Characteristics of Jupiter’s X‐ray auroral hot spot emissions using Chandra

To help understand and determine the driver of jovian auroral X-rays, we present the first statistical study to focus on the morphology and dynamics of the jovian northern hot spot (NHS) using Chandra data. The catalogue we explore dates from 18 December 2000 up to and including 8 September 2019. Using a numerical criterion, we characterize the typical and extreme behaviour of the concentrated NHS emissions across the catalogue. The mean power of the NHS is found to be 1.91 GW with a maximum brightness of 2.02 Rayleighs (R), representing by far the brightest parts of the jovian X-ray spectrum. We report a statistically significant region of emissions at the NHS center which is always present, the averaged hot spot nucleus (AHSNuc), with mean power of 0.57 GW and inferred average brightness of ∼ 1.2 R. We use a flux equivalence mapping model to link this distinct region of X-ray output to a likely source location and find that the majority of mappable NHS photons emanate from the pre-dusk to pre-midnight sector, coincident with the dusk flank boundary. A smaller cluster maps to the noon magnetopause boundary, dominated by the AHSNuc, suggesting that there may be multiple drivers of X-ray emissions. On application of timing analysis techniques (Rayleigh, Monte Carlo, Jackknife), we identify several instances of statistically significant quasi-periodic oscillations (QPOs) in the NHS photons ranging from ∼ 2.3-min to 36.4-min, suggesting possible links with ultra-low frequency activity on the magnetopause boundary (e.g. dayside reconnection, Kelvin-Helmholtz instabilities)

Identifying the Variety of Jovian X-Ray Auroral Structures: Tying the Morphology of X-Ray Emissions to Associated Magnetospheric Dynamics

We define the spatial clustering of X-rays within Jupiter's northern auroral regions by classifying their distributions into “X-ray auroral structures.” Using data from Chandra during Juno's main mission observations (24 May 2016 to 8 September 2019), we define five X-ray structures based on their ionospheric location and calculate the distribution of auroral photons. The morphology and ionospheric location of these structures allow us to explore the possibility of numerous X-ray auroral magnetospheric drivers. We compare these distributions to Hubble Space Telescope (HST) and Juno (Waves and MAG) data, and a 1D solar wind propagation model to infer the state of Jupiter's magnetosphere. Our results suggest that the five sub-classes of “X-ray structures” fall under two broad morphologies: fully polar and low latitude emissions. Visibility modeling of each structure suggests the non-uniformity of the photon distributions across the Chandra intervals are likely associated with the switching on/off of magnetospheric drivers as opposed to geometrical effects. The combination of ultraviolet (UV) and X-ray morphological structures is a powerful tool to elucidate the behavior of both electrons and ions and their link to solar wind/magnetospheric conditions in the absence of an upstream solar monitor. Although much work is still needed to progress the use of X-ray morphology as a diagnostic tool, we set the foundations for future studies to continue this vital research

Net1 and Myeov: computationally identified mediators of gastric cancer

Gastric adenocarcinoma (GA) is a significant cause of mortality worldwide. The molecular mechanisms of GA remain poorly characterised. Our aim was to characterise the functional activity of the computationally identified genes, NET 1 and MYEOV in GA. Digital Differential Display was used to identify genes altered expression in GA-derived EST libraries. mRNA levels of a subset of genes were quantitated by qPCR in a panel of cell lines and tumour tissue. The effect of pro- and anti-inflammatory stimuli on gene expression was investigated. Cell proliferation and invasion were measured using in an in-vitro GA model following inhibition of expression using siRNA. In all, 23 genes not previously reported in association with GA were identified. Two genes, Net1 and Myeov, were selected for further analysis and increased expression was detected in GA tissue compared to paired normal tissue using quantitative PCR. siRNA-mediated downregulation of Net1 and Myeov resulted in decreased proliferation and invasion of gastric cancer cells in vitro. These functional studies highlight a putative role for NET1 and Myeov in the development and progression of gastric cancer. These genes may provide important targets for intervention in GA, evidenced by their role in promoting invasion and proliferation, key phenotypic hallmarks of cancer cells

Comparing Jupiter's equatorial X-ray emissions with solar X-ray flux over 19 years of the Chandra mission

We present a statistical study of Jupiter’s disk X-ray emissions using 19 years of Chandra X-Ray Observatory (CXO) observations. Previous work has suggested that these emissions are consistent with solar X-rays elastically scattered from Jupiter’s upper atmosphere. We showcase a new Pulse Invariant (PI) filtering method that minimises instrumental effects which may produce unphysical trends in photon counts across the nearly-two-decade span of the observations. We compare the CXO results with solar X-ray flux data from the Geostationary Operational Environmental Satellites (GOES) X-ray Sensor (XRS) for the wavelength band 1-8 Å (long channel), to quantify the correlation between solar activity and jovian disk counts. We find a statistically significant Pearson’s Correlation Coefficient (PCC) of 0.9, which confirms that emitted jovian disk X-rays are predominantly governed by solar activity. We also utilise the high spatial resolution of the High Resolution Camera Instrument (HRC-I) on board the CXO to map the disk photons to their positions on Jupiter’s surface. Voronoi tessellation diagrams were constructed with the JRM09 (Juno Reference Model through Perijove 9) internal field model overlaid to identify any spatial preference of equatorial photons. After accounting for area and scattering across the curved surface of the planet, we find a preference of jovian disk emission at 2-3.5 Gauss surface magnetic field strength. This suggests that a portion of the disk X-rays may be linked to processes other than solar scattering: the spatial preference associated with magnetic field strength may imply increased precipitation from the radiation belts, as previously postulated

Loss of microRNA-21 influences the gut microbiota, causing reduced susceptibility in a murine model of colitis

Background and Aims microRNAs regulate gene expression and influence the pathogenesis of human diseases. The present study investigated the role of microRNA-21 [miR-21] in the pathogenesis of intestinal inflammation, because miR-21 is highly expressed in inflammatory bowel disease. Inflammatory bowel disease is associated with intestinal barrier dysfunction and an altered gut microbiota. Recent studies have demonstrated that host microRNAs can shape the microbiota. Thus, we determined the influence of miR-21 on the gut microbiota and observed the subsequent impact in a dextran sodium sulphate [DSS]-induced colitis model. Methods The influence of miR-21 on the gut microbiota and inflammation was assessed in wild-type [WT] and miR-21–/– mice, in co-housed mice, following antibiotic depletion of the microbiota, or by colonization of germ-free [GF] mice with fecal homogenate, prior to DSS administration. We carried out 16S rRNA sequencing on WT and miR-21–/– mice to dissect potential differences in the gut microbiota. Results miR-21–/– mice have reduced susceptibility to DSS-induced colitis compared with WT mice. Co-housing conferred some protection to WT mice, while GF mice colonized with fecal homogenate from miR-21–/– were protected from DSS colitis compared with those colonized with WT homogenate. Further supporting a role for the microbiota in the observed phenotype, the protection afforded by miR-21 depletion was lost when mice were pre-treated with antibiotics. The 16S rRNA sequencing revealed significant differences in the composition of WT and miR-21–/– intestinal microbiota. Conclusions These findings suggest that miR-21 influences the pathogenesis of intestinal inflammation by causing propagation of a disrupted gut microbiota

Loss of microRNA-21 influences the gut microbiota, causing reduced susceptibility in a murine model of colitis

Background and Aims microRNAs regulate gene expression and influence the pathogenesis of human diseases. The present study investigated the role of microRNA-21 [miR-21] in the pathogenesis of intestinal inflammation, because miR-21 is highly expressed in inflammatory bowel disease. Inflammatory bowel disease is associated with intestinal barrier dysfunction and an altered gut microbiota. Recent studies have demonstrated that host microRNAs can shape the microbiota. Thus, we determined the influence of miR-21 on the gut microbiota and observed the subsequent impact in a dextran sodium sulphate [DSS]-induced colitis model. Methods The influence of miR-21 on the gut microbiota and inflammation was assessed in wild-type [WT] and miR-21–/– mice, in co-housed mice, following antibiotic depletion of the microbiota, or by colonization of germ-free [GF] mice with fecal homogenate, prior to DSS administration. We carried out 16S rRNA sequencing on WT and miR-21–/– mice to dissect potential differences in the gut microbiota. Results miR-21–/– mice have reduced susceptibility to DSS-induced colitis compared with WT mice. Co-housing conferred some protection to WT mice, while GF mice colonized with fecal homogenate from miR-21–/– were protected from DSS colitis compared with those colonized with WT homogenate. Further supporting a role for the microbiota in the observed phenotype, the protection afforded by miR-21 depletion was lost when mice were pre-treated with antibiotics. The 16S rRNA sequencing revealed significant differences in the composition of WT and miR-21–/– intestinal microbiota. Conclusions These findings suggest that miR-21 influences the pathogenesis of intestinal inflammation by causing propagation of a disrupted gut microbiota