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Iron overload affects the cell cycle of various cell types, but the effect of iron overload on human pluripotent stem cells (hPSCs) has not yet been reported. Here, we show that the proliferation capacities of human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) were significantly inhibited by ferric ammonium citrate (FAC) in a concentration-dependent manner. Additionally, deferoxamine (DFO) protected hESCs/hiPSCs against FAC-induced cell cycle arrest. However, iron overload did not affect pluripotency in hESCs/hiPSCs. Further, treatment of hiPSCs with FAC resulted in excess reactive oxygen species production and DNA damage. Collectively, our findings provide new insights into the role of iron homeostasis in the maintenance of self-renewal in hPSCs. © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.Renalase is predominantly expressed in the kidney, where it plays a role in catecholamine metabolism and blood pressure regulation. Moderate-intensity exercise has been shown to increase the concentration of renalase in the blood and to reduce renal function in humans. Moreover, such exercise was also reported to increase catecholamine levels. Here, we examined renalase concentration in the blood and renalase expression levels in different organs after moderate-intensity exercise in rats. Twelve male Wistar rats were made to run on a treadmill (moderate exercise (MEX) group) for 60 min at 20 m/min, after resting for 15 min. The control (CON) group rats were euthanized after resting on the treadmill. Tissue and blood samples were analyzed using western blotting, real-time RT-PCR, and ELISA. Overall, the concentrations of renalase in the blood were significantly higher in the MEX group than that in the CON group. Renalase expression was decreased in the kidney after 60 min of exercise, whereas the expression of renalase mRNA and protein the extensor digitorum longus and plantaris muscles, respectively, increased after exercise. However, the expression of renalase in the other tissues examined did not change after acute exercise. In conclusion, we report that moderate-intensity exercise for 60 min increases both renalase concentration in the blood and its expression in skeletal muscle. © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.Previous reports have shown that ketamine triggered apoptosis in immature developing brain involving mitochondrial-mediated pathways. However, no data for ketamine effects on hippocampal and cortical mitochondrial function are available in prepubertal rats. Twenty-one-day-old Sprague-Dawley rats received ketamine (40 mg/kg i.p.) for 3 days and were killed 24 hr after the last injection. Hippocampal mitochondria from ketamine-treated rats showed decreased malate-glutamate state 4 and 3 respiratory rates and an inhibition in complex I and IV activities. Hippocampal mitochondrial membrane depolarization and mitochondrial permeability transition induction were observed. This was not reflected in an increment of H2 O2 production probably due to increased Mn-SOD and catalase activities, 24 hr after treatment. Interestingly, increased H2 O2 production rates and cardiolipin oxidation were found in hippocampal mitochondria shortly after ketamine treatment (45 min). Unlike the hippocampus, ketamine did not affect mitochondrial parameters in the brain cortex, being the area less vulnerable to suffer ketamine-induced oxidative damage. Results provide evidences that exposure of prepubertal rats to ketamine leads to an induction of mitochondrial ROS generation at early stages of treatment that was normalized by the triggering of antioxidant systems. Although hippocampal mitochondria from prepubertal rats were capable of responding to the oxidative stress, they remain partially dysfunctional. © 2020 ISDN. Published by John Wiley & Sons Ltd.Staphylococcus aureus carries a collection of mobile genetic elements that often harbor virulence and antimicrobial resistance genes. Since the introduction of antibiotics, plasmids have become a major genetic element responsible for the distribution of antimicrobial resistance. Under antimicrobial selection, resistance plasmids are maintained within bacterial populations as a means to ensure survival. However, in the absence of selection, large plasmids can be lost due to the fitness costs associated with harboring these genetic elements. pC02 is a previously identified multidrug resistance, conjugative plasmid that is found in S. aureus. In addition to antibiotic resistance, pC02 also carries genes known to be associated with antiseptic resistance. Among these, we previously characterized the contribution of qacA to pC02 mediated reduced chlorhexidine susceptibility. Herein, we demonstrate that pC02 also mediates triclosan resistance, likely due to the presence of fabI, a known triclosan resistance gene. Moreover, we demonstrate that conjugative transfer of pC02 increases triclosan resistance in recipient cells. Competition assays demonstrated a fitness cost associated with carriage of the large pC02 plasmid. However, subinhibitory concentrations of either chlorhexidine or triclosan abrogated this fitness cost. Given the widespread use of these antiseptics, both of which accumulate in wastewater and other environmental reservoirs, indiscriminate use of antiseptics likely imposes a constant selective pressure that promotes maintenance of antimicrobial resistance factors within S. aureus. Tertiapin-Q purchase © 2020 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.A systematic approach to both diagnosis and investigations is essential, when investigating a patient with a suspected perioperative hypersensitivity reaction. The perioperative setting is extremely complex with documented and undocumented exposures to many different drugs and substances. In addition, the effect of anaesthetic drugs and surgical procedure may mimick hypersensitivity. To ensure that all these complexities are addressed, collaboration between allergist and anaesthetist is essential. Also, the current recommendation is, that investigation of these patients should take place in highly specialized centres or in centres investigating a minimum of 20 patients/year, and where close collaboration between allergists and anaesthetists is established. This article is protected by copyright. All rights reserved.