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Groups clapping in unison undergo size-dependent error-induced frequency increase.

ABSTRACT: Humans clapping together in unison is a familiar and robust example of emergent synchrony. We find that in experiments, such groups (from two to a few hundred) always increase clapping frequency, and larger groups increase more quickly. Based on single-person experiments and modeling, an individual tendency to rush is ruled out as an explanation. Instead, an asymmetric sensitivity in aural interactions explains the frequency increase, whereby individuals correct more strongly to match neighbour claps that precede their own clap, than those that follow it. A simple conceptual coupled oscillator model based on this interaction recovers the main features observed in experiments, and shows that the collective frequency increase is driven by the small timing errors in individuals, and the resulting inter-individual interactions that occur to maintain unison.

SUBMITTER: Thomson M

PROVIDER: S-EPMC5770382 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Groups clapping in unison undergo size-dependent error-induced frequency increase.

Thomson Michael M Murphy Kennedy K Lukeman Ryan R

Scientific reports 20180116 1

Humans clapping together in unison is a familiar and robust example of emergent synchrony. We find that in experiments, such groups (from two to a few hundred) always increase clapping frequency, and larger groups increase more quickly. Based on single-person experiments and modeling, an individual tendency to rush is ruled out as an explanation. Instead, an asymmetric sensitivity in aural interactions explains the frequency increase, whereby individuals correct more strongly to match neighbour ...[more]

PMID: 29339736

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Project description:American children consume up to 27% of calories from high-fat and high-sugar snacks. Both sugar and fat consumption have been implicated as a cause of hepatic steatosis and obesity but the effect of meal pattern is largely understudied. We hypothesized that a high meal frequency, compared to consuming large meals, is detrimental in the accumulation of intrahepatic and abdominal fat. To test this hypothesis, we randomized 36 lean, healthy men to a 40% hypercaloric diet for 6 weeks or a eucaloric control diet and measured intrahepatic triglyceride content (IHTG) using proton magnetic resonance spectroscopy ((1) H-MRS), abdominal fat using magnetic resonance imaging (MRI), and insulin sensitivity using a hyperinsulinemic euglycemic clamp with a glucose isotope tracer before and after the diet intervention. The caloric surplus consisted of fat and sugar (high-fat-high-sugar; HFHS) or sugar only (high-sugar; HS) and was consumed together with, or between, the three main meals, thereby increasing meal size or meal frequency. All hypercaloric diets similarly increased body mass index (BMI). Increasing meal frequency significantly increased IHTG (HFHS mean relative increase of 45%; P?=?0.016 and HS mean relative increase of 110%; P?=?0.047), whereas increasing meal size did not (2-way analysis of variance [ANOVA] size versus frequency P?=?0.03). Abdominal fat increased in the HFHS-frequency group (+63.3?±?42.8 mL; P?=?0.004) and tended to increase in the HS-frequency group (+46.5?±?50.7 mL; P?=?0.08). Hepatic insulin sensitivity tended to decrease in the HFHS-frequency group while peripheral insulin sensitivity was not affected.A hypercaloric diet with high meal frequency increased IHTG and abdominal fat independent of caloric content and body weight gain, whereas increasing meal size did not. This study suggests that snacking, a common feature in the Western diet, independently contributes to hepatic steatosis and obesity. (www.clinicaltrials.gov; nr.NCT01297738.)

Project description:ObjectivesThe theoretical basis for minimizing tidal volume during high-frequency oscillatory ventilation may not be appropriate when lung tissue stretch occurs heterogeneously and/or rapidly. The objective of this study was to assess the extent to which increased ventilation heterogeneity may contribute to ventilator-induced lung injury during high-frequency oscillatory ventilation in adults compared with neonates on the basis of lung size, using a computational model of human lungs.DesignComputational modeling study.SettingResearch laboratory.SubjectsHigh-fidelity, 3D computational models of human lungs, scaled to various sizes representative of neonates, children, and adults, with varying injury severity. All models were generated from one thoracic CT image of a healthy adult male.InterventionsOscillatory ventilation was simulated in each lung model at frequencies ranging from 0.2 to 40 Hz. Sinusoidal flow oscillations were delivered at the airway opening of each model and distributed through the lungs according to regional parenchymal mechanics.Measurements and main resultsAcinar flow heterogeneity was assessed by the coefficient of variation in flow magnitudes across all acini in each model. High-frequency oscillatory ventilation simulations demonstrated increasing heterogeneity of regional parenchymal flow with increasing lung size, with decreasing ratio of deadspace to total acinar volume, and with increasing frequency above lung corner frequency and resonant frequency. Potential for resonant amplification was greatest in injured adult-sized lungs with higher regional quality factors indicating the presence of underdamped lung regions.ConclusionsThe potential for ventilator-induced lung injury during high-frequency oscillatory ventilation is enhanced at frequencies above lung corner frequency or resonant frequency despite reduced tidal volumes, especially in adults, due to regional amplification of heterogeneous flow. Measurements of corner frequency and resonant frequency should be considered during high-frequency oscillatory ventilation management.

Project description:BackgroundLipopolysaccharide (LPS) was shown to induce an increase in caveolin-1 (Cav-1) expression in endothelial cells; however, the mechanisms regarding this response and the consequences on caveolae-mediated transcellular transport have not been completely investigated. This study aims to investigate the role of LPS-induced Cav-1 phosphorylation in pulmonary microvascular permeability in pulmonary microvascular endothelial cells (PMVECs).MethodsRat PMVECs were isolated, cultured, and identified. Endocytosis experiments were employed to stain the nuclei by DAPI, and images were obtained with a fluorescence microscope. Permeability of endothelial cultures was measured to analyze the barrier function of endothelial monolayer. Western blot assay was used to examine the expression of Cav-1, pCav-1, triton-insoluble Cav-1, and triton-soluble Cav-1 protein.ResultsThe LPS treatment induced phosphorylation of Cav-1, but did not alter the total Cav-1 level till 60 min in both rat and human PMVECs. LPS treatment also increased the triton-insoluble Cav-1 level, which peaked 15 min after LPS treatment in both rat and human PMVECs. LPS treatment increases the intercellular cell adhesion molecule-1 expression. Src inhibitors, including PP2, PP1, Saracatinib, and Quercetin, partially inhibited LPS-induced phosphorylation of Cav-1. In addition, both PP2 and caveolae disruptor M?CD inhibited LPS-induced increase of triton-insoluble Cav-1. LPS induces permeability by activating interleukin-8 and vascular endothelial growth factor and targeting other adhesion markers, such as ZO-1 and occludin. LPS treatment also significantly increased the endocytosis of albumin, which could be blocked by PP2 or M?CD. Furthermore, LPS treatment for 15 min significantly elevated Evans Blue-labeled BSA transport in advance of a decrease in transendothelial electrical resistance of PMVEC monolayer at this time point. After LPS treatment for 30 min, transendothelial electrical resistance decreased significantly. Moreover, PP2 and M?CD blocked LPS-induced increase in Evans Blue-labeled BSA level.ConclusionOur study demonstrates that LPS-induced Cav-1 phosphorylation may lead to the increase of transcellular permeability prior to the increase of paracellular permeability in a Src-dependent manner. Thus, LPS-induced Cav-1 phosphorylation may be a therapeutic target for the treatment of inflammatory lung disease associated with elevated microvascular permeability.

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Groups clapping in unison undergo size-dependent error-induced frequency increase.

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Groups clapping in unison undergo size-dependent error-induced frequency increase.

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