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Two 2,4,6-trimethylaniline-based trifuloromethanesulfonate (trifluoromethanesulfonate) salts were synthesized and characterized by single-crystal X-ray diffraction. N,2,4,6-Tetramethylanilinium trifluoromethanesulfonate, [C10H14NH2+][CF3O3S−] (1), was synthesized via methylation of 2,4,6-trimethylaniline. N-Isopropylidene-N,2,4,6-tetramethylanilinium trifluoromethanesulfonate, [C13H20N+][CF3O3S−] (2), was synthesized in a two-step reaction where the imine, N-isopropylidene-2,4,6-trimethylaniline, was first prepared via a dehydration reaction to form the Schiff base, followed by methylation using methyl trifluoromethanesulfonate to form the iminium ion. In compound 1, both hydrogen bonding and π–π interactions form the main intermolecular interactions. The primary interaction is a strong N—H...O hydrogen bond with the oxygen atoms of the trifluoromethanesulfonate anions bonded to the hydrogen atoms of the ammonium nitrogen atom to generate a one-dimensional chain. The [C10H14NH2+] cations form dimers where the benzene rings form a π–π interaction with a parallel-displaced geometry. The separation distance between the calculated centroids of the benzene rings is 3.9129 (8) Å, and the interplanar spacing and ring slippage between the dimers are 3.5156 (5) and 1.718 Å, respectively. For 2, the [C13H20N+] cations also form dimers as in 1, but with the benzene rings highly slipped. The distance between the calculated centroids of the benzene rings is 4.8937 (8) Å, and interplanar spacing and ring slippage are 3.3646 (5) and 3.553 Å, respectively. The major intermolecular interactions in 2 are instead a series of weaker C—H...O hydrogen bonds [C...O distances of 3.1723 (17), 3.3789 (18), and 3.3789 (18) Å], an interaction virtually absent in the structure of 1. Fluorine atoms are not involved in strong directional interactions in either structure.

When a material enters the body, it is immediately attacked by hundreds of proteins, organized into complex networks of binding interactions and reactions. How do such complex systems interact with a material, "deciding" whether to attack? We focus on the "complement" system of ∼40 blood proteins that bind microbes, nanoparticles, and medical devices, initiating inflammation. We show a sharp threshold for complement activation upon varying a fundamental material parameter, the surface density of potential complement attachment points. This sharp threshold manifests at scales spanning single nanoparticles to macroscale pathologies, shown here for diverse engineered and living materials. Computational models show these behaviors arise from a minimal subnetwork of complement, manifesting percolation-type critical transitions in the complement response. This criticality switch explains the "decision" of a complex signaling network to interact with a material, and elucidates the evolution and engineering of materials interacting with the body.

Bladder cancer is a histologically and clinically heterogenous disease. Most bladder cancers are urothelial carcinomas, which frequently develop distinct histological subtypes. Several urothelial carcinoma histological subtypes, such as micropapillary, plasmacytoid, small-cell carcinoma and sarcomatoid, show highly aggressive behaviour and pose unique challenges in diagnosis and treatment. Comprehensive genomic characterizations of the urothelial carcinoma subtypes have revealed that they probably arise from a precursor subset of conventional urothelial carcinomas that belong to different molecular subtypes - micropapillary and plasmacytoid subtypes develop along the luminal pathway, whereas small-cell and sarcomatoid subtypes evolve along the basal pathway. The subtypes exhibit distinct genomic alterations, but in most cases their biological properties seem to be primarily determined by specific gene expression profiles, including epithelial-mesenchymal transition, urothelial-to-neural lineage plasticity, and immune infiltration with distinct upregulation of immune regulatory genes. These breakthrough studies have transformed our view of bladder cancer histological subtype biology, generated new hypotheses for therapy and chemoresistance, and facilitated the discovery of new therapeutic targets., (© 2024. Springer Nature Limited.)

Background: Many health professionals report feeling uncomfortable talking with patients who hear voices. Patients who hear voices report feeling a lack of support and empathy from emergency nurses. A local emergency department reported a need for training for nurses in the care of behavioral health patients. Objective: The aim of this study is to implement a quality improvement project using a hearing voices simulation. Empathy was measured using the Toronto Empathy Questionnaire, and a post-intervention survey was used to evaluate emergency nurses' perception of the professional development session. Methods: The quality improvement project included the implementation of a hearing voices simulation with emergency nurses. A paired t -test was used to determine the differences in the nurses empathy levels pre-and post-simulation. Qualitative data was collected on the nurses' experience during the simulation debriefing. A Likert-style questionnaire was used to collect data on the nurses' evaluation of the simulation. Results: The results of the hearing voices simulation were a statistically significant increase ( p < .00) in empathy from baseline ( M = 47.95, SD = 6.55) to post-intervention empathy scores ( M = 48.93, SD = 6.89). The results of the post-simulation survey indicated that nurses felt that the hearing voices simulation was useful ( n = 100; 98%) and helped them to feel more empathetic toward patients who hear voices ( n = 98; 96%). Conclusions: Using a hearing voices simulation may help emergency nurses feel more empathetic toward the behavioral health patients who hear voices. Implications for Nursing: Through the implementation of a hearing voices simulation, clinical staff educators can provide support to staff nurses in the care of behavioral health patients., (© Copyright 2024 Springer Publishing Company, LLC.)