Magic3D: High-Resolution Text-to-3D Content Creation

DreamFusion has recently demonstrated the utility of a pre-trained text-to-image diffusion model to optimize Neural Radiance Fields (NeRF), achieving remarkable text-to-3D synthesis results. However, the method has two inherent limitations: (a) extremely slow optimization of NeRF and (b) low-resolution image space supervision on NeRF, leading to low-quality 3D models with a long processing time. In this paper, we address these limitations by utilizing a two-stage optimization framework. First, we obtain a coarse model using a low-resolution diffusion prior and accelerate with a sparse 3D hash grid structure. Using the coarse representation as the initialization, we further optimize a textured 3D mesh model with an efficient differentiable renderer interacting with a high-resolution latent diffusion model. Our method, dubbed Magic3D, can create high quality 3D mesh models in 40 minutes, which is 2x faster than DreamFusion (reportedly taking 1.5 hours on average), while also achieving higher resolution. User studies show 61.7% raters to prefer our approach over DreamFusion. Together with the image-conditioned generation capabilities, we provide users with new ways to control 3D synthesis, opening up new avenues to various creative applications.Comment: Accepted to CVPR 2023 as highlight. Project website: https://research.nvidia.com/labs/dir/magic3

A Mid-infrared Flare in the Active Galaxy MCG-02-04-026: Dust Echo of a Nuclear Transient Event

We report the discovery of a mid-infrared (MIR) flare using Wide field Infrared Survey Explorer data in the center of the nearby Seyfert 1.9 galaxy MCG-02-04-026. The MIR flare began in the first half of 2014, peaked around the end of 2015, and faded in 2017. During these years, energy of more than 7 × 10⁵⁰ erg was released in the infrared, and the flare's MIR color was generally turning red. We detected neither optical nor ultraviolet (UV) variation corresponding to the MIR flare based on available data. We explained the MIR flare using a dust echo model in which the radiative transfer is involved. The MIR flare can be well explained as thermal reradiation from dust heated by UV–optical photons of a primary nuclear transient event. Although the transient event was not seen directly owing to dust obscuration, we can infer that it may produce a total energy of at least ~10⁵¹ erg, most of which was released in less than ~3 yr. The nature of the transient event could be a stellar tidal disruption event by the central supermassive black hole (SMBH), or a sudden enhancement of the existing accretion flow onto the SMBH, or a supernova that was particularly bright

A Mid-infrared Flare in the Active Galaxy MCG-02-04-026: Dust Echo of a Nuclear Transient Event

We report the discovery of a mid-infrared (MIR) flare using WISE data in the center of the nearby Seyfert 1.9 galaxy MCG-02-04-026. The MIR flare began in the first half of 2014, peaked around the end of 2015, and faded in 2017. During these years, energy more than $7\times10^{50}$ erg was released in the infrared, and the flare's MIR color was generally turning red. We detected neither optical nor ultraviolet (UV) variation corresponding to the MIR flare based on available data. We explained the MIR flare using a dust echo model in which the radiative transfer is involved. The MIR flare can be well explained as thermal reradiation from dust heated by UV-optical photons of a primary nuclear transient event. Although the transient event was not seen directly due to dust obscuration, we can infer that it may produce a total energy of at least $\sim10^{51}$ erg, most of which was released in less than $\sim$3 years. The nature of the transient event could be a stellar tidal disruption event by the central supermassive black hole (SMBH), or a sudden enhancement of the existing accretion flow onto the SMBH, or a supernova which was particularly bright.Comment: 44 pages, 13 figures; Accepted to be published in Ap

ATR/Chk1 signaling induces autophagy through sumoylated RhoB-mediated lysosomal translocation of TSC2 after DNA damage

RhoB作为抑癌蛋白通过诱导肿瘤细胞的凋亡在抑制肿瘤的发生发展中发挥着重要作用，并且与肿瘤耐药性密切相关，但关于RhoB如何促进细胞死亡的分子机理的研究仍不清楚。在本研究中，该团队发现在DNA单链损伤情况下，ATR-Chk1信号通路的激活，会使RhoB被Chk1磷酸化，该磷酸化修饰会使RhoB从细胞质膜解离下来进入细胞质中，进而被SUMO化修饰。SUMO化修饰后的RhoB会与TSC2形成复合物，并将TSC2复合物带到溶酶体上，引起细胞自噬的发生。 该文共同第一作者为刘明冬、曾涛玲和张新，通讯作者为王洪睿教授和赵同金教授。【Abstract】DNA damage can induce autophagy; however, the underlying mechanism remains largely unknown. Here we report that DNA damage leads to autophagy through ATR/Chk1/RhoB-mediated lysosomal recruitment of TSC complex and subsequent mTORC1 inhibition. DNA damage caused by ultraviolet light (UV) or alkylating agent methyl methanesulphonate (MMS) results in phosphorylation of small GTPase RhoB by Chk1. Phosphorylation of RhoB enhances its interaction with the TSC2, and promotes its sumoylation by PIAS1, which is required for RhoB/TSC complex to translocate to lysosomes. As a result, mTORC1 is inhibited, and autophagy is activated. Knockout of RhoB severely attenuates lysosomal translocation of TSC complex and the DNA damage-induced autophagy. Reintroducing wild-type but not sumoylation-resistant RhoB into RhoB−/− cells restores the onset of autophagy. Hence, our study identifies a molecular mechanism for translocation of TSC complex to lysosomes in response to DNA damage, which depends on ATR/Chk1-mediated RhoB phosphorylation and sumoylation.This work was supported by the National Natural Science Foundation of China (U1605222, 81472459, 31671223), the National Key Research and Development Project of China (2016YFC1302400, 2016YFA0502003), the Fundamental Research Funds for the Central Universities (20720140550, 20720160070), the National Science Foundation for Fostering Talents in Basic Research of the National Natural Science Foundation of China (J1310027), the Project 111 sponsored by the State Bureau of Foreign Experts and Ministry of Education (B12001), the National Natural Science Foundation of China (31601132) to T.Z., the National Natural Science Foundation of China (81402290) to Q.L., and the National Natural Science Foundation of China (U1405223) to X.D