Plant-derived exosome-like nanovesicles (PELNs), characterized by a natural lipid bilayer membrane, have rapidly emerged as a prominent research frontier in medicine owing to their unique biological properties and robust therapeutic potential. This review comprehensively examines the biological profiles, mechanistic functions, and recent engineering advancements of PELNs. In terms of composition, PELNs are uniquely enriched in plant-specific glycolipids, phosphatidylserine, secondary metabolites, and highly stable 2'-O-methylated miRNAs. This distinct molecular makeup endows them with exceptional biocompatibility, negligible immunogenicity, and the capacity for cross-species molecular communication. Mechanistically, PELNs demonstrate profound anti-inflammatory efficacy by suppressing the NF-κB and NLRP3 inflammasome pathways. They also serve as potent immune modulators, driving macrophage M1/M2 polarization and regulating T cell activity. Additionally, PELNs exhibit promising antitumor capabilities, targeting malignancies via reactive oxygen species (ROS) induction, TRAIL pathway activation, and tumor microenvironment remodeling. Crucially, the plant miRNAs encapsulated within PELNs remain highly stable in the gastrointestinal tract, allowing them to selectively alter gene expression in specific gut microbiota communities. This interaction deeply influences host immunity and metabolism, highlighting the vital role in cross-species regulation. Advancements in bioengineering have further expanded the clinical utility of PELNs. Targeted delivery efficiency can be significantly amplified via surface functionalization (e.g., folate and RGD sequences) and state-of-the-art drug loading technologies such as sonication and electroporation. Consequently, engineered PELNs surpass traditional synthetic nanocarriers in penetrating natural physiological barriers, particularly for oral and transdermal drug administration. Despite these advantages, clinical translation is currently hindered by the lack of standardized isolation protocols, challenges in scalable manufacturing, and the need for robust quality control frameworks. Looking forward, the integration of multi-omics approaches and AI-driven “molecular fingerprinting”—coupled with the design of synthetic biomimetic vesicles—will be instrumental in overcoming these bottlenecks, ultimately establishing PELNs as a next-generation platform for precision medicine and targeted nanotherapeutic delivery.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveThis paper aims to investigate the distribution patterns of traditional Chinese medicine syndromes in patients with chronic hepatitis B （CHB） comorbid with metabolically associated fatty liver disease （MAFLD） and analyze their correlation with clinical characteristics and the progression of liver fibrosis. MethodsA cross-sectional study method was employed， and 506 patients with CHB comorbid with MAFLD who attended the Hepatology Outpatient Department of Public Health Clinical Center of Chengdu from June 2024 to December 2024 were enrolled. General information， traditional Chinese medicine syndromes information， laboratory indicators， and imaging examination results were collected using case report forms （CRF）. Tongue images of patients were acquired using a tongue diagnosis instrument， and tongue feature parameters were extracted using computer image processing technology. Frequency analysis， factor analysis， and cluster analysis， and other methods were used to explore syndrome categories and distribution patterns. Non-parametric tests were used to compare the differences in clinical characteristics among different syndromes. Univariate and multivariate logistic regression analyses were performed to investigate the correlation between traditional Chinese medicine syndromes and the progression of liver fibrosis. ResultsThe main traditional Chinese medicine syndromes in patients with CHB comorbid with MAFLD were mainly dominated by damp-heat accumulation syndrome， liver stagnation and spleen deficiency syndrome， and phlegm-blood stasis syndrome， with damp-heat accumulation syndrome accounting for the highest proportion （41.89%）. Compared with those without damp-heat accumulation syndrome， patients with damp-heat accumulation syndrome had significantly lower tongue proper H value， tongue coating H value， and tongue coating a^* value （P<0.05）， significantly higher tongue coating b^* value （P<0.05）， significantly increased levels of white blood cell （WBC）， red blood cell （RBC）， hemoglobin （HGB）， and glucose （GLU）， increased CAP values （P<0.05）， a higher proportion of males （P<0.05）， and a younger age （P<0.05）. Univariate and multivariate logistic regression analyses show that age， hepatitis B surface antigen （HBsAg）， diabetes， and damp-heat accumulation syndrome are independent risk factors for liver fibrosis （P<0.05）， and that damp-heat accumulation syndrome is predominantly distributed in liver fibrosis stage F0-F1. ConclusionDamp-heat accumulation syndrome is a typical syndrome in patients with CHB comorbid with MAFLD， which is significantly associated with enhanced inflammatory response， metabolic disorders， and early liver fibrosis， and is a key link in disease progression. Clinical attention and early intervention are needed.

In this study, there were three toxoplasmosis patients, two of whom developed symptoms in both eyes. One patient had a slight deviation of the lesion from the central fovea, which had a minor impact on vision. The diagnosis of this disease requires not only a close pet contact history and typical clinical manifestations, but also serology and the gold standard Goldmann-Witmer coefficient(GWC). However, the GWC of some patients cannot be detected at the initial stage, such as the first patient′s GWC, which did not meet the standard. All three patients underwent metagenomic testing to assist with diagnosis.

Objective To explore the medication rules of Professor Hua Baojin in the treatment of subsolid pulmonary nodules through retrospective analysis and data mining techniques. Methods The prescriptions of patients with subsolid pulmonary nodules who were diagnosed and treated by Professor Hua Baojin at Guang’anmen Hospital of the Chinese Academy of Chinese Medical Sciences from January 1, 2021 to December 31, 2024 were retrospectively collected. Data were imported into the Ancient and Modern Medical Case Cloud Platform for analysis of drug frequency, four natures and five flavors, meridian tropism, drug association, and hierarchical clustering. Results A total of 455 prescriptions were included, containing 205 kinds of traditional Chinese medicines, with a total frequency of 12048 times. Fifty-seven commonly used drugs were screened out, among which drugs with high frequencies included astragalus membranaceus (raw) and hawthorn fruit (charred). The nature of the drugs was mainly warm, cold, and neutral. The flavor of the drugs was mostly sweet, bitter, and pungent. The meridians they belonged to mainly included the lung, spleen, and liver meridians. Their efficacy was mainly tonifying deficiency, clearing heat, resolving phlegm, and relieving cough and asthma. Association analysis obtained 19 pairs of drug combinations, 21 groups of three-drug combinations, and four groups of four-drug combinations. Hierarchical clustering obtained 10 groups of drug combinations. Conclusion On the basis of the core pathogenesis of subsolid pulmonary nodule, Professor Hua applies the theory of regulating qi and detoxifying; regulating the qi of the liver, spleen, and lung; and detoxifying the toxins of phlegm and blood stasis, providing valuable experience for the clinical treatment of SSN.

Objective To explore the clinical information of female patients with pulmonary nodules and the distribution of traditional Chinese medicine (TCM) syndromes and their elements. Methods A cross-sectional study was conducted to collect the basic information, medical history data, image data, and four diagnostic information of female patients with pulmonary nodules. The distribution characteristics of TCM syndromes and their elements in female patients with pulmonary nodules were determined by KMO test, Bartlett spherical test, systematic cluster analysis, chi-square test, and other methods. Results A total of 721 female patients with pulmonary nodules were included in this study. The patients were mainly 45-59 years old, had secondary school education or above, and had a history of oil smoke exposure as clinical characteristics. The pulmonary nodules were mainly 6-10 mm in size and appeared as multiple and ground glass nodules. The clinical symptoms were mainly fatigue, emotional irritability, and shortness of breath. The main syndromes of disease location were the spleen, liver, and lung; and the main syndromes of disease were phlegm, dampness, and qi deficiency. The main complex syndromes were spleen deficiency and dampness, liver stagnation, and qi/yin deficiency. Conclusion Middle age, high education, and multiple small ground glass nodules are the clinical characteristics of female patients with pulmonary nodules. Exposure to oil smoke is an important cause of the occurrence of female pulmonary nodules. During treatment, attention should be paid to strengthening the spleen, removing dampness, soothing the liver, regulating and tonifying qi, and nourishing yin.

Perceptual decision making refers to the process by which individuals make choices and judgments based on sensory information, serving as a fundamental ability for human adaptation to complex environments. While traditional research has focused on perceptual decision making in isolated contexts, growing evidence highlights the profound influence of social contexts prevalent in real-world scenarios. As a crucial factor supporting individual survival and development, social context not only provides rich information sources but also shapes perceptual decision making through top-down processing mechanisms, prompting researchers to recognize the inherently social nature of human decisions. Empirical studies have demonstrated that social information, such as others’ choices or group norms, can systematically bias individuals’ perceptual decisions, often manifesting as conformity behaviors. Social influence can also facilitate performance under certain conditions, particularly when individuals can accurately identify and adopt high-quality social information. The impact of social context on perceptual decisions is modulated by a variety of external and internal factors, including group characteristics(e.g., group size, response consistency), attributes of peers (e.g., familiarity, social status, distinctions between human and artificial agents), as well as individual differences such as confidence, personality traits, and developmental stage. The motivations driving social influence encompass three primary mechanisms: improving decision accuracy through informational influence, gaining social acceptance through normative influence, and maintaining positive self-concept. Recent computational approaches have employed diverse theoretical frameworks to provide valuable insights into the cognitive mechanisms underlying social influence in perceptual decision making. Reinforcement learning models demonstrate how social feedback shapes future choices through reward-based updating. Bayesian inference frameworks describe how individuals integrate personal beliefs with social information based on their respective reliabilities, dynamically updating beliefs to optimize decisions under uncertainty. Drift diffusion models offer powerful tools to decompose social influence into distinct cognitive components, allowing researchers to differentiate between changes in perceptual processing and shifts in decision criteria. Collectively, these models establish a comprehensive methodological foundation for disentangling the multiple pathways by which social context shapes perceptual decisions. Neuroimaging and electrophysiological studies provide converging evidence that social context influences perceptual decision making through multi-level neural mechanisms. At early perceptual processing stages, social influence modulates sensory evidence accumulation in parietal cortex and directly alters primary visual cortex activity, while guiding selective attention to stimulus features consistent with social norms through attentional alignment mechanisms. At higher cognitive levels, the reward system (ventral striatum, ventromedial prefrontal cortex) is activated during group-consistent decisions; emotion-processing networks (anterior cingulate cortex, insula, amygdala) regulate experiences of social acceptance and rejection; and mentalizing-related brain regions (dorsomedial prefrontal cortex, temporoparietal junction) support inference of others’ mental states and social information integration. These neural circuits work synergistically to achieve top-down multi-level modulation of perceptual decision making. Understanding the mechanisms by which social context shapes perceptual decision making has broad theoretical and practical implications. These insights inform the optimization of collective decision-making, the design of socially adaptive human-computer interaction systems, and interventions for cognitive disorders such as autism spectrum disorder and anorexia nervosa. Future studies should combine computational modeling and neuroimaging approaches to systematically investigate the multi-level and dynamic nature of social influences on perceptual decision making.

ObjectiveThis study aims to develop and validate a novel multimodal predictive model， termed criss-cross network（CCNet）-directed graph neural network（DGNN）（CGN）， for accurate assessment of pulmonary nodule progression in high-risk individuals for lung cancer， by integrating longitudinal chest computed tomography（CT） imaging with both traditional Chinese and western clinical evaluation data. MethodsA cohort of 4 432 patients with pulmonary nodules was retrospectively analyzed. A twin CCNet was employed to extract spatiotemporal representations from paired sequential CT scans. Structured clinical assessment and imaging-derived features were encoded via a multilayer perceptron， and a similarity-based alignment strategy was adopted to harmonize multimodal imaging features across temporal dimensions. Subsequently， a DGNN was constructed to integrate heterogeneous features， where nodes represented modality-specific embeddings and edges denoted inter-modal information flow. Finally， model optimization was performed using a joint loss function combining cross-entropy and cosine similarity loss， facilitating robust classification of nodule progression status. ResultsThe proposed CGN model demonstrated superior predictive performance on the held-out test set， achieving an area under the receiver operating characteristic curve（AUC） of 0.830， accuracy of 0.843， sensitivity of 0.657， specificity of 0.712， Cohen's Kappa of 0.417， and F₁ score of 0.544. Compared with unimodal baselines， the CGN model yielded a 36%-48% relative improvement in AUC. Ablation studies revealed a 2%-22% increase in AUC when compared to simplified architectures lacking key components， substantiating the efficacy of the proposed multimodal fusion strategy and modular design. Incorporation of traditional Chinese medicine （TCM）-specific symptomatology led to an additional 5% improvement in AUC， underscoring the complementary value of integrating TCM and western clinical data. Through gradient-weighted activation mapping visualization analysis， it was found that the model's attention predominantly focused on nodule regions and effectively captured dynamic associations between clinical data and imaging-derived features. ConclusionThe CGN model， by synergistically combining cross-attention encoding with directed graph-based feature integration， enables effective alignment and fusion of heterogeneous multimodal data. The incorporation of both TCM and western clinical information facilitates complementary feature enrichment， thereby enhancing predictive accuracy for pulmonary nodule progression. This approach holds significant potential for supporting intelligent risk stratification and personalized surveillance strategies in lung cancer prevention.

To address the common clinical problems associated with warm needling moxibustion, such as burns, bending of needle handles, and the inability to perform moxibustion during oblique needling, an adjustable warm needling moxibustion device is designed and has been granted a national patent. This device consists of five components: a moxa cylinder, an adjustable arm, a supporting tube, a temperature alarm, and a fixing strap. It allows infrared heat radiation from the moxa to pass through while blocking falling ash, thereby ensuring therapeutic efficacy and preventing burns. The device accommodates both perpendicular and oblique needling angles and adapts to various body positions, effectively avoiding deformation of the needle handle. It is easy to operate and offers high safety.
Moxibustion/methods* ; Humans ; Equipment Design ; Needles