Hippocampus, Amygdala and Basal Ganglia Based Navigation Control

In this paper we present a novel robot navigation system aimed at testing hypotheses about the roles of key brain areas in foraging behavior of rats. The key components of the control network are: 1. a Hippocampus inspired module for spatial localization based on associations between sensory inputs and places; 2. an Amygdala inspired module for the association of values with places and sensory stimuli; 3. a Basal Ganglia inspired module for the selection of actions based on the evaluated sensory inputs. By implementing this Hippocampus-Amygdala-Basal Ganglia based control network with a simulated rat embodiment we intend to test not only our understanding of the individual brain areas but especially the interaction between them. Understanding the neural circuits that allows rats to efficiently forage for food will also help to improve the ability of robots to autonomously evaluate and select navigation targets

The Role of Radioactivities in Astrophysics

I present both a history of radioactivity in astrophysics and an introduction to the major applications of radioactive abundances to astronomy

Search for gravitational waves from Scorpius X-1 in the second Advanced LIGO observing run with an improved hidden Markov model

We present results from a semicoherent search for continuous gravitational waves from the low-mass x-ray binary Scorpius X-1, using a hidden Markov model (HMM) to track spin wandering. This search improves on previous HMM-based searches of LIGO data by using an improved frequency domain matched filter, the J-statistic, and by analyzing data from Advanced LIGO's second observing run. In the frequency range searched, from 60 to 650 Hz, we find no evidence of gravitational radiation. At 194.6 Hz, the most sensitive search frequency, we report an upper limit on gravitational wave strain (at 95% confidence) of h095%=3.47×10-25 when marginalizing over source inclination angle. This is the most sensitive search for Scorpius X-1, to date, that is specifically designed to be robust in the presence of spin wandering. © 2019 American Physical Society

Firn cold content evolution at nine sites on the Greenland ice sheet between 1998 and 2017

Current sea-level rise partly stems from increased surface melting and meltwater runoff from the Greenland ice sheet. Multi-year snow, also known as firn, covers about 80% of the ice sheet and retains part of the surface meltwater. Since the firn cold content integrates its physical and thermal characteristics, it is a valuable tool for determining the meltwater-retention potential of firn. We use gap-filled climatological data from nine automatic weather stations in the ice-sheet accumulation area to drive a surface-energy-budget and firn model, validated against firn density and temperature observations, over the 1998-2017 period. Our results show a stable top 20 m firn cold content (CC20) at most sites. Only at the lower-elevation Dye-2 site did CC20 decrease, by 24% in 2012, before recovering to its original value by 2017. Heat conduction towards the surface is the main process feeding CC20 at all nine sites, while CC20 reduction occurs through low-cold-content fresh-snow addition at the surface during snowfall and latent-heat release when meltwater refreezes. Our simulations suggest that firn densification, while reducing pore space for meltwater retention, increases the firn cold content, enhances near-surface meltwater refreezing and potentially sets favourable conditions for ice-slab formation.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Epithelial-specific A2B adenosine receptor signaling protects the colonic epithelial barrier during acute colitis

Central to inflammatory bowel disease (IBD) pathogenesis is loss of mucosal barrier function. Emerging evidence implicates extracellular adenosine signaling in attenuating mucosal inflammation. We hypothesized that adenosinemediated protection from intestinal barrier dysfunction involves tissue-specific signaling through the A2B adenosine receptor (Adora2b) at the intestinal mucosal surface. To address this hypothesis, we combined pharmacologic studies and studies in mice with global or tissue-specific deletion of the Adora2b receptor. Adora2b / mice experienced a significantly heightened severity of colitis, associated with a more acute onset of disease and loss of intestinal epithelial barrier function. Comparison of mice with Adora2b deletion on vascular endothelial cells (Adora2bfl/flVeCadCre þ ) or intestinal epithelia (Adora2bfl/flVillinCre þ ) revealed a selective role for epithelial Adora2b signaling in attenuating colonic inflammation. In vitro studies with Adora2b knockdown in intestinal epithelial cultures or pharmacologic studies highlighted Adora2b-driven phosphorylation of vasodilator-stimulated phosphoprotein (VASP) as a specific barrier repair response. Similarly, in vivo studies in genetic mouse models or treatment studies with an Adora2b agonist (BAY 60-6583) recapitulate these findings. Taken together, our results suggest that intestinal epithelial Adora2b signaling provides protection during intestinal inflammation via enhancing mucosal barrier responses