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4,738 result(s) for "Kong, Yan"
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دراسات حول الفضاء العالمي و\الحزام والطريق\ : (مجلد الثقافة)
ينطلق هذا المجلد من العلاقة الهيكلية بين \"الفضاء\" و\"الثقافة\"، ويجمع بين مفهوم \"الفضاء\" في الجغرافيا ومفهوم \"السياق\" في الدراسات الثقافية وغيرهم من المفاهيم الأخرى، ويشرح نماذج ودلالات وأهداف مبادرة \"الحزام والطريق\" في سياق الحضارة الحديثة، ويصف صورة امتداد الحضارة على المحور التاريخي لـ \"الحزام والطريق\"، ويحلل الدلالة الثقافية في كل من اتجاه القيمة وبناء القوة الناعمة وإنشاء السياق الشرقي الخاصين بمبادرة \"الحزام والطريق\"، ويفسر علاقة الارتباط بين الثقافة الوطنية لـ \"الحزام والطريق\" والفضاء الوطني، ويكشف عن السرد عبر الفضاء للرموز الثقافية لـ \"الحزام والطريق\" ويوضح التعبير الرقمي والمرئي لواقع \"الحزام والطريق\"
Underlying the Mechanisms of Doxorubicin-Induced Acute Cardiotoxicity: Oxidative Stress and Cell Death
Cancer is a destructive disease that causes high levels of morbidity and mortality. Doxorubicin (DOX) is a highly efficient antineoplastic chemotherapeutic drug, but its use places survivors at risk for cardiotoxicity. Many studies have demonstrated that multiple factors are involved in DOX-induced acute cardiotoxicity. Among them, oxidative stress and cell death predominate. In this review, we provide a comprehensive overview of the mechanisms underlying the source and effect of free radicals and dependent cell death pathways induced by DOX. Hence, we attempt to explain the cellular mechanisms of oxidative stress and cell death that elicit acute cardiotoxicity and provide new insights for researchers to discover potential therapeutic strategies to prevent or reverse doxorubicin-induced cardiotoxicity.
دراسات حول الفضاء العالمي و\الحزام والطريق\ : (مجلد السياحة)
إن استراتيجية \"الحزام والطريق\" هي عملية طويلة الأمد، ولا يمكن وصف دورها في تعزيز تنمية السياحة ببساطة. يحلل \"الفضاء العالمي و\"حزام واحد وطريق واحد\" حجم السياحة\" الوضع الحالي لتنمية السياحة العالمية في سياق استراتيجية \"حزام واحد وطريق واحد\"، ويقدم بالتفصيل تطور السياحة العالمية والخلفية السياحية. \"حزام وطريق\"، بما في ذلك نظرة عامة على صناعة السياحة العالمية، والاتجاهات الجديدة في تنمية السياحة العالمية ونمط السياحة العالمية، وما إلى ذلك، واستنادا إلى تحليل فرص وتحديات تنمية السياحة العالمية والصينية، والتأثير الترويجي لـ \"حزام واحد وطريق واحد\"، وتم تفسير استراتيجية \"الحزام والطريق\" لتنمية السياحة.
FNDC5 alleviates oxidative stress and cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity via activating AKT
Oxidative stress and cardiomyocyte apoptosis play critical roles in doxorubicin (DOX)-induced cardiotoxicity. Previous studies indicated that fibronectin type III domain-containing 5 (FNDC5) and its cleaved form, irisin, could preserve mitochondrial function and attenuate oxidative damage as well as cell apoptosis, however, its role in DOX-induced cardiotoxicity remains unknown. Our present study aimed to investigate the role and underlying mechanism of FNDC5 on oxidative stress and cardiomyocyte apoptosis in DOX-induced cardiotoxicity. Cardiomyocyte-specific FNDC5 overexpression was achieved using an adeno-associated virus system, and then the mice were exposed to a single intraperitoneal injection of DOX (15 mg/kg) to generate DOX-induced cardiotoxicity. Herein, we found that FNDC5 expression was downregulated in DOX-treated murine hearts and cardiomyocytes. Fndc5 deficiency resulted in increased oxidative damage and apoptosis in H9C2 cells under basal conditions, imitating the phenotype of DOX-induced cardiomyopathy in vitro, conversely, FNDC5 overexpression or irisin treatment alleviated DOX-induced oxidative stress and cardiomyocyte apoptosis in vivo and in vitro. Mechanistically, we identified that FNDC5/Irisin activated AKT/mTOR signaling and decreased DOX-induced cardiomyocyte apoptosis, and moreover, we provided direct evidence that the anti-oxidant effect of FNDC5/Irisin was mediated by the AKT/GSK3β/FYN/Nrf2 axis in an mTOR-independent manner. And we also demonstrated that heat shock protein 20 was responsible for the activation of AKT caused by FNDC5/Irisin. In line with the data in acute model, we also found that FNDC5/Irisin exerted beneficial effects in chronic model of DOX-induced cardiotoxicity (5 mg/kg, i.p., once a week for three times, the total cumulative dose is 15 mg/kg) in mice. Based on these findings, we supposed that FNDC5/Irisin was a potential therapeutic agent against DOX-induced cardiotoxicity.
دراسات حول الفضاء العالمي و\الحزام والطريق\ : (مجلد البيئة الإيكولوجية)
إن معظم الدول والمناطق على طول «الحزام والطريق» هي دول نامية، وتعاني جميعا من مشكلات في البيئة الإيكولوجية أكثر أو أقل، كما إنها تواجه تحديات ضخمة في التوازن بين التنمية وحماية البيئة. وتواجه هذه البلدان النامية فرصا غير مسبوقة أتاحها المفهوم الاستراتيجي لمبادرة «الحزام والطريق»، كما أن كيفية التعامل مع التحدي المتمثل في حماية البيئة الإيكولوجية أثناء بناء وتطوير «الحزام والطريق» هي المهمة الأساسية التي تواجهها البلدان النامية بما فيها الصين. ويناقش هذا الكتاب ويلخص الخلفية البيئية الإيكولوجية للبلدان/ المناطق المشاركة في مبادرة \"الحزام والطريق\" والمشكلات الرئيسية في هذا الجانب.
Vertical transmission of Zika virus targeting the radial glial cells affects cortex development of offspring mice
The recent Zika virus (ZIKV) epidemic in Latin America coincided with a marked increase in microcephaly in newborns. However, the causal link between maternal ZIKV infection and malformation of the fetal brain has not been firmly established. Here we show a vertical transmission of ZIKV in mice and a marked effect on fetal brain development. We found that intraperitoneal (i.p.) injection of a contemporary ZIKV strain in pregnant mice led to the infection of radial gila cells (RGs) of dorsal ventricular zone of the fetuses, the primary neural progenitors responsi- ble for cortex development, and caused a marked reduction of these cortex founder cells in the fetuses. Interestingly, the infected fetal mice exhibited a reduced cavity of lateral ventricles and a discernable decrease in surface areas of the cortex. This study thus supports l;he conclusion that vertically transmitted ZIKV affects fetal brain development and provides a valuable animal model for the evaluation of potential therapeutic or preventative strategies.
دراسات حول الفضاء العالمي و\الحزام والطريق\ : (مجلد الموانئ البحرية)
ينقسم الكتاب إلى خمسة فصول، يقدم الفصل الأول نظام الموانئ العالمي والعلاقات بين المدن الساحلية والتعاون في مجال الموانئ، ويناقش الفصل الثاني الخدمات اللوجستية البحرية العالمية وتطوير لوجستيات الموانئ الرئيسية، ويتناول الفصل الثالث نظام الموانئ في الصين وخصائصه. الاستجابة العالمية: يحلل الفصل الرابع بشكل رئيسي مؤشر البلطيق، وهو مؤشر تقييم مراكز الشحن الدولية، ويناقش الفصل الخامس نمط الموانئ العالمية وتغيرات النظام وتطور النقل البحري بناءً على منظور عالمي.
Random forest model in tax risk identification of real estate enterprise income tax
The text describes improvements made to the random forest model to enhance its distinctiveness in addressing tax risks within the real estate industry, thereby tackling issues related to tax losses. Firstly, the paper introduces the potential application of the random forest model in identifying tax risks. Subsequently, the experimental analysis focuses on the selection of indicators for tax risk. Finally, the paper develops and utilizes actual taxpayer data to test a risk identification model, confirming its effectiveness. The experimental results indicate that the model’s output report includes basic taxpayer information, a summary of tax compliance risks, value-added tax refund situations, directions of suspicious items, and detailed information on common indicators. This paper comprehensively presents detailed taxpayer data, providing an intuitive understanding of tax-related risks. Additionally, the paper reveals the level of enterprise risk registration assessment, risk probability, risk value, and risk assessment ranking. Further analysis shows that enterprise risk points primarily exist in operating income, selling expenses, financial expenses, and total profit. Additionally, the results indicate significant differences between the model’s judgment values and declared values, especially in the high-risk probability of total operating income and profit. This implies a significant underreporting issue concerning corporate income tax for real estate enterprises. Therefore, this paper contributes to enhancing the identification of tax risks for real estate enterprises. Using the optimized random forest model makes it possible to accurately assess enterprises’ tax compliance risks and identify specific risk points.
Fibronectin type III domain‐containing 5 improves aging‐related cardiac dysfunction in mice
Aging is an important risk factor for cardiovascular diseases, and aging‐related cardiac dysfunction serves as a major determinant of morbidity and mortality in elderly populations. Our previous study has identified fibronectin type III domain‐containing 5 (FNDC5) and its cleaved form, irisin, as the cardioprotectant against doxorubicin‐induced cardiomyopathy. Herein, aging or matched young mice were overexpressed with FNDC5 by adeno‐associated virus serotype 9 (AAV9) vectors, or subcutaneously infused with irisin to uncover the role of FNDC5 in aging‐related cardiac dysfunction. To verify the involvement of nucleotide‐binding oligomerization domain‐like receptor with a pyrin domain 3 (NLRP3) and AMP‐activated protein kinase α (AMPKα), Nlrp3 or Ampkα2 global knockout mice were used. Besides, young mice were injected with AAV9‐FNDC5 and maintained for 12 months to determine the preventive effect of FNDC5. Moreover, neonatal rat cardiomyocytes were stimulated with tumor necrosis factor‐α (TNF‐α) to examine the role of FNDC5 in vitro. We found that FNDC5 was downregulated in aging hearts. Cardiac‐specific overexpression of FNDC5 or irisin infusion significantly suppressed NLRP3 inflammasome and cardiac inflammation, thereby attenuating aging‐related cardiac remodeling and dysfunction. In addition, irisin treatment also inhibited cellular senescence in TNF‐α‐stimulated cardiomyocytes in vitro. Mechanistically, FNDC5 activated AMPKα through blocking the lysosomal degradation of glucagon‐like peptide‐1 receptor. More importantly, FNDC5 gene transfer in early life could delay the onset of cardiac dysfunction during aging process. We prove that FNDC5 improves aging‐related cardiac dysfunction by activating AMPKα, and it might be a promising therapeutic target to support cardiovascular health in elderly populations. FNDC5 is downregulated in aging hearts, and cardiac‐specific overexpression of FNDC5 or irisin infusion attenuates aging‐related inflammation, cardiac remodeling, and dysfunction. Mechanistically, FNDC5 activates AMPKα through blocking the lysosomal degradation of GLP‐1R.
Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis
Semaglutide, a glucagon-like peptide-1 receptor agonist, is clinically used as a glucose-lowering and weight loss medication due to its effects on energy metabolism. In heart failure, energy production is impaired due to altered mitochondrial function and increased glycolysis. However, the impact of semaglutide on cardiomyocyte metabolism under pressure overload remains unclear. Here we demonstrate that semaglutide improves cardiac function and reduces hypertrophy and fibrosis in a mouse model of pressure overload-induced heart failure. Semaglutide preserves mitochondrial structure and function under chronic stress. Metabolomics reveals that semaglutide reduces mitochondrial damage, lipid accumulation, and ATP deficiency by promoting pyruvate entry into the tricarboxylic acid cycle and increasing fatty acid oxidation. Transcriptional analysis shows that semaglutide regulates myocardial energy metabolism through the Creb5/NR4a1 axis in the PI3K/AKT pathway, reducing NR4a1 expression and its translocation to mitochondria. NR4a1 knockdown ameliorates mitochondrial dysfunction and abnormal glucose and lipid metabolism in the heart. These findings suggest that semaglutide may be a therapeutic agent for improving cardiac remodeling by modulating energy metabolism. Semaglutide is used for glucose control and weight reduction. Here, the authors show that it enhances myocardial metabolism by targeting Creb5/NR4a1, protecting against cardiac remodeling and offering a therapeutic approach for heart failure through metabolic regulation.