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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 1,261 records · Page 70
All sourcesNASA NTRSDOE OSTI
DOE OSTI2021

Integrin alpha 6 as a stemness driver is a novel promising target for HPV (+) head and neck squamous cell carcinoma

Although the incidence rates of head and neck squamous cell carcinoma (HNSCC) associated with human papilloma virus (HPV) infection have recently been on the rise, the underlying mechanism of its tumorigenesis remains largely unknown. Here, we investigated whether HNSCC cells with high expression of integrin alpha 6 (ITGα6), one of the HPV receptors, have a preference during HPV infection. In addition, we examined the gain or loss of function of the ITGα6 gene in HPV + ve HNSCC cells, as well as its prognostic value in patients with HNSCC. HPV pseudovirus was found to be more infective, with HNSCC cells featuring an overexpressed ITGα6 gene compared to the control cells. Overexpression and suppression of ITGα6 respectively increases and decreases stemness phenotypes of HPV + ve HNSCC cells. Furthermore, ITGα6 can regulate stemness by partially mediating AKT pathway in HPV + ve HNSCC cells. Finally, patients with HPV + ve HNSCC had a poor prognosis in cases of elevated ITGα6 expression; however, the expression levels of ITGα6 did not influence the survival rates of HPV-negative HNSCC patients. In conclusion, ITGα6 can serve as a potential therapeutic target for HPV + ve HNSCC cancer-like stem cells (CSCs).

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

EP300/CBP is crucial for cAMP-PKA pathway to alleviate podocyte dedifferentiation via targeting Notch3 signaling

Podocyte injury is the hallmark of proteinuric glomerular diseases. Notch3 is neo-activated simultaneously in damaged podocytes and podocyte's progenitor cells of FSGS, indicating a unique role of Notch3. We previously showed that activation of cAMP-PKA pathway alleviated podocyte injury possibly via inhibiting Notch3 expression. However, the mechanisms are unknown. In the present study, Notch3 signaling was significantly activated in ADR-induced podocytes in vitro and in PAN nephrosis rats and patients with idiopathic FSGS in vivo, concomitantly with podocyte dedifferentiation. In cultured podocytes, pCPT-cAMP, a selective cAMP-PKA activator, dramatically blocked ADR-induced activation of Notch3 signaling as well as inhibition of cAMP-PKA pathway, thus alleviating the decreased cell viability and podocyte dedifferentiation. Bioinformatics analysis revealed EP300/CBP, a transcriptional co-activator, as a central hub for the crosstalk between these two signaling pathways. Additionally, CREB/KLF15 in cAMP-PKA pathway competed with RBP-J the major transcriptional factor of Notch3 signaling for binding to EP300/CBP. EP300/CBP siRNA significantly inhibited these two signaling transduction pathways and disrupted the interactions between the above major transcriptional factors. These data indicate a crucial role of EP300/CBP in regulating the crosstalk between cAMP-PKA pathway and Notch3 signaling and modulating the phenotypic change of podocytes, and enrich the reno-protective mechanisms of cAMP-PKA pathway.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

HMGA2 contributes to vascular development and sprouting angiogenesis by promoting IGFBP2 production

Highlights: • Our findings demonstrates that HMGA2 promotes central arteries formation in zebrafish. • HMGA2 induces vascular development through modulation of IGFBP2 whatever in vivo or in vitro. • The mRNA expressions of HMGA2 and IGFBP2 increased significantly in peripheral blood of Hemangioma patients. • HMGA2-IGFBP2 are promising candidates towards therapeutical vascularization in vascular diseases like Hemangioma. Angiogenesis is the process by which new blood vessels form from preexisting vessels and regulates the processes of embryonic development, wound healing and tumorigenesis. HMGA2 is involved in the occurrence of several cancers, but its biological role and the exact downstream genes involved in vascular development and sprouting angiogenesis remain largely unknown. Here, we first found that HMGA2 knockdown in zebrafish embryos resulted in defects of central artery formation. RNA sequencing revealed that IGFBP2 was significantly downregulated by interference with HMGA2, and IGFBP2 overexpression reversed the inhibition of brain vascular development caused by HMGA2 deficiency. In vitro, we further found that HMGA2 knockdown blocked the migration, tube formation and branching of HUVECs. Similarly, IGFBP2 protein overexpression attenuated the impairments induced by HMGA2 deficiency. Moreover, the promotion of angiogenesis by HMGA2 overexpression was verified in a Matrigel plug assay. We next found that HMGA2 bound directly to a region in the IGFBP2 promoter and positively regulated IGFBP2 expression. Interestingly, the mRNA expression levels of HMGA2 and IGFBP2 were increased significantly in the peripheral blood of hemangioma patients, indicating that overexpression of HMGA2 and IGFBP2 results in vessel formation, consistent with the results of the in vivo and in vitro experiments. In summary, our findings demonstrate that HMGA2 promotes central artery formation by modulating angiogenesis via IGFBP2 induction.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

SIRT3 mediates mitofusin 2 ubiquitination and degradation to suppress ischemia reperfusion-induced acute kidney injury

Ischemia reperfusion-induced acute kidney injury (IR-induced AKI) is a life-threatening disease with many complications. Mitofusin 2 (Mfn2) ubiquitination is related to AKI. But the underlying molecular mechanisms remain unknown. This study aimed to probe the mechanism of Mfn2 ubiquitination in IR-induced AKI development. In IR-induced AKI mouse models, orbital blood and urine were collected for assessing kidney function. The kidney injury, ultrastructure of mitochondria, and histopathology in mice were evaluated after injection of G5, an ubiquitination inhibitor. Oxygen glucose deprivation/reoxygenation (OGD/R) models were established in HK-2 cells, and the mitochondria were extracted. Cell viability, apoptosis, oxidative stress, inflammatory reaction, mitochondrial membrane potential, and ATP production were measured. Mfn2 ubiquitination in mouse and cell models was evaluated. si-SIRT3 and pcDNA3.1-SIRT3 were transfected into cell models. Consequently, kidney function in mice was impaired by IR-induced AKI. Mfn2 ubiquitination and degradation promoted IR-induced AKI. OGD/R induced renal tubular epithelial cell injury and disrupted mitochondrial dynamics and functions through promoting Mfn2 ubiquitination. SIRT3 knockdown led to Mfn2 ubiquitination by binding to UBC; while its overexpression alleviated tubular epithelial cell injury. Briefly, SIRT3 mediates Mfn2 ubiquitination to relieve IR-induced AKI. This investigation may offer new insights for the treatment of IR-induced AKI injury.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Role of karyopherin nuclear transport receptors in nuclear transport by nuclear trafficking peptide

Nuclear trafficking peptide (NTP), a cell-penetrating peptide (CPP) composed of 10 amino acids (aa) (RIFIHFRIGC), has potent nuclear trafficking activity. Recently, we established a protein-based cell engineering system by using NTP, but it remained elusive how NTP functions as a CPP with nuclear orientation. In the present study, we identified importin subunit β1 (IMB1) and transportin 1 (TNPO1) as cellular proteins underlying the activity of NTP. These karyopherin nuclear transport receptors were identified as candidate molecules by liquid chromatography/mass spectrometry analysis, and downregulation of each protein by small interfering RNA significantly reduced NTP activity (P < 0.01). Biochemical analyses revealed that NTP bound directly to both molecules, and the forced expression of an IMB1 fragment (296–516 aa) or TNPO1 fragment (1–297 aa), which both contain binding sites to NTP, reduced nuclear NTP-green fluorescent protein (GFP) levels when it was added to cell culture medium. NTP is derived from viral protein R (Vpr) of human immunodeficiency virus-1, and Vpr enters the nucleus and exerts pleiotropic functions. Notably, Vpr bound directly to IMB1 and TNPO1, and its function was significantly impaired by the forced expression of the 296–516-aa fragment of IMB1 and 1–297-aa fragment of TNPO1. Interestingly, NTP completely blocked the physical association of Vpr with IMB1 and TNPO1. Although the nuclear localization mechanism of Vpr remains unknown, our data suggest that NTP functions as a novel nuclear localization signal of Vpr.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

HNRNPU promotes the progression of hepatocellular carcinoma by enhancing CDK2 transcription

Highlights: • The expression of HNRNPU is upregulated in hepatocellular carcinoma. • HNRNPU knockdown significantly inhibits HCC cell proliferation. • HNRNPU knockdown induces cell cycle arrest. • HNRNPU regulates CDK2 transcription by directly binding to the CDK2 gene locus. The nuclear matrix-associated protein Heterogeneous Nuclear Ribonucleoprotein U (HNRNPU), also known as SAF-A, is known to maintain active chromatin structure in mouse hepatocytes. However, the functional roles and molecular mechanisms of HNRNPU in the development of hepatocellular carcinoma (HCC) remain largely unknown. Herein, we found that HNRNPU was upregulated in HCC, and the proliferation of HCC cells was inhibited in vitro and in vivo upon HNRNPU knockdown. Moreover, the upregulation of HNRNPU was correlated with poor prognosis in HCC. Mechanistically, HNRNPU bound to the CDK2 gene locus, a key factor in cell cycle regulation, where it was enriched with H3K27 acetylation (H3K27ac), H3K9 acetylation (H3K9ac), and H3K4 mono-methylation (H3K4me1). Furthermore, HNRNPU knockdown reduced the levels of H3K27ac and H3K9ac at the binding site, where the levels of H3K27 tri-methylation (H3K27me3) were increased, eventually leading to the downregulation of CDK2. Collectively, our results provide a new mechanism whereby HNRNPU promotes HCC development by enhancing the transcription of CDK2.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Long noncoding RNA AK023096 interacts with hnRNP-K and contributes to the maintenance of self-renewal in bladder cancer stem-like cells

Highlights: • BCSLCs play a critical role for the high risk of recurrence and we identified that lncRNA-AK023096 was required for controls stemness of BCSLCs. • LncRNA-AK023096 recruits hnRNP-K and epigenetically upregulated SOX2 expression by modulating H3K4 trimethylation of SOX2 promoter. • Overexpression of lncRNA-AK023096 expression in the tumor tissue was significantly associated with high risk of recurrence following TUR-Bt. LncRNA contribution to self-renewal of bladder cancer stem-like cells (CSLCs) remains largely unknown. We investigated the expression profile and biological function of lncRNAs in urothelial CSLCs by microarray analysis. Among these, lncRNA-AK023096 was identified as potentially playing a role in maintaining self-renewal of CSLCs. Knockdown of this transcript inhibited spheroid formation and tumor formation. We found that AK023096 mediates recruitment of hnRNP-K to SOX2 promoter and increases H3K4 trimethylation status on SOX2 promoter, leading to a robust change in SOX2 mRNA and protein levels. Moreover, AK023096 expression in primary tumors was found to be a powerful predictor of recurrence following transurethral resection in patients with nonmuscle-invasive bladder cancer, highlighting the critical role of lncRNA in the bladder cancer regulatory network.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Incomplete radiofrequency ablation induced chemoresistance by up-regulating heat shock protein 70 in hepatocellular carcinoma

Highlights: • iRFA treatment inhibited cisplatin-induced pyroptosis of HCC cells. • Heat shock protein 70 was involved in the suppression of NLRP3 activation. • iRFA treatment decreased the cisplatin sensitivity of HCC through regulating HSP70. Radiofrequency ablation (RFA) is a common minimally invasive treatment for hepatocellular carcinoma (HCC). Incomplete RFA (iRFA) due to the sub-lethal heat shock challenge of some cell populations leads to the generation of transformed survivor cells with enhanced chemoresistance. However, the underlying mechanism of iRFA on HCCs chemoresistance remains unknown. In the present study, we investigated the effect of iRFA on HCCs sensitivity to cisplatin. Cells treated with the sub-lethal heat shock challenge were used to mimic iRFA treatment in vitro. An orthotopic implantation HCC model was established and also performed iRFA treatment. Flow cytometry, transwell assay, and cell counting kit-8 assay were used to determine the effect of iRFA treatment on cisplatin-induced HCC cell apoptosis, invasion, and cell viability. ELISA and Western blot were used to detect the effect of iRFA treatment on cisplatin-induced HCC cell pyroptosis. We found that iRFA treatment increased the HCC cell proliferation and invasion ability, and inhibited cisplatin-induced pyroptosis. Further experiments showed that iRFA treatment induced upregulation of HSP70, which inhibited the cisplatin-induced NLRP3 inflammasome activation, leading to inhibition of pyroptosis. HSP70 knockdown or NLRP3 overexpression could reverse the effect of iRFA treatment in vitro. In vivo, HSP70 knockdown reversed the chemosensitivity of HCC to cisplatin, which was decreased by iRFA. In conclusion, we demonstrated that iRFA induced drug resistance by HSP70-mediated inhibition of cell pyroptosis in HCC.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2021

Computational design and analysis of modular cells for large libraries of exchangeable product synthesis modules

Microbial metabolism can be harnessed to produce a large library of useful chemicals from renewable resources such as plant biomass. However, it is laborious and expensive to create microbial biocatalysts to produce each new product. To tackle this challenge, we have recently developed modular cell (ModCell) design principles that enable rapid generation of production strains by assembling a modular (chassis) cell with exchangeable production modules to achieve overproduction of target molecules. Previous computational ModCell design methods are limited to analyze small libraries of around 20 products. In this study, we developed a new computational method, named ModCell-HPC, that can design modular cells for large libraries with hundreds of products with a highly-parallel and multi-objective evolutionary algorithm and enable us to elucidate modular design properties. We demonstrated ModCell-HPC to design Escherichia coli modular cells towards a library of 161 endogenous production modules. From these simulations, we identified E. coli modular cells with few genetic manipulations that can produce dozens of molecules in a growth-coupled manner with different types of fermentable sugars. These designs revealed key genetic manipulations at the chassis and module levels to accomplish versatile modular cells, involving not only in the removal of major by-products but also modification of branch points in the central metabolism. We further found that the effect of various sugar degradation on redox metabolism results in lower compatibility between a modular cell and production modules for growth on pentoses than hexoses. To better characterize the degree of compatibility, we developed a method to calculate the minimal set cover, identifying that only three modular cells are all needed to couple with up 85 compatible production modules. By determining the unknown compatibility contribution metric, we further elucidated the design features that allow an existing modular cell to be re-purposed towards production of new molecules. Altogether, ModCell-HPC is a useful tool for understanding modularity of biological systems and guiding more efficient and generalizable design of modular cells that help reduce research and development cost in biocatalysis.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2022

Assessing the impact of substrate-level enzyme regulations limiting ethanol titer in Clostridium thermocellum using a core kinetic model

Clostridium thermocellum is a promising candidate for consolidated bioprocessing because it can directly ferment cellulose to ethanol. Despite significant efforts, achieved yields and titers fall below industrially relevant targets. This implies that there still exist unknown enzymatic, regulatory, and/or possibly thermodynamic bottlenecks that can throttle back metabolic flow. By (i) elucidating internal metabolic fluxes in wild-type C. thermocellum grown on cellobiose via 13 C-metabolic flux analysis ( 13 C-MFA), (ii) parameterizing a core kinetic model, and (iii) subsequently deploying an ensemble-docking workflow for discovering substrate-level regulations, this paper aims to reveal some of these factors and expand our knowledgebase governing C. thermocellum metabolism. Generated 13 C labeling data were used with 13 C-MFA to generate a wild-type flux distribution for the metabolic network. Notably, flux elucidation through MFA alluded to serine generation via the mercaptopyruvate pathway. Using the elucidated flux distributions in conjunction with batch fermentation process yield data for various mutant strains, we constructed a kinetic model of C. thermocellum core metabolism (i.e. k-ctherm138). Subsequently, we used the parameterized kinetic model to explore the effect of removing substrate-level regulations on ethanol yield and titer. Upon exploring all possible simultaneous (up to four) regulation removals we identified combinations that lead to many-fold model predicted improvement in ethanol titer. In addition, by coupling a systematic method for identifying putative competitive inhibitory mechanisms using K-FIT kinetic parameterization with the ensemble-docking workflow, we flagged 67 putative substrate-level inhibition mechanisms across central carbon metabolism supported by both kinetic formalism and docking analysis.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2025

Disruption of acyl-acyl carrier protein (acyl-ACP) synthetase in cyanobacteria impairs lipid remodeling as revealed by acyl-ACP measurements

Free fatty acid (FFA) production in bacteria is a key target for metabolic engineering. The knockout of the acyl-ACP synthetase (AAS) prevents reincorporation of FFA into the fatty acid biosynthetic cycle and is widely used to enhance their secretion. However, the role of AAS in membrane lipid remodeling under environmental stress, such as altered temperature, remains poorly understood. In cyanobacteria, temperature shifts are known to affect fatty acid desaturation and membrane fluidity, yet it is unclear whether AAS contributes to these adaptive responses through re-esterification of membrane-released acyl chains. We elucidated unique aspects of fatty acid metabolism in response to temperature changes in biotechnologically relevant microbes with the development of an efficient method for quantifying acyl-ACP intermediates using anion exchange chromatography (AEX). In Escherichia coli, which performs desaturation during fatty acid biosynthesis, we detected saturated and unsaturated acyl-ACPs that confirm biosynthetic pathway operation. In the cyanobacteria, Picosynechococcus sp. PCC 7002 and the Δaas strain, changes between two temperatures were interpreted with support from proteomic and lipidomic analyses and indicated that the AAS is tied to membrane lipid remodeling. Further, polyunsaturated acyl-ACPs were detected in the Δaas strain, which was unexpected because fatty acid synthesis does not produce polyunsaturates in cyanobacteria, suggesting the presence of alternative acyl-activating enzymes or unknown acyl-ACP desaturases. This study highlights the possible link between acyl chain recycling and lipid remodeling in cyanobacteria and demonstrates the utility of AEX-based acyl-ACP profiling in dissecting fatty acid metabolism.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2020

Novel strategies for modal-based structural material identification

Here, we present modal-based methods for model calibration in structural dynamics, and address several key challenges in the solution of gradient-based optimization problems with eigenvalues and eigenvectors, including the solution of singular Helmholtz problems encountered in sensitivity calculations, non-differentiable objective functions caused by mode swapping during optimization, and cases with repeated eigenvalues. Unlike previous literature that relied on direct solution of the eigenvector adjoint equations, we present a parallel iterative domain decomposition strategy (Adjoint Computation via Modal Superposition with Truncation Augmentation) for the solution of the singular Helmholtz problems. For problems with repeated eigenvalues we present a novel Mode Separation via Projection algorithm, and in order to address mode swapping between inverse iterations we present a novel Injective mode ordering metric. We present the implementation of these methods in a massively parallel finite element framework with the ability to use measured modal data to extract unknown structural model parameters from large complex problems. A series of increasingly complex numerical examples are presented that demonstrate the implementation and performance of the methods in a massively parallel finite element framework [7], [5], using gradient-based optimization techniques in the Rapid Optimization Library (ROL) [21].

36 MATERIALS SCIENCE↗
DOE OSTI2025

Reduced Order Modeling conditioned on monitored features for response and error bounds estimation in engineered systems

Reduced Order Models (ROMs) form essential tools across engineering domains by virtue of their function as surrogates for computationally intensive digital twinning simulators. Although purely data-driven methods are available for ROM construction, schemes that allow to retain a portion of the physics tend to enhance the interpretability and generalization of ROMs. However, physics-based techniques can adversely scale when dealing with nonlinear systems that feature parametric dependencies. This study introduces a generative physics-based ROM that is suited for nonlinear systems with parametric dependencies and is additionally able to provide numerical error bounds associated with the respective estimates. A main contribution of this work is the conditioning of these parametric ROMs to features that can be derived from monitoring measurements, feasibly in an online fashion. This is contrary to most existing ROM schemes, which remain restricted to the prescription of the physics-based, and usually a priori unknown, system parameters. Our work utilizes conditional Variational Autoencoders to continuously map the required reduction bases to a feature vector extracted from limited output measurements, while additionally allowing for a probabilistic assessment of the ROM-estimated Quantities of Interest. An auxiliary task using a neural network-based parametrization of suitable probability distributions is introduced to re-establish the link with physical model parameters. We verify the proposed scheme on a series of simulated case studies incorporating effects of geometric and material nonlinearity under parametric dependencies related to system properties and input load characteristics.

Conditional VAEs↗
DOE OSTI2026

Pareto-optimal target definition for multi-axis random vibration testing

In random vibration testing with multiple control channels, existing control laws require specification of a complete spectral density matrix at each control frequency. Spectral density matrices include autospectral densities on the diagonal and cross-spectral densities on the off-diagonal. In practice, the off-diagonal terms are often unknown, and recent vibration testing research has focused on fixing the diagonal and specifying the off-diagonal to minimize the required control energy, subject to a constraint that the target matrix is positive semidefinite. This paper shows that, even with a fixed diagonal, off-diagonal terms strongly affect control residuals. This overlooked effect occurs in both square and rectangular systems. By jointly considering input energy and control residuals, open-loop inputs are derived directly from the diagonal without specifying the off-diagonal terms. Vibration targets that can be used in closed-loop control are then derived using the optimal inputs, with positive semidefinite constraints applied during the derivation. The result is a set of Pareto-optimal control solutions. For each solution in the set, any other possible solution produces greater control error, greater input energy, or both. A balanced solution is selected automatically, though others can be chosen based on test needs. Simulations and experiments show that the proposed method outperforms state-of-the-art energy-minimizing approaches, achieving significant reductions in both control error and input energy.

Autospectral density↗
DOE OSTI2022

Flow in additively manufactured super-rough channels

Metal additive manufacturing has enabled geometrically complex internal cooling channels for turbine and heat exchanger applications, but the process gives rise to large-scale roughness whose size is comparable to the channel height (which is 500 $\mathrm {\mu }$ m). These super-rough channels pose previously unseen challenges for experimental measurements, data interpretation and roughness modelling. First, it is not clear if measurements at a particular streamwise and spanwise location still provide accurate representation of the mean (time- and plane-averaged) flow. Second, we do not know if the logarithmic layer survives. Third, it is unknown how well previously developed rough-wall models work for these large-scale roughnesses. To answer the above practical questions, we conduct direct numerical simulations of flow in additively manufactured super-rough channels. Three rough surfaces are considered, all of which are obtained from computed tomography scans of additively manufactured surfaces. The roughness’ trough to peak sizes are 0.1 $h$ , 0.3 $h$ and 0.8 $h$ , respectively, where $h$ is the intended half-channel height. Each rough surface is placed opposite a smooth wall and the other two rough surfaces, leading to six rough-wall channel configurations. Two Reynolds numbers are considered, namely $Re_\tau =180$ and $Re_\tau =395$ . We show first that measurements at one streamwise and spanwise location are insufficient due to strong mean flow inhomogeneity across the entire channel, second that the logarithmic law of the wall survives despite the mean flow inhomogeneity and third that the established roughness sheltering model remains accurate.

Altland, Samuel↗
DOE OSTI2024

Evanescent and inertial-like waves in rigidly rotating odd viscous liquids

Three-dimensional non-rotating odd viscous liquids give rise to Taylor columns and support axisymmetric inertial-like waves ( J. Fluid Mech ., vol. 973, 2023, A30). When an odd viscous liquid is subjected to rigid-body rotation however, there arise in addition a plethora of other phenomena that need to be clarified. In this paper, we show that three-dimensional incompressible or two-dimensional compressible odd viscous liquids, rotating rigidly with angular velocity 𝛺, give rise to both oscillatory and evanescent inertial-like waves or a combination thereof (which we call of mixed type) that can be non-axisymmetric. By evanescent, we mean that along the radial direction, typically when moving away from a solid boundary, the velocity field decreases exponentially. These waves precess in a prograde or retrograde manner with respect to the rotating frame. The oscillatory and evanescent waves resemble respectively the body and wall-modes observed in (non-odd) rotating Rayleigh–Bénard convection ( J. Fluid Mech ., vol. 248, 1993, pp. 583–604). We show that the three types of waves (wall, body or mixed) can be classified with respect to pairs of planar wavenumbers 𝜅 which are complex, real or a combination, respectively. Experimentally, by observing the precession rate of the patterns, it would be possible to determine the largely unknown values of the odd viscosity coefficients. This formulation recovers as special cases recent studies of equatorial or topological waves in two-dimensional odd viscous liquids which provided examples of the bulk–interface correspondence at frequencies 𝜔 < 2⁢𝛺. We finally point out that the two- and three-dimensional problems are formally equivalent. Their difference then lies in the way data propagate along characteristic rays in three dimensions, which we demonstrate by classifying the resulting Poincaré–Cartan equations.

Mechanics↗
DOE OSTI2025

Molecular fluctuations inhibit intermittency in compressible turbulence

In the standard picture of fully developed turbulence, highly intermittent hydrodynamic fields are nonlinearly coupled across scales, where local energy cascades from large scales into dissipative vortices and large density gradients. Microscopically, however, constituent fluid molecules are in constant thermal (Brownian) motion, but the role of molecular fluctuations in large-scale turbulence is largely unknown, and with rare exceptions, it has historically been considered irrelevant at scales larger than the molecular mean free path. Recent theoretical and computational investigations have shown that molecular fluctuations can impact energy cascade at Kolmogorov length scales. Here, we show that molecular fluctuations not only modify energy spectrum at wavelengths larger than the Kolmogorov length in compressible turbulence, but also significantly inhibit spatio-temporal intermittency across the entire dissipation range. Using large-scale direct numerical simulations of computational fluctuating hydrodynamics, we demonstrate that the extreme intermittency characteristic of turbulence models is replaced by nearly Gaussian statistics in the dissipation range. These results demonstrate that the compressible Navier–Stokes equations should be augmented with molecular fluctuations to accurately predict turbulence statistics across the dissipation range. Our findings have significant consequences for turbulence modelling in applications such as astrophysics, reactive flows and hypersonic aerodynamics, where dissipation-range turbulence is approximated by closure models.

compressible turbulence↗