Contested Chinese dreams of AI? Public discourse about artificial intelligence on WeChat and people’s daily online

Artificial intelligence (AI) has become a prominent public issue, particularly in China, where the government has announced plans to turn the country into a global AI power. This study analyses public discourse about AI in China through the conceptual lens of public spheres theory and counter-public spheres. It compares the official AI narrative on People’s Daily Online with public discussion about AI on the social medium WeChat, where we assumed that official views would be challenged. Using a combination of qualitative and computational methods, 140,000 AI-related articles published between 2015 and 2018 were studied. Findings reveal that AI-related discourse on WeChat is surprisingly similar to that on People’s Daily Online. That is, it is dominated by industry and political actors, such as government agencies and technology companies, and is mostly characterized by discussions about the economic potential of the technology, with strongly positive evaluations, and little critical debate

Diode Like Attributes in Magnetic Domain Wall Devices via Geometrical Pinning for Neuromorphic Computing

Neuromorphic computing (NC) is considered as a potential vehicle for implementing energy-efficient artificial intelligence (AI). To realize NC, several materials systems are being investigated. Among them, the spin-orbit torque (SOT) -driven domain wall (DW) devices are one of the potential candidates. To implement these devices as neurons and synapses, the building blocks of NC, researchers have proposed different device designs. However, the experimental realization of DW device-based NC is only at the primeval stage. In this study, we have proposed and investigated pine-tree-shaped DW devices, based on the Laplace force on the elastic DWs, for achieving the synaptic functionalities. We have successfully observed multiple magnetization states when the DW was driven by the SOT current. The key observation is the asymmetric pinning strength of the device when DW moves in two opposite directions (defined as, xhard and xeasy). This shows the potential of these DW devices as DW diodes. We have used micromagnetic simulations to understand the experimental findings and to estimate the Laplace pressure for various design parameters. The study leads to the path of device fabrication, where synaptic properties are achieved with asymmetric pinning potential

Computer-Aided Diagnosis with Deep Learning Architecture: Applications to Breast Lesions in US Images and Pulmonary Nodules in CT Scans

This paper performs a comprehensive study on the deep-learning-based computer-aided diagnosis (CADx) for the differential diagnosis of benign and malignant nodules/lesions by avoiding the potential errors caused by inaccurate image processing results (e.g., boundary segmentation), as well as the classification bias resulting from a less robust feature set, as involved in most conventional CADx algorithms. Specifically, the stacked denoising auto-encoder (SDAE) is exploited on the two CADx applications for the differentiation of breast ultrasound lesions and lung CT nodules. The SDAE architecture is well equipped with the automatic feature exploration mechanism and noise tolerance advantage, and hence may be suitable to deal with the intrinsically noisy property of medical image data from various imaging modalities. To show the outperformance of SDAE-based CADx over the conventional scheme, two latest conventional CADx algorithms are implemented for comparison. 10 times of 10-fold cross-validations are conducted to illustrate the efficacy of the SDAE-based CADx algorithm. The experimental results show the significant performance boost by the SDAE-based CADx algorithm over the two conventional methods, suggesting that deep learning techniques can potentially change the design paradigm of the CADx systems without the need of explicit design and selection of problem-oriented features

Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma

Abstract Background The mechanisms by which viruses cause asthma exacerbations are not precisely known. Previously, we showed that, in ovalbumin (OVA)-sensitized and -challenged mice with allergic airway inflammation, rhinovirus (RV) infection increases type 2 cytokine production from alternatively-activated (M2) airway macrophages, enhancing eosinophilic inflammation and airways hyperresponsiveness. In this paper, we tested the hypothesis that IL-4 signaling determines the state of macrophage activation and pattern of RV-induced exacerbation in mice with allergic airways disease. Methods Eight week-old wild type or IL-4 receptor knockout (IL-4R KO) mice were sensitized and challenged with OVA and inoculated with RV1B or sham HeLa cell lysate. Results In contrast to OVA-treated wild-type mice with both neutrophilic and eosinophilic airway inflammation, OVA-treated IL-4R KO mice showed increased neutrophilic inflammation with few eosinophils in the airways. Like wild-type mice, IL-4R KO mice showed OVA-induced airway hyperreactivity which was further exacerbated by RV. There was a shift in lung cytokines from a type 2-predominant response to a type 1 response, including production of IL-12p40 and TNF-α. IL-17A was also increased. RV infection of OVA-treated IL-4R KO mice further increased neutrophilic inflammation. Bronchoalveolar macrophages showed an M1 polarization pattern and ex vivo RV infection increased macrophage production of TNF-α, IFN-γ and IL-12p40. Finally, lung cells from OVA-treated IL-4R KO mice showed reduced CD206+ CD301+ M2 macrophages, decreased IL-13 and increased TNF-α and IL-17A production by F4/80+, CD11b+ macrophages. Conclusions OVA-treated IL-4R KO mice show neutrophilic airway inflammation constituting a model of allergic, type 1 cytokine-driven neutrophilic asthma. In the absence of IL-4/IL-13 signaling, RV infection of OVA-treated mice increased type 1 cytokine and IL-17A production from conventionally-activated macrophages, augmenting neutrophilic rather than eosinophilic inflammation. In mice with allergic airways inflammation, IL-4R signaling determines macrophage activation state and the response to subsequent RV infection.http://deepblue.lib.umich.edu/bitstream/2027.42/109511/1/12931_2014_Article_1503.pd

Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma

Abstract Background The mechanisms by which viruses cause asthma exacerbations are not precisely known. Previously, we showed that, in ovalbumin (OVA)-sensitized and -challenged mice with allergic airway inflammation, rhinovirus (RV) infection increases type 2 cytokine production from alternatively-activated (M2) airway macrophages, enhancing eosinophilic inflammation and airways hyperresponsiveness. In this paper, we tested the hypothesis that IL-4 signaling determines the state of macrophage activation and pattern of RV-induced exacerbation in mice with allergic airways disease. Methods Eight week-old wild type or IL-4 receptor knockout (IL-4R KO) mice were sensitized and challenged with OVA and inoculated with RV1B or sham HeLa cell lysate. Results In contrast to OVA-treated wild-type mice with both neutrophilic and eosinophilic airway inflammation, OVA-treated IL-4R KO mice showed increased neutrophilic inflammation with few eosinophils in the airways. Like wild-type mice, IL-4R KO mice showed OVA-induced airway hyperreactivity which was further exacerbated by RV. There was a shift in lung cytokines from a type 2-predominant response to a type 1 response, including production of IL-12p40 and TNF-α. IL-17A was also increased. RV infection of OVA-treated IL-4R KO mice further increased neutrophilic inflammation. Bronchoalveolar macrophages showed an M1 polarization pattern and ex vivo RV infection increased macrophage production of TNF-α, IFN-γ and IL-12p40. Finally, lung cells from OVA-treated IL-4R KO mice showed reduced CD206+ CD301+ M2 macrophages, decreased IL-13 and increased TNF-α and IL-17A production by F4/80+, CD11b+ macrophages. Conclusions OVA-treated IL-4R KO mice show neutrophilic airway inflammation constituting a model of allergic, type 1 cytokine-driven neutrophilic asthma. In the absence of IL-4/IL-13 signaling, RV infection of OVA-treated mice increased type 1 cytokine and IL-17A production from conventionally-activated macrophages, augmenting neutrophilic rather than eosinophilic inflammation. In mice with allergic airways inflammation, IL-4R signaling determines macrophage activation state and the response to subsequent RV infection.http://deepblue.lib.umich.edu/bitstream/2027.42/134573/1/12931_2014_Article_1503.pd

All-Electrical Skyrmionic Bits in a Chiral Magnetic Tunnel Junction

Topological spin textures such as magnetic skyrmions hold considerable promise as robust, nanometre-scale, mobile bits for sustainable computing. A longstanding roadblock to unleashing their potential is the absence of a device enabling deterministic electrical readout of individual spin textures. Here we present the wafer-scale realization of a nanoscale chiral magnetic tunnel junction (MTJ) hosting a single, ambient skyrmion. Using a suite of electrical and multi-modal imaging techniques, we show that the MTJ nucleates skyrmions of fixed polarity, whose large readout signal - 20-70% relative to uniform states - corresponds directly to skyrmion size. Further, the MTJ exploits complementary mechanisms to stabilize distinctly sized skyrmions at zero field, thereby realizing three nonvolatile electrical states. Crucially, it can write and delete skyrmions using current densities 1,000 times lower than state-of-the-art. These results provide a platform to incorporate readout and manipulation of skyrmionic bits across myriad device architectures, and a springboard to harness chiral spin textures for multi-bit memory and unconventional computing.Comment: 8 pages, 5 figure

Targeting cancer addiction for SALL4 by shifting its transcriptome with a pharmacologic peptide

Sal-like 4 (SALL4) is a nuclear factor central to the maintenance of stem cell pluripotency and is a key component in hepatocellular carcinoma, a malignancy with no effective treatment. In cancer cells, SALL4 associates with nucleosome remodeling deacetylase (NuRD) to silence tumor-suppressor genes, such as PTEN. Here, we determined the crystal structure of an amino-terminal peptide of SALL4(1-12) complexed to RBBp4, the chaperone subunit of NuRD, at 2.7 Å, and subsequent design of a potent therapeutic SALL4 peptide (FFW) capable of antagonizing the SALL4-NURD interaction using systematic truncation and amino acid substitution studies. FFW peptide disruption of the SALL4-NuRD complex resulted in unidirectional up-regulation of transcripts, turning SALL4 from a dual transcription repressor-activator mode to singular transcription activator mode. We demonstrate that FFW has a target affinity of 23 nM, and displays significant antitumor effects, inhibiting tumor growth by 85% in xenograft mouse models. Using transcriptome and survival analysis, we discovered that the peptide inhibits the transcription-repressor function of SALL4 and causes massive up-regulation of transcripts that are beneficial to patient survival. This study supports the SALL4-NuRD complex as a drug target and FFW as a viable drug candidate, showcasing an effective strategy to accurately target oncogenes previously considered undruggable