This study aimed to investigate the mechanism of liquiritin (LQ) in the improvement of ventricular remodeling (VR) after acute myocardial infarction (AMI). Molecular docking was used to predict the binding affinity of liquiritin to thioredoxin-interacting protein (TXNIP). After 2 weeks of modeling, the rats were randomly divided into a model group, a low-dose liquiritin group (20 mg/kg LQ), and a high-dose liquiritin group (40 mg/kg LQ). Liquiritin was administered by gavage once a day, and the sham group and model group were given the same volume of 0.5% sodium carboxymethylcellulose (CMC-Na), with intervention of 4 consecutive weeks. Echocardiography was employed to detect the cardiac function, HE staining was used to observe cardiological changes, ELISA was used to detect the activity of serum creatine kinase-MB (CK-MB) activity, and the colorimetric method was adopted to detect serum malondialdehyde (MDA), total superoxide dismutase (T-SOD) and catalase (CAT) activities. RT-qPCR was used to detect the gene expressions of TXNIP, thioredoxin (TRX) and NACHT, LRR, and PYD domains-containing protein 3(NLRP3). Western blot was used to detect the protein expressions of TXNIP, TRX and NLRP3 in rat myocardial tissue. Molecular docking results showed that liquiritin had a good binding affinity to TNXIP target. After 20 and 40 mg/kg liquiritin intervention, the levels of ejection fraction (EF) and fractional shortening (FS) were significantly increased (P<0.01), and the levels of LVIDs, LVIDd, LVESV, and LVEDV were decreased (P<0.01). The myocardial structure was significantly improved, the cell arrangement tended to be regular, and the area of inflammatory cell infiltration and necrosis was reduced. Liquiritin significantly reduced the level of CK-MB (P<0.01), decreased the activity of MDA, and increased the activities of CAT and T-SOD (P<0.01). Liquiritin effectively inhibited the overexpression of TXNIP and NLRP3 genes and proteins, and enhanced the expression of TRX genes and proteins in the myocardial tissues of AMI rats. In conclusion, liquiritin has a regulatory effect on the TXNIP/TRX signaling pathway, inhibits the activation of the NLRP3 inflammasome, and thus improves ventricular remodeling after acute myocardial infarction.

The prescription of Qidong Yixin oral liquid is derived from the experience of national medical master Ren Jixue in treating viral myocarditis （VMC）. It has the functions of tonifying Qi， nourishing the heart，calming the mind， and relieving palpitations. It is used to treat VMC and angina pectoris of coronary heart disease caused by deficiency of both Qi and Yin. However，the understanding of its efficacy evidence， advantageous aspects， dosage and administration， and medication safety remains insufficient in clinical practice. Therefore，the development of the Expert Consensus on the Clinical Application of Qidong Yixin Oral Liquid （hereinafter referred to as consensus） was initiated. Consensus strictly followed the process and methods of the expert consensus on the clinical application of Chinese patent medicines of the China Association of Chinese Medicine，successively completing multiple tasks such as the consensus project initiation，determination of clinical problems，evidence search and evaluation，formation of recommendation opinions and consensus suggestions，solicitation of opinions，peer review， submission for review and release， and so on. Consensus formed a total of 10 recommendation opinions and 12 consensus suggestions，clarifying the clinical positioning，efficacy advantages，syndrome differentiation，dosage and administration，combination therapy，timing of medication，adverse reactions，contraindications， and precautions of Qidong Yixin oral liquid，indicating that it has good clinical advantages and safety in the treatment of VMC and angina pectoris of coronary heart disease，providing norms and references for physicians to safely and rationally apply Qidong Yixin oral liquid. Consensus was reviewed and approved for release by the Standardization Office of the China Association of Chinese Medicine on December 23， 2024. Standard number：GSCACM-376-2024.

The philosophy of “treating disease before its onset” is a fundamental concept of traditional Chinese medicine (TCM), permeating its diagnostic and therapeutic framework, and is central to clinical practice. However, current TCM diagnostic and treatment models for the “pre-disease to disease” window period face several limitations, including the lack of comprehensive clinical parameters, difficulties in characterizing and integrating heterogeneous multimodal data, and insufficient dynamic precision in interventions and efficacy evaluations. To address these issues, guided by Professor Candong Li’s theory of TCM stateology, this study focuses on integrating objective multimodal data. It proposes a new model for personalized TCM diagnosis and treatment targeting the “pre-disease to disease” window period. This approach first proposes the idea of restructuring the conceptual framework of “symptom” and integrating multi-source heterogeneous data at macroscopic, mesoscopic, and microscopic levels to form a three-dimensional assessment indicator system. By integrating graph neural networks, convolutional neural networks, attention mechanisms, and knowledge graph-guided weight allocation, this approach enables collaborative representation, alignment, and fusion of multi-source data. Subsequently, it plans to construct a multimodal fusion model at both feature and decision levels, in order to establish mappings between indicators and TCM state elements, and to screen key indicators characterizing pathological evolution during the window period. Furthermore, it proposes a technical path for enhancing model interpretability using methods such as SHapley Additive exPlanations (SHAP) and Ablation-CAM++. Finally, with state assessment as the core, it proposes the concept of constructing a dynamic evaluation method for individualized diagnosis and treatment based on time-series data analysis using algorithms such as long short-term memory (LSTM) networks and gated recurrent units (GRUs). Moreover, a causal inference framework and semi-supervised learning strategies are introduced to enable quantitative evaluation of individual intervention effects and to provide interpretable therapeutic feedback, forming a complete technical path from data representation and fusion, weight adjustment, and interpretability analysis, to dynamic diagnosis feedback. This study aims to address deficiencies in the current TCM diagnosis and treatment model during the “pre-disease to disease” window period and to provide an operational framework for the clinical practice of TCM’s “treating disease before its onset”.

This paper has summarized current studies on retinitis pigmentosa （RP） from two perspectives， which were disease mechanism insights from western medicine， and etiology， pathogenesis and therapeutic principles in traditional Chinese medicine （TCM）. From the perspective of western medicine， the understanding of RP has evolved from an early single-factor explanation focusing on pathogenic gene mutations to a more comprehensive， multifactorial model involving genetic abnormalities， photoreceptor cell degeneration， retinal pigment epithelium dysfunction， oxidative stress， inflammatory responses， microenvironmental imbalance， and vascular insufficiency. In TCM， RP is considered to be a disorder manifested in the eyes but rooted in dysfunction of the zang-fu （脏腑） organs. Its pathogenesis is primarily associated with congenital insufficiency， liver-kidney depletion， impaired spleen function of transportation and transformation， and stasis obstructing the meridians. The core pathological mechanism can be summarized as "deficiency complicated by stasis"， emphasizing holistic imbalance， dynamic disease progression， and syndrome differentiation and treatment. The differences and complementarities between the two medical systems in understanding disease progression are further discussed. RP is proposed to be more appropriately regarded as a complex disease characterized by long-term progression， stage-dependent evolution， and persistent decompensation. Western medicine contributes to elucidating the molecular mechanisms underlying RP and provides the foundation for targeted therapeutic interventions， whereas TCM offers a holistic perspective for understanding disease evolution through the assessment of overall functional status， disease-stage stratification， and long-term syndrome-based regulation.

This paper has summarized current studies on retinitis pigmentosa （RP） from two perspectives， which were disease mechanism insights from western medicine， and etiology， pathogenesis and therapeutic principles in traditional Chinese medicine （TCM）. From the perspective of western medicine， the understanding of RP has evolved from an early single-factor explanation focusing on pathogenic gene mutations to a more comprehensive， multifactorial model involving genetic abnormalities， photoreceptor cell degeneration， retinal pigment epithelium dysfunction， oxidative stress， inflammatory responses， microenvironmental imbalance， and vascular insufficiency. In TCM， RP is considered to be a disorder manifested in the eyes but rooted in dysfunction of the zang-fu （脏腑） organs. Its pathogenesis is primarily associated with congenital insufficiency， liver-kidney depletion， impaired spleen function of transportation and transformation， and stasis obstructing the meridians. The core pathological mechanism can be summarized as "deficiency complicated by stasis"， emphasizing holistic imbalance， dynamic disease progression， and syndrome differentiation and treatment. The differences and complementarities between the two medical systems in understanding disease progression are further discussed. RP is proposed to be more appropriately regarded as a complex disease characterized by long-term progression， stage-dependent evolution， and persistent decompensation. Western medicine contributes to elucidating the molecular mechanisms underlying RP and provides the foundation for targeted therapeutic interventions， whereas TCM offers a holistic perspective for understanding disease evolution through the assessment of overall functional status， disease-stage stratification， and long-term syndrome-based regulation.

ObjectiveTo investigate the effect of sorafenib and donafenib on the pharmacokinetics of ertugliflozin in rats， and to provide a theoretical basis for drug combination in clinical practice. MethodsA total of 24 male Sprague-Dawley rats were randomly divided into groups A， B， C， and D， with 6 rats in each group. The rats in groups A and B were given sorafenib control solvent and sorafenib （100 mg/kg）， respectively， by gavage for 7 consecutive days， followed by ertugliflozin （1.5 mg/kg） by gavage on day 7. Blood samples were collected from the angular vein plexus at different time points， and ultra-performance liquid chromatography-tandem mass spectrometry was used to determine the mass concentration of ertugliflozin and plot the plasma concentration-time curves， while the non-compartment model in DAS 2.1.1 software was used to calculate related pharmacokinetic parameters. The independent-samples t test was used for comparison of normally distributed continuous data between two groups， and the Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups. ResultsCompared with group A， group B had significant increases in the AUC_0-t and AUC_0-∞ of the plasma concentration-time curve of ertugliflozin （both P<0.05）， significant prolongation of t_1/2， MRT_0-t， and MRT_0-∞ （all P<0.05）， and a significant reduction in CL_Z/F （P<0.05）. Compared with group C， group D had significant increases in the AUC_0-t and AUC_0-∞ of ertugliflozin （both P<0.05）， significant prolongation of T_max， t_1/2， MRT_0-t， and MRT_0-∞ （all P<0.01）， and significant reductions in V_Z/F and CL_Z/F （both P<0.05）. ConclusionBoth sorafenib and donafenib can affect the pharmacokinetics of ertugliflozin in rats and significantly increase the plasma exposure of ertugliflozin. The efficacy and adverse drug reactions of ertugliflozin should be closely monitored during combined use in clinical practice and the dose should be adjusted when necessary to avoid the potential risk of drug interaction.

Objective:To investigate whether intermittent fasting alleviates insulin resistance in a polycystic ovary syndrome(PCOS) mouse model through the regulation of autophagy.Methods:Fifty 3-week-old female C57BL/6J mice were randomly assigned into the following groups using a random number table: normal control(NC) group( n=10), maintained on a standard chow diet; high-fat diet(HFD) group( n=10) fed a diet with 60% of calories derived from fat; and PCOS model group( n=30), established by combining a HFD with dehydroepiandrosterone(DHEA) administration. Successful modeling was confirmed by disrupted estrous cycles, hyperandrogenism, and polycystic ovarian morphology. The PCOS model mice were further divided into three groups: PCOS group( n=9), PCOS with intermittent fasting group(PCOS+ IF, n=9), and PCOS with intermittent fasting plus the autophagy inhibitor 3-methyladenine(3-MA) group(PCOS+ IF+ 3-MA, n=9). Autophagy levels were assessed by detecting markers LC3 and p62 and observing autophagosomes via transmission electron microscopy. Glucose tolerance test(GTT) and insulin tolerance test(ITT) were performed, and the area under the curve(AUC) was calculated to evaluate insulin resistance. Western blotting was used to detect phosphorylation levels of phosphatidylinositol 3-kinase(PI3K), protein kinase B(Akt), mammalian target of rapamycin(mTOR), and p70S6 kiase(p70S6K). Results:Compared with the NC group, the PCOS model group showed absent estrous cycles, significantly elevated serum testosterone, sex hormone binding globulin, and luteinizing hormone(LH) levels( P<0.001), and polycystic ovarian changes on hematoxylin-eosin staining, confirming successful model establishment. Immunohistochemistry, transmission electron microscopy, and Western blotting demonstrated that autophagy levels were increased in the PCOS+ IF group compared with the PCOS group, while 3-MA administration reduced the intermittent fasting - induced autophagy. The AUC values for both GTT and ITT were significantly lower in the PCOS+ IF group than those in the PCOS group( P<0.001, P=0.003), but increased in the PCOS+ IF+ 3-MA group compared to the PCOS+ IF group( P<0.001, P=0.020). Western blotting analysis showed that phosphorylation levels of PI3K, Akt, mTOR, and p70S6K were significantly decreased in the PCOS+ IF group compared with the PCOS group( P=0.002, P=0.001, P=0.001, and P<0.001, respectively), and increased in the PCOS+ IF+ 3-MA group compared with the PCOS+ IF group( P=0.021, P=0.041, P=0.047, and P=0.024, respectively). Conclusions:Intermittent fasting alleviates insulin resistance in a PCOS mouse model through inhibitiing PI3K/Akt/mTOR signaling pathway and promoting autophagy.

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.

Objective:To investigate the treatment and management of patients with endemic fluorosis (referred to as fluorosis) in Ankang City, Shaanxi Province, and to provide a scientific basis for adjusting and optimizing treatment and management strategies for fluorosis patients.Methods:A retrospective analysis was conducted on patient information collected from county-level disease prevention and control centers in Ankang City from 2019 to 2023. Data included demographic information, clinical treatment, chronic disease management, treatment records, work reports, and summaries. The study aimed to learn about the treatment willingness, methods, and effects of patients with fluorosis, and to evaluate the disease management situation of patients with fluorosis.Results:From 2019 to 2023, the proportion of fluorosis patients who were willing to receive treatment in Ankang City had increased from 76.80% (1 089/1 418) in 2019 to 100% (1 408/1 408) in 2023, showing an upward trend year by year (χ 2trend = 971.15, P < 0.001). A total of 6 876 patients received treatment, with a treatment rate of 100%. The majority of patients received drug treatment (99.64%, 6 851/6 876), with an effective rate of 94.90% (6 525/6 876). The effective rate of treatment for patients with fluorosis had increased from 88.71% (966/1 418) in 2019 to 94.67% (1 333/1 408) in 2023, showing an upward trend (χ 2trend = 1 002.92, P < 0.001). The adverse reaction rate of drug treatment was 0.36% (25/6 876). The combination of oral medication and local treatment had the highest effective rate (97.62%, 3 566/3 653). The management rate and contracted service rate of fluorosis patients were 100% each year, and the standardized management rate was above 99%. Conclusions:Fluorosis patients in Ankang City have a high willingness to receive treatment, with good treatment outcomes. The contracted services and management of patients are well implemented. In the future, continuous efforts should be made to improve the prevention, management, and health education of fluorosis patients.

Objective:To conduct a study on pricing by service unit to address the problems of hospice and palliative care pricing and fee system in China.Methods:Combining theoretical research and empirical evidence,this study organized the pricing mechanism of initiative hospice and palliative care services and established a graded and categorized pricing strategy.Empirical research was conducted based on real-world data from 36 pilot institutions in typical areas.Results:This study developed a comprehensive pricing framework for value-based classification price standard of initiative hospice and palliative care services from the perspective of incentive regulation.We proposed a pricing plan based on service units,with inpatient bed fee ranging from 459 to 606 yuan or 459 to 1 102 yuan,and home visit fee ranging from 89 to 264 yuan.Conclusions and suggestions:This study proposes a pricing scheme based on the technique and service value with a gradient fluctuation by service unit,and forms a set of price standards with high economic and technical feasibility,which can provide scientific evidences for solving the pricing problem of hospice care.In addition,there is still a need to establish a multi-level incentive compensation mechanism to motivate all levels and types of organisations and healthcare provider,and to promote the high-quality and sustainable development of hospice and palliative care.