Thymic epithelial tumors (TETs) represent the most common primary neoplasms of the anterior mediastinum, yet thymic carcinoma (TC) stands out as an exceptionally rare and biologically aggressive subtype. Unlike thymomas, TCs exhibit marked cytologic atypia, early invasive potential, and a high predisposition for extrathoracic metastasis. We report the case of a 59-year-old male who presented with a seven-month history of progressive, refractory lumbar pain and functional limitation. Initial clinical and laboratory evaluation revealed normocytic anemia, leukocytosis, elevated inflammatory markers, and increased lactate dehydrogenase and beta-2 microglobulin levels. These findings, combined with systemic bone marrow infiltration observed on spinal magnetic resonance imaging, initially suggested a lymphoproliferative disorder. A subsequent thoracic computed tomography scan identified an anterior mediastinal mass with lymphadenopathy. A bone marrow biopsy evidenced infiltration by a poorly differentiated malignant neoplasm, and an immunohistochemical profile of the mediastinal mass confirmed the diagnosis of stage IVb TC, showing positivity for pan-cytokeratin, tumor protein p63, cluster of differentiation 5 (CD5), epithelial membrane antigen (EMA), and cluster of differentiation 117 (CD117), with a Ki-67 proliferation index of 20%, while remaining negative for hematolymphoid, neuroendocrine, and lung-specific markers. The patient was managed through a multidisciplinary approach with systemic palliative chemotherapy. This case highlights a critical diagnostic challenge where TC mimicked a hematological malignancy. The systemic dissemination of TC, particularly the diffuse bone marrow infiltration, is a rare clinical phenotype that obscures the primary mediastinal origin. Our report emphasizes the necessity of including TC in the differential diagnosis of patients presenting with refractory bone pain and systemic hematological abnormalities, even in the absence of respiratory symptoms. Early diagnostic recognition through strategic immunohistochemical profiling is imperative to avoid clinical bias, prevent the initiation of inappropriate therapies, and facilitate a prompt, evidence-based management strategy for patients with advanced, non-resectable disease.

Myoepithelioma-like tumor of the vulvar region (MELTVR) is a rare mesenchymal subcutaneous tumor of low malignant potential that occurs in adult women and has typical histological features, including loss of SMARCB1 (INI1) expression. This report describes the case of a 23-year-old woman with a painful vulvar subcutaneous nodule and a diagnosis of MELTVR and describes the challenges in the approach to definitive diagnosis. A 23-year-old woman presented with a three-month history of right pubic pain. Imaging revealed a 25-mm inguinal lesion without metastasis. Biopsy demonstrated spindle and plasmacytoid tumor cells in myxoid and hypercellular areas, suggesting myoepithelioma. Although necrosis and mitotic activity were not evaluable in the biopsy specimen, malignant potential could not be excluded. Complete surgical excision was subsequently performed. The resected tumor measured 45 × 35 × 15 mm and showed multilocular solid and gelatinous areas. Histologically, lobulated growth, marked atypia, necrosis, and mitotic activity (9/10 HPF) were identified. Immunohistochemically, tumor cells showed positivity for estrogen receptor (ER) and progesterone receptor (PgR), along with loss of SMARCB1 (INI1) expression. Other markers, such as neural and myoepithelial markers, were negative. Fluorescence in situ hybridization (FISH) analysis showed no Ewing sarcoma breakpoint region 1 (EWSR1) rearrangement. MELTVR was diagnosed based on integrated clinicopathological and molecular findings. Biopsy specimens may fail to capture key diagnostic features of MELTVR because of intratumoral heterogeneity. Definitive diagnosis requires comprehensive evaluation of resection specimens with immunohistochemical and molecular analyses. This case may contribute to establishing diagnostic criteria for this rare entity.

To synthesize qualitative evidence on how financial toxicity is experienced, sustained, and managed at the family level in pediatric cancer.

A qualitative systematic review using meta-aggregation.

PubMed, Web of Science, Embase, PsycINFO, CINAHL, and three major Chinese databases (CNKI, WanFang, VIP) were searched up to May 2025.

Two reviewers independently conducted study screening, data extraction, and quality appraisal following Joanna Briggs Institute (JBI) guidelines. Discrepancies were resolved through discussion and team consensus. Meta-aggregation was applied to synthesize findings.

Fourteen studies of moderate-to-high methodological quality, involving 524 participants (primarily parents of children with cancer) from seven countries, were included. Thirty-eight initial findings were aggregated into 10 categories and further synthesized into three final findings: (1) Financial toxicity arose from the accumulation of direct medical costs, indirect expenses, income loss due to employment disruption, and inadequate insurance or social support; (2) These financial pressures compromised family economic security and were associated with debt, reduced living standards, long-term financial vulnerability, and psychosocial impacts; (3) Families attempted to manage financial toxicity through external financial assistance and reorganization of life around the child's treatment, although such strategies often provided only partial relief.

Financial toxicity in pediatric oncology is a sustained and family-level burden that undermines household stability beyond clinical treatment phases. The limited effectiveness of existing coping strategies highlights structural gaps in supportive care. Early identification of financial risk, family-centered counseling, and coordinated system-level support may mitigate long-term consequences and promote more equitable survivorship outcomes.

No patient or public contribution.

This review was prospectively registered with PROSPERO, the International Prospective Register of Systematic Reviews (CRD42024519179). Available from https://www.crd.york.ac.uk/PROSPERO/view/CRD42024519179 .

PD-1/PD-L1 blockade can produce durable tumor control, yet primary, adaptive, and acquired resistance remain common. Existing accounts often catalogue resistance by cellular compartment, obscuring the coordinated nature of tumor adaptation. Here, we introduce immune-pressure redistribution as a treatment-oriented framework that complements cancer immunoediting by asking where therapeutic immune pressure is diverted after checkpoint release. Resistance is organized into three coupled routes: transfer into tumor-intrinsic escape through antigen-presentation loss, interferon-response defects, oncogenic rewiring, and lineage plasticity; weakening through defective priming, terminal T-cell differentiation, compensatory checkpoints, metabolic constraint, and chronic cytokine signaling; and unloading into stromal, vascular, myeloid, regulatory, microbial, and systemic host compartments. We integrate clinically validated mechanisms with emerging evidence, including the temporal duality of interferon-JAK signaling, the role of tumor-draining lymph nodes in sustaining progenitor-exhausted T cells, and the limited translation of TIGIT, IDO1, TGF-β, and CSF-1R targeting. We further propose a biomarker-guided strategy that combines tumor visibility, immune-cell state, spatial architecture, systemic inflammation, and early treatment dynamics to identify the dominant resistance topology. This framework supports topology-matched combinations and adaptive sequencing rather than uniform escalation, with the aim of restoring productive immune pressure while limiting compensatory escape and toxicity.

Among breast cancer (BC) survivors, overweight and obesity increase the risk of recurrence, underscoring the importance of dietary strategies for weight management. The Mediterranean diet (MD) can promote weight loss and reduce lipid levels. Analyzing alterations at the lipid species level can provide more detailed insights into the metabolic benefits associated with the MD. This study aimed to explore lipid remodeling associated with MD adherence in BC survivors through comprehensive lipidomic analysis.

This exploratory ancillary study was conducted as non-randomized, non-controlled pre-post intervention analysis of serum samples collected before and after an 8-week MD intervention from 12 overweight or obese BC survivors. Fasting paired serum samples (n = 24) were used to profile lipid species using ultra-high-performance liquid chromatography-tandem mass spectrometry in both positive and negative ionization modes. Multivariate and correlation analyses were used to assess overall lipidomic alterations. Participants were further classified into maintainer or improver subgroups based on changes in their Mediterranean diet score (MDS), and subgroup-specific lipidomic responses to the MD intervention were examined.

Participants showed significant reductions in body weight, waist circumference, and clinical triglyceride levels, along with increased quantitative insulin sensitivity check index and MDS following the MD intervention. Forty-three putative lipid species were identified, predominantly characterized by reductions in triacylglycerols (TGs) enriched with saturated fatty acids. TG 16:0_18:0_18:0 and TG 16:0_18:1_24:0 exhibited strong negative correlations with MDS and positive correlations with insulin resistance markers. Significant lipid remodeling was observed only in the maintainer group.

In this exploratory study, adherence to an 8-week MD was associated with changes in body composition, metabolic markers, and the serum lipidomic profile in overweight and obese BC survivors. These findings provide preliminary evidence that MD adherence may be associated with lipidomic and metabolic changes in BC survivors, warranting confirmation in larger, controlled studies.

http://clinicaltrials.gov , NCT03581630.

Severe acute kidney injury (AKI) is frequent in critically ill patients with chronic obstructive pulmonary disease (COPD), but predictive importance does not establish causality.

To model severe AKI (KDIGO stage 3), evaluate temporal robustness at a 24-hour ICU landmark, and explore adjusted exposure-effect estimates.

This retrospective MIMIC-IV v3.1 cohort included 4,705 adults with COPD. The original modeling dataset was split into training (n = 3,294) and testing (n = 1,411) sets. Consensus features from LASSO, Boruta, and random-forest importance informed 15 classifiers; the highest observed test-set AUC was interpreted with SHAP. A 24-hour landmark analysis excluded earlier stage 3 AKI and used pre-landmark predictors for incident stage 3 AKI thereafter. CausalForestDML estimated exploratory adjusted effects of the most recent valid creatinine within 365 days before ICU admission.

Severe AKI occurred in 1,085 patients (23.06%). The original six-feature CatBoost model included total ICU length of stay and had an AUC of 0.848 (95% CI, 0.825-0.872); it is interpreted as a retrospective trajectory model. The landmark cohort included 4,171 patients and 841 events. The temporal five-feature AUC was 0.679 (95% CI, 0.641-0.717); without pre-ICU creatinine it was 0.686 (95% CI, 0.648-0.724; paired difference, -0.0067; P = 0.293). The adjusted creatinine risk difference was 0.0547 per 1 mg/dL (95% CI, -0.0021 to 0.1115) and 0.0705 (95% CI, 0.0022-0.1387) after 1st-99th percentile trimming.

This study establishes a COPD-specific benchmark showing that a parsimonious model can characterize severe-AKI trajectories and that temporal separation materially changes performance and interpretation. Integrating model comparison, SHAP, adjusted-effect estimation, and landmark validation provides a rigorous framework for distinguishing prognostic importance from causal relevance and defines priorities for external validation.

Depression is common among individuals with asthma and is linked to increased mortality. However, whether socioeconomic factors contribute to this association remains unclear. We explored whether income may partially account for the association between depressive symptoms and reduced survival in adults with asthma.

A total of 4945 asthma patients were included using baseline data from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 linked to the National Death Index (NDI) mortality follow-up through December 31, 2019. Depression was assessed using the Patient Health Questionnaire-9 (PHQ-9), and mortality was identified through linkage to the NDI. Cox proportional hazards models were used to evaluate the association between depression symptoms and all-cause mortality, and restricted mean survival time (RMST) analysis quantified survival differences over 15 years. Exploratory mediation analysis with quasi-Bayesian simulation was conducted to evaluate whether the poverty-income ratio (PIR) may partially account for the observed association, adjusting for demographic, behavioral, and clinical covariates.

Depression was associated with all-cause mortality in asthma patients, and the strength of this association decreased after adjustment for demographic, behavioral, and clinical factors. Over a 15-year period, patients with depression symptoms (PHQ-9 ≥ 10) had markedly shorter survival, losing 9.89 months in RMST (155.2 vs. 165.1 months; p < 0.001). In exploratory mediation analysis, PIR accounted for 23.8% of the observed association between depressive symptoms and reduced survival, suggesting a potential socioeconomic contribution to the survival gap.

Depressive symptoms were associated with reduced survival among adults with asthma, and income may partially account for this observed relationship. These findings should be interpreted cautiously because depressive symptoms and income were measured at baseline, limiting causal interpretation of the mediation analysis. Further longitudinal studies are needed to confirm these findings and clarify temporal relationships.

A considerable proportion of patients experience post-acute sequelae of COVID-19 (PASC). Increasing evidence suggests sex-related differences, yet systematic longitudinal analyses remain limited. This study aimed to examine sex-specific differences in symptoms, psychological burden, work productivity and physical activity over ten months following acute COVID-19.

In this prospective, dynamically enrolled cohort study, patients with ongoing symptoms after confirmed SARS-CoV-2 infection were followed over a 10-month observation period. Patients conducted at the post-COVID outpatient clinic of the department of respiratory medicine and infectious diseases at Hannover Medical School, Germany. The assessment included patient-reported outcome measures, pulmonary function tests, six-minute walk tests, and capillary blood gas analysis. All outcome comparisons between sexes were adjusted for age, BMI, COVID-19 severity, and comorbidities using generalised linear mixed-effects models, with sex-by-time interaction terms tested to assess whether differences changed over follow-up, and p-values corrected for multiple testing across all outcome comparisons using the Holm method. A sensitivity analysis was performed in the subgroup of patients with complete follow-up at all four visits.

Five hundred ninety patients attended to our clinic and a total of 433 patients were eligible and consecutively enrolled. Males were older (56 years vs. 52 years, p = 0.002), had more cardiovascular comorbidities (16% vs. 5%, p < 0.001), and experienced more severe COVID-19 (28% vs. 8%, p < 0.001). After adjustment for age, BMI, COVID-19 severity, and comorbidities, and Holm correction for multiple testing across all 27 outcome comparisons, females showed higher fatigue (Fatigue Assessment Scale, adjusted β = 3.3, Holm-adjusted p = 0.006), higher anxiety (GAD-2, β = 0.5, p = 0.021), lower quality of life (EQ-5D-3L, β = -0.6, p = 0.004), and greater work productivity impairment, both as a continuous score (WPAI-VAS, β = 1.3, p = 0.031) and as a binary indicator of clinically relevant impairment (OR = 3.0, p = 0.020). Females also had higher percent-predicted (pp) total lung capacity (p < 0.0001) and lower pCO₂ (p < 0.0001), whereas males had higher pp diffusion capacity (p = 0.001). Headache (p < 0.001) and chest tightness (p = 0.011) were reported more frequently by females. None of these differences varied significantly over the 10-month follow-up (all sex-by-time interaction p ≥ 0.41), indicating no evidence that these differences changed over time. No significant sex differences remained after adjustment for depression (PHQ-2), lung function parameters, sex/height-adjusted exercise capacity, post-exercise dyspnoea or oxygen saturation, or most acute-COVID-19 symptoms other than headache and chest tightness. Regression models separately for each sex revealed fever (OR = 2.48, 95% CI: 1.11-5.57, p = 0.027) and diarrhoea (OR 2.33, 95%CI: 1.05-5.16, p = 0.038) during acute COVID-19 were associated with higher odds of work productivity impairment (WPAI-VAS ≥ 2) in males. In females, higher BMI (OR = 2.06, 95% CI: 1.13-3.76, p = 0.018) and dyspnoea during acute COVID-19 (OR = 4.38, 95% CI: 1.55-12.40, p = 0.005) were associated with increased odds. Formal interaction analyses showed a significant interaction only for dyspnoea after Holm correction.

After accounting for baseline imbalance in age, BMI, COVID-19 severity, and comorbidities, and after correcting for multiple testing, sex-specific differences persisted for fatigue, anxiety, quality of life, and work productivity impairment, as well as selected lung function parameters. These differences did not change significantly across the 10-month observation period and did not show a significant sex-by-time interaction. The findings support the need for individualised, sex-specific follow-up focused on fatigue, psychological burden, and work productivity in patients with PASC.

Direct oral anticoagulants (DOACs) have simplified treatment for venous thromboembolism (VTE), but fewer mandatory monitoring visits may reduce opportunities for structured reassessment. We evaluated temporal changes in hospital-captured documentation of post-VTE care processes during the transition to DOAC-based treatment, including initial anticoagulation, clinical follow-up, laboratory monitoring, and selective imaging reassessment.

We conducted a single-center retrospective electronic health record cohort study using routinely collected vascular surgery outpatient and inpatient records from Peking University People's Hospital between 2009 and 2024. Patients with VTE-related evidence and a definable hospital-captured index date were included. Treatment eras were prespecified as 2009-2014, 2015-2019, and 2020-2024. The study-defined documentation measure comprised therapeutic anticoagulation within 14 days and clinical follow-up, laboratory monitoring, and selective VTE-related ultrasound or imaging reassessment within 15-90 days.

Among 5998 patients with a definable hospital-captured index VTE-related event, the median age was 64.0 years, and 55.3% were female. Documented anticoagulation within 14 days increased from 34.1% in 2009-2014 to 58.0% in 2020-2024. Within 15-90 days, clinical follow-up was documented in 1483 patients (24.7%), laboratory monitoring in 366 (6.1%), and VTE-related ultrasound or imaging reassessment in 578 (9.6%). All four prespecified domains were documented in 149 patients (2.5%) overall and in 3.2% during 2020-2024. In multivariable analysis, the 2020-2024 era, pulmonary embolism presentation, and upper-extremity or catheter-related VTE were associated with higher odds of four-domain documentation completion.

In this 16-year electronic health record cohort, hospital-captured documentation of early anticoagulation increased, whereas documentation of 90-day follow-up processes remained infrequent; incomplete documentation or care delivered outside the hospital system may have contributed. These findings highlight opportunities to strengthen continuity and traceability of post-VTE management through timely clinical review and individualized decisions regarding treatment duration, safety monitoring, and selective imaging when clinically indicated.

Older adults with hypertension commonly experience poor sleep quality and reduced health-related quality of life (HRQoL). Previous studies have mainly examined these associations using total scores, providing limited insight into interactions between specific symptom dimensions. This study aimed to construct a component- and dimension-level network linking sleep quality and HRQoL and to compare network differences across depressive-symptom status.

This study included 2,257 older adults. Sleep quality, HRQoL, and depressive symptoms were assessed using the B-PSQI, EQ-5D-5L, and PHQ-9, respectively. We estimated a component- and dimension-level network based on the EBICGlasso-regularized Gaussian graph model, calculated centrality and bridge centrality metrics, validated stability using the bootstrap method, and compared network differences between the depressive and non-depressive-symptom groups.

The final network included 10 nodes and 32 non-zero edges among 45 possible edges, with a density of 0.711. The strongest associations were between sleep efficiency and sleep duration (SE-ST, 0.793), sleep interruption and subjective sleep quality (SW-SQ, 0.583), and self-care and usual activities (SC-UA, 0.560). Usual activities (UA) showed the highest strength centrality and expected influence, followed by subjective sleep quality (SQ), self-care (SC), and sleep efficiency (SE). Sleep efficiency had the highest bridge expected influence, followed by subjective sleep quality. Centrality indices demonstrated good stability (CS = 0.75). No significant differences were found in network structure (M = 0.224, P > 0.05) or global strength (S = 0.119, P > 0.05); repeated 1:1 subsampling broadly supported these findings.

Sleep components and HRQoL dimensions formed a closely connected network in older adults with hypertension. Usual activities showed the highest centrality, while sleep efficiency and subjective sleep quality showed prominent cross-community. These domains may be useful for screening or hypothesis generation but should not be interpreted as confirmed intervention targets.