241 research outputs found
Trajectory Analysis for Sport and Video Surveillance
In video surveillance and sports analysis applications, object trajectories offer the possibility of extracting rich information on the underlying behavior of the moving targets. To this end we introduce an extension of Point Distribution Models (PDM) to analyze the object motion in their spatial, temporal and spatiotemporal dimensions. These trajectory models represent object paths as an average trajectory and a set of deformation modes, in the spatial, temporal and spatiotemporal domains. Thus any given motion can be expressed in terms of its modes, which in turn can be ascribed to a particular behavior. The proposed analysis tool has been tested on motion data extracted from a vision system that was tracking radio-guided cars running inside a circuit. This affords an easier interpretation of results, because the shortest lap provides a reference behavior. Besides showing an actual analysis we discuss how to normalize trajectories to have a meaningful analysis
Ăvolution des comportements et des reprĂ©sentations sociales liĂ©s Ă la consommation de cannabis chez les adolescents. RĂ©sumĂ©
La recherche, dont les résultats principaux sont
décrits dans ce résumé, visait trois objectifs différents:
a) mieux comprendre l'Ă©volution de la
consommation de substances durant l'adolescence;
b) mesurer les représentations sociales, par
rapport Ă la consommation, dans une population
de consommateurs comparée à une population
«tout-venant»; c) valider un instrument de dépistage
de la consommation.
L'Ă©chantillon, sur lequel porte l'observation du
suivi, est représentatif d'une population de
consommateurs de substances. Le suivi a été
réalisé sur une période de quatre ans, l'ùge des
sujets variant entre 15 et 20 ans au moment du
premier entretien. Pour l'évaluation des représentations
sociales, une population «tout-venant» a
été recrutée, afin de pouvoir comparer les attitudes
et opinions des adolescents en relation avec
la consommation. Enfin, pour la validation de
l'instrument de screening, les deux populations,
suivi et «tout-venant», ont été réunies
Electrical impedance spectroscopy detects skin barrier dysfunction in childhood atopic dermatitis
Background
Skin barrier dysfunction is associated with the development of atopic dermatitis (AD), however methods to assess skin barrier function are limited. We investigated the use of electrical impedance spectroscopy (EIS) to detect skin barrier dysfunction in children with AD of the CARE (Childhood AlleRgy, nutrition, and Environment) cohort.
Methods
EIS measurements taken at multiple time points from 4âmonths to 3âyearâold children, who developed AD (nâ=â66) and those who did not (nâ=â49) were investigated. Using only the EIS measurement and the AD status, we developed a machine learning algorithm that produces a score (EIS/AD score) which reflects the probability that a given measurement is from a child with active AD. We investigated the diagnostic ability of this score and its association with clinical characteristics and age.
Results
Based on the EIS/AD score, the EIS algorithm was able to clearly discriminate between healthy skin and clinically unaffected skin of children with active AD (area under the curve 0.92, 95% CI 0.85â0.99). It was also able to detect a difference between healthy skin and AD skin when the child did not have active AD. There was no clear association between the EIS/AD score and the severity of AD or sensitisation to the tested allergens. The performance of the algorithm was not affected by age.
Conclusions
This study shows that EIS can detect skin barrier dysfunction and differentiate skin of children with AD from healthy skin and suggests that EIS may have the ability to predict future AD development
Electrical impedance spectroscopy detects skin barrier dysfunction in childhood atopic dermatitis.
BACKGROUND
Skin barrier dysfunction is associated with the development of atopic dermatitis (AD), however methods to assess skin barrier function are limited. We investigated the use of electrical impedance spectroscopy (EIS) to detect skin barrier dysfunction in children with AD of the CARE (Childhood AlleRgy, nutrition, and Environment) cohort.
METHODS
EIS measurements taken at multiple time points from 4âmonths to 3-year-old children, who developed AD (nâ=â66) and those who did not (nâ=â49) were investigated. Using only the EIS measurement and the AD status, we developed a machine learning algorithm that produces a score (EIS/AD score) which reflects the probability that a given measurement is from a child with active AD. We investigated the diagnostic ability of this score and its association with clinical characteristics and age.
RESULTS
Based on the EIS/AD score, the EIS algorithm was able to clearly discriminate between healthy skin and clinically unaffected skin of children with active AD (area under the curve 0.92, 95% CI 0.85-0.99). It was also able to detect a difference between healthy skin and AD skin when the child did not have active AD. There was no clear association between the EIS/AD score and the severity of AD or sensitisation to the tested allergens. The performance of the algorithm was not affected by age.
CONCLUSIONS
This study shows that EIS can detect skin barrier dysfunction and differentiate skin of children with AD from healthy skin and suggests that EIS may have the ability to predict future AD development
Molecular Biomarkers of Neovascular Age-Related Macular Degeneration With Incomplete Response to Anti-Vascular Endothelial Growth Factor Treatment.
The standard treatment for neovascular age-related macular degeneration (nAMD) consists of intravitreal anti-vascular endothelial growth factors (VEGF). However, for some patients, even maximal anti-VEGF treatment does not entirely suppress exudative activity. The goal of this study was to identify molecular biomarkers in nAMD with incomplete response to anti-VEGF treatment. Aqueous humor (AH) samples were collected from three groups of patients: 17 patients with nAMD responding incompletely to anti-VEGF (18 eyes), 17 patients affected by nAMD with normal treatment response (21 eyes), and 16 control patients without any retinopathy (16 eyes). Proteomic and multiplex analyses were performed on these samples. Proteomic analyses showed that nAMD patients with incomplete anti-VEGF response displayed an increased inflammatory response, complement activation, cytolysis, protein-lipid complex, and vasculature development pathways. Multiplex analyses revealed a significant increase of soluble vascular cell adhesion molecule-1 (sVCAM-1) [ p = 0.001], interleukin-6 (IL-6) [ p = 0.009], bioactive interleukin-12 (IL-12p40) [ p = 0.03], plasminogen activator inhibitor type 1 (PAI-1) [ p = 0.004], and hepatocyte growth factor (HGF) [ p = 0.004] levels in incomplete responders in comparison to normal responders. Interestingly, the same biomarkers showed a high intercorrelation with r2 values between 0.58 and 0.94. In addition, we confirmed by AlphaLISA the increase of sVCAM-1 [ p < 0.0001] and IL-6 [ p = 0.043] in the incomplete responder group. Incomplete responders in nAMD are associated with activated angiogenic and inflammatory pathways. The residual exudative activity of nAMD despite maximal anti-VEGF treatment may be related to both angiogenic and inflammatory responses requiring specific adjuvant therapy. Data are available via ProteomeXchange with identifier PXD02247
MHC Class II Molecules Enhance Toll-Like Receptor Mediated Innate Immune Responses
BACKGROUND: Major histocompatibility complex (MHC) class II molecules play crucial roles in immune activation by presenting foreign peptides to antigen-specific T helper cells and thereby inducing adaptive immune responses. Although adaptive immunity is a highly effective defense system, it takes several days to become fully operational and needs to be triggered by danger-signals generated during the preceding innate immune response. Here we show that MHC class II molecules synergize with Toll-like receptor (TLR) 2 and TLR4 in inducing an innate immune response.
METHODOLOGY/PRINCIPAL FINDINGS: We found that co-expression of MHC class II molecules and TLR2 or TLR4 in human embryonic kidney (HEK) cells 293 leads to enhanced production of the anti-microbial peptide human-beta-defensin (hBD) 2 after treatment with TLR2 stimulus bacterial lipoprotein (BLP) or TLR4 ligand lipopolysaccharide (LPS), respectively. Furthermore, we found that peritoneal macrophages of MHC class II knock-out mice show a decreased responsiveness to TLR2 and TLR4 stimuli compared to macrophages of wild-type mice. Finally, we show that MHC class II molecules are physically and functionally associated with TLR2 in lipid raft domains of the cell membrane.
CONCLUSIONS/SIGNIFICANCE: These results demonstrate that MHC class II molecules are, in addition to their central role in adaptive immunity, also implicated in generating optimal innate immune responses
An integrated molecular risk score early in life for subsequent childhood asthma risk.
BACKGROUND
Numerous children present with early wheeze symptoms, yet solely a subgroup develops childhood asthma. Early identification of children at risk is key for clinical monitoring, timely patient-tailored treatment, and preventing chronic, severe sequelae. For early prediction of childhood asthma, we aimed to define an integrated risk score combining established risk factors with genome-wide molecular markers at birth, complemented by subsequent clinical symptoms/diagnoses (wheezing, atopic dermatitis, food allergy).
METHODS
Three longitudinal birth cohorts (PAULINA/PAULCHEN, nâ=â190â+â93â=â283, PASTURE, nâ=â1133) were used to predict childhood asthma (age 5-11) including epidemiological characteristics and molecular markers: genotype, DNA methylation and mRNA expression (RNASeq/NanoString). Apparent (ap) and optimism-corrected (oc) performance (AUC/R2) was assessed leveraging evidence from independent studies (NaĂŻve-Bayes approach) combined with high-dimensional logistic regression models (LASSO).
RESULTS
Asthma prediction with epidemiological characteristics at birth (maternal asthma, sex, farm environment) yielded an ocAUCâ=â0.65. Inclusion of molecular markers as predictors resulted in an improvement in apparent prediction performance, however, for optimism-corrected performance only a moderate increase was observed (upto ocAUCâ=â0.68). The greatest discriminate power was reached by adding the first symptoms/diagnosis (up to ocAUCâ=â0.76; increase of 0.08, pâ=â.002). Longitudinal analysis of selected mRNA expression in PASTURE (cord blood, 1, 4.5, 6âyears) showed that expression at age six had the strongest association with asthma and correlation of genes getting larger over time (râ=â.59, pâ<â.001, 4.5-6âyears).
CONCLUSION
Applying epidemiological predictors alone showed moderate predictive abilities. Molecular markers from birth modestly improved prediction. Allergic symptoms/diagnoses enhanced the power of prediction, which is important for clinical practice and for the design of future studies with molecular markers
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Visual function improvement using photocromic and selective blue-violet light filtering spectacle lenses in patients affected by retinal diseases
Background
To evaluate functional visual parameters using photocromic and selective blue-violet light filtering spectacle lenses in patients affected by central or peripheral scotoma due to retinal diseases.
Sixty patients were enrolled in this study: 30 patients affected by central scotoma, group 1, and 30 affected by peripheral scotoma, group 2.
Black on White Best Corrected Visual Acuity (BW-BCVA), White on Black Best Corrected Visual Acuity (WB-BCVA), Mars Contrast Sensitivity (CS) and a Glare Test (GT) were performed to all patients.
Test results with blue-violet filter, a short-pass yellow filter and with no filters were compared.
Results
All scores from test results increased significantly with blue-violet filters for all patients.
The mean BW-BCVA increased from 0.30 ± 0.20 to 0.36 ± 0.21 decimals in group 1 and from 0.44 ± 0.22 to 0.51 ± 0.23 decimals in group 2 (Mean ± SD, p < 0.0001 in both cases).
The mean WB-BCVA increased from 0.31 ± 0.19 to 0.38 ± 0.23 decimals in group 1 and from 0.46 ± 0.20 to 0.56 ± 0.22 decimals in group 2 (Mean ± SD, p < 0.0001 in both cases).
The letter count for the CS test increased from 26.7 ± 7.9 to 30.06 ± 7.8 in group 1 (Mean ± SD, p = 0.0005) and from 31.5 ± 7.6 to 33.72 ± 7.3 in group 2 (Mean ± SD, p = 0.031).
GT was significantly reduced: the letter count increased from 20.93 ± 5.42 to 22.82 ± 4.93 in group 1 (Mean ± SD, p < 0.0001) and from 24.15 ± 5.5 to 25.97 ± 4.7 in group 2 (Mean ± SD, p < 0.0001).
Higher scores were recorded with the Blue filter compared to Yellow filter in all tests (p < 0.05).
No significant differences in any test results could be detected between the Yellow filter and the No filter condition.
Conclusions
The use of a combination of photocromic lens with a selective blue-violet light filter showed functional benefit in all evaluated patients
Acute Hypoglycemia Induces Retinal Cell Death in Mouse
BACKGROUND: Glucose is the most important metabolic substrate of the retina and maintenance of normoglycemia is an essential challenge for diabetic patients. Glycemic excursions could lead to cardiovascular disease, nephropathy, neuropathy and retinopathy. A vast body of literature exists on hyperglycemia namely in the field of diabetic retinopathy, but very little is known about the deleterious effect of hypoglycemia. Therefore, we decided to study the role of acute hypoglycemia in mouse retina. METHODOLOGY/PRINCIPAL FINDINGS: To test effects of hypoglycemia, we performed a 5-hour hyperinsulinemic/hypoglycemic clamp; to exclude an effect of insulin, we made a hyperinsulinemic/euglycemic clamp as control. We then isolated retinas from each group at different time-points after the clamp to analyze cells apoptosis and genes regulation. In parallel, we used 661W photoreceptor cells to confirm in vivo results. We showed herein that hypoglycemia induced retinal cell death in mouse via caspase 3 activation. We then tested the mRNA expression of glutathione transferase omega 1 (Gsto1) and glutathione peroxidase 3 (Gpx3), two genes involved in glutathione (GSH) homeostasis. The expression of both genes was up-regulated by low glucose, leading to a decrease of reduced glutathione (GSH). In vitro experiments confirmed the low-glucose induction of 661W cell death via superoxide production and activation of caspase 3, which was concomitant with a decrease of GSH content. Moreover, decrease of GSH content by inhibition with buthionine sulphoximine (BSO) at high glucose induced apoptosis, while complementation with extracellular glutathione ethyl ester (GSHee) at low glucose restored GSH level and reduced apoptosis. CONCLUSIONS/SIGNIFICANCE: We showed, for the first time, that acute insulin-induced hypoglycemia leads to caspase 3-dependant retinal cell death with a predominant role of GSH content
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