GPGPU computation and visualization of three-dimensional cellular automata

This paper presents a general-purpose simulation approach integrating a set of technological developments and algorithmic methods in cellular automata (CA) domain. The approach provides a general-purpose computing on graphics processor units (GPGPU) implementation for computing and multiple rendering of any direct-neighbor three-dimensional (3D) CA. The major contributions of this paper are: the CA processing and the visualization of large 3D matrices computed in real time; the proposal of an original method to encode and transmit large CA functions to the graphics processor units in real time; and clarification of the notion of top-down and bottom-up approaches to CA that non-CA experts often confuse. Additionally a practical technique to simplify the finding of CA functions is implemented using a 3D symmetric configuration on an interactive user interface with simultaneous inside and surface visualizations. The interactive user interface allows for testing the system with different project ideas and serves as a test bed for performance evaluation. To illustrate the flexibility of the proposed method, visual outputs from diverse areas are demonstrated. Computational performance data are also provided to demonstrate the method’s efficiency. Results indicate that when large matrices are processed, computations using GPU are two to three hundred times faster than the identical algorithms using CPU

Glycolysis Upregulation Is Neuroprotective As A Compensatory Mechanism In Als

Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodegenerative disorder, with TDP-43 inclusions as a major pathological hallmark. Using a Drosophila model of TDP-43 proteinopathy we found significant alterations in glucose metabolism including increased pyruvate, suggesting that modulating glycolysis may be neuroprotective. Indeed, a high sugar diet improves locomotor and lifespan defects caused by TDP-43 proteinopathy in motor neurons or glia, but not muscle, suggesting that metabolic dysregulation occurs in the nervous system. Overexpressing human glucose transporter GLUT-3 in motor neurons mitigates TDP-43 dependent defects in synaptic vesicle recycling and improves locomotion. Furthermore, PFK mRNA, a key indicator of glycolysis, is upregulated in flies and patient derived iPSC motor neurons with TDP-43 pathology. Surprisingly, PFK overexpression rescues TDP-43 induced locomotor deficits. These findings from multiple ALS models show that mechanistically, glycolysis is upregulated in degenerating motor neurons as a compensatory mechanism and suggest that increased glucose availability is protective

PPLook: an automated data mining tool for protein-protein interaction

<p>Abstract</p> <p>Background</p> <p>Extracting and visualizing of protein-protein interaction (PPI) from text literatures are a meaningful topic in protein science. It assists the identification of interactions among proteins. There is a lack of tools to extract PPI, visualize and classify the results.</p> <p>Results</p> <p>We developed a PPI search system, termed PPLook, which automatically extracts and visualizes protein-protein interaction (PPI) from text. Given a query protein name, PPLook can search a dataset for other proteins interacting with it by using a keywords dictionary pattern-matching algorithm, and display the topological parameters, such as the number of nodes, edges, and connected components. The visualization component of PPLook enables us to view the interaction relationship among the proteins in a three-dimensional space based on the OpenGL graphics interface technology. PPLook can also provide the functions of selecting protein semantic class, counting the number of semantic class proteins which interact with query protein, counting the literature number of articles appearing the interaction relationship about the query protein. Moreover, PPLook provides heterogeneous search and a user-friendly graphical interface.</p> <p>Conclusions</p> <p>PPLook is an effective tool for biologists and biosystem developers who need to access PPI information from the literature. PPLook is freely available for non-commercial users at <url>http://meta.usc.edu/softs/PPLook</url>.</p

Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS

Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodegenerative disorder, with TDP-43 inclusions as a major pathological hallmark. Using a Drosophila model of TDP-43 proteinopathy we found significant alterations in glucose metabolism including increased pyruvate, suggesting that modulating glycolysis may be neuroprotective. Indeed, a high sugar diet improves locomotor and lifespan defects caused by TDP-43 proteinopathy in motor neurons or glia, but not muscle, suggesting that metabolic dysregulation occurs in the nervous system. Overexpressing human glucose transporter GLUT-3 in motor neurons mitigates TDP-43 dependent defects in synaptic vesicle recycling and improves locomotion. Furthermore, PFK mRNA, a key indicator of glycolysis, is upregulated in flies and patient derived iPSC motor neurons with TDP-43 pathology. Surprisingly, PFK overexpression rescues TDP-43 induced locomotor deficits. These findings from multiple ALS models show that mechanistically, glycolysis is upregulated in degenerating motor neurons as a compensatory mechanism and suggest that increased glucose availability is protective.National Institutes of Health [T32GM008659, NS091299]; Howard Hughes Medical Institute; University of Arizona; Arnold and Mabel Beckman Foundation; Association pour la Recherche sur la Sclerose Laterale Amyotrophique et autres Maladies du Motoneurone; Target ALS; Barrow Neurological Foundation; Muscular Dystrophy Association [418515]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]