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Cell survival depends on the maintenance of cell homeostasis that involves all the biochemical, genomic and transport processes that take place in all the organelles within a eukaryote cell. In particular, ion homeostasis is required to regulate the membrane potential and solute transport across all membranes, any alteration in these parameters will reflect in the malfunctioning of any organelle, and consequently, in the development of the organism. In plant cells, sodium transporters play a central role in keeping the concentrations of this cation across all membranes under physiological conditions to prevent its toxic effects. HKT transporters are a family of membrane proteins exclusively present in plants, with some homologs present in prokaryotes. HKT transporters have been associated to salt tolerance in plants, retrieving any leak of the cation into the xylem, or removing it from aerial parts, including the flowers, to be transported to the roots along the phloem. This function has been assigned as most of the HKT transporters are located at the plasma membrane. Here, we report the localization of the HKT from Physcomitrium patens to the thylakoid membrane, reminiscent of the prokaryote origin of these family of transporters. Mutation of PpHKT leads to several alterations in the phenotype of the organism, including the lack of sporophyte formation, and changes in expression of many genes. These alterations suggest that the breakdown in chloroplast ion homeostasis triggers a signalling cascade to the nucleus to communicate its status, being important for the moss to complete its life cycle., (© 2025 Society for Experimental Biology and John Wiley & Sons Ltd.)

Cranial radiotherapy can cause lifelong cognitive complications in childhood brain tumor survivors, and reduced hippocampal neurogenesis is hypothesized to contribute to this. Following irradiation (IR), microglia clear dead neural progenitors and give rise to a neuroinflammatory microenvironment, which promotes a switch in surviving progenitors from neuronal to glial differentiation. Recently, depletion and repopulation of microglia were shown to promote neurogenesis and ameliorate cognitive deficits in various brain injury models. In this study, we utilized the Cx3cr1 CreERt2-YFP/+ Rosa26 DTA transgenic mouse model to deplete microglia in the juvenile mouse brain before subjecting them to whole-brain IR and investigated the short- and long-term effects on hippocampal neurogenesis. Within the initial 24 h after IR, the absence of microglia led to an accumulation of dead cells in the subgranular zone, and 50-fold higher levels of the chemokine C-C motif ligand 2 (CCL2) in sham brains and 7-fold higher levels after IR. The absence of microglia, and the subsequent repopulation within 10 days, did neither affect the loss of proliferating or doublecortin-positive cells, nor the reduced growth of the granule cell layer. Our results argue against a role for a pro-inflammatory microenvironment in the dysregulation of hippocampal neurogenesis and suggest that the observed reduction of neurogenesis was solely due to IR./+ transgenic mouse model to deplete microglia in the juvenile mouse brain before subjecting them to whole-brain IR and investigated the short- and long-term effects on hippocampal neurogenesis. Within the initial 24 h after IR, the absence of microglia led to an accumulation of dead cells in the subgranular zone, and 50-fold higher levels of the chemokine C-C motif ligand 2 (CCL2) in sham brains and 7-fold higher levels after IR. The absence of microglia, and the subsequent repopulation within 10 days, did neither affect the loss of proliferating or doublecortin-positive cells, nor the reduced growth of the granule cell layer. Our results argue against a role for a pro-inflammatory microenvironment in the dysregulation of hippocampal neurogenesis and suggest that the observed reduction of neurogenesis was solely due to IR., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: Many hospitals and surgery centers have focused improvement efforts on operating room inefficiencies. A common inefficiency is missing and unusable surgical instrumentation, which can result in case delays and decreased effectiveness. Lean Six Sigma methodology, a set of process improvement tools focused on the reduction of waste and variation, has been used to identify and correct root causes of missing and unusable instrumentation., Methods: An analysis of current operations was performed within the Sterile Processing Department (SPD). The team assessed physical workflows, including decontamination, assembly, sterilization, and sterile storage, as well as digital processes. The team identified five drivers of defects: (1) staffing and training, (2) inventory management, (3) equipment and SPD physical environment, (4) standard workflows and communication, and (5) governance structure. A root cause was established for each driver, and Lean Six Sigma principles were applied. Two metrics were established to assess accuracy and efficiency in the SPD. First pass yield was defined as the proportion of trays processed that were usable after the first cycle. Tray defect rate was defined as the proportion of requested instruments that were missing or unusable., Results: After implementation, the SPD increased first pass yield from 81.0% to 97.4% (p < 0.001) and reduced the defect rate from 2.2% to < 0.10% (p < 0.001) with sustainment for more than a year., Conclusion: Application of Lean Six Sigma methodology improved tray accuracy in a hospital's SPD. It is feasible and beneficial to apply improvement methodology developed for manufacturing in the hospital setting to reduce missing and unusable instrumentation., (Copyright © 2024 The Joint Commission. Published by Elsevier Inc. All rights reserved.)