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 This study used The Cancer Genome Atlas (TCGA) database to investigate the methylation levels of PCDHGB7 in lung adenocarcinoma tissues and analyze its association with clinical pathological features of lung adenocarcinoma, and its prognostic predictive value. Methods Methylation data of PCDHGB7 from 473 lung adenocarcinoma tissues and 32 normal tissues in the TCGA database were derived and analyzed to assess between-group variance and determine the correlation of methylation levels with clinical pathological features and overall survival. Results PCDHGB7 exhibited significantly higher methylation levels in lung adenocarcinoma tissues than in normal tissues (P<0.001), demonstrating a strong discriminative ability for lung adenocarcinoma (AUC=0.926, P<0.001). The methylation level was strongly associated with gender (P=0.047) and T stage (P=0.013). The critical prognostic sites of PCDHGB7 were identified through univariate Cox regression analysis. We found significant differences in overall survival between patient groups with low or high methylation levels (P=0.0099). Conclusion PCDHGB7 shows significantly elevated methylation in lung adenocarcinoma, which correlates with tumor malignancy and possesses certain prognostic predictive potential.

BackgroundAnxiety exhibits a rising prevalence among college students. Investigating the mechanisms through which family function relates to anxiety and examining the moderating role of emotion regulation strategies within this context hold substantial implications for promoting mental health among college students. However， existing research has not sufficiently elucidated the complex interplay among family function， emotion regulation， and anxiety among college students. Further research is warranted to clarify the underlying mechanisms linking family function to anxiety outcomes and to examine the potential moderating role of emotion regulation strategies in this causal pathway. ObjectiveTo explore the relationship between family function and anxiety among lower-grade college students， and to validate the moderating role of emotion regulation strategies in this relationship， thereby offering evidence-based insights for anxiety reduction interventions in this population. MethodsIn March 2023， a total of 1 980 first- and second-year students from a comprehensive university in Shanghai were selected using the cluster sampling method. A self-designed demographic questionnaire， the Emotion Regulation Questionnaire （ERQ）， the Family Adaptability and Cohesion Evaluation Scale Ⅱ-Chinese Version （FACES Ⅱ-CV）， and the Symptom Checklist-90 （SCL-90） were utilized for assessment. Pearson correlation analysis and Spearman correlation analysis were employed to test the correlations of each variable. Hierarchical linear regression analysis was conducted to certify the moderating role of emotion regulation strategies in the relationship between family function and anxiety. ResultsCompared with female students， male students scored significantly lower on ERQ cognitive reappraisal （t=-5.793， P<0.01） but significantly higher on ERQ expressive suppression （t=8.359， P<0.01）. For lower-grade college students， scores on adaptability and cohesion subscales of FACES Ⅱ-CV showed a positive association with cognitive reappraisal in ERQ （r=0.251， 0.302， P<0.01）， while simultaneously displaying negative correlations with both expressive suppression in ERQ （r=-0.113， -0.154， P<0.01） and anxiety in SCL-90 （r=-0.243， -0.202， P<0.01）. Notably， anxiety scores in SCL-90 were inversely related to cognitive reappraisal scores in ERQ （r=-0.159， P<0.01） but directly associated with expressive suppression scores in ERQ （r=0.171， P<0.01）. Hierarchical regression analysis indicated that cognitive reappraisal significantly moderated the relationship between family cohesion and anxiety （β=-0.421， P<0.01）. ConclusionThe cognitive reappraisal strategy serves as a moderator in the relationship between family cohesion and anxiety， potentially mitigating the escalation of anxiety levels associated with family dysfunction. ［Funded by Science and Technology Development Fund of Shanghai Pudong New Area （number， PKJ2023-Y21）］

In this work,with tris(4-aminophenyl)amine(TAPA)and 1,3,5-tris(4-formylphenyl)benzene(TFPB)as monomers,an imine-type porous organic polymer,TAPA-TFPB,was synthesized using a simple method under the catalysis of acetic acid.The material TAPA-TFPB was used as solid-phase extraction adsorbent and combined with ultra-performance liquid chromatography/quadrupole time-of-flight-tandem mass spectrometry(UHPLC-QTOF-MS)to establish a detection method for four kinds of nitrofuran metabolites(NFMs)residues in meat samples.The parameters of the adsorbent dosage,the pH value and volume of sample,and the type and volume of washing and eluent solvents were optimized,respectively.Under the optimal extraction conditions,low detection limits(0.11-1.60 μg/kg)were achieved for four kinds of NFMs.At three different spiked levels,the intra-day and inter-day precisions(Relative standard deviations)were 2.8% -10.9% and 4.3% -16.2%,respectively,and the spiked recoveries were 72.0% -107.2%.The results showed that the method chould be used for efficient extraction and analysis of trace NFMs residues in meat samples,indicating that TAPA-TFPB was a kind of promising SPE adsorbent.

Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*

The mandibular condyle is a critical growth center in craniofacial bone development, especially during postnatal stages. Postnatal condyle osteogenesis requires precise spatiotemporal coordination of growth factor signaling cascades and hierarchical gene regulatory networks. Plagl1, which encodes a zinc finger transcription factor, is a paternally expressed gene. We demonstrate that PLAGL1 is highly expressed in cranial neural crest cell (CNCC)-derived lineage cells in mouse condyles. Using the CNCC-derived lineage-specific Plagl1 knockout mouse model, we evaluate the function of PLAGL1 during postnatal mouse condyle development. Our findings show that PLAGL1 contributes significantly to osteoblast differentiation, and its deficiency impairs osteogenic lineage differentiation, which consequently disrupts mandibular condyle development. Mechanistically, insulin-like growth factor 2 (IGF2) in complex with IGF-binding proteins (IGFBPs) has been identified as the principal PLAGL1 effector responsible for osteogenic regulation during postnatal condyle morphogenesis. Plagl1 deficiency significantly downregulates the IGF2/IGFBP pathway, leading to disordered glucose metabolism, defective extracellular matrix organization, and impaired ossification. Exogenous IGF2 treatment rescues impaired osteoblast differentiation caused by Plagl1 deficiency. In conclusion, the PLAGL1-IGF2 axis is a critical regulator of osteogenesis during mandibular condyle development.
Animals ; Osteogenesis/genetics* ; Insulin-Like Growth Factor II/metabolism* ; Mice ; Transcription Factors/metabolism* ; Mice, Knockout ; Cell Differentiation ; DNA-Binding Proteins/genetics* ; Mandibular Condyle/growth & development* ; Osteoblasts/cytology* ; Signal Transduction ; Neural Crest/cytology*

ObjectiveTo investigate the preventive effect and mechanism of Dendrobium officinale （DO） on non-alcoholic fatty liver disease （NAFLD） by network pharmacology and animal experiments. MethodsDO components in blood after administration were identified and analyzed using ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap high-resolution mass spectrometry （UPLC-QE-HF-MS/MS）. Network pharmacology and molecular docking methods were employed to obtain active ingredients and potential targets of DO for NAFLD control. High-fat feeds were used to replicate the NAFLD rat model. Biochemical kits were used for detecting the expression levels of blood lipids， hepatic lipids， and liver functions of rats. Hematoxylin-eosin （HE） staining and oil red O staining were employed to observe pathological changes in rat liver， and real-time fluorescence quantitative PCR （Real-time PCR） assay was performed to validate potential targets obtained from the network pharmacology analysis. ResultsA total of 13 DO components were identified in blood， including berberine， dihydrosanguinarine， and oxypeucedanin. A total of 14 potential targets were screened through network pharmacology， including Forkhead box protein O1 （FoxO1）， epidermal growth factor receptor （EGFR）， and insulin-like growth factor 1 （IGF-1R）， involving pathways such as the advanced glycation end product （AGE）/receptor for AGE （RAGE） signaling pathway， blood lipids and atherosclerosis， insulin resistance， and FoxO signaling. The results of animal experiments showed that the NAFLD rat model was successfully replicated. After the preventive treatment with DO for NAFLD rats， the indexes of blood lipids， hepatic lipids， and liver function were normalized； lipid deposition and lesions in the liver were significantly improved； the expression level of FoxO1 mRNA in the liver was significantly reduced （P<0.05）， and the mRNA expression levels of phosphatidylinositide 3-kinases （PI3K）， protein kinase B （Akt）， EGFR， and IGF-1R were significantly increased （P<0.05）. ConclusionDO has a preventive effect on NAFLD rats， and the mechanism of action may be related to the modulation of IGF1R and EGFR targets and activation of the PI3K/Akt/FoxO1 signaling pathway.