126 research outputs found

    Synthesizing Coherent Story with Auto-Regressive Latent Diffusion Models

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    Conditioned diffusion models have demonstrated state-of-the-art text-to-image synthesis capacity. Recently, most works focus on synthesizing independent images; While for real-world applications, it is common and necessary to generate a series of coherent images for story-stelling. In this work, we mainly focus on story visualization and continuation tasks and propose AR-LDM, a latent diffusion model auto-regressively conditioned on history captions and generated images. Moreover, AR-LDM can generalize to new characters through adaptation. To our best knowledge, this is the first work successfully leveraging diffusion models for coherent visual story synthesizing. Quantitative results show that AR-LDM achieves SoTA FID scores on PororoSV, FlintstonesSV, and the newly introduced challenging dataset VIST containing natural images. Large-scale human evaluations show that AR-LDM has superior performance in terms of quality, relevance, and consistency.Comment: Technical Repor

    Theoretical EXAFS studies of a model of the oxygen-evolving complex of photosystem II obtained with the quantum cluster approach

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    The oxygen-evolving complex (OEC) of photosystem II is the only natural system that can form O2 from water and sunlight and it consists of a Mn4Ca cluster. In a series of publications, Siegbahn has developed a model of the OEC with the quantum mechanical (QM) cluster approach that is compatible with available crystal structures, able to form O2 with a reasonable energetic barrier, and has a significantly lower energy than alternative models. In this investigation, we present a method to restrain a QM geometry optimization toward experimental polarized extended X-ray absorption fine structure (EXAFS) data. With this method, we show that the cluster model is compatible with the EXAFS data and we obtain a refined cluster model that is an optimum compromise between QM and polarized EXAFS data. (C) 2012 Wiley Periodicals, Inc

    Extraordinary Thermoelectric Properties of Topological Surface States in Quantum-Confined Cd3As2 Thin Films

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    Topological insulators and semimetals have been shown to possess intriguing thermoelectric properties promising for energy harvesting and cooling applications. However, thermoelectric transport associated with the Fermi arc topological surface states on topological Dirac semimetals remains less explored. In this work, we systematically examine thermoelectric transport in a series of topological Dirac semimetal Cd3As2 thin films grown by molecular beam epitaxy. Surprisingly, we find significantly enhanced Seebeck effect and anomalous Nernst effect at cryogenic temperatures when the Cd3As2 layer is thin. Combining angle-dependent quantum oscillation analysis, magnetothermoelectric measurement, transport modelling and first-principles simulation, we isolate the contributions from bulk and surface conducting channels and attribute the unusual thermoeletric properties to the topological surface states. Our analysis showcases the rich thermoelectric transport physics in quantum-confined topological Dirac semimetal thin films and suggests new routes to achieving high thermoelectric performance at cryogenic temperatures

    TLR3 Regulated Poly I:C-Induced Neutrophil Extracellular Traps and Acute Lung Injury Partly Through p38 MAP Kinase

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    Acute lung injury (ALI) is the leading cause of morbidity and mortality in critically ill patients. Neutrophil extracellular traps (NETs) have been well documented in the ALI model of bacterial infection. In the present study, we demonstrated that poly I:C could induce pulmonary NETs. Upon poly I:C intratracheal inoculation, neutrophil infiltration in the bronchoalveolar lavage fluid (BALF) was significantly increased. Furthermore, the inflammatory cytokines IL-1β, IL-6, and TNF-α in the lung were also significantly elevated. Neutrophil depletion abolished NETs and decreased both neutrophil infiltration and IL-1β in the lung. As expected, DNase I, an inhibitor of MPO and NADPH, decreased pulmonary inflammation and NETs. Blocking of the poly I:C receptor TLR3 reduced lung inflammation and NETs. The MAPK kinase inhibitor p38 diminished the formation of NETs and restored the expression of the tight junction protein claudin-5 in the mouse lung when challenged with poly I:C. In summary, poly I:C induced the formation of pulmonary NETs and ALI, which may be associated with the activation of p38 MAPK and the decreased expression of claudin-5

    The competition and equilibrium in power markets under decarbonization and decentralization

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    Equilibrium analysis has been widely studied as an effective tool to model gaming interactions and predict market results. However, as competition modes are fundamentally changed by the decarbonization and decentralization of power systems, analysis techniques must evolve. This article comprehensively reviews recent developments in modelling methods, practical settings and solution techniques in equilibrium analysis. Firstly, we review equilibrium in the evolving wholesale power markets which feature new entrants, novel trading products and multi-stage clearing. Secondly, the competition modes in the emerging distribution market and distributed resource aggregation are reviewed, and we compare peer-to-peer clearing, cooperative games and Stackelberg games. Furthermore, we summarize the methods to treat various information acquisition degrees, risk preferences and rationalities of market participants. To deal with increasingly complex market settings, this review also covers refined analytical techniques and agent-based models used to compute the equilibrium. Finally, based on this review, this paper summarizes key issues in the gaming and equilibrium analysis in power markets under decarbonization and decentralization

    Fumarylacetoacetate Hydrolase Knock-out Rabbit Model for Hereditary Tyrosinemia Type 1.

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    Hereditary tyrosinemia type 1 (HT1) is a severe human autosomal recessive disorder caused by the deficiency of fumarylacetoacetate hydroxylase (FAH), an enzyme catalyzing the last step in the tyrosine degradation pathway. Lack of FAH causes accumulation of toxic metabolites (fumarylacetoacetate and succinylacetone) in blood and tissues, ultimately resulting in severe liver and kidney damage with onset that ranges from infancy to adolescence. This tissue damage is lethal but can be controlled by administration of 2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione (NTBC), which inhibits tyrosine catabolism upstream of the generation of fumarylacetoacetate and succinylacetone. Notably, in animals lacking FAH, transient withdrawal of NTBC can be used to induce liver damage and a concomitant regenerative response that stimulates the growth of healthy hepatocytes. Among other things, this model has raised tremendous interest for the in vivo expansion of human primary hepatocytes inside these animals and for exploring experimental gene therapy and cell-based therapies. Here, we report the generation of FAH knock-out rabbits via pronuclear stage embryo microinjection of transcription activator-like effector nucleases. FAH-/- rabbits exhibit phenotypic features of HT1 including liver and kidney abnormalities but additionally develop frequent ocular manifestations likely caused by local accumulation of tyrosine upon NTBC administration. We also show that allogeneic transplantation of wild-type rabbit primary hepatocytes into FAH-/- rabbits enables highly efficient liver repopulation and prevents liver insufficiency and death. Because of significant advantages over rodents and their ease of breeding, maintenance, and manipulation compared with larger animals including pigs, FAH-/- rabbits are an attractive alternative for modeling the consequences of HT1.Wellcome Trus

    Current evidence, clinical applications, and future directions of transcranial magnetic stimulation as a treatment for ischemic stroke

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    Transcranial magnetic stimulation (TMS) is a non-invasive brain neurostimulation technique that can be used as one of the adjunctive treatment techniques for neurological recovery after stroke. Animal studies have shown that TMS treatment of rats with middle cerebral artery occlusion (MCAO) model reduced cerebral infarct volume and improved neurological dysfunction in model rats. In addition, clinical case reports have also shown that TMS treatment has positive neuroprotective effects in stroke patients, improving a variety of post-stroke neurological deficits such as motor function, swallowing, cognitive function, speech function, central post-stroke pain, spasticity, and other post-stroke sequelae. However, even though numerous studies have shown a neuroprotective effect of TMS in stroke patients, its possible neuroprotective mechanism is not clear. Therefore, in this review, we describe the potential mechanisms of TMS to improve neurological function in terms of neurogenesis, angiogenesis, anti-inflammation, antioxidant, and anti-apoptosis, and provide insight into the current clinical application of TMS in multiple neurological dysfunctions in stroke. Finally, some of the current challenges faced by TMS are summarized and some suggestions for its future research directions are made

    Small-Molecule RORγt Antagonists Inhibit T Helper 17 Cell Transcriptional Network by Divergent Mechanisms

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    SummaryWe identified three retinoid-related orphan receptor gamma t (RORγt)-specific inhibitors that suppress T helper 17 (Th17) cell responses, including Th17-cell-mediated autoimmune disease. We systemically characterized RORγt binding in the presence and absence of drugs with corresponding whole-genome transcriptome sequencing. RORγt acts as a direct activator of Th17 cell signature genes and a direct repressor of signature genes from other T cell lineages; its strongest transcriptional effects are on cis-regulatory sites containing the RORα binding motif. RORγt is central in a densely interconnected regulatory network that shapes the balance of T cell differentiation. Here, the three inhibitors modulated the RORγt-dependent transcriptional network to varying extents and through distinct mechanisms. Whereas one inhibitor displaced RORγt from its target loci, the other two inhibitors affected transcription predominantly without removing DNA binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity
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