181st Hospital of Chinese People's Liberation Army

Background: Early venous outflow dysfunction is a leading cause of early failure after finger replantation. This study evaluated whether preoperative serum markers of endothelial activation and inflammation can predict early venous outflow dysfunction and developed a serum-based risk model. Methods: This retrospective cohort included 150 patients who underwent finger replantation between January 2022 and October 2025. Peripheral venous blood was collected 2 h before surgery. Serum von Willebrand factor (vWF), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured. Early venous outflow dysfunction was defined as venous congestion requiring intervention within 72 h postoperatively. Independent markers were identified using multivariable logistic regression. Model performance was assessed by receiver operating characteristic analysis (AUC with 95% confidence intervals by the DeLong method and between-model comparison by the DeLong test), calibration by the Hosmer–Lemeshow test, and internal validation using bootstrap resampling (200 iterations). Results: All seven biomarkers were higher in cases (n=74) than controls (n=76) (P<0.05) and were positively correlated with crisis duration (all P<0.01). vWF, E-selectin, and TNF-α remained independently associated with early venous outflow dysfunction. The resulting panel achieved an AUC of 0.811 (95% CI, 0.738–0.883), with 72.97% sensitivity and 84.21% specificity. Calibration was acceptable (Hosmer–Lemeshow P=0.093), and the optimism-corrected AUC was 0.802. A clinical-variable model showed poorer discrimination (AUC 0.618; 95% CI, 0.527–0.709), and the biomarker panel improved discrimination significantly (DeLong P=0.001). Conclusions: A preoperative serum panel combining vWF, E-selectin, and TNF-α showed good discrimination for early venous outflow dysfunction after finger replantation. External validation is needed before routine clinical use.

Background: This study aimed to analyze the clinical and ultrasonographic features of 6 pathologically confirmed cases of uterine inflammatory myofibroblastic tumors (UIMT) and to enhance clinicians’ ability to achieve timely diagnosis and treatment. Methods: This retrospective case series included 6 patients with pathologically confirmed UIMT who were admitted to our hospital between January 2019 and January 2025. Clinical, ultrasonographic, and pathological data were collected and analyzed retrospectively. Results: All 6 tumors were solid and originated from the myometrium. 3 were confined to the myometrium, 2 extended toward the submucosa, and 1 toward the subserosa. 5 lesions were hypoechoic and 1 was hyperechoic, all showing heterogeneous internal echoes and a characteristic “blurred halo sign”. The median maximum diameter was 6.9 cm. Color Doppler flow imaging (CDFI) showed an Adler grade ≥2, demonstrating a “colorful mosaic sign”. During follow-up, 2 lesions increased in size by 1 cm and 2 cm, respectively, within 2–4 months. No extrauterine metastasis was observed. All cases were positive for anaplastic lymphoma kinase (ALK), as confirmed by fluorescence in situ hybridization (FISH). All patients underwent surgical treatment, including 1 total hysterectomy and 5 local resections. No recurrence or metastasis was observed during 21–57 months of follow-up. Conclusions: UIMT exhibits characteristic sonographic features, including solid masses with heterogeneous internal echoes (“blurred halo sign”) and abundant blood flow signals (“colorful mosaic sign”). Recognizing these distinctive imaging patterns is critical for improving diagnostic accuracy and guiding appropriate clinical management.

Patients with uremia undergoing long-term hemodialysis are prone to multi-organ complications, but the underlying molecular mechanisms remain unclear. Ferroptosis, an iron-dependent form of cell death, has been linked to inflammation and organ damage. Its role in hemodialysis-related pathology, however, has not been well characterized. In this study, we systematically profiled low-abundance plasma proteins from six hemodialysis patients and eight healthy controls using a protein corona-based enrichment technique to enhance detection sensitivity. A total of 183 differentially expressed proteins (DEPs) were defined based on a fold-change threshold (≤ 0.25 or ≥ 4), including 101 upregulated and 82 downregulated proteins. Notably, pathway enrichment analysis highlighted the ferroptosis pathway, with altered abundance of proteins including TFRC, ALOX15, PRNP, CYBB, and ACSL1, suggesting a potential association of ferroptosis-related signals with hemodialysis-related complications. To complement the proteomic analysis, enzyme-linked immunosorbent assay (ELISA) was performed in an independent cohort. ALOX15 showed a significant and reproducible increase in plasma levels (P < 0.0001), consistent with the proteomic results. Other ferroptosis-related candidates warrant further evaluation and independent validation in larger cohorts. Furthermore, drug target prediction based on DEP data identified N-oleoyldopamine, luteolin, and catechol as potential compounds targeting the five ferroptosis-related molecules. Collectively, this study provides an exploratory plasma proteomic resource and suggests that ferroptosis-associated plasma protein changes may be relevant to hemodialysis-related complications, warranting further validation. Collectively, this study provides an exploratory plasma proteomic resource and offers initial insights into ferroptosis-associated plasma protein changes in hemodialysis patients.

To correlate the Osteoporosis Self-assessment Tool for Asians (OSTA) index with lumbar QCT-measured bone mineral density (BMD) and bone mineral content (BMC), and assess its utility in evaluating lumbar spine BMD/BMC. From Jan 2023 to Jun 2024, 366 patients scheduled for lumbar spine surgery were enrolled. All underwent lumbar CT, QCT, and DXA. Spearman correlation analyzed OSTA vs. QCT-BMD and QCT-BMC. Patients were categorized by DXA T-scores into osteoporotic or non-osteoporotic groups. ROC curves were plotted to determine AUC, optimal cutoff, sensitivity, and specificity. The OSTA index showed a moderate, statistically significant correlation with QCT-BMD and QCT-BMC (P < 0.01). Based on DXA diagnosis, QCT-BMC yielded AUCs of 0.712 (men) and 0.745 (women) for osteoporosis, indicating moderate diagnostic value. The optimal cutoffs were 663.86 mg for men and 521.65 mg for women, with sensitivities of 57.6% and 59.5%, respectively. As a screening tool, the OSTA index can help identify high-risk individuals undergoing spinal surgery who are likely to have low lumbar trabecular BMD and BMC as measured by QCT. Diagnostic thresholds for osteoporosis may be set at lumbar QCT-BMC <663.86 mg in men or <521.65 mg in women.

BackgroundOxidized regenerated cellulose (ORC) is a topical hemostatic agent, but its efficacy and safety in arthroplasty remain inconclusive. This meta-analysis aimed to comprehensively assess its role in this procedure.MethodsWe systematically searched multiple databases up to July 30, 2025, for cohort studies and randomized controlled trials investigating the use of ORC in arthroplasty. Study quality was assessed using standard tools, and data were analyzed using Stata software.ResultsA total of 33 articles were retrieved. After removing 27 duplicates, six high-quality studies involving 684 participants were included in the analysis. The analysis revealed that ORC significantly reduced total blood loss (WMD = -102.50 mL, 95% CI: -201.75, -3.26, I2 = 69.9%) and hemoglobin drop (WMD = -3.99 g/L, 95% CI: -6.19, -1.79, I2 = 39.8%) compared with the control group. No significant differences were found in other secondary outcomes, such as intraoperative blood loss, risk of thrombosis, operative time, or wound complications.ConclusionORC is an effective and safe hemostatic agent that reduces total blood loss and hemoglobin drop during arthroplasty. Future research should focus on determining the optimal timing of ORC and long-term functional outcomes.

Breast cancer is one of the most common and deadly diseases that threaten women’s health worldwide, and early and accurate breast nodule segmentation is of great significance for the early detection, diagnosis and treatment of breast cancer. However, due to the limitation of medical annotated data, the training segmentation models for medical images is still challenging. The Segment Anything Model (SAM) is a foundational model that interactively segments target objects. Although significant achievements have been made in natural images, there are still challenges in the application in medical images. In this paper, the effect of SAM on breast nodule segmentation was studied from three aspects: initial weight, organ (breast) mask and prompt box, so as to explore the feasibility of breast nodule segmentation. Through a series of experiments on the data collected in this paper, it is found that the use of MedSAM initial weights and the use of single individual fixed prompt boxes can obtain better segmentation results, and can take into account practical application problems.

BackgroundProstate cancer (PCa) is the most common male reproductive malignancy, with traditional Chinese medicine (TCM) offering potential complementary treatments. Aidi injection, used for liver, lung, and colorectal cancers, shows promise for PCa, but its mechanisms are unclear. This study aims to uncover the molecular pathways through which Aidi injection affects PCa using network pharmacology and experiments.MethodsThe study used network pharmacology to identify active components of Aidi injection and their targets from various databases. These targets were cross-referenced with PCa-related targets to uncover therapeutic possibilities. Protein-protein interaction (PPI) and KEGG pathway analyses highlighted key molecular pathways affected by Aidi injection. Molecular docking examined ingredient-target binding. In vitro tests evaluated effects on PCa cell proliferation, apoptosis, and IL-6/STAT3 signaling, while in vivo studies assessed tumor growth and immune response in mice.ResultsThe study identified 58 active components and 804 PCa-related target genes, with 49 overlapping therapeutic targets. Key compounds such as quercetin, kaempferol, isorhamnetin, and cantharidin were highlighted. Core targets included ESR1, IL-6, STAT3, HSP90AA1, EGFR, and VEGFA. KEGG analysis revealed the IL-6/STAT3 and EGFR pathways as significant in PCa treatment. In vitro, Aidi injection inhibited PCa cell proliferation, induced apoptosis, and suppressed IL-6/STAT3 activation. In vivo, Aidi injection reduced tumor growth and enhanced immune response in mice.ConclusionsAidi injection influences the IL-6/STAT3 and EGFR pathways, suppressing PCa cell growth, inducing apoptosis, and reducing migration and invasion. These findings offer valuable insights into the therapeutic potential of Aidi injection for prostate cancer.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12575-025-00299-w.

Gallbladder cancer (GBC) is an aggressive malignant tumor that seriously threatens the survival of GBC patients. Laminin-γ2 (LAMC2), an important component of laminins, has been reported to facilitate cancer development and chemoresistance in several cancers. However, the biological effect of LAMC2 on GBC is still unclear. LAMC2 expression was assessed in GBC specimens through proteomics and RNA-seq data. To evaluate the biological effects of LAMC2, we performed colony formation, sphere formation, wound healing, and transwell and invasion assays, along with an in vivo metastasis model. Additionally, we also explored the role of LAMC2 in GBC organoid. Finally, Western blot and RT-qPCR were employed to identify the molecular mechanism underlying LAMC2-mediated regulation of aggressive behavior in GBC. Here, we revealed that LAMC2 was overexpressed in GBC tissues and was positively correlated with poor patient outcomes. Furthermore, the genetic silencing of LAMC2 significantly inhibited GBC cell colony formation, sphere formation, and organoid growth. Additionally, LAMC2 deficiency impaired GBC cell metastasis in vitro and in vivo, accompanied by a reversal of the epithelial-mesenchymal transition (EMT) phenotype. Mechanistically, LAMC2 expression was induced by the canonical TGF-β/SMAD2 signaling pathway, and in turn, LAMC2 feedback enhanced the activity of TGF-β signaling by binding to TGF-β receptor II (TGF-βRII). Our findings suggest that LAMC2 promotes GBC progression and metastasis, potentially by regulating the TGF-β signaling pathway. Therefore, LAMC2 could serve as a potential prognostic biomarker and therapeutic target for GBC.

Coronary microembolization (CME) is a serious cardiovascular complication that causes severe cardiac dysfunction and arrhythmias. Glutathione (GSH) exhaustion-induced oxidative stress is a key contributor to CME. Here, we explore the molecular mechanisms underlying GSH imbalance during CME. We show that CME induces myocardial injury by disturbing GSH homeostasis, which is ameliorated by glutamate-cysteine ligase modifier subunit (GCLM) or glutaminase (GLS) overexpression. Lysine-specific histone demethylase 1A (KDM1A) removes H3K9me1/2 from the promoter regions of GCLM and GLS to promote their epigenetic expression, thereby maintaining GSH homeostasis in CME. KDM1A is ubiquitinated at the K355 site during CME via inhibiting ubiquitin-specific peptidase 16 (USP16)-mediated deubiquitination. Inducible nitric oxide synthase (iNOS) facilitates S-nitrosylation (SNO) of USP16 at the C731 site, contributing to KDM1A ubiquitination and causing GSH imbalance during CME. Altogether, SNO-USP16 inhibition stabilizes the KDM1A protein to epigenetically activate GCLM and GLS, thus maintaining GSH homeostasis and relieving CME-induced myocardial injury.