15,745 research outputs found
Spectroscopic evidence of charge exchange X-ray emission from galaxies
What are the origins of the soft X-ray line emission from non-AGN galaxies?
XMM-Newton RGS spectra of nearby non-AGN galaxies (including starforming ones:
M82, NGC 253, M51, M83, M61, NGC 4631, M94, NGC 2903, and the Antennae
galaxies, as well as the inner bulge of M31) have been analyzed. In particular,
the K{\alpha} triplet of O VII shows that the resonance line is typically
weaker than the forbidden and/or inter-combination lines. This suggests that a
substantial fraction of the emission may not arise directly from optically thin
thermal plasma, as commonly assumed, and may instead originate at its interface
with neutral gas via charge exchange. This latter origin naturally explains the
observed spatial correlation of the emission with various tracers of cool gas
in some of the galaxies. However, alternative scenarios, such as the resonance
scattering by the plasma and the relic photo-ionization by AGNs in the recent
past, cannot be ruled out, at least in some cases, and are being examined. Such
X-ray spectroscopic studies are important to the understanding of the
relationship of the emission to various high-energy feedback processes in
galaxies.Comment: 5 pages, published in Astronomical Notes, for "Charge exchange in the
Universe" workshop, Paris 201
The Impact of IT spending and Vendor Interaction on Innovation Deployment in Hospitals
This paper examines the impact of financial investment and vendor interactions on the availability of electronic health record (EHR) systems to healthcare workers and patients, which in turn impacts technology usage and hospital performance. We used hospital‐level data from the American Hospital Association (AHA) IT Supplemental Survey, the AHA Annual Survey Database, and the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey to test the EHR systems deployment model. The results show that both financial investment and vendor interactions significantly influence the availability of the HER in hospitals. Especially, collaboration with dominant vendors can lead to the high availability of the system and better performance
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Metabolic Pathways Enhancement Confers Poor Prognosis in p53 Exon Mutant Hepatocellular Carcinoma.
RNA-Sequencing (RNA-Seq), the most commonly used sequencing application tool, is not only a method for measuring gene expression but also an excellent media to detect important structural variants such as single nucleotide variants (SNVs), insertion/deletion (Indels), or fusion transcripts. The Cancer Genome Atlas (TCGA) contains genomic data from a variety of cancer types and also provides the raw data generated by TCGA consortium. p53 is among the top 10 somatic mutations associated with hepatocellular carcinoma (HCC). The aim of the present study was to analyze concordant different gene profiles and the priori defined set of genes based on p53 mutation status in HCC using RNA-Seq data. In the study, expression profile of 11 799 genes on 42 paired tumor and adjacent normal tissues was collected, processed, and further stratified by the mutated versus normal p53 expression. Furthermore, we used a knowledge-based approach Gene Set Enrichment Analysis (GSEA) to compare between normal and p53 mutation gene expression profiles. The statistical significance (nominal P value) of the enrichment score (ES) genes was calculated. The ranked gene list that reflects differential expression between p53 wild-type and mutant genotypes was then mapped to metabolic process by KEGG, an encyclopedia of genes and genomes to assign functional meanings. These approaches enable us to identify pathways and potential target gene/pathways that are highly expressed in p53 mutated HCC. Our analysis revealed 2 genes, the hexokinase 2 (HK2) and Enolase 1 (ENO1), were conspicuous of red pixel in the heatmap. To further explore the role of these genes in HCC, the overall survival plots by Kaplan-Meier method were performed for HK2 and ENO1 that revealed high HK2 and ENO1 expression in patients with HCC have poor prognosis. These results suggested that these glycolysis genes are associated with mutated-p53 in HCC that may contribute to poor prognosis. In this proof-of-concept study, we proposed an approach for identifying novel potential therapeutic targets in human HCC with mutated p53. These approaches can take advantage of the massive next-generation sequencing (NGS) data generated worldwide and make more out of it by exploring new potential therapeutic targets
microRNA-33a-5p increases radiosensitivity by inhibiting glycolysis in melanoma.
Glycolysis was reported to have a positive correlation with radioresistance. Our previous study found that the miR-33a functioned as a tumor suppressor in malignant melanoma by targeting hypoxia-inducible factor1-alpha (HIF-1α), a gene known to promote glycolysis. However, the role of miR-33a-5p in radiosensitivity remains to be elucidated. We found that miR-33a-5p was downregulated in melanoma tissues and cells. Cell proliferation was downregulated after overexpression of miR-33a-5p in WM451 cells, accompanied by a decreased level of glycolysis. In contrast, cell proliferation was upregulated after inhibition of miR-33a-5p in WM35 cells, accompanied by increased glycolysis. Overexpression of miR-33a-5p enhanced the sensitivity of melanoma cells to X-radiation by MTT assay, while downregulation of miR-33a-5p had the opposite effects. Finally, in vivo experiments with xenografts in nude mice confirmed that high expression of miR-33a-5p in tumor cells increased radiosensitivity via inhibiting glycolysis. In conclusions, miR-33a-5p promotes radiosensitivity by negatively regulating glycolysis in melanoma
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