The Methane Diurnal Variation and Microseepage Flux at Gale Crater, Mars as Constrained by the ExoMars Trace Gas Orbiter and Curiosity Observations

The upper bound of 50 parts per trillion by volume for Mars methane above 5 km established by the ExoMars Trace Gas Orbiter, substantially lower than the 410 parts per trillion by volume average measured overnight by the Curiosity Rover, places a strong constraint on the daytime methane flux at the Gale crater. We propose that these measurements may be largely reconciled by the inhibition of mixing near the surface overnight, whereby methane emitted from the subsurface accumulates within meters of the surface before being mixed below detection limits at dawn. A model of this scenario allows the first precise calculation of microseepage fluxes at Gale to be derived, consistent with a constant 1.5 à 10â 10 kg·mâ 2·solâ 1 (5.4 à 10â 5 tonnes·kmâ 2·yearâ 1) source at depth. Under this scenario, only 2.7 à 104 km2 of Mars’s surface may be emitting methane, unless a fast destruction mechanism exists.Plain Language SummaryThe ExoMars Trace Gas Orbiter and the Curiosity Rover have recorded different amounts of methane in the atmosphere on Mars. The Trace Gas Orbiter measured very little methane (<50 parts per trillion by volume) above 5 km in the sunlit atmosphere, while Curiosity measured substantially more (410 parts per trillion by volume) near the surface at night. In this paper we describe a framework which explains both measurements by suggesting that a small amount of methane seeps out of the ground constantly. During the day, this small amount of methane is rapidly mixed and diluted by vigorous convection, leading to low overall levels within the atmosphere. During the night, convection lessens, allowing methane to build up near the surface. At dawn, convection intensifies and the nearâ surface methane is mixed and diluted with much more atmosphere. Using this model and methane concentrations from both approaches, we are ableâ for the first timeâ to place a single number on the rate of seepage of methane at Gale crater which we find equivalent to 2.8 kg per Martian day. Future spacecraft measuring methane near the surface of Mars could determine how much methane seeps out of the ground in different locations, providing insight into what processes create that methane in the subsurface.Key PointsNighttime SAMâ TLS seasonal cycle enrichment measurements and TGO sunset/sunrise measurements are not in oppositionMicroseepage fluxes must be local to Gale, range from 0.82 to 4.6 kg/sol, and are consistent with a constant source at depthLittle of Mars experiences microseepage unless a fast destruction mechanism exists or Gale is very unusualPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/151840/1/grl59471-sup-0001-2019GL083800-SI.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151840/2/grl59471_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151840/3/grl59471.pd

Stability of hydrated minerals on Mars

The validity of recent identification of various hydrated minerals (kieserite, gypsum, hexahydrite, nontronite, chamosite, and montmorillonite) on Mars was assessed by exposing these minerals to simulated Martian surface conditions of atmospheric composition and pressure, temperature, and ultraviolet light irradiation. When exposed to such conditions the hydrated minerals exhibit in general, greater losses of interlayer H2O than structural OH. Minerals such as gypsum that contain structural H2O are more resistant to H2O loss than phyllosilicates. The partial loss of OH in some of the phyllosilicates is not accompanied by a measurable and systematic change in the wavelength position or intensity of metal-OH absorption bands. The characteristic absorption features that allow for identification of these minerals on Mars may be reduced in intensity, but are nevertheless largely preserved.This study was supported with grants from the University of Winnipeg, the Canadian Space Agency. Funding for our spectrometer and Mars environment chamber facility at the University of Winnipeg (HOSERLab) was provided by the Canada Foundation for Innovation, the Manitoba Research and Innovation Fund and the Canadian Space Agency.https://agupubs.onlinelibrary.wiley.com/doi/abs/10.1029/2007GL03126

Assessment of β-amyloid deposits in human brain: a study of the BrainNet Europe Consortium

β-Amyloid (Aβ) related pathology shows a range of lesions which differ both qualitatively and quantitatively. Pathologists, to date, mainly focused on the assessment of both of these aspects but attempts to correlate the findings with clinical phenotypes are not convincing. It has been recently proposed in the same way as ι and α synuclein related lesions, also Aβ related pathology may follow a temporal evolution, i.e. distinct phases, characterized by a step-wise involvement of different brain-regions. Twenty-six independent observers reached an 81% absolute agreement while assessing the phase of Aβ, i.e. phase 1 = deposition of Aβ exclusively in neocortex, phase 2 = additionally in allocortex, phase 3 = additionally in diencephalon, phase 4 = additionally in brainstem, and phase 5 = additionally in cerebellum. These high agreement rates were reached when at least six brain regions were evaluated. Likewise, a high agreement (93%) was reached while assessing the absence/presence of cerebral amyloid angiopathy (CAA) and the type of CAA (74%) while examining the six brain regions. Of note, most of observers failed to detect capillary CAA when it was only mild and focal and thus instead of type 1, type 2 CAA was diagnosed. In conclusion, a reliable assessment of Aβ phase and presence/absence of CAA was achieved by a total of 26 observers who examined a standardized set of blocks taken from only six anatomical regions, applying commercially available reagents and by assessing them as instructed. Thus, one may consider rating of Aβ-phases as a diagnostic tool while analyzing subjects with suspected Alzheimer’s disease (AD). Because most of these blocks are currently routinely sampled by the majority of laboratories, assessment of the Aβ phase in AD is feasible even in large scale retrospective studies

Toward an Open-Access Global Database for Mapping, Control, and Surveillance of Neglected Tropical Diseases

There is growing interest in the scientific community, health ministries, and other organizations to control and eventually eliminate neglected tropical diseases (NTDs). Control efforts require reliable maps of NTD distribution estimated from appropriate models and survey data on the number of infected people among those examined at a given location. This kind of data is often available in the literature as part of epidemiological studies. However, an open-access database compiling location-specific survey data does not yet exist. We address this problem through a systematic literature review, along with contacting ministries of health, and research institutions to obtain disease data, including details on diagnostic techniques, demographic characteristics of the surveyed individuals, and geographical coordinates. All data were entered into a database which is freely accessible via the Internet (http://www.gntd.org). In contrast to similar efforts of the Global Atlas of Helminth Infections (GAHI) project, the survey data are not only displayed in form of maps but all information can be browsed, based on different search criteria, and downloaded as Excel files for further analyses. At the beginning of 2011, the database included over 12,000 survey locations for schistosomiasis across Africa, and it is continuously updated to cover other NTDs globally

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Mutational processes molding the genomes of 21 breast cancers

All cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed "kataegis," was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed

The life history of 21 breast cancers.

Cancer evolves dynamically as clonal expansions supersede one another driven by shifting selective pressures, mutational processes, and disrupted cancer genes. These processes mark the genome, such that a cancer's life history is encrypted in the somatic mutations present. We developed algorithms to decipher this narrative and applied them to 21 breast cancers. Mutational processes evolve across a cancer's lifespan, with many emerging late but contributing extensive genetic variation. Subclonal diversification is prominent, and most mutations are found in just a fraction of tumor cells. Every tumor has a dominant subclonal lineage, representing more than 50% of tumor cells. Minimal expansion of these subclones occurs until many hundreds to thousands of mutations have accumulated, implying the existence of long-lived, quiescent cell lineages capable of substantial proliferation upon acquisition of enabling genomic changes. Expansion of the dominant subclone to an appreciable mass may therefore represent the final rate-limiting step in a breast cancer's development, triggering diagnosis

Mutational processes molding the genomes of 21 breast cancers

All cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed “kataegis,” was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed

The fusion crust of the Winchcombe meteorite: vigorous degassing during atmospheric entry

Introduction: Fusion crusts form during the atmospheric entry heating of meteorites and preserve a record of the conditions that occurred in the last few seconds of their deceleration in the atmosphere [1]. Although fusion crusts are ubiquitous they are rarely characterised and studied because they obscure the primary features of meteorites. Here we report the results of a study of the fusion crust of the Winchcombe CM2 chondrite. The Winchcombe meteorite fell at 21:54 hours on 28 February 2021 in Gloucestershire in the UK and was recovered over the next week. The fall was observed on UKFAll network cameras and recorded by CCTV. The meteoroid had a low entry velocity compared to other observed falls of 13.5 km/s. Study of the fusion crust reveals unique textural features that testify to previously unknown processes related to vigorous degassing of this intensely altered CM2 chondrite. Methods: Six polished blocks of Winchcombe were studied using backscattered electron imaging, elemental mapping, energy dispersive spectroscopy (EDS), electron backscatter diffraction (EBSD) and micro-X-ray fluorescence (XRF). Apparent size distributions and abundances were obtained by threshold analysis using ImageJ. Results: The fusion crust consists of an inner thermally altered substrate and outer melted crust. The altered substrate exhibits unusually abundant dehydration cracks extending up to 5 mm into the meteorite. The crack network encompasses fragments up to 70 µm in diameter (dense rock equivalent) with increasing abundance with decreasing size. Loss of sheet-like habits for phyllosilicates and tochilinite testifies to progressive dehydration towards the exterior. The outer melted crust has a vesicular porphyritic texture with olivine phenocrysts and magnetite in a glassy mesostasis. Grain-size and magnetite abundance increase outwards similar to other CI/CM2 fusion crusts [2]. High Ni (<80 wt%) sulphide-metal droplets occur – often as menisci on vesicles. A magnetite rim occurs on the exterior surface and some vesicles, and include some tabular, rim-parallel magnetite crystals. Unique features in the fusion crust are oscillatory zoned olivine crystals, monolayers of magnetite and silicate warts. Monolayers form chains of magnetite crystals within the mesostasis that have tabular crystals similar to magnetite rims. EBSD data reveals [111] is parallel to the length of tabular crystals and is layer parallel in rims and monolayers. Oscillatory zoned crystals are equant with up to 4 Mg-rich zones. Silicate warts form lenticular features on the surface of the fusion crust and contain dendritic olivine – their compositions are, however, similar to the rest of the crust. Magnetite monolayers lie between warts and the underlying crust. Discussion: The unusualy high abundance of dehydration cracks suggests the tochlinite-rich matrix of the Winchcombe meteorite is particularly sensitive to dehydration, owing to the low decomposition temperature of this mineral (250oC [3]). Mechanical failure of the substrate, in part driven by gas pressure, is likely to inject large abundances of particulates into the meteoroid gas stream. Observations of episodic pulsed plasma in the trail of the fireball may be a phenomena associated with calving of the dehydrated substrate and generate thermal pulses explaining the presence of oscillatory zoning. Other features also are consistent with vigorous degassing. Magnetite monolayers appear to have formed as surface magnetite rims – owing to their similar alignment of tabular crystals. Trapping of surface magneite rims through collapse of melt protrusions is likely to explain how these layers become buried within the crust and is probably driven by perturbation of surface melt by rapid vesicle loss. Finally, silicate warts are likely to be droplets attached to the crust surface. Their dendritic textures suggest higher peak temperatures and strongly suggest they represent droplets removed from other stones in the shower. Warts represent the first discovery of intershower transport of ablation materials, possibly owing to enhanced ablation as a result of vigorous degassing. Implications: The fusion crust of the Winchcombe meteorite illustrates the complexity of processes affecting meteorites during atmospheric flight. Features such as magnetite monolayers and silicate warts have not previously been described, and may be unique to tochlinite-rich CM2 chondrites, which experience vigorous degassing. They may also allow ablation debris to be related to particular types of meteorite, thus providing a distributed record of the meteorite flux. Winchcombe underlines the utility of fusion crust, which should be routinely characterised in addition to meteorite interiors. References: [1] Ramsdohr P. (1967) EPSL 2, 593-598, [2] Genge M. J. & Grady M. M. (1999) MAPS 34 (3).341-356. [3] Fuchs, L. H et al. (1973) Smithsonian Contrib. Earth Sci. 1–3

Recurrent De Novo Dominant Mutations in SLC2SA4 Cause Severe Early-Onset Mitochondrial Disease and Loss of Mitochondrial DNA Copy Number

Mutations in SLC25A4 encoding the mitochondrial ADP/ATP carrier AAC1 are well-recognized causes of mitochondrial disease. Several heterozygous SLC25A4 mutations cause adult-onset autosomal-dominant progressive external ophthalmoplegia associated with multiple mitochondrial DNA deletions, whereas recessive SLC25A4 mutations cause childhood-onset mitochondrial myopathy and cardiomyopathy. Here, we describe the identification by whole-exome sequencing of seven probands harboring dominant, de novo SLC25A4 mutations. All affected individuals presented at birth, were ventilator dependent and, where tested, revealed severe combined mitochondria' respiratory chain deficiencies associated with a marked loss of mitochondria' DNA copy number in skeletal muscle. Strikingly, an identical c.239G>A (p.Arg80His) mutation was present in four of the seven subjects, and the other three case subjects harbored the same c.703C>G (p.Arg235Gly) mutation. Analysis of skeletal muscle revealed a marked decrease of AAC1 protein levels and loss of respiratory chain complexes containing mitochondria' DNA-encoded subunits. We show that both recombinant AAC1 mutant proteins are severely impaired in ADP/ATP transport, affecting most likely the substrate binding and mechanics of the carrier, respectively. This highly reduced capacity for transport probably affects mitochondria' DNA maintenance and in turn respiration, causing a severe energy crisis. The confirmation of the pathogenicity of these de novo SLC25A4 mutations highlights a third distinct clinical phenotype associated with mutation of this gene and demonstrates that early-onset mitochondria' disease can be caused by recurrent de novo mutations, which has significant implications for the application and analysis of whole-exome sequencing data in mitochondrial disease.Peer reviewe