Spatiotemporal analysis of the UPR transition induced by methylmercury in the mouse brain

Methylmercury (MeHg), an environmental toxicant, induces neuronal cell death and injures a specific area of the brain. MeHg-mediated neurotoxicity is believed to be caused by oxidative stress and endoplasmic reticulum (ER) stress but the mechanism by which those stresses lead to neuronal loss is unclear. Here, by utilizing the ER stress-activated indicator (ERAI) system, we investigated the signaling alterations in the unfolded protein response (UPR) prior to neuronal apoptosis in the mouse brain. In ERAI transgenic mice exposed to MeHg (25 mg/kg, S.C.), the ERAI signal, which indicates activation of the cytoprotective pathway of the UPR, was detected in the brain. Interestingly, detailed ex vivo analysis showed that the ERAI signal was localized predominantly in neurons. Time course analysis of MeHg exposure (30 ppm in drinking water) showed that whereas the ERAI signal was gradually attenuated at the late phase after increasing at the early phase, activation of the apoptotic pathway of the UPR was enhanced in proportion to the exposure time. These results suggest that MeHg induces not only ER stress but also neuronal cell death via a UPR shift. UPR modulation could be a therapeutic target for treating neuropathy caused by electrophiles similar to MeHg

Revision Plan of ISO11227 Considering Oblique Impact Tests

The number of space debris is continuously increasing, and the risk of collision with a spacecraft is also increasing Secondary debris called ejecta is specifically threat to spacecraft, so an international standardization of the test procedure to evaluate ejecta, was developed and published as ISO11227 on September 15, 2012. This paper intends to show the necessity of oblique impact test by comparing spacecraft material oblique impact with normal impact and to consider the experimental condition of oblique impact test to revise this standard.2015 Hypervelocity Impact Symposium (HVIS 2015), April 26-30, 2015, Boulder, Colorad

Computational modeling of braided-stent deployment for interpreting the mechanism of stent flattening

This study develops a computational model of the braided stent for interpreting the mechanism of stent flattening during deployment into curved arteries. Stent wires are expressed using Kirchhoff's rod theory and their mechanical behavior is treated using a corotational beam formulation. The equation of motion of the braided stent is solved in a step-by-step manner using the resultant elastic force and mechanical interactions of wires with friction. Examples of braided-stent deployment into idealized arteries with various curvatures are numerically simulated. In cases of low curvature, the braided stent expands from a catheter by releasing the bending energy stored in stent wires, while incomplete expansion is found at both stent ends (ie, the fish-mouth phenomenon), where relatively little bending energy is stored. In cases of high curvature, much torsional energy is stored in stent wires locally in the midsection of the curvature and the bending energy for stent self-expansion is not fully released even after deployment, leading to stent flattening. These findings suggest that the mechanical state of the braided stent and its transition during deployment play an important role in the underlying mechanism of stent flattening. Novelty Statement: This study developed a computational mechanical model of the braided stent for interpreting stent flattening, which is a critical issue observed during deployment into highly curved arteries. Mechanical behaviors of the stent wires are appropriately treated by corotational beam element formulation with considering multiple contacts. We conducted numerical examples of the stent deployment into curved arteries and found that the mechanical state of the braided stent during deployment associated with occurrences of the stent flattening. We believe this finding gives new insight into the mechanism of stent flattening and would advance the design of the stent and its deployment protocol.This is the peer reviewed version of the following article: Shiozaki, S, Otani, T, Fujimura, S, Takao, H, Wada, S. Computational modeling of braided-stent deployment for interpreting the mechanism of stent flattening. Int J Numer Meth Biomed Engng. 2021; 37:e3335., which has been published in final form at https://doi.org/10.1002/cnm.3335. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited