Étude du comportement poroélastique incompressible d’un disque intervertébral sous chargement externe

Le Disque InterVertébral (DIV) est un fibrocartilage hétérogène qui assure d’une part la mobilité du rachis et d’autre part la distribution des contraintes mécaniques entre les vertèbres. Ces deux propriétés principales sont liées à la fois au contenu hydrique et à la présence des protéoglycanes (PG) dans le DIV. Les contenus en eau et en PGs diminuent selon un processus naturel durant la vie. Ce processus dégénératif est dans certains cas accéléré et conduit à des maladies dégénératives. Plusieurs études [M. Alini, S.M. Eisenstein, K. Ito, C. Little, A. Kettler, K. Masuda, J. Melrose, J. Ralphs, I. Stokes, H.J. Wilke, Eur. Spine J. 17 (2008) 2–19; E.C. Bass, N.A. Duncan, J.S. Hariharan, J. Dusick, H.U. Bueff, J.C. Lotz, Spine (Phila. Pa. 1976) 22 (1997) 2867–2876; H. Ohshima, H. Tsuji, N. Hirano, H. Ishihara, Y. Katoh, H. Yamada, Spine (Phila. Pa. 1976) 14 (1989) 1234–1244; N.D. Panagiotacopulos, Spine (Phila. Pa. 1976) 12 (1987) 912–918; N.D. Panagiotacopulos, Spine (Phila. Pa. 1976) 12 (1987) 918–924] ont montré l’importance de la teneur en eau du DIV sur son comportement biomécanique. Le but de notre étude est de suivre, avec une méthode d’Imagerie de Résonance Magnétique (IRM), les variations de morphologie et d’hydratation sous un chargement mécanique. Les campagnes de mesure complétées par un post-traitement ont permis de reconstruire la déformation volumique du DIV et d’obtenir ainsi l’évolution de la porosité au cours du chargement. Les résultats ainsi obtenus sont conformes avec la littérature et le comportement retenu adhère parfaitement avec le cadre expérimental. Ce travail d’exploration de la viabilité discale permettra d’apporter des informations importantes dans la compréhension du comportement osmotico-mécanique du DIV

Quantitative MRI water content mapping of porcine intervertebral disc during uniaxial compression

International audienceBackground: Intervertebral disc (IVD) diseases are major public health problem in industrialized countries where they affect a large proportion of the population. In particular, IVD degeneration is considered to be one of the leading causes of pain consultation and sick leave. The aim of this study was to develop a new method for assessing the functionality of IVD in order to diagnose IVD degeneration. Methods: For this purpose, we have designed a specific device that enables to mechanically load porcine IVD ex vivo in the 4.7-Tesla horizontal superconducting magnet of a magnetic resonance (MR) scanner. Proton density weighted imaging (rho(H)-MRI) of the samples was acquired. Findings: The post-processing on MR images allowed (1) to reconstruct the 3D deformation under a known mechanical load and (2) to infer the IVD porosity assuming an incompressible poroelastic model. Interpretation: This study demonstrates the ability to follow the change in morphology and hydration of an IVD using MR measurements, thereby providing valued information for a better understanding of IVD function

Reconfigurable Secure Video Codec Based on DWT and AES Processor

In this paper, we proposed a secure video codec based on the discrete wavelet transformation (DWT) and the Advanced Encryption Standard (AES) processor. Either, use of video coding with DWT or encryption using AES is well known. However, linking these two designs to achieve secure video coding is leading. The contributions of our work are as follows. First, a new method for image and video compression is proposed. This codec is a synthesis of JPEG and JPEG2000,which is implemented using Huffman coding to the JPEG and DWT to the JPEG2000. Furthermore, an improved motion estimation algorithm is proposed. Second, the encryptiondecryption effects are achieved by the AES processor. AES is aim to encrypt group of LL bands. The prominent feature of this method is an encryption of LL bands by AES-128 (128-bit keys), or AES-192 (192-bit keys), or AES-256 (256-bit keys).Third, we focus on a method that implements partial encryption of LL bands. Our approach provides considerable levels of security (key size, partial encryption, mode encryption), and has very limited adverse impact on the compression efficiency. The proposed codec can provide up to 9 cipher schemes within a reasonable software cost. Latency, correlation, PSNR and compression rate results are analyzed and shown

Deficit of Resolution Receptor Magnifies Inflammatory Leukocyte directed Cardiorenal and Endothelial Dysfunction with Signs of Cardiomyopathy of Obesity

Chronic unresolved inflammation is the primary determinant of cardiovascular disease. Precise mechanisms that define the genesis of unresolved inflammation in heart failure with preserved ejection fraction (HFpEF) are of interest due to the obesity epidemic. To examine the obesity phenotype and its direct/indirect consequences, multiple approaches were employed using the lipoxin receptor (abbreviated as ALX) dysfunction mouse model. Indirect calorimetry analyses revealed that the deletion of ALX dysregulated energy metabolism driving toward age‐related obesity. Heart function data suggest that obesity‐prone ALX deficient mice had impaired myocardium strain. Comprehensive measurement of chemokines, extracellular matrix, and arrhythmogenic arrays confirmed the dysregulation of multiple ion channels gene expression with amplified inflammatory chemokines and cytokines response at the age of 4 months compared with WT counterparts. Quantitative analyses of leukocytes demonstrated an increase of proinflammatory Ly6ChiCCR2+ macrophages in the spleen and heart at a steady‐state resulting in an inflamed splenocardiac axis. Signs of subtle inflammation were marked with cardiorenal, endothelial defects with decreased CD31 and eNOS and an increased iNOS and COX2 expression. Thus, ALX receptor deficiency serves as an experimental model that defines multiple cellular and molecular mechanisms in HFpEF that could be a target for the development of HFpEF therapy in cardiovascular medicine

Lack of Resolution Sensor Drives Age-Related Cardiometabolic and Cardiorenal Defects and Impedes Inflammation-Resolution in Heart Failure

Objective: Recently, we observed that the specialized proresolving mediator (SPM) entity resolvin D1 activates lipoxin A4/formyl peptide receptor 2 (ALX/FPR2), which facilitates cardiac healing and persistent inflammation is a hallmark of impaired cardiac repair in aging. Splenic leukocyte-directed SPMs are essential for the safe clearance of inflammation and cardiac repair after injury; however, the target of SPMs remains undefined in cardiac healing and repair. Methods: To define the mechanistic basis of ALX/FPR2 as a resolvin D1 target, ALX/FPR2-null mice were examined extensively. The systolic-diastolic heart function was assessed using echocardiography, leukocytes were phenotyped using flow cytometry, and SPMs were quantitated using mass spectrometry. The presence of cardiorenal syndrome was validated using histology and renal markers. Results: Lack of ALX/FPR2 led to the development of spontaneous obesity and diastolic dysfunction with reduced survival with aging. After cardiac injury, ALX/FPR2−/− mice showed lower expression of lipoxygenases (−5, −12, −15) and a reduction in SPMs in the infarcted left ventricle and spleen, indicating nonresolving inflammation. Reduced SPM levels in the infarcted heart and spleen are suggestive of impaired cross-talk between the injured heart and splenic leukocytes, which are required for the resolution of inflammation. In contrast, cyclooxygenases (−1 and −2) were over amplified in the infarcted heart. Together, these results suggest interorgan signaling in which the spleen acts as both an SPM biosynthesizer and supplier in acute heart failure. ALX/FPR2 dysfunction magnified obesogenic cardiomyopathy and renal inflammation (↑NGAL, ↑TNF-α, ↑CCL2, ↑IL-1β) with elevated plasma creatinine levels in aging mice. At the cellular level, ALX/FPR2−/− mice showed impairment of macrophage phagocytic function ex-vivo with expansion of neutrophils after myocardial infarction. Conclusions: Lack of ALX/FPR2 induced obesity, reduced the life span, amplified leukocyte dysfunction, and facilitated profound interorgan nonresolving inflammation. Our study shows the integrative and indispensable role of ALX/FPR2 in lipid metabolism, cardiac inflammation–resolution processes, obesogenic aging, and renal homeostasis