Segmentation d'images échocardiographiques par contours actifs implicites : exploitation de descripteurs statistiques de régions

Le problème traité concerne la segmentation d'images échocardiographiques par contour actifs implicites utilisant des descripteurs statistiques de région basés sur les K-distributions. La quasi totalité des auteurs traitant ce sujet exploite la statistique de Rayleigh, qui est un modèle limité pour la caractérisation de certain milieux tissulaires, tel que le myocarde. Ainsi, l'originalité de la méthode proposée réside en l'exploitation du formalisme récemment développé par Jehan-Besson et al. afin d'utiliser un paramètre statistique issu du modèle des K-distributions qui reflète plus fidèlement les propriétés des images ultrasonores du myocarde

Automatic Extraction of Hiatal Dimensions in 3-D Transperineal Pelvic Ultrasound Recordings

The aims of this work were to create a robust automatic software tool for measurement of the levator hiatal area on transperineal ultrasound (TPUS) volumes and to measure the potential reduction in variability and time taken for analysis in a clinical setting. The proposed tool automatically detects the C-plane (i.e., the plane of minimal hiatal dimensions) from a 3-D TPUS volume and subsequently uses the extracted plane to automatically segment the levator hiatus, using a convolutional neural network. The automatic pipeline was tested using 73 representative TPUS volumes. Reference hiatal outlines were obtained manually by two experts and compared with the pipeline's automated outlines. The Hausdorff distance, area, a clinical quality score, C-plane angle and C-plane Euclidean distance were used to evaluate C-plane detection and quantify levator hiatus segmentation accuracy. A visual Turing test was created to compare the performance of the software with that of the expert, based on the visual assessment of C-plane and hiatal segmentation quality. The overall time taken to extract the hiatal area with both measurement methods (i.e., manual and automatic) was measured. Each metric was calculated both for computer–observer differences and for inter-and intra-observer differences. The automatic method gave results similar to those of the expert when determining the hiatal outline from a TPUS volume. Indeed, the hiatal area measured by the algorithm and by an expert were within the intra-observer variability. Similarly, the method identified the C-plane with an accuracy of 5.76 ± 5.06° and 6.46 ± 5.18 mm in comparison to the inter-observer variability of 9.39 ± 6.21° and 8.48 ± 6.62 mm. The visual Turing test suggested that the automatic method identified the C-plane position within the TPUS volume visually as well as the expert. The average time taken to identify the C-plane and segment the hiatal area manually was 2 min and 35 ± 17 s, compared with 35 ± 4 s for the automatic result. This study presents a method for automatically measuring the levator hiatal area using artificial intelligence-based methodologies whereby the C-plane within a TPUS volume is detected and subsequently traced for the levator hiatal outline. The proposed solution was determined to be accurate, relatively quick, robust and reliable and, importantly, to reduce time and expertise required for pelvic floor disorder assessment

Modest phenotypic improvements in ASA-deficient mice with only one UDP-galactose:ceramide-galactosyltransferase gene

BACKGROUND: Arylsulfatase A (ASA)-deficient mice are a model for the lysosomal storage disorder metachromatic leukodystrophy. This lipidosis is characterised by the lysosomal accumulation of the sphingolipid sulfatide. Storage of this lipid is associated with progressive demyelination. We have mated ASA-deficient mice with mice heterozygous for a non-functional allele of UDP-galactose:ceramide-galactosyltransferase (CGT). This deficiency is known to lead to a decreased synthesis of galactosylceramide and sulfatide, which should reduce sulfatide storage and improve pathology in ASA-deficient mice. RESULTS: ASA-/- CGT+/- mice, however, showed no detectable decrease in sulfatide storage. Neuronal degeneration of cells in the spiral ganglion of the inner ear, however, was decreased. Behavioural tests showed small but clear improvements of the phenotype in ASA-/- CGT+/- mice. CONCLUSION: Thus the reduction of galactosylceramide and sulfatide biosynthesis by genetic means overall causes modest improvements of pathology

Unravelling the wavelength dependency of anthracene photoinitiated reactions

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Quinolinic acid injection in mouse medial prefrontal cortex affects reversal learning abilities, cortical connectivity and hippocampal synaptic plasticity.

Intracerebral injection of the excitotoxic, endogenous tryptophan metabolite, quinolinic acid (QA), constitutes a chemical model of neurodegenerative brain disease. Complementary techniques were combined to examine the consequences of QA injection into medial prefrontal cortex (mPFC) of C57BL6 mice. In accordance with the NMDAR-mediated synapto- and neurotoxic action of QA, we found an initial increase in excitability and an augmentation of hippocampal long-term potentiation, converting within two weeks into a reduction and impairment, respectively, of these processes. QA-induced mPFC excitotoxicity impaired behavioral flexibility in a reversal variant of the hidden-platform Morris water maze (MWM), whereas regular, extended MWM training was unaffected. QA-induced mPFC damage specifically affected the spatial-cognitive strategies that mice use to locate the platform during reversal learning. These behavioral and cognitive defects coincided with changes in cortical functional connectivity (FC) and hippocampal neuroplasticity. FC between various cortical regions was assessed by resting-state fMRI (rsfMRI) methodology, and mice that had received QA injection into mPFC showed increased FC between various cortical regions. mPFC and hippocampus (HC) are anatomically as well as functionally linked as part of a cortical network that controls higher-order cognitive functions. Together, these observations demonstrate the central functional importance of rodent mPFC as well as the validity of QA-induced mPFC damage as a preclinical rodent model of the early stages of neurodegeneration

Absence of thrombospondin-2 causes age-related dilated cardiomyopathy

BACKGROUND: The progressive shift from a young to an aged heart is characterized by alterations in the cardiac matrix. The present study investigated whether the matricellular protein thrombospondin-2 (TSP-2) may affect cardiac dimensions and function with physiological aging of the heart. METHODS AND RESULTS: TSP-2 knockout (KO) and wild-type mice were followed up to an age of 60 weeks. Survival rate, cardiac function, and morphology did not differ at a young age in TSP-2 KO compared with wild-type mice. However, >55% of the TSP-2 KO mice died between 24 and 60 weeks of age, whereas <10% of the wild-type mice died. In the absence of TSP-2, older mice displayed a severe dilated cardiomyopathy with impaired systolic function, increased cardiac dilatation, and fibrosis. Ultrastructural analysis revealed progressive myocyte stress and death, accompanied by an inflammatory response and replacement fibrosis, in aging TSP-2 KO animals, whereas capillary or coronary morphology or density was not affected. Importantly, adeno-associated virus-9 gene-mediated transfer of TSP-2 in 7-week-old TSP-2 KO mice normalized their survival and prevented dilated cardiomyopathy. In TSP-2 KO animals, age-related cardiomyopathy was accompanied by increased matrix metalloproteinase-2 and decreased tissue transglutaminase-2 activity, together with impaired collagen cross-linking. At the cardiomyocyte level, TSP-2 deficiency in vivo and its knockdown in vitro decreased the activation of the Akt survival pathway in cardiomyocytes. CONCLUSIONS: TSP-2 expression in the heart protects against age-dependent dilated cardiomyopath