Objective To investigate the radon activity concentrations in subways of Nanning City and assess the average annual effective doses for subway staff and passengers due to radon exposure. Methods Sixty-three stations across the subway lines 2, 3, and 5 were selected as study sites. Radon activity concentrations were measured using the scintillation counting method with scintillation vials. Results The radon activity concentrations in subway lines 2, 3, and 5 were 7.9-24.4, 12.0-26.2, and 12.6-18.2 Bq/m³, respectively. The average radon activity concentrations for these three lines were (17.4 ± 4.6), (19.1 ± 4.1), and (14.6 ± 1.7) Bq/m³, respectively. Statistical analysis using SPSS 26.0 software revealed a significant difference in radon activity concentrations among these stations (P<0.01). Considering the data in previous research, the average radon activity concentration across all stations in the subway lines of Nanning City was determined to be 17.4 Bq/m³. The estimated average annual effective dose due to radon exposure was 0.131 mSv for subway staff and 0.033 mSv for passengers. Conclusion The radon activity concentrations in the subway lines of Nanning City were significantly lower than the national standard limit (400 Bq/m³). The annual effective doses from radon exposure for both subway staff and passengers were below the limits specified in the Basic Standards for Protection Against Ionizing Radiation and for the Safety of Radiation Sources (GB18871—2002). The health impact of radon and its progeny on subway staff and passengers in the subway lines of Nanning City was extremely low and can be considered negligible.

ObjectiveTo investigate the suppressive effect of 23-hydroxybetulinic acid （23-HBA）， a key constituent of Pulsatillae Radix， on the pulmonary inflammation-related carcinogenesis induced by the combined exposure of 4-（methylnitrosamino）-1-（3-pyridyl）-1-butanone （NNK） and lipopolysaccharide （LPS） in mice， alongside exploring its influence on immune cells and delving into the underlying mechanisms. MethodsA murine model of pulmonary inflammation-related carcinogenesis induced by NNK combined with LPS was established. Mice were randomly assigned into blank control， model， aspirin （10 mg·kg^-1）， and low-， medium-， and high-dose （3.75， 7.5， 15 mg·kg^-1， respectively） 23-HBA groups. The treatment lasted for 26 weeks， after which the spleen， lung， and peripheral blood samples were collected. Lung and spleen indices were calculated. Histopathological changes in the lung tissue were observed by hematoxylin-eosin staining. Immunohistochemistry was employed to assess the expression levels of thyroid transcription factor-1 （TTF-1）， neuron-specific enolase （NSE）， and proliferating cell nuclear antigen （Ki-67） in the lung tissue. High-throughput protein microarray was employed to measure the levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in the mouse serum. Flow cytometry was employed to evaluate the expression of macrophages， myeloid-derived suppressor cells （MDSCs）， and exhausted T lymphocytes in the lung and spleen tissue. Molecular docking was performed to predict the binding affinity of 23-HBA to Janus kinase 2 （JAK2）， Src homology 2 domain-containing phosphatase 2 （SHP2）， and suppressor of cytokine signaling 3 （SOCS3）. Western blot was performed to assess the protein levels of phosphorylated-signal transducer and activator of transcription 3 （p-STAT3）， p53， and SHP2 in the M1-activated macrophages and A549 lung adenocarcinoma cells treated with 23-HBA. ResultsCompared with the normal group， the lung and spleen indexes of the model group were increased to varying degrees （P<0.05， P<0.01）， the expression of TTF-1， NSE and Ki-67 protein was significantly increased （P<0.05， P<0.01）， and the serum levels of TNF-α， IL-1β and IL-6 were significantly increased （P<0.01）. The number of macrophages in the model group was significantly decreased （P<0.01）， and the number of exhausted T cells and MDSCs was significantly increased （P<0.05， P<0.01）. Compared with the model group， the spleen and thymus index of mice in each dose group of 23-HBA decreased significantly （P<0.05）， and the lung index of mice in the middle dose group of 23-HBA decreased significantly （P<0.05）. The high and middle dose groups of 23-HBA could improve the occurrence of inflammatory infiltration and malignant lesions in the lungs of mice induced by NNK combined with LPS in the model group. The expression of TTF-1 in the middle and high dose groups of 23-HBA was significantly lower than that in the model group （P<0.05， P<0.01）. The expression of NSE and Ki-67 protein in each dose group of 23-HBA was significantly lower than that in the model group （P<0.05， P<0.01）. The contents of IL-1β in the low and high dose groups of 23-HBA were significantly decreased （P<0.05）， and the contents of IL-6 and TNF-α in each dose of 23-HBA were significantly decreased （P<0.05， P<0.01）. The number of macrophages in the lung of the middle dose group of 23-HBA was significantly increased （P<0.05）， and the number of exhausted T cells and MDSCs expressing PD-1 in the lung was significantly decreased （P<0.05， P<0.01）. In addition， 23-HBA had strong molecular docking ability to SHP2， SOCS3 and JAK2 （≥7 kcal·mol^-1）， and significantly down-regulated the protein levels of p-STAT3， SHP2 and p53 in M1 macrophages and A549 lung adenocarcinoma （P<0.01）. Conclusion23-HBA holds promise as a potential therapeutic agent for mitigating pulmonary inflammation and inhibiting malignant transformation induced by the combination of LPS and NNK. It may exert effects by regulating immune cell responses， improving the tumor immune microenvironment， and regulating key signaling pathways.

Objective:To explore applications of adjusting timing of nebulization and analgesic usage in patients after lung cancer surgery, to provide reference for postoperative rehabilitation of lung cancer.Methods:Adopting a prospective randomized controlled study design, a total of 84 patients with lung cancer who underwent surgery in affiliated hospital of Jining Medical University from September 2020 to June 2023 were enrolled by a convenience sampling method, they were randomly divided into experimental group and control group according to random number table method. Two groups was given routine perioperative care, on this basis, the control group received lip and abdomen contraction breathing training according to the conventional process, and the experimental group adjusted timing of nebulization and analgesic usage and received respiratory function training when nebulization and analgesics were at the peak of blood drug concentration. Pain level and exercise self-efficacy of two groups were compared.Results:There were 27 males and 15 females in the control group, aged (54.52 ± 14.06) years; and 24 males and 18 females in the experimental group, aged (53.33 ± 12.02) years. At one day, two days and three days after operation, the scores of Numerical Rating Scale (NRS) were (5.07 ± 0.84), (3.40 ± 0.49), (2.93 ± 0.87) in the experimental group, lower than (5.86 ± 1.05), (4.09 ± 0.88), (3.33 ± 0.65) in the control group, the differences were statistically significant ( t=3.79, 4.44.2.42, all P<0.05), and for both groups, the differences in the time effect, between-group effect, and the interaction effect were all statistically significant ( F=582.92, 44.65, 3.82, all P<0.05). Three days after operation, the dimensions of efficacy expectation, outcome expectation and total self-efficacy scores were (28.62 ± 6.75), (33.71 ± 7.04) and (62.33 ± 9.07) in the experimental group, and (25.52 ± 6.66), (30.43 ± 6.80) and (55.95 ± 9.34) in the control group, the differences were statically significant ( t=2.12, 2.18, 3.18, all P<0.05). Conclusions:Adjusting timing of nebulization and analgesic usage and giving respiratory function training for lung cancer surgery when nebulization and analgesics at the peak of blood drug concentration can effectively alleviate the pain caused by respiratory exercise and improve training self-efficacy of patients after lung cancer surgery.

Lung cancer is a serious pulmonary tumor,with exacerbation of chronic lung inflammation being a precursor to the development of lung cancer.Relevant animal models are widely used in experimental research,to gain a deeper understanding of the pathogenesis of lung cancer and to develop preventive treatment strategies.Induced lung cancer animal models are of particular importance for understanding the transition from chronic lung inflammation to lung cancer.Early intervention is crucial for the prevention and treatment of lung cancer.Here we review the recent literature regarding the inducing factors for lung cancer,including carcinogens(e.g.nicotine-derived nitrosamine ketone,benzopyrene,diethylnirtosamine atmospheric fine particulate matter(PM2.5),coal smoke,heavy metal ions,radiation,and biological infections).We also summarize animal models of lung inflammation and cancer transformation induced by these factors,discuss the mechanisms by which relevant carcinogens induce lung cancer,analyze the advantages and limitations of the animal models,and consider future development directions.This review aims is to provide a valuable reference for the future establishment of relevant models.

Lung cancer is a serious pulmonary tumor,with exacerbation of chronic lung inflammation being a precursor to the development of lung cancer.Relevant animal models are widely used in experimental research,to gain a deeper understanding of the pathogenesis of lung cancer and to develop preventive treatment strategies.Induced lung cancer animal models are of particular importance for understanding the transition from chronic lung inflammation to lung cancer.Early intervention is crucial for the prevention and treatment of lung cancer.Here we review the recent literature regarding the inducing factors for lung cancer,including carcinogens(e.g.nicotine-derived nitrosamine ketone,benzopyrene,diethylnirtosamine atmospheric fine particulate matter(PM2.5),coal smoke,heavy metal ions,radiation,and biological infections).We also summarize animal models of lung inflammation and cancer transformation induced by these factors,discuss the mechanisms by which relevant carcinogens induce lung cancer,analyze the advantages and limitations of the animal models,and consider future development directions.This review aims is to provide a valuable reference for the future establishment of relevant models.

Objective:To explore applications of adjusting timing of nebulization and analgesic usage in patients after lung cancer surgery, to provide reference for postoperative rehabilitation of lung cancer.Methods:Adopting a prospective randomized controlled study design, a total of 84 patients with lung cancer who underwent surgery in affiliated hospital of Jining Medical University from September 2020 to June 2023 were enrolled by a convenience sampling method, they were randomly divided into experimental group and control group according to random number table method. Two groups was given routine perioperative care, on this basis, the control group received lip and abdomen contraction breathing training according to the conventional process, and the experimental group adjusted timing of nebulization and analgesic usage and received respiratory function training when nebulization and analgesics were at the peak of blood drug concentration. Pain level and exercise self-efficacy of two groups were compared.Results:There were 27 males and 15 females in the control group, aged (54.52 ± 14.06) years; and 24 males and 18 females in the experimental group, aged (53.33 ± 12.02) years. At one day, two days and three days after operation, the scores of Numerical Rating Scale (NRS) were (5.07 ± 0.84), (3.40 ± 0.49), (2.93 ± 0.87) in the experimental group, lower than (5.86 ± 1.05), (4.09 ± 0.88), (3.33 ± 0.65) in the control group, the differences were statistically significant ( t=3.79, 4.44.2.42, all P<0.05), and for both groups, the differences in the time effect, between-group effect, and the interaction effect were all statistically significant ( F=582.92, 44.65, 3.82, all P<0.05). Three days after operation, the dimensions of efficacy expectation, outcome expectation and total self-efficacy scores were (28.62 ± 6.75), (33.71 ± 7.04) and (62.33 ± 9.07) in the experimental group, and (25.52 ± 6.66), (30.43 ± 6.80) and (55.95 ± 9.34) in the control group, the differences were statically significant ( t=2.12, 2.18, 3.18, all P<0.05). Conclusions:Adjusting timing of nebulization and analgesic usage and giving respiratory function training for lung cancer surgery when nebulization and analgesics at the peak of blood drug concentration can effectively alleviate the pain caused by respiratory exercise and improve training self-efficacy of patients after lung cancer surgery.

BACKGROUND:Traumatic spinal cord injury primarily relies on scale assessment and imaging examinations in clinical practice.However,there are limitations in predicting the prognosis of the injury.Therefore,the use of metabolomics technology for biomarker screening is significant for estimating the extent of damage,injury and recovery,as well as developing new therapies. OBJECTIVE:To characterize the metabolic features of patients with traumatic spinal cord injury using metabolomics technology and explore potential biomarkers and disrupted metabolic pathways. METHODS:Serum and urine samples were collected from 20 patients with traumatic spinal cord injury(observation group)and 10 healthy subjects(control group).Metabolites were analyzed and multivariate statistical analysis was then performed for data processing to screen differential metabolites.Metabolic pathway enrichment was performed using MetaboAnalyst software.Logistic regression was applied to construct a biomarker combination model,and its relationship with the American Spinal Injury Association grading was analyzed. RESULTS AND CONCLUSION:Significant differences in 160 and 73 metabolites were detected in the serum and urine samples of the two groups,respectively.Pathway enrichment analysis showed evident disturbances in lipid metabolism after traumatic spinal cord injury,including sphingolipid,arachidonic acid,α-linolenic acid,and arachidonic acid metabolism,as well as glycerophospholipid and inositol phosphate biosynthesis.The combination of two identified biomarkers,telmisartan and quercetin glycoside,showed a correlation with the American Spinal Injury Association grading in both serum and urine levels.Thus,metabolomics technology provides assistance in further understanding the pathological mechanisms of traumatic spinal cord injury and screening therapeutic targets.The identified metabolic biomarker combination may serve as a reference for assessing the severity of traumatic spinal cord injury.

Objective To study the distribution and significance of CD1a and CD83 positive dendritic cells(DCs)in lung tissue of chronic obstructive pulmonary disease(COPD)mice.Methods Twenty C57BL/6 mice were randomly divided into the air control group and the smoked COPD group(n=10 for each group).COPD mouse model was established using cigarette smoking method.Mice were executed within 24 h after the last cigarette smoking,and right lower lung was collected.Body mass changes and lung histopathological changes of mice were observed in two groups.Mean linear intercept(MLI)was measured,and expression levels of CD1a+and CD83+DCs in lung tissue were detected by immunohistochemistry.Results The body mass of mice at 7,14,21 and 28 d after modeling was lower in the smoked COPD group than that in the air control group(P＜0.05).HE staining showed that the normal alveolar structure of lung tissue of mice in the smoked group was disrupted,with multiple alveoli fused with each other to form a larger alveolar lumen,a large number of inflammatory cells infiltrated in alveolar intervals,and walls of the alveoli were thickened.COPD modeling was successful.Compared with the air control group,MLI values(μm)increased in the smoked COPD group(28.30±3.47 vs.50.40±3.60),and the number of CD1a+DCs(per field of view)in lung tissue increased(9.58±2.18 vs.17.08±3.67),while the number of CD83+DCs(per field of view)decreased(19.78±4.95 vs.8.02±3.30)(all P＜0.05).Conclusion The number of CD1a+DCs in lung tissue is increased and the number of CD83+DCs in lung tissue is decreased in the smoked COPD group of mice,and cigarette smoking may have impaired DC maturation.

ObjectiveTo screen the differential markers by analyzing volatile components in Dalbergia odorifera and its counterfeits， in order to provide reference for authentication of D. odorifera. MethodThe volatile components in D. odorifera and its counterfeits were detected by headspace gas chromatography-mass spectrometry（HS-GC-MS）， and the GC conditions were heated by procedure（the initial temperature of the column was 50 ℃， the retention time was 1 min， and then the temperature was raised to 300 ℃ at 10 ℃ for 10 min）， the carrier gas was helium， and the flow rate was 1.0 mL·min^-1， the split ratio was 10∶1， and the injection volume was 1 mL. The MS conditions used electron bombardment ionization（EI） with the scanning range of m/z 35-550. The compound species were identified by database matching， the relative content of each component was calculated by the peak area normalization method， and principal component analysis（PCA）， orthogonal partial least squares-discrimination analysis（OPLS-DA） and cluster analysis were performed on the detection results by SIMCA 14.1 software， and the differential components of D. odorifera and its counterfeits were screened out according to the variable importance in the projection（VIP） value>2 and P<0.05. ResultA total of 26， 17， 8， 22， 24 and 7 volatile components were identified from D. odorifera， D. bariensis， D. latifolia， D. benthamii， D. pinnata and D. cochinchinensis， respectively. Among them， there were 11 unique volatile components of D. odorifera， 6 unique volatile components of D. bariensis， 3 unique volatile components of D. latifolia， 6 unique volatile components of D. benthamii， 8 unique volatile components of D. pinnata， 4 unique volatile components of D. cochinchinensis. The PCA results showed that， except for D. latifolia and D. cochinchinensis， which could not be clearly distinguished， D. odorifera and other counterfeits could be distributed in a certain area， respectively. The OPLS-DA results showed that D. odorifera and its five counterfeits were clustered into one group each， indicating significant differences in volatile components between D. odorifera and its counterfeits. Finally， a total of 31 differential markers of volatile components between D. odoriferae and its counterfeits were screened. ConclusionHS-GC-MS combined with SIMCA 14.1 software can systematically elucidate the volatile differential components between D. odorifera and its counterfeits， which is suitable for rapid identification of them.

Objective This study aimed to explore the differences in global and local brain network topological properties between deficient pattern(DP)and excess pattern(EP)of mild vascular cognitive impairment caused by subcortical small vessel disease based on graph theory network.Methods Patients were recruited prospectively and were classified with DP and EP subtype.The global small-world topological attributes and local nodes were calculated for the comparison of DP,EP,and healthy controls(CN)using the GRETNA platform.Results The three groups all had small-world attributes,but only the patients in EP had a significantly lower small world attribute δ in the range of 0.05-0.26 than the control group(P<0.05).The node efficiency and node strength indicators of multiple brain region were able to significantly distinguish the DP group from the EP group.However,there was no positive brain region in the node efficiency of the DP patients(P>0.05),and only a few brain regions showed increased node strength efficiency(P<0.05).Conclusion The results indicate that the syndrome of DP and EP have significantly different neuroimaging phenotypes,providing a basis for further research of biological classification based on Chinese Medicine syndromes.