Sec-Lib: Protecting Scholarly Digital Libraries From Infected Papers Using Active Machine Learning Framework

Researchers from academia and the corporate-sector rely on scholarly digital libraries to access articles. Attackers take advantage of innocent users who consider the articles\u27 files safe and thus open PDF-files with little concern. In addition, researchers consider scholarly libraries a reliable, trusted, and untainted corpus of papers. For these reasons, scholarly digital libraries are an attractive-target and inadvertently support the proliferation of cyber-attacks launched via malicious PDF-files. In this study, we present related vulnerabilities and malware distribution approaches that exploit the vulnerabilities of scholarly digital libraries. We evaluated over two-million scholarly papers in the CiteSeerX library and found the library to be contaminated with a surprisingly large number (0.3-2%) of malicious PDF documents (over 55% were crawled from the IPs of US-universities). We developed a two layered detection framework aimed at enhancing the detection of malicious PDF documents, Sec-Lib, which offers a security solution for large digital libraries. Sec-Lib includes a deterministic layer for detecting known malware, and a machine learning based layer for detecting unknown malware. Our evaluation showed that scholarly digital libraries can detect 96.9% of malware with Sec-Lib, while minimizing the number of PDF-files requiring labeling, and thus reducing the manual inspection efforts of security-experts by 98%

Type Three Secretion System-Dependent Microvascular Thrombosis and Ischemic Enteritis in Human Gut Xenografts Infected with Enteropathogenic Escherichia coli

Enteropathogenic Escherichia coli (EPEC) is a leading cause of severe intestinal disease and infant mortality in developing countries. Virulence is mediated by a type three secretion system (T3SS), causing the hallmark attaching and effacing (AE) lesions and actin-rich pedestal formation beneath the infecting bacteria on the apical surface of enterocytes. EPEC is a human-specific pathogen whose pathogenesis cannot be studied in animal models. We therefore established an EPEC infection model in human gut xenografts in SCID mice and used it to study the role of T3SS in the pathogenesis of the disease. Following EPEC O127: H6 strain E2348/69 infection, T3SS-dependent AE lesions and pedestals were demonstrated in all infected xenografts. We report here the development of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis in similar to 50% of infected human gut xenografts. Using species-specific CD31 immunostaining, we showed that iTMA was limited to the larger human-mouse chimeric blood vessels, which are located between the muscularis mucosa and circular muscular layer of the human gut. These blood vessels were massively invaded by bacteria, which adhered to and formed pedestals on endothelial cells and aggregated with mouse neutrophils in the lumen. We conclude that endothelial infection, iTMA, and ischemic enteritis might be central mechanisms underlying severe EPEC-mediated disease

Cold Forming of Al-TiB2 Composites Fabricated by SPS: A Computational Experimental Study

The mechanical response and failure of Al-TiB2 composites fabricated by Spark Plasma Sintering (SPS) were investigated. The effective flow stress at room temperature for different TiB2 particle volume fractions between 0% and 15% was determined using compression experiments on cylindrical specimens in conjunction with an iterative computational methodology. A different set of experiments on tapered specimens was used to validate the effective flow curves by comparing experimental force–displacement curves and deformation patterns to the ones obtained from the computations. Using a continuum damage mechanics approach, the experiments were also used to construct effective failure curves for each material composition. It was demonstrated that the fracture modes observed in the different experiments could be reproduced in the computations. The results show that increasing the TiB2 particle volume fraction to 10% results in an increase in material effective yield stress and a decrease in hardening. For a particle volume fraction of 15%, the effective yield stress decreases with no significant influence on the hardening slope. The ductility (workability) of the composite decreases with increasing particle volume fraction

Modeling SARS-CoV-2 Infection in Mice Using Lentiviral hACE2 Vectors Infers Two Modes of Immune Responses to SARS-CoV-2 Infection

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused a severe global pandemic. Mice models are essential to investigate infection pathology, antiviral drugs, and vaccine development. However, wild-type mice lack the human angiotensin-converting enzyme 2 (hACE2) that mediates SARS-CoV-2 entry into human cells and consequently are not susceptible to SARS-CoV-2 infection. hACE2 transgenic mice could provide an efficient COVID-19 model, but are not always readily available, and practically restricted to specific strains. Therefore, there is a dearth of additional mouse models for SARS-CoV-2 infection. We applied lentiviral vectors to generate hACE2 expression in interferon receptor knock-out (IFNAR1−/−) mice. Lenti-hACE2 transduction supported SARS-CoV-2 replication in vivo, simulating mild acute lung disease. Gene expression analysis revealed two modes of immune responses to SARS-CoV-2 infection: one in response to the exposure of mouse lungs to SARS-CoV-2 particles in the absence of productive viral replication, and the second in response to productive SARS-CoV-2 infection. Our results infer that immune response to immunogenic elements on incoming virus or in productively infected cells stimulate diverse immune effectors, even in absence of type I IFN signaling. Our findings should contribute to a better understanding of the immune response triggered by SARS-CoV-2 and to further elucidate COVID-19