Virtual Cell (VC) technology, as an interdisciplinary frontier at the intersection of systems biology and computational biology, aims to precisely simulate cellular biological behaviors through computer models. This paper systematically explores the potential applications of virtual cell technology in the study of Human Immunodeficiency Syndrome (AIDS), the current key challenges, and future development directions. By reviewing existing literature and research findings, we find that while the term "Virtual Cell" has not been widely and standardized applied in Human Immunodeficiency Virus (HIV) research, its core concept simulating HIV infection, immune responses, and therapeutic interventions through multi-scale, multi-modal computational models has deeply rooted in the forefront of this field. This paper will focus on analyzing the potential of "virtual cell-like" (VCL) models, such as agent-based models, cellular automata, mechanistic mathematical models, etc. in revealing HIV pathogenesis, accelerating drug development and evaluating treatment strategies, and promoting personalized precision medicine. Simultaneously, this paper will explore the technical challenges in practical applications, such as model complexity and biological fidelity, data integration and validation standards, computational resource demands, and ethical dilemmas such as data privacy, clinical decision reliability, and regulatory framework gaps. Finally, we look forward to the integration of artificial intelligence (AI) and virtual cell models, emphasizing the importance of establishing standardized validation processes and ethical governance frameworks to promote the healthy development of this technology and ultimately contribute to conquering HIV/AIDS.

Chronic obstructive pulmonary disease (COPD) represents a prevalent respiratory ailment, which is distinguished by enduring airflow obstruction and a tendency to progress over time. Over 400 million people globally are currently impacted. Alveolar epithelial cells, airway epithelial cells, and important inflammatory cell populations are all actively involved in the pathological development of COPD. These cells' interactions have wide-ranging physiological effects on the body, such as aggravating lung damage and inducing inflammation, which are the pathogenic causes of COPD. In the present review, numerous programmed cell death (PCD) modes are addressed with a focus on molecular mechanisms and crosstalk of seven PCD processes-apoptosis, necroptosis, ferroptosis, autophagy, pyroptosis, cuproptosis, and disulfidptosis-in COPD pathogenesis and initiation. It also refers to clinical treatment strategies for the acute and stable phases of COPD based on PCD regulation. From the cellular perspective, we may have a more exact understanding of disease phenotypes; demystification of cell-type-specific mechanisms is aimed at providing theoretical guidance for further probing of COPD's molecular pathology and development of novel therapeutic strategies against PCD.

Background and aim: As an auxiliary therapy, acupuncture is effective in ameliorating myocardial ischemia (MI). Selecting correct acupoints is widely acknowledged to be key for therapeutic effects of acupuncture, and traditional acupuncturists believe that selecting acupoints whose pressure pain threshold (PPT) change with disease, for instance selecting PC6 (Neiguan) when MI occurs, usually leads to better therapeutic effects. In this study, we aimed to identify the molecular mechanism of PPT regulation at PC6 in MI rats. Experimental procedure: Firstly, we established MI models by intraperitoneal injection of ISO and evaluated PPT changes and mast cell degranulation (MCD) at PC6 during MI. Then, we performed high-throughput sequencing and overlapped the differentially expressed miRNAs in plasma and skin tissue from the left PC6 (L-PC6). Through bioinformatics analysis and dual-luciferase reporter assays, we tried to find the downstream molecules of miRNA. Subsequently, miRNA agonists were injected intramusculally at L-PC6, and we paid attention to changes in PPT and MCD at L-PC6 as well as the relationship between local mast cells (MCs) and nerve axons. Result and conclusion: PPT decreased and MCD increased at PC6 in MI rats and miR-144-3p is a key molecule in the induction of these phenomenon. Furthermore, miR-144-3p targeting Interleukin-1(3 (IL-1(3) leads to local MCD, neurogenic inflammation and peripheral nociceptor hypersensitization, finally resulting in PPT change at PC6. Innovatively, our study also provides a new direction for investigating the relationship between MCs, PPT and sensitivity of acupoints, which is mediated by miR-144-3p.

Purpose Acupoints are fundamental to the efficacy of acupuncture. When the body is diseased, the pressure pain threshold (PPT) of the corresponding acupoints typically exhibits significant changes. Clinically, selecting acupoints with marked PPT changes often enhances therapeutic efficacy. Mast cells are involved in changes in the PPT at acupoints, but the regulatory mechanism remains unclear. We aimed to identify microRNAs (miRNAs) that regulate mast cells to elucidate the mechanisms underlying PPT changes, thereby guiding clinical acupuncture practice. Methods We evaluated changes in PPT and differentially expressed miRNAs at the ST36 acupoint in a rat model of knee osteoarthritis. miRNA agonists and antagonists were injected to observe changes in the PPT at the ST36 acupoint. Subsequently, the functions of differentially expressed miRNA in regulating degranulation and their possible targets of action were evaluated using in vitro and in vivo experiments. Results PPT decreased in knee osteoarthritis (KOA) rats, accompanied by increased degranulation of local skin mast cells. rno-miR-199a-3p played a key role in this process. Overexpression of rno-miR-199a-3p increased mast cell degranulation. Furthermore, the overexpression of neural precursor cell expressed developmentally down-regulated 4 (Nedd4) is suppressed by rno-miR-199a-3p, which modulated mast cells. Conclusion Pathological changes in the body lead to changes in the PPT, manifested by altered local pain thresholds and mast cell degranulation. rno-miR-199a-3p targets Nedd4, leading to mast cell degranulation, which probably underlies this mechanism.

Objective:Pre-mRNA alternative splicing(AS)is an important post-transcriptional regulation mechanism.The abnormal splicing of genes can lead to cardiovascular diseases.Acupuncture has been shown to alleviate myocardial ischemia-reperfusion injury(MIRI),but most studies have focused on the regulation of gene expression by acupuncture.Previously,we reported that electroacupuncture(EA)can relieve angina by regulating the AS of GABARG2;however,the genome-wide regulation of AS by EA remains unknown. Methods:We explored the protective effects of EA on MIRI.We then studied the AS profiles retrieved from the previously submitted to Gene Expression Omnibus(GEO)database and analyzed the data using the replicate multivariate analysis of transcript splicing(rMATS)tool.Subsequently,we conducted validation experiments on splicing regulatory factors and their target genes modulated by EA,as identified through bioinformatics analysis. Results:The results showed that EA at PC6 point could effectively alleviate MIRI.More than 200 differential alternative splicing events(ASEs)changed following MIRI.The differential ASEs underwent protein-protein interaction(PPI)network analysis,gene ontology(GO)enrichment,and pathway analysis,and were shown to be involved in distinct biological functions,especially in the maintenance of synaptic structure.Enrichment analysis also identified several pathways that are potentially associated with the progression of MIRI.Importantly,we identified critical ASEs and pathways that could be completely rescued by EA treatment.In the validation experiments,we found that AS of the key gene CAMK2G,associated with synaptic function,is regulated by the expression level of the MBNL1 protein modulated by EA. Conclusions:Our results indicate that EA is not only an effective procedure to protect against MIRI by rescuing gene expression but also rescues abnormal ASEs.This study is a major contribution to a genome-wide comprehensive analysis of the regulation of AS by EA in MIRI.

BackgroundMyocardial ischemia-reperfusion injury (MIRI) presents a significant challenge to the effectiveness of reperfusion therapy in severe ischemic heart disease. One of the core pathological mechanisms of MIRI is NLRP3 inflammasome-mediated cardiomyocyte pyroptosis. While electroacupuncture (EA) has demonstrated efficacy in mitigating MIRI, its potential to target and inhibit NLRP3 inflammasome-mediated cardiomyocyte pyroptosis in the context of MIRI remains unclear. Additionally, the mechanism through which local EA may remotely influence the heart to alleviate MIRI is not well understood.ObjectiveThis study aims to explore the protective effects and molecular mechanisms of EA targeting NLRP3 inflammasome-mediated myocardial cell death in MIRI, focusing on the role of serum exosomes.Methods and resultsAn animal model of MIRI was established by ligating the left anterior descending coronary artery, and EA was applied at the Neiguan (PC6) acupoint. Cardiac function, myocardial infarction area, serum myocardial enzymes, inflammatory factors, and myocardial cell pathological changes were assessed using echocardiography, Evans-TTC staining, ELISA, and H&E staining to confirm the therapeutic effect of EA in reducing MIRI. The NLRP3 agonist Nigericin was applied, and the expression levels of key genes and proteins related to NLRP3-mediated apoptosis were measured by Western blotting and RT-qPCR, confirming that EA alleviates MIRI by targeting and inhibiting NLRP3-mediated myocardial apoptosis. The role of serum exosomes in inhibiting NLRP3 inflammasome-mediated cardiomyocyte pyroptosis was then tested in a cardiomyocyte hypoxia/reoxygenation model. Exosomes from serum samples of AMI-PCI patients (with or without standard EA) and from MIRI model rats were isolated. Small RNA sequencing was performed to identify key effector miRNAs post-EA. Our findings revealed that miR-22-3p was significantly upregulated in serum exosomes following EA. Further validation demonstrated that miR-22-3p mitigates MIRI by targeting NLRP3 to inhibit cardiomyocyte pyroptosis, as confirmed through target gene prediction, in vitro cell experiments, and in vivo animal studies.ConclusionThis study provides evidence that EA reduces MIRI by upregulating miR-22-3p in serum exosomes, which in turn targets and inhibits NLRP3 inflammasome-mediated cardiomyocyte pyroptosis, thereby reducing severe myocardial injury.

Acupuncture has demonstrated consistent clinical efficacy in treating pain, autonomic dysfunction, and immune-mediated disorders, yet its integration into mainstream evidence-based medicine remains limited by the absence of a unified, anatomically defined mechanism of action. To address this gap, we propose the neuro-vascular-immune (NVI) functional unit as a hypothetical framework to understand the structural and functional substrate underlying acupoints. This specialized perivascular microdomain, enriched in sensory nerve endings, perivascular mast cells, and immune-stromal elements, acts as a mechanosensitive interface transducing physical stimuli into biological signals. Our model suggests that acupuncture exerts its effects primarily through targeted mechanical activation of these NVI units, converting local physical inputs into coordinated regional and systemic neuro-immune responses. Mast cells within the NVI unit are proposed to function as central signal integrators, mediating context-dependent modulation of innate immunity, adaptive immune polarization, and tissue microenvironments. This framework aims to complement traditional meridian theory by providing a testable, biologically grounded foundation for precision acupuncture. The heterogeneous spatial distribution of NVI units may help explain acupoint functional specificity: The heterogeneous spatial distribution of NVI units forms the basis of a working hypothesis regarding acupoint functional specificity. We hypothesize that distal acral points, enriched in glomus bodies, may be preferentially suited for rapid neuromodulation in acute conditions, while proximal and trunk points may favor sustained neuro-immune regulation for chronic disorders. This distal–proximal gradient is proposed as a working hypothesis rather than a rigid dichotomy, acknowledging that every acupoint engages the full NVI triad simultaneously. NVI mechanosensitivity may also provide a rationale for optimizing stimulation parameters to enhance efficacy. By connecting peripheral tissue responses to systemic homeostatic regulation, the NVI model offers a unifying paradigm for standardizing protocols, improving clinical reproducibility, and expanding evidence-based acupuncture applications in complex neuro-immune disorders, facilitating its integration into global precision medicine.

To observe the effect of electro-acupuncture (EA) on cardiomyocytes ferroptosis induced by myocardial ischemia/reperfusion injury (MIRI) in mice and to investigate whether this effect occurs via the nuclear factor-E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) signalling pathway. Firstly, Fe2+ in the hearts and serum of mice from both the sham-operated (SO) group and MIRI group was measured to ascertain whether ferroptosis had occurred in the cardiomyocytes of mice in MIRI group. In the second phase, EA was administered, with sham acupuncture (SA) group as the comparator, to investigate the protective effects of EA on ferroptosis in MIRI cardiomyocytes and cardiac function. Additionally, we studied the levels of Nrf2 and HO-1 within the myocardium. In the third phase, Nrf2 inhibitor ML385 and agonist DMF were applied to observe the impact of inhibiting Nrf2 on the therapeutic efficacy of EA. Compared with SO group, MIRI group showed increased iron deposition, along with a significant decrease in Nrf2 and HO-1 levels. Compared with MIRI group, MIRI + EA group exhibited significantly improved cardiac function and reduced cardiac iron deposition, accompanied by increased Nrf2 and HO-1 levels. Furthermore, the therapeutic effect of MIRI + EA group was superior to that of MIRI + SA group. Administration of ML385 partially blocked the anti-ferroptotic and cardioprotective effects of EA, while EA treatment exhibited similar effects to dimethyl fumarate (DMF) intervention. EA alleviates ferroptosis-induced damage in MIRI in mice via the Nrf2/HO-1 pathway, providing modern scientific evidence for the application of acupuncture in the treatment of cardiovascular diseases.

Purpose: This systematic review and meta-analysis of randomized controlled trials (RCTs) is aimed at assessing the clinical efficacy and safety of stellate ganglion block (SGB) for angina pectoris (AP). Methods: PubMed, Embase, Cochrane Library, Web of Science, Chinese National Knowledge Infrastructure, China Science and Technology Journal Database, and Wanfang databases were comprehensively searched for RCTs investigating SGB treatment for AP. The retrieval time was from the establishment date of each database to October 10, 2024. The Cochrane risk of bias assessment tool was used to determine the methodological quality. Review Manager 5.4 software was employed for data analysis, and GRADEpro GDT software was utilized to evaluate the quality of evidence. Results: Ultimately, six RCTs were included, encompassing 373 patients with angina. The overall methodological quality of the included studies was moderate, with the evaluation of evidence quality showing 12 low-quality and five extremely low-quality studies. The meta-analysis results demonstrated that compared with the control group, the experimental group had lower frequency and duration of AP, visual analog scale score, heart rate, detection rate of S-T segment elevation ≥ 0.1 mV on electrocardiogram (ECG) after 24 h of treatment, detection rate of abnormal T waves on ECG after 24 h of treatment, and S-T segment displacement on ECG after treatment. Furthermore, the experimental group exhibited lower serum Cardiac Troponin I levels, a decreased incidence of acute myocardial infarction (AMI) and rehospitalization, and improved clinical efficacy. However, none of the included studies reported SGB-related adverse events. Conclusion: SGB is effective in alleviating myocardial injury and reducing the incidence of AMI and rehospitalization in patients with AP. Nevertheless, the limited number and relatively low quality of included studies emphasize the requirement for more high-quality research to verify these conclusions.

Migraine is a highly prevalent and disabling neurological disorder characterized by abnormal encoding of pain perception, linked to structural and functional abnormalities in the insula. Insular subregions play critical but distinct roles in this process, however, the specific patterns and mechanisms remain elusive in migraineurs. In this study, voxel-based morphometry and seed-based functional connectivity (FC) were employed to investigate structural and functional alterations in insula subdivisions in 44 patients with migraine without aura (MWoA) compared with 51 matched healthy controls. Pain perception was evaluated using the intensity, frequency, and duration of migraine. Compared with healthy controls, patients exhibited(1) reduced gray matter volume in the bilateral dorsal anterior insula (dAI);(2) increased FC between the dAI/posterior insula and bilateral precuneus, the left dAI and left middle temporal gyrus, the left ventral AI and superior/middle frontal gyrus;(3) decreased FC between the left dAI and left middle frontal gyrus, left middle occipital gyrus and right pallidum. Moreover, the left dAI was correlated with the duration and frequency of migraine, the right dAI was correlated with the intensity and duration of migraine. Our results provide novel evidence in support of the insula abnormality hypothesis in migraine and highlight the pivotal role of alterations in the dAI in pain perception in migraineurs.

Background To review the biological functions of ergothioneine (ERGO), its correlation with plasma levels in cognitive frailty, and research progress in treating frailty and cognitive impairment, with the aim of providing a reference for ERGO application in cognitive frailty treatment.Methods A comprehensive review of existing literature on ERGO’s chemical structure, sources, antioxidant and anti-inflammatory effects, and its role in cognitive frailty was conducted. Clinical trial data and metabolomic studies were also analyzed to understand ERGO’s therapeutic potential.Results ERGO, a naturally occurring antioxidant, exhibits strong antioxidant, anti-inflammatory, and immunomodulatory activities. Age-related declines in plasma ERGO levels are observed, particularly in individuals with cognitive impairment. Metabolomic analyses confirm ERGO’s beneficial effects on cognition and memory. Preclinical studies demonstrate ERGO’s capacity to enhance cognitive function and neuronal health through oxidative stress reduction and neuroprotection.Conclusion Preclinical studies have underscored ERGO’s potent antioxidant, anti-inflammatory, and neuroprotective effects, suggesting its potential as a therapeutic agent for cognitive frailty. However, the translation of these findings into clinical benefits necessitates validation through well-designed clinical trials. While existing evidence is promising, suggesting ERGO as a viable complementary intervention, comprehensive and rigorous studies are imperative to establish its clinical efficacy and safety in managing cognitive frailty.

Background and aim As an auxiliary therapy, acupuncture is effective in ameliorating myocardial ischemia (MI). Selecting correct acupoints is widely acknowledged to be key for therapeutic effects of acupuncture, and traditional acupuncturists believe that selecting acupoints whose pressure pain threshold (PPT) change with disease, for instance selecting PC6 (Neiguan) when MI occurs, usually leads to better therapeutic effects. In this study, we aimed to identify the molecular mechanism of PPT regulation at PC6 in MI rats. Experimental procedure Firstly, we established MI models by intraperitoneal injection of ISO and evaluated PPT changes and mast cell degranulation (MCD) at PC6 during MI. Then, we performed high-throughput sequencing and overlapped the differentially expressed miRNAs in plasma and skin tissue from the left PC6 (L-PC6). Through bioinformatics analysis and dual-luciferase reporter assays, we tried to find the downstream molecules of miRNA. Subsequently, miRNA agonists were injected intramusculally at L-PC6, and we paid attention to changes in PPT and MCD at L-PC6 as well as the relationship between local mast cells (MCs) and nerve axons. Result and conclusion PPT decreased and MCD increased at PC6 in MI rats and miR-144-3p is a key molecule in the induction of these phenomenon. Furthermore, miR-144-3p targeting Interleukin-1β (IL-1β) leads to local MCD, neurogenic inflammation and peripheral nociceptor hypersensitization, finally resulting in PPT change at PC6. Innovatively, our study also provides a new direction for investigating the relationship between MCs, PPT and sensitivity of acupoints, which is mediated by miR-144-3p.

Objectives: This study systematically reviewed and meta-analyzed randomized controlled trials (RCTs) evaluating the efficacy and safety of acupuncture in myocardial ischemia/reperfusion (I/R) injury. Methods: A comprehensive literature search was conducted in PubMed, Cochrane Library, Web of Science, Chinese National Knowledge Infrastructure, China Science and Technology Journal Database, and Wanfang from database inception to November 3, 2024. Eligible RCTs assessing acupuncture for myocardial I/R injury were included. Statistical analyses were performed using Review Manager 5.3 and Stata 16. Results: A total of 26 RCTs of moderate methodological quality were included. Acupuncture significantly reduced myocardial enzyme levels compared to controls. Inflammatory markers (hs-CRP, TNF-α, IL-6, IL-8, and IL-1) were suppressed, while anti-inflammatory and immunoregulatory factors (IL-10 and IL-2) increased. Oxidative stress parameters showed improvements, with reductions in MDA and SOD levels. Echocardiographic findings demonstrated enhanced cardiac function, reflected by increased LVEF and LVESV, along with reductions in LVFS, LVEDD, LVEDV, and LVESD. Additionally, acupuncture alleviated TCM chest pain symptoms, shortened ICU stays, lowered MACE incidence, and improved 6MWT and SAQ indicators. No adverse reactions were reported. Conclusion: Acupuncture attenuates myocardial injury, inflammation, and oxidative stress while activating anti-inflammatory and immune responses, enhancing cardiac function, and mitigating ventricular remodeling. Furthermore, it alleviates chest pain, shortens ICU stays, reduces adverse cardiovascular events, and improves 6MWT and SAQ indicators.

INTRODUCTION:The enduring presence of HIV reservoirs represents an important obstacle to clinical management. Extensive research has been conducted in this field, but there are no bibliometric analyses focusing on HIV reservoir research. AIM:This study aimed to present the current status and global trends in HIV reservoir research through bibliometric analysis. METHODS:Studies on HIV reservoirs published from 1 January 1994 to 31 December 2023 were included in the Web of Science Core Collection database, and annual publication numbers, institutions, countries, and authors were analysed using CiteSpace bibliometric software. Furthermore, popular research topics and trends were analysed using co-cited references and keywords. From 1994 to 2023, 5778 publications on HIV reservoirs were included, with the United States producing the most publications, citations, and research funding. The most productive individual author was Nicolas Chomont. Cell was the journal publishing the most publications, while Nat Med had the best total link strength. The University of California System was the institution that made the greatest contribution. Keyword clustering analysis of the extracted publications indicated that the research areas over the past three decades have primarily focused on "central nervous system," "histone deacetylase," "multiple Epstein‒Barr virus infection," and "dendritic cell." RESULTS:Moreover, keyword emergence analysis indicates that "provirus" and "identification" are likely to become central themes in future research. Future investigations should prioritize elucidating the specific mechanisms underlying proviral persistence and the identification of novel biomarkers in HIV reservoirs. Additionally, exploring the role of proviral dynamics in therapeutic development and reservoir targeting could offer new insights into potential treatment strategies. CONCLUSION:This study makes a significant contribution to the understanding of HIV reservoirs, shedding light on key characteristics and emerging trends while also pointing to future research directions.

Objective:To observe the effect of electroacupuncture (EA) on the intestinal flora in rats with chronic obstructive pulmonary disease (COPD) and explore its possible mechanism based on the gut-lung axis theory. Methods:A total of 30 male SD rats of SPF grade were randomly divided into a normal control (NC) group, a model group and an EA group, 10 rats in each one. In the model group and the EA group, COPD model was established by intratracheal instillation of lipopolysaccharide combined with cigarette fumigation. In the EA group, EA was applied at bilateral "Feishu" (BL13) and "Zusanli" (ST36), with disperse-dense waves, in frequency of 4 Hz/20 Hz, current of 1-3 mA, 20 min a time, once a day for 14 days continuously. Before and after modeling, as well as after intervention, body weight was observed; after intervention, the lung function indexes (forced expiratory volume in 0.1 second [FEV0.1], FEV0.1/forced vital capacity [FVC]%, forced expiratory volume in 0.3 second [FEV0.3] and FEV0.3/FVC%) were measured, serum levels of inflammatory factors (tumor necrosis factor-α[TNF-α], interleukin-6[IL-6], interleukin-1β[IL-1β] and interleukin-10[IL-10]) were detected by ELISA, histopathology of lung and colon tissues was observed by HE staining, the intestinal flora were analyzed by 16S rRNA, and the correlations between lung function and intestinal flora were analyzed. Results:Compared with the NC group, in the COPD group, the body weight and lung function indexes were reduced (P<0.01); the lung and colon tissues were damaged, the mean linear intercept (MLI) of alveolus and inflammatory cell numbers of 100 μm2 in lung tissue were increased (P<0.01); the serum levels of TNF-α, IL-6 and IL-1β were increased (P<0.01, P<0.05), and the serum level of IL-10 was decreased (P<0.01); α-diversity indexes of intestinal flora were increased (P<0.01); the relative abundance of Bacteroidetes, Proteobacteria and Oscillospira, Bacteroides, Coprococcus was increased (P<0.01), the relative abundance of Firmicutes, Actinobacteria, Tenericutes, TM7 and Lactobacillus, Allobaculum, Bifidobacterium, YRC22 was decreased (P<0.01, P<0.05); 31 different expressed metabolic pathways were identified between the two groups. Compared with the COPD group, in the EA group, the body weight and lung function indexes were increased (P<0.01); the damage of lung and colon tissues was improved, the MLI of alveolus was decreased (P<0.05); the serum levels of TNF-α, IL-6 and IL-1β were decreased (P<0.05), and the serum level of IL-10 was increased (P<0.05); α-diversity indexes of intestinal flora were decreased (P<0.01); the relative abundance of Bacteroidetes, Proteobacteria and Oscillospira, Bacteroides, Coprococcus was decreased (P<0.01, P<0.05), the relative abundance of Firmicutes, Actinobacteria, Tenericutes, TM7 and Lactobacillus, Allobaculum, Bifidobacterium, YRC22 was increased (P<0.01); 35 different expressed metabolic pathways were identified between the two groups. The lung function was positive related with Actinobacteria, Tenericutes, TM7 and YRC22, and was negative related with Bacteroidetes, Proteobacteria and Oscillospira, Bacteroides, Coprococcus. Conclusion:EA may ameliorate lung function and tissue injury of COPD by regulating intestinal flora dysbiosis and inflammatory response, suggesting an anti-inflammatory effect mediated via "gut-lung" axis.

This study employed representative data from the U.S. and China to delve into the correlation among migraine prevalence, the triglyceride‒glucose index, a marker of insulin resistance, and the composite indicator of obesity. Cross–sectional data were acquired from the National Health and Nutrition Examination Survey conducted between 1999 and 2004, as well as from the China Longitudinal Study of Health and Retirement (CHARLS) performed from 2011 to 2012. Weighted logistic regression analysis, subgroup analysis, smooth curve fitting and threshold effect analysis were used to ascertain the intricate relationships among triglyceride glucose–body mass index (TyG–BMI), triglyceride glucose–waist circumference (TyG–WC), triglyceride glucose–waist height ratio (TyG–WHtR) and migraine. Boruta’s algorithm and nine machine learning models were applied. SHapley Additive Explanations (SHAP) values were used to analyze leading models, highlighting influential features. The analysis included 6,204 U.S. participants and 9,401 Chinese participants. TyG–BMI as well as TyG–WHtR were shown to be strongly correlated with the incidence of migraine among U.S. adults (TyG–BMI: OR = 1.28, 95

The meridian theory is an important component of traditional Chinese medicine, playing a crucial role in disease diagnosis, treatment, and health preservation. Serving as the media for the effects of acupuncture, moxibustion, herbal medicine, and acupressure massage, meridians exert undeniable impact on the human body. However, the essence of meridians remains a topic of debate. Recent research has primarily focused on their anatomical structures, leading to numerous hypotheses. Simultaneously, other researchers have approached this subject from an energetic perspective, discovering information interactions within the meridian system. These findings suggest that meridians possess both physical and information dimensions, indicating that a singular approach to their study is insufficient. To bridge this gap, a shift from purely structural research toward an exploration of the information aspects of meridians is necessary. By integrating this information approach with traditional meridian theory, it may be possible to develop a new, modernized meridian theory that is aligned with contemporary concepts, making it more accessible and applicable in clinical settings.

ST-elevation myocardial infarction (STEMI) is a common acute ischemia heart disease that causes serious damage to human health worldwide. Even though morbidity and mortality have significantly decreased by percutaneous coronary intervention (PCI), an additional cardiac protection strategy is still required. Acupuncture therapy has presented a dominant cardiac protection in many studies lately. Thus, we aim to evaluate the effect and safety of acupuncture as an adjunctive therapy in STEMI patients after PCI through a randomized controlled trial. This study describes a protocol of multicenter, double-blinded, parallel-controlled, randomized controlled trial. Ninety-six patients with STEMI aged 18–85 years who undergoing PCI will be recruited from the Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, The Affiliated Third Hospital of Chengdu Traditional Chinese Medicine University/Chengdu Pidu District Hospital of Traditional Chinese Medicine, and Zhaotong Municipal Hospital of Traditional Chinese Medicine. Participants will be randomly assigned (1:1 ratio) to the verum acupuncture plus basic therapy (i.e., treatment) group or the sham acupuncture plus basic therapy (i.e., control) group. These participants will be treated for 5 days and then will be followed up for 24 weeks. Any adverse events will be recorded throughout the study to evaluate safety. The present study aims to investigate the effect and safety of acupuncture for patients with STEMI after PCI and set up standardized treatment programs for acupuncture of these patients. This study was registered in the Chinese Clinical Trial Registry (Registration ID: [ChiCTR2400081117]), on February 22, 2024.

Background:Electroacupuncture (EA), with varying stimulation intensities, has demonstrated therapeutic potentials in both animal and clinical studies for the treatment of chronic obstructive pulmonary disease (COPD). However, a comprehensive investigation of the intensity-related effects, particularly 1mA and 3mA of EA, and the underlying mechanisms remains lacking.Methods:A COPD rat model was established by prolonged exposure to cigarette smoke and intermittent intratracheal instillation of lipopolysaccharide. EA treatment was administered at acupoints BL13 (Feishu) and ST36 (Zusanli), 20 minutes daily for 2 weeks, with intensities of 1mA and 3mA. EA effectiveness was evaluated by pulmonary function, histopathological change, serum level of inflammatory cytokines, and level of oxidative stress markers in serum and lung tissues. Transcriptome profiling and weighted gene co-expression network analysis (WGCNA) were performed to reveal gene expression patterns and identify hub genes. Real-time quantitative PCR (RT-qPCR) and Western blot (WB) were performed to detect the mRNA and protein expression levels, respectively.Results:EA at both 1mA and 3mA exerted differing therapeutic effects by improving lung function and reducing inflammation and oxidative stress in COPD rats. Transcriptome analysis revealed distinct expression patterns between the two groups, functionally corresponding to shared and intensity-specific (1mA and 3mA) enriched pathways. Eight candidate genes were identified, including Aqp9, Trem1, Mrc1, and Gpnmb that were downregulated by EA and upregulated in COPD. Notably, Msr1 and Slc26a4 exclusively downregulated in EA-1mA, while Pde3a and Bmp6 upregulated solely in EA-3mA. WGCNA constructed 5 key modules and elucidated the module-trait relationship, with the aforementioned 8 genes being highlighted. Additionally, their mRNA and protein levels were validated by RT-qPCR and WB.Conclusion:Our results demonstrated that 1mA and 3mA intensities induce distinct gene expression patterns at the transcriptional level, associated with shared and 1mA vs 3mA-specific enriched pathways. Genes Mrc1, Gpnmb, Trem1, and Aqp9 emerge as promising targets, and further studies are needed to elucidate their functional consequences in COPD.

This study explored how the weight-adjusted waist index (WWI) and a body shape index (ABSI) are related to serum neurofilament light chain (sNfL) levels among U.S. adults. We aimed to evaluate sNfL, which plays key roles in neuronal injury in neurological diseases, given its understudied connection to obesity. We used cross-sectional data from the 2013–2014 National Health and Nutrition Examination Survey (NHANES) of people with complete information on the weight-adjusted waist index (WWI), a body shape index (ABSI), and serum neurofilament light chain (sNfL). Multiple linear regression analysis allowed us to investigate the separate connections among the WWI, ABSI, and sNfL. Moreover, interaction testing and subgroup analysis were performed to improve the general validity of our results. To assess any nonlinear correlations, we also performed threshold effect analysis and smoothed curve fitting. WWI and ABSI were positively linked with sNfL (WWI: β = 0.05, 95