Multiframe Scene Flow with Piecewise Rigid Motion

We introduce a novel multiframe scene flow approach that jointly optimizes the consistency of the patch appearances and their local rigid motions from RGB-D image sequences. In contrast to the competing methods, we take advantage of an oversegmentation of the reference frame and robust optimization techniques. We formulate scene flow recovery as a global non-linear least squares problem which is iteratively solved by a damped Gauss-Newton approach. As a result, we obtain a qualitatively new level of accuracy in RGB-D based scene flow estimation which can potentially run in real-time. Our method can handle challenging cases with rigid, piecewise rigid, articulated and moderate non-rigid motion, and does not rely on prior knowledge about the types of motions and deformations. Extensive experiments on synthetic and real data show that our method outperforms state-of-the-art.Comment: International Conference on 3D Vision (3DV), Qingdao, China, October 201

Characterizing preclinical sub-phenotypic models of acute respiratory distress syndrome:An experimental ovine study

Abstract The acute respiratory distress syndrome (ARDS) describes a heterogenous population of patients with acute severe respiratory failure. However, contemporary advances have begun to identify distinct sub‐phenotypes that exist within its broader envelope. These sub‐phenotypes have varied outcomes and respond differently to several previously studied interventions. A more precise understanding of their pathobiology and an ability to prospectively identify them, may allow for the development of precision therapies in ARDS. Historically, animal models have played a key role in translational research, although few studies have so far assessed either the ability of animal models to replicate these sub‐phenotypes or investigated the presence of sub‐phenotypes within animal models. Here, in three ovine models of ARDS, using combinations of oleic acid and intravenous, or intratracheal lipopolysaccharide, we investigated the presence of sub‐phenotypes which qualitatively resemble those found in clinical cohorts. Principal Component Analysis and partitional clustering identified two clusters, differentiated by markers of shock, inflammation, and lung injury. This study provides a first exploration of ARDS phenotypes in preclinical models and suggests a methodology for investigating this phenomenon in future studies

A clinically relevant sheep model of orthotopic heart transplantation 24 h after donor brainstem death

BACKGROUND: Heart transplantation (HTx) from brainstem dead (BSD) donors is the gold-standard therapy for severe/end-stage cardiac disease, but is limited by a global donor heart shortage. Consequently, innovative solutions to increase donor heart availability and utilisation are rapidly expanding. Clinically relevant preclinical models are essential for evaluating interventions for human translation, yet few exist that accurately mimic all key HTx components, incorporating injuries beginning in the donor, through to the recipient. To enable future assessment of novel perfusion technologies in our research program, we thus aimed to develop a clinically relevant sheep model of HTx following 24 h of donor BSD. METHODS: BSD donors (vs. sham neurological injury, 4/group) were hemodynamically supported and monitored for 24 h, followed by heart preservation with cold static storage. Bicaval orthotopic HTx was performed in matched recipients, who were weaned from cardiopulmonary bypass (CPB), and monitored for 6 h. Donor and recipient blood were assayed for inflammatory and cardiac injury markers, and cardiac function was assessed using echocardiography. Repeated measurements between the two different groups during the study observation period were assessed by mixed ANOVA for repeated measures. RESULTS: Brainstem death caused an immediate catecholaminergic hemodynamic response (mean arterial pressure, p = 0.09), systemic inflammation (IL-6 - p = 0.025, IL-8 - p = 0.002) and cardiac injury (cardiac troponin I, p = 0.048), requiring vasopressor support (vasopressor dependency index, VDI, p = 0.023), with normalisation of biomarkers and physiology over 24 h. All hearts were weaned from CPB and monitored for 6 h post-HTx, except one (sham) recipient that died 2 h post-HTx. Hemodynamic (VDI - p = 0.592, heart rate - p = 0.747) and metabolic (blood lactate, p = 0.546) parameters post-HTx were comparable between groups, despite the observed physiological perturbations that occurred during donor BSD. All p values denote interaction among groups and time in the ANOVA for repeated measures. CONCLUSIONS: We have successfully developed an ovine HTx model following 24 h of donor BSD. After 6 h of critical care management post-HTx, there were no differences between groups, despite evident hemodynamic perturbations, systemic inflammation, and cardiac injury observed during donor BSD. This preclinical model provides a platform for critical assessment of injury development pre- and post-HTx, and novel therapeutic evaluation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s40635-021-00425-4

Interaction entre assistance extracorporelle veino-artérielle (ECMO VA) et cerveau : exemple de l'hypoxie différentielle

Femoral-arterial V-A ECMO can cause "differential hypoxemia", a situation where the hyperoxic laminar flow of the ECMO going up the aorta meets the hypoxemic pulsatile flow of the native heart going down the aorta. This encounter occurs in a zone called the "mixing zone" (or watershed). The objectives of this work were to create an ex vivo and an in vivo models to study the parameters and consequences of differential hypoxemia. Thus, in a first step, we modified an existing mock circulation loop to add an aortic arch and a V-A ECMO circuit. In this ex vivo model, only temperature variations in the right subclavian artery (accessible through the radial artery in clinical practice) were predictive of the position of the mixing zone. In a second step, to define the appropriate in vivo model, we performed a meta-analysis of animal models of cardiogenic shock under V-A ECMO. Nineteen studies were included in our analysis and show that methods and data were very poorly reported, and that a very large variability regarding models of cardiogenic shock, animals used and management of ECMO existed. Thus, we chose to perform an ovine model of cardiogenic shock induced by intraventricular injection of ethanol. This model - respecting strict criteria for the definition of cardiogenic shock - had the advantage of being titratable and reproducible. We thus obtained a model supported by V- A ECMO with hypoxemia through the reduction of mechanical ventilation, creating a model of differential hypoxemia confirmed on a clinical, biological and histological level. Finally, in the last step, we randomized our sheep in two groups according to the level of ECMO support: low flow (2.5 L/min) or high flow (4.5 L/min). In the low-flow group, the brain was fully perfused by the native heart. In the high-flow group, the brain was partially perfused by the ECMO. We observed lesions compatible with ischemic-hypoxic damage after only a few hours of differential hypoxemia. These lesions were significantly reduced in the high flow group, explained by a switch to an aerobic mechanism.L’ECMO VA fémoro-fémorale peut être à l’origine d’une « hypoxémie différentielle » lorsque le flux laminaire hyperoxique de l’ECMO remontant le long de l'aorte rencontre le flux pulsatile hypoxémique du cœur natif descendant le long de l’aorte. Cette rencontre a lieu dans la « zone de mélange ». Les objectifs de ce travail étaient de créer des modèles ex vivo et in vivo d’étude des paramètres et des conséquences de l’hypoxémie différentielle. Ainsi, dans un premier temps, nous avons modifié une boucle de circulation (mock loop) afin d’y adjoindre une crosse aortique et un circuit d’ECMO-VA. Dans ce modèle ex vivo, seule la variation de température de l’artère sous-clavière droite (accessible en radial en pratique clinique) était prédictive de la position de la zone de mélange. Dans un second temps, afin de définir le modèle in vivo adéquat, nous avons réalisé une méta-analyse des modèles animaux de choc cardiogénique sous ECMO- VA. Les dix-neuf études inclues dans notre analyse montrent que les méthodes et données étaient très mal rapportées et qu’il existait une très grande variabilité concernant les modèles, les animaux et la gestion de l’ECMO. Ainsi, nous avons créé un modèle ovin de choc cardiogénique induit par l’injection intra-ventriculaire d’éthanol. Ce modèle respectait des critères stricts de choc cardiogénique et avait l’avantage d’être titrable et reproductible. L’hypoxémie était induite par diminution de la ventilation mécanique, résultant en un modèle d’hypoxémie différentielle confirmé cliniquement, biologiquement et histologiquement. Enfin, dans un dernier temps, nous avons randomisé nos brebis en deux groupes: bas débit (2,5 L/min) ou haut débit (4,5 L/min) d’ECMO. Dans le groupe bas débit, le cerveau était entièrement perfusé par le cœur natif. Dans le groupe haut débit, le cerveau était lui partiellement perfusé par l’ECMO. Nous avons observé des lésions de type ischémie-hypoxie après seulement quelques heures d’hypoxémie différentielle. Ces lésions étaient significativement moindres dans le groupe haut débit avec un retour vers un mécanisme aérobie

Interaction between venoarterial extracorporeal membrane oxygenation (V-A ECMO) and the brain : example of differential hypoxemia.

L’ECMO VA fémoro-fémorale peut être à l’origine d’une « hypoxémie différentielle » lorsque le flux laminaire hyperoxique de l’ECMO remontant le long de l'aorte rencontre le flux pulsatile hypoxémique du cœur natif descendant le long de l’aorte. Cette rencontre a lieu dans la « zone de mélange ». Les objectifs de ce travail étaient de créer des modèles ex vivo et in vivo d’étude des paramètres et des conséquences de l’hypoxémie différentielle. Ainsi, dans un premier temps, nous avons modifié une boucle de circulation (mock loop) afin d’y adjoindre une crosse aortique et un circuit d’ECMO-VA. Dans ce modèle ex vivo, seule la variation de température de l’artère sous-clavière droite (accessible en radial en pratique clinique) était prédictive de la position de la zone de mélange. Dans un second temps, afin de définir le modèle in vivo adéquat, nous avons réalisé une méta-analyse des modèles animaux de choc cardiogénique sous ECMO- VA. Les dix-neuf études inclues dans notre analyse montrent que les méthodes et données étaient très mal rapportées et qu’il existait une très grande variabilité concernant les modèles, les animaux et la gestion de l’ECMO. Ainsi, nous avons créé un modèle ovin de choc cardiogénique induit par l’injection intra-ventriculaire d’éthanol. Ce modèle respectait des critères stricts de choc cardiogénique et avait l’avantage d’être titrable et reproductible. L’hypoxémie était induite par diminution de la ventilation mécanique, résultant en un modèle d’hypoxémie différentielle confirmé cliniquement, biologiquement et histologiquement. Enfin, dans un dernier temps, nous avons randomisé nos brebis en deux groupes: bas débit (2,5 L/min) ou haut débit (4,5 L/min) d’ECMO. Dans le groupe bas débit, le cerveau était entièrement perfusé par le cœur natif. Dans le groupe haut débit, le cerveau était lui partiellement perfusé par l’ECMO. Nous avons observé des lésions de type ischémie-hypoxie après seulement quelques heures d’hypoxémie différentielle. Ces lésions étaient significativement moindres dans le groupe haut débit avec un retour vers un mécanisme aérobie.Femoral-arterial V-A ECMO can cause "differential hypoxemia", a situation where the hyperoxic laminar flow of the ECMO going up the aorta meets the hypoxemic pulsatile flow of the native heart going down the aorta. This encounter occurs in a zone called the "mixing zone" (or watershed). The objectives of this work were to create an ex vivo and an in vivo models to study the parameters and consequences of differential hypoxemia. Thus, in a first step, we modified an existing mock circulation loop to add an aortic arch and a V-A ECMO circuit. In this ex vivo model, only temperature variations in the right subclavian artery (accessible through the radial artery in clinical practice) were predictive of the position of the mixing zone. In a second step, to define the appropriate in vivo model, we performed a meta-analysis of animal models of cardiogenic shock under V-A ECMO. Nineteen studies were included in our analysis and show that methods and data were very poorly reported, and that a very large variability regarding models of cardiogenic shock, animals used and management of ECMO existed. Thus, we chose to perform an ovine model of cardiogenic shock induced by intraventricular injection of ethanol. This model - respecting strict criteria for the definition of cardiogenic shock - had the advantage of being titratable and reproducible. We thus obtained a model supported by V- A ECMO with hypoxemia through the reduction of mechanical ventilation, creating a model of differential hypoxemia confirmed on a clinical, biological and histological level. Finally, in the last step, we randomized our sheep in two groups according to the level of ECMO support: low flow (2.5 L/min) or high flow (4.5 L/min). In the low-flow group, the brain was fully perfused by the native heart. In the high-flow group, the brain was partially perfused by the ECMO. We observed lesions compatible with ischemic-hypoxic damage after only a few hours of differential hypoxemia. These lesions were significantly reduced in the high flow group, explained by a switch to an aerobic mechanism

Outcomes and survival prediction models for severe adult acute respiratory distress syndrome treated with extracorporeal membrane oxygenation

International audienceExtracorporeal membrane oxygenation (ECMO) for severe acute respiratory distress syndrome (ARDS) has known a growing interest over the last decades with promising results during the 2009 A(H1N1) influenza epidemic. Targeting populations that can most benefit from this therapy is now of major importance. Survival has steadily improved for a decade, reaching up to 65% at hospital discharge in the most recent cohorts. However, ECMO is still marred by frequent and significant complications such as bleeding and nosocomial infections. In addition, physiological and psychological symptoms are commonly described in long-term follow-up of ECMO-treated ARDS survivors. Because this therapy is costly and exposes patients to significant complications, seven prediction models have been developed recently to help clinicians identify patients most likely to survive once ECMO has been initiated and to facilitate appropriate comparison of risk-adjusted outcomes between centres and over time. Higher age, immunocompromised status, associated extra-pulmonary organ dysfunction, low respiratory compliance and non-influenzae diagnosis seem to be the main determinants of poorer outcome

COVID-19: Brief overview of therapeutic strategies

International audienceNo abstract availabl

Predatory journals in anaesthesiology and critical care

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Enhanced recovery after cardiac surgery under CPB or off pump

International audienc

COVID-19 vaccines: A race against time

International audienceNo abstract availabl