3D-Spatiotemporal Forecasting the Expansion of Supernova Shells Using Deep Learning toward High-Resolution Galaxy Simulations

Supernova (SN) plays an important role in galaxy formation and evolution. In high-resolution galaxy simulations using massively parallel computing, short integration timesteps for SNe are serious bottlenecks. This is an urgent issue that needs to be resolved for future higher-resolution galaxy simulations. One possible solution would be to use the Hamiltonian splitting method, in which regions requiring short timesteps are integrated separately from the entire system. To apply this method to the particles affected by SNe in a smoothed-particle hydrodynamics simulation, we need to detect the shape of the shell on and within which such SN-affected particles reside during the subsequent global step in advance. In this paper, we develop a deep learning model, 3D-MIM, to predict a shell expansion after a SN explosion. Trained on turbulent cloud simulations with particle mass $m_{\rm gas}=1$M$_\odot$, the model accurately reproduces the anisotropic shell shape, where densities decrease by over 10 per cent by the explosion. We also demonstrate that the model properly predicts the shell radius in the uniform medium beyond the training dataset of inhomogeneous turbulent clouds. We conclude that our model enables the forecast of the shell and its interior where SN-affected particles will be present.Comment: 14 pages, 14 figures, 3 tables, accepted for MNRA

Surrogate Modeling for Computationally Expensive Simulations of Supernovae in High-Resolution Galaxy Simulations

Some stars are known to explode at the end of their lives, called supernovae (SNe). The substantial amount of matter and energy that SNe release provides significant feedback to star formation and gas dynamics in a galaxy. SNe release a substantial amount of matter and energy to the interstellar medium, resulting in significant feedback to star formation and gas dynamics in a galaxy. While such feedback has a crucial role in galaxy formation and evolution, in simulations of galaxy formation, it has only been implemented using simple {\it sub-grid models} instead of numerically solving the evolution of gas elements around SNe in detail due to a lack of resolution. We develop a method combining machine learning and Gibbs sampling to predict how a supernova (SN) affects the surrounding gas. The fidelity of our model in the thermal energy and momentum distribution outperforms the low-resolution SN simulations. Our method can replace the SN sub-grid models and help properly simulate un-resolved SN feedback in galaxy formation simulations. We find that employing our new approach reduces the necessary computational cost to $\sim$ 1 percent compared to directly resolving SN feedback.Comment: 11 pages, 9 figures, Accepted for the NeurIPS 2023 AI4Science Worksho

Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings

The types of voltage-dependent calcium channels (VDCCs) present in the cholinergic terminals isolated from the electric organ of the ray, Narke japonica, were characterized on the basis of their pharmacological sensitivity to specific antagonists. Inhibition of these channel types by autoantibodies from patients with the Lambert-Eaton syndrome (LES) was then studied to determine the specificity of the pathogenic IgG. In normal untreated synaptosomal preparations, maximal doses of N- and P and/or Q-type Ca2+ channel antagonists, -conotoxin GVIA and -agatoxin IVA, inhibited depolarization-evoked ACh release by 47 % and 43 %, respectively. Calciseptine, an L-type VDCC antagonist, caused a 20 % reduction in the release. This indicates that the exocytotic release process is predominantly mediated by N- and P/Q-type VDCCs. LES IgG or sera caused an inhibition of ACh release by 39-45 % in comparison with the control antibody-treated preparations. The ionomycin-induced ACh release, however, was not altered by the antibodies. Additionally, the same LES antibodies inhibited whole-cell calcium currents (ICa) in bovine adrenal chromaffin cells. Thus, the pathogenic antibodies exert their action on VDCCs present in the synaptosomes. The efficacy of three Ca2+ channel antagonists in blocking ACh release was determined in preparations pretreated with LES IgG. -Agatoxin IVA produced only an additional 3-5 % reduction in release beyond that obtained with LES antibodies. Despite the pretreatment with LES IgG, -conotoxin GVIA and calciseptine inhibited the release to nearly their control levels. These results indicate that LES antibodies mainly downregulate P/Q-type Ca2+ channels which contribute to presynaptic transmitter release from the cholinergic nerve terminals of electric organ. The present findings are consistent with the hypothesis that P/Q-type VDCCs at the neuromuscular junction are the target of LES antibodies and that their inhibition by the antibodies produces the characteristic neuromuscular defect in this disease

Japan Carotid Atherosclerosis Study : JCAS (EBM of Neurosurgical Disease in Japan)

The recent randomized trials, North American Symptomatic Carotid Endarterectomy Trial, European Carotid Surgery Trial, and Asymptomatic Carotid Atherosclerosis Study, have demonstrated the effectiveness of carotid endarterectomy to reduce the incidence of cerebral infarction in patients with symptomatic and asymptomatic high-grade carotid artery stenosis. However, no studies on Japanese patients have been done until now, and recent progress in endovascular stent treatment has been made. The present prospective, multicenter (not randomized) trial, the Japan Carotid Atherosclerosis Study, has started to analyze present practice and propose treatment guidelines for Japanese patients. Here, the protocol and early results of 565 patients registered until the end of January 2004 are presented

Vertebrobasilar Insufficiency in a Patient with Persistent Trigeminal Artery and Stenosis of the Ipsilateral Carotid Bifurcation : Case Report

A 69-year-old female with frequent episodes of vertigo was found to have persistent trigeminal artery and ulcerative stenosis of the ipsilateral carotid bifurcation. The clinical symptoms, pathogenesis, and treatment of this anomaly are discussed