Animal experimentation constitutes a critical link between basic research and clinical application, making its research quality and translational efficiency paramount. Although considerable progress has been made in standardizing operational procedures and ethical guidelines, the standardization of outcome evaluation systems has significantly lagged, creating a key bottleneck that constrains the quality of biomedical research and evidence synthesis. This deficiency is manifested by pronounced heterogeneity in outcome selection across similar studies, incomplete methodological reporting, and disparate criteria for result interpretation, which severely impairs the comparability of findings and the evidence integration. To cope with this challenge, this paper systematically introduces a mature methodological tool from clinical research–the core outcome set (COS)–and explores its construction strategies and application potential in the field of animal experimentation. Given the extensive diversity of animal experiments, a pragmatic strategy of "focusing on key areas, implementing phased pilots, and promoting gradual expansion" should be adopted. This approach prioritizes the development of domain-specific COS for disease areas characterized by high research volume, urgent translational needs, and well-established animal models. A multi-source integration pathway for COS development is detailed, comprising systematic literature searches, methodological appraisals, and expert consensus, with the feasibility of leveraging artificial intelligence (AI) to enhance efficiency also being examined. The development and promotion of such COS are not intended to restrict scientific exploration; rather, they aim to establish a new, tiered evaluation paradigm consisting of "core outcomes" (mandatory), "recommended outcomes" (encouraged), and "exploratory outcomes" (optional). This framework is expected not only to enhance research quality through standardization and to adhere to the "3R" principles but also to accelerate the accumulation of high-quality evidence. This, in turn, provides a solid foundation for higher-level evidence synthesis, ultimately facilitating the effective translation of basic research findings into clinical practice and providing an essential methodological framework for scientific advancement in relevant disciplines.

ObjectiveTo explore the possible mechanism of Tongbian Decoction （通便汤， TD） in treating slow transit constipation （STC）. MethodsTwenty-four SD rats were randomly divided into normal group， model group， TD group， and mosapride group， with 6 rats per group. Except for the normal group， STC models were established by intragastric administration of loperamide hydrochloride combined with normal saline. On the day following successful model establishment， rats in the TD group received 18.63 g·kg⁻¹ of TD by gavage， while those in the mosapride group received 1.605 mg·d⁻¹ of mosapride， and those in the normal group and the model group received 10 ml·kg⁻¹ of normal saline by gavage. All treatments were administered once daily for 7 consecutive days. Twenty-four hours after the last administration， fecal pellet number and fecal water content were measured. After intragastric administration of a 10% activated charcoal suspension， the small intestinal transit rate was calculated 30 minutes later. Serum levels of gastrin （GAS） and motilin （MTL） were measured by ELISA. Colonic histopathology was observed by HE staining， and mucus secretion by Alcian blue-periodic acid-Schiff （AB-PAS） staining. Ultrastructure of colon tissue was examined using transmission electron microscopy. Protein expression levels of C-kit， stem cell factor （SCF）， autophagy-related protein 5 （ATG5）， Beclin1， vesicle-associated membrane protein B （VAPB）， and protein tyrosine phosphatase interacting protein 51 （VAPB-PTPIP51） were measured by Western Blot， and the mRNA levels were detected by real-time PCR. Immunohistochemistry was used to detect SCF， C-kit， Beclin1， and ATG5 expression. The calcium content in colon tissue was determined by ELISA. ResultsCompared to the normal group， rats in the model group showed significantly reduced fecal pellet number， fecal water content， small intestinal transit rate， and serum GAS and MTL levels （P＜0.01）； the number of goblet cells decreased， and the mucosal and muscular layers of the colon became thinner； mRNA and protein expression levels of ATG5 and Beclin1 in colon tissue significantly increased， while calcium content decreased （P＜0.05 or P＜0.01）； and electron microscopy revealed vacuolar degeneration and increased autophagosomes in colonic cells. Compared to the model group， both TD group and mosapride group showed increased fecal pellet number， fecal water content， small intestinal transit rate， serum GAS and MTL levels， and colonic calcium content， along with decreased Beclin1 and ATG5 protein levels （P＜0.05 or P＜0.01）； the mucosal thickness and goblet cell number increased significantly， and autophagosomes decreased； in the TD group， ATG5 and Beclin1 mRNA levels decreased； in the mosapride group， SCF， VAPB， and PTPIP51 mRNA levels increased， while Beclin1 mRNA decreased （P＜0.05 or P＜0.01）. Compared to the mosapride group， the TD group showed higher fecal pellet number， fecal water content， serum GAS levels， colonic calcium content， and C-kit expression， along with lower ATG5 and Beclin1 levels （P＜0.05 or P＜0.01）. ConclusionTD may improve constipation symptoms by upregulating the VAPB-PTPIP51 complex during mitochondria-endoplasmic reticulum interactions， reducing autophagy of interstitial cells of Cajal， and promoting intestinal motility.

ObjectiveTo explore the possible mechanism of Tongbian Decoction （通便汤， TD） in treating slow transit constipation （STC）. MethodsTwenty-four SD rats were randomly divided into normal group， model group， TD group， and mosapride group， with 6 rats per group. Except for the normal group， STC models were established by intragastric administration of loperamide hydrochloride combined with normal saline. On the day following successful model establishment， rats in the TD group received 18.63 g·kg⁻¹ of TD by gavage， while those in the mosapride group received 1.605 mg·d⁻¹ of mosapride， and those in the normal group and the model group received 10 ml·kg⁻¹ of normal saline by gavage. All treatments were administered once daily for 7 consecutive days. Twenty-four hours after the last administration， fecal pellet number and fecal water content were measured. After intragastric administration of a 10% activated charcoal suspension， the small intestinal transit rate was calculated 30 minutes later. Serum levels of gastrin （GAS） and motilin （MTL） were measured by ELISA. Colonic histopathology was observed by HE staining， and mucus secretion by Alcian blue-periodic acid-Schiff （AB-PAS） staining. Ultrastructure of colon tissue was examined using transmission electron microscopy. Protein expression levels of C-kit， stem cell factor （SCF）， autophagy-related protein 5 （ATG5）， Beclin1， vesicle-associated membrane protein B （VAPB）， and protein tyrosine phosphatase interacting protein 51 （VAPB-PTPIP51） were measured by Western Blot， and the mRNA levels were detected by real-time PCR. Immunohistochemistry was used to detect SCF， C-kit， Beclin1， and ATG5 expression. The calcium content in colon tissue was determined by ELISA. ResultsCompared to the normal group， rats in the model group showed significantly reduced fecal pellet number， fecal water content， small intestinal transit rate， and serum GAS and MTL levels （P＜0.01）； the number of goblet cells decreased， and the mucosal and muscular layers of the colon became thinner； mRNA and protein expression levels of ATG5 and Beclin1 in colon tissue significantly increased， while calcium content decreased （P＜0.05 or P＜0.01）； and electron microscopy revealed vacuolar degeneration and increased autophagosomes in colonic cells. Compared to the model group， both TD group and mosapride group showed increased fecal pellet number， fecal water content， small intestinal transit rate， serum GAS and MTL levels， and colonic calcium content， along with decreased Beclin1 and ATG5 protein levels （P＜0.05 or P＜0.01）； the mucosal thickness and goblet cell number increased significantly， and autophagosomes decreased； in the TD group， ATG5 and Beclin1 mRNA levels decreased； in the mosapride group， SCF， VAPB， and PTPIP51 mRNA levels increased， while Beclin1 mRNA decreased （P＜0.05 or P＜0.01）. Compared to the mosapride group， the TD group showed higher fecal pellet number， fecal water content， serum GAS levels， colonic calcium content， and C-kit expression， along with lower ATG5 and Beclin1 levels （P＜0.05 or P＜0.01）. ConclusionTD may improve constipation symptoms by upregulating the VAPB-PTPIP51 complex during mitochondria-endoplasmic reticulum interactions， reducing autophagy of interstitial cells of Cajal， and promoting intestinal motility.

OBJECTIVE To investigate the therapeutic effect and mechanism of Qiwei dongqingye powder （QDP） on bronchial asthma in mice. METHODS The mice were divided into blank group （normal saline）， model group （normal saline）， dexamethasone group （2 mg/kg）， and QDP low-， medium-， and high-dose groups （200， 400， 800 mg/kg）， with 14 mice in each group. Except for the blank group， mice in all other groups were given ovalbumin via intraperitoneal injection followed by aerosol inhalation to induce a bronchial asthma model. During the modeling process， mice in each group were administered corresponding drug solutions or normal saline intragastrically/intraperitoneally. After the last medication， the number of cells in the bronchoalveolar lavage fluid （BALF） of the mice was observed and counted； the pathological changes of the bronchus and lung tissue were observed； the levels of malondialdehyde （MDA）， nitric oxide （NO）， total superoxide dismutase （T-SOD）， and glutathione peroxidase （GSH-Px） in the lung tissue of the mice were determined， and the level of interleukin-17 （IL-17） in the BALF and serum was determined. Transcriptomics was employed to predict and validate the mechanism of action of QDP against bronchial asthma. RESULTS Compared with the model group， the total cell count， neutrophil count， lymphocyte count， and macrophage counts in the BALF of the QDP high-dose group were all significantly reduced （ P ＜0.05）； the levels of MDA and NO in the lung tissue， and the levels of IL-17 in the BALF and serum were all decreased significantly （ P ＜0.05）； the levels of T-SOD and GSH-Px were significantly increased （ P ＜0.05）； the arrangement of lung tissue cells tended to normalize， with reduced infiltration of inflammatory cells and decreased exfoliation of bronchial simple columnar epithelial cells. The transcriptomic results revealed that the differentially expressed genes were B-cell receptor signaling pathway， nuclear factor κB （NF-κB） signaling pathway， ferroptosis signaling pathway， and others. Further validation revealed that， compared with the model group， the expression levels of NF-κB p65 and chemokine ligand 20， as well as the phosphorylation level of NF-κB inhibitor protein α， were significantly decreased in the lung tissues of the mice in all QDP groups （ P ＜0.05）. Conversely， the protein expression of nuclear factor erythroid 2-related factor 2 （Nrf2） and heme oxygenase 1 （HO-1） were significantly increased （ P ＜0.05）. CONCLUSIONS QDP can effectively alleviate bronchial asthma by inhibiting the NF-κB signaling pathway， activating the Nrf2/HO-1 signaling pathway， regulating oxidative stress， and reducing inflammatory responses.

Acute lung injury （ALI） is a life-threatening condition characterized by uncontrolled pulmonary inflammatory responses， presenting high morbidity and mortality rates that pose serious threats to patient health. The pathogenesis of ALI involves complex interactions among pathological mechanisms including immune-inflammatory responses， disruption of the alveolar-capillary barrier， mesenchymal stem cell dysfunction， metabolic disorders， ferroptosis， and alterations in the gut microbiota. The dysregulation of programmed cell death （PCD） has increasingly emerged as a research focus. PCD represents a genetically regulated autonomous process of cell death， crucial for maintaining the internal stability of organisms. Recent studies indicate that multiple PCD modes， including apoptosis， pyroptosis， necroptosis， autophagy， and ferroptosis， participate in the development and progression of ALI by mediating pathological processes such as alveolar epithelial cell injury and vascular endothelial barrier disruption. Current therapeutic approaches for ALI encompass lung-protective ventilation， body fluid management， mesenchymal stem cell therapy， and pharmacological interventions. While these measures may alleviate clinical symptoms， they remain unable to reverse the pathological progression of lung injury. Traditional Chinese medicine （TCM） possesses the unique advantages of a holistic perspective and syndrome differentiation-based treatment， achieving breakthrough progress in targeted PCD intervention for ALI. It can mitigate pulmonary tissue injury by suppressing inflammatory responses， regulating immune function， and improving coagulation disorders， thereby delaying the onset and progression of ALI. This paper delves into the molecular mechanisms of PCD in ALI， systematically reviewing the effects of TCM extracts， active constituents （terpenoids， saponins， flavonoids， and phenols）， and compound formulas （e.g.， Qingjie Huagong prescription， Maxing Kugan Tang， and Yifei Jianpi prescription） in improving pulmonary epithelial cell function and mitigating lung injury by modulating PCD pathways. This review aims to provide theoretical underpinnings and novel directions for drug development in the clinical prevention and treatment of ALI.

Acute lung injury （ALI） is a life-threatening condition characterized by uncontrolled pulmonary inflammatory responses， presenting high morbidity and mortality rates that pose serious threats to patient health. The pathogenesis of ALI involves complex interactions among pathological mechanisms including immune-inflammatory responses， disruption of the alveolar-capillary barrier， mesenchymal stem cell dysfunction， metabolic disorders， ferroptosis， and alterations in the gut microbiota. The dysregulation of programmed cell death （PCD） has increasingly emerged as a research focus. PCD represents a genetically regulated autonomous process of cell death， crucial for maintaining the internal stability of organisms. Recent studies indicate that multiple PCD modes， including apoptosis， pyroptosis， necroptosis， autophagy， and ferroptosis， participate in the development and progression of ALI by mediating pathological processes such as alveolar epithelial cell injury and vascular endothelial barrier disruption. Current therapeutic approaches for ALI encompass lung-protective ventilation， body fluid management， mesenchymal stem cell therapy， and pharmacological interventions. While these measures may alleviate clinical symptoms， they remain unable to reverse the pathological progression of lung injury. Traditional Chinese medicine （TCM） possesses the unique advantages of a holistic perspective and syndrome differentiation-based treatment， achieving breakthrough progress in targeted PCD intervention for ALI. It can mitigate pulmonary tissue injury by suppressing inflammatory responses， regulating immune function， and improving coagulation disorders， thereby delaying the onset and progression of ALI. This paper delves into the molecular mechanisms of PCD in ALI， systematically reviewing the effects of TCM extracts， active constituents （terpenoids， saponins， flavonoids， and phenols）， and compound formulas （e.g.， Qingjie Huagong prescription， Maxing Kugan Tang， and Yifei Jianpi prescription） in improving pulmonary epithelial cell function and mitigating lung injury by modulating PCD pathways. This review aims to provide theoretical underpinnings and novel directions for drug development in the clinical prevention and treatment of ALI.

Objective:To explore the clinical efficacy of retrograde tibial intramedullary nail (RTN) combined with less invasive stabilization system (LISS) in the treatment of distal femoral fractures.Methods:A retrospective analysis was conducted on the data of 11 patients with distal femoral fractures who underwent RTN combined with LISS locking plate treatment at the 909th Hospital from June 2021 to December 2022. There were 5 males and 6 females, with an average age of 56.5±17.5 years. The fracture types were AO/OTA 33A2 in 2 cases, A3 in 2 cases, C1 in 2 cases, and C2 in 2 cases. There were 3 cases of periprosthetic femoral fractures after total knee arthroplasty (TKA), all classified as Rorabeck type Ⅱ. They were treated with retrograde intramedullary nailing of the tibia combined with a minimally invasive lateral internal fixation system. The operation time, intraoperative blood loss, fracture healing time, full weight-bearing time, femorotibial angle, range of motion (ROM) of the knee joint, Hospital for Special Surgery (HSS) score, visual analogue scale (VAS) for pain, and complications were recorded.Results:The operation was successfully completed in all 11 cases. The operation time was 98.3±9.0 min (range 83-115 min), and the intraoperative blood loss was 167.8±24.3 ml (range 120-210 ml). All 11 cases were followed up for 11.0±1.9 months (range 9-15 months). The healing time of 11 cases was 5.3±0.8 months (range 4-6 months) after operation. The time of complete weight-bearing activity after operation was 55.7±6.5 d (range 46-67 d). At the last follow-up, the femoral-tibial angle of 11 cases was 171.2°±1.8° (range 169°-174°), the ROM of knee joint was 129.5°±4.7° (range 120°-135°), and the HSS score was 86.8±6.9 points (range 69-95 points). There were no major complications except for one case of superficial infection of surgical incision after operation.Conclusion:RTN combined with lateral LISS locking plate showed good clinical effect with the advantages of less trauma, reliable fixation, rapid recovery, less postoperative complications.

Objective:To investigate the clinicopathological characteristics and diagnostic criteria of cutaneous melanocytic tumor with CRTC1::TRIM11 fusion (CMTCT), and to improve understanding of this entity.Methods:The clinical features, histology, immunohistochemistry (IHC) and molecular characteristics of 3 CMTCT cases were analyzed, supplemented by a literature review.Results:All patients were female, aged 53, 46 and 46 years, respectively. Grossly, the lesions presented as dermal/subcutaneous nodules protruding from the skin surface. Histologically, tumor cells were arranged in nested and fascicular patterns separated by delicate fibrous septa. Tumor cell infiltration was observed in the epidermis of case 1, but not in that of cases 2 and 3. Tumor cells exhibited epithelioid, spindle-shaped, or oval morphology, with eosinophilic or pale cytoplasm and mild to moderate nuclear atypia. Tumor mitotic figure was <5/10 HPF. Scant melanin pigment was observed in case 2. IHC demonstrated diffuse and strong positivity for SOX-10, S-100 protein and MITF. HMB45 was negative in two cases (case 1 and case 3) and focally positive in case 2; Melan A was negative in two cases (case 1 and case 3) and partially positive in case 2. The Ki-67 proliferation index was approximately 5%-8%. Molecular analysis revealed CRTC1::TRIM11 fusion in three cases via RNA sequencing, and CRTC1 rearrangement in two cases (case 1 and case 3) via fluorescence in situ hybridization.Conclusions:CMTCT shares histological and immunophenotypic features with melanoma and clear cell sarcoma but is defined by the presence of CRTC1::TRIM11 fusion, necessitating molecular confirmation for definitive diagnosis. Complete excision with clear margins is recommended. While most of the CMTCTs exhibit indolent biological behaviors, rare cases may recur locally or metastasize, warranting close follow-up.

Objective To conduct a comparative study on the biomechanical performance of using sutures for repairing inferior pole patellar fractures.Methods Compared to the normal patellar structure(Group A),four repair methods,namely,'Krackow'suture(Group B),"Kessler"fixation(Group C),'8-figure'mesh method(Group D),and modified suture bridge(Group E)were adopted.The static stiffness and dynamic stability of inferior pole patellar fractures fixed by each repair method were measured at 30°,60°,and 90° knee flexion.Results The stiffness at all flexion angles in Group E was closer to that in Group A,compared to other repair groups,followed by Group B,then Group D,and finally Group C.After the first cycle,at 30° knee flexion,Group C showed the greatest displacement,while Groups B and E had slightly larger displacements than the Group A,and the displacement of Group D was smaller than that of Group A.At 60° and 90° knee flexion,the displacement in all repair groups was smaller than that of Group A.After 200 cycles in the subsequent three cycles,displacement changes in all repair groups were smaller than those in Group A.Conclusions All repair methods were effective.In terms of biomechanical fixation performance,the modified suture bridge was superior to the'Krackow'suture and'8-figure'mesh,with Kessler fixation being the least effective.However,factors such as the injury severity,incision location,and surgical time should be comprehensively considered in actual clinical use,and it is recommended that the repair method should be selected in the following order:E,B,D,and C.

Objective To investigate the expression levels of serum hemoglobin β(HBB)in hepatocellular carcinoma(HCC)patients and its correlation with topoisomeraseⅡα(TOP2A)gene.Methods A total of 48 HCC patients visited the Second Affiliated Hospital of Nantong University from August 2023 to September 2024 were selected as the HCC group,and 32 healthy individuals who underwent physical examination during the same period were selected as the healthy control group.Their blood samples were collected,and the ex-pression levels of serum HBB and TOP2A genes were detected by real-time fluorescence quantitative polymerase chain reaction(qRT-PCR).Then,the relationship between the expression of HBB gene and clinicopathological parameters of the patients was ana-lyzed.The Kaplan-Meier Plotter database was used to evaluate the relationship between the expression of HBB gene and the prognosis of HCC.The diagnostic value of the expressions of serum HBB and TOP2A genes for HCC was assessed by the receiver operating charac-teristic(ROC)curve.Spearman rank correlation analysis was used to evaluate the correlation between the expressions of serum HBB and TOP2A genes in HCC patients.The regulatory effect of HBB gene on TOP2A gene was verified by the cell experiment.Results The expression levels of serum HBB gene in HCC patients(0.097[0.055,0.155])were significantly lower than that in healthy controls(1.029[0.625,1.434],U=19,P＜0.001).The expression levels of serum TOP2A gene in HCC patients(1.810[0.825,3.623])were significantly higher than that in healthy controls(1.047[0.604,1.364],U=495,P=0.007).The expression level of serum HBB gene in HCC patients was significantly negatively correlated with that of TOP2A gene(ρ=-0.384,P=0.007).The analysis results of clinicopathological parameters showed that the expression level of HBB gene was only related to tumor size(χ2=4.090,P＜0.05).The Kaplan-Meier survival analysis showed that the 5-year overall survival rate of the patients with low expression of HBB gene was signifi-cantly lower than that with high expression(HR=0.680,95%CI:0.470-0.970,P＜0.05).The analysis of the ROC curve showed that the area under the ROC curve(AUCROC)of HBB gene in diagnosing HCC was 0.987(95%CI:0.963-1.000).When the cut-off value was 0.228,its sensitivity was 100%and specificity was 97%.The AUCROC of TOP2A gene for the diagnosis of HCC was 0.677(95%CI:0.559-0.797).When the cut-off value was 1.285,its sensitivity was 65%and specificity was 75%.The combined detection of HBB and TOP2A genes for the diagnosis of HCC had an AUCROC of 0.988(95%CI:0.965-1.000).When the cut-off value was 0.657,its sensitivity was 100%and specificity was 97%.The cell experiment results showed that the overexpression of HBB gene could inhibit the expression of TOP2A gene,while the knockout of HBB gene had the opposite effect.Conclusion HBB gene is lowly expressed in the serum of HCC patients and is significantly negatively correlated with the expression of TOP2A gene.