On the Coding of Negative Quantities in Cortical Circuits

Mullers Law of specific nerve energies introduced the idea that nerves transmit information about specific sensory features. This concept has been refined by the notion of 'labeled lines,' specific cells that capture sub-features of a sensory or motor stimulus, such as Hubel and Weisel's opponent color cells. Such features can be visualized as coding a signed quantity that has positive and negative components that are encoded with separate nerve cells. We show that there are two important consequences when learning receptive field using signed codings in circuits. The first is that in feedback circuits even simple operations need to be distributed across multiple distinct pathways. The second consequence is that such pathways are necessarily dynamic. Synaptic weights change during learning and must break and grow new circuit connections because the weights need to change sign during receptive field formation

Dual Roles for Spike Signaling in Cortical Neural Populations

A prominent feature of signaling in cortical neurons is that of randomness in the action potential. The output of a typical pyramidal cell can be well fit with a Poisson model, and variations in the Poisson rate repeatedly have been shown to be correlated with stimuli. However while the rate provides a very useful characterization of neural spike data, it may not be the most fundamental description of the signaling code. Recent data showing γ frequency range multi-cell action potential correlations, together with spike timing dependent plasticity, are spurring a re-examination of the classical model, since precise timing codes imply that the generation of spikes is essentially deterministic. Could the observed Poisson randomness and timing determinism reflect two separate modes of communication, or do they somehow derive from a single process? We investigate in a timing-based model whether the apparent incompatibility between these probabilistic and deterministic observations may be resolved by examining how spikes could be used in the underlying neural circuits. The crucial component of this model draws on dual roles for spike signaling. In learning receptive fields from ensembles of inputs, spikes need to behave probabilistically, whereas for fast signaling of individual stimuli, the spikes need to behave deterministically. Our simulations show that this combination is possible if deterministic signals using γ latency coding are probabilistically routed through different members of a cortical cell population at different times. This model exhibits standard features characteristic of Poisson models such as orientation tuning and exponential interval histograms. In addition, it makes testable predictions that follow from the γ latency coding

De plaats van de grote zaal in het Oost-Indisch Huis te Amsterdam: Wat zegt het gebouw nu zelf?

In last year\u27s Bulletin there was a discussion on the place of the \u27large hall\u27 in the East-India House in Amsterdam drawn by Simon Fokke in 1771. On the basis of building-historical research carried out during the restoration in 1978, this hall must have been situated on the ground floor. It concerns the eastern room between the staircase and the former arsenal on the side of the courtyard. This room was two beam sections wide with two windows giving on to the courtyard. The large corbels, clearly depicted by Fokke, and the fireplace against the arsenal can only be situated there. In order to make the room look as large as possible, the draughtsman stood in the central space near the staircase, as it were. This way of drawing can also be demonstrated elsewhere. The only question remaining now is: was Simon Fokke\u27s company in the \u27hall\u27 in question, which was the subject of the earlier discussion, or did he draw a room in this building after all? A kind of reception room may be thought of. However, this does not alter the fact that the back room on the ground floor occupied the most important place in the building then, because of its greater height

De plaats van de grote zaal in het Oost-Indisch Huis te Amsterdam: Wat zegt het gebouw nu zelf?

In last year's Bulletin there was a discussion on the place of the 'large hall' in the East-India House in Amsterdam drawn by Simon Fokke in 1771. On the basis of building-historical research carried out during the restoration in 1978, this hall must have been situated on the ground floor. It concerns the eastern room between the staircase and the former arsenal on the side of the courtyard. This room was two beam sections wide with two windows giving on to the courtyard. The large corbels, clearly depicted by Fokke, and the fireplace against the arsenal can only be situated there. In order to make the room look as large as possible, the draughtsman stood in the central space near the staircase, as it were. This way of drawing can also be demonstrated elsewhere. The only question remaining now is: was Simon Fokke's company in the 'hall' in question, which was the subject of the earlier discussion, or did he draw a room in this building after all? A kind of reception room may be thought of. However, this does not alter the fact that the back room on the ground floor occupied the most important place in the building then, because of its greater height

The scalable mammalian brain: emergent distributions of glia and neurons

In this paper, we demonstrate that two characteristic properties of mammalian brains emerge when scaling-up modular, cortical structures. Firstly, the glia-to-neuron ratio is not constant across brains of different sizes: large mammalian brains have more glia per neuron than smaller brains. Our analyses suggest that if one assumes that glia number is proportional to wiring, a particular quantitative relationship emerges between brain size and glia-to-neuron ratio that fits the empirical data. Secondly, many authors have reported that the number of neurons underlying one mm2 of mammalian cortex is remarkably constant, across both areas and species. Here, we will show that such a constancy emerges when enlarging modular, cortical brain structures. Our analyses thus corroborate recent studies on the mammalian brain as a scalable architecture, providing a possible mechanism to explain some of the principles, constancies and rules that hold across brains of different size

Functionality-Driven Musculature Retargeting

We present a novel retargeting algorithm that transfers the musculature of a reference anatomical model to new bodies with different sizes, body proportions, muscle capability, and joint range of motion while preserving the functionality of the original musculature as closely as possible. The geometric configuration and physiological parameters of musculotendon units are estimated and optimized to adapt to new bodies. The range of motion around joints is estimated from a motion capture dataset and edited further for individual models. The retargeted model is simulation-ready, so we can physically simulate muscle-actuated motor skills with the model. Our system is capable of generating a wide variety of anatomical bodies that can be simulated to walk, run, jump and dance while maintaining balance under gravity. We will also demonstrate the construction of individualized musculoskeletal models from bi-planar X-ray images and medical examinations.Comment: 15 pages, 20 figure

Infection of Enteromyxum leei in cultured starry flounder Platichthys stellatus

Enteromyxum leei has been identified as the causative agent of emaciation disease in a wide range of marine fish hosts. In this study, we aimed to determine the effect of the parasitic infection of Enteromyxum species on starry flounder that were cultured in aquaculture farms of Jeju island in Korea. As the mortality of cultured olive flounder Paralichthys olivaceus because of E. leei infection increased, some fish farms on Jeju island attempted to culture the starry flounder Platichthys stellatus, as an alternative. Myxosporeans with a developmental stage similar to E. leei were found in the intestines of cultured starry flounders. The partial 18S rDNA of myxosporeans showed 100% similarity with E. leei. To reveal the effect of E. leei infection on starry flounder, the intensity of E. leei infection measured using quantitative polymerase chain reaction, and the condition factor (CF) of fish were measured and analyzed statistically. The results showed that high-intensity E. leei infection significantly decreased the CF of the starry flounder. However, the pathogenicity of E. leei to starry flounder is low, considering its mortality and clinical signs

Viperin mutation is linked to immunity, immune cell dynamics, and metabolic alteration during VHSV infection in zebrafish

Viperin is a prominent antiviral protein found in animals. The primary function of Viperin is the production of 3’-deoxy-3’,4’-didehydro-cytidine triphosphate (ddhCTP), an inhibitory nucleotide involved in viral RNA synthesis. Studies in mammalian models have suggested that ddhCTP interferes with metabolic proteins. However, this hypothesis has yet to be tested in teleost. In this study, the role of Viperin in regulating metabolic alterations during viral hemorrhagic septicemia virus (VHSV) infection was tested. When infected with VHSV, viperin-/- fish showed considerably higher mortality rates. VHSV copy number and the expression of the NP gene were significantly increased in viperin-/- fish. Metabolic gene analysis revealed significant differences in soda, hif1a, fasn, and acc expression, indicating their impact on metabolism. Cholesterol analysis in zebrafish larvae during VHSV infection showed significant upregulation of cholesterol production without Viperin. In vitro analysis of ZF4 cells suggested a considerable reduction in lipid production and a significant upregulation of reactive oxygen species (ROS) generation with the overexpression of viperin. Neutrophil and macrophage recruitment were significantly modulated in viperin-/- fish compared to the wild-type (WT) fish. Thus, we have demonstrated that Viperin plays a role in interfering with metabolic alterations during VHSV infection

Using a combination of MLPA kits to detect chromosomal imbalances in patients with multiple congenital anomalies and mental retardation is a valuable choice for developing countries

Conventional karyotyping detects anomalies in 3-15% of patients with multiple congenital anomalies and mental retardation (MCA/MR). Whole-genome array screening (WGAS) has been consistently suggested as the first choice diagnostic test for this group of patients, but it is very costly for large-scale use in developing countries. We evaluated the use of a combination of Multiplex Ligation-dependent Probe Amplification (MLPA) kits to increase the detection rate of chromosomal abnormalities in MCA/MR patients. We screened 261 MCA/MR patients with two subtelomeric and one microdeletion kits. This would theoretically detect up to 70% of all submicroscopic abnormalities. Additionally we scored the de Vries score for 209 patients in an effort to find a suitable cut-off for MLPA screening. Our results reveal that chromosomal abnormalities were present in 87 (33.3%) patients, but only 57 (21.8%) were considered causative. Karyotyping detected 15 abnormalities (6.9%), while MLPA identified 54 (20.7%). Our combined MLPA screening raised the total detection number of pathogenic imbalances more than three times when compared to conventional karyotyping. We also show that using the de Vries score as a cutoff for this screening would only be suitable under financial restrictions. A decision analytic model was constructed with three possible strategies: karyotype, karyotype + MLPA and karyotype + WGAS. Karyotype + MLPA strategy detected anomalies in 19.8% of cases which account for 76.45% of the expected yield for karyotype + WGAS. Incremental Cost Effectiveness Ratio (ICER) of MLPA is three times lower than that of WGAS, which means that, for the same costs, we have three additional diagnoses with MLPA but only one with WGAS. We list all causative alterations found, including rare findings, such as reciprocal duplications of regions deleted in Sotos and Williams-Beuren syndromes. We also describe imbalances that were considered polymorphisms or rare variants, such as the new SNP that confounded the analysis of the 22q13.3 deletion syndrome. (C) 2011 Elsevier Masson SAS. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)CEPID (Centro de Pesquisa, Inovacao e Difusao)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Inst Biociencias, Dept Genet & Biol Evolut, Ctr Estudos Genoma Humano, BR-05508900 São Paulo, BrazilUniv São Paulo, Fac Med, Dept Oncol, BR-05508 São Paulo, BrazilUniv Fed Campina Grande, Campina Grande, PB, BrazilUniversidade Federal de São Paulo, Dept Ginecol, Lab Ginecol Mol, São Paulo, BrazilAssoc Beneficente Coleta Sangue, São Paulo, BrazilUniv São Paulo, Fac Med, Inst Crianca, BR-05508 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Ginecol, Lab Ginecol Mol, São Paulo, BrazilWeb of Scienc