Revisiting Pseudo-Haptics for Psychomotor Skills Development in Online Teaching.

In a centralized model of simulation-based education (Ce-SBE), the trainees practice clinical skills in simulated laboratories based on physical models, while in a decentralized model (De-SBE), the trainees practice these skills outside of these laboratories. Attention to De-SBE has drastically shifted to virtual learning environments (VLEs), serious games, and virtual simulations employing various digital technologies, including virtual, augmented, and mixed reality. In particular, remote learning has grown immensely during the COVID-19 pandemic as traditional in-person teaching and training activities are conducted online as a form of facilitating continuity in education. VLEs allow trainees to learn from virtual simulated health experiences in an interactive, engaging, and ethically safe manner, while providing educators the opportunity to implement simulated experiences to a larger number of learners. Despite these benefits, for certain types of clinical skills, such as psychomotor skills, VLEs have not yet reached their potential. This is primarily due to technical limitations and cost issues with the haptic devices required to simulate the sense of touch. Pseudo-haptic refers to the illusion of haptic stimulation in the absence of mechanical haptic interfaces and often combines the use of a passive input device (e.g., mouse) with visual and auditory feedback to simulate haptic properties (stiffness or friction of an object). Although the application of pseudo-haptics for psychomotor skills development is still in its infancy and currently trending due to the availability of consumer-level technologies, the potential to present haptic cues in the absence of active haptic devices may allow trainees to practice some tasks outside of research and training labs. The implications of pseudo-haptics are tremendous, particularly as remote learning becomes more widespread, and warrant further discussion.

Cardiac and renal nitrosative-oxidative stress after acute poisoning by a nerve agent Tabun.

We hypothesized that Tabun poisoning, as well as other organophosphorous treatment, cause specific organs' oxidative changes that have not previously been substantiated investigated. In this regard, a marker for nitrosative-oxidative stress in the main haemodynamic organs (heart and kidney) could reveal the existence of such changes. In this study, for the first time we studied the nitrosative/oxidative stress in heart and kidney after acute Tabun (Ethyl N,N- Dimethylphosphoramidocyanidate) poisoning measuring by immunohistochemistry the expression of 3-nitrotyrosine--a marker for nitrosative-oxidative stress. We investigated nitrotyrozine expression in three different groups of animals (with at least 3 animals in each group): the first group was treated with 0.5 LD50 Tabun and organs were collected after 24 h; the second group received vehicle for the same period; in the third group a highly specific re-activator was applied immediately after Tabun application. Heart and kidney were collected after 24 h. The levels of nitrotyrozine production significantly increased (more than 3 times) in cardiomyocytes after Tabun. The application of re-activator slightly reduced these levels not reaching the basal heart levels. Nitrotyrozine expression in kidney increased more than 2 times after Tabun and application of re-activator did not change it significantly. In conclusion, our study evidently demonstrated that Tabun trigger oxidative-nitrosative stress in heart and kidney and these cellular effects should be protected by an additional anti-oxidant therapy, since acetylcholinesterase re-activator is not efficient in this manner.

Correlation between butyrylcholinesterase variants and sensitivity to soman toxicity.

Butyrylcholinesterase (BChE) is synthesized in the liver and found in high concentrations in blood plasma, liver, heart, pancreas, vascular endothelium, skin, brain white matter, smooth muscle cells and adipocytes. BChE is a non specific enzyme that hydrolyzes different choline esters (succinylcholine, mivacurium) and many other drugs such as aspirin, cocaine and procaine. The enzyme is also considered as a bioscavenger due to its ability to neutralize the toxic effects of organophosphorus compounds (nervous system fs agents) such as soman. BChE displays several polymorphisms that influence its serum activity; therefore they could determine the individual sensitivity to chemical nerve agents. In this study, we investigated the correlation between BChE variants and the degree of enzyme inhibition and reactivation after soman application on blood samples of 726 individuals. The blood samples of individuals expressing abnormal variants, were more sensitive to soman compared to variants of homozygotes and heterozygotes for U-allele. We found significant differences in the degree of enzyme reactivation between different variants (with and without U-presence).