A survey of machine learning wall models for large eddy simulation

This survey investigates wall modeling in large eddy simulations (LES) using data-driven machine learning (ML) techniques. To this end, we implement three ML wall models in an open-source code and compare their performances with the equilibrium wall model in LES of half-channel flow at eleven friction Reynolds numbers between $180$ and $10^{10}$. The three models have ''seen'' flows at only a few Reynolds numbers. We test if these ML wall models can extrapolate to unseen Reynolds numbers. Among the three models, two are supervised ML models, and one is a reinforcement learning ML model. The two supervised ML models are trained against direct numerical simulation (DNS) data, whereas the reinforcement learning ML model is trained in the context of a wall-modeled LES with no access to high-fidelity data. The two supervised ML models capture the law of the wall at both seen and unseen Reynolds numbers--although one model requires re-training and predicts a smaller von K\'arm\'an constant. The reinforcement learning model captures the law of the wall reasonably well but has errors at both low ($Re_\tau<10^3$) and high Reynolds numbers ($Re_\tau>10^6$). In addition to documenting the results, we try to ''understand'' why the ML models behave the way they behave. Analysis shows that the errors of the supervised ML model is a result of the network design and the errors in the reinforcement learning model arise due to the present choice of the ''states'' and the mismatch between the neutral line and the line separating the action map. In all, we see promises in data-driven machine learning models

Log-law recovery through reinforcement-learning wall model for large-eddy simulation

This paper focuses on the use of reinforcement learning (RL) as a machine-learning (ML) modeling tool for near-wall turbulence. RL has demonstrated its effectiveness in solving high-dimensional problems, especially in domains such as games. Despite its potential, RL is still not widely used for turbulence modeling and is primarily used for flow control and optimization purposes. A new RL wall model (WM) called VYBA23 is developed in this work, which uses agents dispersed in the flow near the wall. The model is trained on a single Reynolds number ($Re_\tau = 10^4$) and does not rely on high-fidelity data, as the back-propagation process is based on a reward rather than output error. The states of the RLWM, which are the representation of the environment by the agents, are normalized to remove dependence on the Reynolds number. The model is tested and compared to another RLWM (BK22) and to an equilibrium wall model, in a half-channel flow at eleven different Reynolds numbers ($Re_\tau \in [180;10^{10}]$). The effects of varying agents' parameters such as actions range, time-step, and spacing are also studied. The results are promising, showing little effect on the average flow field but some effect on wall-shear stress fluctuations and velocity fluctuations. This work offers positive prospects for developing RLWMs that can recover physical laws, and for extending this type of ML models to more complex flows in the future.Comment: arXiv admin note: text overlap with arXiv:2211.0361

Defective endoplasmic reticulum-mitochondria contacts and bioenergetics in SEPN1-related myopathy

SEPN1-related myopathy (SEPN1-RM) is a muscle disorder due to mutations of the SEPN1 gene, which is characterized by muscle weakness and fatigue leading to scoliosis and life-threatening respiratory failure. Core lesions, focal areas of mitochondria depletion in skeletal muscle fibers, are the most common histopathological lesion. SEPN1-RM underlying mechanisms and the precise role of SEPN1 in muscle remained incompletely understood, hindering the development of biomarkers and therapies for this untreatable disease. To investigate the pathophysiological pathways in SEPN1-RM, we performed metabolic studies, calcium and ATP measurements, super-resolution and electron microscopy on in vivo and in vitro models of SEPN1 deficiency as well as muscle biopsies from SEPN1-RM patients. Mouse models of SEPN1 deficiency showed marked alterations in mitochondrial physiology and energy metabolism, suggesting that SEPN1 controls mitochondrial bioenergetics. Moreover, we found that SEPN1 was enriched at the mitochondria-associated membranes (MAM), and was needed for calcium transients between ER and mitochondria, as well as for the integrity of ER-mitochondria contacts. Consistently, loss of SEPN1 in patients was associated with alterations in body composition which correlated with the severity of muscle weakness, and with impaired ER-mitochondria contacts and low ATP levels. Our results indicate a role of SEPN1 as a novel MAM protein involved in mitochondrial bioenergetics. They also identify a systemic bioenergetic component in SEPN1-RM and establish mitochondria as a novel therapeutic target. This role of SEPN1 contributes to explain the fatigue and core lesions in skeletal muscle as well as the body composition abnormalities identified as part of the SEPN1-RM phenotype. Finally, these results point out to an unrecognized interplay between mitochondrial bioenergetics and ER homeostasis in skeletal muscle. They could therefore pave the way to the identification of biomarkers and therapeutic drugs for SEPN1-RM and for other disorders in which muscle ER-mitochondria cross-talk are impaired

Building leaders for the UN Ocean Science Decade : a guide to supporting early career women researchers within academic marine research institutions

Diverse and inclusive marine research is paramount to addressing ocean sustainability challenges in the 21st century, as envisioned by the UN Decade of Ocean Science for Sustainable Development. Despite increasing efforts to diversify ocean science, women continue to face barriers at various stages of their career, which inhibits their progression to leadership within academic institutions. In this perspective, we draw on the collective experiences of thirty-four global women leaders, bolstered by a narrative review, to identify practical strategies and actions that will help empower early career women researchers to become the leaders of tomorrow. We propose five strategies: (i) create a more inclusive culture, (ii) ensure early and equitable career development opportunities for women ECRs, (iii) ensure equitable access to funding for women ECRs, (iv) offer mentoring opportunities and, (v) create flexible, family-friendly environments. Transformational, meaningful, and lasting change will only be achieved through commitment and collaborative action across various scales and by multiple stakeholders.Peer reviewe

Building leaders for the UN Ocean Science Decade: a guide to supporting early career women researchers within academic marine research institutions

Diverse and inclusive marine research is paramount to addressing ocean sustainability challenges in the 21st century, as envisioned by the UN Decade of Ocean Science for Sustainable Development. Despite increasing efforts to diversify ocean science, women continue to face barriers at various stages of their career, which inhibits their progression to leadership within academic institutions. In this perspective, we draw on the collective experiences of thirty-four global women leaders, bolstered by a narrative review, to identify practical strategies and actions that will help empower early career women researchers to become the leaders of tomorrow. We propose five strategies: (i) create a more inclusive culture, (ii) ensure early and equitable career development opportunities for women ECRs, (iii) ensure equitable access to funding for women ECRs, (iv) offer mentoring opportunities and, (v) create flexible, family-friendly environments. Transformational, meaningful, and lasting change will only be achieved through commitment and collaborative action across various scales and by multiple stakeholders

Lipodystrophic laminopathy: Lamin A mutation relaxes chromatin architecture to impair adipogenesis

The familial partial Dunnigan lipodystrophy, characterized by subcutaneous fat loss, is frequently caused by an R482W mutation in lamin A. In this issue, Oldenburg et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201701043) demonstrate that this mutation impairs the ability of lamin A to repress the anti-adipogenic miR-335, providing a potential molecular mechanism for the disease

The beneficial effect of myostatin deficiency on maximal muscle force and power is attenuated with age

International audienceThe prolonged effect of myostatin deficiency on muscle performance in knockout mice has as yet been only poorly investigated. We have demonstrated that absolute maximal force is increased in 6-month old female and male knockout mice and 2-year old female knockout mice as compared to age- and sex-matched wildtype mice. Similarly, absolute maximal power is increased by myostatin deficiency in 6-month old female and male knockout mice but not in 2-year old female knockout mice. The increases we observed were greater in 6-month old female than in male knockout mice and can primarily result from muscle hypertrophy. In contrast, fatigue resistance was decreased in 6-month old knockout mice of both sexes as compared to age- and sex-matched wildtype mice. Moreover, in contrast to 2-year old female wildtype mice, aging in 2-year old knockout mice reduced absolute maximal force and power of both sexes as compared to their younger counterparts, although muscle weight did not change. These age- related decreases were lower in 2-year old female than in 2-year old male knockout mice. Together these results suggest that the beneficial effect of myostatin deficiency on absolute maximal force and power is greater in young (versus old) mice and female (versus male) mice. Most of these effects of myostatin deficiency are related neither to changes in the concentration of myofibrillar proteins nor to the slow to fast fiber type transition

Expression des enzymes de la stéroïdogenèse dans une tumeur surrénalienne oncocytaire sécrétant des androgènes

International audienceExpression des enzymes de la stéroïdogenèse dans une tumeur surrénalienne oncocytaire sécrétant des androgènes Milène Tetsi Nomigni, Sophie Ouzounian, Alice Benoit, Jacqueline Vadrot, Frédérique Tissier, Sylvie Renouf, Hervé Lefebvre, Sophie Christin-Maitre, et Estelle LouisetL’hirsutisme est induit par un hyperandrogénisme associé à un syndrome des ovaires polykystiques, un déficit en 21-hydroxylase ou une tumeur ovarienne ou surrénalienne sécrétant des androgènes. Les tumeurs surrénaliennes productrices d’androgènes sont le plus souvent malignes et très rarement des oncocytomes. Nous avons caractérisé in vitro les profils sécrétoire et d’expression des enzymes de la stéroïdogenèse d’une tumeur surrénalienne oncocytaire bénigne, ôtée chez une jeune femme présentant un hirsutisme associé à des taux plasmatiques élevés de Δ4-androstènedione et testostérone. Les expériences de Q-PCR et d’immunohistochimie montrent que parmi les enzymes requises pour la synthèse du cortisol, la 17α-hydroxylase (OH) et la 3β-hydroxystéroïde deshydrogénase (HSD) 2 étaient fortement exprimées, alors que la 21-OH et la 11β-OH n’étaient que faiblement produites dans la tumeur. Les enzymes indispensables à la synthèse de testostérone, les 17β-HSD5 et 17β-HSD3, ont également été détectées. Le récepteur de l’ACTH était présent dans l’oncocytome mais pas celui de la LH. Les cellules tumorales en culture sécrétaient du cortisol et des androgènes, majoritairement de la Δ4-androstènedione et plus faiblement de la testostérone. Les sécrétions hormonales étaient stimulées in vitro par l’ACTH. Les résultats montrent que l’hypersécretion de Δ4-androstènedione résultait d’une forte expression de 17α-OH et 3β-HSD2 combinée à une faible expression de 21-OH et 11β-OH. La synthèse de testostérone était due aux activités des 17β-HSD5 et 17β-HSD3. Finalement, nos données indiquent que cette tumeur très rare présentait à la fois un phénotype de cellules des zones fasciculée et réticulée mais n’avait pas les caractéristiques de cellules stéroïdogènes gonadiques