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"Dong, Yuan"
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Synergy of Pd atoms and oxygen vacancies on In2O3 for methane conversion under visible light
Methane (CH
4
) oxidation to high value chemicals under mild conditions through photocatalysis is a sustainable and appealing pathway, nevertheless confronting the critical issues regarding both conversion and selectivity. Herein, under visible irradiation (420 nm), the synergy of palladium (Pd) atom cocatalyst and oxygen vacancies (OVs) on In
2
O
3
nanorods enables superior photocatalytic CH
4
activation by O
2
. The optimized catalyst reaches ca. 100 μmol h
−1
of C1 oxygenates, with a selectivity of primary products (CH
3
OH and CH
3
OOH) up to 82.5%. Mechanism investigation elucidates that such superior photocatalysis is induced by the dedicated function of Pd single atoms and oxygen vacancies on boosting hole and electron transfer, respectively. O
2
is proven to be the only oxygen source for CH
3
OH production, while H
2
O acts as the promoter for efficient CH
4
activation through ·OH production and facilitates product desorption as indicated by DFT modeling. This work thus provides new understandings on simultaneous regulation of both activity and selectivity by the synergy of single atom cocatalysts and oxygen vacancies.
CH4 oxidation to high value chemicals under mild conditions through photocatalysis confronts critical issues regarding both conversion and selectivity. Here, atomic Pd and oxygen vacancies were integrated on In2O3 nanorods, leading to visible-driven CH4 conversion with a remarkable yield of oxygenates and high selectivity of primary products.
Journal Article
Temperature Forecasting via Convolutional Recurrent Neural Networks Based on Time-Series Data
Today, artificial intelligence and deep neural networks have been successfully used in many applications that have fundamentally changed people’s lives in many areas. However, very limited research has been done in the meteorology area, where meteorological forecasts still rely on simulations via extensive computing resources. In this paper, we propose an approach to using the neural network to forecast the future temperature according to the past temperature values. Specifically, we design a convolutional recurrent neural network (CRNN) model that is composed of convolution neural network (CNN) portion and recurrent neural network (RNN) portion. The model can learn the time correlation and space correlation of temperature changes from historical data through neural networks. To evaluate the proposed CRNN model, we use the daily temperature data of mainland China from 1952 to 2018 as training data. The results show that our model can predict future temperature with an error around 0.907°C.
Journal Article
A high-resolution summary of Cambrian to Early Triassic marine invertebrate biodiversity
One great challenge in understanding the history of life is resolving the influence of environmental change on biodiversity. Simulated annealing and genetic algorithms were used to synthesize data from 11,000 marine fossil species, collected from more than 3000 stratigraphic sections, to generate a new Cambrian to Triassic biodiversity curve with an imputed temporal resolution of 26 ± 14.9 thousand years. This increased resolution clarifies the timing of known diversification and extinction events. Comparative analysis suggests that partial pressure of carbon dioxide (PCO2) is the only environmental factor that seems to display a secular pattern similar to that of biodiversity, but this similarity was not confirmed when autocorrelation within that time series was analyzed by detrending. These results demonstrate that fossil data can provide the temporal and taxonomic resolutions necessary to test (paleo)biological hypotheses at a level of detail approaching those of long-term ecological analyses.
Journal Article
Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
Alzheimer’s disease (AD) is one of the most common causes of dementia. Its pathogenesis is characterized by the aggregation of the amyloid-β (Aβ) protein in senile plaques and the hyperphosphorylated tau protein in neurofibrillary tangles in the brain. Current medications for AD can provide temporary help with the memory symptoms and other cognitive changes of patients, however, they are not able to stop or reverse the progression of AD. New medication discovery and the development of a cure for AD is urgently in need. In this review, we summarized drugs for AD treatments and their recent updates, and discussed the potential of microglia induced neuroinflammation as a target for anti-AD drug development.
Journal Article
Synthesis of a CFD Benchmark Exercise: Examining Fluid Flow and Residence-Time Distribution in a Water Model of Tundish
Computational Fluid Dynamics (CFD) has become an indispensable tool that can potentially predict many phenomena of practical interest in the tundish. Model verification and validation (V&V) are essential parts of a CFD model development process if the models are to be used with sufficient confidence in real industrial tundish applications. The crucial aspects of CFD simulations in the tundish are addressed in this study, such as the selection of the turbulence models, meshing, boundary conditions, and selection of discretization schemes. A series of CFD benchmarking exercises are presented serving as selected examples of appropriate modelling strategies. A tundish database, initiated by German Steel Institute VDEH working group “Fluid Mechanics and Fluid Simulation”, was revisited with the aim of establishing a comprehensive set of best practice guidelines (BPG) in CFD simulations for tundish applications. These CFD benchmark exercises yield important results for the sensible application of CFD models and contribute to further improving the reliability of CFD applications in metallurgical reactors.
Journal Article
HDAC3 inhibition ameliorates ischemia/reperfusion-induced brain injury by regulating the microglial cGAS-STING pathway
Rationale: It is known that neuroinflammation plays a critical and detrimental role in the development of cerebral ischemia/reperfusion (I/R), but the regulation of the cyclic GMP-AMP synthase (cGAS)-mediated innate immune response in I/R-induced neuroinflammation is largely unexplored. This study aimed to investigate the function and regulatory mechanism of cGAS in I/R-induced neuroinflammation and brain injury, and to identify possible strategies for the treatment of ischemic stroke. Methods: To demonstrate that microglial histone deacetylase 3 (HDAC3) regulates the microglial cGAS-stimulator of interferon genes (cGAS-STING) pathway and is involved in I/R-induced neuroinflammation and brain injury, a series of cell biological, molecular, and biochemical approaches were utilized. These approaches include transient middle cerebral artery occlusion (tMCAO), real-time polymerase chain reaction (PCR), RNA sequencing, western blot, co-immunoprecipitation, chromosome-immunoprecipitation, enzyme-linked immunosorbent assay (ELISA), dual-luciferase reporter assay, immunohistochemistry, and confocal imaging. Results: The microglial cGAS- STING pathway was activated by mitochondrial DNA, which promoted the formation of a pro-inflammatory microenvironment. In addition, we revealed that HDAC3 transcriptionally promoted the expression of cGAS and potentiated the activation of the cGAS-STING pathway by regulating the acetylation and nuclear localization of p65 in microglia. Our in vivo results indicated that deletion of cGAS or HDAC3 in microglia attenuated I/R-induced neuroinflammation and brain injury. Conclusion: Collectively, we elucidated that the HDAC3-p65-cGAS-STING pathway is involved in the development of I/R-induced neuroinflammation, identifying a new therapeutic avenue for the treatment of ischemic stroke.
Journal Article
NPFs-mediated actin cytoskeleton: a new viewpoint on autophagy regulation
Macroautophagy/autophagy is a lysosome-dependent catabolic process induced by various cellular stress conditions, maintaining the homeostasis of cells, tissues and organs. Autophagy is a series of membrane-related events involving multiple autophagy-related (ATG) proteins. Most studies to date have focused on various signaling pathways affecting ATG proteins to control autophagy. However, mounting evidence reveals that the actin cytoskeleton acts on autophagy-associated membranes to regulate different events of autophagy. The actin cytoskeleton assists in vesicle formation and provides the mechanical forces for cellular activities that involve membrane deformation. Although the interaction between the actin cytoskeleton and membrane makes the role of actin in autophagy recognized, how the actin cytoskeleton is recruited and assembles on membranes during autophagy needs to be detailed. Nucleation-promoting factors (NPFs) activate the Arp2/3 complex to produce actin cytoskeleton. In this review, we summarize the important roles of the actin cytoskeleton in autophagy regulation and focus on the effect of NPFs on actin cytoskeleton assembly during autophagy, providing new insights into the occurrence and regulatory mechanisms of autophagy.
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Video Abstract
Journal Article
Inhibition of Drp1 SUMOylation by ALR protects the liver from ischemia-reperfusion injury
Hepatic ischemic reperfusion injury (IRI) is a common complication of liver surgery. Although an imbalance between mitochondrial fission and fusion has been identified as the cause of IRI, the detailed mechanism remains unclear. Augmenter of liver regeneration (ALR) was reported to prevent mitochondrial fission by inhibiting dynamin-related protein 1 (Drp1) phosphorylation, contributing partially to its liver protection. Apart from phosphorylation, Drp1 activity is also regulated by small ubiquitin-like modification (SUMOylation), which accelerates mitochondrial fission. This study aimed to investigate whether ALR-mediated protection from hepatic IRI might be associated with an effect on Drp1 SUMOylation. Liver tissues were harvested from both humans and from heterozygous
ALR
knockout mice, which underwent IRI. The SUMOylation and phosphorylation of Drp1 and their modulation by ALR were investigated. Hepatic Drp1 SUMOylation was significantly increased in human transplanted livers and IRI-livers of mice.
ALR-
transfection significantly decreased Drp1 SUMOylation, attenuated the IRI-induced mitochondrial fission and preserved mitochondrial stability and function. This study showed that the binding of transcription factor Yin Yang-1 (YY1) to its downstream target gene
UBA
2, a subunit of SUMO-E1 enzyme heterodimer, was critical to control Drp1 SUMOylation. By interacting with YY1, ALR inhibits its nuclear import and dramatically decreases the transcriptional level of
UBA
2. Consequently, mitochondrial fission was significantly reduced, and mitochondrial function was maintained. This study showed that the regulation of Drp1 SUMOylation by ALR protects mitochondria from fission, rescuing hepatocytes from IRI-induced apoptosis. These new findings provide a potential target for clinical intervention to reduce the effects of IRI during hepatic surgery.
Journal Article
Microglial deletion and inhibition alleviate behavior of post-traumatic stress disorder in mice
Background
Alteration of immune status in the central nervous system (CNS) has been implicated in the development of post-traumatic stress disorder (PTSD). However, the nature of overall changes in brain immunocyte landscape in PTSD condition remains unclear.
Methods
We constructed a mouse PTSD model by electric foot-shocks followed by contextual reminders and verified the PTSD-related symptoms by behavior test (including contextual freezing test, open-field test, and elevated plus maze test). We examined the immunocyte panorama in the brains of the naïve or PTSD mice by using single-cell mass cytometry. Microglia number and morphological changes in the hippocampus, prefrontal cortex, and amygdala were analyzed by histopathological methods. The gene expression changes of those microglia were detected by quantitative real-time PCR. Genetic/pharmacological depletion of microglia or minocycline treatment before foot-shocks exposure was performed to study the role of microglia in PTSD development and progress.
Results
We found microglia are the major brain immune cells that respond to PTSD. The number of microglia and ratio of microglia to immunocytes was significantly increased on the fifth day of foot-shock exposure. Furthermore, morphological analysis and gene expression profiling revealed temporal patterns of microglial activation in the hippocampus of the PTSD brains. Importantly, we found that genetic/pharmacological depletion of microglia or minocycline treatment before foot-shock exposure alleviated PTSD-associated anxiety and contextual fear.
Conclusion
Our results demonstrated a critical role for microglial activation in PTSD development and a potential therapeutic strategy for the clinical treatment of PTSD in the form of microglial inhibition.
Journal Article