1,098 research outputs found

    Cannibalism as a life boat mechanism

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    Under certain conditions a cannibalistic population can survive when food for the adults is too scarce to support a non-cannibalistic population. Cannibalism can have this lifeboat effect if (i) the juveniles feed on a resource inaccessible to the adults; and (ii) the adults are cannibalistic and thus incorporate indirectly the inaccessible resource. Using a simple model we conclude that the mechanism works when, at low population densities, the average yield, in terms of new offspring, due to the energy provided by one cannibalized juvenile is larger than one

    Statistical mechanics of Beltrami flows in axisymmetric geometry: Equilibria and bifurcations

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    We characterize the thermodynamical equilibrium states of axisymmetric Euler-Beltrami flows. They have the form of coherent structures presenting one or several cells. We find the relevant control parameters and derive the corresponding equations of state. We prove the coexistence of several equilibrium states for a given value of the control parameter like in 2D turbulence [Chavanis and Sommeria, J. Fluid Mech. 314, 267 (1996)]. We explore the stability of these equilibrium states and show that all states are saddle points of entropy and can, in principle, be destabilized by a perturbation with a larger wavenumber, resulting in a structure at the smallest available scale. This mechanism is therefore reminiscent of the 3D Richardson energy cascade towards smaller and smaller scales. Therefore, our system is truly intermediate between 2D turbulence (coherent structures) and 3D turbulence (energy cascade). We further explore numerically the robustness of the equilibrium states with respect to random perturbations using a relaxation algorithm in both canonical and microcanonical ensembles. We show that saddle points of entropy can be very robust and therefore play a role in the dynamics. We evidence differences in the robustness of the solutions in the canonical and microcanonical ensembles. A scenario of bifurcation between two different equilibria (with one or two cells) is proposed and discussed in connection with a recent observation of a turbulent bifurcation in a von Karman experiment [Ravelet et al., Phys. Rev. Lett. 93, 164501 (2004)].Comment: 25 pages; 16 figure

    Isolation and damping properties of magnetorheologic elastomers

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    Abstract. This paper considers two systems based on a magnetorheological elastomer (MRE): a MRE isolator under a frequency varying harmonic excitation and a MRE Dynamic Vibration Absorber (DVA) mounted on a frequency-varying structure under a random excitation. It is shown that the commandability of the elastomer improves the isolation performances in the first case, and decreases the stress level in the structure in the second case

    Early brainstem [18F]THK5351 uptake is linked to cortical hyper-excitability in healthy aging

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    BACKGROUND: Neuronal hyper-excitability characterizes the early stages of Alzheimer's disease (AD). In animals, early misfolded tau and amyloid-beta (Aβ) protein accumulation, both central to AD neuropathology, promote cortical excitability and neuronal network dysfunction. In healthy humans, misfolded tau and Aβ aggregates are first detected, respectively, in the brainstem and frontomedial and temporobasal cortices, decades prior to the onset of AD cognitive symptoms. Whether cortical excitability is related to early brainstem tau, and its associated neuroinflammation, and cortical Aβ aggregations remains unknown. METHODS: We probed frontal cortex excitability, using transcranial magnetic stimulation combined with electroencephalography, in a sample of 64 healthy late middle-aged individuals (50-69 y; 45 women). We assessed whole-brain [18F]THK5351 positron emission tomography (PET) uptake as a proxy measure of tau/neuroinflammation, and whole-brain Aβ burden with [18F]Flutemetamol or [18F]Florbetapir radiotracers. RESULTS: We find that higher [18F]THK5351 uptake in a brainstem monoaminergic compartment is associated with increased cortical excitability (r = .29, p = .02). By contrast, [18F]THK5351 PET signal in the hippocampal formation, although strongly correlated with brainstem signal in whole-brain voxel-based quantification analyses (pFWE-corrected < .001), was not significantly associated with cortical excitability (r = .14, p = .25). Importantly, no significant association was found between early Aβ cortical deposits and cortical excitability (r = -.20, p = .11). CONCLUSION: These findings reveal potential brain substrates for increased cortical excitability in preclinical AD and may constitute functional in vivo correlates of early brainstem tau accumulation and neuroinflammation in humans. TRIAL REGISTRATION: EudraCT 2016-001436-35. FUNDING: F.R.S.-FNRS Belgium, Wallonie-Bruxelles International, ULiège, Fondation Simone et Pierre Clerdent, European Regional Development Fund

    VGLL2-NCOA2 leverages developmental programs for pediatric sarcomagenesis

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    Clinical sequencing efforts are rapidly identifying sarcoma gene fusions that lack functional validation. An example is the fusion of transcriptional coactivators, VGLL2-NCOA2, found in infantile rhabdomyosarcoma. To delineate VGLL2-NCOA2 tumorigenic mechanisms and identify therapeutic vulnerabilities, we implement a cross-species comparative oncology approach with zebrafish, mouse allograft, and patient samples. We find that VGLL2-NCOA2 is sufficient to generate mesenchymal tumors that display features of immature skeletal muscle and recapitulate the human disease. A subset of VGLL2-NCOA2 zebrafish tumors transcriptionally cluster with embryonic somitogenesis and identify VGLL2-NCOA2 developmental programs, including a RAS family GTPase, ARF6. In VGLL2-NCOA2 zebrafish, mouse, and patient tumors, ARF6 is highly expressed. ARF6 knockout suppresses VGLL2-NCOA2 oncogenic activity in cell culture, and, more broadly, ARF6 is overexpressed in adult and pediatric sarcomas. Our data indicate that VGLL2-NCOA2 is an oncogene that leverages developmental programs for tumorigenesis and that reactivation or persistence of ARF6 could represent a therapeutic opportunity

    Supporting the Specification and Runtime Validation of Asynchronous Calling Patterns in Reactive Systems

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    Wireless sensor networks (“sensornets”) are highly distributed and concurrent, with program actions bound to external stimuli. They exemplify a system class known as reactive systems, which comprise execution units that have “hidden” layers of control flow. A key obstacle in enabling reactive system developers to rigorously validate their implementations has been the absence of precise software component specifications and tools to assist in leveraging those specifications at runtime. We address this obstacle in three ways: (i) We describe a specification approach tailored for reactive environments and demonstrate its application in the context of sensornets. (ii) We describe the design and implementation of extensions to the popular nesC tool-chain that enable the expression of these specifications and automate the generation of runtime monitors that signal violations, if any. (iii) Finally, we apply the specification approach to a significant collection of the most commonly used software components in the TinyOS distribution and analyze the overhead involved in monitoring their correctness

    Contrasting prefrontal cortex contributions to episodic memory dysfunction in behavioural variant frontotemporal dementia and alzheimer's disease

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    Recent evidence has questioned the integrity of episodic memory in behavioural variant frontotemporal dementia (bvFTD), where recall performance is impaired to the same extent as in Alzheimer's disease (AD). While these deficits appear to be mediated by divergent patterns of brain atrophy, there is evidence to suggest that certain prefrontal regions are implicated across both patient groups. In this study we sought to further elucidate the dorsolateral (DLPFC) and ventromedial (VMPFC) prefrontal contributions to episodic memory impairment in bvFTD and AD. Performance on episodic memory tasks and neuropsychological measures typically tapping into either DLPFC or VMPFC functions was assessed in 22 bvFTD, 32 AD patients and 35 age- and education-matched controls. Behaviourally, patient groups did not differ on measures of episodic memory recall or DLPFC-mediated executive functions. BvFTD patients were significantly more impaired on measures of VMPFC-mediated executive functions. Composite measures of the recall, DLPFC and VMPFC task scores were covaried against the T1 MRI scans of all participants to identify regions of atrophy correlating with performance on these tasks. Imaging analysis showed that impaired recall performance is associated with divergent patterns of PFC atrophy in bvFTD and AD. Whereas in bvFTD, PFC atrophy covariates for recall encompassed both DLPFC and VMPFC regions, only the DLPFC was implicated in AD. Our results suggest that episodic memory deficits in bvFTD and AD are underpinned by divergent prefrontal mechanisms. Moreover, we argue that these differences are not adequately captured by existing neuropsychological measures
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