To explore the value of general information and rapid laboratory tests obtained from the emergency department in the early diagnosis and prevention of young patients with acute myocardial infarction and acute myocarditis, in order to prevent the disease from progressing to a critical stage. This study employs a retrospective observational study, compiling clinical data from young patients diagnosed with acute myocardial infarction or acute myocarditis who were admitted to the Department of Cardiology or Emergency Department of the Second Affiliated Hospital of Soochow University from January 2015 to September 2024. Demographic information and laboratory test results from both the outpatient and emergency departments were retrieved. The acute myocardial infarction group comprised 267 patients (257 males, 10 females) aged 23-44 ys, while the acute myocarditis group included 134 patients (93 males, 41 females) aged 18-44 ys. A comparative analysis of the clinical data between the two groups was conducted, encompassing variables such as age, gender, comorbidities, high-risk factors, emergency blood routine tests, high-sensitivity C-reactive protein levels, coagulation profiles, renal function tests, NT-proBNP levels, myocardial injury markers, electrocardiogram readings, blood pressure, and heart rate. The results showed that:Compared with the young myocarditis group, the myocardial infarction group was older (ys)[38(35, 42) vs 30(25, 37), U=7 893, P<0.001], more male [257(96.3%) vs 93(69.4%), χ2=57.95, P<0.001], more smoking [211(79.0%) vs 38(28.4%), χ2=97.32, P<0.001], drinking history [125(46.8%) vs 22(16.4%), χ2=35.51, P<0.001], family history of coronary heart disease [45(16.9%) vs 3(2.2%), χ2=18.09, P<0.001], hypertension [100(37.5%) vs 12(9.0%), χ2=36, P<0.001] and diabetes [42(15.7%) vs 4(3.0%), χ2=14.27, P<0.001]. Systolic blood pressure (mmHg)[126(114, 144) vs 119(101, 126), U=11 389.50, P<0.001], diastolic blood pressure (mmHg)[80(70, 93) vs 72(62, 81), U=12 220.50, P<0.001], total white blood cell count (10 9/L)[11.3(9.2, 14.1) vs 8.5(6.6, 11.2), U=10 825.50, P<0.001], hemoglobin (g/L)[157(147, 166) vs 143(129, 154), U=9 404.50, P<0.001], platelet count (10 9/L)[244(206, 297) vs 207(173, 253), U=11 680, P<0.001], uric acid (μmol/L)[380(315, 446) vs 347(265, 412), U=14 805.50, P=0.005], ST segment elevation [204(76.4%) vs 57(42.5%), χ2=73.03, P<0.001] and Q wave formation [76(28.5%) vs 17(12.7%), χ2=12.47, P<0.001] in ECG were higher than those in myocarditis group. The duration of onset (hs) [6(3, 25) vs 48(24, 73), U=27911, P<0.001], heart rate (beats/min)[82(74, 92) vs 92(78, 103), U=22 347, P<0.001], D-dimer (μg/ml)[0.23(0.17, 0.51) vs 0.61(0.30, 1.38), U=25 806, P<0.001], High-sensitivity troponin T/99th percentile upper reference limit [5(1, 36) vs 16(8, 39), U=22 577, P<0.001], NT-proBNP (pg/ml) [204(64, 644) vs 824(189, 4 043), U=25 134, P<0.001], C-reactive protein (mg/L)[6(3, 9) vs 24(6, 55), U=26 349.50, P<0.001] and body temperature (℃) [36.50(36.30, 36.60) vs 37.35(36.50, 38.50), U=26 961, P<0.001] were significantly lower than those in myocarditis group, the symptoms of chest pain in myocardial infarction group was significantly higher than those in myocarditis group [262(98.1%) vs 83(61.9%), χ2=97.24, P<0.001], and the history of prodromal infection [12(4.5%) vs 112(83.6%), χ2=261.26, P<0.001], syncope [11(4.1%) vs 18(13.4%), χ2=11.53, P<0.001] and shock [6(2.2%) vs 22(16.4%), χ2=27.59, P<0.001] in myocardial infarction group were significantly lower than those in myocarditis group. With acute myocardial infarction as the target outcome, 8 influencing factors selected by LASSO regression, and 5 independent influencing factors were found after multiple Logistic regression, those were age ( OR=1.21, 95% CI: 1.12-1.31; P<0.001), pre-infection ( OR=0.02, 95% CI: 0.01-0.06; P<0.001), body temperature ( OR=0.37, 95% CI: 0.18-0.77; P=0.008), chest pain ( OR=26.75, 95% CI: 5.87-121.81; P<0.001) and white blood cell count ( OR=1.27, 95% CI: 1.12-1.44; P<0.001). Younger age, high body temperature and pre-infection are independent predictors for acute myocarditis, while chest pain and elevated white blood cell count are independent predictors for acute myocardial infarction. The five influencing factors selected by multivariate logistic regression and their combined diagnostic model were subjected to ROC analysis. The AUC reached 0.969, sensitivity reached 0.940 and specificity reached 0.925. Calibration curve and decision curve analysis(DCA) demonstrate that the model possesses excellent clinical application value. In conclusion, age, chest pain, pre-infection, body temperature and white blood cell count were independent factors in distinguishing acute myocardial infarction and acute myocarditis in young people. The clinical differential diagnosis model based on 5 independent factors may has high efficiency and good clinical practicability.

To explore the value of general information and rapid laboratory tests obtained from the emergency department in the early diagnosis and prevention of young patients with acute myocardial infarction and acute myocarditis, in order to prevent the disease from progressing to a critical stage. This study employs a retrospective observational study, compiling clinical data from young patients diagnosed with acute myocardial infarction or acute myocarditis who were admitted to the Department of Cardiology or Emergency Department of the Second Affiliated Hospital of Soochow University from January 2015 to September 2024. Demographic information and laboratory test results from both the outpatient and emergency departments were retrieved. The acute myocardial infarction group comprised 267 patients (257 males, 10 females) aged 23-44 ys, while the acute myocarditis group included 134 patients (93 males, 41 females) aged 18-44 ys. A comparative analysis of the clinical data between the two groups was conducted, encompassing variables such as age, gender, comorbidities, high-risk factors, emergency blood routine tests, high-sensitivity C-reactive protein levels, coagulation profiles, renal function tests, NT-proBNP levels, myocardial injury markers, electrocardiogram readings, blood pressure, and heart rate. The results showed that:Compared with the young myocarditis group, the myocardial infarction group was older (ys)[38(35, 42) vs 30(25, 37), U=7 893, P<0.001], more male [257(96.3%) vs 93(69.4%), χ2=57.95, P<0.001], more smoking [211(79.0%) vs 38(28.4%), χ2=97.32, P<0.001], drinking history [125(46.8%) vs 22(16.4%), χ2=35.51, P<0.001], family history of coronary heart disease [45(16.9%) vs 3(2.2%), χ2=18.09, P<0.001], hypertension [100(37.5%) vs 12(9.0%), χ2=36, P<0.001] and diabetes [42(15.7%) vs 4(3.0%), χ2=14.27, P<0.001]. Systolic blood pressure (mmHg)[126(114, 144) vs 119(101, 126), U=11 389.50, P<0.001], diastolic blood pressure (mmHg)[80(70, 93) vs 72(62, 81), U=12 220.50, P<0.001], total white blood cell count (10 9/L)[11.3(9.2, 14.1) vs 8.5(6.6, 11.2), U=10 825.50, P<0.001], hemoglobin (g/L)[157(147, 166) vs 143(129, 154), U=9 404.50, P<0.001], platelet count (10 9/L)[244(206, 297) vs 207(173, 253), U=11 680, P<0.001], uric acid (μmol/L)[380(315, 446) vs 347(265, 412), U=14 805.50, P=0.005], ST segment elevation [204(76.4%) vs 57(42.5%), χ2=73.03, P<0.001] and Q wave formation [76(28.5%) vs 17(12.7%), χ2=12.47, P<0.001] in ECG were higher than those in myocarditis group. The duration of onset (hs) [6(3, 25) vs 48(24, 73), U=27911, P<0.001], heart rate (beats/min)[82(74, 92) vs 92(78, 103), U=22 347, P<0.001], D-dimer (μg/ml)[0.23(0.17, 0.51) vs 0.61(0.30, 1.38), U=25 806, P<0.001], High-sensitivity troponin T/99th percentile upper reference limit [5(1, 36) vs 16(8, 39), U=22 577, P<0.001], NT-proBNP (pg/ml) [204(64, 644) vs 824(189, 4 043), U=25 134, P<0.001], C-reactive protein (mg/L)[6(3, 9) vs 24(6, 55), U=26 349.50, P<0.001] and body temperature (℃) [36.50(36.30, 36.60) vs 37.35(36.50, 38.50), U=26 961, P<0.001] were significantly lower than those in myocarditis group, the symptoms of chest pain in myocardial infarction group was significantly higher than those in myocarditis group [262(98.1%) vs 83(61.9%), χ2=97.24, P<0.001], and the history of prodromal infection [12(4.5%) vs 112(83.6%), χ2=261.26, P<0.001], syncope [11(4.1%) vs 18(13.4%), χ2=11.53, P<0.001] and shock [6(2.2%) vs 22(16.4%), χ2=27.59, P<0.001] in myocardial infarction group were significantly lower than those in myocarditis group. With acute myocardial infarction as the target outcome, 8 influencing factors selected by LASSO regression, and 5 independent influencing factors were found after multiple Logistic regression, those were age ( OR=1.21, 95% CI: 1.12-1.31; P<0.001), pre-infection ( OR=0.02, 95% CI: 0.01-0.06; P<0.001), body temperature ( OR=0.37, 95% CI: 0.18-0.77; P=0.008), chest pain ( OR=26.75, 95% CI: 5.87-121.81; P<0.001) and white blood cell count ( OR=1.27, 95% CI: 1.12-1.44; P<0.001). Younger age, high body temperature and pre-infection are independent predictors for acute myocarditis, while chest pain and elevated white blood cell count are independent predictors for acute myocardial infarction. The five influencing factors selected by multivariate logistic regression and their combined diagnostic model were subjected to ROC analysis. The AUC reached 0.969, sensitivity reached 0.940 and specificity reached 0.925. Calibration curve and decision curve analysis(DCA) demonstrate that the model possesses excellent clinical application value. In conclusion, age, chest pain, pre-infection, body temperature and white blood cell count were independent factors in distinguishing acute myocardial infarction and acute myocarditis in young people. The clinical differential diagnosis model based on 5 independent factors may has high efficiency and good clinical practicability.

OBJECTIVE: To investigate the effects of removing microglia from spinal cord on nerve repair and functional recovery after spinal cord injury (SCI) in mice. METHODS: Thirty-nine 6-week-old female C57BL/6 mice were randomly divided into control group ( n=12), SCI group ( n=12), and PLX3397+SCI group ( n=15). The PLX3397+SCI group received continuous feeding of PLX3397, a colony-stimulating factor 1 receptor inhibitor, while the other two groups were fed a standard diet. After 14 days, both the SCI group and the PLX3397+SCI group were tested for ionized calcium binding adapter molecule 1 (Iba1) to confirm that the PLX3397+SCI group had completely depleted the spinal cord microglia. The SCI model was then prepared by clamping the spinal cord in both the SCI group and the PLX3397+SCI group, while the control group underwent laminectomy. Preoperatively and at 1, 3, 7, 14, 21, and 28 days postoperatively, the Basso Mouse Scale (BMS) was used to assess the hind limb function of mice in each group. At 28 days, a footprint test was conducted to observe the gait of the mice. After SCI, spinal cord tissue from the injury site was taken, and Iba1 immunofluorescence staining was performed at 7 days to observe the aggregation and proliferation of microglia in the spinal cord. HE staining was used to observe the formation of glial scars at the injury site at 28 days; glial fibrillary acidic protein (GFAP) immunofluorescence staining was applied to astrocytes to assess the extent of the injured area; neuronal nuclei antigen (NeuN) immunofluorescence staining was used to evaluate neuronal survival. And 5-hydroxytryptamine (5-HT) immunofluorescence staining was performed to assess axonal survival at 60 days. RESULTS: All mice survived until the end of the experiment. Immunofluorescence staining revealed that the microglia in the spinal cord of the PLX3397+SCI group decreased by more than 95% compared to the control group after 14 days of continuous feeding with PLX3397 ( P<0.05). Compared to the control group, the BMS scores in the PLX3397+SCI group and the SCI group significantly decreased at different time points after SCI ( P<0.05). Moreover, the PLX3397+SCI group showed a further decrease in BMS scores compared to the SCI group, and exhibited a dragging gait. The differences between the two groups were significant at 14, 21, and 28 days ( P<0.05). HE staining at 28 days revealed that the SCI group had formed a well-defined and dense gliotic scar, while the PLX3397+SCI group also developed a gliotic scar, but with a more blurred and loose boundary. Immunofluorescence staining revealed that the number of microglia near the injury center at 7 days increased in the SCI group than in the control group, but the difference between groups was not significant ( P>0.05). In contrast, the PLX3397+SCI group showed a significant reduction in microglia compared to both the control and SCI groups ( P<0.05). At 28 days after SCI, the area of spinal cord injury in the PLX3397+SCI group was significantly larger than that in SCI group ( P<0.05); the surviving neurons significantly reduced compared with the control group and SCI group ( P<0.05). The axonal necrosis and retraction at 60 days after SCI were more obvious. CONCLUSION The removal of microglia in the spinal cord aggravate the tissue damage after SCI and affecte the recovery of motor function in mice, suggesting that microglia played a neuroprotective role in SCI.
Animals ; Spinal Cord Injuries/surgery* ; Microglia/pathology* ; Female ; Mice ; Mice, Inbred C57BL ; Nerve Regeneration/drug effects* ; Spinal Cord/pathology* ; Pyrroles/administration & dosage* ; Aminopyridines/administration & dosage* ; Recovery of Function ; Disease Models, Animal ; Calcium-Binding Proteins/metabolism* ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors* ; Microfilament Proteins/metabolism* ; Glial Fibrillary Acidic Protein/metabolism*

Objective: To elucidate the biological basis of the heart qi deficiency (HQD) pattern, an in-depth understanding of which is essential for improving clinical herbal therapy. Methods: We predicted and characterized HQD pattern genes using the new strategy, TCM-HIN2Vec, which involves heterogeneous network embedding and transcriptomic experiments. First, a heterogeneous network of traditional Chinese medicine (TCM) patterns was constructed using public databases. Next, we predicted HQD pattern genes using a heterogeneous network-embedding algorithm. We then analyzed the functional characteristics of HQD pattern genes using gene enrichment analysis and examined gene expression levels using RNA-seq. Finally, we identified TCM herbs that demonstrated enriched interactions with HQD pattern genes via herbal enrichment analysis. Results: Our TCM-HIN2Vec strategy revealed that candidate genes associated with HQD pattern were significantly enriched in energy metabolism, signal transduction pathways, and immune processes. Moreover, we found that these candidate genes were significantly differentially expressed in the transcriptional profile of mice model with heart failure with a qi deficiency pattern. Furthermore, herbal enrichment analysis identified TCM herbs that demonstrated enriched interactions with the top 10 candidate genes and could potentially serve as drug candidates for treating HQD. Conclusion Our results suggested that TCM-HIN2Vec is capable of not only accurately identifying HQD pattern genes, but also deciphering the basis of HQD pattern. Furthermore our finding indicated that TCM-HIN2Vec may be further expanded to develop other patterns, leading to a new approach aimed at elucidating general TCM patterns and developing precision medicine.

Objective To establish a lipid differentiation model of primary rat bone marrow mesenchymal stem cells(rBMSCs)in vitro using homocysteine(Hcy),and analyze the specific effects of Hcy on lipid and bone differentiation of BMSCs;to comprehensively explore the effects of mangiferin on lipid and bone differentiation of BMSCs,and further reveal the potential mechanism of mangiferin in the treatment of osteoporosis through the inter-vention of Hcy-induced BMSCs by different concentrations of mangiferin.Methods First,rBMSCs were extracted and isolated.The rBMSCs that were well-cultured to a certain generation were placed in culture medium containing different concentrations of Hcy(0.125,0.250,0.5,1,2,4 mmol/L)to establish lipid differentiation model of rBMSCs.Then,different concentrations of mangiferin(37.5,75,150 μmol/L)were applied to the experimental cells for intervention.After culture for a certain period of time,the cells were collected for the following tests:The accumulation of lipids in the cells was detected by semi-quantitative method of oil red 0 dye solution to evaluate the degree of lipid differentiation;The activity of alkaline phosphatase(ALP)was measured by pNPP method;The expression of bone morphogenetic protein-2(BMP-2)and type Ⅰ collagen(Col Ⅰ)were detected by western blot assay to evaluate the degree of bone differentiation.Results Mangiferin could significantly up-regulate the expression of BMP-2 and Col Ⅰ in vitro,increase the level of ALP,and promote bone differentiation of rBMSCs.Hcy promoted lipid differentiation of rBMSCs by increasing lipid accumulation,and down-regulated the expression of BMP-2 and Col Ⅰ,reduced the intracellular ALP level,thereby inhibiting bone differentiation of rBMSCs.How-ever,the above Hcy-related effects could be successfully reversed by mangiferin.Conclusion Mangiferin can sig-nificantly promote bone differentiation of rBMSCs in vitro,while Hcy can inhibit bone differentiation of rBMSCs and promote its lipid differentiation.Mangiferin has the ability to reverse this effect,indicating that mangiferin has certain potential in the treatment of osteoporosis-related diseases.

Objective To analyze the predictive value of dynamic changes of multiple inflammatory factors in early screening of sepsis risk in patients with abdominal trauma.Methods A total of 360 patients with abdominal trauma admitted to the Department of Surgery of Jiangsu Provincial Corps Hospital of the Chinese People's Armed Police Force from January 2018 to January 2022 were studied.Patients were divided into sepsis group and control group according to whether sepsis occurred.The general data and dynamic changes of inflammatory indicators were compared between the two groups.Multivariate Logistic regression was used to analyze the related factors of sepsis in patients with abdominal trauma,and ROC curve was used to analyze the value of dynamic changes of multiple inflammatory factors in predicting sepsis in patients with abdominal trauma.Results Among the patients included in the study,13 cases fell out,leaving 347 cases,of which 51 patients with sepsis were classified as sepsis group,and the remaining 296 cases were classified as control group.The incidence of sepsis was 14.70％.There was no significant difference in age,blood glucose and white blood cell at admission between the two groups(P＞0.05).But the SOFA score in sepsis group(1.86±0.45)was higher than that in control group(1.54±0.36).In sepsis group,the difference of C-reactive protein(CRP)was(5.67±1.17)mg/L,the PCT was(0.12±0.05)ng/ml,the PCT variation rate was(36.43±8.02)％,and the difference of serum amylase A protein(SAA)was(8.62±1.05)m g/L,the difference of neutrophil percentage was(9.31±1.09)％,which was higher than that of control group[(4.79±0.63)mg/L,(0.10±0.04)ng/ml,(28.04±6.21)％,(7.11±0.84)mg/L,(8.41±0.92)％],the difference was statistically significant(P＜0.05).Multivariate Logistic regression analysis showed that:SOFA score(OR=1.648),CRP change difference(OR=2.338),PCT variation rate(OR=1.096),SAA change difference(OR=6.043),neutrophil percentage change difference(OR=3.355)were independent risk factors for sepsis in patients with abdominal trauma.ROC curve showed that SAA difference was more effective in predicting the risk of sepsis in patients with abdominal trauma than CRP difference,PCT variation rate,neutrophil percentage change difference and SOFA score.Conclusion Dynamic analysis of multiple inflammatory factors is valuable for early screening of sepsis risk in patients with abdominal trauma,and monitoring the changes of inflammatory factors is helpful for early adjustment of treatment.

Objective To establish a lipid differentiation model of primary rat bone marrow mesenchymal stem cells(rBMSCs)in vitro using homocysteine(Hcy),and analyze the specific effects of Hcy on lipid and bone differentiation of BMSCs;to comprehensively explore the effects of mangiferin on lipid and bone differentiation of BMSCs,and further reveal the potential mechanism of mangiferin in the treatment of osteoporosis through the inter-vention of Hcy-induced BMSCs by different concentrations of mangiferin.Methods First,rBMSCs were extracted and isolated.The rBMSCs that were well-cultured to a certain generation were placed in culture medium containing different concentrations of Hcy(0.125,0.250,0.5,1,2,4 mmol/L)to establish lipid differentiation model of rBMSCs.Then,different concentrations of mangiferin(37.5,75,150 μmol/L)were applied to the experimental cells for intervention.After culture for a certain period of time,the cells were collected for the following tests:The accumulation of lipids in the cells was detected by semi-quantitative method of oil red 0 dye solution to evaluate the degree of lipid differentiation;The activity of alkaline phosphatase(ALP)was measured by pNPP method;The expression of bone morphogenetic protein-2(BMP-2)and type Ⅰ collagen(Col Ⅰ)were detected by western blot assay to evaluate the degree of bone differentiation.Results Mangiferin could significantly up-regulate the expression of BMP-2 and Col Ⅰ in vitro,increase the level of ALP,and promote bone differentiation of rBMSCs.Hcy promoted lipid differentiation of rBMSCs by increasing lipid accumulation,and down-regulated the expression of BMP-2 and Col Ⅰ,reduced the intracellular ALP level,thereby inhibiting bone differentiation of rBMSCs.How-ever,the above Hcy-related effects could be successfully reversed by mangiferin.Conclusion Mangiferin can sig-nificantly promote bone differentiation of rBMSCs in vitro,while Hcy can inhibit bone differentiation of rBMSCs and promote its lipid differentiation.Mangiferin has the ability to reverse this effect,indicating that mangiferin has certain potential in the treatment of osteoporosis-related diseases.

Objective To analyze the predictive value of dynamic changes of multiple inflammatory factors in early screening of sepsis risk in patients with abdominal trauma.Methods A total of 360 patients with abdominal trauma admitted to the Department of Surgery of Jiangsu Provincial Corps Hospital of the Chinese People's Armed Police Force from January 2018 to January 2022 were studied.Patients were divided into sepsis group and control group according to whether sepsis occurred.The general data and dynamic changes of inflammatory indicators were compared between the two groups.Multivariate Logistic regression was used to analyze the related factors of sepsis in patients with abdominal trauma,and ROC curve was used to analyze the value of dynamic changes of multiple inflammatory factors in predicting sepsis in patients with abdominal trauma.Results Among the patients included in the study,13 cases fell out,leaving 347 cases,of which 51 patients with sepsis were classified as sepsis group,and the remaining 296 cases were classified as control group.The incidence of sepsis was 14.70％.There was no significant difference in age,blood glucose and white blood cell at admission between the two groups(P＞0.05).But the SOFA score in sepsis group(1.86±0.45)was higher than that in control group(1.54±0.36).In sepsis group,the difference of C-reactive protein(CRP)was(5.67±1.17)mg/L,the PCT was(0.12±0.05)ng/ml,the PCT variation rate was(36.43±8.02)％,and the difference of serum amylase A protein(SAA)was(8.62±1.05)m g/L,the difference of neutrophil percentage was(9.31±1.09)％,which was higher than that of control group[(4.79±0.63)mg/L,(0.10±0.04)ng/ml,(28.04±6.21)％,(7.11±0.84)mg/L,(8.41±0.92)％],the difference was statistically significant(P＜0.05).Multivariate Logistic regression analysis showed that:SOFA score(OR=1.648),CRP change difference(OR=2.338),PCT variation rate(OR=1.096),SAA change difference(OR=6.043),neutrophil percentage change difference(OR=3.355)were independent risk factors for sepsis in patients with abdominal trauma.ROC curve showed that SAA difference was more effective in predicting the risk of sepsis in patients with abdominal trauma than CRP difference,PCT variation rate,neutrophil percentage change difference and SOFA score.Conclusion Dynamic analysis of multiple inflammatory factors is valuable for early screening of sepsis risk in patients with abdominal trauma,and monitoring the changes of inflammatory factors is helpful for early adjustment of treatment.

Despite exciting achievements with some malignancies, immunotherapy for hypoimmunogenic cancers, especially glioblastoma (GBM), remains a formidable clinical challenge. Poor immunogenicity and deficient immune infiltrates are two major limitations to an effective cancer-specific immune response. Herein, we propose that an injectable signal-amplifying nanocomposite/hydrogel system consisting of granulocyte-macrophage colony-stimulating factor and imiquimod-loaded antigen-capturing nanoparticles can simultaneously amplify the chemotactic signal of antigen-presenting cells and the "danger" signal of GBM. We demonstrated the feasibility of this strategy in two scenarios of GBM. In the first scenario, we showed that this simultaneous amplification system, in conjunction with local chemotherapy, enhanced both the immunogenicity and immune infiltrates in a recurrent GBM model; thus, ultimately making a cold GBM hot and suppressing postoperative relapse. Encouraged by excellent efficacy, we further exploited this signal-amplifying system to improve the efficiency of vaccine lysate in the treatment of refractory multiple GBM, a disease with limited clinical treatment options. In general, this biomaterial-based immune signal amplification system represents a unique approach to restore GBM-specific immunity and may provide a beneficial preliminary treatment for other clinically refractory malignancies.

The incidence rate of liver cancer has been rising in recent years. Traditional cell line culture and human patient-derived tumor xenograft models, which are commonly used tools to simulate the occurrence of human liver cancer, have deepened the understanding of tumor occurrence, development, and drug resistance mechanisms. However, they cannot reflect the accurate state of cancer cells, the tumor microenvironment, or spatial structural characteristics. Recently, more in vitro-produced physiological liver organoids have been applied in the study of liver cancer. Liver organoid models have made breakthroughs in the occurrence and development mechanisms of liver cancer, personalized drug screening and biomarker identification, immunotherapy, and regenerative medicine applications. This paper mainly summarizes the progress and application of liver organoids processed in the study of liver cancer.