Doxorubicin (DOX)-induced cardiotoxicity and sepsis-induced myocardial injury (SIMI) represent significant clinical challenges in patients undergoing chemotherapy, sharing a common pathological basis of oxidative stress and mitochondrial dysfunction. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently been shown to play a critical role in DOX-induced cardiotoxicity and lipopolysaccharide (LPS)-induced SIMI. This article systematically reviews the mechanisms underlying myocardial injury caused by DOX and sepsis, identifying ferroptosis as a central common pathway. DOX triggers a burst of reactive oxygen species within mitochondria and inhibits glutathione peroxidase 4 (GPX4) activity through redox cycling of its quinone group and high-affinity accumulation in mitochondrial cardiolipin. LPS, by activating pattern recognition receptors and related inflammatory signaling pathways, provokes a cytokine storm and mitochondrial dysfunction. Both can disrupt the core regulatory axis of cysteine-glutathione (GSH)-GPX4, synergistically promoting ferroptosis in cardiomyocytes. Moreover, epigenetic regulation plays a key role in DOX- and LPS-induced cardiomyocyte ferroptosis and may serve as a promising therapeutic target. A deeper understanding of the ferroptosis mechanism and its epigenetic regulatory network in the synergistic injury induced by DOX and sepsis is of great importance for developing novel strategies to mitigate chemotherapy-related cardiotoxicity and improve outcomes in cancer patients with concurrent infections.

Objective To explore the non-invasive diagnostic criteria of magnetocardiography (MCG) for coronary microvascular dysfunction (CMVD), and its value in dynamically assessing drug treatment for CMVD. Methods Patients who presented with chest tightness or chest pain at Zhongshan Hospital, Fudan University from September 2024 to March 2025 were consecutively enrolled, and all of whom had non-obstructive coronary arteries on angiography. Using the coronary angiography-derived index of microcirculatory resistance (caIMR) as the gold standard, patients were divided into a normal microcirculation group (caIMR≤40 U) and a CMVD group (caIMR＞40 U). MCG testing was performed using a domestic device (MD-U041001, Mind Medical). Patients in the CMVD group received adenosine treatment and underwent repeat MCG after medication. Differences in MCG parameters between the two groups were analyzed, and a diagnostic model was established. The value of the diagnostic model was analyzed using receiver operating characteristic (ROC) curves. Results A total of 311 patients were included, with 135 in the normal microcirculation group and 176 in the CMVD group. The CMVD group had a significantly higher proportion of males (61.9% vs 47.4%, P＝0.012), and lower high-density lipoprotein cholesterol (HDL-C) levels ([1.16±0.31] mmol/L vs [1.24±0.29] mmol/L, P＝0.029) than the normal group. Eleven MCG parameters showed significant differences between the two groups (P＜0.05), among which increased values of mfm_QR_epav, mfm_RS_epmse, space_zeroRTrot, as well as decreased value of mfm_QR_v1 were independent predictors of CMVD. The diagnostic model based on these 11 MCG parameters yielded an area under the curve (AUC) of 0.688 (95%CI 0.629-0.747). The integrated diagnostic model combining clinical risk factors (male, smoking history, HDL-C) with MCG parameters had an AUC of 0.701 (95%CI 0.643-0.759). After adenosine treatment, patients in the CMVD group showed significant decreases in mfm_QR_epav (P＝0.010), mfm_RS_sad (P＝0.013), and mfm_RS_epmse (P＝0.046). Conclusions The model based on MCG parameters demonstrates good diagnostic ability for CMVD; dynamic changes in MCG parameters following adenosine intervention may serve as potential objective indicators for evaluating microcirculatory treatment efficacy.

ObjectiveTo investigate the effects of Schisandrae Chinensis Fructus lignans on schizophrenia induced by dizocilpine maleate （MK-801） in mice and to clarify its mechanism. MethodsMale mice of 4-6 weeks old were randomized into blank， model， positive drug， and low-， medium-， and high-dose （40， 80， 160 mg·kg^-1， respectively） Schisandrae Chinensis Fructus lignans groups. The blank group was administrated with distilled water， and the other groups were injected with 0.5 mg·kg^-1 MK-801 to induce schizophrenia symptoms. Meanwhile， risperidone was injected at 0.2 mg·kg^-1 in the positive drug group， and mice in the intervention groups were injected with corresponding drugs for 14 consecutive days. The behavioral changes of mice were observed by autonomous activity test， open field test， forced swimming test， and water maze test. The levels of dopamine （DA） and 5-hydroxytryptamine （5-HT） in the brain and tumor necrosis factor-α （TNF-α） and nuclear factor-κB （NF-κB） in peripheral blood were quantified by enzyme-linked immunosorbent assay （ELISA）. The changes in the prefrontal lobe of mice were observed by hematoxylin-eosin staining， and the changes of the hippocampal tissue were observed by Nissl staining. The protein levels of silencing information regulatory factor 1 （SIRT1） and forkhead box protein O3a （FoxO3a） in the hippocampus of mice were determined by Western blot. ResultsCompared with the model group， low， medium， and high doses of Schisandrae Chinensis Fructus lignans reduced the total number of autonomous activities， total distance in the open field test， immobile time in the forced swimming test， and levels of TNF-α and NF-κB in peripheral blood （P<0.05）， while increasing the number of platform crossings in the water maze test and DA and 5-HT levels in the brain tissue （P<0.05）. Compared with the model group， risperidone and low， medium， and high doses of Schisandrae Chinensis Fructus lignans improve the neural cell morphology in the CA1 region， with full cells in neatly dense arrangement and exhibiting clear membrane boundary. Schisandrae Chinensis Fructus lignans inhibited the expression of SIRT 1 and FoxO3a in the hippocampus （P<0.05）. ConclusionTo sum up， Schisandrae Chinensis Fructus lignans may improve the behavior of schizophrenic mice by activating the SIRT1/FoxO3a signaling pathway to exert neuroprotective effects.

Objective To investigate the role and regulatory mechanism of LINC00657 in the progression of cervical cancer. Methods Bioinformatics analysis predicted potential binding sites between LINC00657 and miR-30a-5p and between miR-30a-5p and Skp2. These sites were verified by using RNA immunoprecipitation and dual-luciferase reporter experiments. LINC00657, miR-30a-5p, and Skp2 mRNA expression levels in cervical cancer tissues and cell lines were assessed by utilizing RT-qPCR. Western blot analysis was employed to examine the protein levels of Skp2 in cells and subcutaneous xenograft tumor models in nude mice. Immunohistochemistry was applied to analyze Skp2 expression in animal tissues. The cellular processes of cervical cancer cell lines were evaluated through CCK-8, scratch, and Transwell assays. Results LINC00657 and Skp2 presented binding sites for miR-30a-5p. In cervical cancer, LINC00657 and Skp2 showed high expression levels (P<0.05), whereas miR-30a-5p displayed low expression (P<0.05). Functional experiments demonstrated that linc00657 upregulates Skp2 expression, a process that is dependent on its sequestration of miR-30a-5p. Conclusion LINC00657 promoted the malignant progression of cervical cancer by upregulating Skp2 expression through specifically sequestering miR-30a-5p, thereby relieving its inhibitory effect on the target gene Skp2.

Current formulation of objective performance criteria （OPC） in traditional Chinese medicine （TCM） faces methodological challenges， including poor reporting quality， insufficient standardization of methods， limited comparability of study populations， and inadequate consideration of the genetic and environment particularities of ethnic minority populations. In response to these issues， this paper proposes optimization strategies for setting OPC in TCM， with particular attention to ethnic minority medicine. These include improving methodological techniques and statistical descriptions， ensuring transparency in meta-analyses and data sources； standardizing the estimation of point estimates and confidence intervals， and incorporating multidisciplinary expert consensus for value determination； introducing local real-world data from the same period， especially cohort study evidence， to compensate for the lack of high-quality randomized controlled trial data. Through process transparency and dynamic updating mechanisms， the credibility of OPC method can be enhanced， thereby providing methodological support for strengthening evidence-based research capacity in this field.

Objective To investigate the expression characteristics, prognostic value, and correlation with immune infiltration of vasoactive intestinal peptide receptor 2 (VIPR2) in esophageal adenocarcinoma (ESAD). Methods Transcriptome data of 80 ESAD and 10 normal tissues were retrieved from the TCGA database. Immune-related differential genes were identified by integrating the ImmPort database. Cox regression analysis was applied to evaluate the prognostic significance of VIPR2. GSVA and ssGSEA were employed to assess the association between VIPR2 and immune-cell infiltration. Functional enrichment was performed using GO, KEGG, and GSEA. Results VIPR2 expression was significantly downregulated in ESAD tissues (P<0.05). High VIPR2 expression was associated with prolonged overall survival (HR=0.246, P=0.047), serving as an independent prognostic factor. Fifteen immune-cell types, including CD8⁺ T cells, NK cells, and dendritic cells, showed significantly higher infiltration in the VIPR2-high group, whereas Th17-cell abundance was decreased (P<0.05). Enrichment analyses revealed that VIPR2 participated in multiple tumor-immune pathways and was positively correlated with PD-1 and CTLA-4 expression (P<0.01). Conclusion VIPR2 may serve as a potential biomarker in the prognostic assessment and could modulate the tumor-immune microenvironment in ESAD.

AIM:To evaluate the accuracy of a portable non-contact tonometer(PNCT)compared with a traditional non-contact tonometer(NCT)in measuring intraocular pressure(IOP)at different levels.METHODS:Patients who presented to Ningbo Eye Hospital between January 2025 and January 2026 were retrospectively included. All patients underwent measurements using PNCT, NCT, and Goldmann applanation tonometry(GAT). Based on the GAT measurements, the patients were categorized into a low IOP group(IOP≤16 mmHg), a moderate IOP group(16 mmHg0.05). Spearman correlation analysis revealed that the IOP values measured by both PNCT and NCT were positively correlated with those measured by GAT(rs=0.86 and 0.84, respectively, P<0.05). Intraclass correlation coefficient(ICC)analysis demonstrated an ICC of 0.89 between PNCT and GAT(P<0.05), and 0.88 between NCT and GAT(P<0.05), with an overall ICC of 0.88 among the three instruments(P<0.05). Bland-Altman analysis indicated a mean bias of 0.1 mmHg [95% limits of agreement(LoA): -7.3 to 7.6 mmHg] between PNCT and GAT, and a mean bias of 0.1 mmHg(95%LoA: -8.4 to 8.6 mmHg)between NCT and GAT. Based on the GAT measurements, the eyes were categorized into a low IOP group(60 eyes, 32.6%, IOP≤16 mmHg), a moderate IOP group(63 eyes, 34.2%, 16 mmHg0.05), whereas the difference between NCT and GAT showed a positive correlation with CCT(rs=0.23, P<0.05).CONCLUSION:The IOP measurements obtained by PNCT, NCT, and GAT demonstrated strong correlation and good agreement, with PNCT being less influenced by CCT. However, as IOP levels increased, the measurement errors of both PNCT and NCT also increased. Therefore, PNCT and NCT readings should only serve as references and cannot replace GAT.

ObjectiveTo construct an interleukin-9 （Il9） gene knockout mouse model on a C57BL/6N background， establish a reliable genotyping method， and provide a standardized animal model for investigating Il9-related immune mechanisms and diseases. MethodsIl9 knockout mouse strain （C57BL/6N-Il9^em1Cya） was generated using conventional gene knockout technology. The method for DNA extraction from mouse tails was optimized to ensure template quality. Two sets of specific primers （F1/R1 and F1/R2） were designed to amplify target fragments by PCR， and mouse genotypes were determined by agarose gel electrophoresis. Specifically， primer pair F1/R1 targeted the knockout sequence with an expected product of 465 bp， while F1/R2 targeted the wild-type sequence with an expected product of 703 bp. Subsequently， Western blot was performed to verify the knockout efficiency of Il9 in primary immune cells and key organs of the offspring mice， and flow cytometry was used to assess the effects of Il9 deficiency on the function of the immune system in major immune cell populations. ResultsIl9 knockout mice were successfully bred and genotyped. PCR identification showed that homozygous mice （-/-） exhibited only a 465 bp band， wild-type mice （+/+） displayed only a 703 bp band， and heterozygous mice （+/-） showed both bands simultaneously. Meanwhile， Western blot analysis revealed significantly decreased IL-9 expression in various organs of the offspring mice （P<0.001）. Flow cytometric results demonstrated that Il9 deficiency exerted no obvious effects on the proportions of peripheral blood lymphocytes， splenic lymphocytes， and peritoneal macrophages. ConclusionAn Il9 gene knockout mouse model on a C57BL/6N background is successfully constructed. The established PCR genotyping system is highly efficient and accurate， which can effectively distinguish mice of different genotypes. This model provides a stable and reliable experimental basis for subsequent functional studies of Il9 and exploration of the mechanisms underlying Il9-related diseases.

With a growing public emphasis on oral health, efficacy-focused toothpastes have become mainstream. By combining chemical active ingredients with mechanical cleaning, these products deliver multifunctional benefits, such as caries prevention, dentin hypersensitivity relief, whitening, and anti-inflammation. This article systematically reviews recent advances in key efficacious ingredients across four functional domains: fluoride, often supplemented with calcium-phosphorus compounds, probiotics, and herbal preparations, primarily prevents caries; antibacterial and anti-inflammatory effects arise from multi-ingredient synergy; anti-hypersensitivity works via physical occlusion and nerve inhibition, with herbal extracts as natural alternatives; and whitening involves mechanical abrasion, chemical action, and optical modification. However, current research remains fragmented and repetitive, lacking a systematic evidence base. This complicates evidence-based consumer choice, while studies on precision and personalized formulations are still limited. Future efforts should establish comprehensive efficacy evaluation systems, investigate multi-component synergies, and advance precision toothpaste development tailored to individual oral microbiomes and needs. By summarizing ingredients, mechanisms, efficacy, and safety elements, this review aims to support optimized toothpaste formulation and clinical application, thereby contributing to oral healthcare precision.

The disease-syndrome combination model of spleen deficiency with dampness pattern in ulcerative colitis（SDDP-UC） is an important experimental carrier for traditional Chinese medicine （TCM） research on the prevention and treatment of ulcerative colitis （UC）， and the quality of model construction and evaluation directly influences the scientific rigor and translational value of related research conclusions. However， this field still lacks methodological synthesis and a standardized consensus. Based on a comprehensive review of existing literature， this paper summarized isomorphic cues between the spleen deficiency with dampness pattern and UC across four dimensions， including energy metabolism， immune homeostasis， mucosal barrier， and intestinal microecology. The cues were mainly involved in impaired mitochondrial energy supply and glucose metabolic reprogramming， a lowered pro-inflammatory threshold of innate immunity with insufficient adaptive immune regulation， disruption of epithelial barrier gating accompanied by compromised repair capacity， and attenuation of the luminal hypoxia barrier with accumulation of toxic metabolites. A mutually reinforcing process between local "form damage" and systemic "Qi depletion" was further interpreted from a holistic perspective. Regarding modeling strategies， existing studies predominantly use rats as the carrier， apply combined interventions such as improper diet， external damp exposure， and fatigue-related dysregulation to establish the spleen deficiency with dampness pattern background， and subsequently superimpose chemical stimulation to induce UC-like colonic damage， with a total modeling period generally spanning three to four weeks. In terms of the evaluation system， a multidimensional framework integrating syndrome assessment， histopathology， mechanistic indices， and pharmacodynamic counter-verification was outlined. On this basis， current methodological bottlenecks of models were systematically identified， including syndrome drift risk and compounded stress dilemma in temporal sequencing， syndrome confounding from etiological simulation， cross-sectional evaluation bias related to modeling duration， inadequate disease-syndrome linkage and control design within the evaluation system， and limited controls with overly single-track decision logic in formula-based syndrome verification. To address the above issues， a construction and evaluation strategy emphasizing streamlining of core etiological factors， multi-node dynamic monitoring， integration of core disease-syndrome indicator clusters， and establishment of a formula-based syndrome verification system was proposed， providing a reference for the standardized construction and scientific evaluation of the SDDP-UC model.