OBJECTIVE To study the quality standard of the ethnic medicine Diplazium lanceum， and to provide reference for its quality control.METHODS The medicinal material of D. lanceum was identified by properties， microscopy， and thin-layer chromatography（TLC）， and its moisture， ash， and extract contents were determined. The contents of chlorogenic acid and rutin in 10 batches of D. lanceum were determined by high-performance liquid chromatography . RESULTS The rhizome of D. lanceum is slender and creeping， the leaf is leathery and shriveled， and yellow sporangia are borne on the abaxial surface of the leaf. The transverse section of the leaf shows inclusions， sclerenchyma， phloem cells， etc.； the transverse section of the petiole shows ground tissue， sclerenchyma， endodermis， etc.； the transverse section of the rhizome shows ground tissue， tracheids， vascular bundles， etc.； and the powder shows spiral vessels and brown inclusions. The TLC identification results showed that the chromatogram of the test sample exhibited spots of the same color at the corresponding positions as the chromatogram of the chlorogenic acid reference substance. The content ranges of moisture， total ash， acid-insoluble ash， extract， chlorogenic acid， and rutin in the 10 batches of samples were 10.18%-12.43%， 7.08%-19.12%， 0.95%-10.62%， 14.13%-26.05%， 0.113 1-1.015 9 mg/g， and 0.009 9-0.208 9 mg/g， respectively. CONCLUSIONS In the quality standard of D. lanceum， the moisture content should be ≤12.5%， total ash content should be ≤20.0%， acid-insoluble ash content should be ≤11.0%， extract content should be ≥14.0%， and chlorogenic acid content should be ≥0.11 mg/g. The established method is simple， specific， and reproducible， and can provide a scientific basis for the quality control of D. lanceum.

ObjectiveThis study aimed to investigate the mechanism by which Luoshi Neiyi prescription treats endometriosis （EMs） through regulating ferroptosis， and to screen key metabolites and analyze their association with ferroptosis. MethodsClinical samples of normal endometrium from patients without EMs and eutopic and ectopic endometrium from EMs patients （10 cases each） were collected and divided into control group， eutopic group， and EMs group. Hematoxylin-eosin （HE） staining was performed to observe ectopic lesions of EMs. Immunohistochemistry was used to detect the expression of solute carrier family 7 member 11 （SLC7A11） and glutathione peroxidase 4 （GPX4）. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of malondialdehyde （MDA）， ferrous ion （Fe²⁺）， GPX4 and glutathione （GSH） in endometrial tissues， as well as serum levels of Fe²⁺， GPX4 and GSH. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of SLC7A11， GPX4， transferrin receptor （TFR） and ferritin heavy chain 1 （FTH1）. In the in vitro experiment， primary stromal cells were isolated from ectopic lesions of EMs patients. Cell counting kit-8 （CCK-8） was used to determine the optimal concentration of drug-containing serum for intervention. The level of reactive oxygen species （ROS） was measured， and Real-time PCR was applied to detect ferroptosis-related indicators. In the animal experiments， an EM rat model was established， and the rats were randomly assigned to the sham operation group， EMs group， low-dose Luoshi Neiyi Formula group （7.87 g·kg^-1）， high-dose Luoshi Neiyi prescription group （15.74 g·kg^-1）， and danazol group （42 mg·kg^-1）. Untargeted metabolomics detection and pathway enrichment analysis were conducted on serum samples from patients and rats. Spearman correlation analysis was performed to assess the relationship between differential metabolites and ferroptosis indicators. The correlations between differential metabolites in patient endometrium and serum and key ferroptosis indicators （GPX4， Fe²⁺， MDA， GSH） as well as ferroptosis-related mRNAs （GPX4， SLC7A11， FTH1） were analyzed， and correlation heatmaps were generated accordingly. ResultsCompared with normal eutopic endometrium， ectopic lesions in EMs patients showed glandular disorganization and stromal fibrosis. In ectopic endometrium， the contents of MDA， ROS， and Fe²⁺ decreased， while GPX4 level increased， and the mRNA expression of SLC7A11 and GPX4 was upregulated （P<0.05， P<0.01）. In serum， the levels of GPX4 and Fe²⁺ were elevated， whereas the GSH level declined， suggesting abnormalities in ferroptosis-related pathways in ectopic lesions （P<0.05， P<0.01）. After intervention with Luoshi Neiyi prescription-containing serum， the intracellular ROS level in ectopic endometrial stromal cells was elevated， the mRNA expression of SLC7A11 and GPX4 was downregulated， and TFR mRNA expression was upregulated （P<0.05， P<0.01）. Metabolomics analysis revealed 1104 and 198 differential metabolites in EMs patients and EMs rats， respectively， compared with their corresponding control groups， and both low-dose and high-dose Luoshi Neiyi prescription were found to regulate this metabolic disturbance， with the core regulatory pathways mainly involving arginine and proline metabolism. Correlation analysis showed that the glycerophospholipids including PI（16∶0/17∶0） and PI［18∶2（9Z，12Z）］ were negatively correlated with GPX4 and positively correlated with MDA， while 17α-hydroxyprogesterone was positively correlated with GPX4， SLC7A11， and FTH1 q<0.05）. ConclusionLuoshi Neiyi prescription may systematically ameliorate disease-associated metabolic dysregulation via modulation of the serum arginine and proline metabolism pathway， and may regulate ferroptosis in ectopic lesions through a mechanism potentially linked to the serum glycerophospholipid and steroid metabolism pathways. Collectively， these findings provide experimental evidence for the clinical application of Luoshi Neiyi prescription.

ObjectiveThis study aimed to investigate the mechanism by which Luoshi Neiyi prescription treats endometriosis （EMs） through regulating ferroptosis， and to screen key metabolites and analyze their association with ferroptosis. MethodsClinical samples of normal endometrium from patients without EMs and eutopic and ectopic endometrium from EMs patients （10 cases each） were collected and divided into control group， eutopic group， and EMs group. Hematoxylin-eosin （HE） staining was performed to observe ectopic lesions of EMs. Immunohistochemistry was used to detect the expression of solute carrier family 7 member 11 （SLC7A11） and glutathione peroxidase 4 （GPX4）. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of malondialdehyde （MDA）， ferrous ion （Fe²⁺）， GPX4 and glutathione （GSH） in endometrial tissues， as well as serum levels of Fe²⁺， GPX4 and GSH. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of SLC7A11， GPX4， transferrin receptor （TFR） and ferritin heavy chain 1 （FTH1）. In the in vitro experiment， primary stromal cells were isolated from ectopic lesions of EMs patients. Cell counting kit-8 （CCK-8） was used to determine the optimal concentration of drug-containing serum for intervention. The level of reactive oxygen species （ROS） was measured， and Real-time PCR was applied to detect ferroptosis-related indicators. In the animal experiments， an EM rat model was established， and the rats were randomly assigned to the sham operation group， EMs group， low-dose Luoshi Neiyi Formula group （7.87 g·kg^-1）， high-dose Luoshi Neiyi prescription group （15.74 g·kg^-1）， and danazol group （42 mg·kg^-1）. Untargeted metabolomics detection and pathway enrichment analysis were conducted on serum samples from patients and rats. Spearman correlation analysis was performed to assess the relationship between differential metabolites and ferroptosis indicators. The correlations between differential metabolites in patient endometrium and serum and key ferroptosis indicators （GPX4， Fe²⁺， MDA， GSH） as well as ferroptosis-related mRNAs （GPX4， SLC7A11， FTH1） were analyzed， and correlation heatmaps were generated accordingly. ResultsCompared with normal eutopic endometrium， ectopic lesions in EMs patients showed glandular disorganization and stromal fibrosis. In ectopic endometrium， the contents of MDA， ROS， and Fe²⁺ decreased， while GPX4 level increased， and the mRNA expression of SLC7A11 and GPX4 was upregulated （P<0.05， P<0.01）. In serum， the levels of GPX4 and Fe²⁺ were elevated， whereas the GSH level declined， suggesting abnormalities in ferroptosis-related pathways in ectopic lesions （P<0.05， P<0.01）. After intervention with Luoshi Neiyi prescription-containing serum， the intracellular ROS level in ectopic endometrial stromal cells was elevated， the mRNA expression of SLC7A11 and GPX4 was downregulated， and TFR mRNA expression was upregulated （P<0.05， P<0.01）. Metabolomics analysis revealed 1104 and 198 differential metabolites in EMs patients and EMs rats， respectively， compared with their corresponding control groups， and both low-dose and high-dose Luoshi Neiyi prescription were found to regulate this metabolic disturbance， with the core regulatory pathways mainly involving arginine and proline metabolism. Correlation analysis showed that the glycerophospholipids including PI（16∶0/17∶0） and PI［18∶2（9Z，12Z）］ were negatively correlated with GPX4 and positively correlated with MDA， while 17α-hydroxyprogesterone was positively correlated with GPX4， SLC7A11， and FTH1 q<0.05）. ConclusionLuoshi Neiyi prescription may systematically ameliorate disease-associated metabolic dysregulation via modulation of the serum arginine and proline metabolism pathway， and may regulate ferroptosis in ectopic lesions through a mechanism potentially linked to the serum glycerophospholipid and steroid metabolism pathways. Collectively， these findings provide experimental evidence for the clinical application of Luoshi Neiyi prescription.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

China has become the country with the highest global burden of heart failure(HF).Despite the widespread use of prognostic-improving medications today,the mortality rate of HF remains high,reaching 13.7％at one year-particularly among patients with heart failure with reduced ejection fraction(HFrEF).HF interventional device therapy(structural intervention)targets the structural factors underlying HF,including atrial pressure,ventricular remodeling,and valvular intervention.It leverages the heart's intrinsic physiological properties and pathological progression mechanisms to deliver treatments through interventions without external active forces,achieving anatomical or functional repair.This field has emerged as a rapidly growing area and plays an increasingly critical role in HF management.This article provides a comprehensive review and summary of the latest advancements in HF and cardiomyopathy interventional therapy over the past year.It covers various novel technologies and products currently in the research phase,aiming to provide an in-depth analysis of the current status and future directions of HF interventional therapy,and further advance the development of this discipline.

BACKGROUND:Studies have found that inhibition of tumor necrosis factor receptor-associated factor 6 improves myocardial function and promotes myocardial autophagy in sepsis,but the specific mechanism is not clear.OBJECTIVE:To explore the effect of inhibiting tumor necrosis factor receptor-associated factor 6-regulated mTORC1/ULK1 autophagy signaling pathway on myocardial injury in sepsis mice.METHODS:Thirty male Kunming mice were randomly divided into sham operation group,cecal ligation and puncture group(model group),model+tumor necrosis factor receptor-associated factor 6 specific inhibitor C25-140(model+C)group,model+C25-140+autophagy inhibitor 3-methyladenine(model+C+3-MA)group,and model+C25-140+mTORC1-specific agonist MHY1485(model+C+M)group.The cecum of mice in the sham operation group was not ligated or punctured.The mice in the other groups underwent cecum ligation and puncture to establish the mouse sepsis model.C25-140,3-methyladenine,and MHY1485 were intraperitoneally injected 0.5 hours after surgery according to the grouping.Myocardial tissue was obtained 24 hours after surgery.Hematoxylin-eosin staining was used to evaluate myocardial inflammatory lesions.Transmission electron microscopy was used to observe the changes in the autophagic bodies and mitochondrial microstructures of myocardial cells.TUNEL assay was used to detect myocardial cell apoptosis.PCR was used to detect the relative expression of tumor necrosis factor receptor-associated factor 6 mRNA.Western blot assay was used to detect the expression of related proteins.RESULTS AND CONCLUSION:(1)Compared with sham operation group,myocardial inflammatory cell infiltration and fibrous edema were observed in the model group.The mitochondria of the cells were obviously swollen,and autophagosomes were occasionally seen;cardiomyocyte apoptosis increased significantly;the expression of tumor necrosis factor receptor-associated factor 6,phosphorylated nuclear factor κB P65/P65,p-mTOR/mTOR,p-ULK1/ULK1,P62 and Bax protein increased,and the expression of Bcl2 protein decreased(P＜0.05).(2)Compared with the model group,myocardial inflammation and fibrous edema were alleviated in the model+C group.Myocardial mitochondrial swelling was reduced and autophagosomes increased;cardiomyocyte apoptosis decreased;the expression of phosphorylated nuclear factor κB P65/nuclear factor-κB P65,p-mTOR/mTOR,p-ULK1/ULK1,P62,and Bax protein decreased,while the Beclin-1 and Bcl2 protein increased(P＜0.05).(3)Compared with the model+C group,myocardial autophagosomes decreased and myocardial mitochondrial swelling was more obvious in the model+C+3-MA group.Myocardial inflammation was aggravated;myocardial cell apoptosis increased;the expression of phosphorylated nuclear factor κB P65/nuclear factor κB P65,P62,and Bax protein increased,and the Beclin-1 and Bcl2 protein decreased(P＜0.05).(4)Compared with the model+C group,the expression of p-mTOR/mTOR and p-ULK1/ULK1 in the model+C+M group increased,and the Beclin-1 and microtubule-associated protein 1 light chain 3 Ⅱ/Ⅰ protein expression decreased(P＜0.05).It is concluded that inhibition of tumor necrosis factor receptor-associated factor 6 regulates mTORC1/ULK1 autophagy signal to promote myocardial autophagy and participate in the protection of myocardial injury in sepsis.

China has become the country with the highest global burden of heart failure(HF).Despite the widespread use of prognostic-improving medications today,the mortality rate of HF remains high,reaching 13.7％at one year-particularly among patients with heart failure with reduced ejection fraction(HFrEF).HF interventional device therapy(structural intervention)targets the structural factors underlying HF,including atrial pressure,ventricular remodeling,and valvular intervention.It leverages the heart's intrinsic physiological properties and pathological progression mechanisms to deliver treatments through interventions without external active forces,achieving anatomical or functional repair.This field has emerged as a rapidly growing area and plays an increasingly critical role in HF management.This article provides a comprehensive review and summary of the latest advancements in HF and cardiomyopathy interventional therapy over the past year.It covers various novel technologies and products currently in the research phase,aiming to provide an in-depth analysis of the current status and future directions of HF interventional therapy,and further advance the development of this discipline.

Juvenile idiopathic arthritis(JIA)is the most prevalent joint disease in childhood.The disease is defined as arthritis of unknown etiology,involving one or more joints,with onset before the age of 16 years and symptomatic duration of more than 6 weeks.Temporomandibular joint(TMJ)arthritis is a common manifestation of JIA,but it often develops insidiously.Failing to diag-nose and treat it promptly may lead to maxillofacial dysfunction and dentofacial deformity,and negatively affect the patient's quality of life.Therefore,early diagnosis and disease management of TMJ arthritis are crucial.This article reviews the occurrence of JIA-TMJ arthritis and its progress in clinical diagnosis and disease treatment in recent years,aiming to provide some reference for den-tists in the clinical diagnosis and treatment of JIA.

BACKGROUND:Studies have found that inhibition of tumor necrosis factor receptor-associated factor 6 improves myocardial function and promotes myocardial autophagy in sepsis,but the specific mechanism is not clear.OBJECTIVE:To explore the effect of inhibiting tumor necrosis factor receptor-associated factor 6-regulated mTORC1/ULK1 autophagy signaling pathway on myocardial injury in sepsis mice.METHODS:Thirty male Kunming mice were randomly divided into sham operation group,cecal ligation and puncture group(model group),model+tumor necrosis factor receptor-associated factor 6 specific inhibitor C25-140(model+C)group,model+C25-140+autophagy inhibitor 3-methyladenine(model+C+3-MA)group,and model+C25-140+mTORC1-specific agonist MHY1485(model+C+M)group.The cecum of mice in the sham operation group was not ligated or punctured.The mice in the other groups underwent cecum ligation and puncture to establish the mouse sepsis model.C25-140,3-methyladenine,and MHY1485 were intraperitoneally injected 0.5 hours after surgery according to the grouping.Myocardial tissue was obtained 24 hours after surgery.Hematoxylin-eosin staining was used to evaluate myocardial inflammatory lesions.Transmission electron microscopy was used to observe the changes in the autophagic bodies and mitochondrial microstructures of myocardial cells.TUNEL assay was used to detect myocardial cell apoptosis.PCR was used to detect the relative expression of tumor necrosis factor receptor-associated factor 6 mRNA.Western blot assay was used to detect the expression of related proteins.RESULTS AND CONCLUSION:(1)Compared with sham operation group,myocardial inflammatory cell infiltration and fibrous edema were observed in the model group.The mitochondria of the cells were obviously swollen,and autophagosomes were occasionally seen;cardiomyocyte apoptosis increased significantly;the expression of tumor necrosis factor receptor-associated factor 6,phosphorylated nuclear factor κB P65/P65,p-mTOR/mTOR,p-ULK1/ULK1,P62 and Bax protein increased,and the expression of Bcl2 protein decreased(P＜0.05).(2)Compared with the model group,myocardial inflammation and fibrous edema were alleviated in the model+C group.Myocardial mitochondrial swelling was reduced and autophagosomes increased;cardiomyocyte apoptosis decreased;the expression of phosphorylated nuclear factor κB P65/nuclear factor-κB P65,p-mTOR/mTOR,p-ULK1/ULK1,P62,and Bax protein decreased,while the Beclin-1 and Bcl2 protein increased(P＜0.05).(3)Compared with the model+C group,myocardial autophagosomes decreased and myocardial mitochondrial swelling was more obvious in the model+C+3-MA group.Myocardial inflammation was aggravated;myocardial cell apoptosis increased;the expression of phosphorylated nuclear factor κB P65/nuclear factor κB P65,P62,and Bax protein increased,and the Beclin-1 and Bcl2 protein decreased(P＜0.05).(4)Compared with the model+C group,the expression of p-mTOR/mTOR and p-ULK1/ULK1 in the model+C+M group increased,and the Beclin-1 and microtubule-associated protein 1 light chain 3 Ⅱ/Ⅰ protein expression decreased(P＜0.05).It is concluded that inhibition of tumor necrosis factor receptor-associated factor 6 regulates mTORC1/ULK1 autophagy signal to promote myocardial autophagy and participate in the protection of myocardial injury in sepsis.

Juvenile idiopathic arthritis(JIA)is the most prevalent joint disease in childhood.The disease is defined as arthritis of unknown etiology,involving one or more joints,with onset before the age of 16 years and symptomatic duration of more than 6 weeks.Temporomandibular joint(TMJ)arthritis is a common manifestation of JIA,but it often develops insidiously.Failing to diag-nose and treat it promptly may lead to maxillofacial dysfunction and dentofacial deformity,and negatively affect the patient's quality of life.Therefore,early diagnosis and disease management of TMJ arthritis are crucial.This article reviews the occurrence of JIA-TMJ arthritis and its progress in clinical diagnosis and disease treatment in recent years,aiming to provide some reference for den-tists in the clinical diagnosis and treatment of JIA.