A critical review on the performance of pile-supported rail embankments under cyclic loading: Numerical modeling approach

Searching for economical and practical solutions to increase any transport substructures protection and stability is critical for ensuring the long-term viability and adequate load-bearing capacity. Piles are increasingly being used as an economical and environmentally sustainable solution to enhance the strength of soft subgrade soils on which embankments are raised. As per the available literature, there are two main strategies used to explain railway embankments performance: experimental approaches and numerical simulations on a broad scale. The purpose of this study is to examine the state-of-the-art literature on numerical modeling methods adopted to assess the performance of pile-supported rail embankments subjected to cyclic loading. The paper addresses the main results from various numerical methods to explain the appropriate mechanisms associated with the load deformation response. It also presents the key issues and drawbacks of these numerical methods concerning rail embankment development while outlining the specific shortcomings and research gaps relevant to enhanced future design and analysis. (c) 2021 by the authors. Licensee MDPI, Basel, Switzerland

An adaptive distributed Intrusion detection system architecture using multi agents

Intrusion detection systems are used for monitoring the network data, analyze them and find the intrusions if any. The major issues with these systems are the time taken for analysis, transfer of bulk data from one part of the network to another, high false positives and adaptability to the future threats. These issues are addressed here by devising a framework for intrusion detection. Here, various types of co-operating agents are distributed in the network for monitoring, analyzing, detecting and reporting. Analysis and detection agents are the mobile agents which are the primary detection modules for detecting intrusions. Their mobility eliminates the transfer of bulk data for processing. An algorithm named territory is proposed to avoid interference of one analysis agent with another one. A communication layout of the analysis and detection module with other modules is depicted. The inter-agent communication reduces the false positives significantly. It also facilitates the identification of distributed types of attacks. The co-ordinator agents log various events and summarize the activities in its network. It also communicates with co-ordinator agents of other networks. The system is highly scalable by increasing the number of various agents if needed. Centralized processing is avoided here to evade single point of failure. We created a prototype and the experiments done gave very promising results showing the effectiveness of the system

Establishing a COVID-19 lemmatized word list for journalists and ESP learners

The aim of this research is two-fold; first, to explore the most frequent COVID-19 inspired words in medical news reporting contexts, and second, to classify them into different categories. This paper adopts a corpus-based approach to build a lemmatized academic word list (AWL) inspired by the COVID-19 pandemic. Factiva was used to retrieve the pandemic-related articles published in News Rx from January 1 - October 31, 2020. A total number of 18,249,093-word corpus was compiled. The corpus linguistic software program Wordsmith (WS-6) (Scott, 2012) was used to generate a word list based on the complied corpus. Subsequent to compiling, lemmatizing, and analyzing the AWL, six categories were identified, namely, acronyms and abbreviation, diseases, COVID-19, biology, medicine, and scientific disciplines, all of which are of essential use for media workers, ESP learners of journalism, medicine, nursing, pharmacy, and allied health sciences. Building such a discipline-specific glossary will be of special pedagogical value for health journalists, textbook writers and curriculum designers, instructors, and ESP learners in the health sciences field. One of the major contributions of this research is establishing lemmas of a large set of AWL. This set can be utilized by news media workers, health communication specialists, and ESP learners. Lemmatization will ensure rapid dissemination of the word list and its integration in the linguistic system through derivation and other word-formation processes

Identification of Genes and Pathways Regulated by Lamin A in Heart

Background Mutations in the LMNA gene, encoding LMNA (lamin A/C), causes distinct disorders, including dilated cardiomyopathies, collectively referred to as laminopathies. The genes (coding and noncoding) and regulatory pathways controlled by LMNA in the heart are not completely defined. Methods and Results We analyzed cardiac transcriptome from wild-type, loss-of-function (Lmna-/-), and gain-of-function (Lmna-/- injected with adeno-associated virus serotype 9 expressing LMNA) mice with normal cardiac function. Deletion of Lmna (Lmna-/-) led to differential expression of 2193 coding and 629 long noncoding RNA genes in the heart (q<0.05). Re-expression of LMNA in the Lmna-/- mouse heart, completely rescued 501 coding and 208 non-coding and partially rescued 1862 coding and 607 lncRNA genes. Pathway analysis of differentially expressed genes predicted activation of transcriptional regulators lysine-specific demethylase 5A, lysine-specific demethylase 5B, tumor protein 53, and suppression of retinoblastoma 1, paired-like homeodomain 2, and melanocyte-inducing transcription factor, which were completely or partially rescued upon reexpression of LMNA. Furthermore, lysine-specific demethylase 5A and 5B protein levels were increased in the Lmna-/- hearts and were partially rescued upon LMNA reexpression. Analysis of biological function for rescued genes identified activation of tumor necrosis factor-α, epithelial to mesenchymal transition, and suppression of the oxidative phosphorylation pathway upon Lmna deletion and their restoration upon LMNA reintroduction in the heart. Restoration of the gene expression and transcriptional regulators in the heart was associated with improved cardiac function and increased survival of the Lmna-/- mice. Conclusions The findings identify LMNA-regulated cardiac genes and their upstream transcriptional regulators in the heart and implicate lysine-specific demethylase 5A and B as epigenetic regulators of a subset of the dysregulated genes in laminopathies

Unveiling the interplay between NSAID-induced dysbiosis and autoimmune liver disease in children: insights into the hidden gateway to autism spectrum disorders. Evidence from ex vivo, in vivo, and clinical studies

Autism spectrum disorders (ASD) represent a diverse group of neuropsychiatric conditions, and recent evidence has suggested a connection between ASD and microbial dysbiosis. Immune and gastrointestinal dysfunction are associated with dysbiosis, and there are indications that modulating the microbiota could improve ASD-related behaviors. Additionally, recent findings highlighted the significant impact of microbiota on the development of autoimmune liver diseases, and the occurrence of autoimmune liver disease in children with ASD is noteworthy. In the present study, we conducted both an in vivo study and a clinical study to explore the relationship between indomethacin-induced dysbiosis, autoimmune hepatitis (AIH), and the development of ASD. Our results revealed that indomethacin administration induced intestinal dysbiosis and bacterial translocation, confirmed by microbiological analysis showing positive bacterial translocation in blood cultures. Furthermore, indomethacin administration led to disturbed intestinal permeability, evidenced by the activation of the NLRP3 inflammasomes pathway and elevation of downstream biomarkers (TLR4, IL18, caspase 1). The histological analysis supported these findings, showing widened intestinal tight junctions, decreased mucosal thickness, inflammatory cell infiltrates, and collagen deposition. Additionally, the disturbance of intestinal permeability was associated with immune activation in liver tissue and the development of AIH, as indicated by altered liver function, elevated ASMA and ANA in serum, and histological markers of autoimmune hepatitis. These results indicate that NSAID-induced intestinal dysbiosis and AIH are robust triggers for ASD existence. These findings were further confirmed by conducting a clinical study that involved children with ASD, autoimmune hepatitis (AIH), and a history of NSAID intake. Children exposed to NSAIDs in early life and complicated by dysbiosis and AIH exhibited elevated serum levels of NLRP3, IL18, liver enzymes, ASMA, ANA, JAK1, and IL6. Further, the correlation analysis demonstrated a positive relationship between the measured parameters and the severity of ASD. Our findings suggest a potential link between NSAIDs, dysbiosis-induced AIH, and the development of ASD. The identified markers hold promise as indicators for early diagnosis and prognosis of ASD. This research highlights the importance of maintaining healthy gut microbiota and supports the necessity for further investigation into the role of dysbiosis and AIH in the etiology of ASD.Peer Reviewe

Atomic Resonance and Scattering

Contains reports on six research projects.National Science Foundation (PHY83-06273)Joint Services Electronics Program (DAAL03-86-K-0002)National Science Foundation (PHY84-11483)U.S. Navy-Office of Naval Research (Grant N00014-79-C-0183)Joint Services Electronics Program (Contract DAAG29-83-K-0003)National Science Foundation (Grant PHY83-07172-A01)U.S. Navy - Office of Naval Research (Grant N00014-83-K-0695)National Science Foundation (Grant CHE84-21392

Atomic Resonance and Scattering

Contains reports on six research projects.National Science Foundation (Grant PHY 83-06273)U.S. Navy - Office of Naval Research (Contract N00014-79-C-0183)Joint Services Electronics Program (Contract DAALO03-86-K-0002)National Science Foundation (Grant PHY 84-11483)National Science Foundation (Grant PHY 86-05893)National Science Foundation (Grant ECS 84-21392)U.S. Navy - Office of Naval Research (Contract N00014-83-K-0695)National Science Foundation (Grant CHE 84-21392

Atomic Resonance and Scattering

Contains reports on nine research projects.National Science Foundation (Grant PHY79-09743)National Science Foundation (Grant PHY82-10486)Joint Services Electronics Program (Contract DAAG29-83-K-0003)U.S. Navy - Office of Naval Research (Contract N00014-79-C-0183)National Bureau of Standards (Grant NB83-NAHA-4058)National Science Foundation (Grant CHE79-02967-A04)National Science Foundation (Grant PHY83-07172)Joint Services Electronics Program (Grant DAAG29-83-K-0003

Atomic Resonance and Scattering

Contains reports on eight research projects.National Science Foundation (Grant PHY83-06273)National Bureau of Standards (Grant NB83-NAHA-4058)National Science Foundation (Grant PHY84-11483)Joint Services Electronics Program (Contract DAAG29-83-K-0003)U.S. Navy - Office of Naval Research (Contract NO0014-79-C-0183)U.S. Navy - Office of Naval Research (Contract N00014-83-K-0695)National Science Foundation (Grant PHY83-07172-A01

Unveiling the interplay between NSAID-induced dysbiosis and autoimmune liver disease in children: insights into the hidden gateway to autism spectrum disorders. Evidence from ex vivo, in vivo, and clinical studies

Autism spectrum disorders (ASD) represent a diverse group of neuropsychiatric conditions, and recent evidence has suggested a connection between ASD and microbial dysbiosis. Immune and gastrointestinal dysfunction are associated with dysbiosis, and there are indications that modulating the microbiota could improve ASD-related behaviors. Additionally, recent findings highlighted the significant impact of microbiota on the development of autoimmune liver diseases, and the occurrence of autoimmune liver disease in children with ASD is noteworthy. In the present study, we conducted both an in vivo study and a clinical study to explore the relationship between indomethacin-induced dysbiosis, autoimmune hepatitis (AIH), and the development of ASD. Our results revealed that indomethacin administration induced intestinal dysbiosis and bacterial translocation, confirmed by microbiological analysis showing positive bacterial translocation in blood cultures. Furthermore, indomethacin administration led to disturbed intestinal permeability, evidenced by the activation of the NLRP3 inflammasomes pathway and elevation of downstream biomarkers (TLR4, IL18, caspase 1). The histological analysis supported these findings, showing widened intestinal tight junctions, decreased mucosal thickness, inflammatory cell infiltrates, and collagen deposition. Additionally, the disturbance of intestinal permeability was associated with immune activation in liver tissue and the development of AIH, as indicated by altered liver function, elevated ASMA and ANA in serum, and histological markers of autoimmune hepatitis. These results indicate that NSAID-induced intestinal dysbiosis and AIH are robust triggers for ASD existence. These findings were further confirmed by conducting a clinical study that involved children with ASD, autoimmune hepatitis (AIH), and a history of NSAID intake. Children exposed to NSAIDs in early life and complicated by dysbiosis and AIH exhibited elevated serum levels of NLRP3, IL18, liver enzymes, ASMA, ANA, JAK1, and IL6. Further, the correlation analysis demonstrated a positive relationship between the measured parameters and the severity of ASD. Our findings suggest a potential link between NSAIDs, dysbiosis-induced AIH, and the development of ASD. The identified markers hold promise as indicators for early diagnosis and prognosis of ASD. This research highlights the importance of maintaining healthy gut microbiota and supports the necessity for further investigation into the role of dysbiosis and AIH in the etiology of ASD