ObjectiveTo investigate whether Huanglian Jiedutang （HLJD） and its major active constituents （geniposide， baicalin， and berberine） can inhibit the inflammatory response of BV2 cells under lipopolysaccharide （LPS） stimulation via the high-mobility group protein B1 （HMGB1）/Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway， and to explore differences in therapeutic efficacy among the three monomers， their combined formula， and HLJD under equal content ratios. MethodsBV2 microglial cells were used as the primary experimental model. Cell viability was assessed using the cell counting kit-8 （CCK-8） method to examine the effects of different concentrations of dimethyl sulfoxide （DMSO， 0.8%， 0.4%， 0.2%， 0.1%， and 0.05%） on cell viability. IncuCyte was employed to monitor the growth of cells under different concentrations of HLJD （200， 100， 50， 25， 12.5， 6.25 mg·L^-1）. Nitric oxide （NO） assay was used to screen the optimal HLJD concentration. High-performance liquid chromatography （HPLC） determined the content of geniposide， baicalin， and berberine in HLJD， and experimental groups were subsequently established according to the relative proportions of these constituents. CCK-8 assay evaluated cell viability under different treatments. Enzyme-linked immunosorbent assay （ELISA） measured levels of inflammatory factors （TNF-α， IL-1β， IL-6， IL-10） in the supernatant. Flow cytometry assessed the effects of treatments on M1-type polarization of BV2 cells. Western blot determined the expression levels of HMGB1， TLR4， and NF-κB-related proteins. ResultsCompared with the blank group， DMSO at concentrations ≤0.2% did not affect cell viability within 48 h. BV2 cell growth plateaued at 24 h after treatment with 200 mg·L^-1 HLJD. Under stimulation with 2 mg·L^-1 LPS， this concentration of HLJD effectively reduced NO release， and 6 h pre-treatment had a stronger inhibitory effect on NO than direct administration. HPLC results showed that 1 mg of HLJD freeze-dried powder contained approximately 24 μg of geniposide， 15 μg of baicalin， and 30 μg of berberine. Based on these ratios， experimental groups were blank， LPS （2 mg·L^-1）， HLJD （200 mg·L^-1）， monomer combination， geniposide （4.8 mg·L^-1）， baicalin （3 mg·L^-1）， and berberine （6 mg·L^-1）. The monomer combination group consisted of all three active constituents dissolved together. LPS and HLJD or its active constituents did not affect cell viability compared with the blank group. LPS significantly increased TNF-α， IL-1β， IL-6， and IL-10 in the supernatant （P<0.01）. HLJD and its active constituents significantly reduced pro-inflammatory factors TNF-α， IL-1β， and IL-6 （P<0.05， P<0.01） while upregulating anti-inflammatory IL-10 （P<0.01）， with the monomer combination showing the strongest effect （P<0.05， P<0.01）. Compared with the blank group， LPS significantly increased the proportion of CD80⁺CD86⁺ （M1-type） BV2 cells （P<0.01）. HLJD and its constituents partially inhibited M1 polarization （P<0.05， P<0.01）， with the monomer combination exhibiting the most pronounced effect （P<0.05， P<0.01）. Compared with the blank group， LPS upregulated HMGB1， TLR4， and NF-κB-related proteins （P<0.01）， whereas HLJD and its active constituents significantly reduced their expression （P<0.05， P<0.01）， with the monomer combination having the strongest regulatory effect （P<0.05， P<0.01）. ConclusionHLJD and its major active constituents （geniposide， baicalin， berberine） can inhibit LPS-induced inflammatory responses in BV2 cells. The combination of the three active constituents demonstrates the most potent anti-inflammatory effect， significantly attenuating M1-type polarization of BV2 cells via the HMGB1/TLR4/NF-κB signaling pathway.

Objective To explore the feasibility of magnetic compression technique (MCR) in the treatment of severe single mid-ureteral stricture in a rabbit model. Methods After 10 female New Zealand rabbits were selected, the distal end of the right ureter was ligated with silk thread. Two weeks after the operation, when the right ureter was dilated, the mid-ureter was ligated again with silk thread to create a severe single mid-ureteral stricture animal model. Longitudinal incisions were made at the upper and lower ends of the ligation site, and cylindrical NdFeB magnets with central holes (sub-magnets and main magnets) were placed to anastomose and recanalize the mid-ureteral stricture. The magnets were adjusted to the appropriate position to automatically align and attract each other. The longitudinal incision sites of the ureter were sutured with 6-0 Prolene thread, and the abdominal cavity was closed layer by layer. The operation time was recorded. X-ray films were taken every two days to confirm the position of the magnets and record the time of magnet detachment. Three weeks after the operation, the anastomotic specimens were obtained, and the formation of the anastomosis was evaluated with gross observation and histological staining. Results Two weeks after ligation, all experimental rabbits showed obvious dilation of the right ureter. The mid-ureteral ligation and placement of the male and female magnets were successfully completed in all 10 experimental rabbits, with an operation time of (24.00±5.15)minutes. The male and female magnets attracted each other well. X-ray examination showed that the magnets detached and entered the distal ureter (14.0±1.9) days after magnetic compression. The recanalization of the severe single mid-ureteral stricture was successfully achieved. The gross specimens and histological examination of the anastomosis showed that the anastomosis remained patent and the mucosal healing was good. All experimental rabbits survived well after the operation without serious complications. Conclusion MCT provides a new idea and novel method for the treatment of mid-ureteral stricture. This study confirmed the feasibility of this technique in treating severe single mid-ureteral stricture in a rabbit model. The operation is relatively simple and has potential for clinical application.

Objective: To analyze the mortality trend of chronic respiratory diseases in Lianyungang City, Jiangsu Province from 2011 to 2024, and predict the mortality from 2025 to 2029, so as to provide the evidence for developing forward-looking prevention and control strategies and targeted intervention measures. Methods: Chronic respiratory disease death surveillance data in Lianyungang City from 2011 to 2024 were collected through the Jiangsu Chronic Disease Management Information Platform. The crude mortality was calculated and standardized using the data of the Sixth National Population Census in 2010. Average annual percent change (AAPC) was used to analyze the mortality trends of chronic respiratory diseases by gender, region, and age in Lianyungang City from 2011 to 2024. The GM (1,1) grey model was established using the crude mortality of chronic respiratory diseases from 2011 to 2024 to predict the crude mortality of chronic respiratory diseases from 2025 to 2029. Results: From 2011 to 2024, the crude mortality and standardized mortality of chronic respiratory diseases in Lianyungang City were 52.20/105 and 36.57/105, respectively. The crude mortality and standardized mortality were 53.14/105 and 43.79/105 in males, respectively, which were higher than 51.17/105 and 30.14/105 in females (both P<0.05). The crude mortality and standardized mortality were 55.62/105 and 39.85/105 in rural areas, respectively, which were higher than 38.11/105 and 24.15/105 in urban areas (both P<0.05). From 2011 to 2024, the standardized mortality of chronic respiratory diseases showed downward trends in the total population, males, females, urban areas, and rural areas (AAPC=-6.956%, -5.175%, -8.659%, -4.290%, and -7.369%, all P<0.05). The crude mortality of chronic respiratory diseases in the total population showed an upward trend with increasing age (P<0.05), reaching a peak of 1 371.20/105 in the ≥80 years group. The top two causes of chronic respiratory disease deaths were chronic obstructive pulmonary disease and bronchial asthma, with 31 792 cases and 3 254 cases, accounting for 82.40% and 8.43%, respectively. The GM (1,1) grey model prediction results showed that the crude mortality of chronic respiratory diseases in the total population from 2025 to 2029 would be 37.91/105, 36.32/105, 34.80/105, 33.34/105, and 31.95/105, respectively (average relative error=8.76%). Conclusions From 2011 to 2024, the mortality of chronic respiratory diseases in Lianyungang City showed a downward trend. The risk of death from chronic respiratory diseases was higher in males, rural areas, and the elderly. It is predicted that the mortality of chronic respiratory diseases will decrease year by year from 2025 to 2029.

Objective:To investigate the specific expressions of Delta like non-canonical Notch ligand 1 ( DLK1) and Maternally expressed gene 3 ( MEG3) in POU class 1 homeobox 1 (POU1F1) spectrum pituitary tumors and their correlation with prognosis. Methods:A retrospective case-control study method was adopted. A total of 167 patients with POU1F1 lineage pituitary adenomas who were diagnosed and underwent pituitary adenoma resection at Tangshan People′s Hospital from April 2021 to April 2023 were collected as the research subjects. There were 98 males and 69 females with an average age of (63.05±7.51) years, ranging from 52 to 82 years. They were divided into good prognosis group ( n=111) and poor prognosis group ( n=56) according to postoperative follow-up. A multiple linear regression analysis was performed to examine the relationships between the levels of DLK1 mRNA and MEG3 mRNA and the immune function indicators (Complement 3/Complement 4/Immunoglobulin M/Immunoglobulin A). Multivariate Logistic regression analysis was used to investigate the correlation between DLK1 mRNA and MEG3 mRNA levels and poor prognosis of patients. The odds ratio (OR) of multivariate Logistic regression analysis was calculated. RCS model was used to analyze the dose-response relationship between DLK1 mRNA and MEG3 mRNA and poor prognosis of pituitary tumor resection in POU1F1 spectrum patients. The measurement data following a normal distribution were presented as mean±standard deviation ( ± s), and the t-test was used for comparison between groups. The count data were presented as the number of cases and percentages (%), and the chi-square test was used for comparison between groups. Results:Before treatment, the levels of DLK1 mRNA and MEG3 mRNA in the serum of patients in the good prognosis group were 0.142±0.047 and 0.075±0.024 respectively, and after treatment, they were 0.019±0.003 and 0.577±0.067 respectively. Before treatment, the levels of DLK1 mRNA and MEG3 mRNA in the serum of patients in the poor prognosis group were 0.109±0.035 and 0.067±0.016 respectively, and after treatment, they were 0.057±0.011 and 0.298±0.047 respectively. Before and after treatment the level of DLK1 mRNA in the good prognosis group was significantly lower than that in the poor prognosis group, and the level of MEG3 mRNA in the good prognosis group was significantly higher than that in the poor prognosis group ( P< 0.05). Moreover, the serum DLK1 mRNA and MEG3 mRNA of patients after treatment were significantly different from those before treatment ( P<0.05). The levels of adrenocorticotropin (ACTH), growth hormone, prolactin, complement 3, mean visual field defect and weighted visual field index in the good prognosis group were (42.15±4.68) ng/L, (13.47±2.17) ng/L, (8.28±1.76) ng/L, (1.38±0.34) g/L, (5.26±1.15) dB, (89.14±17.23)%. In the poor prognosis group, there were (56.64±6.42) ng/L, (18.06±3.11) ng/L, (11.49±2.93) ng/L, (1.12±0.45) g/L and (7.96±1.52) dB, (73.65±15.28)%, and there was statistical significance in the above indexes between the two groups ( P< 0.05). There was no independent correlation between the expression of DLK1 mRNA and MEG3 mRNA and immune function indexes (Complement 3/Complement 4、IgM、IgA) ( P>0.05). There was an independent positive correlation between high level of DLK1 mRNA and poor prognosis ( OR=0.521, 95% CI: 0.466-0.738), and a stable correlation between low level of MEG3 mRNA and poor prognosis ( OR=0.761, 95% CI: 0.526-0.883). There is a negative nonlinear dose-response relationship between MEG3 and risk of poor prognosis, and a positive nonlinear dose-response relationship between DLK1 and risk-poor prognosis. The area under ROC curve (AUC) of DLK1 mRNA and MEG3 mRNA for predicting poor prognosis were 0.685(0.504-0.797) and 0.710 (0.611-0.806), respectively. Conclusion:There are significant differences between serum DLK1 mRNA and MEG3 mRNA after treatment and before treatment. DLK1 mRNA were positively nonlinear independent correlated with poor prognosis, and MEG3 mRNA was negatively nonlinear independent correlated with poor prognosis.

Objective To explore the risk factors for 28-day mortality of sepsis-associated acute kidney injury(SA-AKI)patients and to develop a nomogram risk prediction model.Methods A retrospective cohort study was conducted,involving 184 patients with SA-AKI admitted to the intensive care unit(ICU)of the 940th Hospital of Joint Logistic Support Force of PLA between January 2017 and December 2022.Patients were categorized into survival(n=135)and non-survival(n=49)groups based on 28-day mortality.Clinical data were collected,and statistically significant risk factors were preliminarily screened.Multivariate stepwise logistic regression analysis was performed to identify independent risk factors for 28-day mortality of SA-AKI patients.A nomogram predictive model was constructed using these factors,and internally validated with the Bootstrap method.The receiver operating characteristic curve(ROC curve)was drawn,and the area under the ROC curve(AUC)was calculated to verify the predictive value and accuracy of the model.Results The 28-day mortality rate among 184 SA-AKI patients was 26.6％(49/184).Multivariate stepwise logistic regression analysis identified multiple organ dysfunction syndrome(MODS)(OR=16.393,95％CI 4.317-62.254,P＜0.001),high acute physiology and chronic health evaluation Ⅱ(APACHE Ⅱ)score(OR=1.097,95％CI 1.036-1.161,P=0.002),low oxygenation index(OR=0.992,95％CI 0.986-0.998,P=0.015),low neutrophil count(OR=0.912,95％CI 0.860-0.968,P=0.002)and low fibrinogen concentration(OR=0.733,95％CI 0.549-0.978,P=0.034)as independent risk factors.The prediction model equation was P=1/1+e-logit(P),logit(P)=-1.626+2.797×MODS+0.092×AP ACHE Ⅱ+(-0.311)×fibrinogen+(-0.092)×neutrophil count+(-0.008)×oxygenation index.Internal validation with 1000 Bootstrap resamples showed high consistency between predicted and actual values.ROC analysis showed an AUC of 0.911(95％CI 0.868-0.955,P＜0.05)for the model,with 93.9％sensitivity and 78.5％specificity at a cut-off of 0.194.The Hosmer-Lemeshow test confirmed good calibration(P=0.62),and decision-making curve analysis demonstrated clinical utility within the high-risk threshold range(0.1-0.9).Conclusions MODS,high APACHE Ⅱ score,low oxygenation index,low neutrophil count,and low fibrinogen concentration are independent risk factors for 28-day mortality in SA-AKI patients.The developed nomogram risk prediction model may provide important guidance for predicting 28-day mortality in SA-AKI patients.

Objective To screen metabolic core genes in colon cancer based on machine learning algorithms and analyze their functional mechanisms.Methods Data were obtained from The Cancer Genome Atlas(TCGA)database and the Gene Expression Omnibus(GEO)database.The TCGA co-hort included 375 tumor samples and 32 adjacent normal tissue samples,while the GSE39582 cohort comprised 419 tumor samples.Univariate Cox regression analysis combined with random forest,sup-port vector machine recursive feature elimination(SVM-RFE),and least absolute shrinkage and selec-tion operator(LASSO)regression algorithms were employed to screen for metabolic core genes.Re-ceiver operating characteristic(ROC)curves were plotted,and the area under the curve(AUC)was used to evaluate the predictive efficacy of the core genes.Real-time fluorescent quantitative polymerase chain reaction(qRT-PCR)and immunohistochemistry(IHC)methods were adopted to detect the ex-pression of the core genes.The core genes were knocked down to explore their roles in colon cancer.Results Three core genes,namely CPT2,SCP2 and NR3C2,were screened based on machine learning algorithms.According to the comparison results of the AUCs of the ROC curves,NR3C2 exhibited the best predictive efficacy.qRT-PCR detection results showed that NR3C2 mRNA was lowly ex-pressed in colon cancer cell lines;IHC detection results revealed that NR3C2 was lowly expressed in colon cancer tissues.Knocking down NR3C2 significantly promoted the proliferation and migration of colon cancer cells.Conclusion NR3C2 is identified as a core metabolic inhibitory gene in colon cancer by cross-applying three machine learning algorithms,which may provide a new strategy for metabolic targeted therapy.

Numerous c-mesenchymal-epithelial transition(c-MET)inhibitors have been reported as potential anticancer agents.However,most fail to enter clinical trials owing to poor efficacy or drug resistance.To date,the scaffold-based chemical space of small-molecule c-MET inhibitors has not been analyzed.In this study,we constructed the largest c-MET dataset,which included 2,278 molecules with different struc-tures,by inhibiting the half maximal inhibitory concentration(IC50)of kinase activity.No significant differences in drug-like properties were observed between active molecules(1,228)and inactive mol-ecules(1,050),including chemical space coverage,physicochemical properties,and absorption,distri-bution,metabolism,excretion,and toxicity(ADMET)profiles.The higher chemical diversity of the active molecules was downscaled using t-distributed stochastic neighbor embedding(t-SNE)high-dimensional data.Further clustering and chemical space networks(CSNs)analyses revealed commonly used scaffolds for c-MET inhibitors,such as M5,M7,and M8.Activity cliffs and structural alerts were used to reveal"dead ends"and"safe bets"for c-MET,as well as dominant structural fragments consisting of pyr-idazinones,triazoles,and pyrazines.Finally,the decision tree model precisely indicated the key structural features required to constitute active c-MET inhibitor molecules,including at least three aromatic het-erocycles,five aromatic nitrogen atoms,and eight nitrogen-oxygen atoms.Overall,our analyses revealed potential structure-activity relationship(SAR)patterns for c-MET inhibitors,which can inform the screening of new compounds and guide future optimization efforts.

Objective:To explore the correlation between metabolic syndrome (MS), serum high-sensitivity C-reactive protein (hs-CRP) levels, their combination and the risk of digestive system malignancies.Methods:A prospective cohort study was conducted in the participants from the Kailuan cohort who took health examination in July 2006. Anthropometric parameters, epidemiological information, and laboratory test results were collected. Incidence and mortality of digestive system malignant tumors were collected through biennial health examinations and questionnaires. The follow-up period ended on December 31, 2021.According to MS status and hs-CRP levels (hs-CRP≤3 or >3 mg/L), the cohort was divided into 4 groups, induding MS -hs-CRP -, MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + group. Chi-squared test, one analysis of variance, and the Kruskal-Wallis H test were used for inter-group comparison among groups. Kaplan-Meier method was used to calculate the cumulative incidence of digestive system malignant tumors, and log-rank test was performed to compare the cumulative incidence among groups. Multivariable Cox proportional hazards regression models were used to evaluate the effects of MS and hs-CRP levels on the overall risk of digestive system malignant tumors, as well as the effects of their combination on the risk of digestive system malignant tumors of different site, and relevant confounding factors were adjusted.A sensitivity analysis was conducted by excluding individuals diagnosed with digestive system malignancies within one year of follow-up, as well as those taking antihypertensive, antidiabetic, or lipid-lowering medications. Results:A total of 92 916 participants were included in this study. Among them, 57 933 cases were in the MS -hs-CRP - group, 10 949 cases in the MS -hs-CRP + group, 18 412 cases in the MS + hs-CRP - group, and 5 622 cases in the MS + hs-CRP + group.The median follow-up period was 15.01 years (14.66 to 15.20 years). By the end of follow-up, these were 1 992 cases of new-onset digestive system malignant tumors. The cumulative incidence rates of digestive system malignant tumors of MS -hs-CRP -, MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + groups were 2.0%(1 164/57 933), 2.3%(249/10 949), 2.4%(440/18 412), and 2.5%(139/5 622), respectively. The difference in the cumulative incidence among the 4 groups was statistically significant ( χ2=14.09, P=0.003).The results of multivariate Cox analysis showed that, after hs-CRP level and other confounding factors were adjusted, the risk of developing digestive system malignant tumors in participants with MS was 21.4% higher than that in those without MS ( HR=1.214 (95% confidence interval (95% CI): 1.086 to 1.340), P<0.001). After MS status and other confounding factors were adjusted, the risk of developing digestive system malignant tumors in participants with high hs-CRP level (>3 mg/L) was 17.2% higher than those with low hs-CRP level (≤3 mg/L) ( HR=1.172 (95% CI: 1.042 to 1.303), P=0.008). After relevant confounding factors were adjusted, the risks of developing digestive system malignant tumors in the MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + groups increased by 17.2%, 21.4%, and 35.9%, respectively, as compared with that of the MS -hs-CRP - group ( HR=1.172 (95% CI: 1.017 to 1.399), P=0.028; HR=1.214 (95% CI: 1.074 to 1.356), P=0.002; HR=1.359 (95% CI: 1.135 to 1.635), P=0.001). Among the 4 groups, the overall risk of developing digestive system malignant tumors of MS + hs-CRP + group was the highest. After relevant confounding factors were adjusted, the risks of colorectal cancer, liver cancer, and pancreatic cancer of the MS + hs-CRP + group increased by 46.2%, 35.7%, and 88.3%, respectively, as compared with those of the MS -hs-CRP - group ( HR=1.462 (95% CI: 1.088 to 1.956), HR=1.357 (95% CI: 1.132 to 2.089), HR=1.883 (95% CI: 1.052 to 3.342)), suggesting that MS combined with high hs-CRP was a significant risk factor for increased incidences of colorectal cancer, liver cancer, and pancreatic cancer ( P=0.012, 0.016 and 0.033). After participants diagnosed with new digestive system malignancies within one year of follow-up and those taking antihypertensive, antidiabetic, or lipid-lowering medications (108 cases, 10 680 cases, 2 344 cases, 906 cases) were excluded, the results of sensitivity analysis indicated the increased risk of digestive system malignant tumors in the MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + groups were 12.1%, 21.4%, 28.7%; 18.2%, 21.4%, 24.8%; 16.4%, 21.4%, 32.2%; 17.3%, 20.4%, 35.8%. Among the 3 groups, the increased risk of developing digestive system malignant tumors of MS + hs-CRP + group was the highest. Conclusion:MS and hs-CRP >3 mg/L are both independent risk factors for developing digestive system malignant tumors, and their combination further increases the risk of developing digestive system malignant tumors.

BACKGROUND:Exosomes have been confirmed to be closely related to cartilage degeneration in osteoarthritis.However,the role and mechanism of exosome-derived genes in cartilage degeneration of osteoarthritis have not been fully elucidated.OBJECTIVE:Bioinformatics analyses were used to screen the genes related to cartilage degeneration in the synovial exosomes of patients with osteoarthritis,and to determine their biological functions and signaling pathways in order to provide new therapeutic targets for delaying cartilage degeneration in osteoarthritis.METHODS:Firstly,osteoarthritis-related exosome dataset GSE185059 and cartilage degeneration dataset GSE114007 were downloaded from Gene Expression Omnibus(GEO)database to screen exosome-derived cartilage degeneration related genes.GO functional and KEGG pathway enrichment analyses were performed based on the screened exosome-derived cartilage degeneration related genes.Protein-protein interaction network was drawn and Ingenuity Pathway Analysis(IPA)was conducted to screen and obtain key exosome-derived cartilage degeneration-related genes.Finally,qRT-PCR was used to verify the expression of key genes in osteoarthritis cartilage tissue and interleukin-1β stimulated chondrocyte models.RESULTS AND CONCLUSION:(1)There were 831 differentially expressed genes in the GSE185059 dataset and 5 323 differentially expressed genes in the GSE114007 dataset.A total of 94 exosome-derived cartilage degeneration related genes were screened after the intersection of these differentially expressed genes,of which 51 genes were down-regulated and 43 genes were up-regulated.(2)GO functional enrichment analysis showed that the up-regulated genes were mainly involved in the positive regulation of cell-cell adhesion,the positive regulation of T cell activation,and chronic inflammatory response,while the down-regulated genes were mainly involved in biological processes such as cell aggregation,cartilage differentiation and development,and skeletal system morphogenesis.(3)KEGG pathway enrichment analysis showed that exosome-derived cartilage degeneration-related genes were mainly involved in tryptophan enrichment metabolism,vitamin B6 metabolism,and leukocyte transendothelial migration.(4)The constructed protein-protein interaction network confirmed the existence of multiple interaction relationships among exosome-derived cartilage degeneration-related genes.Combined with five algorithms in CytoHubba software,four key exosome-derived cartilage degeneration-related genes were further screened,namely THY1,CYP1A1,NFKB2,and COL6A3.(5)The results of qRT-PCR showed that compared with normal cartilage,the expressions of THY1 and COL6A3 in osteoarthritic cartilage were increased,while the expression of CYP1A1 and NFKB2 was decreased.Similarly,compared with the unstimulated group,the expression of THY1 and COL6A3 in the interleukin-1β induced chondrocytes was upregulated,while the expression of CYP1A1 and NFKB2 was downregulated.(6)These results indicate that THY1,CYP1A1,NFKB2,and COL6A3 are genes related to cartilage degeneration in the exosomes of synovial fluid of patients with osteoarthritis,and may participate in the pathogenesis of osteoarthritis by regulating biological processes such as protein tyrosine kinase activity and lipid metabolism,as well as nuclear factor-κB signaling pathway and focal adhesion signaling pathway.However,the specific regulatory roles and molecular mechanisms of these key genes in cartilage degeneration need to be further verified by experiments.

Cervical spinal cord injury without fracture-dislocation (CSCIWFD) is referred to as a special type of cervical spinal cord injury characterized by traumatic spinal cord dysfunction and no significant bony structural abnormalities on imagines. Duo to the high risk of missed diagnosis during the initial consultation, CSCIWFD may lead to progressive neurological deterioration or even complete paralysis, severely impacting patients′ prognosis. Currently, there are no established consensuses over the diagnosis and treatment of CSCIWFD, such as the lack of evidence-based standards for indications of non-surgical treatment and risk of secondary neurological injury, as well as debates over the optimal timing for surgical intervention and indications for different surgical approaches. To address these issues, the Spine Trauma Group of the Orthopedic Branch of the Chinese Medical Doctor Association organized experts in the relevant fields to formulate Diagnosis and treatment guideline for acute cervical spinal cord injury without fracture- dislocation in adults ( version 2025) . Based on evidence-based medicine and the principles of scientific rigor and clinical applicability, the guidelines proposed 11 recommendations covering terminology, diagnosis, evaluation treatment, and rehabilitation, etc., aiming to standardize the management of CSCIWFD.