Search Results Heading

MBRLSearchResults

mbrl.module.common.modules.added.book.to.shelf
Title added to your shelf!
View what I already have on My Shelf.
Oops! Something went wrong.
Oops! Something went wrong.
While trying to add the title to your shelf something went wrong :( Kindly try again later!
Are you sure you want to remove the book from the shelf?
Oops! Something went wrong.
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
    Done
    Filters
    Reset
  • Discipline
      Discipline
      Clear All
      Discipline
  • Is Peer Reviewed
      Is Peer Reviewed
      Clear All
      Is Peer Reviewed
  • Item Type
      Item Type
      Clear All
      Item Type
  • Subject
      Subject
      Clear All
      Subject
  • Year
      Year
      Clear All
      From:
      -
      To:
  • More Filters
      More Filters
      Clear All
      More Filters
      Source
    • Language
120 result(s) for "Yang, Qiumei"
Sort by:
Tryptophan hydroxylase 1 drives glioma progression by modulating the serotonin/L1CAM/NF-κB signaling pathway
Background Glioma is one of the main causes of cancer-related mortality worldwide and is associated with high heterogeneity. However, the key players determining the fate of glioma remain obscure. In the present study, we shed light on tumor metabolism and aimed to investigate the role of tryptophan hydroxylase 1 (TPH-1) in the advancement of glioma. Method Herein, the levels of TPH-1 expression in glioma tissues were evaluated using The Cancer Genome Atlas (TCGA) database. Further, the proliferative characteristics and migration ability of TPH-1 overexpressing LN229/T98G cells were evaluated. Additionally, we performed a cytotoxicity analysis using temozolomide (TMZ) in these cells. We also examined the tumor growth and survival time in a mouse model of glioma treated with chemotherapeutic agents and a TPH-1 inhibitor. Results The results of both clinical and experimental data showed that excess TPH-1 expression resulted in sustained glioma progression and a dismal overall survival in these patients. Mechanistically, TPH-1 increased the production of serotonin in glioma cells. The elevated serotonin levels then augmented the NF-κB signaling pathway through the upregulation of the L1-cell adhesion molecule (L1CAM), thereby contributing to cellular proliferation, invasive migration, and drug resistance. In vivo experiments demonstrated potent antitumor effects, which benefited further from the synergistic combination of TMZ and LX-1031. Conclusion Taken together, these data suggested that TPH-1 facilitated cellular proliferation, migration, and chemoresistance in glioma through the serotonin/L1CAM/NF-κB pathway. By demonstrating the link of amino acid metabolic enzymes with tumor development, our findings may provide a potentially viable target for therapeutic manipulation aimed at eradicating glioma.
α‐Synuclein aggregation causes muscle atrophy through neuromuscular junction degeneration
Background Sarcopenia is common in patients with Parkinson's disease (PD), showing mitochondrial oxidative stress in skeletal muscle. The aggregation of α‐synuclein (α‐Syn) to induce oxidative stress is a key pathogenic process of PD; nevertheless, we know little about its potential role in regulating peripheral nerves and the function of the muscles they innervate. Methods To investigate the role of α‐Syn aggregation on neuromuscular system, we used the Thy1 promoter to overexpress human α‐Syn transgenic mice (mThy1‐hSNCA). hα‐Syn expression was evaluated by western blot, and its localization was determined by confocal microscopy. The impact of α‐Syn aggregation on the structure and function of skeletal muscle mitochondria and neuromuscular junctions (NMJs), as well as muscle mass and function were characterized by flow cytometry, transmission electron microscopy, Seahorse XF24 metabolic assay, and AAV9 in vivo injection. We assessed the regenerative effect of mitochondrial‐targeted superoxide dismutase (Mito‐TEMPO) after skeletal muscle injury in mThy1‐hSNCA mice. Results Overexpressed hα‐Syn protein localized in motor neuron axons and NMJs in muscle and formed aggregates. α‐Syn aggregation increased the number of abnormal mitochondrial in the intramuscular axons and NMJs by over 60% (P < 0.01), which inhibited the release of acetylcholine (ACh) from presynaptic vesicles in NMJs (P < 0.05). The expression of genes associated with NMJ activity, neurotransmission and regulation of reactive oxygen species (ROS) metabolic process were significantly decreased in mThy1‐hSNCA mice, resulting in ROS production elevated by ~220% (P < 0.05), thereby exacerbating oxidative stress. Such process altered mitochondrial spatial relationships to sarcomeric structures, decreased Z‐line spacing by 36% (P < 0.05) and increased myofibre apoptosis by ~10% (P < 0.05). Overexpression of α‐Syn altered the metabolic profile of muscle satellite cells (MuSCs), including basal respiratory capacity (~170% reduction) and glycolytic capacity (~150% reduction) (P < 0.05) and decreased cell migration and fusion during muscle regeneration (~60% and ~40%, respectively) (P < 0.05). We demonstrated that Mito‐TEMPO treatment could restore the oxidative stress status (the complex I/V protein and enzyme activities increased ~200% and ~150%, respectively), which caused by α‐Syn aggregation, and improve the ability of muscle regeneration after injury. In addition, the NMJ receptor fragmentation and ACh secretion were also improved. Conclusions These results reveal that the α‐synuclein aggregation plays an important role in regulating acetylcholine release from neuromuscular junctions and induces intramuscular mitochondrial oxidative stress, which can provide new insights into the aetiology of muscle atrophy in patients with Parkinson's disease.
A Long-Term Video Tracking Method for Group-Housed Pigs
Pig tracking provides strong support for refined management in pig farms. However, long and continuous multi-pig tracking is still extremely challenging due to occlusion, distortion, and motion blurring in real farming scenarios. This study proposes a long-term video tracking method for group-housed pigs based on improved StrongSORT, which can significantly improve the performance of pig tracking in production scenarios. In addition, this research constructs a 24 h pig tracking video dataset, providing a basis for exploring the effectiveness of long-term tracking algorithms. For object detection, a lightweight pig detection network, YOLO v7-tiny_Pig, improved based on YOLO v7-tiny, is proposed to reduce model parameters and improve detection speed. To address the target association problem, the trajectory management method of StrongSORT is optimized according to the characteristics of the pig tracking task to reduce the tracking identity (ID) switching and improve the stability of the algorithm. The experimental results show that YOLO v7-tiny_Pig ensures detection applicability while reducing parameters by 36.7% compared to YOLO v7-tiny and achieving an average video detection speed of 435 frames per second. In terms of pig tracking, Higher-Order Tracking Accuracy (HOTA), Multi-Object Tracking Accuracy (MOTP), and Identification F1 (IDF1) scores reach 83.16%, 97.6%, and 91.42%, respectively. Compared with the original StrongSORT algorithm, HOTA and IDF1 are improved by 6.19% and 10.89%, respectively, and Identity Switch (IDSW) is reduced by 69%. Our algorithm can achieve the continuous tracking of pigs in real scenarios for up to 24 h. This method provides technical support for non-contact pig automatic monitoring.
Effect of Ultrasonic-Assisted Casting on Hot Deformation Mechanism and Microstructure of 35CrMo Steel Ingot
Hot compression tests were performed with strain rates (0.01–10 s−1) and temperatures (850–1150 °C). The power law relationship between the critical stress and critical strain and Zener–Hollomon parameters was determined by θ-σ curves. Microstructure was investigated by electron backscattered diffraction. The results showed that the flow behavior and microstructure of 35CrMo steel was affected by ultrasonic-assisted casting. The activation energy of non-ultrasonic and ultrasonic-assisted 35CrMo steel were 410 ± 9.9 and 386 ± 9.4 kJ/mol, respectively, and the activation energy of ultrasonic-assisted specimens was reduced by 6%. In addition, the ultrasonic-assisted treatment refines the grains to some extent and makes the softening process of ultrasonic-assisted samples progress faster, which promoted the development of dynamic recrystallization and the production of Σ3 boundaries. The discontinuous dynamic recrystallization was the main DRX nucleation mechanism of the 35CrMo steel.
Effect of Hot Deformation Process Parameters on Microstructure and Corrosion Behavior of 35CrMoV Steel
Hot deformation experiments of as-cast 35CrMoV steel, with strain rates of 0.01 s−1 and 10 s−1, deformation temperatures of 850, 950, and 1050 °C, and an extreme deformation reaching 50%, were carried out using a Gleeble-3810 thermal simulator. Electrochemical corrosion experiments were conducted on the deformed specimens. The microstructure was observed by optical microscope (OM), and the corrosion morphology and corrosion products of the specimens were investigated by scanning electron microscopy (SEM), energy disperse spectroscopy (EDS), confocal laser scanning microscopy (CLSM), and X-ray diffraction (XRD) techniques. The results show that the grain size increased gradually with an increase in the deformation temperature at the same strain rate, whereas the corrosion resistance deteriorated. At the same deformation temperature, the grain size becomes smaller as the strain rate increases, which enhances the corrosion resistance. This is mainly attributed to the fine grains, which can form more grain boundaries, increase the grain boundary area, and accelerate the formation of the inner rust layer at the beginning of corrosion. Moreover, fine grains can also refine the rust particles and enhance the bonding strength between the inner rust layer and the matrix. The denseness and stability of the inner rust layer increases as the corrosion process progresses, thereby improving corrosion resistance.
Group-housed pigs and their body parts detection with Cascade Faster R-CNN
The detection of individual pigs and their parts is a key step to realizing automatic recognition of group-housed pigs' behavior by video monitoring. However, it is still difficult to accurately locate each individual pig and their body parts from video images of groups-housed pigs. To solve this problem, a Cascade Faster R-CNN Pig Detector (C-FRPD) was designed to detect the individual pigs and different parts of their body. Firstly, the features were extracted by 101-layers Residual Networks (ResNet-101) from video images of group-housed pigs, and the features were input into the region proposal networks (RPN) to obtain the region proposals. Then classification and bounding box regression on region proposals were performed to get the location of each pig. Finally, the body parts of the pig were determined by using the Cascade structure to search on the feature map of the pig body area. These operations completed the detection of the whole body of each pig and its different parts of the body, and established the association between the whole and parts of body in the end-to-end detection. In this study, 1500 pig pen images were trained and tested. The test results showed that the detection accuracy of C-FRPD reached 98.4%. Compared with the Faster R-CNN without cascade structure, the average detection accuracy was increased by 4.3 percentage points. The average detection time of a single image was 259 ms. The method in this study could accurately detect and correlate the individual pig with its head, back, and tail in the image. This method can provide a technical reference for recognizing the behavior of group-housed pigs.
Tryptophan hydroxylase 1 drives glioma progression by modulating the serotonin/L1CAM/NF-?B signaling pathway
Glioma is one of the main causes of cancer-related mortality worldwide and is associated with high heterogeneity. However, the key players determining the fate of glioma remain obscure. In the present study, we shed light on tumor metabolism and aimed to investigate the role of tryptophan hydroxylase 1 (TPH-1) in the advancement of glioma. Herein, the levels of TPH-1 expression in glioma tissues were evaluated using The Cancer Genome Atlas (TCGA) database. Further, the proliferative characteristics and migration ability of TPH-1 overexpressing LN229/T98G cells were evaluated. Additionally, we performed a cytotoxicity analysis using temozolomide (TMZ) in these cells. We also examined the tumor growth and survival time in a mouse model of glioma treated with chemotherapeutic agents and a TPH-1 inhibitor. The results of both clinical and experimental data showed that excess TPH-1 expression resulted in sustained glioma progression and a dismal overall survival in these patients. Mechanistically, TPH-1 increased the production of serotonin in glioma cells. The elevated serotonin levels then augmented the NF-?B signaling pathway through the upregulation of the L1-cell adhesion molecule (L1CAM), thereby contributing to cellular proliferation, invasive migration, and drug resistance. In vivo experiments demonstrated potent antitumor effects, which benefited further from the synergistic combination of TMZ and LX-1031. Taken together, these data suggested that TPH-1 facilitated cellular proliferation, migration, and chemoresistance in glioma through the serotonin/L1CAM/NF-?B pathway. By demonstrating the link of amino acid metabolic enzymes with tumor development, our findings may provide a potentially viable target for therapeutic manipulation aimed at eradicating glioma.
Regulation of myonuclear positioning and muscle function by the skeletal muscle-specific CIP protein
The appropriate arrangement of myonuclei within skeletal muscle myofibers is of critical importance for normal muscle function, and improper myonuclear localization has been linked to a variety of skeletal muscle diseases, such as centronuclear myopathy and muscular dystrophies. However, the molecules that govern myonuclear positioning remain elusive. Here, we report that skeletal muscle-specific CIP (sk-CIP) is a regulator of nuclear positioning. Genetic deletion of sk-CIP in mice results in misalignment of myonuclei along the myofibers and at specialized structures such as neuromuscular junctions (NMJs) and myotendinous junctions (MTJs) in vivo, impairing myonuclear positioning after muscle regeneration, leading to severe muscle dystrophy in mdx mice, a mouse model of Duchenne muscular dystrophy. sk-CIP is localized to the centrosome in myoblasts and relocates to the outer nuclear envelope in myotubes upon differentiation. Mechanistically, we found that sk-CIP interacts with the Linker of Nucleoskeleton and Cytoskeleton (LINC) complex and the centriole Microtubule Organizing Center (MTOC) proteins to coordinately modulate myonuclear positioning and alignment. These findings indicate that sk-CIP may function as a muscle-specific anchoring protein to regulate nuclear position in multinucleated muscle cells.
Bergaptol Alleviates LPS-Induced Neuroinflammation, Neurological Damage and Cognitive Impairment via Regulating the JAK2/STAT3/p65 Pathway
Purpose: Neuroinflammation is considered a critical pathological process in various central nervous system (CNS) diseases and is closely related to neuronal death and dysfunction. Bergaptol is a natural 5-hydroxyfurocoumarin found in lemon, bergamot and other plants. Some studies have confirmed its anti-cancer, anti-inflammatory and anti-atherogenic functions, indicating that it may have significant medicinal value. In this study, we investigated the potential effect of Bergaptol in vitro and in vivo neuroinflammatory models. Methods: Mice were injected with LPS (40 μg/kg) into the hippocampal CA1 region and then injected intraperitoneally with Bergaptol (10, 20 and 40 mg/kg) once a day for two weeks. In addition, to verify the effect of Bergaptol on BV2 cells, Bergaptol with different concentrations (5, 10 and 20 μg/mL) was firstly incubated for 1 hour, then LPS with a concentration of 1 μg/mL was added and incubated for 23 hours. Results: Bergaptol treatment significantly improved the cognitive impairment induced by LPS. In addition, Bergaptol significantly inhibited the reduction of dendritic spines and the mRNA level of inflammatory factors (TNF-α, IL-6 and IL-1β) in hippocampal induced by LPS. In vitro, Bergaptol inhibited the production of TNF-α, IL-6 and IL-1β from LPS-treated BV-2 cells. In addition, Bergaptol treatment significantly reduced the phosphorylation levels of JAK2, STAT3 and p65 in LPS-stimulated BV-2 cells. Conclusion: In conclusion, our results suggest that Bergaptol alleviates LPS-induced neuroinflammation, neurological damage and cognitive impairment by regulating the JAK2/STAT3/P65 pathway, suggesting that Bergaptol is a promising neuroprotective agent.
Trade liberalization, fiscal federalism, and foreign capital inflows in the context of the Chinese reforms
In recent years China is increasingly considered as a successful example for a transition towards a market economy. The growth rate of the Chinese economy has averaged 9.5 percent in the past fifteen years. What are the secrets behind the Chinese story? This dissertation aims to answer this question by analyzing three important areas in the Chinese economic reform--trade liberalization, the central-local governmental fiscal relation, and foreign investment. The first essay describes the extensive reforms to China's external sector from 1979 to 1994. It then estimates an econometric model to test the empirical effect of trade liberalization on exports employing unit root, cointegration, and recursive coefficient stability tests. The major result found in this paper is that after 1984, six years after China embarked its historical economic reform, the paper finds some evidence of structural break of liberalization of exports which is contrast to previous studies. In the second essay, I employ the Principal-Agent Model to discuss the impact of corruption in local tax administration on the tax revenue of the central government in China. When the central government does not have the information about the true income of firms and local governments have great discretion in manipulating the tax administration system, the tax revenue of the central government is subject to erosion due to collusion between firms and local governments. To solve the problem, the central government needs to design incentive-compatible tax revenue sharing schemes for local governments. The third essay provides empirical evidence of the determinants of foreign direct investment inflows into China. It first shows that including human capital in the neoclassical growth model does not resolve the question: \"Why doesn't capital flow from rich to poor countries?\" posed by Lucas (1990). Twenty nine provinces in China are tested with the result that predicted rates of return to physical capital in some poor provinces are more than 600 percent of those in Shanghai, the representative rich province. The paper finds that the size of the market and the growth of private economy are the main factors that determine the foreign capital investment in China.