Mechanism Elucidation of High-Pressure Generation in Cellular Metal at High-Velocity Impact

Cellular metals exhibit diverse properties, depending on their geometries and base materials. This study investigated the mechanism of high-pressure generation during the high-velocity impact of unidirectional cellular (UniPore) materials. Cubic UniPore copper samples were mounted on a projectile and subjected to impact loading using a powder gun to induce direct impact of samples. The specimens exhibited a unique phenomenon of high-pressure generation near the pores during compression. We elucidate the mechanism of the high-pressure phenomenon and discuss the pore geometries that contribute to the generation of high pressures.

Intracellular Accumulation of Staphylopine Can Sensitize Staphylococcus aureus to Host-Imposed Zinc Starvation by Chelation-Independent Toxicity

ABSTRACT The host restricts the availability of zinc to prevent infection. To overcome this defense, Staphylococcus aureus and Pseudomonas aeruginosa rely on zincophore-dependent zinc importers. Synthesis of the zincophore staphylopine by S. aureus and its import are both necessary for the bacterium to cause infection. In this study, we sought to elucidate how loss of zincophore efflux impacts bacterial resistance to host-imposed zinc starvation. In culture and during infection, mutants lacking CntE, the staphylopine efflux pump, were more sensitive to zinc starvation imposed by the metal-binding immune effector calprotectin than those lacking the ability to import staphylopine. However, disruption of staphylopine synthesis reversed the enhanced sensitivity phenotype of the ΔcntE mutant to calprotectin, indicating that intracellular toxicity of staphylopine is more detrimental than the impaired ability to acquire zinc. Unexpectedly, intracellular accumulation of staphylopine does not increase the expression of metal importers or alter cellular metal concentrations, suggesting that, contrary to prevailing models, the toxicity associated with staphylopine is not strictly due to intracellular chelation of metals. As P. aeruginosa and other pathogens produce zincophores with similar chemistry, our observations on the crucial importance of zincophore efflux are likely to be broadly relevant. IMPORTANCE Staphylococcus aureus and many other bacterial pathogens rely on metal-binding small molecules to obtain the essential metal zinc during infection. In this study, we reveal that export of these small molecules is critical for overcoming host-imposed metal starvation during infection and prevents toxicity due to accumulation of the metal-binding molecule within the cell. Surprisingly, we found that intracellular toxicity of the molecule is not due to chelation of cellular metals.

A novel calcium-concentrating compartment drives biofilm formation and persistent infections

Bacterial biofilms produce a robust internal mineral layer, composed of calcite, which strengthens the colony and protects the residing bacteria from antibiotics. In this work, we provide evidence that the assembly of a functional mineralized macro-structure begins with mineral precipitation within a defined cellular compartment in a differentiated subpopulation of cells. Transcriptomic analysis of a model organism, Bacillus subtilis, revealed that calcium was essential for activation of the biofilm state, and highlighted the role of cellular metal homeostasis and carbon metabolism in biomineralization. The molecular mechanisms promoting calcite formation were conserved in pathogenic Pseudomonas aeruginosa biofilms, resulting in formation of calcite crystals tightly associated with bacterial cells in sputum samples collected from cystic fibrosis patients. Biomineralization inhibitors targeting calcium uptake and carbonate accumulation significantly reduced the damage inflicted by P. aeruginosa biofilms to lung tissues. Therefore, better understanding of the conserved molecular mechanisms promoting biofilm calcification can path the way to the development of novel classes of antibiotics to combat otherwise untreatable biofilm infections.

CALCIUM AND IRON ABSORPTION: INVITRO STUDIES

Studies on human subjects have shown that Ca (Ca) will inhibit iron (Fe) absorption, regardless of whether or not it's given as Ca salts or in dairy farm products. This has caused concern as increased Ca intake usually is usually recommended for kids and girls, similar populations that are in danger of metal deficiency. However, a radical review of studies on humans during which Ca intake was considerably increased for long periods shows no changes in hematologic measures or indicators of iron standing. Thus, the repressing impact additionally be|is also} of short period and there also is also counteractive mechanisms. The interaction between Ca and metal is also a lumenal event, poignant metal uptake through DMT1 (divalent metal transporter 1) at the top membrane. However, it's additionally attainable that inhibition happens throughout metal transfer into circulation, suggesting roles for the serosal bourgeois ferroportin (FPN) and hephaestin. We explored these prospects in human enteral Caco-2 cells cultivated in monolayers. Iron transport (fifty nine Fe) and expression of DMT1, FPN, and hephaestin were assessed when one.5 and four hours with zero or a hundred μM CaCl 2. though Ca failed to have an effect on metal uptake or DMT1 expression at one.5 hours, FPN abundance at the basolateral membrane remittent, leading to increased cellular metal retention and remittent metal efflux. when four hours, DMT1 and FPN expression increased and there was an increased FPN.