-
Wang Yichun, Ding Ning, Wu Ting, Lu Shan, Liu Yun
2025,6(4):1-6, DOI: 10.12287/j.issn.2096-8965.20250401
Abstract:
The swift evolution of technology has spurred extensive research into brain-computer interfaces (BCIs), encompassing their fundamental principles, technological innovations, and practical applications across different domains. Within healthcare, BCI research has predominantly centered on motor rehabilitation, brain recovery, and neurodegenerative diseases. Given that sleep is vital for human health and well-being, the escalating incidence of sleep disorders presents a substantial risk to both physical and psychological health. Conventional sleep monitoring and intervention techniques are limited, which has driven scientists to seek more effective alternatives. As a cutting-edge neuroscience tool, BCI technology is increasingly making its mark in sleep-related research and showing great promise for real-world use. BCIs that rely on electroencephalography (EEG) have attracted significant interest due to their high temporal resolution, affordability, and portability, which make them suitable for sleep monitoring, intervention, and disease diagnosis. This review offers an in-depth analysis of the latest progress in BCIs for sleep monitoring and intervention, while also addressing the existing hurdles and future directions in this field.
-
Wang Yingzi, Shi Xueying, Bian Ziwei, Gao Ruoyan, Sun Hongtao, Zhang Guanyi
2025,6(4):7-13, DOI: 10.12287/j.issn.2096-8965.20250402
Abstract:
Traumatic Brain Injury (TBI) is a severe neurological injury with an extremely complex pathological mechanism, centrally characterized by abnormal activation of the immune microenvironment— triggering persistent inflammatory responses that severely impair post-TBI repair processes. Immune cells and their secreted inflammatory factors play a pivotal role in shaping and regulating the post-TBI immune microenvironment. This paper aims to review recent research advances on the role of the immune microenvironment in TBI, exploring its critical functions and association with disease prognosis, while highlighting current limitations: how to precisely regulate macrophage polarization, maintain the dynamic balance between pro-and anti-inflammatory effects, and modulate the temporal functional switching of inflammatory factors. These insights provide new perspectives for TBI treatment from an immune regulation standpoint. Futureresearch should prioritize developing targeted regulatory strategies for specific immune cell subsets, optimizing stem cell transplantation for therapeutic purposes and addressing immune rejection, elucidating the synergistic mechanisms of multi-component traditional Chinese medicine, and establishing biomarker-based personalized treatment regimens.
-
Lou Jiale, Chen Jiongfei, Chen Yitong, Ying Shibo
2025,6(4):14-20, DOI: 10.12287/j.issn.2096-8965.20250403
Abstract:
Malignant mesothelioma is an occupational cancer closely associated with asbestos exposure, characterized by poor prognosis and limited efficacy of conventional chemotherapy, which urgently necessitates the development of novel alternative therapeutic strategies. In recent years, molecular targeted therapy has emerged as a research hotspot in this field, offering new hope for the prevention and treatment of malignant mesothelioma. With in-depth investigations into its molecular mechanisms, several therapeutic targets have been identified and progressively translated into clinical applications. This review systematically summarizes the molecular pathogenesis of malignant mesothelioma, advances in targeted molecular therapies, and progress alongside future challenges in clinical trials. It aims to provide new insights for disease prevention, early intervention, and the development of targeted therapeutics in occupational asbestos-exposed populations.
-
Zhu Enpeng, Yin Jiaojiao, Ma Dengqin, Ha Xiaoqin
2025,6(4):21-26, DOI: 10.12287/j.issn.2096-8965.20250404
Abstract:
Exosomes, as natural nanoscale vesicles, demonstrate breakthrough potential in the treatment of venous thromboembolism (VTE) due to their low immunogenicity, ability to penetrate biological barriers, and diverse cargo. This review systematically elucidates the regulatory mechanisms of exosomes in venous thrombosis formation, including surface molecule-mediated thrombus initiation and amplification, nucleic acid-mediated regulation of coagulation-inflammation networks, immune cell interactions, and the remodeling of the thrombus microenvironment, effects on endothelial cells, and promotion of fibrinolysis. It also covers the advancements in the application of exosomes in treating venous thrombosis, including the advantages and disadvantages of natural exosomes, breakthroughs in engineered modifications, innovations in intelligent delivery systems, and challenges in clinical translation. This provides new perspectives for future treatments of venous thrombosis.
-
Chen Lijun, Wang Hong, Wu Fanqi, Liu Jiaxin
2025,6(4):27-35, DOI: 10.12287/j.issn.2096-8965.20250405
Abstract:
Pheochromocytoma / paraganglioma (PPGL) is a rare neuroendocrine tumor with metastatic potential that is often overlooked due to atypical clinical presentations. With advances in biochemical assays for catecholamines and their metabolites, combined with improved imaging techniques, the diagnostic rate of PPGL has been steadily increasing. Nevertheless, precise diagnosis continues to face major challenges including significant molecular heterogeneity and the limited sensitivity of conventional imaging modalities. This review systematically elucidates the pathogenesis, clinical manifestations, diagnostic approaches, and classification systems of PPGL, aiming to support and improve its diagnosis.
-
2025,6(4):36-43, DOI: 10.12287/j.issn.2096-8965.20250406
Abstract:
Bronchial asthma is a chronic inflammatory respiratory disease that significantly impairs lung function. In recent years, the rapid advancement of artificial intelligence (AI) technology in the medical field has created new opportunities for diagnosing, treating, and prognosis of bronchial asthma. This paper provides a comprehensive review of AI applications in bronchial asthma, highlighting the use of machine learning, deep learning, and other technologies for efficient and intelligent prediction, precise diagnosis and classification, treatment decision-making, and prognosis assessment. It also explores current challenges and potential future directions for development.
-
Zhang Bing, Yang Tingting, Li Shuwen, He Rongxia
2025,6(4):44-49, DOI: 10.12287/j.issn.2096-8965.20250407
Abstract:
Preeclampsia is characterized by multisystem dysfunction, and its pathogenesis involves oxidative stress induced by the placental ischemia-hypoxia microenvironment, angiogenic factor imbalance and systemic endothelial injury, etc. However, the key molecular regulatory networks have not been fully elucidated. As epigenetics has become a hot research topic in recent years, aberrant regulation of RNA methylation leading to imbalanced gene expression may be involved in the development of preeclampsia. This paper explores the regulatory roles of three types of RNA methylations (m6A, m5C, and m7G) in preeclampsia and their molecular interaction mechanisms with key pathological processes, with the aim of providing a theoretical basis for the prevention and epigenetically targeted therapy of this disease.
-
2025,6(4):50-59, DOI: 10.12287/j.issn.2096-8965.20250408
Abstract:
Osteoporosis is a metabolic bone disease characterized by decreased bone mass and deterioration of bone microarchitecture. Its essence is pathological bone loss caused by an imbalance in bone remodeling, marked by osteoclast-mediated bone resorption exceeding osteoblast-mediated bone formation. This article systematically reviews the pathophysiological mechanisms of osteoporosis, focusing on key signaling pathways regulating the activity of osteoblasts, osteoclasts, and mesenchymal stem cells, and provides a detailed overview of current drugs and therapeutic strategies. This review aims to offer clinicians and researchers an indepth analysis of the pathogenesis of osteoporosis and the mechanisms of drug therapy, to support evidence-based medical decisions and improve patient outcomes.
-
Meng Jing, Liu Manqi, Cui Xiang, Cai Yue, Liu Fangchao, Xia Changfa, Zhang Yang, Zeng Hongmei
2025,6(4):60-66, DOI: 10.12287/j.issn.2096-8965.20250409
Abstract:
Objective To identify and prioritize key intervention targets for improving healthy life expectancy (HLE) within the Healthy China Action, providing a scientific basis for optimizing resource allocation and adjusting action strategies. Methods A three-stage mixed-methods design was adopted, consisting of the following stages. (1) Delphi method: Twenty experts in fields including public health, clinical medicine, and health policy were invited to rate 15 selected actions using a 5-point Likert scale across five dimensions: HLE improvement potential, implementation feasibility, equity impact, cost-effectiveness, and feasibility of data-based estimation. Key strategies were screened based on criteria of a mean score ＞ 3.5 and a coefficient of variation ＜ 0.30. (2) Analytic Hierarchy Process (AHP): The AHP was then used for pairwise comparisons of these dimensions to determine their overall weights. (3) Focus group interviews were conducted with 5 experts to provide in-depth interpretation of the priority ranking. Results The Delphi process achieved an expert authority coefficient of 0.82. The AHP results indicated the following weights for the criteria, in descending order: implementation feasibility (31.23%), cost-effectiveness (19.62%), HLE improvement potential (17.81%), data estimation feasibility (17.27%), and equity impact (14.07%). The top six prioritized intervention strategies were: prevention and control of cardiovascular and cerebrovascular diseases, prevention and control of diabetes, tobacco control, maternal and child health promotion, cancer prevention and control, and health knowledge popularization. Conclusion In the selection of intervention strategies for the Healthy China Action, "implementation feasibility" and "cost-effectiveness" exert greater influence on decision-making than the theoretical "health improvement potential. " A series of actions focusing on the prevention and control of chronic diseases constitute the priority areas for enhancing HLE. These findings can inform decisions regarding the allocation of primary healthcare resources and the dynamic adjustment of strategies for the Healthy China Action during the '15th Five-Year Plan' period.
-
Chen Zhuo, Yang Guodong, Luo Gaochao
2025,6(4):67-76, DOI: 10.12287/j.issn.2096-8965.20250410
Abstract:
Objective This study aims to evaluate the therapeutic efficacy of radioactive iodine-131 (I-131) combined with PD-1 neutralizing antibody or PI3K inhibitor LY294002 in the treatment of thyroid cancer, as well as its impact on the immune microenvironment, especially its effects on tumor antigen release, immune checkpoint regulation and immune cell activation. Methods BCPAP and TPC1 cells were divided into a control group, a group treated with I-131 alone, a group treated with I-131 combined with a PD-1 neutralizing antibody, and a group treated with I-131 combined with PI3K inhibitor LY294002. CCK8 was used to detect cell proliferation, Transwell assay was employed to assess cell migration and invasion, ELISA kits were applied to monitor tumor antigen (CEA, TG) levels in the cell culture supernatant, qRT-PCR and Western blotting were used to analyze the expression of immune-related molecules (e.g., PD-L1, MHC-I, FoxP3, γH2AX, p-STAT1, STAT1, HLA-ABC). In the immune cell co-culture experiment, I-131-treated thyroid cancer cells were co-cultured with PBMCs from healthy volunteers to detect immune cell activation, and ELISA was performed to measure cytokines including IFN-γ, IL-2, TNF-α, and IL-10. In addition, TCGA database was utilized to further analyze the protein expression of PDCD1(PD-1) and CD274(PD-L1) in thyroid cancer tissues across different stages. Results I-131 treatment significantly reduced the proliferation, migration, and invasion of BCPAP and TPC1 cells, as well as the release of tumor antigens CEA and TG. Combination treatment with PD-1-neutralizing antibody or LY294002 further reduced the release of tumor antigens, demonstrating an obvious synergistic effect. Regarding the expression of immune-related molecules, I-131 treatment significantly downregulated PD-L1 expression while significantly upregulating the expression of HLA-A, HLA-B, HLA-C, and MHC-I. Combination treatment with a PD-1-neutralizing antibody or LY294002 could further enhance this regulatory effect. Western blotting results showed that γH2AX, p-STAT1, and HLA-ABC were decreased after I-131 treatment, while total STAT1 remained largely unchanged. I-131 treatment significantly increased IFN-γ concentrations in immune cell co-culture experiments, and combination treatment significantly increased IFN-γ levels. Meanwhile, IL-2 and TNF-α levels were significantly elevated, whereas IL-10 was decreased, indicating enhanced immune activation. In addition, changes in the expression of PD-1 / PD-L1 / FoxP3 further confirmed that I-131 enhanced the immune response. TCGA database analysis showed that the expression level of PDCD1 in normal tissues was higher than that in tumor tissues, and decreased with advancing stage. Conclusion I-131 inhibits the proliferation, migration, invasion of BCPAP and TPC1 cells, suppresses the expression of immune checkpoint molecules, and upregulates antigen-presenting molecules, accompanied by downregulation of γH2AX and p-STAT1 expression, and changes in cytokine concentrations. Combined immunotherapy (PD-1 neutralizing antibody /LY294002) can further improve the immune enhancement effect. Therefore, this combined immunotherapy modality may be one of the new treatment methods for thyroid cancer.
-
Gulijiamali Niyazi, Sun Longfei, Liao Jun
2025,6(4):77-83, DOI: 10.12287/j.issn.2096-8965.20250411
Abstract:
Objective Atherosclerosis (AS) is an aging-related disease characterized by vascular endothelial injury, inflammation, and endothelial cell senescence. Recent studies increasingly indicate that abnormal opening of the mitochondrial permeability transition pore (mPTP) not only causes severe mitochondrial dysfunction but also plays a critical role in cellular senescence. However, the relationship and role of mPTP in vascular endothelial cell senescence during the pathogenesis and progression of AS remain insufficiently clear. This study aims to elucidate the role of mPTP in vascular endothelial cell senescence and to determine whether targeted intervention of mPTP can effectively mitigate endothelial cell senescence and injury. Methods An in vitro model of atherosclerosis-related endothelial injury was established using lipopolysaccharide (LPS)-induced human coronary artery endothelial cells (HCAECs). Senescence status and mitochondrial function were systematically evaluated using SA -β-gal senescence staining, Western blotting, mPTP fluorescence staining, ATP level measurement, and quantitative real-time PCR. Furthermore, by inhibiting mPTP opening, its regulatory effects on mitochondrial function, endothelial cell senescence, and associated inflammatory responses were investigated. Results In the in vitro LPS-induced HCAEC injury model, abnormal mitochondrial mPTP opening was observed, accompanied by a significant decrease in cellular ATP levels and a marked increase in mtDNA release into the cytosol. Concurrently, SA-β-gal staining intensity was significantly enhanced, protein levels of senescence-associated markers P16, P21, and P53 were significantly upregulated, and the expression of the senescence-associated secretory phenotype (SASP) marker gene IL-6 was significantly elevated. Inhibition of mPTP using the inhibitor VBIT-4 in this model restored mitochondrial membrane potential and ATP levels. Furthermore, VBIT-4 treatment reversed the LPS-induced upregulation of senescence-associated P16, P21, P53, and IL-6. Conclusion During the pathological process of AS, abnormal mPTP opening in vascular endothelial cells contributes to endothelial dysfunction by promoting cellular senescence. Inhibition of mPTP alleviates endothelial cell senescence, reduces inflammatory levels, and ameliorates mitochondrial function. These findings provide new insights into potential diagnostic and therapeutic strategies for AS.
-
Beijing Cancer Prevention & Treatment Society
2025,6(4):84-92, DOI: 10.12287/j.issn.2096-8965.20250412
Abstract:
Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. Postoperative adjuvant therapy is essential. However, CRC exhibits significant heterogeneity, resulting in variable drug sensitivity profiles. Traditional in vitro tumor models have many limitations. In recent years, Chinese researchers have invented a patient-derived tumor-like cell cluster (PTC) model utilizing matrix-free, serum-free, and suspended three-dimensional culture techniques. This innovative approach overcomes the technical limitations of conventional models, offering advantages including minimal, safe, accurate, and timely. On December 28, 2023, the “Chinese Expert Consensus on the Construction of Patient-Derived Tumor-Like Cell Cluster (PTC) Model and Anti-Tumor Drug Sensitivity Detection Technology (2023 Version)” was published. To precisely guide the construction of colorectal cancer PTC models and standardize its application in colorectal cancer clinical practice, the Beijing Cancer Prevention & Treatment Society convened domestic experts from related fields and, based on the latest domestic and international research data, formulated this expert consensus and operating guidelines. This guideline provides a comprehensive overview of the PTC model. It covers the model’s definition, application, sample selection criteria, drug types, and criteria for interpreting drug sensitivity results. Additionally, it details the operating procedures for constructing the model and conducting drug sensitivity tests. The aim of this consensus is to offer individualized and precise guidance for colorectal cancer drug treatment and to promote the clinical application of this technology.
Volume 6,2025 Issue 4
· Review ·
· Original Research ·
· Guidelines and Consensus ·
-
Zhang Huafeng, Tang Ke, Ma Jingwei, Chen Jie, Zhou Yabo, Huang Bo
2024,4(2):30-35, DOI: 10.12287/j.issn.2096-8965.20240204
Abstract:
Glycogen, a polysaccharide composed of glucose molecules linked by α-1,4-glycosidic and α-1,6- glycosidic bonds, is one of the primary energy storage forms in human body. Glycogen is primarily stored in the liver (as liver glycogen) and skeletal muscles (as muscle glycogen), with smaller amounts present in tissues such as myocardium, kidneys, and brain. When the body requires energy, liver glycogen can be broken down into glucose, which is then utilized by various tissues and organs. During exercise, muscle glycogen is consumed by skeletal muscles to meet the energy demands of the muscles. Beyond its crucial roles in maintaining blood glucose levels and providing energy, recent research has revealed that glycogen metabolism also regulates biological processes such as cell differentiation, signal transduction, and redox reactions. This review focuses on the latest research advancements in the regulatory mechanisms of glycogen metabolism in metabolic diseases, tumors, and immune cell responses, highlighting new regulatory modes and mechanisms.
-
Chen Dongping, Huang Chunxiang, Wu Caiyuan, Wei Yuan, Kuang Dongming
2024,4(2):46-57,66, DOI: 10.12287/j.issn.2096-8965.20240206
Abstract:
The tumor immune microenvironment plays a crucial role in the initiation and progression of tumors, and is closely related to the long-term effectiveness of treatments. Notably, while being influenced by the microenvironment, treatment can also actively reshape the composition of the microenvironment. In recent years, with the help of emerging technologies such as single-cell sequencing, the interactions between various therapeutic approaches and the immune microenvironment, as well as their impact on therapeutic efficacy, have been revealed in various tumors. This review summarizes the impact of primary tumor immune microenvironments on therapeutic efficacy, introduces the remodeling of microenvironment by different therapeutic approaches, and explores the intricate regulatory mechanisms governing secondary immune microenvironments' interactions with tumors and their implications on treatment outcomes. Clarifying the mechanisms of interactions between the tumor immune microenvironment and treatments has profound implications for monitoring and predicting treatment outcomes, as well as for optimizing cancer therapy.
-
Liu Feng, Zhuang Wanxin, Yang Yuan, Gao Chengjiang
2024,4(2):2-11,35, DOI: 10.12287/j.issn.2096-8965.20240201
Abstract:
NLRP3 inflammasome is a vital component of the innate immune system, crucial in combatting pathogenic infections and responding to danger signals. At the same time, the aberrant activation of NLRP3 inflammasome is intricately linked with diseases such as diabetes, Alzheimer's disease, and lupus erythematosus. Therefore, regulation and intervention of inflammasome activation processes are pivotal for sustaining immune homeostasis and functionality. This review comprehensively summarizes recent progress in elucidating the regulatory mechanisms governing NLRP3 inflammasome activation, including post-translational modifications of NLRP3, interacting molecules, alterations in organelle and cellular localization, as well as metabolic processes and associated metabolites associated with NLRP3 function. Its objective is to offer novel perspectives on understanding inflammasome activation occurrences, inflammatory responses, and therapeutic approaches for inflammation-related disorders.
-
Li Huixia, Che Ruochen, Zhang Aihua
2021,2(1):55-63, DOI: 10.12287/j.issn.2096-8965.20210108
Abstract:
As the major threat of poor renal outcome and survival quality, the mechanism of acute kidney injury (AKI) progressing to chronic kidney disease (CKD) has aroused much attention. The cell cycle arrest, one of the major culprits, accelerates the AKI-to-CKD transition through maladaptive repair that involved overwhelming cytokines excretion and inflammation storm, epithelial-mesenchymal transition, organelles stress/crosstalk, aging activation as well as peritubular capillary rarefaction. Therefore, the cell cycle regulation can serve as a novel potential therapeutic target for the prevention, alleviation and even interruption of AKI -to- CKD transition.
-
Sun Luying, Sun Weiwei, Zhou Shaofeng, Tian Lei, Zhang Meiling, Ai Sinan, Zheng Huijuan, Li Yaotan, Li Danting, Liu Weijing, Zhou Jingwei, Wang Zhen, Wang Yaoxian
2022,3(3):31-44,63, DOI: 10.12287/j.issn.2096-8965.20220306
Abstract:
Chronic kidney disease (CKD) is a major disease that seriously endangers human health. Traditional Chinese medicine (TCM) has certain characteristic effect in the prevention and treatment of CKD, especially in reducing urinary proteins, protecting renal function, delaying the progress of CKD and alleviating related complications. This study reviews the new understanding of TCM theory of CKD in recent years, and summarizes the evidence-based medical evidence of the efficacy of TCM in the treatment of CKD and the new progress related to the effect mechanism of TCM treatment of CKD, summarizing the current situation of clinical and basic research and achievements transformation of CKD, and proposes future research prospects, in order to contribute to the further innovation and development of TCM in the prevention and treatment of CKD.
Expert Demeanor
