Sichuan Cancer Hospital

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.

Motivation: Accurate cancer survival prediction requires modeling tumor heterogeneity across both population and cell levels. Most cancer survival analyses use tumor transcriptomes only, since cohorts are usually measured with bulk RNA-seq but are rarely recorded with single-cell RNA-seq. This prevents the direct use of cell-level transcriptomes in cancer survival analysis. Results: To bridge this gap, we propose using bulk RNA-seq deconvolution algorithms to reconstruct each subject's scRNA-seq profile from their bulk data. Then, by combining both scRNA-seq and bulk RNA-seq together with their survival labels (paired to bulk), we perform multimodal transcriptome-based survival analysis. We built this framework as DeSCENT and evaluated it with common survival models on eight TCGA cancer cohorts. Results showed notable and consistent improvements in C-index over bulk-only models or models using cellular information alone. Availability: Our code is available at GitHub: https://github.com/YonghaoZhao722/DeSCENT.

Pancreatic exocrine insufficiency (PEI), presenting as bloating or diarrhea, affects 26%-100% of patients after gastrectomy, delaying recovery and impairing quality of life. Pancreatic enzyme replacement therapy (PERT) is the standard PEI management, yet its efficacy after gastric cancer surgery remains controversial. This study evaluates PERT's effectiveness in alleviating postoperative gastrointestinal symptoms. In this multicenter randomized controlled trial, 204 patients undergoing radical gastrectomy will be randomized 1:1 to PERT or control. The PERT group will receive Pancreatin Enteric-coated Capsules (containing 450mg pancrelipase microgranules) three times daily with meals for 1month post-discharge. The primary outcome is the incidence of gastrointestinal symptoms at 1month post-surgery, assessed using the MD Anderson Symptom Inventory Gastrointestinal Cancer Module (MDASI-GI). Secondary outcomes include nutritional status and treatment compliance. This protocol establishes a framework for definitively evaluating PERT in gastric cancer patients. Results will inform evidence-based PEI management, with significant implications for survivorship care. By integrating patient-reported outcomes and nutritional metrics, we aim to validate a patient-centered strategy optimizing functional recovery after curative resection. This study was registered with the Chinese Clinical Trial Registry (ChiCTR; registry number: ChiCTR2500102557). Date of registration: 16 May 2025.

Germline pathogenic alleles predispose carriers to malignancies; failure to recognize the underlying cancer susceptibility and subsequent delayed diagnosis may lead to severe health impairment. It remains largely undetermined what the somatic mutation characteristics are in colorectal cancer (CRC) patients with pathogenic/likely pathogenic (P/LP) germline mutations and whether, and how, these germline mutations typically located in non-mismatch repair genes, are associated with CRC tumorigenesis. From 8,676 Chinese patients with CRC, we initially screened those who had undergone both germline and somatic mutation testing. We analyzed the relationship between germline mutations and the somatic mutational landscape in this cohort. Germline alterations were examined with a 556- or 105- gene next-generation sequencing panel, and somatic alterations were examined with a 556-gene panel. Overall, 80 CRC patients were identified as carriers of P/LP germline mutations. After excluding 6 patients lacking somatic mutation testing data, 74 patients with P/LP germline mutations and 100 patients without germline mutations were finally enrolled in this study. Twenty-one germline genes were detected in the 74 patients. Compared with patients without P/LP mutations (non-P group), those in the P/LP mutations (P group) had significantly lower age and a higher ratio of microsatellite instability. Patients harboring P/LP germline mutations in MMR genes (P-MMR) were significantly younger and more frequently exhibited high tumor mutational burden. The most frequent somatic variations were KRAS and TP53. The somatic mutational landscape revealed a significantly higher mutational frequency in the P group than in the non-P group, and in the P-MMR group than in the P-non-MMR group. The MAPK pathway was significantly enriched in the P and P-MMR groups. Our data showed lower mutation rate of MSH2 among all MMR genes than in the Western population. Population-based risk analysis indicated that the odds ratio of BRCA2 and ATM mutations exceeded 10. Our findings offer a comprehensive overview of genetic susceptibility in Chinese CRC, which may help to shape a more comprehensive understanding of genetic structure of CRC and generate accurate individualized risk management strategies for mutation carriers.

A 51-year-old man presented with a 3-month history of progressive lower extremity weakness and numbness, starting distally and progressing proximally, accompanied by mild gait difficulty but no bowel/bladder symptoms.Examination revealed mild hypoesthesia starting at T10 and grade 4/5 lower extremity weakness suggesting a spinal lesion.Thoracolumbosacral MRI revealed longitudinally extensive edema from T8 to the conus medullaris (CM) with prominent vascular flow voids on the spinal cord surface; and magnetic resonance angiography (MRA) revealed a dilated intradural vein from the S1 level to the CM, concerning for a sacral dural arteriovenous fistula ([DAVF]; Figure 1, A-C).Spinal angiography confirmed a sacral DAVF

Cerebral palsy (CP) is the leading cause of childhood motor disability, often requiring intensive, long-term rehabilitation to improve motor function and independence in daily activities. Robot-assisted therapy has emerged as a promising intervention, as it can deliver high-intensity, task-specific, and motivating treatment. However, evidence for its superiority over conventional rehabilitation interventions (CRIs) is inconsistent, and a comprehensive quantitative synthesis is lacking. This protocol details a systematic review and meta-analysis to evaluate the effectiveness of robot-assisted therapy on motor outcomes in children with CP. This protocol has been developed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) statement. We will conduct a comprehensive search of five electronic databases (PubMed, Embase, Web of Science, CINAHL, and the Cochrane Library) from their inception to June 2025. The review will include randomized controlled trials (RCTs) comparing robot-assisted therapy with CRIs in children with CP. Two independent reviewers will screen titles, abstracts, and full texts and extract relevant data. Primary outcomes will include measures of gross motor function, activities of daily living (ADL), gait, and balance. Secondary outcomes will include upper limb function and quality of life. Where appropriate, we will perform a meta-analysis using a random-effects model in Stata 14.0. We will investigate sources of heterogeneity using subgroup and sensitivity analyses. Publication bias will be assessed with funnel plots and Egger's test. Furthermore, Trial Sequential Analysis will be employed to assess the robustness of the findings and control for risks of random error. The overall quality of evidence will be evaluated using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) framework. PROSPERO CRD420250652267.

Resistance to 5-fluorouracil-based chemotherapies presents a major clinical challenge in colorectal cancer (CRC) treatment, leading to elevated recurrence rates. Recent findings indicate that enhanced metabolic plasticity in cancer cells plays a crucial role in drug resistance development, though the exact mechanisms remain uncertain. In this study, we demonstrate that the lipophagy-triggered fatty acid oxidation (FAO) is involved in maintaining the adenosine triphosphate (ATP) levels upon drug administration. Using mass spectrometric imaging, we identified arachidonic acid (AA) as a critical lipid mediator of intracellular selective autophagy and energy balance in resistant cancer cells. The high level of arachidonate metabolism was associated with poor response to chemotherapy in clinical practice. Mechanistically, accumulated AA induced phosphorylation of PLINs via the LOXs/PKCζ pathway and stimulated the production of free fatty acid (FFA) driven by lipophagy. Importantly, we further certified that inhibition of AA-associated lipophagy specifically sensitize drug-resistant colorectal cancer cells to chemotherapy. This study offers insights into the mechanism of acquired chemoresistance, suggesting that targeting AA-associated lipophagy could be a potential therapeutic strategy to overcome drug resistance in colorectal cancer.