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Denoising diffusion probabilistic models are a promising new class of generative models that mark a milestone in high-quality image generation. This paper showcases their ability to sequentially generate video, surpassing prior methods in perceptual and probabilistic forecasting metrics. We propose an autoregressive, end-to-end optimized video diffusion model inspired by recent advances in neural video compression. The model successively generates future frames by correcting a deterministic next-frame prediction using a stochastic residual generated by an inverse diffusion process. We compare this approach against six baselines on four datasets involving natural and simulation-based videos. We find significant improvements in terms of perceptual quality and probabilistic frame forecasting ability for all datasets.

We use first-principles methods to study doped strong ferroelectrics (taking BaTiO 3 as a prototype). Here, we find a strong coupling between itinerant electrons and soft polar phonons in doped BaTiO 3 , contrary to Anderson/Blount’s weakly coupled electron mechanism for \"ferroelectric-like metals”. As a consequence, across a polar-to-centrosymmetric phase transition in doped BaTiO 3 , the total electron-phonon coupling is increased to about 0.6 around the critical concentration, which is sufficient to induce phonon-mediated superconductivity of about 2 K. Lowering the crystal symmetry of doped BaTiO 3 by imposing epitaxial strain can further increase the superconducting temperature via a sizable coupling between itinerant electrons and acoustic phonons. Our work demonstrates a viable approach to modulating electron-phonon coupling and inducing phonon-mediated superconductivity in doped strong ferroelectrics and potentially in polar metals. Our results also show that the weakly coupled electron mechanism for \"ferroelectric-like metals” is not necessarily present in doped strong ferroelectrics. Usually the coupling between polar phonons and itinerant electrons is weak in polar metals. Here, the authors show that in doped ferroelectrics (approximate polar metals), this coupling can be increased across the structural phase transition and as a result, phonon-mediated superconductivity emerges.

The film series “White Snake” of Light Chaser Animation is an attempt to internationalize Chinese comics in terms of cultural elements, characterization and core spirit.However, in the midst of continuous innovation, Chinese comics also face new dilemmas, and how to get out of this dilemma is the key to further development of Chinese comics in current era. By using both documentary and case study methods, I review the literature on the “White Snake” series to understand how the film has been received by audiences in China and the overseas market. What’s more, to gain a comprehensive understanding of the current state of adaptation of Chinese comics base on the various aspects of the adaptation and innovation of “White Snake” in the literature of others.Then, in the part of the study on new dilemmas, I use the method of comparative thinking to compare “White Snake” with the success of foreign films called “Kung Fu Panda” and “Dragon Ball” respectively, and come to the conclusion that national comics already have good innovation in terms of cultural elements and characterization, but in order to further develop Chinese comics, we need to combine the core spirit with the current trend of the times, and through the localization of foreign culture to arouse the cultural resonance of the new era.

Background. Venous thromboembolism (VTE) is considered a common complication in lung cancer patients. Despite its widespread use, the Khorana score performed moderately in predicting VTE risk. This study aimed to determine the diagnostic utility of the Systemic Immunoinflammatory Index (SII) and to create a novel nomogram for predicting VTE in patients with pulmonary carcinoma. Materials and Methods. The data, like clinical features and laboratory indicators, of inpatients diagnosed with lung cancer from March 2019 to March 2020 were collected and analyzed. Univariate and multivariate logistic analyses were performed to confirm the risk factors and then construct a nomogram model. The calibration curve and clinical decision curve analysis (DCA) were used to assess the model’s fitting performance. The receiver-operating characteristic (ROC) curve and the area under the ROC curve (AUC) were used to evaluate the diagnostic value of SII and the nomogram. Results. This study enrolled 369 lung patients with a VTE morbidity rate of 23.33%. The patients with VTE had higher SII levels than the non-VTE group (1441.47 ± 146.28 vs. 626.76 ± 26.04, P<0.001). SII is the stronger correlator for VTE among inflammatory markers, of which the optimal cut-off value was 851.51. Univariate and multivariate analysis revealed that the age, metastasis, antitumor treatment, hemoglobin<100 g/L, SII>851.51 × 109/L, and D-dimer>2 folds were independent risk factors for lung cancer-related VTE, and a new prediction nomogram model was constructed based on them. ROC curve analysis showed the AUC of the new model and Khorana score were 0.708 (0.643-0.772) and 0.600 (0.531-0.699). Conclusion. The SII was a simple and valuable biomarker for VTE, and the new nomogram model based on it can accurately forecast the occurrence of VTE. They can be utilized in clinical practice to identify those at high risk of VTE in lung cancer patients.

Biomass gasification serves as a key carbon-neutral technology. To effectively address the challenge of tar treatment during biomass gasification, the National Institute of Clean and low-carbon Energy developed a fluidized bed coupled with an entrained-flow bed. A steady-state Aspen Plus V12 model was designed to assess the compatibility between the two beds and optimize operating parameters. The model divides the process into three main zones: fluidized bed gasification, entrained-flow bed gasification, and bottom slag treatment, employing a reaction-restricted equilibrium assumption. Simulation results indicate that an increase in pressure leads to a reduction in the concentration of syngas components (CO and H2), an insignificant rise in gas low heating value (LHV), and a notable decline in cold gas efficiency (η). A higher equivalence ratio (ER) results in decreased syngas components, along with a significant reduction in both LHV and η. The introduction of carbon dioxide reduces syngas components and lowers LHV. Similarly, the addition of steam reduces the CO content of the syngas and decreases its LHV. When the fluidized bed temperature exceeds 900 °C, changes in LHV and gas yield become negligible, while variations remain minimal when the entrained-flow bed temperature exceeds 1200 °C.

ObjectiveTo report a case of autoimmune nodopathy (AN) with concurrent serum and CSF immunoglobulin (Ig)G4 anti-neurofascin 155 (NF155) and anti-GD1b antibodies.MethodsA 20-year-old male presented distal weakness of the 4 limbs, hypoesthesia, absent tendon reflexes and sensory ataxia. Nerve conduction studies (NCS), MRI, and autoantibody tests were performed.ResultsNCS revealed a diffuse demyelinating neuropathy in the peripheral nerve with motor and sensory involvement. MRI of the cervical and lumbar plexus showed diffuse enlargement. IgG4 anti-NF155 antibodies in both serum and CSF and IgG anti-GD1b antibodies in serum were positive. After treatment with IVIg, rituximab, and plasma exchange, the titer of the patient’s anti-NF155 antibodies decreased, but symptoms did not significantly improve.DiscussionThis patient presented a typical clinical feature of AN with serum and CSF anti-NF155 antibodies and serum anti-GD1b antibodies coexistent but poor response to IVIg, rituximab and plasma exchange. Early detection of antibodies may be helpful in both diagnosis and therapy of the disease. And prospective studies are necessary to demonstrate the potential role of anti-NF155 antibodies in CSF and help further understand this complex and heterogeneous disease.

F-box and WD repeat domain-containing 7 (FBXW7), formerly known as hCdc4, hAGO Fbw7, or SEL10, plays a specific recognition function in SCF-type E3 ubiquitin ligases. FBXW7 is a well-established cancer suppressor gene that specifically controls proteasomal degradation and destruction of many key oncogenic substrates. The FBXW7 gene is frequently abnormal in human malignancies especially in gastrointestinal cancers. Accumulating evidence reveals that mutations and deletions of FBXW7 are participating in the occurrence, progression and treatment resistance of human gastrointestinal cancers. Considering the current therapeutic challenges faced by gastrointestinal cancers, elucidating the biological function and molecular mechanism of FBXW7 can provide new perspectives and references for future personalized treatment strategies. In this review, we elucidate the key molecular mechanisms by which FBXW7 and its substrates are involved in gastrointestinal cancers. Furthermore, we discuss the consequences of FBXW7 loss or dysfunction in tumor progression and underscore its potential as a prognostic and therapeutic biomarker. Lastly, we propose potential therapeutic strategies targeting FBXW7 to guide the precision treatment of gastrointestinal cancers.

Background Neurite dystrophy is a pathologic hallmark of Alzheimer’s disease (AD). However, drug discovery targeting neurite protection in AD remains largely unexplored. Methods Aβ-induced neurite and mitochondrial damage assays were used to evaluate Aβ toxicity and the neuroprotective efficacy of a natural compound salidroside (SAL). The 5×FAD transgenic mouse model of AD was used to study the neuroprotective function of SAL. To verify the direct target of SAL, we used surface plasmon resonance and cellular thermal shift assays to analyze the drug-protein interaction. Results SAL ameliorates Aβ-mediated neurite damage in cell culture. We further reveal that SAL represses mitochondrial damage in neurites by promoting mitophagy and maintaining mitochondrial homeostasis, dependent on an NAD-dependent deacetylase SIRT3. In AD mice, SAL protects neurite morphology, mitigates Aβ pathology, and improves cognitive function, which are all SIRT3-dependent. Notably, SAL directly binds to transcription factor NRF2, inhibits its degradation by blocking its interaction with KEAP1 ubiquitin ligase, and then advances NRF2-mediated SIRT3 transcription. Conclusions Overall, we demonstrate that SAL, a potential anti-aging drug candidate, attenuates AD pathology by targeting NRF2/SIRT3 pathway for mitochondrial and neurite protection. Drug discovery strategies focusing on SAL may thus provide promising therapeutics for AD.

Background Ectodysplasin-A (EDA), a skin-specific TNF ligand, interacts with its membrane receptor EDAR to trigger EDA signaling in skin appendage formation. Gene mutations in EDA signaling cause Anhidrotic/Hypohidrotic Ectodermal Dysplasia (A/HED), which affects the formation of skin appendages including hair, teeth, and several exocrine glands. Results We report that EDA triggers the translocation of its receptor EDAR from a cytosolic compartment into the plasma membrane. We use protein affinity purification to show that upon EDA stimulation EDAR associates with SNAP23-STX6-VAMP1/2/3 vesicle trafficking complexes. We find that EDA-dependent PKA activation is critical for the association. Notably, either of two HED-linked EDAR mutations, T346M and R420W, prevents EDA-induced EDAR translocation; and both EDA-induced PKA activation and SNAP23 are required for Meibomian gland (MG) growth in a skin appendage model. Conclusions Overall, in a novel regulatory mechanism, EDA increases plasma membrane translocation of its own receptor EDAR, augmenting EDA-EDAR signaling in skin appendage formation. Our findings also provide PKA and SNAP23 as potential targets for the intervention of HED.

•Dynamic switches between strategies are uncovered by HMM.•A novel model of dynamic effective connectivity is proposed to estimate the information flow between key brain regions.•The rTPJ-rDLPFC interaction is stronger for strategic deception compared with the social heuristic strategies.•The top-down control from the BA10 to the rTPJ is correlated with the level of deception. Information exchange between brain regions is key to understanding information processing for social decision-making, but most analyses ignore its dynamic nature. New insights on this dynamic might help us to uncover the neural correlates of social cognition in the healthy population and also to understand the malfunctioning neural computations underlying dysfunctional social behavior in patients with mental disorders. In this work, we used a multi-round bargaining game to detect switches between distinct bargaining strategies in a cohort of 76 healthy participants. These switches were uncovered by dynamic behavioral modeling using the hidden Markov model. Proposing a novel model of dynamic effective connectivity to estimate the information flow between key brain regions, we found a stronger interaction between the right temporoparietal junction (rTPJ) and the right dorsolateral prefrontal cortex (rDLPFC) for the strategic deception compared with the social heuristic strategies. The level of deception was associated with the information flow from the Brodmann area 10 to the rTPJ, and this association was modulated by the rTPJ-to-rDLPFC information flow. These findings suggest that dynamic bargaining strategy is supported by dynamic reconfiguration of the rDLPFC-and-rTPJ interaction during competitive social interactions.