Stroke is one of the leading causes of disability and mortality worldwide. Research into its mechanisms and the development of therapeutic strategies heavily rely on animal models that accurately replicate the pathological features of human disease. An ideal animal model for stroke should not only reproduce the neurological deficits and pathological changes observed in clinical patients but also demonstrate good reproducibility and translational value. This review focuses on the preparation and evaluation methods of ischemic stroke animal models. Firstly, it elaborates on the selection criteria, advantages, and disadvantages of experimental animals, including rodents (rats, mice) and non-rodents (non-human primates, miniature pigs, rabbits, zebrafish). Secondly, it provides a detailed overview of the modeling principles, key procedures, and application scopes for ischemic stroke models and hemorrhagic stroke models. Furthermore, the review summarizes advances in the applications of emerging technologies—including gene editing [e.g., clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing], multimodal imaging (e.g., two-photon microscopy, photoacoustic imaging), artificial intelligence, optogenetics, 3D bioprinting, organoid models, and multi-omics–in model optimization, precise assessment, and mechanistic investigation. Finally, based on a systematic analysis of relevant domestic and international literature from 2019 to 2024, this review discusses model selection strategies based on research objectives, a multidimensional evaluation system encompassing behavioral, imaging, and molecular pathological assessments, and envisions future directions involving technological integration to achieve model precision and individualization. This article aims to provide a comprehensive methodological reference to help researchers select appropriate animal models of stroke according to specific scientific questions.

Objective: To investigate the factors influencing the co-prevalence of allergic rhinitis and obesity among primary and secondary school students in Inner Mongolia, so as to provide a data foundation and theoretical basis for developing targeted intervention measures. Methods: In September and October 2024, a stratified cluster random sampling method was employed to select 139 102 students from 539 schools across 12 leagues/cities and 103 banners/counties in Inner Mongolia Autonomous Region. Participants who were diagnosed with allergic rhinitis by a doctor at least once within one year and had a body mass index ≥ 28 kg/m 2 were considered to have comorbid conditions. Results: The coprevalence rate of allergic rhinitis and obesity among primary and secondary school students in Inner Mongolia was 6.4% (8 931 cases). Lasso-Logistic regression revealed that nonboarding status, higher maternal education, consuming high protein foods ≥1 time daily, occasionally or never eating breakfast, engaging in moderate to vigorous physical activity for ≥60 minutes on fewer than half of holidays, and having been exposed to second hand smoke in person within the past seven days were associated with higher odds ratios for co-prevalence of allergic rhinitis and obesity( OR = 1.23 , 1.22-1.63, 1.20, 1.19, 1.38, 1.35); being female, higher grade level, residence in flag/county/district areas, non only child status, never having consumed a full glass of alcohol, non hypertensive status, and households without pets were associated with lower co-prevalence risks ( OR =0.65, 0.67-0.77, 0.81, 0.87, 0.73, 0.41, 0.68) (all P <0.05). The ROC curve indicated an area under the curve of 0.64 for the predictive model, demonstrating satisfactory discriminatory ability. The calibration curve showed consistency between predicted and actual occurrence probabilities. Conclusions The co-prevalence of allergic rhinitis and obesity among primary and secondary school students in Inner Mongolia is closely associated with demographic characteristics, dietary behaviours, and lifestyle habits. Future prevention and control strategies should prioritize these factors to implement targeted interventions.

OBJECTIVE To construct a comprehensive evaluation system for oral Chinese patent medicines in children that is compatible with pediatric physiological characteristics and the features of traditional Chinese medicine （TCM）， and provide a basis for the selection， pharmaceutical management， and medical insurance procurement of oral Chinese patent medicines in children.METHODS According to the Guidelines for the Management of Comprehensive Clinical Evaluation of Drugs （ 2021 Trial Edition ） and related policy documents and literatures， six first-level indicators were determined： safety， efficacy， suitability， economy， accessibility， and innovation. An initial indicator pool was constructed through literature retrieval， policy text analysis， and semi-structured expert interviews. A preliminary survey using a 5-point Likert scale was conducted to determine the primary indicator list. Two rounds of Delphi expert consultation were carried out. The analytic hierarchy process （AHP） was used to determine the weights and scores of indicators at all levels， and the methodological quality of the questionnaire and reliability were evaluated. Five oral Chinese patent medicines for pediatric respiratory diseases were selected for empirical evaluation. Two independent blinded reviewers scored the medicines， and the Kappa value was calculated to evaluate inter-rater consistency.RESULTS Both rounds of Delphi consulting had 21 experts， with a positive coefficient of 100% and an authoritative coefficient of 0.89. The Kendall’s W coefficients of concordance for the first and second rounds of Delphi expert consultation were 0.812 and 0.856， respectively （ P ＜0.01）. The consistency ratios of all AHP judgment matrices ranged from 0.032 to 0.087 （all ＜0.10）. The Cronbach’s α coefficient was 0.847. A comprehensive evaluation system for oral Chinese patent medicines in children was established， comprising 6 first-level indicators， 25 second-level indicators， and 78 third-level indicators. The weights of the first-level indicators were 0.32， 0.24， 0.16， 0.13， 0.10 and 0.05， respectively， for safety， effectiveness， suitability， economy， accessibility and innovation. The empirical evaluation showed that Xiao’er chiqiao qingre granules obtained the highest comprehensive score （90.8 points）， followed by Xiao’er feire kechuan oral liquid （86.3 points）， Ertong qingfei oral liquid （82.8 points）， Xiao’er xiaoji zhike oral liquid （82.0 points）， and Jinzhen oral liquid （81.5 points）. The inter-rater consistency Kappa value was 0.91.CONCLUSIONS The comprehensive evaluation system for oral Chinese patent medicines in children constructed in this study， includes 12 pediatric-specific third-level indicators and integrates key evaluation points of both traditional Chinese and Western medicine. It demonstrates good consistency and reliability， with good operability and reproducibility.

Against the backdrop of a continuously rising incidence of breast cancer globally， breast reconstruction surgery represents one of the key measures to improve patients’ quality of life. Ethics of care emphasizes paying attention to patients’ actual needs in doctor-patient interactions and advocates creating a decision-making environment that facilitates the explicit expression of these needs. Focusing on the decision-making process of 16 breast cancer patients who underwent breast reconstruction surgery and stemming from the perspective of ethics of care， this paper explored the realization paths of autonomy for breast cancer patients when confronting medical decisions on breast reconstruction from three aspects， including the situatedness， relationality， and practicality of ethics of care. The study found that under the ethics of care， the organic interaction of contextualized practice， relational negotiation， and subjectivity cultivation jointly constructed a dynamically evolving medical decision-making ecosystem. This ecosystem， with situational response capabilities based on embodied cognition， relational adjustment mechanisms linked by ethical negotiation， and dual-track support networks aimed at subject empowerment， ultimately achieved the in-depth integration of technical practice and humanistic care.

BACKGROUND:Acute exercise tends to cause skeletal muscle tissue damage and lipid metabolism disorders in vivo,but the mechanism by which acute exercise combined with electroacupuncture modulates metabolic and autophagic pathways in vivo is unclear. OBJECTIVE:To observe the changes in metabolic enzymes and autophagy levels in skeletal muscle of rats subjected to acute exercise by electroacupuncture at the acupoints of"Zusanli"and"Huantiao." METHODS:Fifty male Sprague-Dawley rats were randomly divided into three groups:quiet control group(n=10),model group(n=20),and reverse electroacupuncture group(n=20).The latter two groups were set up with two time points,i.e.immediate and 3 hours after exercise groups(n=10 per time point).The model group and the reverse electroacupuncture group underwent acute exercise training after adaptive treadmill training.The rats in the reverse electroacupuncture group underwent electroacupuncture treatment(parameters:electroacupuncture on both sides of the rats at the acupoints of"Zusanli"and"Huantiao,"continuous wave,frequency of 2 Hz,intensity of 2 mA,leaving the needle in the body for 30 minutes,once a day for 7 consecutive days)before treadmill training.Bilateral gastrocnemius muscle tissues were taken under anesthesia immediately after exercise and 3 hours after exercise,and hematoxylin-eosin staining was used to observe the histopathological changes of rat skeletal muscle.ELISA kit was used to detect the activities of hepatic lipase,fatty acid synthase,hormone-sensitive lipase,and carnitine palmitoyltransferase 1 in rat skeletal muscle tissues.Immunohistochemistry and western blot were used to detect the changes in the expression of autophagy genes. RESULTS AND CONCLUSION:After hematoxylin-eosin staining,the arrangement of gastrocnemius muscle fibers in the model group was disturbed,swollen and ruptured immediately after exercise and 3 hours after exercise.In the reverse electroacupuncture group,gastrocnemius muscle fibers were tightly arranged and the number of swollen and ruptured cells was greatly reduced immediately after exercise and 3 hours after exercise,and there was no significant difference when compared with the quiet control group.Compared with the quiet control group,the activities of hepatic lipase and fatty acid synthase were lower while the activities of lipoprotein lipase,hormone-sensitive lipase,and carnitine palmitoyltransferase 1 were higher in the model group and the reverse electroacupuncture group 3 hours after exercise(P＜0.05 or P＜0.01).Compared with the model group,the activities of lipoprotein lipase and carnitine palmitoyltransferase 1 were higher in the reverse electroacupuncture group immediately after exercise(P＜0.05),while the activity of lipoprotein lipase was higher and the activity of hormone-sensitive lipase was lower in the reverse electroacupuncture group 3 hours after exercise(P＜0.01).Immunohistochemical results showed that compared with the quiet control group,the expression of P62,autophagy-related gene 5 and autophagy-related gene 7 was higher in the model group immediately and 3 hours after exercise,as well as in the reverse electroacupuncture group immediately after exercise(P＜0.05 or P＜0.01);compared with the model group,the expression of P62 and autophagy-related gene 7 was lower in the reverse electroacupuncture group immediately and 3 hours after exercise(P＜0.05).Western blot results showed that the protein expression of P62 and autophagy-related gene 7 in the reverse electroacupuncture group was lower than that in the model group immediately after exercise(P＜0.05);the protein expression of Parkin in the model group was higher than that in the quiet control group immediately and 3 hours after exercise(P＜0.05);and the protein expression of Parkin in the reverse electroacupuncture group was lower than that in the model group immediately and 3 hours after exercise(P＜0.05).To conclude,acute exercise induces disorders,swelling and rupture of gastrocnemius muscle fibers in rats and electroacupuncture on both sides of the acupoints of"Zusanli"and"Huantiao"can improve the level of lipid metabolism and regulate autophagy cells in rat skeletal muscle,preventing the disorders of lipid metabolism and damage of gastrocnemius muscle tissues caused by acute exercise.The mechanism may be closely related to the regulation of autophagy-related factor P62,autophagy-related gene 5,autophagy-related gene 7,and Parkin protein expression to promote the occurrence of autophagy or regulate the autophagy pathway in rat skeletal muscle cells.

Objective To observe the improvement effect and mechanism of emodin on lipopolysaccharide(LPS)-induced podocyte injury.Methods Human glomerular podocytes were used as the study object,and they were randomly divided into the blank control group,the LPS group,the emodin low-,medium-,and high-dose groups,and the emodin+lysophosphatidic acid[LP A,RhoA/RhoRho-associatedcoiled-coil kinase(ROCK)activator]group.Cell counting kit 8(CCK8)and 5-ethynyl-2'-deoxyuridine(EdU)staining were applied to detect the proliferation of glomerular podocytes,Transwell assay was used to test the migration of glomerular podocytes,flow cytometry was used to detect apoptosis of glomerular podocytes,and enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of inflammatory factors tumor necrosis factor α(TNF-α),interleukin(IL)-1β,and IL-18 in the supernatant of glomerular podocytes,and the protein expression levels of RhoA and ROCK in glomerular podocytes were determined by Western Blot.Results The optical density(OD)450nm,EdU positive cell rate and migration number of glomerular podocytes in the LPS group were lower than those in the blank control group,and the apoptosis rate,the levels of TNF-α,IL-1β and IL-18 in the supernatant,as well as the protein expression levels of RhoA and ROCK in the cells were higher than those in the blank control group,the differences being statistically significant(P＜0.05);the OD450nm,EdU positive cell rate and migration number of glomerular podocytes in the emodin low-,medium-,and high-dose groups were higher than those in the LPS group,while the apoptosis rate,levels of TNF-α,IL-1 β and IL-18 in supernatant,as well as RhoA and ROCK protein expression levels in cells were reduced compared with those in the LPS group,the differences being statistically significant(P＜0.05);the OD450nm and EdU positive cell rate and migration number of glomerular podocytes in LPA group were lower than those of emodin high-dose group,while the apoptosis rate,levels of TNF-α,IL-1 βand IL-18 in supernatant,as well as RhoA and ROCK protein expression levels in cells were higher than those of emodin high-dose group,the differences being all statistically significant(P＜0.05).Conclusion Emodin can improve LPS-induced podocyte injury,and its mechanism of action may be related to the inhibition of RhoA/ROCK signaling pathway.

Objective To investigate the knee disorders and risk factors in electromechanical soldiers of a warship,so as to provide a basis for prevention and treatment measures.Methods The knee disorders and treatment data of 200 electromechanical soldiers(study group)and 200 soldiers from other departments(control group)were colected by questionnaire survey and medical records.Results The incidence of knee diseases was 37.5%(75 cases)in the study group,which was significantly higher than that in the control group(16.0%,32 cases,P＜0.05).Traumatic and degenerative diseases were the main types of knee disorders.Age and body mass index were the influencing factors of knee disorders in electromechanical soldiers.Conclusion There is a high incidence of knee disorders in electromechanical soldiers,which is related to a variety of factors.Appropriate prevention and treatment measures are of great significance to reduce the incidence of knee disorders,promote rapid recovery,and reduce non-combat casualty.

Objective:To investigate the regulatory role and mechanism of synaptic vesicle protein 2A (SV2A) in apoptosis of drug-resistant epilepsy neurons.Methods:One hundred and fifty specific pathogen-free (SPF) Sprague-Dawley (SD) rats were randomly numbered; 20 rats were selected as a normal control group (NC group), and the remaining 130 rats were subjected to chronic epilepsy models of lithium-pilocarpine. Phenobarbital and phenytoin sodium for 2 weeks were given to these rats after modeling; fanally, 94 rats with chronic epilepsy were divided into a drug-resistant group (phenobarbital and phenytoin sodium-resistant epilepsy [PRE] group, reduction in episodes<50%, n= 55) and a drug-sensitive group (phenobarbital and phenytoin sodium-sensitive epilepsy [PSE] group, reduction in episodes by≥50%, n=38). Rats in the PRE group were further randomly divided into 5 groups, namely a up-regulated-SV2A PRE group (UPRE group), a down-regulated-SV2A PRE group (DPRE group), a up-regulated-SV2A control group (UPRC group), a down-regulated-SV2A control group (DPRC group), and a non-transfected PRE group; different types of lentivirus were given to the first 4 groups via stereotactic brain injection. Ten days after lentiviral transfection, virus detection was performed; and 2 weeks after lentiviral transfection, occurrence of epileptic seizures was observed, and after that, rats were sacrificed and the hippocampal tissues were collected for subsequent experiments. Western blotting was used to detect the expressions of SV2A, cyclophilin A (CyPA), apoptosis-inducing factor (AIF), and superoxide dismutase 2 (SOD2) in the cell nucleus or mitochondria; coimmunoprecipitation experiment was performed to observe the interaction among SV2A, CyPA and AIF proteins; immunofluorescent co-staining was used to observe the CyPA/AIF localization; mitochondrial damage was detected by electron microscopy; ATP content in the hippocampal tissues was detected by luciferase method, 8-hydroxy-2-deoxyguanosine (8-OHDG) expression was detected by immunofluorescent staining, and neuronal apoptosis rate was calculated by double staining with neuron-specific nuclear protein (NeuN) and TUNEL. Results:(1) Confocal microscopy revealed that the hippocampal tissues in the 4 transfected groups showed green fluorescence inherent to the lentivirus, indicating successful viral infection. Compared with the UPRC group, the UPRE group had significantly reduced frequency of epileptic seizures and seizure duration ( P<0.05). (2) Western blotting showed that, in mitochondria, the UPRE group had significantly higher expressions of SV2A (0.475± 0.105 vs. 0.136±0.043), CyPA (0.473±0.041 vs. 0.175±0.047), AIF (0.443±0.058 vs. 0.131±0.037), and SOD2 (0.457±0.037 vs. 0.152±0.038) compared with the UPRC group ( P<0.05); the DPRE group had significantly decreased expressions of SV2A (0.038±0.013 vs. 0.184±0.047), CyPA (0.041±0.010 vs. 0.214±0.040), AIF (0.040±0.019 vs. 0.175±0.046), and SOD2 (0.043±0.017 vs. 0.187±0.039) compared with the DPRC group ( P<0.05). In the cell nucleus, the UPRE group had significantly lower expressions of AIF (0.336±0.084 vs. 0.649±0.209) and CyPA (0.331±0.086 vs. 0.620±0.162) compared with the UPRC group ( P<0.05); the DPRE group had statistically higher expressions of AIF (0.771± 0.180 vs. 0.519±0.144) and CyPA (0.738±0.223 vs. 0.488±0.091) compared with the DPRC group ( P< 0.05). (3) Co-immunoprecipitation experiment results showed that the bidirectional precipitation results of SV2A and AIF, SV2A and CyPA, and AIF and CyPA were all positive, suggesting existence of interactions. (4) Immunofluorescent co-staining showed that the fluorescence changes of CyPA and AIF were consistent. (5) Electron microscopy showed that mitochondria in the NC group had intact structure; mitochondria in the UPRE group, UPRC group, DPRC group and DPRE group showed swelling and cristae fragmentation; among them, injury in the UPRE group was relatively less severe than that in the UPRC group, while that in the DPRC group was more severe than that in the DPRE group. (6) Compared with the UPRC group, the UPRE group had statistically higher ATP content ( P<0.05); compared with the DPRC group, the DPRE group had significantly lower ATP content ( P<0.05).(7) Immunofluorescent staining results showed that the UPRE group had significantly lower 8-OHDG expression than the UPRC group ( P<0.05); compared with the DPRC group, the DPRE group had statistically higher 8-OHDG expression ( P<0.05). (8) The UPRE group had significantly lower NeuN-TUNEL double staining positive rate than the UPRC group ( P<0.05); compared with the DPRC group, the DPRE group had significantly higher NeuN-TUNEL double staining positive rate ( P<0.05). Conclusion:SV2A can play a role in the apoptosis of hippocampal neurons in rats with drug-resistant epilepsy by regulating the nuclear translocation of AIF/CyPA and mitochondrial damage.

Objective To investigate the effects of time in range(TIR)and microRNA-2245P(miR-2245P)interac-tions on the susceptibility and severity of diabetic retinopathy(DR)in the target range of glucose.Methods A prospec-tive study was conducted on 259 patients with DR(DR group)and 259 patients with type 2 diabetes mellitus(T2DM group)admitted to the Ophthalmology Department of Yantai Yeda Hospital from April 2022 to June 2024.TIR and miR-2245P were compared between the two groups,and the multivariate Logistic analysis was used to identify the factors associated with DR susceptibility.The receiver operating characteristic(ROC)curve was used to evaluate the predictive value of TIR,miR-2245 P,and their combination for DR.The interaction coefficient γ was used to analyze the effect of the interaction between TIR and miR-2245P on DR susceptibility.The Spearman correlation analysis was used to evaluate the correlation of TIR and miR-2245P with DR staging.Results The TIR and miR-2245P levels in the DR group were lower than those in the T2DM group(both P＜0.05).The multivariate logistic regression analysis showed that Logit(P)=0.083-0.470 × TIR-0.584 × miR-2245P,high levels of TIR and miR-2245P were independent protective factors of DR susceptibility(all P＜0.05).The areas under the ROC curve(AUC)of TIR,miR-2245P,and their combination for predicting DR were 0.76,0.79,and 0.91,respectively.The AUC of TIR combined with miR-2245P was greater than that of TIR and miR-2245P(both P＜0.05).The interaction analysis showed that the OR values of DR caused by low levels of TIR and miR-2245P alone were 2.05 and 1.92,respectively.The OR value of the interaction between TIR and miR-2245P was 10.69,greater than the prod-uct of OR values of TIR and miR-2245P alone.It indicates that the effect of the interaction of TIR and miR-2245P on suscep-tibility to DR is a super-multiplication model.The interaction coefficient was γ=3.31＞1,indicating a positive relationship of the interaction between the two factors with DR susceptibility.The Spearman correlation analysis showed that TIR and miR-2245P were negatively correlated with DR staging(both P＜0.001).Conclusion Both TIR and miR-2245P are asso-ciated with DR and its severity,and they have interactive effects on DR susceptibility.Combined detection can improve the predictive value of DR.This study provides a new idea and target for the prevention and treatment of DR.

Objective Prepubertal mice are administered subcutaneously with letrozole sustained-release pellets behind the neck and treated with a high-fat diet to establish a mouse model of polycystic ovary syndrome(PCOS).The liver transcriptomes of the model mice are compared with those of the placebo control mice to investigate the underlying mechanisms of liver involvement in the pathogenesis of PCOS.Methods A customized 2 mg dose of letrozole sustained-release pellets with a 40-day release period was used.The control placebo and letrozole pellets were implanted subcutaneously in the dorsal cervical region of 3-4-week-old C57BL/6J mice(8 mice per group)to establish the control group and letrozole-induced PCOS model group.Both groups were treated with a high-fat diet starting the day after administration.The modeling period lasted for 5 weeks,during which body weight and 24-hour food intake were monitored in each group every week.When samples were collected,liver weight was recorded.Pathological changes in ovarian and hepatic tissues were examined by hematoxylin-eosin(HE)staining,while hepatic lipid deposition was observed by Oil Red O staining.The extent of macrophage infiltration in the liver was evaluated via F4/80 immunohistochemical staining,and hepatic fibrosis levels were observed by Masson's trichrome staining.Transcriptomic sequencing was performed to analyze differentially expressed genes(DEGs)in liver tissues between the control and model groups,followed by enrichment analysis of significant DEGs.Quantitative real-time fluorescent quantitative PCR(qPCR)was subsequently used to validate the expression of significant DEGs in liver tissues of both groups.Results Compared with the control group,the model group which received subcutaneous letrozole sustained-release pellets combined with a high-fat diet exhibited significantly increased body weight(P＜0.001),prominent polycystic ovarian morphology,and significantly decreased liver-to-body weight ratio(P＜0.05).However,no significant changes were observed in absolute liver weight(P＞0.05),hepatic histomorphology,or lipid deposition.Transcriptome sequencing identified 119 upregulated and 217 downregulated DEGs in the liver tissues of letrozole-treated mice,which were predominantly enriched in pathways related to cholesterol and steroid biosynthesis,steroid hormone metabolism,and inflammatory responses.qPCR validation demonstrated that mRNA expression of HSD3B2 and HMGCR was significantly upregulated in liver(P＜0.01),while mRNA expression of IL4,CCL2 and COL1A1 was downregulated(P＜0.05)in the model group compared with the control group.However,Masson's trichrome staining and F4/80 immunohistochemical analysis showed no significant changes in hepatic fibrosis or macrophage infiltration.Conclusion Subcutaneous administration of letrozole sustained-release pellets combined with a high-fat diet successfully establishes a mouse model of PCOS.The model mice exhibited significant changes in hepatic gene expression.Liver may contribute to PCOS pathogenesis through regulating cholesterol and steroid metabolism.