X-ray Fluorescence Particle Size and Scattering Angle Considerations Preparatory Experiments for the Calibration and Interpretation of C1XS Data

ISRO’s Chandrayaan-1 mission to the Moon is due to be launched in April 2008. Part of its payload is C1XS, a compact X-ray fluorescence (XRF) spectrometer which will provide high quality elemental mapping of the lunar surface [1]. In flight, the input source (solar X-ray spectrum) will be measured by the accompanying XSM payload [2]. An ‘in-house’ IDL XRF modelling code (referred to as the ‘C1XS XRF code’ [3]), which is based on the methods of [4], will be used to convert the C1XS data from X-ray fluxes into elemental ratios and abundances. This study outlines a plan of testing the accuracy and robustness of the code, using XRF spectral data from well characterised geological samples. We aim to quantify how XRF intensity varies with changing particle size and phase angle (θ in Fig. 1) geometry, in order to simulate changes in the solar aspect angle (angle between the Sun, the lunar surface and the detectors), as well as surface topography. These issues have previously been studied within a materials science context e.g. [5 – 9], but rarely but rarely for heterogeneous, geological samples [10 – 12]

Lunar chemistry from Chandrayaan-1, C1XS results from Southern nearside highlands of the Moon

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A Mercury Lander Mission Concept Study for the Next Decadal Survey

Mariner 10 provided our first closeup reconnaissance of Mercury during its three flybys in 1974 and 1975. MESSENGERs 20112015 orbital investigation enabled numerous discoveries, several of which led to substantial or complete changes in our fundamental understanding of the planet. Among these were the unanticipated, widespread presence of volatile elements (e.g., Na, K, S); a surface with extremely low Fe abundance whose darkening agent is likely C; a previously unknown landformhollows that may form by volatile sublimation from within rocks exposed to the harsh conditions on the surface; a history of expansive effusive and explosive volcanism; substantial radial contraction of the planet from interior cooling; offset of the dipole moment of the internal magnetic field northward from the geographic equator by ~20% of the planets radius; crustal magnetization, attributed at least in part to an ancient field; unexpected seasonal variability and relationships among exospheric species and processes; and the presence in permanently shadowed polar terrain of water ice and other volatile materials, likely to include complex organic compounds. Mercurys highly chemically reduced and unexpectedly volatile-rich composition is unique among the terrestrial planets and was not predicted by earlier hypotheses for the planets origin. As an end-member of terrestrial planet formation, Mercury holds unique clues about the original distribution of elements in the earliest stages of the Solar System and how planets (and exoplanets) form and evolve in close proximity to their host stars. The BepiColombo mission promises to expand our knowledge of this planet and to shed light on some of the mysteries revealed by the MESSENGER mission. However, several fundamental science questions raised by MESSENGERs pioneering exploration of Mercury can only be answered with in situ measurements from the planets surface

Heterogeneous Distribution of Chromium on Mercury

Measurements made with geochemical instruments on the MESSENGER spacecraft revealed that Mercury's crust is surprisingly rich in volatile elements, including S, Na, K, Cl, and C, and that it is enriched in Mg and depleted in Al, Ca, and Fe, relative to other terrestrial planets. Geochemical maps also indicated the presence of a number of distinct geochemical terranes. The MESSENGER X-ray Spectrometer (XRS) detected X-ray fluorescence, induced by incident solar X-rays, from the top approx. 10s of micrometers of Mercury's surface. Like Fe, Cr was only detectable by XRS during large solar flares. However, accurate Cr measurements are more susceptible to systematic errors than other elements measured by the XRS. Therefore, to date, Cr data have been published for only 11 XRS measurements, but we have recently derived a map of Cr/Si across Mercury's surface. This map is based on data acquired through the complete MESSENGER mission and reveals clear spatial heterogeneity in Cr

No FeS layer in Mercury? Evidence from Ti/Al measured by MESSENGER

In this study we investigate the likeliness of the existence of an iron sulfide layer (FeS matte) at the core-mantle boundary (CMB) of Mercury by comparing new chemical surface data obtained by the X-ray Spectrometer onboard the MESSENGER spacecraft with geochemical models supported by high-pressure experiments under reducing conditions. We present a new data set consisting of 233 Ti/Si measurements, which combined with Al/Si data show that Mercury's surface has a slightly subchondritic Ti/Al ratio of 0.035 ± 0.008. Multiphase equilibria experiments show that at the conditions of Mercury's core formation, Ti is chalcophile but not siderophile, making Ti a useful tracer of sulfide melt formation. We parameterize and use our partitioning data in a model to calculate the relative depletion of Ti in the bulk silicate fraction of Mercury as a function of a putative FeS layer thickness. By comparing the model results and surface elemental data we show that Mercury most likely does not have a FeS layer, and in case it would have one, it would only be a few kilometers thick (<13km). We also show that Mercury's metallic Fe(Si) core cannot contain more than ∼1.5 wt.% sulfur and that the formation of this core under reducing conditions is responsible for the slightly subchondritic Ti/Al ratio of Mercury's surface. © 2020 Elsevier B.V

Chromosomal polymorphism of ribosomal genes in the genus Oryza

The genes encoding for 18S–5.8S–28S ribosomal RNA (rDNA) are both conserved and diversified. We used rDNA as probe in the fluorescent in situ hybridization (rDNA-FISH) to localized rDNAs on chromosomes of 15 accessions representing ten Oryza species. These included cultivated and wild species of rice, and four of them are tetraploids. Our results reveal polymorphism in the number of rDNA loci, in the number of rDNA repeats, and in their chromosomal positions among Oryza species. The numbers of rDNA loci varies from one to eight among Oryza species. The rDNA locus located at the end of the short arm of chromosome 9 is conserved among the genus Oryza. The rDNA locus at the end of the short arm of chromosome 10 was lost in some of the accessions. In this study, we report two genome specific rDNA loci in the genus Oryza. One is specific to the BB genome, which was localized at the end of the short arm of chromosome 4. Another may be specific to the CC genome, which was localized in the proximal region of the short arm of chromosome 5. A particular rDNA locus was detected as stretched chromatin with bright signals at the proximal region of the short arm of chromosome 4 in O.grandiglumis by rDNA-FISH. We suggest that chromosomal inversion and the amplification and transposition of rDNA might occur during Oryza species evolution. The possible mechanisms of cyto-evolution in tetraploid Oryza species are discussed

A Yeast Model of FUS/TLS-Dependent Cytotoxicity

FUS/TLS is a nucleic acid binding protein that, when mutated, can cause a subset of familial amyotrophic lateral sclerosis (fALS). Although FUS/TLS is normally located predominantly in the nucleus, the pathogenic mutant forms of FUS/TLS traffic to, and form inclusions in, the cytoplasm of affected spinal motor neurons or glia. Here we report a yeast model of human FUS/TLS expression that recapitulates multiple salient features of the pathology of the disease-causing mutant proteins, including nuclear to cytoplasmic translocation, inclusion formation, and cytotoxicity. Protein domain analysis indicates that the carboxyl-terminus of FUS/TLS, where most of the ALS-associated mutations are clustered, is required but not sufficient for the toxicity of the protein. A genome-wide genetic screen using a yeast over-expression library identified five yeast DNA/RNA binding proteins, encoded by the yeast genes ECM32, NAM8, SBP1, SKO1, and VHR1, that rescue the toxicity of human FUS/TLS without changing its expression level, cytoplasmic translocation, or inclusion formation. Furthermore, hUPF1, a human homologue of ECM32, also rescues the toxicity of FUS/TLS in this model, validating the yeast model and implicating a possible insufficiency in RNA processing or the RNA quality control machinery in the mechanism of FUS/TLS mediated toxicity. Examination of the effect of FUS/TLS expression on the decay of selected mRNAs in yeast indicates that the nonsense-mediated decay pathway is probably not the major determinant of either toxicity or suppression.Fidelity Biosciences (Firm)Fidelity Biosciences (Firm) (Research Inititative)ALS Therapy AllianceNational Institutes of Health (U.S.) (NIH 1RC1NS06839)National Institutes of Health (U.S.) (NIH U01NS05225-03)National Institutes of Health (U.S.) (NIH R01NS050557-05)National Institutes of Health (U.S.) (NIH 1RC2NS070342-01)Pierre L. de Bourgknecht ALS Research FoundationNational Science Foundation (U.S.) (NS614192

Stromelysin-3 over-expression enhances tumourigenesis in MCF-7 and MDA-MB-231 breast cancer cell lines: involvement of the IGF-1 signalling pathway

BACKGROUND: Stromelysin-3 (ST-3) is over-expressed in the majority of human carcinomas including breast carcinoma. Due to its known effect in promoting tumour formation, but its impeding effect on metastasis, a dual role of ST-3 in tumour progression, depending on the cellular grade of dedifferentiation, was hypothesized. METHODS: The present study was designed to investigate the influence of ST-3 in vivo and in vitro on the oestrogen-dependent, non-invasive MCF-7 breast carcinoma cell line as well as on the oestrogen-independent, invasive MDA-MB-231 breast carcinoma cell line. Therefore an orthotopic human xenograft tumour model in nude mice, as well as a 3D matrigel cell culture system, were employed. RESULTS: Using both in vitro and in vivo techniques, we have demonstrated that over-expression of ST-3 in MCF-7 and MDA-MB-231 cells leads to both increased cell numbers and tumour volumes. This observation was dependent upon the presence of growth factors. In particular, the enhanced proliferative capacity was in MCF-7/ST-3 completely and in MDA-MB-231/ST-3 cells partially dependent on the IGF-1 signalling pathway. Microarray analysis of ST-3 over-expressing cells revealed that in addition to cell proliferation, further biological processes seemed to be affected, such as cell motility and stress response. The MAPK-pathway as well as the Wnt and PI3-kinase pathways, appear to also play a potential role. Furthermore, we have demonstrated that breast cancer cell lines of different differentiation status, as well as the non-tumourigenic cell line MCF-10A, have a comparable capability to induce endogenous ST-3 expression in fibroblasts. CONCLUSION: These data reveal that ST-3 is capable of enhancing tumourigenesis in highly differentiated "early stage" breast cancer cell lines as well as in further progressed breast cancer cell lines that have already undergone epithelial-mesenchymal transition. We propose that ST-3 induction in tumour fibroblasts leads to the stimulation of the IGF-1R pathway in carcinoma cells, thus enhancing their proliferative capacity. In addition, further different cellular processes seem to be activated by ST-3, possibly accounting for the dual role of ST-3 in tumour progression and metastasis

The Evolution of Mammalian Gene Families

Gene families are groups of homologous genes that are likely to have highly similar functions. Differences in family size due to lineage-specific gene duplication and gene loss may provide clues to the evolutionary forces that have shaped mammalian genomes. Here we analyze the gene families contained within the whole genomes of human, chimpanzee, mouse, rat, and dog. In total we find that more than half of the 9,990 families present in the mammalian common ancestor have either expanded or contracted along at least one lineage. Additionally, we find that a large number of families are completely lost from one or more mammalian genomes, and a similar number of gene families have arisen subsequent to the mammalian common ancestor. Along the lineage leading to modern humans we infer the gain of 689 genes and the loss of 86 genes since the split from chimpanzees, including changes likely driven by adaptive natural selection. Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives