ObjectiveTo investigate the therapeutic mechanism of Danhe granules in treating mixed hyperlipidemia based on network pharmacology， as well as animal and cell experiments. MethodsThe active compounds and targets of Danhe granules were screened using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and the Encyclopedia of Traditional Chinese Medicine （ETCM）. Related targets for mixed hyperlipidemia were obtained from the GeneCards database. The intersecting targets were subjected to Gene Ontology （GO） functional annotation and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analyses. A high-fat model was established in human hepatocellular carcinoma cells （HepG2） induced by palmitic acid （PA）， followed by intervention with Danhe granules to assess intracellular lipid accumulation and oxidative stress levels. A mixed hyperlipidemia rat model was also established and divided into low-， medium-， and high-dose Danhe granules groups （1.134， 2.268， and 4.536 g·kg^-1， respectively）， as well as a positive control group treated with pravastatin sodium （4.020 mg·kg^-1）. After eight weeks of intervention， serum lipid levels， inflammatory factors， oxidative stress indices， and the expression of key hepatic lipid metabolism-related proteins were determined. ResultsNetwork pharmacology identified 93 intersecting targets between Danhe granules and mixed hyperlipidemia， with peroxisome proliferator-activated receptor gamma （PPARG）， peroxisome proliferator-activated receptor alpha （PPARA）， tumor necrosis factor （TNF）， interleukin-6 （IL-6）， and IL-1B among the key nodes. The PPAR signaling pathway， AGE/RAGE signaling pathway， lipid metabolism， atherosclerosis and non-alcoholic fatty liver disease （NAFLD） were among the most significantly enriched pathways. Cellular experiments demonstrated that Danhe granules significantly reduced reactive oxygen species （ROS） and malondialdehyde （MDA） levels while increasing catalase （CAT） activity （P<0.05）， thereby alleviating intracellular lipid accumulation and triglyceride （TG） content in HepG2. In animal experiments， Danhe granules markedly decreased serum total cholesterol （TC）， TG， and low-density lipoprotein cholesterol （LDL-C） levels （P<0.05）， reduced hepatic MDA levels， and elevated superoxide dismutase （SOD） and CAT levels. Histological analysis showed alleviation of hepatic steatosis， upregulation of hepatic PPARA and lipoprotein lipase （LPL） expressions， and downregulation of sterol regulatory element-binding protein 1 （SREBP1） expression （P<0.05， P<0.01）. ConclusionDanhe granules improve lipid metabolism disorders in mixed hyperlipidemia by reducing MDA levels， enhancing SOD and CAT activities， scavenging excessive ROS， inhibiting oxidative stress， and mitigating liver injury. The underlying mechanism may involve the upregulation of PPARA and LPL and the suppression of SREBP1 expression.

ObjectiveTo investigate the therapeutic mechanism of Danhe granules in treating mixed hyperlipidemia based on network pharmacology， as well as animal and cell experiments. MethodsThe active compounds and targets of Danhe granules were screened using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and the Encyclopedia of Traditional Chinese Medicine （ETCM）. Related targets for mixed hyperlipidemia were obtained from the GeneCards database. The intersecting targets were subjected to Gene Ontology （GO） functional annotation and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analyses. A high-fat model was established in human hepatocellular carcinoma cells （HepG2） induced by palmitic acid （PA）， followed by intervention with Danhe granules to assess intracellular lipid accumulation and oxidative stress levels. A mixed hyperlipidemia rat model was also established and divided into low-， medium-， and high-dose Danhe granules groups （1.134， 2.268， and 4.536 g·kg^-1， respectively）， as well as a positive control group treated with pravastatin sodium （4.020 mg·kg^-1）. After eight weeks of intervention， serum lipid levels， inflammatory factors， oxidative stress indices， and the expression of key hepatic lipid metabolism-related proteins were determined. ResultsNetwork pharmacology identified 93 intersecting targets between Danhe granules and mixed hyperlipidemia， with peroxisome proliferator-activated receptor gamma （PPARG）， peroxisome proliferator-activated receptor alpha （PPARA）， tumor necrosis factor （TNF）， interleukin-6 （IL-6）， and IL-1B among the key nodes. The PPAR signaling pathway， AGE/RAGE signaling pathway， lipid metabolism， atherosclerosis and non-alcoholic fatty liver disease （NAFLD） were among the most significantly enriched pathways. Cellular experiments demonstrated that Danhe granules significantly reduced reactive oxygen species （ROS） and malondialdehyde （MDA） levels while increasing catalase （CAT） activity （P<0.05）， thereby alleviating intracellular lipid accumulation and triglyceride （TG） content in HepG2. In animal experiments， Danhe granules markedly decreased serum total cholesterol （TC）， TG， and low-density lipoprotein cholesterol （LDL-C） levels （P<0.05）， reduced hepatic MDA levels， and elevated superoxide dismutase （SOD） and CAT levels. Histological analysis showed alleviation of hepatic steatosis， upregulation of hepatic PPARA and lipoprotein lipase （LPL） expressions， and downregulation of sterol regulatory element-binding protein 1 （SREBP1） expression （P<0.05， P<0.01）. ConclusionDanhe granules improve lipid metabolism disorders in mixed hyperlipidemia by reducing MDA levels， enhancing SOD and CAT activities， scavenging excessive ROS， inhibiting oxidative stress， and mitigating liver injury. The underlying mechanism may involve the upregulation of PPARA and LPL and the suppression of SREBP1 expression.

ObjectiveThis paper aims to systematically summarize the construction methods and characteristics of Alzheimer's disease （AD） animal models， providing a reference for improving AD animal models. MethodsLiterature related to AD animal models published between January 2022 and April 2025 was retrieved from China National Knowledge Infrastructure （CNKI）， China Biomedical Literature Database （CBM）， Wanfang Data， and VIP Database. Information such as experimental animal species， month of age， sex， modeling methods， and period， as well as evaluation indicators， was collated， extracted， and imported into Microsoft Excel 2024 to establish the database. In addition， various modeling methods and detection means were summarized and compared. ResultsA total of 400 articles were included. Among the AD animal models， amyloid precursor protein/presenilin-1 （APP/PS1） mice were used most frequently， with a predominance of male animals. Typically， 3-4-month-old rats or 5-6-month-old mice were selected. The main modeling methods included natural aging， accelerated aging， surgical intervention， drug induction， and transgenic technology. The modeling period was mainly concentrated in a single day or 6-8 weeks. Detection indicators of the models focused on physiological， behavioral， pathological-morphological， and biochemical phenotypes. ConclusionThe construction methods of AD animal models are relatively mature， with multifactorial interventions effectively simulating human pathology， though certain limitations remain. By systematically reviewing and analyzing recent experimental literature of AD animal models， this study aims to provide theoretical support and a reference for further improving the construction of the AD animal model.

OBJECTIVE To investigate the clinical efficacy and mechanism of Gongliuxiao capsule combined with dienogest （DNG） in the treatment of refractory/recurrent endometriosis （EMT）. METHODS A retrospective analysis was conducted on the clinical data of 94 patients with refractory/recurrent EMT admitted to Qingdao TCM Hospital from January 2022 to January 2025. According to different treatment methods， they were divided into a monotherapy group （47 cases， receiving DNG monotherapy） and a combination group （47 cases， receiving Gongliuxiao capsule combined with DNG）. The cl inical efficacy， symptom and sign scores [Visual Analog Scale （VAS） and Pictorial Blood Loss Assessment Chart （PBAC） scores ] ， vascular endothelial function indicators [serum transforming growth factor-β 1 （TGF-β 1 ）， vascular endothelial growth factor （VEGF）， matrix metalloproteinase-2 （MMP-2）， MMP-9， basic fibroblast growth factor （bFGF） ] ， serum pathological factors [carbohydrate antigen 125 （CA125）， CA199， anti-endometrial antibody （EMAb） ] ， and Th1/Th2 drift indicators [interferon-γ （IFN-γ）， interleukin-4 （IL-4） ] were compared between the two groups before and after 6 months of treatment. RESULTS After treatment， the VAS and PBAC scores， serum levels of TGF-β 1 ， VEGF， MMP-2， MMP-9， bFGF， CA125， CA199， EMAb， and IL-4 in both groups were significantly lower than those before treatment， while IFN-γ levels were significantly higher than those before treatment （ P ＜0.05）. Moreover， the magnitude of increase or decrease in the combination group was significantly greater than that in the monotherapy group （ P ＜0.05）. The total effective rate in the combination group was significantly higher than that in the monotherapy group （93.62% vs. 76.60%， P ＜0.05）. CONCLUSIONS The combination of Gongliuxiao capsule and DNG is effective in treating refractory/recurrent EMT， and can effectively improve the degree of dysmenorrhea and abnormal menstrual volume in patients. The mechanism may be related to improving vascular endothelial function， inhibiting the expression of tumor pathological factors， and correcting Th1/Th2 drift.

Objective To investigate the role of cellular autophagy in medullary thyroid carcinoma (MTC) under doxorubicin (DOX)-induced stress and chemoresistance and to evaluate the synergistic antitumor effect of combining the autophagy inhibitor chloroquine (CQ) with DOX. Methods The human MTC cell line TT was used as an in vitro model and assigned to four groups: control, DOX, CQ, and DOX+CQ combination. Autophagy flux was assessed by Western blot analysis of LC3-Ⅱ protein expression, whereas autophagic structures were observed through transmission electron microscopy (TEM). An MTC xenograft model was established in nude mice, and tumor-bearing mice were randomly allocated to corresponding treatment groups. Tumor growth volume and weight were monitored, and autophagy levels in tumor tissues were detected. Results In vitro experiments showed that DOX treatment considerablyincreased LC3-Ⅱ levels, indicating autophagy induction. The combination of DOX and CQ led to further LC3-Ⅱaccumulation, and TEM revealed numerous undegraded autophagosomes and abnormal autolysosomes, confirming the successful blockade of autophagic flux. In vivo, the DOX+CQ combination therapy inhibited tumor growth significantly more effectively than any single-agent treatment (tumor inhibition rate: 60.0%, P<0.01) without causing considerable systemic toxicity. Marked accumulation of LC3-Ⅱ in tumor tissues from the combination group indicated the effective inhibition of autophagic flux in vivo. Conclusion Functional autophagy flux is a key mechanism underlying DOX chemoresistance in MTC. CQ can effectively reverse this resistance by blocking autophagic flux, and its combination with DOX exhibits a considerable synergistic antitumor effect. These findings suggest a promising therapeutic strategy for the management of advanced MTC.

ObjectiveTo observe the mechanism through which Qige San inhibits tumor angiogenesis in esophageal cancer （EC） by regulating the microRNA-133a （miR-133a）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. MethodsCell experiments were conducted by transfecting miR-133a mimics through liposomes and utilizing PI3K/Akt signaling pathway inhibitors. The effects of 60 mg·L^-1 and 100 mg·L^-1 Qige San on inflammatory factor secretion in the supernatant of EC9706 cells （esophageal cancer cells） were observed. EC9706 cell supernatants were then extracted and used as conditioned media to treat human umbilical vein endothelial cells （HUVECs）. The effects of the conditioned media on the proliferation， migration， tube formation， and apoptosis of HUVECs were examined. Animal experiments involved establishing a subcutaneous tumor model in nude mice with EC9706 cells. After grouping and administration， tumor volumes were measured regularly. At the end of the experiment， tumors were harvested， and histopathological changes were observed under a microscope after hematoxylin-eosin （HE） staining. Real-time polymerase chain reaction （Real-time PCR） was adopted to measure miR-133a expression in the tumor tissue of each group， while Western blotting was employed to analyze the expression of key signaling molecules， such as phosphorylated Akt （p-Akt）， as well as endothelial cell markers， cluster of differentiation 31 （CD31） and cluster of differentiation 34 （CD34）， in the tumor tissue. ResultsCell experiments showed that compared with the blank group， the supernatant of EC9706 cells promoted tube formation of HUVECs （P<0.05）. Both low and high doses of Qige San inhibited tube formation of HUVECs （P<0.05）. All doses of Qige San， PI3K/Akt inhibitor， and the combination reduced the content of interleukin-6 （IL-6） （P<0.05）， while high-dose Qige San， inhibitor， and combination all reduced the content of interleukin-8 （IL-8） （P<0.05）. Compared with the EC9706 blank supernatant group， Qige San-conditioned medium inhibited the proliferation of HUVECs （P<0.05）. Qige San， the inhibitor， and the combination all inhibited the migration and tube formation （P<0.05） and increased the late apoptosis and total apoptosis rates of HUVECs （P<0.05）. In addition， the low-dose combination induced early apoptosis of EC9706 cells （P<0.05）. Compared with the blank supernatant group， the miR-133a mimic combined with Qige San synergistically reduced IL-6/IL-8 （P<0.05）， and enhanced the inhibition on proliferation， migration， and tube formation of HUVECs （P<0.05）. Animal experimental results showed that compared with the model group， both Qige San and cisplatin inhibited the growth of xenograft tumors in nude mice （P<0.05）， promoted tumor cell necrosis， and reduced capillary formation. High-dose Qige San upregulated miR-133a expression （P<0.05）. Moreover， compared with the model group， cisplatin， Qige San， and the combination all downregulated the expression of p-Akt， CD31， and CD34 （P<0.05）. ConclusionQige San upregulates miR-133a expression， inhibit PI3K/Akt signaling pathway activity， and improve the tumor inflammatory microenvironment to suppress the growth and tumor angiogenesis of HUVECs， thereby inhibiting esophageal cancer.

China emerges as a major country in nuclear energy development and the application of nuclear and radiologic technology. The diagnosis and treatment of acute radiation syndrom (ARS) caused by external irradiation represent a core function in the country′s medical rescue of nuclear and radiological emergencies. Clinically, ARS manifests hematopoietic, gastrointestinal, cutaneous, and central nervous system syndromes, with specific clinical manifestations, signs, severity, and prognosis strongly correlated with radiation dose. China has established a number of national and provincial centers for treating radiation-induced damage. Nevertheless, most medical staff have limited experience in ARS treatment. This consensus presents a summary of recent experience in treating ARS of China. In combination with recommendations from international organizations such as the World Health Organization (WHO), this consensus proposes key evidence of critical clinical issues of ARS, covering all links in the rescue of external irradiation-induced ARS. Initially, clinical diagnosis, syndromes, and severe degrees should be determined based on clinical symptoms and dose estimates. It is necessary to normalize clinical treatment measures for hematopoietic recovery, gastrointestinal injury treatment, infection control, symptomatic treatment, and multi-organ function preservation. To this end, this consensus offers cautions. This consensus provides principles of treatment with traditional Chinese medicine, psychological intervention, and follow-up. Additionally, it highlights multidisciplinary collaboration. It is recommended that this consensus be applied in relevant treatment centers.

Turning to critical illness is a common stage of various diseases and injuries before death. Patients usually have complex health conditions, while the treatment process involves a wide range of content, along with high requirements for doctor′s professionalism and multi-specialty teamwork, as well as a great demand for time-sensitive treatments. However, this is not matched with critical care professionals and the current state of medical care in China. Telemedicine, which shortens the distance of medical professionals and the gap of disease diagnosis and treatments in various regions through electronic information, can effectively solve the current problem. Therefore, there is an urgent need to develop a standardized, high-quality visualization telemedicine round system .Therefore, experts have been organized to search domestic and foreign literature on telemedicine round for critically ill patients and to form this consensus based on clinical experiences so as to further improve the level of critical care treatments in regions.

Objective:To assess the real-world triage performance of a dual-marker strategy (DMS) combining copeptin and high-sensitivity cardiac troponin T (hs-cTnT) in patients presenting with chest pain and suspected non-ST-segment elevation myocardial infarction (NSTEMI).Methods:It was conducted a prospective study of 277 consecutive chest pain patients admitted to the Emergency Department of Zhongshan Hospital, Fudan University, between July and August 2023. Admission levels of copeptin and hs-cTnT were measured. The safety, efficacy, and triage efficiency of the DMS (defined as copeptin <10 pmol/L and hs-cTnT <0.014 ng/mL) for excluding NSTEMI were evaluated based on final diagnoses and clinical outcomes.Results:Among 277 patients, 141 (50.9%) had cardiogenic diseases (51 NSTEMI, 37 unstable angina pectoris [UAP], 11 myocardial bridges, and 42 non-coronary artery disease), 29 (10.5%) had non-cardiac conditions, and 107 (38.6%) had low-risk chest pain of unknown etiology. A total of 103 patients (37.2%) were DMS-negative (copeptin and hs-cTnT both below cutoff), including 0 NSTEMI cases, 2 UAP cases, 1 myocardial bridge, 6 non-coronary artery diseases, 4 non-cardiac conditions, and 90 low-risk cases. The DMS demonstrated a negative predictive value (NPV) of 100% for excluding NSTEMI, with no major adverse cardiac events (MACE) observed in DMS-negative patients during 30-day follow-up. Real-world data revealed that only 42.2% of suspected NSTEMI patients received a second troponin test (timing: 1 hour—5.9%, 2 hours—23.9%, ≥3 hours—70.1%). The DMS enabled safe and efficient triage of 37.2% of chest pain patients at 0-hour, outperforming other strategies in applicability and feasibility ( P < 0.05). Conclusions:In real-world clinical practice, the DMS (copeptin combined with hs-cTnT) optimally complements guideline-recommended hs-cTnT algorithms. It provides a simple, rapid, and safe approach to managing acute chest pain, demonstrating superior applicability for improving emergency triage efficiency.

ObjectiveTo explore the mechanism of Huanglian Wendantang on damp-heat type diabetes enteropathy rats based on the G protein coupled bile acid receptor 5/glucagon like peptide-1 （TGR5/GLP-1） signaling pathway and intestinal flora. MethodsA total of 72 male Sprague Dawley （SD） rats were adaptively fed for one week. Twelve SD rats were randomly selected as a blank group and fed with an ordinary diet. The rest of the SD rats were fasted for 12 hours without water. A rat model with damp-heat type diabetes enteropathy was made by left intraperitoneal injection of streptozotocin （55 mg·kg^-1） and high sugar and high fat diet （20% sucrose solution + high fat diet） in a humid and hot environment （artificial climate box： temperature 30-34 ℃， relative humidity： 85%-95%）. After successful modeling， the rats were randomly divided into a model group， a metformin group （200 mg·kg^-1）， low-dose， medium-dose， and high-dose Huanglian Wendantang groups （7.10， 14.20， 28.39 g·kg^-1）， with 12 rats in each group. The normal group and the model group were orally administered with physiological saline once a day for 6 consecutive weeks. During the observation period， the weight and blood glucose levels of rats were measured and recorded weekly. After the administration， fresh feces were collected from rats， and 16S rRNA sequencing technology was used to study the differences and changes in intestinal flora among different groups. The levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in the serum of rats were detected by enzyme-linked immunosorbent assay （ELISA）， and the pathological morphological changes of colon tissue were examined. The expression of TGR5 and GLP-1 in colon tissue was detected by immunohistochemistry， and the expression of TGR5 and GLP-1 proteins in colon tissue was measured by Western blot. ResultsCompared with the blank group， the model group showed a decrease in body weight， an increase in blood glucose， and significant damp-heat symptoms. The levels of IL-6 and TNF-α in serum were significantly increased （P<0.01）. The expression of TGR5 and GLP-1 was decreased （P<0.01）， and the pathogenic bacteria were increased. Compared with the model group， the treatment groups exhibited improvements in body weight， blood glucose levels， and damp-heat syndrome in rats. Among them， the high-dose group of Huanglian Wendantang displayed the most significant improvement effect， with significantly reduced inflammation levels （P<0.01） and elevated expression of TGR5 and GLP-1 （P<0.01）. Colonic pathological sections showed that Huanglian Wendantang could effectively ameliorate colonic pathological changes. The 16S rRNA sequencing result indicated a significant increase in beneficial bacteria in the treatment groups. ConclusionHuanglian Wendantang can effectively ameliorate the damp-heat symptoms and blood glucose levels in rats with damp-heat type diabetes enteropathy， and it may exert an effect by regulating the TGR5/GLP-1 signaling pathway and intestinal flora disorder.