ObjectiveTo systematically evaluate the application of narrative education in undergraduate nursing teaching， to understand the current application status of narrative education， and to provide a theoretical basis for the subsequent establishment of a sound narrative education system. MethodsA systematic search was conducted for studies published in Chinese and English databases on applying narrative education to undergraduate nursing teaching， with the search period ranging from database inception to February 23， 2025. Literature was screened， and relevant information was extracted. A rigorous quality evaluation was conducted on the included studies， and a descriptive analysis was performed on their content. ResultsA total of 20 papers were included， involving 3，180 research subjects， all of whom were undergraduate nursing students. The results of descriptive analysis showed that the teaching model of narrative education primarily encompassed reading narrative works， watching films and videos， performing narrative scenarios， and writing reflective journals. The course setting and content covered pre-teaching preparation and in-teaching implementation. The evaluation of teaching effectiveness included the evaluation of teachers’ teaching methods （student evaluation/self-evaluation） and the evaluation of students’ learning effectiveness （course grade evaluation/humanistic care scale/empathy scale assessment， and others）. ConclusionNarrative education combines abstract concepts with concrete clinical situations， which not only enriches students’ learning experiences but also enhances their humanistic literacy. Meanwhile， it provides teachers with opportunities to develop their narrative teaching skills， which requires them to possess profound professional knowledge and employ narrative techniques to guide students in reflection and critical thinking， thereby improving teaching quality and learning outcomes. Future efforts should consistently deepen the connotation research of narrative education and build a systematic nursing education system.

Objective: To investigate the current status of latent tuberculosis infection (LTBI) among freshmen in junior and senior high schools in Lanzhou, so as to provide scientific basis for improving the tuberculosis prevention and control strategy in schools. Methods: The screening results of 74 516 freshmen in senior and boarding junior high schools in Lanzhou during 2023 and 2024 were collected. The Chi square test and multivariate Logistic regression model were applied to analyze LTBI level, strongly positive risk for tuberculin skin test (TST) and related factors of the freshmen. Results: During 2023 and 2024, the screening rate of tuberculosis among freshmen in senior and boarding junior high schools in Lanzhou was 93.45%, of which the positive rate for TST was 5.71%, the infection rate for LTBI was 3.80%, and the strongly positive rate for TST was 1.24%. There were statistically significant differences in the screening rate of tuberculosis among freshmen in different years, grades, regions, school types and districts ( χ 2=5.34, 2 463.88, 3 516.13, 132.34, 4 436.56, all P <0.05). Multivariate Logistic regression analysis showed that senior high schools ( OR =1.62, 2.18) and urban areas ( OR =2.08, 3.07 ) were all related factors for LTBI and strong positivity for TST among freshmen; schools located in Xigu District, Honggu District, Yongdeng County, Yuzhong County, and Lanzhou New Area ( OR =3.57, 5.67, 9.12, 3.70, 3.64) were related factors of strong positivity for TST among freshmen (all P <0.05). Conclusions The LTBI level among freshmen in senior and boarding junior high schools in Lanzhou is relatively low. Grades and regions are related factors for LTBI and strong positivity for TST.

OBJECTIVE To preliminarily investigate the antiasthmatic effect and mechanism of Ephedrae Herba-Armeniacae Semen Amarum herb pair on the respiratory center. METHODS Male SD rats were randomly divided into blank group， model group， dexamethasone group （positive control）， and Ephedrae Herba-Armeniacae Semen Amarum 2∶1， 1∶1 and 1∶2 groups. Rats in each group were administered different ratios of the herb pair decoction [all at 18 g （crude drug）/kg]， dexamethasone suspension （0.5 mg/kg）， or normal saline intragastrically twice daily for seven consecutive days. Forty minutes after the last administration， medicated cerebrospinal fluid was collected to determine the content of effective components entering the brain. One and a half hours after the last administration， the nucleus tractus solitarius （NTS） was located using a stereotaxic apparatus. Histamine phosphate （1 μL） was injected into the NTS region at a constant rate of 1 μL/min using a 10 μL microsyringe to induce excitation of the respiratory center in rats； the blank group was injected with normal saline. The contents of neurotransmitters [nerve growth factor （NGF）， substance P （SP）， norepinephrine （NA）， 5-hydroxytryptamine （5-HT） and acetylcholine （Ach）] in the medulla oblongata brain tissue were detected. The mRNA expressions of neurokinin-1 receptor （NK-1R）， p38 mitogen-activated protein kinase （MAPK）， and c-fos in the medulla oblongata， as well as the protein expressions of NK-1R， p38 MAPK， and c-fos in the NTS region， were determined. RESULTS The main active components of Ephedrae Herba-Armeniacae Semen Amarum herb pair entering the brain were ephedrine， pseudoephedrine， and methylephedrine. Compared with blank group， the contents of NGF， SP， NA， 5-HT and Ach， and the relative expression levels of NK-1R， p38 MAPK， and c-fos mRNA and protein were significantly increased in the model group （ P ＜0.01）. Compared with model group， Ephedrae Herba-Armeniacae Semen Amarum herb pair groups with different ratios significantly reduced the neurotransmitter contents and the relative expression levels of NK-1R， p38 MAPK， and c-fos mRNA and protein （ P ＜0.01）， with the 2∶1 Ephedrae Herba-Armeniacae Semen Amarum herb pair and 1∶1 mass ratios showing relatively better effects. CONCLUSIONS Ephedrae Herba alkaloids are the main active components in affecting the function of the respiratory center. The herb pair groups with a larger proportion of Ephedrae Herba exhibit stronger effects. Ephedrae Herba-Armeniacae Semen Amarum herb pair can reduce the excitability of the respiratory center by down-regulating the expression of the NK-1R/MAPK/c-fos pathway in the NTS and decreasing the abnormal release of neurotransmitters such as NGF and SP.

ObjectiveTo observe the clinical efficacy and safety of Shenshuai Guanchang prescription in improving the intestinal barrier function，reducing non-indole uremic toxins，ameliorating micro-inflammatory state，and delaying renal function progression in non-dialysis patients with chronic kidney disease （CKD） stage 4-5. MethodsA total of 80 patients with CKD stage 4-5 who did not receive dialysis replacement therapy and were diagnosed with the syndrome of spleen and kidney deficiency，blood stasis and dampness turbidity were randomly assigned into a control group and a treatment group，with 40 patients in each group. The control group received conventional basic treatment and Western medicine symptomatic treatment，while the treatment group received combined intervention with Shenshuai Guanchang prescription through retention enema in addition to the treatment of the control group. Both groups had a treatment course of 4 weeks. The two groups were compared regarding the changes in urine toxin indicators ［p-cresyl sulfate （PCS） and trimethylamine oxide （TMAO）］，intestinal barrier indicators ［D-lactic acid （D-LA），lipopolysaccharide （LPS），and intestinal fatty acid-binding protein （I-FABP）］，renal function indicators ［serum creatinine （SCr），blood urea nitrogen （BUN），and estimated glomerular filtration rate （eGFR）］，and micro-inflammatory state indicators ［interleukin-6 （IL-6），tumor necrosis factor-α （TNF-α），and neutrophil-to-lymphocyte ratio （NLR）］ before and after treatment. The therapeutic effects were evaluated from three aspects：The efficacy regarding traditional Chinese medicine （TCM） symptom scores，the efficacy regarding laboratory indicators，and comprehensive efficacy. The safety of the clinical research drugs used by both groups of patients was also observed. ResultsA total of 37 cases in the treatment group and 38 cases in the control group completed the observation. After treatment，the treatment group showed declined levels of PCS，TMAO，D-LA，SCr，TNF-α，and NLR，spleen and kidney deficiency symptom score，blood stasis and dampness symptom score，and total symptom score （P<0.05），and increased eGFR （P<0.05）. Moreover，the treatment group had lower levels of PCS，TMAO，D-LA，I-FABP，IL-6，and TNF-α，spleen and kidney deficiency symptom score，blood stasis and dampness symptom score，and total symptom score （P<0.05），higher response rate regarding TCM symptoms （χ²=6.68，P<0.05），and higher comprehensive efficacy （χ²=4.08，P<0.05） than the control group. No significant abnormalities were observed in the safety indicators of the two groups of patients. During the treatment period，adverse reactions were reduced after symptomatic treatment，and no serious adverse reactions occurred. ConclusionShenshuai Guanchang prescription can alleviate the clinical symptoms，improve the intestinal barrier function，reduce non-indole-type uremic toxins，alleviate the micro-inflammatory state，and has good clinical application safety of non-dialysis patients with CKD stage 4-5.

Systemic chronic inflammation associated with advancing age is closely linked to the onset and progression of multiple age-related diseases. This persistent inflammatory state, commonly termed inflammaging, reflects complex interactions between accumulated cellular damage and dysregulated immune responses. Inflammasomes are multiprotein complexes of the innate immune system that respond to cellular stress and damage and amplify inflammatory signaling. Their sustained or recurrent activation may contribute to the establishment and maintenance of inflammaging. This review focuses on the NLRP3 inflammasome and summarizes its activation mechanisms, regulatory pathways, and pathological significance within the aging microenvironment. Particular attention is given to neurodegenerative diseases, osteoarthritis, atherosclerosis, and type 2 diabetes, emphasizing shared activation mechanisms and tissue-specific effects. Although initiating stimuli differ among these conditions, several molecular events can contribute to NLRP3 inflammasome activation. Priming mediated by nuclear factor‑κB (NF‑κB) promotes the expression of NLRP3 and pro-interleukin-1β, whereas lysosomal damage, mitochondrial dysfunction, reactive oxygen species accumulation, mitochondrial DNA release, and potassium efflux can participate in activation pathways. These events are interconnected rather than obligatory sequential steps in every setting. Inflammasome assembly promotes caspase-1 activation, which facilitates interleukin-1β and interleukin-18 maturation and gasdermin D cleavage, potentially leading to pyroptosis. The relative contributions of these processes depend on cell type, tissue context, and disease stage. Within aging tissues, persistent damage signals and impaired cellular homeostasis may favor repeated inflammasome activation, establishing a cycle of inflammatory amplification and further tissue injury. However, the pathological consequences vary across organs. In neurodegenerative diseases, inflammasome signaling is associated with neuroinflammation and neuronal vulnerability; in osteoarthritis, it may contribute to joint inflammation and cartilage degeneration. In atherosclerosis, it is implicated in vascular inflammation and plaque progression, whereas in type 2 diabetes, it is linked to metabolic inflammation and impaired glucose homeostasis. These distinctions underscore the importance of interpreting shared molecular mechanisms within specific tissue environments. The review further discusses the therapeutic potential of targeting inflammasomes to mitigate inflammaging and associated disease processes. Strategies include inhibiting NLRP3 activation, modulating upstream stress and priming pathways, and limiting downstream inflammatory signaling or pyroptotic cell death. By interrupting shared mechanisms of inflammatory amplification, these approaches may offer opportunities for coordinated intervention across multiple age-related disorders. Nevertheless, mechanistic overlap does not imply uniform therapeutic responses, and benefits observed in experimental models should not be equated with established clinical efficacy or evidence of delayed human aging.Successful clinical translation will require careful consideration of disease stage, tissue specificity, treatment timing, and the consequences of prolonged interference with innate immune defenses. Long-term safety is particularly important for older populations and preventive applications. The limited availability of validated biomarkers of inflammasome activity also complicates patient stratification, assessment of target engagement, and monitoring of therapeutic responses. Future research should clarify causal relationships, identify contexts in which inflammasome inhibition is most beneficial, and establish reliable translational endpoints. Overall, inflammasomes represent an important link between aging-associated damage and chronic inflammatory amplification, supporting their investigation as shared targets for early intervention in multiple age-related diseases, while highlighting the need for disease-specific evaluation and rigorous assessment of benefits and risks.

ObjectiveTo investigate the inhibitory effects and mechanisms of Yupingfeng San （YPFS） on high-mobility group box protein 1 （HMGB1）-induced angiogenesis in liver cancer. MethodsAn orthotopic liver cancer model was established in 30 C57BL/6 mice. The mice were randomly divided into a model group， YPFS low-， medium-， and high-dose groups （20， 30， 40 g·kg^-1， respectively）， a positive control group （sorafenib， 10 mg·kg^-1）， and a normal control group. After 14 days of medication， tumor and adjacent tissues were harvested. Tumor inhibition rates were calculated based on tumor weight. Microvascular density was determined via immunohistochemistry. HMGB1 and vascular endothelial growth factor （VEGF） expression levels were determined using immunofluorescence. An HMGB1-induced human umbilical vein endothelial cell （HUVEC） proliferation model was established， and cell proliferation was evaluated by a methylthiazolyldiphenyl-tetrazolium bromide （MTT） assay. HUVECs were randomly divided into a blank group， a model group （HMGB1 800 μg·L^-1）， along with YPFS low-， medium-， and high-dose groups （HMGB1 800 μg·L^-1 + YPFS 10， 30， 50 g·L^-1， respectively）. HUVEC migration ability was evaluated via a scratch assay and a Trans well chamber assay. Tube formation ability was detected by a tube formation assay. Microvascular sprouting ability was evaluated by an aortic ring assay. Furthermore， RAGE/MEK1/2/ERK1/2 pathway-related protein expression in HUVECs was measured using Western blot （WB）. ResultsCompared with the model group， all three doses of YPFS significantly reduced tumor weight in mice with orthotopic liver cancer （P<0.01）， with inhibition rates of 31.49% ± 8.27%， 49.60% ± 3.77%， and 56.81% ± 9.70%， respectively. Also， YPFS significantly decreased microvascular density in tumor and adjacent tissues （P<0.05）， as well as VEGF and HMGB1 expression levels （P<0.01）. Compared with the blank group， HMGB1 promoted HUVEC proliferation， migration， tube formation， and microvascular sprouting in aortic rings （P<0.05）. After YPFS administration， the HMGB1-induced proliferation rate， migration rate， number of tube formations， and microvascular sprouting in aortic rings were significantly reduced compared with the model group （P<0.01）. Additionally， YPFS downregulated receptor for advanced glycation end products （RAGE）， mitogen-activated protein kinase kinase 1/2 （MEK1/2）， phosphorylated MEK1/2 （p-MEK1/2）， extracellular signal-regulated kinase 1/2 （ERK1/2）， and phosphorylated ERK1/2 （p-ERK1/2） protein expression in HMGB1-induced HUVECs （P<0.01）. ConclusionYPFS exerts anti-angiogenic effects against HMGB1 induction by suppressing the RAGE/MEK/ERK signaling pathway， thereby inhibiting liver cancer tumor growth.

The pathogenesis of neurodegenerative diseases (NDDs) is fundamentally linked to complex and profound alterations in metabolic networks within the brain, which exhibit marked spatial heterogeneity. While conventional bulk metabolomics is powerful for detecting global metabolic shifts, it inherently lacks spatial resolution. This methodological limitation hampers the ability to interrogate critical metabolic dysregulation within discrete anatomical brain regions and specific cellular microenvironments, thereby constraining a deeper understanding of the core pathological mechanisms that initiate and drive NDDs. To address this critical gap, spatial metabolomics, with mass spectrometry imaging (MSI) at its core, has emerged as a transformative approach. It uniquely overcomes the limitations of bulk methods by enabling high-resolution, simultaneous detection and precise localization of hundreds to thousands of endogenous molecules—including primary metabolites, complex lipids, neurotransmitters, neuropeptides, and essential metal ions—directly in situ from tissue sections. This powerful capability offers an unprecedented spatial perspective for investigating the intricate and heterogeneous chemical landscape of NDD pathology, opening new avenues for discovery. Accordingly, this review provides a comprehensive overview of the field, beginning with a discussion of the technical features, optimal application scenarios, and current limitations of major MSI platforms. These include the widely adopted matrix-assisted laser desorption/ionization (MALDI)-MSI, the ultra-high-resolution technique of secondary ion mass spectrometry (SIMS)-MSI, and the ambient ionization method of desorption electrospray ionization (DESI)-MSI, along with other emerging technologies. We then highlight the pivotal applications of spatial metabolomics in NDD research, particularly its role in elucidating the profound chemical heterogeneity within distinct pathological microenvironments. These applications include mapping unique molecular signatures around amyloid β‑protein (Aβ) plaques, uncovering the metabolic consequences of neurofibrillary tangles composed of hyperphosphorylated tau protein, and characterizing the lipid and metabolite composition of Lewy bodies. Moreover, we examine how spatial metabolomics contributes to constructing detailed metabolic vulnerability maps across the brain, shedding light on the biochemical factors that render certain neuronal populations and anatomical regions selectively susceptible to degeneration while others remain resilient. Looking beyond current applications, we explore the immense potential of integrating spatial metabolomics with other advanced research methodologies. This includes its combination with three-dimensional brain organoid models to recapitulate disease-relevant metabolic processes, its linkage with multi-organ axis studies to investigate how systemic metabolic health influences neurodegeneration, and its convergence with single-cell and subcellular analyses to achieve unprecedented molecular resolution. In conclusion, this review not only summarizes the current state and critical role of spatial metabolomics in NDD research but also offers a forward-looking perspective on its transformative potential. We envision its continued impact in advancing our fundamental understanding of NDDs and accelerating translation into clinical practice—from the discovery of novel biomarkers for early diagnosis to the development of high-throughput drug screening platforms and the realization of precision medicine for individuals affected by these devastating disorders.

Objective To investigate the differences of perineuronal net(PNN)and parvalbumin(PV)-positive neuron distribution across specific brain regions between young and aged mice.Methods Brains from young(45 days)and aged(350 days)mice(n=4 per group)were fixed with 4％paraformaldehyde,sectioned(50 μm)using a vibratome,and stained with Wisteria floribunda agglutinin(WFA)and PV immunofluorescence.Quantitative analyses of PNN-positive and PV-positive neurons,along with PNN encapsulation of PV-positive neurons,were performed in the anterior cingulate cortex(ACC),somatosensory cortex barrel field layer 4(S1BF L4),striatum(STR),and hippocampal CA2 region.Results Aged mice exhibited no significant changes in PNN-positive or PV-positive neuron counts in ACC,S1BF L4,or STR compared to young mice,but showed significantly increased PNN encapsulation of PV-positive neurons.In hippocampal CA2,PNN-positive neurons increased significantly without PV-positive neuron alterations.Conclusion The differences in PNN-PV neuron interactions and PNN density exist in specific brain regions of young and aged mice.

Objective To develop a method of combining electroencephalogram(EEG)/electromyography(EMG)with multi-regional fiber photometry recording to simultaneously capture the changes of neuronal activity in the whole brain and specific brain regions during epileptic seizures.Methods The mouse head was divided into left and right regions based on the middle suture of the skull.EEG electrodes(EEG/EMG)were implanted in one side,while optical fibers were implanted in the striatum,hippocampus,entorhinal cortex,and thalamus on the contralateral side to simultaneously monitor EEG,EMG,and calcium signal dynamics.Results By combining EEG/EMG with multi-regional fiber photometry recording,differences in neuronal activity across brain regions,alongside EEG and EMG,were observed during different behavioral states.In a kainic acid(KA)-induced epilepsy model,abnormal synchronous neuronal discharges in the mouse brain were accompanied by calcium signal changes in the striatum,hippocampus,entorhinal cortex,and thalamus,with the earliest changes occurring in the hippocampus.Conclusion The combined use of EEG/EMG and multi-brain-region fiber photometry is successfully implemented in mice.This method synchronously recordes abnormal calcium signal changes across multiple brain regions,along with EEG and EMG,in the KA-induced epilepsy model.

Objective To investigate the impact of dexmedetomidine on epidural fibrosis after spinal surgery in rats through the transforming growth factor-β1(TGF-β1)signaling pathway.Meth-ods A total of 40 rats were selected,with 10 rats assigned to control group.The remaining 30 rats underwent spinal surgery modeling and were randomly divided into model group,dexmedetomidine group,and dexmedetomidine+TGF-β1 agonist group,with 10 rats in each.Rats with unsuccessful modeling were excluded,resulting in 9 rats in each group for subsequent analysis.Pathological char-acteristics of epidural scar tissue,fibroblast count,PCNA-positive cell expression rate,levels of in-flammatory markers[interleukin(IL)-6,IL-1β,IL-8],stress response indicators[malondialdehyde(MDA),superoxide dismutase(SOD)],and expression levels of mRNAs and proteins related to the TGF-β1 signaling pathway were observed and compared among the groups.Results Compared with the control group,the other three groups showed increased fibroblast count,elevated PCNA-positive cell expression rate,higher levels of IL-6,IL-1β,IL-8,and MDA,lower SOD levels,and increased expression levels of TGF-β1 mRNA,Smad3 mRNA,and TGF-β1 and Smad3 proteins,with statistically significant differences(P＜0.05).Compared with the model group,both the dexmedetomidine group and the dexmedetomidine+TGF-β1 agonist group exhibited decreased fibroblast count,re-duced PCNA-positive cell expression rate,lower levels of IL-6,IL-1 β,IL-8 and MDA,higher SOD levels,and decreased expression levels of TGF-β1 mRNA,Smad3 mRNA,and TGF-β1 and Smad3 proteins,with statistically significant differences(P＜0.05).Compared with the dexmedetomidine group,the dexmedetomidine+TGF-β1 agonist group showed increased fibroblast count,elevated PCNA-positive cell expression rate,higher levels of IL-6,IL-1 β,IL-8 and MDA,lower SOD lev-els,and increased expression levels of TGF-β1 mRNA,Smad3 mRNA,and TGF-β1 and Smad3 proteins,with statistically significant differences(P＜0.05).Conclusion Dexmedetomidine can significantly alleviate the inflammatory response and stress response after spinal surgery in rats and reduce postoperative epidural fibrosis by inhibiting the TGF-β1 signaling pathway.