Dataset Information

Shear shocks in fragile networks.

ABSTRACT: A minimal model for studying the mechanical properties of amorphous solids is a disordered network of point masses connected by unbreakable springs. At a critical value of its mean connectivity, such a network becomes fragile: it undergoes a rigidity transition signaled by a vanishing shear modulus and transverse sound speed. We investigate analytically and numerically the linear and nonlinear visco-elastic response of these fragile solids by probing how shear fronts propagate through them. Our approach, which we tentatively label shear front rheology, provides an alternative route to standard oscillatory rheology. In the linear regime, we observe at late times a diffusive broadening of the fronts controlled by an effective shear viscosity that diverges at the critical point. No matter how small the microscopic coefficient of dissipation, strongly disordered networks behave as if they were overdamped because energy is irreversibly leaked into diverging nonaffine fluctuations. Close to the transition, the regime of linear response becomes vanishingly small: the tiniest shear strains generate strongly nonlinear shear shock waves qualitatively different from their compressional counterparts in granular media. The inherent nonlinearities trigger an energy cascade from low to high frequency components that keep the network away from attaining the quasi-static limit. This mechanism, reminiscent of acoustic turbulence, causes a superdiffusive broadening of the shock width.

SUBMITTER: Ulrich S

PROVIDER: S-EPMC3876272 | biostudies-other | 2013 Dec

REPOSITORIES: biostudies-other

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Shear shocks in fragile networks.

Ulrich Stephan S Upadhyaya Nitin N van Opheusden Bas B Vitelli Vincenzo V

Proceedings of the National Academy of Sciences of the United States of America 20131205 52

A minimal model for studying the mechanical properties of amorphous solids is a disordered network of point masses connected by unbreakable springs. At a critical value of its mean connectivity, such a network becomes fragile: it undergoes a rigidity transition signaled by a vanishing shear modulus and transverse sound speed. We investigate analytically and numerically the linear and nonlinear visco-elastic response of these fragile solids by probing how shear fronts propagate through them. Our ...[more]

PMID: 24309379

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Project description:ImportanceFragile X syndrome (FXS) is an X-linked neurogenetic disorder characterized by a cognitive and behavioral phenotype resembling features of autism spectrum disorder. Until now, research has focused largely on identifying regional differences in brain structure and function between individuals with FXS and various control groups. Very little is known about the large-scale brain networks that may underlie the cognitive and behavioral symptoms of FXS.ObjectiveTo identify large-scale, resting-state networks in FXS that differ from control individuals matched on age, IQ, and severity of behavioral and cognitive symptoms.Design, setting, and participantsCross-sectional, in vivo neuroimaging study conducted in an academic medical center. Participants (aged 10-23 years) included 17 males and females with FXS and 16 males and females serving as controls.Main outcomes and measuresUnivariate voxel-based morphometric analyses, fractional amplitude of low-frequency fluctuations (fALFF) analysis, and group-independent component analysis with dual regression.ResultsPatients with FXS showed decreased functional connectivity in the salience, precuneus, left executive control, language, and visuospatial networks compared with controls. Decreased fALFF in the bilateral insular, precuneus, and anterior cingulate cortices also was found in patients with FXS compared with control participants. Furthermore, fALFF in the left insular cortex was significantly positively correlated with IQ in patients with FXS. Decreased gray matter density, resting-state connectivity, and fALFF converged in the left insular cortex in patients with FXS.Conclusions and relevanceFragile X syndrome results in widespread reductions in functional connectivity across multiple cognitive and affective brain networks. Converging structural and functional abnormalities in the left insular cortex, a region also implicated in individuals diagnosed with autism spectrum disorder, suggests that insula integrity and connectivity may be compromised in FXS. This method could prove useful in establishing an imaging biomarker for FXS.

Project description:BackgroundLoss or disrupted expression of the FMR1 gene causes fragile X syndrome (FXS), the most common monogenetic form of autism in humans. Although disruptions in sensory processing are core traits of FXS and autism, the neural underpinnings of these phenotypes are poorly understood. Using calcium imaging to record from the entire brain at cellular resolution, we investigated neuronal responses to visual and auditory stimuli in larval zebrafish, using fmr1 mutants to model FXS. The purpose of this study was to model the alterations of sensory networks, brain-wide and at cellular resolution, that underlie the sensory aspects of FXS and autism.ResultsCombining functional analyses with the neurons' anatomical positions, we found that fmr1-/- animals have normal responses to visual motion. However, there were several alterations in the auditory processing of fmr1-/- animals. Auditory responses were more plentiful in hindbrain structures and in the thalamus. The thalamus, torus semicircularis, and tegmentum had clusters of neurons that responded more strongly to auditory stimuli in fmr1-/- animals. Functional connectivity networks showed more inter-regional connectivity at lower sound intensities (a - 3 to - 6 dB shift) in fmr1-/- larvae compared to wild type. Finally, the decoding capacities of specific components of the ascending auditory pathway were altered: the octavolateralis nucleus within the hindbrain had significantly stronger decoding of auditory amplitude while the telencephalon had weaker decoding in fmr1-/- mutants.ConclusionsWe demonstrated that fmr1-/- larvae are hypersensitive to sound, with a 3-6 dB shift in sensitivity, and identified four sub-cortical brain regions with more plentiful responses and/or greater response strengths to auditory stimuli. We also constructed an experimentally supported model of how auditory information may be processed brain-wide in fmr1-/- larvae. Our model suggests that the early ascending auditory pathway transmits more auditory information, with less filtering and modulation, in this model of FXS.

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Shear shocks in fragile networks.

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Shear shocks in fragile networks.

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