12 research outputs found

    End-to-End Mobile System for Diabetic Retinopathy Screening Based on Lightweight Deep Neural Network

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    Diabetic Retinopathy (DR) is the leading cause of visual impairment among working-aged adults. Screening and early diagnosis of DR is essential to avoid visual acuity reduction and blindness. However, a worldwide limited access to ophthalmologists may prevent an early diagnosis of this blinding condition. In this paper, we propose a novel method for screening DR from smartphone-captured fundus images. The main challenges are to perform higher accurate detection even with reduced quality of handheld captured fundus images and to provide the result into the smartphone used for acquisition. For such a need, we apply transfer learning to the lightweight deep neural network "NasnetMobile" which is used as a feature descriptor, while configuring a multilayer perceptron classifier to deduce the DR disease, in order to take benefit from their lower complexity. A dataset composed of 440 fundus images is structured, where the acquisition and statement are performed by expert ophthalmologists. A cross-validation process is conducted where 95.91% accuracy, 94.44% sensitivity, 96.92% specificity and 95.71% precision in average are achieved. In addition, the whole processing flowchart is implemented into a mobile device, where the execution time is under one second whatever the fundus image is. Those performances allow deploying the proposed system in a clinical context

    The multi-objective hybridization of particle swarm optimization and fuzzy ant colony optimization

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    In this paper, we illustrate a novel optimization approach based on Multi-objective Particle Swarm Optimization (MOPSO) and Fuzzy Ant Colony Optimization (FACO). The basic idea is to combine these two techniques using the best particle of the Fuzzy Ant algorithm and integrate it as the best local Particle Swarm Optimization (PSO), to formulate a new approach called hybrid MOPSO with FACO (H-MOPSO-FACO). This hybridization solves the multi-objective problem, which relies on both time performance criteria and the shortest path. Experimental results illustrate that the proposed method is efficient.Web of Science27152551

    Genes regulating oxidative-inflammatory response in circulating monocytes and neutrophils in septic syndrome

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    Despite significant progress in the past decades, sepsis still lacks a specific treatment. Under normal conditions, leucocytes play a critical role in controlling infection and it is suggested that their activity is impaired during sepsis which contribute to the dysregulation of immune reactions. Indeed, in response to infection, several intracellular pathways are affected mainly those regulating the oxidative- inflammatory axis. Herein, we focused on the contribution of NF-kB, iNOS, Nrf2, HO-1 and MPO genes in the pathophysiology of septic syndrome, by analyzing the differential expression of their transcripts in circulating monocytes and neutrophils, and monitoring the nitrosative/oxidative status in septic syndrome patients. Circulat- ing neutrophils of septic patients displayed a significant overexpression of NF-kB compared to other groups. In monocytes, patients with septic shock expressed the highest levels of iNOS and NF-kB mRNA. However, genes involved in cytoprotec- tive response had increased expression in patients with sepsis, in particular, the Nrf2 and its target gene HO-1. Moreover, patient monitoring indicates that the iNOS enzyme expression and NO plasma levels may play a role in assessing the severity of septic conditions. Overall, in either monocytes or neutrophils, we pointed out the major role of NF-κB and Nrf2 in the pathophysiological process. Therefore, therapies targeted to redox abnormalities may be useful for better management of septic patients

    Vitamin D status and CYP27B1‐1260 promoter polymorphism in Tunisian patients with systemic lupus erythematosus

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    Abstract Aim An association between serum vitamin D (Vit D) levels and systemic lupus erythematosus (SLE) has been reported by several studies that suggested the involvement of genetically determined characteristics of enzymes of vitamin D metabolism. Our study aimed to evaluate the relationship between 25 hydroxyvitamin D (25[OH]D) level, the most representative metabolite of VitD status, and polymorphism of the cytochrome P450, CYP27B1 gene, which influence vitamin D metabolism, and serum levels, in SLE Tunisian patients. Material and Methods A cross‐sectional study has been conducted in SLE patients (supplemented and not supplemented patients), matched to healthy controls by age and gender. The 25[OH]D serum level was measured by chemiluminescence assay and CYP27B1‐1260 genetic polymorphism was carried out using PCR‐RFLP methods. Statistical analysis was made using Shesis and SPSS.20 Software. Results Controls and Vit D not supplemented patients’ groups presented the highest percentage of hypovitaminosis D. A significant difference in the mean level of circulating 25[OH]D between Vit D supplemented SLE patients and controls was observed (23.91 ng/ml and 7.18 ng/ml, respectively p = 3.4 105). Our results showed a correlation of high 25[OH]D level with complement component 3 levels and prednisolone drug. Moreover, the analysis of CYP27B1‐1260 polymorphism in SLE patients and controls revealed a nonsignificant allelic or genotypic association. Conclusion Despite the sunny climate, the high prevalence of Vit D deficiency is common in Tunisia. This hypovitaminosis D feature may affect the Vit D levels in our SLE patients but a direct association with the disease or with the genetically determined features remains unclear. More studies are needed to establish thresholds and susceptibility genes according to the characteristics of each population

    Evaluation of X chromosome inactivation in endemic Tunisian pemphigus foliaceus

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    Abstract Background Almost 5% of the world's population develops an autoimmune disease (AID), it is considered the fourth leading cause of disability for women, who represent 78% of cases. The sex ratio when it comes to the most prevalent AID varies from 9:1 in systemic lupus erythematosus (SLE) to 13:1 in endemic Tunisian pemphigus foliaceus (PF). Methods To test the potential involvement of skewed x‐inactivation in the pathogenesis of Tunisian PF, we analyzed the methylation status of a highly polymorphic CAG repeat in the androgen receptor gene and evaluated the x chromosome inactivation (XCI) patterns in peripheral blood‐leukocyte‐derived DNA samples of female patients with PF (n = 98) compared to healthy control (HC) subjects (n = 150), as well as female patients with SLE (n = 98) were enrolled as a reference group. Results XCI status was informative for 50 of the 98 PF patients (51%) and 70 of the 150 HC women (47%). Extremely skewed XCI patterns were more frequent in PF and SLEwomen than HC, but the difference was statistically significant only in women with SLE. No statistical difference was observed in XCI patterns between PF and SLE patients. PF phenotype‐XCI correlation analysis revealed that (i) skewed XCI patterns may be involved in the disease's subtype and (ii) it was more pronounced in the endemic group than the sporadic one. Furthermore, preferential XCI showed an increase in heterozygote genotypes of PF's susceptibility polymorphisms in immunity‐related X genes (FOXP3, AR, and TLR7) in PF patients compared to HC. Conclusion Our results suggest that skewed XCI could lead to hemizygosity of X‐linked alleles that might unmask X‐linked deleterious alleles

    Differential Expression of Anti-Inflammatory RNA Binding Proteins in Lupus Nephritis

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    Lupus nephritis (LN) is a type of immunological complex glomerulonephritis characterized by chronic renal inflammation which is exacerbated by infiltrating leukocytes and fueled by a variety of pro-inflammatory cytokines. A profound understanding of the pathogenesis of LN is necessary to identify the optimal molecular targets. The role of RNA-binding proteins (RBPs) in post-transcriptional gene regulation in the immune system is being explored in greater depth to better understand how this regulation is implicated in inflammatory and autoimmune diseases. Tristetraprolin (TTP), Roquin-1/2, and Regnase-1 are 3 RBPs that play a critical role in the regulation of pro-inflammatory mediators by gating the degradation and/or translational silencing of target mRNAs. In this study, we proposed to focus on the differential expression of these RBPs in immune cells and renal biopsies from LN patients, as well as their regulatory impact on a specific target. Herein, we highlight a novel target of anti-inflammatory treatment by revealing the mechanisms underlying RBP expression and the interaction between RBPs and their target RNAs

    HLA Class III: A susceptibility region to systemic lupus erythematosus in Tunisian population

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    <div><p>Background and objectives</p><p>Short tandem repeats (STR) are usually used as informative polymorphic markers for genetic mapping and for disease susceptibility analysis. The involvement of these microsatellite markers localized in the MHC region was reported in many auto-immune diseases.</p><p>In this study we analyzed for the first time eight polymorphisms of microsatellite loci at the HLA region: D6S291, D6S273, TNFa, b and c, MICA, D6S265 and D6S276, in Tunisian systemic lupus erythematosus (SLE) patients.</p><p>Materials and methods</p><p>We performed a case control study in which the microsatellite loci were amplified using specific primers labeled with NED, VIC, PET or 6-FAM and analyzed using GeneScan software 3.7. For the statistical analysis, we used SPSS software and we performed a sub-haplotype scoring test using the haplo.stats software developed in the R language.</p><p>Results</p><p>We found that two mean associated regions existed; the most statistically significant encompassed the 3 TNF markers (p = 0.0003, OR = 19.34); the latter covered the DR region. In fact, when scoring haplotypes in 3 marker- sliding windows, the p value increased as we moved away from the TNF region and decreased again when we approached the DRB1 locus. We also established for the first time the negative association between alleles of D6S291 and SLE. The majority of clinical and serological correlations were noted with TNF alleles.</p><p>Conclusion</p><p>Our results confirm the association between TNF and DRB1 polymorphisms and SLE. The association between alleles of D6S291 and SLE needs however to be verified by the analysis of other markers beyond this region.</p></div
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