Chronic obstructive pulmonary disease（COPD） is a common chronic respiratory disorder frequently accompanied by diaphragmatic dysfunction during its course， which significantly increases respiratory burden and impairs quality of life. As the primary inspiratory muscle， the diaphragm is prone to fatigue， atrophy， inflammation， and fibrosis during the long-term progression of COPD. Its pathological mechanisms involve multiple pathways such as inflammatory responses， oxidative stress， mitochondrial dysfunction， apoptosis， ion channel abnormalities， epigenetic regulation， autophagy disorder， and protein metabolism imbalance. In recent years， traditional Chinese medicine（TCM） has demonstrated multi-targeted and systemic regulatory advantages in improving diaphragmatic function in COPD. However， related studies remain fragmented， and integrated mechanistic understanding is lacking. This paper focuses on the mechanism-target-TCM intervention framework， systematically summarizing the molecular mechanisms of diaphragmatic dysfunction， while incorporating the TCM theory of Zongqi（ancestral Qi）. It highlights the therapeutic effects of Chinese herbal formulas， single herbs， and active components in modulating inflammation， oxidative stress， mitochondrial function， ion channels， epigenetic processes， autophagy， and protein homeostasis. Additionally， the review outlines existing challenges， including insufficient study volume， unbalanced selection of herbal prescriptions， limited mechanistic depth， inconsistent disease models and experimental designs， lack of standardized diaphragmatic function assessment， and weak clinical validation. Future research should strengthen the integration of TCM and modern medicine， identify additional therapeutic targets， deepen mechanistic research， and establish unified and standardized experimental systems to advance the theoretical foundation and clinical application of TCM in the prevention and treatment of COPD-related diaphragmatic dysfunction.

Chronic obstructive pulmonary disease（COPD） is a common chronic respiratory disorder frequently accompanied by diaphragmatic dysfunction during its course， which significantly increases respiratory burden and impairs quality of life. As the primary inspiratory muscle， the diaphragm is prone to fatigue， atrophy， inflammation， and fibrosis during the long-term progression of COPD. Its pathological mechanisms involve multiple pathways such as inflammatory responses， oxidative stress， mitochondrial dysfunction， apoptosis， ion channel abnormalities， epigenetic regulation， autophagy disorder， and protein metabolism imbalance. In recent years， traditional Chinese medicine（TCM） has demonstrated multi-targeted and systemic regulatory advantages in improving diaphragmatic function in COPD. However， related studies remain fragmented， and integrated mechanistic understanding is lacking. This paper focuses on the mechanism-target-TCM intervention framework， systematically summarizing the molecular mechanisms of diaphragmatic dysfunction， while incorporating the TCM theory of Zongqi（ancestral Qi）. It highlights the therapeutic effects of Chinese herbal formulas， single herbs， and active components in modulating inflammation， oxidative stress， mitochondrial function， ion channels， epigenetic processes， autophagy， and protein homeostasis. Additionally， the review outlines existing challenges， including insufficient study volume， unbalanced selection of herbal prescriptions， limited mechanistic depth， inconsistent disease models and experimental designs， lack of standardized diaphragmatic function assessment， and weak clinical validation. Future research should strengthen the integration of TCM and modern medicine， identify additional therapeutic targets， deepen mechanistic research， and establish unified and standardized experimental systems to advance the theoretical foundation and clinical application of TCM in the prevention and treatment of COPD-related diaphragmatic dysfunction.

Growth arrest DNA damage-inducible protein 45 β (GADD45B) has been reported to be a regulatory factor for active DNA demethylation and is implicated in the modulation of synaptic plasticity and chronic stress-related psychopathological processes. However, its precise role and mechanism of action in stress susceptibility remain elusive. In this study, we found a significant reduction in GADD45B expression specifically in the ventral, but not the dorsal hippocampal CA1 (dCA1) of stress-susceptible mice. Furthermore, we demonstrated that GADD45B negatively regulates susceptibility to social stress and NMDA receptor-dependent long-term potentiation (LTP) in the ventral hippocampal CA1 (vCA1). Importantly, through pharmacological inhibition using the NMDA receptor antagonist MK801, we provided further evidence supporting the hypothesis that GADD45B potentially modulates susceptibility to social stress by influencing NMDA receptor-mediated LTP. Collectively, these results suggested that modulation of NMDA receptor-mediated synaptic plasticity is a pivotal mechanism underlying the regulation of susceptibility to social stress by GADD45B.
Animals ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors* ; CA1 Region, Hippocampal/drug effects* ; Male ; Stress, Psychological/physiopathology* ; Mice ; Neuronal Plasticity/drug effects* ; Long-Term Potentiation/drug effects* ; Mice, Inbred C57BL ; Antigens, Differentiation/metabolism* ; Dizocilpine Maleate/pharmacology* ; Excitatory Amino Acid Antagonists/pharmacology* ; GADD45 Proteins

Objective To explore the diagnostic value of 18F-fluorodeoxyglucose(FDG)PET/CT in primary pulmonary enteric adenocarcinoma.Methods The clinical and imaging data of 9 patients with primary pulmonary enteric adenocarcinoma who under-went 18F-FDG PET/CT examination were retrospectively analyzed,including lesion distribution,morphology,maximum standardized uptake value(SUVmax),clinical symptoms and signs,gastroscopy finding,puncture pathological results,and serum tumor markers[carbohydrate antigen 72-4(CA72-4),cytokeratin 19 fragment antigen 21-1(CYFRA21-1),carcinoembryonic antigen(CEA),carbo-hydrate antigen 199(CA199)].Results Pathological examination confirmed a diagnosis of primary pulmonary enteric adenocarcinoma after excluding gastrointestinal primary tumors through clinical evaluation.In all nine patients,18F-FDG PET/CT examination did not reveal any evidence of digestive system malignancies,and gastrointestinal microscopy was negative.Primary lesions were observed as masses or nodular types in 6 cases(5 in the left lung and 1 in the right lung),while 3 cases exhibited diffuse bilateral pulmonary involvement(manifested as multiple patchy opacities,nodules,ground-glass opacities,and consolidations).All pulmonary primary lesions showed increased 18F-FDG uptake,with SUVmax ranging from 2.7 to 12.8,mean 8.6±3.7.The six masses-or nodular-type primary lesions showed maximum diameters ranging from 2.1 to 10.5 cm,mean(5.23±3.06)cm.Four cases demonstrated hilar and mediastinal lymph node metastases,intrapulmonary metastases,and distant metastases,while 1 case showed only distant metastasis.Elevated levels of serum tumor markers were observed as follows:CA72-4 in 7 cases(10-273.3 U/mL),CEA in 7 cases(5-147.4 ng/mL),CA199 in 6 cases(31.22-4 364 U/mL),and CYFRA21-1 in 5 cases(8.31-99.7 ng/mL).Conclusion When pathological biopsy of a pulmonary lesion suggests primary pulmonary enteric adenocarcinoma after excluding gastrointestinal primary tumors,and 18F-FDG PET/CT shows no gastrointestinal masses,this may support the diagnosis of primary pulmonary enteric adenocarcinoma.

Objective:To investigate the impact of different etiologies on the spatial distribution pattern of infarcts and the mapping pattern of focal symptoms in acute ischemic stroke (AIS) using a population-based standardized spatial analysis of MRI.Methods:This was a cross-sectional study. Clinical [age, sex distribution, admission National Institutes of Health Stroke Scale (NIHSS) score and 90-day modified Rankin Scale (mRS) score at discharge, etc.] and imaging data of 2 610 patients with AIS attending 9 Medical Centers from January 2015 to December 2021 were retrospectively analyzed. All patients were categorized into 1 718 cases of large artery atherosclerosis (LAA) type, 335 cases of cardioembolism (CE) type, and 557 cases of small artery occlusion (SAO) type according to TOAST typing. All patients underwent diffusion-weighted imaging, and the detected infarct lesions were segmented and aligned to the standardized space using artificial intelligence-assisted methods, and the spatial distribution frequency heatmaps of lesion locations in patients with different TOAST subtypes were plotted and compared with each other by χ2 test. Lesion-symptom image brain maps with different clinical symptoms were further plotted, and differences of lesion-symptom image relationships among different TOAST subtypes were observed and compared with each other by interaction effect. Results:In all patients, the favored sites of infarct lesions were the bilateral middle cerebral artery region in the anterior circulation and the occipital and brainstem regions in the posterior circulation. Compared with the LAA type, the CE type lesions were more likely to occur in the anterior cerebral artery region, the occipital lobe, and the cerebellum posterior, while the SAO type lesions were more likely to occur in the perforator artery supply area. The lesion-symptom mapping results showed that AIS patients with infarct lesions in the frontoparieto-temporal region in the presence of a left middle cerebral artery supply had higher admission NIHSS scores and higher discharge 90-day mRS scores for the LAA type than for the CE type( P<0.05); AIS patients with infarcted lesions in the brainstem region and some cerebellar regions in the presence of vertebrobasilar artery supply had higher admission NIHSS scores and higher discharge 90-day mRS scores for the CE type than for the LAA type( P<0.05). Conclusion:At the population level, brain mapping reveals specific infarct distribution patterns and differences in lesion-symptom mapping patterns of different etiologies AIS patients, providing imaging evidence for the understanding of AIS pathogenetic mechanisms and clinical management.

Objective:To construct a VP8-mRNA vaccine using human rotavirus spike protein VP8 domain as the immunogen and analyze its immunogenicity in mice.Methods:The VP8-mRNA sequence was designed, optimized, and synthesized. The VP8 gene of rotavirus G1P[8] type was used to construct the plasmid pUC57-VP8-Kan-SapⅠ, which was then sequenced. The plasmid confirmed by sequencing was subjected to large-scale amplification and extraction, followed by linearization, in vitro transcription, and capping. The purified capped products were encapsulated with lipid nanoparticles using a microfluidic control apparatus. The encapsulated VP8-mRNA vaccine was administered intramuscularly to mice at 10, 15, and 20 μg. Serum samples were collected for antibody detection by ELISA. Cellular immune responses were detected by flow cytometry and ELISPOT. Statistical analysis was performed using one-way or two-way analysis of variance and Tukey-Kramer test. Results:The encapsulated VP8-mRNA vaccine was rounded and spherical, with a particle size of about 100 nm, a polymer dispersion index of 0.088, and an encapsulation rate of 92.3%. Two doses of VP8-mRNA vaccine immunization could induce a good immune response in mice. The level of IgG antibody induced after immunization in the 15 μg group was comparable to that of the 20 μg group, and there was no statistical difference ( P>0.05), but the antibody levels in the two groups were significantly higher than that in the 10 μg group ( P<0.000 1). VP8-mRNA vaccine could induce neutralizing antibodies against rotavirus G1 and G9 types. The highest level of neutralizing antibodies against rotavirus type G1 was observed in the 15 μg group, which was significantly higher than that in the 10 μg group ( P<0.05). All immunization groups exhibited good neutralizing ability against rotavirus G9 type. The results of ELISPOT showed that lymphocytes from mice in each vaccine group were able to secrete IFN-γ when stimulated with VP8 peptide. Flow cytometry showed that the proportions of CD8 + T cell subsets in the vaccine groups were higher than that in the control group. Conclusion:The VP8-mRNA vaccine has good immunogenicity in mice and can induce good humoral and T-cell immune responses.

Severe open tibiofibular fractures account for approximately 28.1% of all open fractures. Among them, Gustilo-Anderson type IIIB/C fractures present significant clinical challenges due to associated bone and soft tissue defects, high infection rates, and risk of amputation. Inadequate preoperative assessment may lead to suboptimal emergency surgical planning or intraoperative complications. Historically, external fixation was often preferred, but this approach has been associated with limitations such as restricted joint mobility, delayed bone union, joint stiffness, and disuse osteoporosis, resulting in poor functional recovery. With advancements of debridement techniques, standardization of antibiotic use, and popularization of early soft tissue coverage, early internal fixation has gained broader acceptance. Nevertheless, controversies persist regarding the choice of fixation method, timing of definitive fixation, use of reamed versus unreamed intramedullary nailing, and necessity of fibular fixation. To standardize the diagnosis and early management of severe open tibiofibular fractures, reduce complication rates, and improve functional recovery, the Society of Microsurgery of the Chinese Medical Association organized a panel of domestic experts to develop the Evidence-based guideline for the diagnosis and early fixation of severe open tibiofibular fractures ( version 2025), using evidence-based methodology. The guidelines provided 12 recommendations covering diagnostic and early fixation strategies of severe open tibiofibular fractures, aiming to provide clinicians with scientifically grounded and standardized guidance.

Spinal cord injury represents a severe central nervous system trauma characterized by prolonged treatment duration, limited neural regeneration, and delayed functional recovery, greatly affecting patients′ quality of life. The impaired neural tissue struggles to recover effectively due to both the hostile microenvironment and its own compromised state. Current clinical interventions, including early reduction, laminectomy decompression, and intravenous or intrathecal methylprednisolone administration, fail to simultaneously modulate the microenvironment and improve the neural status. Zinc, a trace element abundant in the central nervous system, plays a critical role in gene expression regulation, synaptic plasticity, and neuronal activity. Clinical evidences have indicated that lower serum zinc concentration in patients with spinal cord injury correlates with poorer outcomes and animal experiments have also demonstrated the neuroprotective effects of zinc. In fact, zinc supplementation therapy has not yet been developed into a mature clinical protocol. Besides, related animal studies still lack comprehensive understanding. To this end, the authors reviewed the biological characteristics of zinc, its administration routes, neuroprotective effects and mechanisms in the management of spinal cord injury, aiming to provide references for future basic research and clinical practice.

Spinal cord injury is a highly disabling central nervous system disorder whose pathological progression is closely associated with blood-spinal cord barrier (BSCB) disruption. Physical trauma to the spine or spinal cord may compromise BSCB integrity, triggering secondary damage including spinal edema, hemorrhage, oxidative stress, and excessive inflammatory responses. For the pivotal role of protecting the spinal cord microenvironment, the repair of BSCB is crucial in the treatment of spinal cord injury. Although present studies have explored BSCB repair strategies such as biological factor regulation, biomaterial applications, and traditional Chinese medicine interventions, most studies focus on improving the overall barrier function and fail to systematically elucidate how these strategies target the core functional units of BSCB, namely the endothelial cells and their junction structures, to achieve functional and structural restoration of the barrier. Therefore, the authors reviewed the composition and key repair targets of BSCB, along with research advances in BSCB repair strategies based on endothelial cells and junction structures, aiming to provide insights for basic research and clinical treatment of spinal cord injury.

OBJECTIVE To investigate the therapeutic effect of Sanhan Huashi Formula(SHF)on respiratory syncytial virus(RSV)-infected mouse models and explore its potential antiviral and anti-inflammatory mechanisms using lipidomics.METHODS Fifty-four BALB/c mice were randomly divided into six groups(n=9):blank group,model group,Ribavirin group(50 mg·kg-1·d-1),and SHF high(15.46 g·kg-1·d-1),medium(7.73 g·kg-1·d-1),and low-dose(3.87 g·kg-1·d-1)groups.A pneumonia model was established by in-tranasal RSV infection,followed by three consecutive days of oral gavage administration.Lung tissues were collected for histopathologi-cal evaluation using hematoxylin-eosin(HE)staining and inflammation scoring.Real-time quantitative polymerase chain reaction(RT-qPCR)was performed to measure mRNA levels of viral gene fusion protein(F),glycoprotein(G),and inflammatory factors tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)to assess lung viral load and inflammation,while immunofluorescence staining was performed to observe the expression of RSV-F protein in lung tissues.Serum lipidomics analysis was conducted using ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap high-resolution mass spectrometry(UPLC-Q Exactive Or-bitrap MS)to identify lipid metabolism changes and differential lipids.RESULTS Compared with the blank group,mice in the model group exhibited marked pulmonary inflammatory cell infiltration and tissue injury,with significantly elevated pulmonary histopa-thology scores and lung index.The lung viral load and the mRNA expression levels of the inflammatory factors TNF-α and IL-6 were significantly increased,and immunofluorescence likewise indicated high expression of RSV-F protein in lung tissue.Relative to the model group,treatment with SHF at all tested doses clearly ameliorated lung tissue injury,effectively suppressed viral gene expression and inflammatory cytokine levels,and reduced the fluorescence signal intensity of RSV-F protein in the lungs.Lipidomics analysis re-vealed that compared with the blank group,the model group exhibited marked disturbances in lipid metabolism-characterized by dys-regulation of triacylglycerol(TG),phosphatidylcholine(PC),lysophosphatidylcholine(LPC),sphingomyelin(SM),diacylglycerol(DG),lysophosphatidylethanolamine(LPE),and phosphatidylethanolamine(PE).High-dose SHF treatment reversed these RSV-induced lipid abnormalities.CONCLUSION SHF effectively alleviates RSV-induced pulmonary inflammation and pathological injury,re-duces pulmonary RSV viral load,and may exert these effects by modulating dysregulated lipid metabolism in peripheral blood.