Browse
Submit Data
Databases
API
Help

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tempo rubato?: animacy speeds up time in the brain.

ABSTRACT: BACKGROUND: How do we estimate time when watching an action? The idea that events are timed by a centralized clock has recently been called into question in favour of distributed, specialized mechanisms. Here we provide evidence for a critical specialization: animate and inanimate events are separately timed by humans. METHODOLOGY/PRINCIPAL FINDINGS: In different experiments, observers were asked to intercept a moving target or to discriminate the duration of a stationary flash while viewing different scenes. Time estimates were systematically shorter in the sessions involving human characters moving in the scene than in those involving inanimate moving characters. Remarkably, the animate/inanimate context also affected randomly intermingled trials which always depicted the same still character. CONCLUSIONS/SIGNIFICANCE: The existence of distinct time bases for animate and inanimate events might be related to the partial segregation of the neural networks processing these two categories of objects, and could enhance our ability to predict critically timed actions.

SUBMITTER: Carrozzo M

PROVIDER: S-EPMC3012081 | biostudies-literature | 2010

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Tempo rubato : animacy speeds up time in the brain.

Carrozzo Mauro M Moscatelli Alessandro A Lacquaniti Francesco F

PloS one 20101229 12

<h4>Background</h4>How do we estimate time when watching an action? The idea that events are timed by a centralized clock has recently been called into question in favour of distributed, specialized mechanisms. Here we provide evidence for a critical specialization: animate and inanimate events are separately timed by humans.<h4>Methodology/principal findings</h4>In different experiments, observers were asked to intercept a moving target or to discriminate the duration of a stationary flash whil ...[more]

PMID: 21206749

Similar Datasets

Nocturnal foraging lifts time constraints in winter for migratory geese but hardly speeds up fueling.

Project description:Climate warming advances the optimal timing of breeding for many animals. For migrants to start breeding earlier, a concurrent advancement of migration is required, including premigratory fueling of energy reserves. We investigate whether barnacle geese are time constrained during premigratory fueling and whether there is potential to advance or shorten the fueling period to allow an earlier migratory departure. We equipped barnacle geese with GPS trackers and accelerometers to remotely record birds' behavior, from which we calculated time budgets. We examined how time spent foraging was affected by the available time (during daylight and moonlit nights) and thermoregulation costs. We used an energetic model to assess onset and rates of fueling and whether geese can further advance fueling by extending foraging time. We show that, during winter, when facing higher thermoregulation costs, geese consistently foraged at night, especially during moonlit nights, in order to balance their energy budgets. In spring, birds made use of the increasing day length and gained body stores by foraging longer during the day, but birds stopped foraging extensively during the night. Our model indicates that, by continuing nighttime foraging throughout spring, geese may have some leeway to advance and increase fueling rate, potentially reaching departure body mass 4 days earlier. In light of rapid climatic changes on the breeding grounds, whether this advancement can be realized and whether it will be sufficient to prevent phenological mismatches remains to be determined.

| S-EPMC8177807 | biostudies-literature

Motor Adaptive Remodeling Speeds Up Bacterial Chemotactic Adaptation.

Project description:Bacterial chemotaxis is a canonical system for the study of signal transduction. One of the hallmarks of this system is its robust adaptive behavior. However, how fast the system adapts remains controversial. The adaptation time measured at the level of the kinase activity was tens of seconds, whereas that measured at the level of the flagellar motor was <10 s. The flagellar motor was recently shown to exhibit adaptive remodeling, its main physiological function being to provide a robust match between the chemoreceptor output and the motor input, whereas its adaptation timescale was thought to be too slow to contribute much to the overall adaptation timescale of the chemotaxis system. Here, through theoretical modeling of the motor adaptive remodeling and experimental tests, we show that this motor adaptation contributes significantly to speeding up the overall chemotactic adaptation, thereby resolving the previous inconsistency.

| S-EPMC5883565 | biostudies-literature

Filling up the heme pocket stabilizes apomyoglobin and speeds up its folding.

Project description:Wild type apomyoglobin folds in at least two steps: the ABGH core rapidly, followed much later by the heme-binding CDEF core. We hypothesize that the evolved heme-binding function of the CDEF core frustrates its folding: it has a smaller contact order and is no more complex topologically than ABGH, and thus, it should be able to fold faster. Therefore, filling up the empty heme cavity of apomyoglobin with larger, hydrophobic side chains should significantly stabilize the protein and increase its folding rate. Molecular dynamics simulations allowed us to design four different mutants with bulkier side chains that increase the native bias of the CDEF region. In vitro thermal denaturation shows that the mutations increase folding stability and bring the protein closer to two-state behavior, as judged by the difference of fluorescence- and circular dichroism-detected protein stability. Millisecond stopped flow measurements of the mutants exhibit refolding kinetics that are over 4 times faster than the wild type's. We propose that myoglobin-like proteins not evolved to bind heme are equally stable, and find an example. Our results illustrate how evolution for function can force proteins to adapt frustrated folding mechanisms, despite having simple topologies.

| S-EPMC4065233 | biostudies-literature

Computational surprisal analysis speeds-up genomic characterization of cancer processes.

Project description:Surprisal analysis is increasingly being applied for the examination of transcription levels in cellular processes, towards revealing inner network structures and predicting response. But to achieve its full potential, surprisal analysis should be integrated into a wider range computational tool. The purposes of this paper are to combine surprisal analysis with other important computation procedures, such as easy manipulation of the analysis results--e.g. to choose desirable result sub-sets for further inspection--, retrieval and comparison with relevant datasets from public databases, and flexible graphical displays for heuristic thinking. The whole set of computation procedures integrated into a single practical tool is what we call Computational Surprisal Analysis. This combined kind of analysis should facilitate significantly quantitative understanding of different cellular processes for researchers, including applications in proteomics and metabolomics. Beyond that, our vision is that Computational Surprisal Analysis has the potential to reach the status of a routine method of analysis for practitioners. The resolving power of Computational Surprisal Analysis is here demonstrated by its application to a variety of cellular cancer process transcription datasets, ours and from the literature. The results provide a compact biological picture of the thermodynamic significance of the leading gene expression phenotypes in every stage of the disease. For each transcript we characterize both its inherent steady state weight, its correlation with the other transcripts and its variation due to the disease. We present a dedicated website to facilitate the analysis for researchers and practitioners.

| S-EPMC4236016 | biostudies-literature

Antagonistic autoregulation speeds up a homogeneous response in Escherichia coli.

Project description:By integrating positive and negative feedback loops, biological systems establish intricate gene expression patterns linked to multistability, pulsing, and oscillations. This depends on the specific characteristics of each interlinked feedback, and thus one would expect additional expression programs to be found. Here, we investigate one such program associated with an antagonistic positive and negative transcriptional autoregulatory motif derived from the multiple antibiotic resistance (mar) system of Escherichia coli. We studied the dynamics of the system by combining a predictive mathematical model with high-resolution experimental measures of the response both at the population and single-cell level. We show that in this motif the weak positive autoregulation does not slow down but rather enhances response speedup in combination with a strong negative feedback loop. This balance of feedback strengths anticipates a homogeneous population phenotype, which we corroborate experimentally. Theoretical analysis also emphasized the specific molecular properties that determine the dynamics of the mar phenotype. More broadly, response acceleration could provide a rationale for the presence of weak positive feedbacks in other biological scenarios exhibiting these interlinked regulatory architectures.

| S-EPMC5086920 | biostudies-literature

Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement.

Project description:Actin and myosin inhibitors often blocked anaphase movements in insect spermatocytes in previous experiments. Here we treat cells with an enhancer of myosin, Calyculin A, which inhibits myosin-light-chain phosphatase from dephosphorylating myosin; myosin thus is hyperactivated. Calyculin A causes anaphase crane-fly spermatocyte chromosomes to accelerate poleward; after they reach the poles they often move back toward the equator. When added during metaphase, chromosomes at anaphase move faster than normal. Calyculin A causes prometaphase chromosomes to move rapidly up and back along the spindle axis, and to rotate. Immunofluorescence staining with an antibody against phosphorylated myosin regulatory light chain (p-squash) indicated increased phosphorylation of cleavage furrow myosin compared to control cells, indicating that calyculin A indeed increased myosin phosphorylation. To test whether the Calyculin A effects are due to myosin phosphatase or to type 2 phosphatases, we treated cells with okadaic acid, which inhibits protein phosphatase 2A at concentrations similar to Calyculin A but requires much higher concentrations to inhibit myosin phosphatase. Okadaic acid had no effect on chromosome movement. Backward movements did not require myosin or actin since they were not affected by 2,3-butanedione monoxime or LatruculinB. Calyculin A affects the distribution and organization of spindle microtubules, spindle actin, cortical actin and putative spindle matrix proteins skeletor and titin, as visualized using immunofluorescence. We discuss how accelerated and backwards movements might arise.

| S-EPMC1847834 | biostudies-other

STAT3 speeds up progression of osteoarthritis through NF-κB signaling pathway.

Project description:Osteoarthritis (OA) is the most common motor system disease in the elderly, with a high incidence and a huge social and economic burden. Therefore, it is urgent to study its potential pathogenesis to improve the therapeutic effect of the disease. In this study, we constructed a number of regulator-mediated OA dysfunction modules, and carried out in-depth analysis in order to examine the disease development process. Differential expression analysis, co-expression analysis and enrichment analysis were combined to screen genes related to disease progression. Subsequently, key regulatory factors in the process of OA were identified based on the pivotal regulators that may manipulate important parts of the module subnetwork. A total of 16 OA dysfunction modules were obtained, involving the aggregation of 3,239 module genes. Then, enrichment analysis showed that module genes were significantly involved in apoptosis, inflammation-related functions and signaling pathways. Finally, we revealed a series of regulators, including 842 ncRNA (miR-132-3p, miR-130a-3p and miR-590-3p), 59 transcription factors (NFKB1, RELA and STAT3). We consider that STAT3 is the core transcription factor and promotes the development of OA through the signal of NF-κB. Overall, our results provide biologists and pharmacists with a new way of thinking to reveal the disease process of OA, and provide a wider range of candidate targets for follow-up research.

| S-EPMC6913305 | biostudies-literature

Sniffing speeds up chemical detection by controlling air-flows near sensors.

Project description:Most mammals sniff to detect odors, but little is known how the periodic inhale and exhale that make up a sniff helps to improve odor detection. In this combined experimental and theoretical study, we use fluid mechanics and machine olfaction to rationalize the benefits of sniffing at different rates. We design and build a bellows and sensor system to detect the change in current as a function of odor concentration. A fast sniff enables quick odor recognition, but too fast a sniff makes the amplitude of the signal comparable to noise. A slow sniff increases signal amplitude but delays its transmission. This trade-off may inspire the design of future devices that can actively modulate their sniffing frequency according to different odors.

| S-EPMC7902652 | biostudies-literature

Michaelis-Menten speeds up tau-leaping under a wide range of conditions.

Project description:This paper examines the benefits of Michaelis-Menten model reduction techniques in stochastic tau-leaping simulations. Results show that although the conditions for the validity of the reductions for tau-leaping remain the same as those for the stochastic simulation algorithm (SSA), the reductions result in a substantial speed-up for tau-leaping under a different range of conditions than they do for SSA. The reason of this discrepancy is that the time steps for SSA and for tau-leaping are determined by different properties of system dynamics.

| S-EPMC3087420 | biostudies-other

Modularity speeds up motor learning by overcoming mechanical bias in musculoskeletal geometry.

Project description:We can easily learn and perform a variety of movements that fundamentally require complex neuromuscular control. Many empirical findings have demonstrated that a wide range of complex muscle activation patterns could be well captured by the combination of a few functional modules, the so-called muscle synergies. Modularity represented by muscle synergies would simplify the control of a redundant neuromuscular system. However, how the reduction of neuromuscular redundancy through a modular controller contributes to sensorimotor learning remains unclear. To clarify such roles, we constructed a simple neural network model of the motor control system that included three intermediate layers representing neurons in the primary motor cortex, spinal interneurons organized into modules and motoneurons controlling upper-arm muscles. After a model learning period to generate the desired shoulder and/or elbow joint torques, we compared the adaptation to a novel rotational perturbation between modular and non-modular models. A series of simulations demonstrated that the modules reduced the effect of the bias in the distribution of muscle pulling directions, as well as in the distribution of torques associated with individual cortical neurons, which led to a more rapid adaptation to multi-directional force generation. These results suggest that modularity is crucial not only for reducing musculoskeletal redundancy but also for overcoming mechanical bias due to the musculoskeletal geometry allowing for faster adaptation to certain external environments.

| S-EPMC6228487 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data