Aim: The aim of this investigation was to assess the efficacy and force decay of elastomeric chains based on their morphology and elongation extent. Methods: Two-hundred-and-seventy elastics from three companies [Ortho Technology (OT), American Orthodontics (AO), G&H, 10 specimens ×27 subgroups] were elongated to 40%, 60%, and 100% and the initial forces were measured. Then after four weeks of incubation in artificial saliva, the residual forces were measured. Forces and force decays were compared across brands, morphologies, and elongation extents (α, =0. 001). Results: Forces degraded significantly over time (repeated-measures ANOVA, P<0. 001). Significant differences existed among the levels of all parameters, in terms of the initial forces, residual forces, and force degradation (3-way ANOVA, P<0. 001). Results of most of the Tukey post hoc tests were significant (P<0. 001). The longer the elongation extent, the higher the force waste (partial correlation coefficient, r=0. 885, P< 0. 001). Conclusion: Initial force was improved when using the OT brand and closed elastics, and by stretching the elastic to 100%. Force loss was minimized when using the G&H brand and open elastics, and by stretching to 40%. Using the OT brand and closed elastics, and 100% stretching caused the highest residual forces after a month. However, the initial forces provided by the 100% elongations were not sound. Force loss was increased by using the OT brand and closed elastics, and with 100% elongations. The lowest residual forces were seen in the AO brand, long elastics, and those elongated to 40%.

This paper is concerned with investigating the spatial decay estimates for linear demped hyperbolic equations in the space-time region Ώ×(0,∞) where Ώ is the semi-infinite prismatic cylinder.

Objective(s): Haemostasis prevents blood loss following vascular injury. It depends on the unique concert of events involving platelets and specific blood proteins, known as coagulation factors. The clotting system requires precise regulation and coordinated reactions to maintain the integrity of the vasculature. Clotting insufficiency mostly occurs due to genetically inherited coagulation factor deficiencies such as hemophilia.Materials and Methods: A relevant literature search of PubMed was performed using the keywords coagulation factors, Nonsense-mediated mRNA decay and premature translation termination codons. Search limitations included English language and human-based studies.Results: Mutations that cause premature translation termination codons probably account for one-third of genetically inherited diseases. Transcripts bearing aberrant termination codons are selectively identified and eliminated by an evolutionarily conserved posttranscriptional pathway known as nonsense-mediated mRNA decay (NMD). There are many pieces of evidence of decay among coagulation factor genes. However, the hemophilia gene (F8) does not seem to be subjected to NMD. Since the F8 gene is located on the X-chromosome, a connection between X-linked traits and mRNA decay could be assumed.Conclusion: Considering that not all genes go through decay, this review focuses on the basics of the mechanism in coagulation genes. It is interesting to determine whether this translation-coupled surveillance system represents a general rule for the genes encoding components of the same physiological cascade.