ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

Malignant gastrointestinal tumors （GT） mainly include laryngeal cancer， esophageal cancer， gastric cancer， pancreatic cancer， hepatocellular carcinoma， bile duct cancer， and colorectal cancer. At present， the morbidity and mortality of GT are high. Tumor immune escape is one of the key reasons for cancer development and treatment failure， and it is also the main direction of current tumor immunotherapy research. Traditional Chinese medicine （TCM） plays a role in treating GT and alleviating systemic symptoms， especially showing potential advantages in regulating the immune escape mechanism. This article elaborates on the immune escape mechanism of GT and systematically reviews that TCM active components or compound prescriptions act on key immune checkpoints such as programmed cell death protein-1 （PD-1） and programmed cell death ligand-1 （PD-L1） to reduce the proportion of marrow-derived suppressor cells （MDSCs）， promote the polarization of M1 macrophages， activate effector immune cells， enhance CD8⁺ T cell recruitment and interferon （IFN）-γ secretion， enhance the killing activity of natural killers （NKs）， and reduce foxhead box protein P3（FoxP3⁺）-positive regulatory T （Treg） cell infiltration. TCM active components or compound prescriptions can remodel the tumor microenvironment （TME）， such as improving immunosuppressive factors， promoting vascular normalization， and regulating intestinal microbiota. Through the regulation of TME， enhancement of antigen presentation， inhibition of immune checkpoint molecules， regulation of cellular network factors and metabolites， etc.， TCM active components or compound prescriptions enhance the immune function， thereby inhibiting the immune escape of GT. This paper summarizes and reflects on the research results of TCM in regulating immune escape to treat GT in recent years， aiming to help transform TCM from empirical medication to precision treatment based on immune regulation， reduce drug resistance and enhance treatment effect.

As a complex autoimmune disease， rheumatoid arthritis （RA） involves immune microenvironment dysregulation resulting from excessive activation of pyroptosis， which is a crucial factor in disease progression. Based on the theory of ying-wei in traditional Chinese medicine， "ying decline and wei attack" is considered the fundamental pathogenesis of RA. Pyroptosis serves as a microscopic manifestation of this concept， suggesting a potential correlation between "ying decline and wei attack" and pyroptosis nd immune microenvironment dysregulation in RA. Accordingly， treatment principles based on this theory are proposed： in the early stage of the disease， boosting wei to consolidate the exterior， and regulating ying to dispel pathogens； in the middle and late stages， harmonizing ying to remove stagnation， and nourishing its transformational source.

Objective:To explore the in vitro radiation levels and in vivo neutron activation after patients receiving boron neutron capture therapy (BNCT). Methods:Totally 29 BNCT treatments were performed for 21 patients with head and neck and brain cancer using the NeuPex accelerator-based boron neutron capture therapy (AB-BNCT) system in Xiamen Humanity Hospital from October, 2022 to April, 2024. The ambient dose equivalent rate around the patients was measured with an X/gamma dose rate survey meter. The gamma radiation dose rates were measured at 0, 0.5, 1.0, and 2.0 m from the irradiation position, at 0, 0.5, 1.0, and 2.0 m from the opposite side of the irradiation position, and at the navel and the affected knee, respectively. Meanwhile, a portable high-purity germanium gamma spectrometer was used to measure the spectrum of activated nuclides in the bodies of patients who had underwent the treatment, and the types of radionuclides generated by neutron activation during each BNCT treatment were analyzed.Results:The radionuclides 24Na, 38Cl, and 49Ca were mainly produced in the bodies of patients treated with BNCT. 20 minutes after BNCT treatment, the ambient dose equivalent rate at a distance of 1.0 m from the irradiation position was lower than 2.5 μSv/h. Conclusions:The dose delivered to the staff and family members by the patients undergoing BNCT is relatively low, and the resulting radiation risk is low. According to the ALARA principle, it is recommended that certain control actions be taken for patients having received BNCT treatment to minimize the exposure doses of both patients and staff as much as possible.

Objective To explore the effects of CDP-diacylglycerol synthase 1(CDS1)on autophagy and amyloid deposition in hippocampal neurons of mice and the related mechanism.Methods Congo red and immunohistochemical staining were used to observe the amyloid deposition in hippocampus of amyloid precursor protein(APP)/presenilin 1(PS1)double-transgenic mice.Lentivirus-mediated overexpression of APP was induced in HT22 cells,and Congo red staining was used to observe the amyloid deposition in HT22 cells.The protein expression levels of microtubule-associated protein 1 light chain 3(LC3)-Ⅱ and P62 in the hippocampus of APP/PS1 double-transgenic mice and APP-overexpressed HT22 cells were detected by Western blotting.The differential protein CDS1 was screened based on the hippocampal proteomics results of APP/PS1 double-transgenic mice.The expression of CDS1 protein in hippocampal tissue of APP/PS1 transgenic mice and APP-overexpressed HT22 cells was detected by Western blotting.After lentivirus-mediated APP overexpression in HT22 cells,CDS1 was overexpressed,and the protein expression levels of LC3-Ⅱ and P62 were detected by Western blotting.Results β-amyloid protein(Aβ)was deposited in the hippocampus of APP/PS1 mice and in HT22 cells overexpressing APP.The levels of LC3-Ⅱ and P62 protein in the hippocampus of APP/PS1 double-transgenic mice and APP-overexpressed HT22 cells were significantly increased.A differential metabolic pathway,glycerophospholipid metabolic pathway,was screened by Kyoto Encyclopedia of Genes and Genomes pathway analysis in the proteomic results of APP/PS1 double-transgenic mice,and the differential protein CDS1 was obtained.Compared with wild-type C57BL/6 mice,APP/PS1 double-transgenic mice exhibited a significantly decrease in CDS1 protein expression in the hippocampus(0.46±0.07 vs 1.00±0.25,P＜0.01).Similarly,lentivirus-mediated overexpression of APP in HT22 cells resulted in decreased CDS1 protein levels compared to cells infected with empty viral vector controls(0.68±0.18 vs 1.00±0.13,P＜0.01).The autophagy flow of nerve cells was significantly restored after the CDS1 overexpression in APP-overexpressed HT22 cells(LC3-Ⅱ:1.00±0.15 vs 0.21±0.05,P＜0.01;P62:1.00±0.16 vs 0.67±0.10,P＜0.01),and Aβ deposition was significantly decreased.Conclusion Downregulation of CDS1 expression can induce dysfusion of autophagosome and lysosome,promoting amyloid deposition in hippocampus of mice with Alzheimer's disease.

In recent years,the incidence and mortality of heatstroke have been increasing annually alongside global warming,with a marked rise in cases exhibiting atypical symptoms.To address the increasingly complex challenges in heatstroke prevention and treatment,Heatstroke Prevention and Treatment Research Center of Chinese PLA,Expert Group of Heatstroke Prevention and Treatment of Chinese PLA,and Chinese PLA Professional Committee of Critical Care Medicine have jointly developed this guideline(2025 edition).Utilizing the Grading of Recommendations Assessment,Development and Evaluation(GRADE)system,Appraisal of Guidelines for Research and Evaluation(AGREE)criteria,and Reporting Items for Practice Guidelines in Healthcare(RIGHT)standards,and based on the 2015 draft"Expert Consensus on the Standardized Diagnosis and Treatment of Heatstroke"and the 2019"Chinese Expert Consensus on the Diagnosis and Treatment of Heatstroke",this guideline has been crafted.This guideline provides 25 evidence-based recommendations to guide the prevention,treatment and research of heatstroke,which thoroughly covers 8 critical domains:clinical classification,pathophysiological mechanisms,clinical manifestations,diagnostic criteria,differential diagnosis,treatment protocols,rehabilitation and return to work,and prevention.

The scientific research and innovation capabilities of medical students are intrinsically linked to the sustained and high-quality development of national healthcare initiatives.Cultivating outstanding medi-cal students with independent scientific capabilities and innovative consciousness is a critical component in the education and training of high-level medical professionals.Our investigation revealed that within the imperfections of the cultivating model,some faculty and students at medical schools have an insufficient understanding of scientific research and innovation and lack motivation for engaging in such activities,which hinder the progression of scientific research activities.Consequently,we initiated a teaching practice and exploratory study on the"tutorial system"aimed at fostering medical students'scientific research and innovation abilities.Based on the principle of"research informing teaching,teaching and research advan-cing together,"this study implements a"tutorial system"coordinated by tutors,supplemented by graduate and undergraduate student mentors,to cultivate innovative thinking,stimulate interest in scientific re-search,and enhance practical and research skills among medical students.Through collaborative efforts within"scientific research innovation teams,"various educational methods—including preliminary re-search,in-class and extracurricular activities,intra-group and inter-group interactions,and theoretical and practical applications—are employed to improve and strengthen the cultivation of medical students'scientif-ic research and innovation abilities.This study aims to provide valuable references for optimizing medical education management systems and enhancing the quality of medical student training.

Objective To investigate the biological function of the proprotein convertase subtilisin/kexin type 9(PCSK9)in prostate cancer(PCa)and its effect on ferroptosis sensitivity Methods Bioinformatics was used to analyze the relationship between the expression of PCSK9 and the prognosis of prostate cancer.The expression of PCSK9 in PCa cell lines were detected using RT-qPCR.PCa cells with PCSK9 knockdown were constructed using siRNA,and the The effect of PCSK9 on cell proliferation,migration,and invasion were detected using CCK-8 assays and Transwell assays.The Cancer Therapeutics Response Portal(CTRP)was employed to investigate the correlation between PCSK9 and ferroptosis drug sensitivity,and PCa cells with PCSK9 knockdown were treated with the ferroptosis inducer(RSL3)to detect the sensitivity to ferroptosis.Results Bioinformatics showed low expression of PCSK9 had longer disease specific survival(P<0.05).The results of the in vitro experiments showed that PCSK9 knockdown significantly inhibited the proliferation,migration,and invasion of PCa cells(P<0.001).Furthermore,CTRP analysis showed that cellular sensitivity to ferroptosis inducers correlated with the expression level of PCSK9.PCSK9 knockdown cells exhibited higher sensitivity to the ferroptosis inducer RSL3.Conclusion Knockdown of PCSK9 inhibits the proliferation,migration,and invasion of PCa cells,and increases the sensitivity of cells to ferroptosis inducers.PCSK9 may provide new insights for the treatment of PCa.

In recent years,the incidence and mortality of heatstroke have been increasing annually alongside global warming,with a marked rise in cases exhibiting atypical symptoms.To address the increasingly complex challenges in heatstroke prevention and treatment,Heatstroke Prevention and Treatment Research Center of Chinese PLA,Expert Group of Heatstroke Prevention and Treatment of Chinese PLA,and Chinese PLA Professional Committee of Critical Care Medicine have jointly developed this guideline(2025 edition).Utilizing the Grading of Recommendations Assessment,Development and Evaluation(GRADE)system,Appraisal of Guidelines for Research and Evaluation(AGREE)criteria,and Reporting Items for Practice Guidelines in Healthcare(RIGHT)standards,and based on the 2015 draft"Expert Consensus on the Standardized Diagnosis and Treatment of Heatstroke"and the 2019"Chinese Expert Consensus on the Diagnosis and Treatment of Heatstroke",this guideline has been crafted.This guideline provides 25 evidence-based recommendations to guide the prevention,treatment and research of heatstroke,which thoroughly covers 8 critical domains:clinical classification,pathophysiological mechanisms,clinical manifestations,diagnostic criteria,differential diagnosis,treatment protocols,rehabilitation and return to work,and prevention.