Inflammation is the body’s response to damage， infection or other stimuli， but its excessive or continuous development can lead to a variety of diseases. Although modern medical anti-inflammatory therapies were widely used， it is often accompanied by limitations such as more adverse reactions. Based on the “holistic view” and “differential treatment”， traditional Chinese medicine （TCM） regards inflammation as a manifestation of the imbalance of yin and yang in the body and the conflict between good and evil. The application of anti-inflammatory TCM is not only aimed at the pathological state of “inflammation”， but also based on the overall consideration of “syndrome”. According to different types of syndrome， anti-inflammatory TCM can be divided into heat-clearing and detoxifying agents （such as Lonicera japonica and Isatis indigotica ）， heat-clearing and drying dampness agents （such as Coptidis Rhizoma）， blood-activating and stasis-dissolving agents （such as Salvia miltiorrhiza ） and vital qi-strengthening and pathogenic factor-expelling agents （such as Panax ginseng ）. Four types of anti-inflammatory TCM restore the body’s immune balance through the systematic regulation of multi-component， multi-target and multi-pathway， exhibiting a good anti-inflammatory effect. Future research should focus on integrating systematic biology， applying artificial intelligence， carrying out high-quality evidence-based research， and combining traditional Chinese medicine and Western medicine， so as to reveal the overall regulatory law of anti-inf lammatory effects of TCM and promote clinical rational use.

Objective To investigate the regulatory mechanism of transforming growth factor-β1 (TGF-β1) in different types of mitral valvular disease (MVD) with atrial fibrillation (AF). Methods From August 2011 to August 2012, patients with moderate to severe MVD accompanied by AF who required mitral valve replacement at the Department of Cardiovascular Surgery, West China Hospital, Sichuan University, were included. Based on echocardiographic results, patients were divided into two groups: a mitral regurgitation (MR) with AF (MR-AF) group and a mitral stenosis (MS) with AF (MS-AF) group. Left atrial tissue samples were collected during surgery. Techniques such as enzyme-linked immunosorbent assay, real-time fluorescence quantitative polymerase chain reaction, immunohistochemistry, and Western blotting were used to detect key molecules in the TGF-β1/JNK pathway. Results Sixteen patients were enrolled. There were 8 patients in the MR-AF group, including 5 males and 3 females, with an average age of (41.38±11.19) years; and 8 patients in the MS-AF group, including 6 males and 2 females, with an average age of (43.12±5.30) years. The left atrial volume load was higher in MR-AF patients, while the left atrial pressure load was higher in MS-AF patients. In MS-AF patients, the relative expression levels of MAPK9, JUN, CASP3, BAX, and BCL2 mRNA in left atrial tissues were significantly upregulated. The serum TGF-β1 protein level and the relative expression levels of p-JNK, p-c-Jun, and Caspase-3 proteins in the left atrial tissues of the MR-AF group were higher. Myocardial cell damage was more severe in the MS-AF group, and the protein expression level of Bcl-2 was higher. Conclusion Different MVD have distinct hemodynamic characteristics. The myocardium of the left atrium in MR-AF patients is more prone to apoptosis, possibly through the activation of the TGF-β1/JNK signaling pathway.

Objective To investigate the perioperative safety of patients with myasthenia gravis who take high doses of oral glucocorticoids. Methods A retrospective analysis was conducted on the clinical data of patients with myasthenia gravis who received oral glucocorticoids and underwent thoracoscopic thymectomy at the Department of Thoracic Surgery, the University of Hong Kong-Shenzhen Hospital from April 2013 to October 2019. Patients were divided into a high-dose steroid group and a medium-to-low dose steroid group based on the dosage of oral steroids, and the clinical data of the two groups were compared. Results A total of 102 patients were included, including 19 (18.62%) males and 83 (81.37%) females, with an average age of (32.25±9.83) years. There were 75 patients in the medium-to-low dose steroid group and 27 patients in the high-dose steroid group. All patients in both groups successfully completed the surgery without major intraoperative bleeding, conversion to open chest surgery, delayed extubation, severe infection, or perioperative death. The daily oral steroid dose for the high-dose steroid group was (35.81±4.29) mg, and for the medium-to-low dose steroid group it was (15.29±2.17) mg. There was no statistical difference in the operation time [(124.69±23.51) min vs. (117.89±21.46) min, P=0.172] and intraoperative blood loss [(21.19±3.48) mL vs. (20.56±3.41) mL, P=0.419] between the two groups. Postoperatively, 12 (11.76%) patients developed complications: one patient of myasthenic crisis (the medium-to-low dose steroid group), which was improved after short-term respiratory support and intravenous immunoglobulin treatment; 11 patients of respiratory/swallowing difficulties (9 in the medium-to-low dose steroid group and 2 in the high-dose steroid group), which were improved after anticholinergic treatment to reduce oral secretions and sputum suction, and the patients were discharged smoothly. There was no statistical difference in the incidence of postoperative complications between the two groups (P=0.637). Conclusion On the basis of good perioperative management, it is safe and feasible for patients with myasthenia gravis who take high dose of oral steroids to undergo thymectomy, and they have the same perioperative safety as patients with medium-to-low dose steroids.

ObjectiveTo investigate the effect of mitochondrial calcium uniporter （MCU） on the cytoskeleton of pancreatic ductal epithelial cells in a mouse model of acute pancreatitis （AP） induced by caerulein （CAE）， to analyze the role of MCU in the development of AP， and to provide a theoretical basis for clinical treatment. MethodsIn the in vivo experiment， wild-type male C57BL6/J mice， aged 4 weeks， were randomly divided into control group and AP group， with 6 mice in each group. The mice in the AP group were given intraperitoneal injection of CAE to establish a model of AP， and those in the control group were given intraperitoneal injection of an equal volume of normal saline. Serum and pancreatic tissue samples were collected after 24 hours of modeling. HE staining was used to observe pancreatic histopathological changes； Western Blot was used to measure the expression levels of MCU， glutathione peroxidase 4 （GPX4）， and acyl-CoA synthetase long chain family member 4 （ASCL4）； kits were used to measure the serum level of amylase. In the in vitro experiment， the human pancreatic ductal epithelial cell line HPDE6-C7 was co-cultured with CAE for 24 hours to establish an in vitro AP model， and the cells were divided into control group， CAE group， RR （an MCU activity inhibitor） group， CAE+RR group， Fer-1 （an ferroptosis inhibitor） group， CAE+Fer-1 group， Erastin （an ferroptosis inducer） group， and CAE+Erastin group. CCK-8 assay was used to observe the influence of different agents on cell viability； Western Blot was used to measure the expression levels of MCU， GPX4， and ASCL4； immunofluorescence assay was used to measure reactive oxygen species （ROS）， actin cytoskeleton， and monolayer permeability； kits were used to measure the concentrations of malondialdehyde （MDA）， glutathione （GSH）， Fe²⁺， and total iron. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for comparison between two groups. ResultsIn the in vivo experiment， compared with the control group， the AP group had significant increases in pancreatic histopathological score， the serum level of amylase， and the expression levels of MCU and ASCL4， as well as a significant reduction in the expression of GPX4 （all P<0.05）. In the in vitro experiment， compared with the control group， the CAE group had significant increases in the expression levels of MCU and ASCL4， a significant reduction in the expression of GPX4， and significant increases in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability， as well as a significant reduction in the concentration of GSH （all P<0.05）， with the presence of actin cytoskeleton disruption. Compared with the CAE group， the CAE+RR group had a significant increase in the expression level of GPX4， a significant reduction in the expression level of ASCL4， and significant reductions in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability and a significant increase in the concentration of GSH （all P<0.05）， with alleviation of actin cytoskeleton disruption. Compared with the CAE group， the CAE+Fer-1 group had significant reductions in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability and a significant increase in the concentration of GSH （all P<0.05）， with alleviation of actin cytoskeleton disruption. Compared with the CAE group， the CAE+Erastin group had significant increases in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability and a significant reduction in the concentration of GSH （all P<0.05）， with aggravation of actin cytoskeleton disruption. ConclusionDuring the onset of AP， MCU mediates oxidative stress-induced ferroptosis and leads to the disruption of the pancreatic ductal epithelial barrier， which may be one of the possible pathogeneses of AP.

OBJECTIVE To investigate the influence of CYP2C19 gene polymorphism on platelet function and inflammatory cytokines in elderly patients with ischemic stroke， and to analyze potential factors associated with poor prognosis. METHODS A retrospective study was conducted on elderly patients with ischemic stroke admitted to our hospital from June 2024 to June 2025， wh o underwent CYP2C19 genotype testing and received antiplatelet therapy with clopidogrel. The levels of platelet function indicators and inflammatory cytokines before and after treatment were compared among patients with different metabolic phenotypes. Based on the prognosis at 6 months post-treatment， patients were divided into poor prognosis group and good prognosis group. Univariate analysis was performed on general data， metabolic phenotype， the levels of platelet function indicators and inflammatory cytokines. Variables with P ＜0.05 and the levels of inflammatory cytokines before treatment were included in a multivariate Logistic regression analysis to identify independent risk factors for poor prognosis. Multiple linear regression was used to further analyze the relationship between metabolic phenotypes and inflammatory cytokines. RESULTS A total of 448 elderly patients with ischemic stroke were included； among them， 162 cases were normal metabolic phenotype， 218 were intermediate metabolic phenotype， and 68 were poor metabolic phenotype. No rapid or ultrarapid metabolic phenotypes were observed. After treatment， platelet aggregation rate， the levels of P-selectin and platelet activated complex-1 （PAC-1）， high-sensitivity C-reactive Protein （hs-CRP）， interleukin-1β （IL-1β）， IL-6 and tumor necrosis factor-α （TNF-α） in the normal metabolic phenotype group， intermediate metabolic phenotype group， and poor metabolic phenotype group （except for platelet aggregation rate， and the levels of P-selectin and PAC-1 in the poor metabolic phenotype group） were significantly lower than those before treatment in the same group. Moreover， the above indicators in the normal metabolic phenotype group were significantly lower than those in the intermediate and poor metabolic phenotype groups at the corresponding time， and the levels of platelet function indicators in the intermediate metabolic phenotype group were significantly lower than those in the poor metabol ic phenotype group at the corresponding time （ P ＜0.05）. Univariate and multivariate Logistic regression analyses showed that combined with hypertension， combined with diabetes mellitus， and intermediate or poor metabolic genotypes were independent risk factors for poor prognosis in elderly patients with ischemic stroke （ P ＜0.05）. Multiple linear regression analysis showed that serum levels of hs-CRP， IL-1β， IL-6 and TNF-α before treatment were significantly higher in patients with intermediate and poor metabolic genotypes compared to those with normal metabolic genotype （ P ＜0.05）， with a greater magnitude of increase in inflammatory cytokines observed in the patients with poor metabolic genotype. CONCLUSIONS The elderly ischemic stroke patients with CYP2C19 intermediate and poor metabolic genotypes have poor inhibition effect on platelet and higher levels of inflammatory cytokines than normal metabolic genotype； CYP2C19 gene polymorphism， and in combination with hypertension and diabetes， can be used as independent predictors of poor prognosis.

Objective To analyze the epidemic characteristics of scarlet fever in Pudong New Area, Shanghai from 2010 to 2023, and to grasp the incidence of scarlet fever in time. Methods The information on the registration of scarlet fever in Pudong New Area, Shanghai from January 1, 2010 to December 31, 2023 was collected through the China Disease Prevention and Control Information System, and descriptive epidemiological methods and Joinpoint regression model were used for data analysis. Results From 2010 to 2023, a total of 5 669 cases of scarlet fever were reported in Pudong New Area, Shanghai, and no deaths were reported. The annual reported incidence rate was 7.2/100 000, and the overall trend was decreasing year by year. In terms of time distribution, the incidence peaks were in spring and winter. The incidence rate in males was higher than that in females, and it mainly affected children, especially those aged 2 to 10 years. Joinpoint regression model analysis showed that the annual percentage change (APC) and average annual percentage change (AAPC) of the reported incidence rate of scarlet fever from 2010 to 2023 showed that the incidence rate was fluctuating, and the incidence rate decreased significantly from 2019 to 2023 (APC was -53.7%). Conclusion The reported incidence rate of scarlet fever in Pudong New Area in Shanghai has decreased year by year from 2010 to 2023, and children remain the focus of prevention and control.

Objective To investigate the detection rate of non-alcoholic fatty liver disease (NAFLD) and influencing factors in the elderly population undergoing physical examination in Nanjing. Methods People who participated in the elderly physical examination in Nanjing from 2018 to 2023 were selected as the study subjects according to the inclusion and exclusion criteria. Basic information and physical examination results were collected. The t-test and Chi-square test were used to compare the detection status of NAFLD in different characteristic populations, and multivariate logistic regression model was used to analyze influencing factors of NAFLD. Results A total of 41 066 people were included in the study, with a detection rate of 39.55%. The detection rate in males (24.12%) was significantly lower than that in females (49.75%) (χ² = 2702.442, P<0.001). Trend χ² test results showed that the detection rate of NAFLD increased gradually with BMI (χ²_trend = 4084.414, P_trend < 0.001). Multivariate logistic regression analysis showed that female (OR = 3.055, 95% CI : 2.911-3.206), primary school or below (OR = 1.075, 95% CI : 1.009-1.146), unmarried (OR = 1.107, 95% CI : 1.039-1.179), BMI (18.5kg/m²-23.9 kg/m²: OR = 4.876, 95% CI :3.340-7.119; 24.0 kg/m²-27.9 kg/m²: OR = 15.324, 95% CI : 10.503-22.358; ≥28.0 kg/m²: OR = 37.433, 95% CI : 25.591-54.753), hypertension (OR = 1.095, 95% CI : 1.040-1.153), diabetes mellitus (OR = 1.317, 95% CI :1.250-1.387), and dyslipidemia (OR = 1.574, 95% CI : 1.501-1.652) were risk factors for NAFLD (all P<0.05). Conclusion The detection rate of NAFLD in the elderly population undergoing physical examinations in Nanjing is relatively high. Women, unmarried people, people with low education, overweight and obesity, and people with hypertension, diabetes, and dyslipidemia are the high-risk groups.

ObjectiveTo clarify the expression of TRIM28 in non-M3 acute myeloid leukemia （AML） and its correlation with clinical indicators and prognosis， and to further explore the effect of TRIM28 expression levels on the proliferation and apoptosis of AML cells using small interfering RNA. MethodsThe GSE34577 dataset was analyzed using R software to compare TRIM28 expression between healthy controls and non-M3 acute myeloid leukemia （AML） patients. Clinical samples from non-M3 AML patients were collected， with TRIM28 expression levels measured using real-time quantitative PCR （qPCR）. The analysis focused on correlations between TRIM28 expression and various clinical indicators， treatment efficacy， and patient prognosis. Furthermore， small interfering RNA （siRNA） technology was employed to downregulate TRIM28 expression in human primary AML cells （HL60 cell line）. The effects on cell proliferation and apoptosis were then assessed through CCK-8 assays and flow cytometry， respectively. ResultsThe results showed that TRIM28 was up-regulated in non-M3 AML of both online database GSE34577 and clinical samples （P<0.000 1）， TRIM28 expression of new diagnosis group and relapsed refractory group was higher than iron deficiency anemia group （P<0.01）， and there was no significance between different French-American-British classification systems subtype. TRIM28 expression was higher in non-M3 AML patients with a poor genetic prognosis stratified as moderate than in the good prognosis group， and TRIM28 expression was associated with NPM1 combined with the FLT3-ITD mutation， positively correlated with age， bone marrow blast， peripheral blood blast and white blood cell， negatively correlated with hemoglobin. In addition， interference TRIM28 greatly inhibited cell proliferation and promoted cell apoptosis. ConclusionThis study reveals that TRIM28 is highly expressed in non-M3 AML and associated with prognosis， and plays a key role in the proliferation and apoptosis of AML cells， suggesting that TRIM28 may serve as a novel therapeutic target for non-M3 AML.

Prostate cancer is one of the most common malignant tumors of male genitourinary system. Prostate cancer has the following characteristics： insidious onset， early asymptomatic or not obvious symptoms， complex etiology and pathogenesis， long incubation period and so on. Therefore， the realization of its early diagnosis and treatment is of great significance to the prognosis of patients. Prostate-specific membrane antigen （PSMA） is a type 2 transmembrane glycoprotein that is highly expressed on the membrane of almost all primary and metastatic prostate cancer cells， and is an ideal target for prostate cancer imaging and treatment. In recent years， with the approval of urea-containing small molecule PET （positron emission computed tomography） radiopharmaceutical based on PSMA （⁶⁸Ga-PSMA-11， ¹⁸F-PSMA-1007）， PET-CT （positron emission computed tomography/computed tomography） has shown new potential for early diagnosis and accurate staging of prostate cancer patients. This review mainly summarizes the research progress of urea-containing PSMA PET imaging agents and finds that they have defects such as uptake in non-target tissues like the kidneys， lacrimal glands， and salivary glands. Thus， further optimizing their structure to reduce the uptake in non-target tissues， providing provide convenience for the labeling of therapeutic radiopharmaceuticals， thereby achieving the goal of integrated diagnosis and treatment， is an important development direction in this field.

Organoid-on-a-chip technology represents a promising interdisciplinary advancement that merges two cutting-edge biomedical platforms: stem cell-derived organoids and microfluidics-based organ-on-a-chip systems. Organoids are self-organizing three-dimensional (3D) cell cultures that mimic the key structural and functional features of in vivo organs. However, traditional organoid culture systems are often static, lacking dynamic environmental cues and suffering from limitations such as batch-to-batch variability, low stability, and low throughput. Organ-on-a-chip platforms, by contrast, utilize microfluidic technologies to simulate the dynamic physiological microenvironment of human tissues and organs, enabling more controlled cell growth and differentiation. By integrating the advantages of organoids and organ-on-a-chip technologies, organoid-on-a-chip systems transcend the limitations of conventional 3D culture models, offering a more physiologically relevant and controllable in vitro platform. In organoid-on-a-chip systems, stem cells or pre-formed organoids are cultured in micro-engineered environments that mimic in vivo conditions, enabling precise control over fluid flow, mechanical forces, and biochemical cues. Specifically, these platforms employ advanced strategies including bio-inspired 3D scaffolds for structural support, precise spatial cell patterning via 3D bioprinting, and integrated biosensors for real-time monitoring of metabolic activities. These synergistic elements recreate complex extracellular matrix signals and ensure high structural fidelity. Based on structural complexity, organoid-on-a-chip systems are classified into single-organoid and multi-organoid types, forming a trajectory from unit biomimicry to systemic simulation. Single-organoid chips focus on highly biomimetic units by integrating vascular, immune, or neural functions. Multi-organoid chips simulate inter-organ crosstalk and systemic homeostasis, advancing complex disease modeling and PK/PD evaluation. This emerging technology has demonstrated broad application potential in multiple fields of biomedicine. Organoid-on-a-chip systems can recapitulate organ developmentin vitro, facilitating research in developmental biology. They mimic organ-specific physiological activities and mechanisms, showing promising applications in regenerative medicine for tissue repair or replacement. In disease modeling, they support the reconstruction of models for neurodegenerative, inflammatory, infectious, metabolic diseases, and cancers. These platforms also enable in vitro drug testing and pharmacokinetic studies (ADME). Patient-derived chips preserve genetic and pathological features, offering potential for precision medicine. Additionally, they reduce species differences in toxicology, providing human-relevant data for environmental, food, cosmetic, and drug safety assessments. Despite progress, organoid-on-a-chip systems face challenges in dynamic simulation, extracellular matrix (ECM) variability, and limited real-time 3D imaging, requiring improved materials and the integration of developmental signals. Current bottlenecks also include the high technical threshold for automation and the lack of standardized validation frameworks for regulatory adoption. Meanwhile, the concept of a “human-on-a-chip” has been proposed to mimic whole-body physiology by integrating multiple organoid modules. This approach enables systemic modeling of drug responses and toxicity, with the potential to reduce animal testing and revolutionize drug development. Future advancements in bio-responsive hydrogels and flexible biosensors will further empower these platforms to bridge the gap between bench-side research and personalized clinical interventions. In conclusion, organoid-on-a-chip technology offers a transformative in vitro model that closely recapitulates the complexity of human tissues and organ systems. It provides an unprecedented platform for advancing biomedical research, clinical translation, and pharmaceutical innovation. Continued development in biomaterials, microengineering, and analytical technologies will be essential to unlocking the full potential of this powerful tool.