A Terrain Elevation Map Generation Method Based on Self-Attention Mechanism and Multifeature Sketch.

To address the issues of low efficiency in manual terrain feature map annotating and poor realism in terrain elevation map generation, this paper proposes a terrain elevation map generation method based on self-attention mechanism and multifeature sketch. Firstly, the proposed method extracts features from a terrain elevation map using an adaptive feature enhancement method. Afterwards, our method adds a self-attention mechanism to the generator and discriminator of conditional generative adversarial network to capture the global spatial features and generates a realistic terrain elevation map.

Neuroprotection Effect of Astragaloside IV from 2-DG-Induced Endoplasmic Reticulum Stress.

Objective: Astragaloside IV shows neuroprotective activity, but its mechanism remains unclear. To investigate whether astragaloside IV protects from endoplasmic reticulum stress (ERS), we focus on the regulation of glycogen synthase kinase-3 (GSK-3) and mitochondrial permeability transition pore (mPTP) by astragaloside IV in neuronal cell PC12.

Methods And Results: PC12 cells treated with different concentrations of ERS inductor 2-deoxyglucose (2-DG) (25-500 M) showed a significant increase of glucose-regulated protein 78 (GRP 78) and GRP 94 expressions and a decrease of tetramethylrhodamine ethyl ester (TMRE) fluorescence intensity and mitochondrial membrane potential (∆m), with the peak effect seen at 50 M, indicating that 2-DG induces ERS and the mPTP opening.

Zn and mPTP mediate resveratrol-induced myocardial protection from endoplasmic reticulum stress.

Resveratrol displays cardioprotective activity; however, its mechanism of action remains unclear. In the current study, resveratrol-induced myocardial protection from endoplasmic reticulum stress (ERS) was investigated, focusing on the roles of Zn2+ and the mitochondrial permeability transition pore (mPTP). We found, using the MTT/LDH kit, that 2-DG-induced ERS significantly decreased H9c2 cell viability.

Tauroursodeoxycholic acid inhibits endoplasmic reticulum stress, blocks mitochondrial permeability transition pore opening, and suppresses reperfusion injury through GSK-3ß in cardiac H9c2 cells.

This study investigates whether inhibition of endoplasmic reticulum (ER) stress prevents opening of the mitochondrial permeability transition pore (mPTP) and evaluates the corresponding signaling pathways involved in this process. Exposure of cardiac H9c2 cells to 800 µM HO for 20 min opened mPTP in response to oxidative stress, as demonstrated by quenching of tetramethylrhodamine ethyl ester (TMRE) fluorescence. Oxidative stress-induced mPTP opening was rescued by the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) in a dose-dependent manner at low concentrations.