Abstract-Emotion recognition is a crucial problem in Human-Computer Interaction (HCI).Various techniques were applied to enhance the robustness of the emotion recognition systems using electroencephalogram (EEG) signals especially the problem of spatiotemporal features learning. In this paper, a novel EEG-based emotion recognition approach is proposed. In this approach, the use of the 3-Dimensional Convolutional Neural Networks (3D-CNN) is investigated using a multi-channel EEG data for emotion recognition. A data augmentation phase is developed to enhance the performance of the proposed 3D-CNN approach. And, a 3D data representation is formulated from the multi-channel EEG signals, which is used as data input for the proposed 3D-CNN model. Extensive experimental works are conducted using the DEAP (Dataset of Emotion Analysis using the EEG and Physiological and Video Signals) data. It is found that the proposed method is able to achieve recognition accuracies 87.44% and 88.49% for valence and arousal classes respectively, which is outperforming the state of the art methods.

BackgroundSteroid-sensitive nephrotic syndrome (SSNS), the most common form of nephrotic syndrome in childhood, is considered an autoimmune disease with an established classic HLA association. However, the precise etiology of the disease is unclear. In other autoimmune diseases, the identification of loci outside the classic HLA region by genome-wide association studies (GWAS) has provided critical insights into disease pathogenesis. Previously conducted GWAS of SSNS have not identified non-HLA loci achieving genome-wide significance.MethodsIn an attempt to identify additional loci associated with SSNS, we conducted a GWAS of a large cohort of European ancestry comprising 422 ethnically homogeneous pediatric patients and 5642 ethnically matched controls.ResultsThe GWAS found three loci that achieved genome-wide significance, which explain approximately 14% of the genetic risk for SSNS. It confirmed the previously reported association with the HLA-DR/DQ region (lead single-nucleotide polymorphism [SNP] rs9273542, P=1.59×10−43; odds ratio [OR], 3.39; 95% confidence interval [95% CI], 2.86 to 4.03) and identified two additional loci outside the HLA region on chromosomes 4q13.3 and 6q22.1. The latter contains the calcium homeostasis modulator family member 6 gene CALHM6 (previously called FAM26F). CALHM6 is implicated in immune response modulation; the lead SNP (rs2637678, P=1.27×10−17; OR, 0.51; 95% CI, 0.44 to 0.60) exhibits strong expression quantitative trait loci effects, the risk allele being associated with lower lymphocytic expression of CALHM6.ConclusionsBecause CALHM6 is implicated in regulating the immune response to infection, this may provide an explanation for the typical triggering of SSNS onset by infections. Our results suggest that a genetically conferred risk of immune dysregulation may be a key component in the pathogenesis of SSNS.

Background Acute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19). The reported incidence of AKI, however, varies among studies. We aimed to evaluate the incidence of AKI and its association with mortality and morbidity in children infected with severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) who required hospital admission. Methods This was a multicenter retrospective cohort study from three tertiary centers, which included children with confirmed COVID-19. All children were evaluated for AKI using the Kidney Disease Improving Global Outcomes (KDIGO) definition and staging. Results Of 89 children included, 19 (21 %) developed AKI (52.6 % stage I). A high renal angina index score was correlated with severity of AKI. Also, multisystem inflammatory syndrome in children (MIS-C) was increased in children with AKI compared to those with normal kidney function (15 % vs. 1.5 %). Patients with AKI had significantly more pediatric intensive care admissions (PICU) (32 % vs. 2.8 %, p < 0.001) and mortality (42 % vs. 0 %, p < 0.001). However, AKI was not associated with prolonged hospitalization (58 % vs. 40 %, p = 0.163) or development of MIS-C (10.5 % vs. 1.4 %, p = 0.051). No patient in the AKI group required renal replacement therapy. Residual renal impairment at discharge occurred in 9 % of patients. This was significantly influenced by the presence of comorbidities, hypotension, hypoxia, heart failure, acute respiratory distress, hypernatremia, abnormal liver profile, high C-reactive protein, and positive blood culture. Conclusions AKI occurred in one-fifth of children with SARS-CoV-2 infection requiring hospital admission, with one-third of those requiring PICU. AKI was associated with increased morbidity and mortality, and residual renal impairment at time of discharge.

AKI occurred in more than half of all NICU admissions, was associated with an increased risk of mortality, and had a higher incidence among smaller and sicker infants. Therefore, close monitoring of renal function during hospitalization and after discharge is warranted in such infants.

Urinary schistosomiasis is a preventable disease through nationwide snail control and mass therapy with oral antibilharzial drugs. If not properly treated, long-standing urinary complications may result in serious sequelae that may lead to mortality from renal failure or bladder cancer.

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Schimke immuno-osseous dysplasia (SIOD) is a rare multisystem disorder with early mortality and steroid-resistant nephrotic syndrome (SRNS) progressing to end-stage kidney disease. We hypothesized that next-generation gene panel sequencing may unsurface oligosymptomatic cases of SIOD with potentially milder disease courses. We analyzed the renal and extrarenal phenotypic spectrum and genotype-phenotype associations in 34 patients from 28 families, the largest SMARCAL1-associated nephropathy cohort to date. In 11 patients the diagnosis was made unsuspectedly through SRNS gene panel testing. Renal disease first manifested at median age 4.5 yrs, with focal segmental glmerulosclerosis or minimal change nephropathy on biopsy and rapid progression to end-stage kidney disease (ESKD) at median age 8.7 yrs. Whereas patients diagnosed by phenotype more frequently developed severe extrarenal complications (cerebral ischemic events, septicemia) and were more likely to die before age 10 years than patients identified by SRNS-gene panel screening (88 vs. 40%), the subgroups did not differ with respect to age at proteinuria onset and progression to ESKD. Also, 10 of 11 children diagnosed unsuspectedly by Next Generation Sequencing were small at diagnosis and all showed progressive growth failure. Severe phenotypes were usually associated with biallelic truncating mutations and milder phenotypes with biallelic missense mutations. However, no genotype-phenotype correlation was observed for the renal disease course. In conclusion, while short stature is a reliable clue to SIOD in children with SRNS, other systemic features are highly variable. Our findings support routine SMARCAL1 testing also in non-syndromic SRNS.

Quantum systems with variables in Z(d) are considered. The properties of lines in the Z(d) × Z(d) phase space of these systems, are studied. Weak mutually unbiased bases in these systems are defined as bases for which the overlap of any two vectors in two different bases, is equal to d −1/2 or alternatively to one of the d −1/2 i , 0 (where di is a divisor of d apart from d, 1). They are designed for the geometry of the Z(d) × Z(d) phase space, in the sense that there is a duality between the weak mutually unbiased bases and the maximal lines through the origin. In the special case of prime d, there are no divisors of d apart from 1, d and the weak mutually unbiased bases are mutually unbiased bases.form the group Sp(2, Z(d)). The cardinality of this group is dJ 2 (d).Acting with the matrix g(κ, λ|µ, ν) on a point (ρ, σ) ∈ Z(d) × Z(d) we get the point (κρ + λσ, µρ + νσ). Acting with the symplectic matrix g(κ, λ|µ, ν) on all the points of a line L(ρ, σ) we get all the points of the line L(κρ + λσ, µρ + νσ) for which we also use the notation g(κ, λ|µ, ν)L(ρ, σ).In [28] we have proved various properties for lines in Z(d) × Z(d). For completeness below we give these properties together with several new properties, but we prove only the new ones.Definition II.1. Lines L(ν, µ) through the origin, with exactly d points are called maximal lines.Proposition II.2.