that if the background electron density is too high, the gas may not penetrate, suggesting a possible explanation for the recent results of Reux et al in JET (2015 Nucl. Fusion 55 093013)
Whole-genome sequencing reveals host factors underlying critical COVID-19
Get PDFCritical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
SARS-CoV-2-specific nasal IgA wanes 9 months after hospitalisation with COVID-19 and is not induced by subsequent vaccination
Get PDFBACKGROUND: Most studies of immunity to SARS-CoV-2 focus on circulating antibody, giving limited insights into mucosal defences that prevent viral replication and onward transmission. We studied nasal and plasma antibody responses one year after hospitalisation for COVID-19, including a period when SARS-CoV-2 vaccination was introduced. METHODS: In this follow up study, plasma and nasosorption samples were prospectively collected from 446 adults hospitalised for COVID-19 between February 2020 and March 2021 via the ISARIC4C and PHOSP-COVID consortia. IgA and IgG responses to NP and S of ancestral SARS-CoV-2, Delta and Omicron (BA.1) variants were measured by electrochemiluminescence and compared with plasma neutralisation data. FINDINGS: Strong and consistent nasal anti-NP and anti-S IgA responses were demonstrated, which remained elevated for nine months (p < 0.0001). Nasal and plasma anti-S IgG remained elevated for at least 12 months (p < 0.0001) with plasma neutralising titres that were raised against all variants compared to controls (p < 0.0001). Of 323 with complete data, 307 were vaccinated between 6 and 12 months; coinciding with rises in nasal and plasma IgA and IgG anti-S titres for all SARS-CoV-2 variants, although the change in nasal IgA was minimal (1.46-fold change after 10 months, p = 0.011) and the median remained below the positive threshold determined by pre-pandemic controls. Samples 12 months after admission showed no association between nasal IgA and plasma IgG anti-S responses (R = 0.05, p = 0.18), indicating that nasal IgA responses are distinct from those in plasma and minimally boosted by vaccination. INTERPRETATION: The decline in nasal IgA responses 9 months after infection and minimal impact of subsequent vaccination may explain the lack of long-lasting nasal defence against reinfection and the limited effects of vaccination on transmission. These findings highlight the need to develop vaccines that enhance nasal immunity. FUNDING: This study has been supported by ISARIC4C and PHOSP-COVID consortia. ISARIC4C is supported by grants from the National Institute for Health and Care Research and the Medical Research Council. Liverpool Experimental Cancer Medicine Centre provided infrastructure support for this research. The PHOSP-COVD study is jointly funded by UK Research and Innovation and National Institute of Health and Care Research. The funders were not involved in the study design, interpretation of data or the writing of this manuscript
Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease
Get PDFOne in ten severe acute respiratory syndrome coronavirus 2 infections result in prolonged symptoms termed long coronavirus disease (COVID), yet disease phenotypes and mechanisms are poorly understood1. Here we profiled 368 plasma proteins in 657 participants ≥3 months following hospitalization. Of these, 426 had at least one long COVID symptom and 233 had fully recovered. Elevated markers of myeloid inflammation and complement activation were associated with long COVID. IL-1R2, MATN2 and COLEC12 were associated with cardiorespiratory symptoms, fatigue and anxiety/depression; MATN2, CSF3 and C1QA were elevated in gastrointestinal symptoms and C1QA was elevated in cognitive impairment. Additional markers of alterations in nerve tissue repair (SPON-1 and NFASC) were elevated in those with cognitive impairment and SCG3, suggestive of brain–gut axis disturbance, was elevated in gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2-specific immunoglobulin G (IgG) was persistently elevated in some individuals with long COVID, but virus was not detected in sputum. Analysis of inflammatory markers in nasal fluids showed no association with symptoms. Our study aimed to understand inflammatory processes that underlie long COVID and was not designed for biomarker discovery. Our findings suggest that specific inflammatory pathways related to tissue damage are implicated in subtypes of long COVID, which might be targeted in future therapeutic trials
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