Moserhigh4698

These results indicate that nickel-induced cytotoxicity of astrocytes is mediated by the activation of apoptotic pathway and disruption of cell cycle regulation.Regulatory protein genes and microRNAs (miRNAs) play important roles in response to abiotic and biotic stress, and the biosynthesis of secondary metabolites in plants. However, their responses to selenium (Se) stimuli have not been comprehensively studied in Pueraria lobata (Willd.) Ohwi, a selenocompound-rich medicinal and edible plant. In this study, we identified a total of 436/556/1161/624 transcription factors, 134/157/308/172 transcriptional regulators, and 341/456/250/518 protein kinases, which were co-expressed with at least one selenocompound-related structural gene/sulfate transporter or phosphate transporter/reactive oxygen species (ROS) scavenging structural gene/isoflavone-related structural gene, respectively. Then, we identified a total of 87 expressed miRNAs by Se disposure, in which 11 miRNAs, including miR171f-3p, miR390b-3P, miR-N111b, miR-N118, miR-N30, miR-N38-3P, miR-N61a, miR-N61b, miR-N80-3p, miR-N84-3P, and miR-N90.2-3P, were significantly upregulated. We also identified a total of 1172 target genes for the 87 expressed miRNAs. Gene Ontology enrichment analysis of these target genes showed that regulation of transcription, DNA-templated, integral component of membrane, nucleus, ATP binding, and plasma membrane are the top five subclassifications. Finally, we revealed that 5 miRNAs targeted 10 regulatory protein genes, which are highly correlated with at least one selenocompound-related structural gene or transporter gene; 5 miRNAs targeted 10 regulatory protein genes, which are highly correlated with at least one ROS scavenging structural gene; and 5 miRNAs targeted 9 regulatory protein genes, which are potentially involved in the isoflavone biosynthesis. Overall, the study provides us the comprehensive insight into the roles of regulatory proteins and miRNAs in response to Se stimuli in P. lobata.The antibacterial properties of silver have been known for centuries and the threat of antibiotic-resistant bacteria has led to renewed focus on the noble metal. Silver is now commonly included in a range of household and medical items to imbue them with bactericidal properties. Despite this, the chemical fate of the metal in biological systems is poorly understood. Selleckchem Canagliflozin Silver(I) is a soft metal with high affinity for soft donor atoms and displays much similarity to the chemistry of Cu(I). In bacteria, interaction of silver with the cell wall/membrane, DNA, and proteins and enzymes can lead to cell death. Additionally, the intracellular generation of reactive oxygen species by silver is posited to be a significant antimicrobial action. While the antibacterial action of silver is well known, bacteria found in silver mines display resistance against it through use of a protein ensemble thought to have been specifically developed for the metal, highlighting the need for judicious use. In mammals, ∼10-20% of ingested silver is retained by the body and thought to predominantly localize in the liver or kidneys. Chronic exposure can result in argyria, a condition characterized by blue staining of the skin, resulting from subdermal deposition of silver [as Ag(0)/sulfides], but more insidious side effects, such as inclusions in the brain, seizures, liver/kidney damage, and immunosuppression, have also been reported. Here, we hope to highlight the current understanding of the biological chemistry of silver and the necessity for continued study of these systems to fill existing gaps in knowledge.Cerium (Ce) is a rare earth element that is incorporated in numerous consumer products, either in its cationic form or as engineered nanoparticles (ENPs). Given the propensity of small oxide particles to dissolve, it is unclear whether biological responses induced by ENPs will be due to the nanoparticles themselves or rather due to their dissolution. This study provides the foundation for the development of transcriptomic biomarkers that are specific for ionic Ce in the freshwater alga, Chlamydomonas reinhardtii, exposed either to ionic Ce or to two different types of small Ce ENPs (uncoated, ∼10 nm, or citrate-coated, ∼4 nm). Quantitative reverse transcription PCR was used to analyse mRNA levels of four ionic Ce-specific genes (Cre17g.737300, MMP6, GTR12, and HSP22E) that were previously identified by whole transcriptome analysis in addition to two oxidative stress biomarkers (APX1 and GPX5). Expression was characterized for exposures to 0.03-3 µM Ce, for 60-360 min and for pH 5.0-8.0. Near-linear concentration-response curves were obtained for the ionic Ce and as a function of exposure time. Some variability in the transcriptomic response was observed as a function of pH, which was attributed to the formation of metastable Ce species in solution. Oxidative stress biomarkers analysed at transcriptomic and cellular levels confirmed that different effects were induced for dissolved Ce in comparison to Ce ENPs. The measured expression levels confirmed that changes in Ce speciation and the dissolution of Ce ENPs greatly influence Ce bioavailability.Epsilonproteobacteria are a diverse class of eubacteria within the Proteobacteria phylum that includes environmental sulfur-reducing bacteria and the human pathogens, Campylobacter jejuni and Helicobacter pylori. These pathogens infect and proliferate within the gastrointestinal tracts of multiple animal hosts, including humans, and cause a variety of disease outcomes. While infection of these hosts provides nutrients for the pathogenic Epsilonproteobacteria, many hosts have evolved a variety of strategies to either sequester metals from the invading pathogen or exploit the toxicity of metals and drive their accumulation as an antimicrobial strategy. As a result, C. jejuni and H. pylori have developed mechanisms to sense changes in metal availability and regulate their physiology in order to respond to either metal limitation or accumulation. In this review, we will discuss the challenges of metal availability at the host-pathogen interface during infection with C. jejuni and H. pylori and describe what is currently known about how these organisms alter their gene expression and/or deploy bacterial virulence factors in response to these environments.