Investment Opportunities Forecasting: Extending the Grammar of a GP-based Tool

In this paper we present a new version of a GP financial forecasting tool, called EDDIE 8. The novelty of this version is that it allows the GP to search in the space of indicators, instead of using pre-specified ones. We compare EDDIE 8 with its predecessor, EDDIE 7, and find that new and improved solutions can be found. Analysis also shows that, on average, EDDIE 8's best tree performs better than the one of EDDIE 7. The above allows us to characterize EDDIE 8 as a valuable forecasting tool

Some Spinor-Curvature Identities

We describe a class of spinor-curvature identities which exist for Riemannian or Riemann-Cartan geometries. Each identity relates an expression quadratic in the covariant derivative of a spinor field with an expression linear in the curvature plus an exact differential. Certain special cases in 3 and 4 dimensions which have been or could be used in applications to General Relativity are noted.Comment: 5 pages Plain TeX, NCU-GR-93-SSC

A Quadratic Spinor Lagrangian for General Relativity

We present a new finite action for Einstein gravity in which the Lagrangian is quadratic in the covariant derivative of a spinor field. Via a new spinor-curvature identity, it is related to the standard Einstein-Hilbert Lagrangian by a total differential term. The corresponding Hamiltonian, like the one associated with the Witten positive energy proof is fully four-covariant. It defines quasi-local energy-momentum and can be reduced to the one in our recent positive energy proof. (Fourth Prize, 1994 Gravity Research Foundation Essay.)Comment: 5 pages (Plain TeX), NCU-GR-94-QSL

Ashtekar's New Variables and Positive Energy

We discuss earlier unsuccessful attempts to formulate a positive gravitational energy proof in terms of the New Variables of Ashtekar. We also point out the difficulties of a Witten spinor type proof. We then use the special orthonormal frame gauge conditions to obtain a locally positive expression for the New Variables Hamiltonian and thereby a ``localization'' of gravitational energy as well as a positive energy proof.Comment: 12 pages Plain Te

The effects of peripheral and central high insulin on brain insulin signaling and amyloid-β in young and old APP/PS1 mice

Hyperinsulinemia is a risk factor for late-onset Alzheimer's disease (AD). In vitro experiments describe potential connections between insulin, insulin signaling, and amyloid-β (Aβ), but in vivo experiments are needed to validate these relationships under physiological conditions. First, we performed hyperinsulinemic-euglycemic clamps with concurrent hippocampal microdialysis in young, awake, behaving APP(swe)/PS1(dE9) transgenic mice. Both a postprandial and supraphysiological insulin clamp significantly increased interstitial fluid (ISF) and plasma Aβ compared with controls. We could detect no increase in brain, ISF, or CSF insulin or brain insulin signaling in response to peripheral hyperinsulinemia, despite detecting increased signaling in the muscle. Next, we delivered insulin directly into the hippocampus of young APP/PS1 mice via reverse microdialysis. Brain tissue insulin and insulin signaling was dose-dependently increased, but ISF Aβ was unchanged by central insulin administration. Finally, to determine whether peripheral and central high insulin has differential effects in the presence of significant amyloid pathology, we repeated these experiments in older APP/PS1 mice with significant amyloid plaque burden. Postprandial insulin clamps increased ISF and plasma Aβ, whereas direct delivery of insulin to the hippocampus significantly increased tissue insulin and insulin signaling, with no effect on Aβ in old mice. These results suggest that the brain is still responsive to insulin in the presence of amyloid pathology but increased insulin signaling does not acutely modulate Aβ in vivo before or after the onset of amyloid pathology. Peripheral hyperinsulinemia modestly increases ISF and plasma Aβ in young and old mice, independent of neuronal insulin signaling. SIGNIFICANCE STATEMENT The transportation of insulin from blood to brain is a saturable process relevant to understanding the link between hyperinsulinemia and AD. In vitro experiments have found direct connections between high insulin and extracellular Aβ, but these mechanisms presume that peripheral high insulin elevates brain insulin significantly. We found that physiological hyperinsulinemia in awake, behaving mice does not increase CNS insulin to an appreciable level yet modestly increases extracellular Aβ. We also found that the brain of aged APP/PS1 mice was not insulin resistant, contrary to the current state of the literature. These results further elucidate the relationship between insulin, the brain, and AD and its conflicting roles as both a risk factor and potential treatment

2021 occultations and transits of Linus orbiting (22) Kalliope: I. Polygonal and `cliptracing' algorithm

The satellite Linus orbiting the main-belt asteroid (22) Kalliope exhibited occultation and transit events in late 2021. A photometric campaign was organized and observations were taken by the TRAPPIST-South, SPECULOOS-Artemis, OWL-Net, and BOAO telescopes, with the goal to constrain models of this system. Our dynamical model is complex, with multipoles (up to the order $\ell = 2$), internal tides, and external tides. The model was constrained by astrometry (spanning 2001--2021), occultations, adaptive-optics imaging, calibrated photometry, as well as relative photometry. Our photometric model was substantially improved. A new precise (${<}\,0.1\,{\rm mmag}$) light curve algorithm was implemented, based on polygon intersections, which are computed exactly -- by including partial eclipses and partial visibility of polygons. Moreover, we implemented a `cliptracing' algorithm, based again on polygon intersections, in which partial contributions to individual pixels are computed exactly. Both synthetic light curves and synthetic images are then very smooth. Based on our combined solution, we confirmed the size of Linus, $(28\pm 1)\,{\rm km}$. However, this solution exhibits some tension between the light curves and the PISCO speckle-interferometry dataset. In most solutions, Linus is darker than Kalliope, with the albedos $A_{\rm w} = 0.40$ vs. $0.44$. This is confirmed on deconvolved images. A~detailed revision of astrometric data allowed us to revise also the $J_2 \equiv -C_{20}$ value of Kalliope. Most importantly, a~homogeneous body is excluded. For a differentiated body, two solutions exist: low-oblateness ($C_{20} \simeq -0.12$), with a~spherical iron core, and alternatively, high-oblateness ($C_{20} \simeq -0.22$) with an elongated iron core. These correspond to the low- and high-energy collisions, respectively, studied by means of SPH simulations in our previous work.Comment: Astronomy and Astrophysics, accepte

Hyperglycemia modulates extracellular amyloid-β concentrations and neuronal activity in vivo

Epidemiological studies show that patients with type 2 diabetes (T2DM) and individuals with a diabetes-independent elevation in blood glucose have an increased risk for developing dementia, specifically dementia due to Alzheimer’s disease (AD). These observations suggest that abnormal glucose metabolism likely plays a role in some aspects of AD pathogenesis, leading us to investigate the link between aberrant glucose metabolism, T2DM, and AD in murine models. Here, we combined two techniques — glucose clamps and in vivo microdialysis — as a means to dynamically modulate blood glucose levels in awake, freely moving mice while measuring real-time changes in amyloid-β (Aβ), glucose, and lactate within the hippocampal interstitial fluid (ISF). In a murine model of AD, induction of acute hyperglycemia in young animals increased ISF Aβ production and ISF lactate, which serves as a marker of neuronal activity. These effects were exacerbated in aged AD mice with marked Aβ plaque pathology. Inward rectifying, ATP-sensitive potassium (K(ATP)) channels mediated the response to elevated glucose levels, as pharmacological manipulation of K(ATP) channels in the hippocampus altered both ISF Aβ levels and neuronal activity. Taken together, these results suggest that K(ATP) channel activation mediates the response of hippocampal neurons to hyperglycemia by coupling metabolism with neuronal activity and ISF Aβ levels