Associations between Dietary Acid Load and Biomarkers of Inflammation and Hyperglycemia in Breast Cancer Survivors.

Metabolic acidosis can lead to inflammation, tissue damage, and cancer metastasis. Dietary acid load contributes to metabolic acidosis if endogenous acid-base balance is not properly regulated. Breast cancer survivors have reduced capacities to adjust their acid-base balance; yet, the associations between dietary acid load and inflammation and hyperglycemia have not been examined among them. We analyzed data collected from 3042 breast cancer survivors enrolled in the Women's Healthy Eating and Living (WHEL) Study who had provided detailed dietary intakes and measurements of plasma C-reactive protein (CRP) and hemoglobin A1c (HbA1c). Using a cross-sectional design, we found positive associations between dietary acid load and plasma CRP and HbA1c. In the multivariable-adjusted models, compared to women with the lowest quartile, the intakes of dietary acid load among women with the highest quartile showed 30-33% increases of CRP and 6-9% increases of HbA1c. Our study is the first to demonstrate positive associations between dietary acid load and CRP and HbA1c in breast cancer survivors. Our study identifies a novel dietary factor that may lead to inflammation and hyperglycemia, both of which are strong risk factors for breast cancer recurrence and comorbidities

Extreme star formation events in quasar hosts over 0.5<z<4{\bf0.5<\textit{z}<4}

We explore the relationship between active galactic nuclei and star formation in a sample of 513 optically luminous type 1 quasars up to redshifts of $\sim$4 hosting extremely high star formation rates (SFRs). The quasars are selected to be individually detected by the \textit{Herschel} SPIRE instrument at $>$3$\sigma$ at 250 $\mu$m, leading to typical SFRs of order of 1000 M$_{\odot}$yr$^{-1}$. We find the average SFRs to increase by almost a factor 10 from $z\sim0.5$ to $z\sim3$, mirroring the rise in the comoving SFR density over the same epoch. However, we find that the SFRs remain approximately constant with increasing accretion luminosity for accretion luminosities above 10$^{12}$ L$_{\odot}$. We also find that the SFRs do not correlate with black hole mass. Both of these results are most plausibly explained by the existence of a self-regulation process by the starburst at high SFRs, which controls SFRs on time-scales comparable to or shorter than the AGN or starburst duty cycles. We additionally find that SFRs do not depend on Eddington ratio at any redshift, consistent with no relation between SFR and black hole growth rate per unit black hole mass. Finally, we find that high-ionisation broad absorption line (HiBAL) quasars have indistinguishable far-infrared properties to those of classical quasars, consistent with HiBAL quasars being normal quasars observed along a particular line of sight, with the outflows in HiBAL quasars not having any measurable effect on the star formation in their hosts.Comment: 12 pages, 6 figure

Exoplanets Torqued by the Combined Tides of a Moon and Parent Star

In recent years, there has been interest in Earth-like exoplanets in the habitable zones of low mass stars ($\sim0.1-0.6\,M_\odot$). Furthermore, it has been argued that a large moon may be important for stabilizing conditions on a planet for life. If these two features are combined, then an exoplanet can feel a similar tidal influence from both its moon and parent star, leading to potentially interesting dynamics. The moon's orbital evolution depends on the exoplanet's initial spin period $P_0$. When $P_0$ is small, transfer of the exoplanet's angular momentum to the moon's orbit can cause the moon to migrate outward sufficiently to be stripped by the star. When $P_0$ is large, the moon migrates less and the star's tidal torques spin down the exoplanet. Tidal interactions then cause the moon to migrate inward until it is likely tidally disrupted by the exoplanet and potentially produces rings. While one may think that these findings preclude the presence of moons for the exoplanets of low mass stars, in fact a wide range of timescales are found for the loss or destruction of the moon; it can take $\sim10^6-10^{10}\,{\rm yrs}$ depending on the system parameters. When the moon is still present, the combined tidal torques force the exoplanet to spin asynchronously with respect to both its moon and parent star, which tidally heats the exoplanet. This can produce heat fluxes comparable to those currently coming through the Earth, arguing that combined tides may be a method for driving tectonic activity in exoplanets.Comment: 10 pages, 9 figures, updated with minor changes to match version accepted for publication in A

Beta-arrestin inhibits CAMKKbeta-dependent AMPK activation downstream of protease-activated-receptor-2

<p>Abstract</p> <p>Background</p> <p>Proteinase-activated-receptor-2 (PAR₂) is a seven transmembrane receptor that can activate two separate signaling arms: one through Gαq and Ca²⁺mobilization, and a second through recruitment of β-arrestin scaffolds. In some cases downstream targets of the Gαq/Ca²⁺signaling arm are directly inhibited by β-arrestins, while in other cases the two pathways are synergistic; thus β-arrestins act as molecular switches capable of modifying the signal generated by the receptor.</p> <p>Results</p> <p>Here we demonstrate that PAR₂can activate adenosine monophosphate-activated protein kinase (AMPK), a key regulator of cellular energy balance, through Ca²⁺-dependent Kinase Kinase β (CAMKKβ), while inhibiting AMPK through interaction with β-arrestins. The ultimate outcome of PAR₂activation depended on the cell type studied; in cultured fibroblasts with low endogenous β-arrestins, PAR₂activated AMPK; however, in primary fat and liver, PAR₂only activated AMPK in β-arrestin-2^-/-mice. β-arrestin-2 could be co-immunoprecipitated with AMPK and CAMKKβ under baseline conditions from both cultured fibroblasts and primary fat, and its association with both proteins was increased by PAR₂activation. Addition of recombinant β-arrestin-2 to in vitro kinase assays directly inhibited phosphorylation of AMPK by CAMKKβ on Thr172.</p> <p>Conclusions</p> <p>Studies have shown that decreased AMPK activity is associated with obesity and Type II Diabetes, while AMPK activity is increased with metabolically favorable conditions and cholesterol lowering drugs. These results suggest a role for β-arrestin in the inhibition of AMPK signaling, raising the possibility that β-arrestin-dependent PAR₂signaling may act as a molecular switch turning a positive signal to AMPK into an inhibitory one.</p

Assigning Creative Commons Licenses to Research Metadata: Issues and Cases

This paper discusses the problem of lack of clear licensing and transparency of usage terms and conditions for research metadata. Making research data connected, discoverable and reusable are the key enablers of the new data revolution in research. We discuss how the lack of transparency hinders discovery of research data and make it disconnected from the publication and other trusted research outcomes. In addition, we discuss the application of Creative Commons licenses for research metadata, and provide some examples of the applicability of this approach to internationally known data infrastructures.Comment: 9 pages. Submitted to the 29th International Conference on Legal Knowledge and Information Systems (JURIX 2016), Nice (France) 14-16 December 201