Machine Learning-Based Methods for Enhancement of UAV-NOMA and D2D Cooperative Networks.

The cooperative aerial and device-to-device (D2D) networks employing non-orthogonal multiple access (NOMA) are expected to play an essential role in next-generation wireless networks. Moreover, machine learning (ML) techniques, such as artificial neural networks (ANN), can significantly enhance network performance and efficiency in fifth-generation (5G) wireless networks and beyond. This paper studies an ANN-based unmanned aerial vehicle (UAV) placement scheme to enhance an integrated UAV-D2D NOMA cooperative network.

Nanosized Drug Delivery Systems in Gastrointestinal Targeting: Interactions with Microbiota.

The new age of nanotechnology has signaled a stream of entrepreneurial possibilities in various areas, form industry to medicine. Drug delivery has benefited the most by introducing nanostructured systems in the transport and controlled release of therapeutic molecules at targeted sites associated with a particular disease. As many nanosized particles reach the gastrointestinal tract by various means, their interactions with the molecular components of this highly active niche are intensively investigated.

Microglial brain region-dependent diversity and selective regional sensitivities to aging.

Microglia have critical roles in neural development, homeostasis and neuroinflammation and are increasingly implicated in age-related neurological dysfunction. Neurodegeneration often occurs in disease-specific, spatially restricted patterns, the origins of which are unknown. We performed to our knowledge the first genome-wide analysis of microglia from discrete brain regions across the adult lifespan of the mouse, and found that microglia have distinct region-dependent transcriptional identities and age in a regionally variable manner.

Host microbe interactions: a licence to interfere?

Through many millennia of continuous evolution hosts and microorganisms have developed sophisticated and sometimes extremely complex mechanisms of coexisting through symbiosis and mutualism. It is now known that in humans, the population of commensal bacteria on or inside the body significantly outnumbers the host cells. Despite their numerical superiority, microorganisms have adjusted their physiological clocks to benefit themselves and at the same time their host through the maintenance of a healthy state.

Multidirectional chemical signalling between Mammalian hosts, resident microbiota, and invasive pathogens: neuroendocrine hormone-induced changes in bacterial gene expression.

Host-pathogen communication appears to be crucial in establishing the outcome of bacterial infections. There is increasing evidence to suggest that this communication can take place by bacterial pathogens sensing and subsequently responding to host neuroendocrine (NE) stress hormones. Bacterial pathogens have developed mechanisms allowing them to eavesdrop on these communication pathways within their hosts.

Pathogen espionage: multiple bacterial adrenergic sensors eavesdrop on host communication systems.

The interactions between bacterial pathogens and their eukaryotic hosts are vital in determining the outcome of infections. Bacterial pathogens employ molecular sensors to detect and facilitate adaptation to changes in their niche. The sensing of these extracellular signals enables the pathogen to navigate within mammalian hosts.

The bacterial cytoskeleton modulates motility, type 3 secretion, and colonization in Salmonella.

Although there have been great advances in our understanding of the bacterial cytoskeleton, major gaps remain in our knowledge of its importance to virulence. In this study we have explored the contribution of the bacterial cytoskeleton to the ability of Salmonella to express and assemble virulence factors and cause disease. The bacterial actin-like protein MreB polymerises into helical filaments and interacts with other cytoskeletal elements including MreC to control cell-shape.

Interkingdom crosstalk: host neuroendocrine stress hormones drive the hemolytic behavior of Salmonella typhi.

The ability of bacterial pathogens to sense their immediate environment plays a significant role on their capacity to survive and cause disease. Salmonella enterica serovar typhi (S. typhi) is an exclusively human pathogen that causes typhoid fever.

Salmonella Typhi sense host neuroendocrine stress hormones and release the toxin haemolysin E.

Salmonella enterica serovar Typhi (S. typhi) causes typhoid fever. We show that exposure of S.

LuxS-based quorum sensing does not affect the ability of Salmonella enterica serovar Typhimurium to express the SPI-1 type 3 secretion system, induce membrane ruffles, or invade epithelial cells.

Bacterial species can communicate by producing and sensing small autoinducer molecules by a process known as quorum sensing. Salmonella enterica produces autoinducer 2 (AI-2) via the luxS synthase gene, which is used by some bacterial pathogens to coordinate virulence gene expression with population density. We investigated whether the luxS gene might affect the ability of Salmonella enterica serovar Typhimurium to invade epithelial cells.

Genetic detoxification of an aroA Salmonella enterica serovar Typhimurium vaccine strain does not compromise protection against virulent Salmonella and enhances the immune responses towards a protective malarial antigen.

Live Salmonella vaccines are limited in use by the inherent toxicity of the lipopolysaccharide. The waaN gene encodes a myristyl transferase required for the secondary acylation of lipid A in lipopolysaccharide. A waaN mutant exhibits reduced induction of the inflammatory cytokines associated with lipopolysaccharide toxicity.

Role of the universal stress protein UspA of Salmonella in growth arrest, stress and virulence.

Pathogenic bacteria employ a variety of mechanisms to resist a barrage of stresses they encounter during active growth in or outside the host as well as during growth stasis. An in silico screen of the Salmonella genome sequence revealed that Salmonella typhimurium LT2 possesses a homologue belonging to the universal stress protein A (UspA) family. We assessed the transcriptional profile of uspA in S.

Role and regulation of the superoxide dismutases of Staphylococcus aureus.

Staphylococcus aureus has two superoxide dismutases (SODs), encoded by the sodA and sodM genes, which inactivate harmful superoxide radicals () encountered during host infection or generated from aerobic metabolism. The transcriptional start sites have been mapped and expression analysis on reporter fusions in both genes has been carried out. Under standard growth conditions, manganese (Mn), a mineral superoxide scavenger, elevated total SOD activity but had no effect on the transcription of either gene.

Manganese: elemental defence for a life with oxygen.

The presence of enzymes such as catalase, peroxidase and superoxide dismutase (SOD) obviates the problems associated with life in an aerobic environment by eliminating the harmful reactive oxygen species (ROS) that arise from respiration. Enzymic detoxification of ROS might not, however, be the only mechanism at work in bacteria. The accumulation of manganese (Mn), an abundant element in many environments, via several, recently identified transporters is thought to form the basis for an alternative, catalytic detoxification of ROS.