Influence of the Pecking Motion Frequency on the Cyclic Fatigue Resistance of Endodontic Rotary Files

Purpose: To analyze the influence of the pecking motion frequency on the cyclic fatigue resistance of endodontic rotary files. Material and Methods: Sixty PlexV 25.06 endodontic rotary files were selected and distributed into three groups: 30 movements/min (n = 20), 60 movements/min (n = 20), and 120 movements/min (n = 20). A dynamic cyclic fatigue device was designed using Computer Aided Design/ Computer Aided Engineering (CAD/CAE) technology and manufactured by 3D impressions to simulate the pecking motion performed by an operator. Failures of the endodontic rotary files were detected by a Light-Emitting Diode (LED)/Light-Dependent Resistor (LDR) system controlled by an Arduino-Driver complex and management software. Endodontic rotary files were tested on an artificial root canal manufactured by wire electrical discharge machining (EDM), with similar dimensions to those of the instrument under examination. Endodontic rotary files were used following the manufacturer's recommendations. The results were analyzed by ANOVA and Weibull statistics. Results: All pairwise comparisons revealed statistically significant differences in all three variables, except for the difference in the number of cycles between the groups with 60 and 120 movements/min (p = 0.298). The scale distribution parameter of Weibull statistics showed statistically significant differences in all three variables, except for the differences in the number of cycles between groups with 30 and 60 movements/min (p = 0.0722). No statistically significant differences in the three variables were observed for the shape distribution parameter. Conclusion: A low frequency of pecking motion is recommended to reduce the risk of failure of endodontic rotary files associated with cyclic fatigue

Changes in lipid metabolism driven by steroid signalling modulate proteostasis in C. elegans

Alzheimer's, Parkinson's and Huntington's diseases can be caused by mutations that enhance protein aggregation, but we still do not know enough about the molecular players of these pathways to develop treatments for these devastating diseases. Here, we screen for mutations that might enhance aggregation in Caenorhabditis elegans, to investigate the mechanisms that protect against dysregulated homeostasis. We report that the stomatin homologue UNC-1 activates neurohormonal signalling from the sulfotransferase SSU-1 in ASJ sensory/endocrine neurons. A putative hormone, produced in ASJ, targets the nuclear receptor NHR-1, which acts cell autonomously in the muscles to modulate polyglutamine repeat (polyQ) aggregation. A second nuclear receptor, DAF-12, functions oppositely to NHR-1 to maintain protein homeostasis. Transcriptomics analyses of unc-1 mutants revealed changes in the expression of genes involved in fat metabolism, suggesting that fat metabolism changes, controlled by neurohormonal signalling, contribute to protein homeostasis. Furthermore, the enzymes involved in the identified signalling pathway are potential targets for treating neurodegenerative diseases caused by disrupted protein homeostasis.Peer reviewe