People's Hospital of Bishan District

This study aimed to make a direct comparison of four tumor burden-related prognostic systems in predicting prognoses in patients with colorectal liver metastasis (CRLM) undergoing hepatectomy. Clinicopathological and survival data of 197 consecutive CRLM patients were extracted from a public database. Clinical Risk Score-derived N1S5 (lesion number of 1 and the largest size of 5cm are cutoffs for risk stratification), tumor burden score (TBS), modified TBS (mTBS) and total tumor volume (TTV) were calculated, and patients were stratified to different risk groups. Kaplan-Meier plots were adopted to depict the survival probabilities. Cox regression analyses were performed to evaluate the association between these systems and overall survival (OS) and disease-free survival (DFS). N1S5 and TTV systems effectively stratified patients into distinct risk groups with significantly different OS and DFS (p<0.05), but TBS and mTBS did not. Multivariable Cox regression analysis demonstrated N1S5 and TTV as independent variables associated with OS (HRs: 1.43 to 1.97, 1.59 to 1.76, respectively) and DFS (HRs: 1.34 to 2.09, and 1.80 to 2.51, respectively) (p<0.05). Compared with the other three systems, TTV showed a relatively higher time-dependent area under the curve (median: 0.60) and C-index (median: 0.64) for predicting OS. N1S5 had the highest C-index (median: 0.63) for predicting DFS. Total tumor volume seems to be a robust and effective tool for risk stratification and prognosis prediction in CRLM patients undergoing liver resection. N1S5 may provide a pragmatic simplified alternative to total tumor volume for prognostic prediction.

The clinical significance of Candida infection in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) remains poorly defined. This multicenter cohort study analyzed 11,925 hospitalized AECOPD patients from ten centers in China, grouped by Candida infection status. Subgroups were analyzed by Candida species and invasiveness. Primary outcome was 3-year all-cause mortality; secondary outcomes included in-hospital mortality, invasive mechanical ventilation (IMV), non-invasive ventilation (NIV), and intensive care unit (ICU) admission. Propensity score matching and Cox regression were used to adjust for confounders. Candida-positive AECOPD patients showed significantly worse short-term outcomes, including increased IMV (7.2% vs 3.8%) and NIV use (31.8% vs 18.2%), more ICU admissions (12.7% vs 8.9%), and prolonged hospitalization (15.97 vs 11.16 days, P < 0.001). No significant difference was observed in 30-day mortality between groups (aHR 1.13, 95% CI 0.63-2.03), but 3-year mortality was significantly higher (41.2% vs 30.5%, P < 0.001) in Candida positive group. Subgroup analyses showed no significant differences by species or invasiveness. Respiratory Candida infection is associated with worse short-term clinical outcomes and increased 3-year mortality in AECOPD patients, but is not an independent risk factor for in-hospital mortality. Neither species nor invasiveness classification offered prognostic value. Screening may identify high-risk patients, but evidence does not support species-specific or β-d-glucan (BDG)-guided therapy among this population.

In children with American Society of Anesthesiologists (ASA) physical status I-II undergoing flexible bronchoscopy, the novel nasal cannula was more effective than the conventional face mask in preventing hypoxemia and reducing procedural interruptions. The Chinese Clinical Trial Registry (chiCTR.gov): No. ChiCTR2500113734, Retrospectively registered, Date of registration: December 2, 2025. • Maintaining adequate oxygenation is essential for ensuring patient safety and procedural success during pediatric flexible bronchoscopy. • Conventional face masks (CMO) are widely used for oxygen delivery; however, they may be insufficient in preventing intraoperative hypoxemia. • A novel nasal cannula (NNO) significantly reduces the incidence of hypoxemia (6.0% vs. 18.2%) compared to CMO in children undergoing flexible bronchoscopy. • The use of NNO is associated with higher minimum SpO₂ levels, a longer time to onset of first hypoxemic event, and fewer procedural interruptions due to rescue ventilation, thereby providing a less invasive and more effective oxygenation strategy.

Vitamin D deficiency (VD-deficiency) has been implicated in various autoimmune diseases, including uveitis, yet its mechanistic role remains unclear. Emerging evidence suggests that gut microbial dysbiosis and metabolic disturbances may serve as critical intermediates linking VD-deficiency and autoimmune disease pathogenesis. Here, using an experimental autoimmune uveitis (EAU) model induced in B10RIII mice, we demonstrate that VD-deficiency exacerbates EAU severity, accompanied by enhanced Th1 and Th17 responses, suppressed regulatory T cells, and disruption of both intestinal and blood–retinal barrier integrity. Integrated microbiota and metabolomic profiling revealed a coordinated pattern of gut dysbiosis, characterized by enrichment of opportunistic pathogens and depletion of beneficial commensals, together with host metabolic reprogramming in VD-deficient EAU mice. KEGG analysis highlighted disruption of vitamin-related pathways, particularly the vitamin digestion and absorption pathway. Mechanistically, VD-deficiency associated disturbances were linked to LRAT downregulation in retinal pigment epithelial (RPE) cells, accompanied by a pro-inflammatory intraocular microenvironment characterized by increased IL-6 and CXCL family chemokines expression. Gain- and loss-of-function studies in complementary in vivo and in vitro RPE-based models further demonstrated that LRAT functions as a negative regulator of retinal inflammatory responses, with LRAT knockdown enhancing, whereas LRAT overexpression suppressing, the production of IL-6, CXCL1, CXCL2, and CXCL8. Collectively, our findings suggest that VD-deficiency exacerbates autoimmune uveitis by disrupting effector–regulatory T cell balance and compromising blood–retinal barrier and intestinal integrity, accompanied by considerable alterations in gut microbiota and systemic metabolism, while identifying LRAT as a potential regulator linking VD-deficiency to retinal inflammatory amplification.

International Practice Guidelines Registry Platform (PREPARE-2024CN606).

Breast cancer progression is influenced not only by intrinsic tumor alterations but also by reciprocal interactions with the tumor microenvironment (TME), a complex ecosystem comprising fibroblasts, immune and endothelial cells, adipocytes, extracellular matrix components, soluble mediators, and extracellular vesicles. This review synthesizes recent basic and translational research on how TME-derived signals activate dysregulated signaling pathways, including the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR), transforming growth factor beta/SMAD (TGF-β/SMAD), Janus kinase/signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), Wingless-related integration site/beta-catenin (Wnt/β-catenin), Notch, Yes-associated protein/transcriptional co-activator with PDZ-binding motif (YAP/TAZ), and nuclear factor kappa B (NF-κB). These pathways promote key processes such as invasion, angiogenesis, adaptation to hypoxia, epithelial–mesenchymal transition, immune evasion, cancer stemness, and therapy resistance. We emphasize convergent findings that indicate the feedback loop between tumor cells and the TME sustains plasticity and drug-tolerant states. Additionally, we summarize emerging therapeutic strategies, including stromal and extracellular matrix normalization, immunotherapy combinations, pathway-targeted inhibitors, and nanotechnology-enabled drug delivery. A comprehensive understanding of TME–signaling crosstalk is crucial for overcoming therapeutic resistance in breast cancer.

Background/Objectives: Breast cancer survivors face elevated risk of treatment-related bone loss, yet routine bone health assessment remains underutilized. Opportunistic bone density extraction from routine CT may address this gap. This study validated AI-derived vertebral bone mineral density (AI-vBMD) from non-contrast thoracoabdominal CT for osteoporosis screening and assessed its diagnostic value beyond clinical variables. Methods: This retrospective study included 332 breast cancer patients; AI-vBMD was successfully extracted in 325 (98%). Quantitative CT (QCT) served as reference standard. Agreement between AI-vBMD and QCT-vBMD was assessed using Pearson correlation, Bland-Altman analysis, and weighted kappa for QCT-defined osteoporosis (<80 mg/cm3). Nested logistic regression models compared a clinical model with and without AI-vBMD. Discrimination [area under the curve (AUC)], calibration, and clinical utility [decision-curve analysis (DCA)] were evaluated. Results: AI-vBMD showed strong correlation with QCT-vBMD (r = 0.98, p < 0.001), minimal bias (mean difference +1.82 mg/cm3), and excellent agreement for osteoporosis classification (weighted κ = 0.90). AI-vBMD alone achieved excellent discrimination for osteoporosis (AUC = 0.986). Integrating AI-vBMD into the clinical model yielded significantly higher diagnostic performance (AUC 0.988 vs. 0.879; p < 0.001) and demonstrated superior net benefit across relevant decision thresholds. Conclusions: AI-derived vertebral BMD from routine CT serves as a reliable QCT-aligned imaging biomarker for opportunistic osteoporosis assessment in breast cancer patients and adds significant incremental diagnostic value beyond clinical information alone.