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30,108 result(s) for "Li, Ning"
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Regulation of short-chain fatty acids in the immune system
A growing body of research suggests that short-chain fatty acids (SCFAs), metabolites produced by intestinal symbiotic bacteria that ferment dietary fibers (DFs), play a crucial role in the health status of symbiotes. SCFAs act on a variety of cell types to regulate important biological processes, including host metabolism, intestinal function, and immune function. SCFAs also affect the function and fate of immune cells. This finding provides a new concept in immune metabolism and a better understanding of the regulatory role of SCFAs in the immune system, which impacts the prevention and treatment of disease. The mechanism by which SCFAs induce or regulate the immune response is becoming increasingly clear. This review summarizes the different mechanisms through which SCFAs act in cells. According to the latest research, the regulatory role of SCFAs in the innate immune system, including in NLRP3 inflammasomes, receptors of TLR family members, neutrophils, macrophages, natural killer cells, eosinophils, basophils and innate lymphocyte subsets, is emphasized. The regulatory role of SCFAs in the adaptive immune system, including in T-cell subsets, B cells, and plasma cells, is also highlighted. In addition, we discuss the role that SCFAs play in regulating allergic airway inflammation, colitis, and osteoporosis by influencing the immune system. These findings provide evidence for determining treatment options based on metabolic regulation.
Altered metabolism in cancer: insights into energy pathways and therapeutic targets
Cancer cells undergo significant metabolic reprogramming to support their rapid growth and survival. This study examines important metabolic pathways like glycolysis, oxidative phosphorylation, glutaminolysis, and lipid metabolism, focusing on how they are regulated and their contributions to the development of tumors. The interplay between oncogenes, tumor suppressors, epigenetic modifications, and the tumor microenvironment in modulating these pathways is examined. Furthermore, we discuss the therapeutic potential of targeting cancer metabolism, presenting inhibitors of glycolysis, glutaminolysis, the TCA cycle, fatty acid oxidation, LDH, and glucose transport, alongside emerging strategies targeting oxidative phosphorylation and lipid synthesis. Despite the promise, challenges such as metabolic plasticity and the need for combination therapies and robust biomarkers persist, underscoring the necessity for continued research in this dynamic field. Graphical Abstract
Hypofractionated versus conventional fractionated postmastectomy radiotherapy for patients with high-risk breast cancer: a randomised, non-inferiority, open-label, phase 3 trial
To our knowledge, no randomised study has compared postmastectomy hypofractionated radiotherapy with conventional fractionated radiotherapy in patients with breast cancer. This study aimed to determine whether a 3-week schedule of postmastectomy hypofractionated radiotherapy is as efficacious and safe as a 5-week schedule of conventional fractionated radiotherapy. This randomised, non-inferiority, open-label, phase 3 study was done in a single academic hospital in China. Patients aged 18–75 years who had undergone mastectomy and had at least four positive axillary lymph nodes or primary tumour stage T3–4 disease were eligible to participate. Patients were randomly assigned (1:1) according to a computer-generated central randomisation schedule, without stratification, to receive chest wall and nodal irradiation at a dose of 50 Gy in 25 fractions over 5 weeks (conventional fractionated radiotherapy) or 43·5 Gy in 15 fractions over 3 weeks (hypofractionated radiotherapy). The modified intention-to-treat population (including all eligible patients who underwent randomisation but excluding those who were considered ineligible or withdrew consent after randomisation) was used in primary and safety analyses. The primary endpoint was 5-year locoregional recurrence, and a 5% margin was used to establish non-inferiority (equivalent to a hazard ratio <1·883). This trial is registered at ClinicalTrials.gov, number NCT00793962. Between June 12, 2008, and June 16, 2016, 820 patients were enrolled and randomly assigned to the conventional fractionated radiotherapy group (n=414) or hypofractionated radiotherapy group (n=406). 409 participants in the conventional fractionated radiotherapy group and 401 participants in the hypofractionated radiotherapy group were included in the modified intention-to-treat analyses. At a median follow-up of 58·5 months (IQR 39·2–81·8), 60 (7%) patients had developed locoregional recurrence (31 patients in the hypofractionated radiotherapy group and 29 in the conventional fractionated radiotherapy group); the 5-year cumulative incidence of locoregional recurrence was 8·3% (90% CI 5·8–10·7) in the hypofractionated radiotherapy group and 8·1% (90% CI 5·4–10·6) in the conventional fractionated radiotherapy group (absolute difference 0·2%, 90% CI −3·0 to 2·6; hazard ratio 1·10, 90% CI 0·72 to 1·69; p<0·0001 for non-inferiority). There were no significant differences between the groups in acute and late toxicities, except that fewer patients in the hypofractionated radiotherapy group had grade 3 acute skin toxicity than in the conventional fractionated radiotherapy group (14 [3%] of 401 patients vs 32 [8%] of 409 patients; p<0·0001). Postmastectomy hypofractionated radiotherapy was non-inferior to and had similar toxicities to conventional fractionated radiotherapy in patients with high-risk breast cancer. Hypofractionated radiotherapy could provide more convenient treatment and allow providers to treat more patients. National Key Projects of Research and Development of China; the Chinese Academy of Medical Science Innovation Fund for Medical Sciences; and Beijing Marathon of Hope, Cancer Foundation of China.
Fostering creative thinking through gamified intercultural communication: innovative pedagogical strategies in higher education English programs
With the acceleration of globalization, fostering intercultural communication competence has emerged as a crucial objective for higher education, particularly for English majors. This study explores the integration of gamified pedagogical strategies into intercultural communication courses and evaluates their impact on enhancing creative thinking, engagement and intercultural competence. By incorporating game elements, such as point systems, badge rewards, leaderboards and task challenges, an innovative course was meticulously designed and implemented. A mixed-method approach, encompassing questionnaires, in-depth interviews and pre- and post-course assessments, was employed to comprehensively evaluate the course's effectiveness. Results demonstrate that gamification significantly boosts student motivation, engagement and intercultural communication skills, with creative thinking showing measurable improvements. Moreover, students expressed high satisfaction with the gamified course, highlighting its practicality in bridging theoretical knowledge with experiential learning. This research not only enriches the theoretical discourse on gamification in education but also provides actionable strategies for enhancing intercultural communication teaching practices in diverse educational contexts. The findings underline the potential of gamification to address cultural diversity challenges and propose directions for future research on its application in cross-cultural education. In today's interconnected world, effective communication across cultures is vital for collaboration and innovation. This study investigates how gamified teaching methods - using game-like elements, such as points, badges and challenges - can make learning intercultural communication more engaging and effective for university students. By transforming traditional classroom activities into interactive, playful experiences, students not only gain cultural awareness but also develop creative problem-solving skills essential for global careers. Results show that these gamified strategies boost motivation, teamwork and adaptability in cross-cultural scenarios, offering practical benefits for educators and learners alike. For the public, this research highlights the power of innovative teaching tools to prepare future professionals for a diverse world, bridging cultural gaps and fostering mutual understanding. Whether in education, business or everyday interactions, such approaches can inspire more inclusive and creative ways to navigate cultural differences.
Artificial intelligence-enhanced audiovisual translation for global dissemination of Chinese film and television
This study investigates how artificial intelligence (AI) technologies intersect with audiovisual translation (AVT) to support the global dissemination of Chinese television dramas. Focusing on the Viki streaming platform, which relies on fan-based community subtitling, the research adopts a qualitative case study design to assess whether AI-assisted translations effectively meet the cultural and emotional expectations of international viewers. Data were collected from four popular Chinese dramas and analyzed through multimodal discourse analysis and user-generated commentaries. The findings reveal that while AI technologies enhance translation speed and accessibility, they often struggle with preserving narrative coherence, cultural nuance, and emotional resonance—especially in the absence of human intervention. Human translators play a crucial role in restoring idiomatic meaning, symbolic references, and character identity, thereby improving audience immersion. The study highlights the importance of human–AI collaboration in subtitling workflows and proposes a hybrid model that integrates automated processing with targeted human refinement. These insights contribute to ongoing debates in AVT and offer practical implications for enhancing intercultural understanding through more culturally sensitive media translation practices.
Globalization and capital disembedding: the decline of the developmental state in South Korea
This study examines how globalization has engendered capital disembeddedness and consequently eroded the foundational features of developmental states. Focusing on South Korea, this study traces three key steps in this process. First, international organizations forced Korea to open its domestic markets, marking the beginning of capital disembedding. Second, financial globalization prompted the government to develop alternative financing sources for enterprises amid deregulation, effectively diminishing the state’s control over capital. Furthermore, global production networks provided enterprises opportunities for technological advancement and hands-on learning, reducing their reliance on government support. Taken together, globalization has empowered capital to evade state oversight and reshaped the government-business relationship. Paradoxically, the economic crisis and market failures triggered by globalization have compelled the Korean government to re-regulate its markets and revitalize the economy. However, its regulatory ability remains weaker than that of a classic developmental state, and state-business relations have not rebounded to their former heights.
Cryo-EM structure of an amyloid fibril formed by full-length human prion protein
Prion diseases are caused by the misfolding of prion protein (PrP). Misfolded PrP forms protease-resistant aggregates in vivo (PrPSc) that are able to template the conversion of the native form of the protein (PrPC), a property shared by in vitro–produced PrP fibrils. Here we produced amyloid fibrils in vitro from recombinant, full-length human PrPC (residues 23–231) and determined their structure using cryo-EM, building a model for the fibril core comprising residues 170−229. The PrP fibril consists of two protofibrils intertwined in a left-handed helix. Lys194 and Glu196 from opposing subunits form salt bridges, creating a hydrophilic cavity at the interface of the two protofibrils. By comparison with the structure of PrPC, we propose that two α-helices in the C-terminal domain of PrPC are converted into β-strands stabilized by a disulfide bond in the PrP fibril. Our data suggest that different PrP mutations may play distinct roles in modulating the conformational conversion.A cryo-EM structure of amyloid fibrils formed in vitro with recombinant human PrP provides insights into fibril architecture and the potential role of disease mutations.
The significance of exosomes in the development and treatment of hepatocellular carcinoma
Hepatocellular carcinoma (HCC) is the most commonmalignancy. Exsome plays a significant role in the elucidation of signal transduction pathways between hepatoma cells, angiogenesis and early diagnosis of HCC. Exosomes are small vesicular structures that mediate interaction between different types of cells, and contain a variety of components (including DNA, RNA, and proteins). Numerous studies have shown that these substances in exosomes are involved in growth, metastasis and angiogenesis in liver cancer, and then inhibited the growth of liver cancer by blocking the signaling pathway of liver cancer cells. In addition, the exosomal substances could also be used as markers for screening early liver cancer. In this review, we summarized to reveal the significance of exosomes in the occurrence, development, diagnosis and treatment of HCC, which in turn might help us to further elucidate the mechanism of exosomes in HCC, and promote the use of exosomes in the clinical diagnosis and treatment of HCC.
Molecular mechanisms underlying the BIRC6-mediated regulation of apoptosis and autophagy
Procaspase 9 is the initiator caspase for apoptosis, but how its levels and activities are maintained remains unclear. The gigantic Inhibitor-of-Apoptosis Protein BIRC6/BRUCE/Apollon inhibits both apoptosis and autophagy by promoting ubiquitylation of proapoptotic factors and the key autophagic protein LC3, respectively. Here we show that BIRC6 forms an anti-parallel U-shaped dimer with multiple previously unannotated domains, including a ubiquitin-like domain, and the proapoptotic factor Smac/DIABLO binds BIRC6 in the central cavity. Notably, Smac outcompetes the effector caspase 3 and the pro-apoptotic protease HtrA2, but not procaspase 9, for binding BIRC6 in cells. BIRC6 also binds LC3 through its LC3-interacting region, probably following dimer disruption of this BIRC6 region. Mutation at LC3 ubiquitylation site promotes autophagy and autophagic degradation of BIRC6. Moreover, induction of autophagy promotes autophagic degradation of BIRC6 and caspase 9, but not of other effector caspases. These results are important to understand how the balance between apoptosis and autophagy is regulated under pathophysiological conditions. The balance between apoptosis and autophagy is critical for normal development, proper tissue function, and disease pathogenesis. Here, the authors show previously unannotated BIRC6 domains, including a ubiquitin-like domain, and how it utilizes its ubiquitylation function to regulate both apoptosis and autophagy.