Reasoning mechanism for cardinal direction relations

In the classical Projection-based Model for cardinal directions [6], a two-dimensional Euclidean space relative to an arbitrary single-piece region, a, is partitioned into the following nine tiles: North-West, NW(a); North, N(a); North-East, NE(a); West, W(a); Neutral Zone, O(a);East, E(a); South-West, SW(a); South, S(a); and South-East,SE(a). In our Horizontal and Vertical Constraints Model [9], [10] these cardinal directions are decomposed into sets corresponding to horizontal and vertical constraints. Composition is computed for these sets instead of the typical individual cardinal directions. In this paper, we define several whole and part direction relations followed by showing how to compose such relations using a formula introduced in our previous paper [10]. In order to develop a more versatile reasoning system for direction relations, we shall integrate mereology, topology, cardinal directions and include their negations as well. © 2010 Springer-Verlag

Quantized spin waves in the metallic state of magnetoresistive manganites

High resolution spin waves measurements have been carried out in ferromagnetic (F) La(1-x)(Sr,Ca)xMnO3 with x(Sr)=0.15, 0.175, 0.2, 0.3 and x(Ca)=0.3. In all q-directions, close to the zone boundary, the spin wave spectra consist of several energy levels, with the same values in the metallic and the x\approx 1/8 ranges. Mainly the intensity varies, jumping from the lower energy levels determined in the x\approx 1/8 range to the higher energy ones observed in the metallic state. On the basis of a quantitative agreement found for x(Sr)=0.15 in a model of ordered 2D clusters, the spin wave anomalies of the metallic state can be interpreted in terms of quantized spin waves within the same 2D clusters, embedded in a 3D matrix.Comment: 4 pages, 5 figure

Finding genetically-supported drug targets for Parkinson’s disease using Mendelian randomization of the druggable genome

Parkinson’s disease is a neurodegenerative movement disorder that currently has no disease-modifying treatment, partly owing to inefficiencies in drug target identification and validation. We use Mendelian randomization to investigate over 3,000 genes that encode druggable proteins and predict their efficacy as drug targets for Parkinson’s disease. We use expression and protein quantitative trait loci to mimic exposure to medications, and we examine the causal effect on Parkinson’s disease risk (in two large cohorts), age at onset and progression. We propose 23 drug-targeting mechanisms for Parkinson’s disease, including four possible drug repurposing opportunities and two drugs which may increase Parkinson’s disease risk. Of these, we put forward six drug targets with the strongest Mendelian randomization evidence. There is remarkably little overlap between our drug targets to reduce Parkinson’s disease risk versus progression, suggesting different molecular mechanisms. Drugs with genetic support are considerably more likely to succeed in clinical trials, and we provide compelling genetic evidence and an analysis pipeline to prioritise Parkinson’s disease drug development

SNCA and mTOR Pathway Single Nucleotide Polymorphisms Interact to Modulate the Age at Onset of Parkinson's Disease

Neurological Motor Disorder