ObjectiveAge-related macular degeneration （AMD） is one of the leading causes of low vision and blindness in people over 50 years old， and dry AMD （dAMD） is one type for which there is currently no clear treatment. On the basis of the diagnosis and clinical characteristics of dAMD in traditional Chinese and Western medicine， this paper evaluated the fitting degrees of existing animal models of dAMD with clinical characteristics according to the evaluation methods of animal models， and put forward suggestions and prospects. MethodsLiterature on animal models of dAMD was searched against database， and the characteristics of the models were assigned according to the diagnosis criteria of diseases and syndromes of traditional Chinese and Western medicine， and the fitting degrees of the models with clinical characteristics were analyzed and evaluated. ResultsAt present， the animal models of dAMD are mainly established targeting complement factors， chemokines， oxidative damage， lipid/glucose metabolism， and natural strains. Most of the models can simulate the major pathological changes of dAMD， showing the fitting degree of 25%-50% with clinical characteristics in Western medicine. However， the evaluation of traditional Chinese medicine （TCM） syndromes， especially the evaluation of secondary syndromes， is missing， and the models present low fitting degrees with the clinical characteristics in TCM. ConclusionExisting animal models of dAMD are mostly established under the guidance of Western diagnostic standards， which reproduce the main disease characteristics of Western medicine and lack observation of TCM syndromes. Future studies can pay attention to the intervention factors and evaluation systems of spleen deficiency Qi deficiency and liver-kidney Yin deficiency syndrome and build the animal model of dAMD with integration of disease and syndrome based on clinical characteristics of traditional Chinese and Western medicine.

ObjectiveAge-related macular degeneration （AMD） is one of the leading causes of low vision and blindness in people over 50 years old， and dry AMD （dAMD） is one type for which there is currently no clear treatment. On the basis of the diagnosis and clinical characteristics of dAMD in traditional Chinese and Western medicine， this paper evaluated the fitting degrees of existing animal models of dAMD with clinical characteristics according to the evaluation methods of animal models， and put forward suggestions and prospects. MethodsLiterature on animal models of dAMD was searched against database， and the characteristics of the models were assigned according to the diagnosis criteria of diseases and syndromes of traditional Chinese and Western medicine， and the fitting degrees of the models with clinical characteristics were analyzed and evaluated. ResultsAt present， the animal models of dAMD are mainly established targeting complement factors， chemokines， oxidative damage， lipid/glucose metabolism， and natural strains. Most of the models can simulate the major pathological changes of dAMD， showing the fitting degree of 25%-50% with clinical characteristics in Western medicine. However， the evaluation of traditional Chinese medicine （TCM） syndromes， especially the evaluation of secondary syndromes， is missing， and the models present low fitting degrees with the clinical characteristics in TCM. ConclusionExisting animal models of dAMD are mostly established under the guidance of Western diagnostic standards， which reproduce the main disease characteristics of Western medicine and lack observation of TCM syndromes. Future studies can pay attention to the intervention factors and evaluation systems of spleen deficiency Qi deficiency and liver-kidney Yin deficiency syndrome and build the animal model of dAMD with integration of disease and syndrome based on clinical characteristics of traditional Chinese and Western medicine.

ObjectiveTo examine the influences of Shenfu injection on the endogenous metabolic byproducts in the myocardium of the rat model exhibiting chronic heart failure， thus deciphering the therapeutic mechanism of the Qi-reinforcing and Yang-warming method. MethodsSD rats were randomly allocated into a control group and a modeling group. Chronic heart failure with heart-Yang deficiency syndrome in rats was modeled by multi-point subcutaneous injection of isoproterenol， and the rats were fed for 14 days after modeling. The successfully modeled rats were randomized into model， Shenfu injection （6.0 mL·kg^-1）， and trimetazidine （10 mg·kg^-1） groups and treated with corresponding agents for 15 days. The control group and the model group were injected with equal doses of normal saline， and the samples were collected after the intervention was completed. Cardiac color ultrasound was performed. Hematoxylin-eosin （HE） staining was used to observe histopathological morphology， and the serum level of N-terminal pro-brain natriuretic peptide （NT-proBNP） was assessed by enzyme-linked immunosorbent assay （ELISA）. The mitochondrial morphological and structural changes of cardiomyocytes were observed by transmission electron microscopy， and the metabolic profiling was carried out by ultra high performance liquid chromatography-quantitative exactive-mass spectrometry （UHPLC-QE-MS）. Differential metabolites were screened and identified by orthogonal partial least squares-discriminant analysis （OPLS-DA） and other methods， and then the MetaboAnalyst database was used for further screening. The relevant biological pathways were obtained through pathway enrichment analysis. The receiver operating characteristic （ROC） curve was established to evaluate the diagnostic value of each potential biomarker for myocardial injury and the evaluation value for drug efficacy. ResultsThe results of color ultrasound showed that Shenfu Injection improved the cardiac function indexes of model rats （P<0.05）. The results of HE staining showed that Shenfu injection effectively alleviated the pathological phenomena such as myocardial tissue structure disorder and inflammatory cell infiltration in model rats. The results of ELISA showed that Shenfu injection effectively regulated the serum NT-proBNP level in the model rats. Transmission electron microscopy （TEM） showed that Shenfu injection effectively restored the mitochondrial morphological structure. The results of metabolomics showed that the metabolic phenotypes of myocardial samples presented markedly differences between groups. Nine differential metabolites could be significantly reversed in the Shenfu injection group， involving three metabolic pathways： pyruvate metabolism， histidine metabolism， and citric acid cycle （TCA cycle）. The results of ROC analysis showed that the area under the curve （AUC） values of all metabolites were between 0.75 and 1.0， indicating that the differential metabolites had high diagnostic accuracy for myocardial injury， and the changes in their expression levels could be used as potential markers for efficacy evaluation. ConclusionShenfu injection significantly alleviated the damage of cardiac function， myocardium， and mitochondrial structure in the rat model of chronic heart failure with heart-Yang deficiency syndrome by ameliorating energy metabolism remodeling. Reinforcing Qi and warming Yang is a key method for treating chronic heart failure with heart-Yang deficiency syndrome.

Abstract The prevention and control of myopia in Chinese children and adolescents has become a major public health issue. While maintaining increased outdoor activity as a cornerstone intervention, there is an urgent need to explore new complementary approaches that can be effectively implemented in both indoor and outdoor settings. In recent years, environmental spatial frequency has gained increasing attention as one of the key environmental factors influencing the development and progression of myopia. Both animal studies and human research have confirmed that indoor environments lacking mid to high spatial frequency components, often characterized as "visually impoverished", can promote axial elongation and myopia through mechanisms such as disruption of retinal neural signaling, impaired accommodative function, and altered expression of related molecules. Based on the scientific consensus, it is recommended that "enriching of environmental spatial frequency" should be integrated into the myopia prevention and control framework. Following the principles of schoolled organization, family cooperation, community involvement, and student participation, specific measures are put forward in three areas：optimizing school visual settings, improving home spatial environments, and promoting healthy visual behavior. The aim is to create "visually friendly" indoor environments as an important supplement to outdoor activity, thereby providing a novel perspective and strategy for comprehensively advancing myopia prevention and control among children and adolescents.

ObjectiveTo observe the influence and therapeutic effect of quercetin on cuproptosis in rheumatoid arthritis rats and to explore its possible mechanism based on the solute carrier family 31 member 1 （SLC31A1）/ferredoxin 1 （FDX1） pathway. MethodsSixty male SD rats were divided into six groups： A control group， a model group， high- and low-dose quercetin groups （150 and 50 mg·kg^-1）， a cuproptosis inhibitor （tetrathiomolybdate， TTM） group （10 mg·kg^-1）， and a methotrexate group （2 mg·kg^-1）， 10 rats in each group. Except for the control group， the model of rheumatoid arthritis （CIA） rats was established by type Ⅱ collagen induction method. After successful modeling， each drug group was intervened according to the corresponding dose of drugs， and the control group and the model group were given the same amount of normal saline by gavage， once a day， which lasted for 4 weeks. The swelling degree of rats' feet was observed， and the clinical arthritis scores were determined. The levels of serum rheumatoid factor （RF）， matrix metalloproteinase-3 （MMP-3）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-10 （IL-10）， and ceruloplasmin （Cp） were detected by enzyme-linked immunosorbent assay （ELISA）. The content of copper ion （Cu）， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） in joint tissue was detected. Hematoxylin-eosin （HE） staining was used to observe the pathological changes of joint tissue. The levels of reactive oxygen species （ROS） and dihydrolipoic acid transacetylase （DLAT） were detected by immunofluorescence （IF）. The protein and mRNA expression of SLC31A1， FDX1， lipoic acid synthase （LIAS）， heat shock protein 70 （HSP70）， pyruvate dehydrogenase E1 subunit β （PDHB）， and copper transporting P-type ATPase β （ATP7B） was detected by immunohistochemistry （IHC） and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared to the control group， the model group exhibited joint swelling and deformity， significantly increased clinical arthritis scores， obvious bone destruction， synovial hyperplasia， and inflammatory cell infiltration in joint tissue. In addition， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp showed significant elevation， while the level of IL-10 was significantly reduced. The levels of Cu， MDA， ROS， and DLAT in joint tissue were markedly increased， whereas SOD and GSH content was significantly decreased. The protein and mRNA expression of SLC31A1 and HSP70 was significantly up-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was significantly down-regulated （P<0.01）. Compared to the model group， each treatment group exhibited varying degrees of improvement in joint swelling and deformation as well as clinical arthritis scores in rats. Additionally， there was a reduction in joint bone destruction， inflammatory cell infiltration， and synovial hyperplasia in rats. Furthermore， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp significantly decreased， while the level of IL-10 increased significantly. In joint tissue， the levels of Cu， MDA， ROS， and DLAT showed significant decreases， while SOD and GSH content exhibited significant increases. The protein and mRNA expression of SLC31A1 and HSP70 was down-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was up-regulated （P<0.05）. ConclusionQuercetin effectively reduces synovial hyperplasia and inflammatory infiltration in rats with rheumatoid arthritis， thereby alleviating pathological damage to joint tissue. This effect may be attributed to the blockade of the SLC31A1/FDX1 signaling pathway activation and inhibition of excessive cuproptosis.

ObjectiveTo investigate the effects of Yiqi Wenyang Huoxue Lishui components on the cardiac function and mitochondrial energy metabolism in the rat model of chronic heart failure （CHF） and explore the underlying mechanism. MethodsThe rat model of CHF was prepared by transverse aortic constriction （TAC）. Eight of the 50 SD rats were randomly selected as the sham group， and the remaining 42 underwent TAC surgery. The 24 SD rats successfully modeled were randomized into model， trimetazidine （6.3 mg·kg^-1）， and Yiqi Wenyang Huoxue Lishui components （60 mg·kg^-1 total saponins of Astragali Radix， 10 mg·kg^-1 total phenolic acids of Salviae Miltiorrhizae Radix et Rhizoma， 190 mg·kg^-1 aqueous extract of Lepidii Semen， and 100 mg·kg^-1 cinnamaldehyde） groups. The rats were administrated with corresponding agents by gavage， and those in the sham and model groups were administrated with the same amount of normal saline at a dose of 10 mL·kg^-1 for 8 weeks. Echocardiography was used to examine the cardiac function in rats. Enzyme-linked immunosorbent assay was employed to determine the serum levels of N-terminal pro-B-type natriuretic peptide （NT-ProBNP）， hypersensitive troponin（cTnI）， creatine kinase （CK）， lactate dehydrogenase （LD）， free fatty acids （FFA）， superoxide dismutase （SOD）， and malondialdehyde （MDA）. The colorimetric assay was employed to measure the levels of adenosine triphosphate （ATP）， adenosine diphosphate （ADP）， and adenosine monophosphate （AMP） in the myocardial tissue. The pathological changes in the myocardial tissue were observed by hematoxylin-eosin staining and Masson staining. The Na⁺-K⁺-ATPase and Ca²⁺-Mg²⁺-ATPase activities in the myocardial tissue were determined by the colorimetric assay. The ultrastructural changes of myocardial mitochondria were observed by transmission electron microscopy. Western blot was employed to determine the protein levels of ATP synthase subunit delta （ATP5D）， glucose transporter 4 （GLUT4）， and carnitine palmitoyltransferase-1 （CPT-1）. The mitochondrial complex assay kits were used to determine the activities of mitochondrial complexes Ⅰ， Ⅱ， Ⅲ， and Ⅳ. ResultsCompared with the sham group， the model group showed a loosening arrangement of cardiac fibers， fracture and necrosis of partial cardiac fibers， inflammatory cells in necrotic areas， massive blue fibrotic tissue in the myocardial interstitium， increased collagen fiber area and myocardial fibrosis， destroyed mitochondria， myofibril disarrangement， sparse myofilaments， and fractured and reduced cristae. In addition， the rats in the model group showed declined ejection fraction （EF） and fractional shortening （FS）， risen left ventricular end-diastolic diameter （LVIDd）， left ventricular end-systolic diameter （LVIDs）， left ventricular end-diastolic posterior wall thickness （LVPWd）， left ventricular end-systolic posterior wall thickness （LVPWs）， left ventricular end-diastolic volume （LVVOLd）， and left ventricular end-systolic volume （LVVOLs）， elevated levels of NT-ProBNP， cTnI， CK， MDA， FFA， and LD， lowered level of SOD， down-regulated protein levels of GLUT4 and CPT-1， decreased activities of Na⁺-K⁺-ATPase， Ca²⁺-Mg²⁺-ATPase， and respiratory complexes Ⅰ-Ⅳ， and declined levels of ATP5D， ATP， ADP， and AMP （P<0.05， P<0.01）. Compared with the model group， the Yiqi Wenyang Huoxue Lishui components and trimetazidine groups showed alleviated pathological damage of the mitochondria and mycardial tissue， risen EF and FS， declined LVIDd， LVIDs， LVPWd， LVPWs， LVVOLd， and LVVOLs， lowered levels of NT-ProBNP， cTnI， CK， MDA， FFA， and LD， elevated level of SOD， up-regulated protein levels of GLUT4 and CPT-1， increased activities of Na⁺-K⁺-ATPase， Ca²⁺-Mg²⁺-ATPase， and respiratory complexes Ⅰ-Ⅳ， and elevated levels of ATP5D， ATP， ADP， and AMP （P<0.05， P<0.01）. ConclusionYiqi Wenyang Huoxue Lishui components can improve the cardiac function， reduce myocardial injury， regulate glucose and lipid metabolism， optimize the utilization of substrates， and alleviate the damage of mitochondrial structure and function， thus improving the energy metabolism of the myocardium in the rat model of CHF.

Chronic heart failure （CHF） is the final stage of cardiovascular diseases. It is a complex syndrome， with dyspnea and edema as the main clinical manifestations， and it is characterized by complex disease conditions， difficult cure， and high mortality. Ferroptosis， a new type of programmed cell death， is different from other types of programmed cell death. Ferroptosis is iron-dependent， accompanied by lipid peroxide accumulation and mitochondrial shrinkage， becoming a hot research topic. Studies have confirmed that ferroptosis plays a key role in the occurrence and development of CHF. The regulation of ferroptosis may become a potential target for the treatment of CHF in the future. The theory of Qi deficiency and stagnation refers to the pathological state of original Qi deficiency and abnormal transportation and distribution of Qi， blood， and body fluid， which has guiding significance for revealing the pathogenesis evolution of some chronic diseases. We believe that Qi deficiency and stagnation is a summary of the pathogenesis of ferroptosis in CHF. Deficiency of Qi （heart Qi） is the root cause of CHF， and stagnation （phlegm turbidity and blood stasis） is the branch of this disease. The two influence each other in a vicious circle to promote the development of this disease. Traditional Chinese medicine （TCM） plays an important role in the treatment of CHF， improving the prognosis and quality of life of CHF patients. This paper explores the correlation between the theory of Qi deficiency and stagnation and the mechanism of ferroptosis in CHF. Furthermore， this paper reviews the mechanism of Chinese medicines and compound prescriptions in preventing and treating CHF by regulating ferroptosis according to the principles of replenishing Qi and dredging to remove stagnation， aiming to provide new ideas and methods for the treatment of CHF with TCM.

Objective To develop an artificial intelligence (AI)-driven lung cancer database by structuring and standardizing clinical data, enabling advanced data mining for lung cancer research, and providing high-quality data for real-world studies. Methods Building on the extensive clinical data resources of the Department of Thoracic Surgery at Peking Union Medical College Hospital, this study utilized machine learning techniques, particularly natural language processing (NLP), to automatically process unstructured data from electronic medical records, examination reports, and pathology reports, converting them into structured formats. Data governance and automated cleaning methods were employed to ensure data integrity and consistency. Results As of September 2024, the database included comprehensive data from 18 811 patients, encompassing inpatient and outpatient records, examination and pathology reports, physician orders, and follow-up information, creating a well-structured, multi-dimensional dataset with rich variables. The database’s real-time querying and multi-layer filtering functions enabled researchers to efficiently retrieve study data that meet specific criteria, significantly enhancing data processing speed and advancing research progress. In a real-world application exploring the prognosis of non-small cell lung cancer, the database facilitated the rapid analysis of prognostic factors. Research findings indicated that factors such as tumor staging and comorbidities had a significant impact on patient survival rates, further demonstrating the database’s value in clinical big data mining. Conclusion The AI-driven lung cancer database enhances data management and analysis efficiency, providing strong support for large-scale clinical research, retrospective studies, and disease management. With the ongoing integration of large language models and multi-modal data, the database’s precision and analytical capabilities are expected to improve further, providing stronger support for big data mining and real-world research of lung cancer.

A 71-year-old male presented with esophageal cancer and severe aortic valve regurgitation. Treatment strategies for such patients are controversial. Considering the risks of cardiopulmonary bypass and potential esophageal cancer metastasis, we successfully performed transcatheter aortic valve implantation and minimally invasive three-incision thoracolaparoscopy combined with radical resection of esophageal cancer (McKeown) simultaneously in the elderly patient who did not require neoadjuvant treatment. This dual minimally invasive procedure took 6 hours and the patient recovered smoothly without any surgical complications.

ObjectiveTo investigate vitamin D level in children with cholestatic liver disease， and to provide a theoretical basis for vitamin D supplementation therapy in children with this disease. MethodsA total of 116 children with cholestatic liver disease who attended Department of Traditional Chinese Medicine， Beijing Children’s Hospital， Capital Medical University， for the first time from January 2022 to January 2024 were enrolled and divided into groups for comparison based on sex， age， vitamin D supplementation dose， course of the disease， and etiology. The data on the serum level of 25-hydroxyvitamin D （25-OH-D） and related biochemical parameters were collected to assess the correlation between vitamin D level and biochemical parameters. The chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups， and the Spearman rank correlation test was used for correlation analysis. ResultsAmong the 116 children， 76 （65.5%） had vitamin D deficiency or insufficiency. The children with vitamin D deficiency or insufficiency accounted for 65.7% （46/70） among boys and 65.2% （30/46） among girls， with no significant difference between boys and girls （χ²=0.003， P=0.956）. The children with vitamin D deficiency or insufficiency accounted for 83.3% （25/30） among the children who had never received vitamin D supplementation， 58.7% （27/46） among the children with a daily supplementation dose of 500 IU， 64.3% （18/28） among the children with a daily supplementation dose of 700 IU， and 50.0% （6/12） among the children with a daily supplementation dose of>700 IU， and there was no significant difference between these groups （χ²=6.460， P=0.091）. Comparison between the groups with different etiologies showed that the children with vitamin D deficiency or insufficiency accounted for 57.7% （15/26） in the infectious disease group， 66.7% （10/15） in the inherited metabolic disease group， 66.7% （6/9） in the drug-induced liver injury group， 100.0% （8/8） in the group with abnormal structure of the biliary system， and 63.8% （37/58） in the group with unknown etiology， and there was no significant difference between these groups （χ²=5.304， P=0.252）. Comparison between the groups with different courses of the disease showed that the children with vitamin D deficiency or insufficiency accounted for 78.4% （29/37） in the<1 month group， 54.3% （25/46） in the 1‍ — ‍3 months group， 53.3% （8/15） in the 3‍ — ‍6 months group， and 77.8% （14/18） in the>6 months group， with no significant difference between these groups （χ²=7.432， P=0.059）. Comparison between different age groups showed that compared with the infant group， the children group had a significantly higher proportion of children with vitamin D deficiency or insufficiency （χ²=9.504， P=0.018）. The correlation analysis showed that serum aspartate aminotransferase and alanine aminotransferase had no significant correlation with 25-OH-D （P>0.05）； serum alkaline phosphatase （ALP） （r=-0.286， P=0.002）， gamma-glutamyl transpeptidase （GGT） （r=-0.248， P=0.007）， total bilirubin （TBil） （r=-0.353， P<0.001）， direct bilirubin （DBil） （r=-0.299， P=0.001）， and total bile acid （r=-0.236， P=0.011） were negatively correlated with 25-OH-D， while serum calcium （r=0.263， P=0.004） and phosphorus （r=0.385， P<0.001） were positively correlated with 25-OH-D. ConclusionMost children with cholestatic liver disease have vitamin D deficiency or insufficiency， and the increase in serum ALP， GGT， TBil， DBil or total bile acid and the reduction in calcium or phosphorus may suggest vitamin D deficiency or insufficiency.