Dynamic Key-Value Memory Networks for Knowledge Tracing

Knowledge Tracing (KT) is a task of tracing evolving knowledge state of students with respect to one or more concepts as they engage in a sequence of learning activities. One important purpose of KT is to personalize the practice sequence to help students learn knowledge concepts efficiently. However, existing methods such as Bayesian Knowledge Tracing and Deep Knowledge Tracing either model knowledge state for each predefined concept separately or fail to pinpoint exactly which concepts a student is good at or unfamiliar with. To solve these problems, this work introduces a new model called Dynamic Key-Value Memory Networks (DKVMN) that can exploit the relationships between underlying concepts and directly output a student's mastery level of each concept. Unlike standard memory-augmented neural networks that facilitate a single memory matrix or two static memory matrices, our model has one static matrix called key, which stores the knowledge concepts and the other dynamic matrix called value, which stores and updates the mastery levels of corresponding concepts. Experiments show that our model consistently outperforms the state-of-the-art model in a range of KT datasets. Moreover, the DKVMN model can automatically discover underlying concepts of exercises typically performed by human annotations and depict the changing knowledge state of a student.Comment: To appear in 26th International Conference on World Wide Web (WWW), 201

Y-chromosome polymorphisms in the United Arab Emirates population

Y chromosome short tandem repeats (Y-STR) has been widely used in forensic DNA profiling and lineages analysis. The aim of this study is to establish a database of an extensive Y-STR profiles of the United Arab Emirates (UAE) population and to investigate the distribution of 17 Y-STR loci. Samples of 345 Emirati males using 17 Y-STR loci included in the AmpFLSTR® Y-filer® PCR Amplification kit (Life Technologies) (DYS456, DYS3891, DYS390, DYS389II, DYS458, DYS19, DYS385a/b, DYS393, DYS391, DYS439, DYS635, DYS392, GATA-H4, DYS437, DYS438 and DYS448). Statistical analysis of allele frequency, haplotype diversity and discrimination capacity were performed for the samples using Arlequin software version 3.5 A total of 301 unique haplotypes were identified, 271 haplotypes were found to be unique and 22 haplotypes were shared between two individuals. In addition, there were four different haplotypes shared between more than two individuals. The haplotype diversity (HD) was found to be equal to 0.99885. The highest gene diversity was estimated to be 0.94142 for DYS385a/b whereas the lowest was estimated to be 0.4369 for DYS392. The discrimination capacity (DC) was calculated to be 90.03

Ang-(1-7)/ MAS1 receptor axis inhibits allergic airway inflammation via blockade of Src-mediated EGFR transactivation in a murine model of asthma

The angiotensin-(1�7) [Ang-(1�7)]/MAS1 receptor signaling axis is a key endogenous anti-inflammatory signaling pathway. However, the mechanisms by which its mediates the anti-inflammatory effects are not completely understood. Using an allergic murine model of asthma, we investigated whether Ang-1(1�7)/MAS1 receptor axis a): inhibits allergic inflammation via modulation of Src-dependent transactivation of the epidermal growth factor receptor (EGFR) and downstream signaling effectors such as ERK1/2, and b): directly inhibits neutrophil and/or eosinophil chemotaxis ex vivo. Ovalbumin (OVA)-induced allergic inflammation resulted in increased phosphorylation of Src kinase, EGFR, and ERK1/2. In addition, OVA challenge increased airway cellular influx, perivascular and peribronchial inflammation, fibrosis, goblet cell hyper/metaplasia and airway hyperresponsiveness (AHR). Treatment with Ang-(1�7) inhibited phosphorylation of Src kinase, EGFR, ERK1/2, the cellular and histopathological changes and AHR. Ang-(1�7) treatment also inhibited neutrophil and eosinophil chemotaxis ex vivo. These changes were reversed following pretreatment with A779. These data show that the anti-inflammatory actions of Ang-(1�7)/ MAS1 receptor axis are mediated, at least in part, via inhibition of Src-dependent transactivation of EGFR and downstream signaling molecules such as ERK1/2. This study therefore shows that inhibition of the Src/EGRF/ERK1/2 dependent signaling pathway is one of the mechanisms by which the Ang-(1�7)/ MAS1 receptor axis mediates it anti-inflammatory effects in diseases such as asthma. - 2019 El-Hashim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.This study was supported by Kuwait University Research Sector - grant # PT01/12. Parts of this work were supported by the research grant # SRUL02/12 to the Research Unit for Genomics, Proteomics and Cellomics Studies through the Research Core Facility. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors are thankful to the support of Mr. Sunny Ojoko and Mr. Hecktor Velasco from the Animal Resources Center of Health Sciences Center. The authors are also very grateful to Dr. Ananthalakshmi KV, Ms. Sowmya Balakrishnan and Ms. Preethi Tobin for their excellent work with the immunofluorescence studies and histological studies.Scopu

NLRP3 inflammasome plays a key role in the regulation of intestinal homeostasis.

BACKGROUND:: Attenuated innate immune responses to the intestinal microbiota have been linked to the pathogenesis of Crohn's disease (CD). Recent genetic studies have revealed that hypofunctional mutations of NLRP3, a member of the NOD-like receptor (NLR) superfamily, are associated with an increased risk of developing CD. NLRP3 is a key component of the inflammasome, an intracellular danger sensor of the innate immune system. When activated, the inflammasome triggers caspase-1-dependent processing of inflammatory mediators, such as IL-1β and IL-18. METHODS:: In the current study we sought to assess the role of the NLRP3 inflammasome in the maintenance of intestinal homeostasis through its regulation of innate protective processes. To investigate this role, Nlrp3(-/-) and wildtype mice were assessed in the dextran sulfate sodium and 2,4,6-trinitrobenzenesulfonic acid models of experimental colitis. RESULTS:: Nlrp3(-/-) mice were found to be more susceptible to experimental colitis, an observation that was associated with reduced IL-1β, reduced antiinflammatory cytokine IL-10, and reduced protective growth factor TGF-β. Macrophages isolated from Nlrp3(-/-) mice failed to respond to bacterial muramyl dipeptide. Furthermore, Nlrp3-deficient neutrophils exhibited reduced chemotaxis and enhanced spontaneous apoptosis, but no change in oxidative burst. Lastly, Nlrp3(-/-) mice displayed altered colonic β-defensin expression, reduced colonic antimicrobial secretions, and a unique intestinal microbiota. CONCLUSIONS:: Our data confirm an essential role for the NLRP3 inflammasome in the regulation of intestinal homeostasis and provide biological insight into disease mechanisms associated with increased risk of CD in individuals with NLRP3 mutations. (Inflamm Bowel Dis 2010)