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21,903 result(s) for "Sun, Jing"
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Linewidth Measurement of a Narrow-Linewidth Laser: Principles, Methods, and Systems
Narrow-linewidth lasers mainly depend on the development of advanced laser linewidth measurement methods for related technological progress as key devices in satellite laser communications, precision measurements, ultra-high-speed optical communications, and other fields. This manuscript provides a theoretical analysis of linewidth characterization methods based on the beat frequency power spectrum and laser phase noise calculations, and elaborates on existing research of measurement technologies. In addition, to address the technical challenges of complex measurement systems that commonly rely on long optical fibers and significant phase noise jitter in the existing research, a short-delay self-heterodyne method based on coherent envelope spectrum demodulation was discussed in depth to reduce the phase jitter caused by 1/f noise. We assessed the performance parameters and testing conditions of different lasers, as well as the corresponding linewidth characterization methods, and analyzed the measurement accuracy and error sources of various methods.
Early childhood education in Chinese societies
This volume provides an up-to-date account of relevant early childhood policy and practice in five Chinese societies: the People's Republic of China or Mainland China, Hong Kong, Macao, Singapore, and Taiwan. It analyses how traditional Chinese values, Eastern and Western curricular approaches, and socio-political, economic, cultural and demographic changes influence current policies, services and practice.
Self-operation and low-carbon scheduling optimization of solar thermal power plants with thermal storage systems
Photo thermal power generation, as a renewable energy technology, has broad development prospects. However, the operation and scheduling of photo thermal power plants rarely consider their internal structure and energy flow characteristics. Therefore, this study explains the structure of a solar thermal power plant with a thermal storage system and analyzes its main energy flow modes to establish a self-operation and low-carbon scheduling optimization model for the solar thermal power plant. The simulation results of the example showed that for the self-operating model oriented towards power generation planning and peak valley electricity prices, the existence of a thermal storage system could improve the power generation capacity and revenue of the photovoltaic power plant. For example, when the capacity of the thermal storage system was greater than 6 h, the penalty for insufficient power generation in the simulation result was 0 $, and the maximum increase in revenue reached 84.9% as the capacity of the thermal storage system increased. In addition, when the capacity of the thermal storage system increased from 0 to 8 h, the comprehensive operating cost decreased from 1635.2 k $ to 1224.6 k $, and the carbon emissions decreased from 26.4 × 10 3  ton to 22.1 × 10 3  ton. Compared with the existing literature, this study provides a more comprehensive and systematic solution through detailed energy flow analysis and optimization model. The research has practical and far-reaching significance for promoting the development of clean energy technology, improving the sustainable utilization of renewable energy, and optimizing the overall performance of the energy system.
The extracellular signal-regulated kinase 1/2 pathway in neurological diseases: A potential therapeutic target (Review)
Signaling pathways are critical modulators of a variety of physiological and pathological processes, and the abnormal activation of some signaling pathways can contribute to disease progression in various conditions. As a result, signaling pathways have emerged as an important tool through which the occurrence and development of diseases can be studied, which may then lead to the development of novel drugs. Accumulating evidence supports a key role for extracellular signal-regulated kinase 1/2 (ERK1/2) signaling in the embryonic development of the central nervous system (CNS) and in the regulation of adult brain function. ERK1/2, one of the most well characterized members of the mitogen-activated protein kinase family, regulates a range of processes, from metabolism, motility and inflammation, to cell death and survival. In the nervous system, ERK1/2 regulates synaptic plasticity, brain development and repair as well as memory formation. ERK1/2 is also a potent effector of neuronal death and neuroinflammation in many CNS diseases. This review summarizes recent findings in neurobiological ERK1/2 research, with a special emphasis on findings that clarify our understanding of the processes that regulate the plethora of isoform-specific ERK functions under physiological and pathological conditions. Finally, we suggest some potential therapeutic strategies associated with agents acting on the ERK1/2 signaling to prevent or treat neurological diseases.
Gq activity- and β-arrestin-1 scaffolding-mediated ADGRG2/CFTR coupling are required for male fertility
Luminal fluid reabsorption plays a fundamental role in male fertility. We demonstrated that the ubiquitous GPCR signaling proteins Gq and β-arrestin-1 are essential for fluid reabsorption because they mediate coupling between an orphan receptor ADGRG2 (GPR64) and the ion channel CFTR. A reduction in protein level or deficiency of ADGRG2, Gq or β-arrestin-1 in a mouse model led to an imbalance in pH homeostasis in the efferent ductules due to decreased constitutive CFTR currents. Efferent ductule dysfunction was rescued by the specific activation of another GPCR, AGTR2. Further mechanistic analysis revealed that β-arrestin-1 acts as a scaffold for ADGRG2/CFTR complex formation in apical membranes, whereas specific residues of ADGRG2 confer coupling specificity for different G protein subtypes, this specificity is critical for male fertility. Therefore, manipulation of the signaling components of the ADGRG2-Gq/β-arrestin-1/CFTR complex by small molecules may be an effective therapeutic strategy for male infertility.
miR-106b-5p upregulation is associated with microglial activation and inflammation in the mouse hippocampus following status epilepticus
To investigate the association of miR-106b-5p with neuroinflammation and microglial activation in a status epilepticus (SE) mouse model. We examined changes in the expression of microRNA-106b-5p (miRNA-106b-5p), repulsive guidance molecule A (RGMa), triggering receptor expressed on myeloid cells 2 (TREM2), and the microglia-related markers interleukin (IL)-1β, IL-4, IL-6, IL-10, inducible nitric oxide synthase (iNOS), and arginase-1 (Arg-1) in the mouse hippocampus of the lithium–pilocarpine-induced SE mouse model. Eighty-four female C57BL/6 mice were randomly divided into a normal control group (n = 12), and six SE groups (n = 12/group), which were monitored at 6 h and at 1, 3, 7, 14, and 21 days (d) post-SE induction. Unlike in the dentate gyrus, immunohistochemical staining revealed prominent neuronal swelling at 6 h, significant neuronal loss and apoptosis on day 3, and recovery by day 14 in the hippocampal cornu ammonis (CA)1 and CA3 pyramidal cells in SE mice. We noted elevated levels of miRNA-106b-5p and all microglia-related markers, which peaked at 3 days post-SE, except IL-4, which peaked at 7 days post-SE, indicating inflammation and microglial activation. RGMa and TREM2 levels decreased at 6 h post-SE. All markers but miRNA-106b-5p, RGMa, and TREM2 returned to baseline levels at 21 days post-SE. Dual luciferase reporter gene assay showed that microRNA-106b-5p can interact with RGMa. We observed that miR-106b-5p level increased while both RGMa and TREM2 levels decreased post-SE and showed associations with microglial activation and inflammation in the mouse hippocampus, suggesting their potential as SE therapeutic targets.
rs1990622 variant associates with Alzheimer’s disease and regulates TMEM106B expression in human brain tissues
Background It has been well established that the TMEM106B gene rs1990622 variant was a frontotemporal dementia (FTD) risk factor. Until recently, growing evidence highlights the role of TMEM106B in Alzheimer’s disease (AD). However, it remains largely unclear about the role of rs1990622 variant in AD. Methods Here, we conducted comprehensive analyses including genetic association study, gene expression analysis, eQTLs analysis, and colocalization analysis. In stage 1, we conducted a genetic association analysis of rs1990622 using large-scale genome-wide association study (GWAS) datasets from International Genomics of Alzheimer’s Project (21,982 AD and 41,944 cognitively normal controls) and UK Biobank (314,278 participants). In stage 2, we performed a gene expression analysis of TMEM106B in 49 different human tissues using the gene expression data in GTEx. In stage 3, we performed an expression quantitative trait loci (eQTLs) analysis using multiple datasets from UKBEC, GTEx, and Mayo RNAseq Study. In stage 4, we performed a colocalization analysis to provide evidence of the AD GWAS and eQTLs pair influencing both AD and the TMEM106B expression at a particular region. Results We found (1) rs1990622 variant T allele contributed to AD risk. A sex-specific analysis in UK Biobank further indicated that rs1990622 T allele only contributed to increased AD risk in females, but not in males; (2) TMEM106B showed different expression in different human brain tissues especially high expression in cerebellum; (3) rs1990622 variant could regulate the expression of TMEM106B in human brain tissues, which vary considerably in different disease statuses, the mean ages at death, the percents of females, and the different descents of the selected donors; (4) colocalization analysis provided suggestive evidence that the same variant contributed to AD risk and TMEM106B expression in cerebellum. Conclusion Our comprehensive analyses highlighted the role of FTD rs1990622 variant in AD risk. This cross-disease approach may delineate disease-specific and common features, which will be important for both diagnostic and therapeutic development purposes. Meanwhile, these findings highlight the importance to better understand TMEM106B function and dysfunction in the context of normal aging and neurodegenerative diseases.
Comparing large language models and search engine responses to common orthodontic questions
Large Language Models (LLMs) highlight their potential in supporting patient education and self-management. Their performance in responses to orthodontic questions has yet to be explored. This study aims to compare the quality, empathy, readability, and satisfaction of responses from LLMs and search engines on common orthodontic questions. Forty-five common orthodontic questions (six categories) and a prompt were developed, and a self-designed multidimensional evaluation questionnaire was constructed. Questions were presented to 5 LLMs and 3 search engines on December,22,2024. The primary outcomes were the median expert-rated scores of LLMs versus search engine responses on quality, empathy, readability, and satisfaction, using 5- or 10-point Likert scales. LLMs scored significantly higher than search engines in quality (4.00 vs. 3.50, p < 0.001), empathy (3.75 vs. 3.50, p < 0.001), readability (4.00 vs. 3.75, p < 0.001), and satisfaction (8.00 vs. 7.25, p < 0.001). LLM-generated responses were rated significantly higher than those from search engines in therapeutic outcomes category, appliance selection category and cost category. In this cross-sectional study, the LLMs, particularly GPT-4o, outperformed search engines. These results indicate the potential of LLMs as supplementary tools for orthodontic patient education and self-management.
Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA mediated miRNA evasion
Thousands of genes have been well demonstrated to play important roles in cancer progression. As genes do not function in isolation, they can be grouped into “networks” based on their interactions. In this study, we discover a network regulating Claudin-4 in gastric cancer. We observe that Claudin-4 is up-regulated in gastric cancer and is associated with poor prognosis. Claudin-4 reinforce proliferation, invasion, and EMT in AGS, HGC-27, and SGC-7901 cells, which could be reversed by miR-596 and miR-3620-3p. In addition, lncRNA-KRTAP5-AS1 and lncRNA-TUBB2A could act as competing endogenous RNAs to affect the function of Claudin-4. Our results suggest that non-coding RNAs play important roles in the regulatory network of Claudin-4. As such, non-coding RNAs should be considered as potential biomarkers and therapeutic targets against gastric cancer. Non-coding RNAs can modify the expression of proteins in cancer networks. Here the authors reveal a regulatory network in gastric cancer whereby claudin-4 expression is reduced by specific miRNAs, which are in turn bound by specific lncRNAs acting as competing endogenous RNAs (ceRNAs), resulting in increased claudin-4 expression.