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Pattern formation by turbulent cascades.

ABSTRACT: Fully developed turbulence is a universal and scale-invariant chaotic state characterized by an energy cascade from large to small scales at which the cascade is eventually arrested by dissipation^1-6. Here we show how to harness these seemingly structureless turbulent cascades to generate patterns. Pattern formation entails a process of wavelength selection, which can usually be traced to the linear instability of a homogeneous state⁷. By contrast, the mechanism we propose here is fully nonlinear. It is triggered by the non-dissipative arrest of turbulent cascades: energy piles up at an intermediate scale, which is neither the system size nor the smallest scales at which energy is usually dissipated. Using a combination of theory and large-scale simulations, we show that the tunable wavelength of these cascade-induced patterns can be set by a non-dissipative transport coefficient called odd viscosity, ubiquitous in chiral fluids ranging from bioactive to quantum systems^8-12. Odd viscosity, which acts as a scale-dependent Coriolis-like force, leads to a two-dimensionalization of the flow at small scales, in contrast with rotating fluids in which a two-dimensionalization occurs at large scales⁴. Apart from odd viscosity fluids, we discuss how cascade-induced patterns can arise in natural systems, including atmospheric flows^13-19, stellar plasma such as the solar wind^20-22, or the pulverization and coagulation of objects or droplets in which mass rather than energy cascades^23-25.

SUBMITTER: de Wit XM

PROVIDER: S-EPMC10954557 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature

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Pattern formation by turbulent cascades.

de Wit Xander M XM Fruchart Michel M Khain Tali T Toschi Federico F Vitelli Vincenzo V

Nature 20240320 8004

Fully developed turbulence is a universal and scale-invariant chaotic state characterized by an energy cascade from large to small scales at which the cascade is eventually arrested by dissipation<sup>1-6</sup>. Here we show how to harness these seemingly structureless turbulent cascades to generate patterns. Pattern formation entails a process of wavelength selection, which can usually be traced to the linear instability of a homogeneous state<sup>7</sup>. By contrast, the mechanism we propose ...[more]

PMID: 38509279

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Project description:Vascular endothelial and hematopoietic cells hold a close relationship that is initiated during development, but that continuously broadens to include new functions aimed at maintaining homeostasis in the adult organism. Here, we report on a population of aortic intimal resident macrophages (MacAIRs) that is a permanent feature of the inner vessel wall (tunica intima) of the aorta in regions of turbulent flow and that shares the luminal surface with the endothelium. MacAIRs were found to be transcriptionally distinct from other macrophages and closely associated with the endothelium in the absence of pathology. Lineage tracing analysis indicated that adult MacAIRs were derived from definitive hematopoietic lineage precursors that migrated from the ductus arteriosus seeding the aorta immediately post-birth in areas of turbulent flow including the lesser curvature of the aortic arch and branch openings. These aortic resident macrophages expanded via direct cell renewal and continued to grow in aged aortae to also populate regions of laminar flow. Binding of MacAIRs relied heavily on expression of endothelial ICAM that interacts with CD11c on macrophages. Genetic deletion of CD11c significantly impaired anchorage of MacAIRs to the endothelium. To clarify the biological significance of this population of macrophages, we used a dual diphtheria toxin induced-depletion system that efficiently eliminated MacAIRs in adult mice. Utilizing this model, we found that absence of MacAIRs led to progressive fibrin accumulation and formation of microclots that, once dislodged, can cause blockade of vessels and organ failure. In fact, 40% of the animals with genetic-mediated depletion of MacAIRs died within 2 weeks post-depletion suggesting that these macrophages were required to clear fibrin deposits in regions of turbulent blood flow. These findings advance our knowledge of how vascular endothelial cells profit from this unique interaction with macrophages to control hemostasis, prevent intravascular clotting, and ensure vascular health.

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Pattern formation by turbulent cascades.

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Pattern formation by turbulent cascades.

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