An Ultraflexible Electrode Array for Large-Scale Chronic Recording in the Nonhuman Primate Brain.

Single-unit (SU) recording in nonhuman primates (NHPs) is indispensible in the quest of how the brain works, yet electrodes currently used for the NHP brain are limited in signal longevity, stability, and spatial coverage. Using new structural materials, microfabrication, and penetration techniques, we develop a mechanically robust ultraflexible, 1 µm thin electrode array (MERF) that enables pial penetration and high-density, large-scale, and chronic recording of neurons along both vertical and horizontal cortical axes in the nonhuman primate brain. Recording from three monkeys yields 2,913 SUs from 1,065 functional recording channels (up to 240 days), with some SUs tracked for up to 2 months. Recording from the primary visual cortex (V1) reveals that neurons with similar orientation preferences for visual stimuli exhibited higher spike correlation. Furthermore, simultaneously recorded neurons in different cortical layers of the primary motor cortex (M1) show preferential firing for hand movements of different directions. Finally, it is shown that a linear decoder trained with neuronal spiking activity across M1 layers during monkey's hand movements can be used to achieve on-line control of cursor movement. Thus, the MERF electrode array offers a new tool for basic neuroscience studies and brain-machine interface (BMI) applications in the primate brain.

UNC93B1 curbs cytosolic DNA signaling by promoting STING degradation.

UNC93B1 is a trafficking chaperone of endosomal Toll-like receptors (TLRs) and plays an essential role in the TLR-mediated innate signaling. However, whether it is also involved in other innate immune sensing or cellular pathways remains largely unexplored. Here we investigated the role of UNC93B1 in cytosolic DNA-triggered cGAS-STING signaling in mouse and human cell lines. We showed that while UNC93B1 deficiency blunts the signal transduction by TLR3, it augments innate immune responses to cytosolic DNA stimulation and DNA virus infection. Mechanistic study reveals a distinct action of UNC93B1 upon STING, but not other parts along the cGAS-STING-TBK1 axis, through regulating the protein level of STING at both resting and cytosolic DNA-stimulated conditions. UNC93B1 can directly interact and traffic along with STING, and the disruption of this interaction causes accumulation of STING that subsequently leads to augmented signaling responses upon its activation. These findings reveal a new function of UNC93B1 in negatively regulating STING-mediated signaling responses.

AttGAN: Facial Attribute Editing by Only Changing What You Want.

Facial attribute editing aims to manipulate single or multiple attributes on a given face image, i.e., to generate a new face image with desired attributes while preserving other details. Recently, the generative adversarial net (GAN) and encoder-decoder architecture are usually incorporated to handle this task with promising results. Based on the encoder-decoder architecture, facial attribute editing is achieved by decoding the latent representation of a given face conditioned on the desired attributes. Some existing methods attempt to establish an attribute-independent latent representation for further attribute editing. However, such attribute-independent constraint on the latent representation is excessive because it restricts the capacity of the latent representation and may result in information loss, leading to over-smooth or distorted generation. Instead of imposing constraints on the latent representation, in this work, we propose to apply an attribute classification constraint to the generated image to just guarantee the correct change of desired attributes, i.e., to change what you want. Meanwhile, the reconstruction learning is introduced to preserve attribute-excluding details, in other words, to only change what you want. Besides, the adversarial learning is employed for visually realistic editing. These three components cooperate with each other forming an effective framework for high quality facial attribute editing, referred as AttGAN. Furthermore, the proposed method is extended for attribute style manipulation in an unsupervised manner. Experiments on two wild datasets, CelebA and LFW, show that the proposed method outperforms the state-of-the-art on realistic attribute editing with other facial details well preserved.

Correction: Hepatitis C virus NS4B induces the degradation of TRIF to inhibit TLR3-mediated interferon signaling pathway.

[This corrects the article DOI: 10.1371/journal.ppat.1007075.].

Hepatitis C virus NS4B induces the degradation of TRIF to inhibit TLR3-mediated interferon signaling pathway.

Toll-like receptor 3 (TLR3) senses dsRNA intermediates produced during RNA virus replication to activate innate immune signaling pathways through adaptor protein TRIF. Many viruses have evolved strategies to block TLR3-mediated interferon signaling via targeting TRIF. Here we studied how hepatitis C virus (HCV) antagonizes the TLR3-mediated interferon signaling. We found that HCV-encoded NS4B protein inhibited TLR3-mediated interferon signaling by down-regulating TRIF protein level. Mechanism studies indicated that the downregulation of TRIF by NS4B was dependent on caspase8. NS4B transfection or HCV infection can activate caspase8 to promote TRIF degradation, leading to suppression of TLR3-mediated interferon signaling. Knockout of caspase8 can prevent TRIF degradation triggered by NS4B, thereby enhancing the TLR3-mediated interferon signaling activation in response to HCV infection. In conclusion, our work revealed a new mechanism for HCV to evade innate immune response by blocking the TLR3-mediated interferon signaling via NS4B-induced TRIF degradation.

[Study on the spectra of Au/CeO2 catalysts modified by La2O3 additive].

For Au-ceria catalysts prepared by deposition-precipitation method, the catalytic performance of water gas shift reaction was studied with different La loadings. In the complete doping range, ceria retains with its cubic fluorite structures. XRD, HRTEM and UV-Vis-DRS, studies showed that La doping can improve the activity of Au-ceria catalyst by stabilizing ceria and modifying its morphology. In addition, the test of catalyst stability evaluation also proved, that a better stability performance of Au-ceria catalyst can be realized by appropriate La doping. The Au/CL5.0 sample with 5 at % La doping showed the best performance in WGS reaction.