University of Bordeaux

About: University of Bordeaux is a education organization based out in Bordeaux, France. It is known for research contribution in the topics: Population & Laser. The organization has 28811 authors who have published 55536 publications receiving 1619635 citations. The organization is also known as: UB.

Spatial Relational Memory Requires Hippocampal Adult Neurogenesis

Abstract: The dentate gyrus of the hippocampus is one of the few regions of the mammalian brain where new neurons are generated throughout adulthood. This adult neurogenesis has been proposed as a novel mechanism that mediates spatial memory. However, data showing a causal relationship between neurogenesis and spatial memory are controversial. Here, we developed an inducible transgenic strategy allowing specific ablation of adult-born hippocampal neurons. This resulted in an impairment of spatial relational memory, which supports a capacity for flexible, inferential memory expression. In contrast, less complex forms of spatial knowledge were unaltered. These findings demonstrate that adult-born neurons are necessary for complex forms of hippocampus-mediated learning.

An adaptive sequential Monte Carlo method for approximate Bayesian computation

Abstract: Approximate Bayesian computation (ABC) is a popular approach to address inference problems where the likelihood function is intractable, or expensive to calculate To improve over Markov chain Monte Carlo (MCMC) implementations of ABC, the use of sequential Monte Carlo (SMC) methods has recently been suggested Most effective SMC algorithms that are currently available for ABC have a computational complexity that is quadratic in the number of Monte Carlo samples (Beaumont et al, Biometrika 86:983---990, 2009; Peters et al, Technical report, 2008; Toni et al, J Roy Soc Interface 6:187---202, 2009) and require the careful choice of simulation parameters In this article an adaptive SMC algorithm is proposed which admits a computational complexity that is linear in the number of samples and adaptively determines the simulation parameters We demonstrate our algorithm on a toy example and on a birth-death-mutation model arising in epidemiology

Lewy body extracts from Parkinson disease brains trigger α‐synuclein pathology and neurodegeneration in mice and monkeys

Abstract: Objective Mounting evidence suggests that α-synuclein, a major protein component of Lewy bodies (LB), may be responsible for initiating and spreading the pathological process in Parkinson disease (PD). Supporting this concept, intracerebral inoculation of synthetic recombinant α-synuclein fibrils can trigger α-synuclein pathology in mice. However, it remains uncertain whether the pathogenic effects of recombinant synthetic α-synuclein may apply to PD-linked pathological α-synuclein and occur in species closer to humans. Methods Nigral LB-enriched fractions containing pathological α-synuclein were purified from postmortem PD brains by sucrose gradient fractionation and subsequently inoculated into the substantia nigra or striatum of wild-type mice and macaque monkeys. Control animals received non-LB fractions containing soluble α-synuclein derived from the same nigral PD tissue. Results In both mice and monkeys, intranigral or intrastriatal inoculations of PD-derived LB extracts resulted in progressive nigrostriatal neurodegeneration starting at striatal dopaminergic terminals. No neurodegeneration was observed in animals receiving non-LB fractions from the same patients. In LB-injected animals, exogenous human α-synuclein was quickly internalized within host neurons and triggered the pathological conversion of endogenous α-synuclein. At the onset of LB-induced degeneration, host pathological α-synuclein diffusely accumulated within nigral neurons and anatomically interconnected regions, both anterogradely and retrogradely. LB-induced pathogenic effects required both human α-synuclein present in LB extracts and host expression of α-synuclein. Interpretation α-Synuclein species contained in PD-derived LB are pathogenic and have the capacity to initiate a PD-like pathological process, including intracellular and presynaptic accumulations of pathological α-synuclein in different brain areas and slowly progressive axon-initiated dopaminergic nigrostriatal neurodegeneration. ANN NEUROL 2014;75:351–362

Grid'5000: A Large Scale And Highly Reconfigurable Experimental Grid Testbed

Abstract: Large scale distributed systems such as Grids are difficult to study from theoretical models and simulators only. Most Grids deployed at large scale are production platforms that are inappropriate research tools because of their limited reconfiguration, control and monitoring capabilities. In this paper, we present Grid'5000, a 5000 CPU nation-wide infrastructure for research in Grid computing. Grid'5000 is designed to provide a scientific tool for computer scientists similar to the large-scale instruments used by physicists, astronomers, and biologists. We describe the motivations, design considerations, architecture, control, and monitoring infrastructure of this experimental platform. We present configuration examples and performance results for the reconfiguration subsystem.