303 Hospital of People's Liberation Army

Adolescent negative emotions are a major public health concern. Physical exercise is often associated with better emotional health, yet the psychological processes underlying this association, particularly in Chinese adolescents, are not fully understood. This study examined whether stress perception and emotional sensitivity are related to the association between physical exercise and negative emotions. A cross-sectional survey was conducted with 1,471 adolescents (54.52% male; Mean age = 13.16, SD = 1.01) from ten middle schools in Guangxi Province, China. Validated Chinese versions of established instruments assessed physical exercise (Youth Physical Activity Rating Scale), negative emotions (PANAS Negative Affect subscale), stress perception (Perceived Stress Scale), and emotional sensitivity operationalized through emotional contagion susceptibility. Path analysis using maximum likelihood estimation with robust standard errors tested the hypothesized sequential mediation model. Bootstrap confidence intervals (5,000 resamples) evaluated indirect effects. Path analysis revealed good model fit (χ²/df = 3.62, CFI = 0.96, TLI = 0.94, SRMR = 0.05, RMSEA = 0.04). Physical exercise demonstrated significant direct (β = -0.13, 95% CI [-0.22, -0.09]) and indirect (β = -0.12, 95% CI [-0.27, -0.08]) associations with negative emotions. Stress perception accounted for 40% of the total association between physical exercise and negative emotions (β = -0.10, 95% CI [-0.16, -0.07]). The sequential indirect association via stress perception and emotional sensitivity accounted for 8% of the total association (β = -0.02, 95% CI [-0.05, -0.01]). The direct path from physical exercise to emotional sensitivity was non-significant (β = -0.04, p = 0.23), which is consistent with an indirect-only pattern via stress perception in the specified model. The findings are consistent with a sequential mediation model in which physical exercise is associated with lower negative emotions both directly and indirectly, primarily through lower stress perception and, to a lesser extent, through a sequential pathway involving emotional sensitivity. Although the cross-sectional design does not permit causal conclusions, the observed pattern of associations highlights physical exercise and stress perception as important contextual factors to consider when developing strategies to support adolescent emotional health.

ObjectiveTo report a well-documented case of cytokine release syndrome (CRS) following the first cycle of amivantamab combined with chemotherapy in a patient with osimertinib-resistant EGFR-mutant non-small cell lung cancer (NSCLC), highlighting its diagnosis, management, and association with a rapid antitumor response.Case summaryA 72-year-old man with metastatic lung adenocarcinoma (epidermal growth factor receptor (EGFR) exon 19 del) progressing on osimertinib initiated treatment with amivantamab, pemetrexed, and carboplatin. Five days post-infusion, he developed a persistent fever unresponsive to broad-spectrum antibiotics. Infection was rigorously excluded based on normal procalcitonin, undetectable endotoxin, and negative cultures. In contrast, inflammatory markers were elevated (peak CRP (C−reactive protein) 16.6 mg/dL), and cytokine profiling revealed significant elevations in IL−6 (interleukin−6) (107 pg/mL), sIL-2R (soluble interleukin−2 receptor), TNF-α (tumor necrosis factor−alpha), and IL-10, accompanied by profound lymphopenia. A computed tomography (CT) scan demonstrated a significant tumor reduction. A diagnosis of grade 1 CRS (by ASTCT (American Society for Transplantation and Cellular Therapy) criteria) was made. The fever and inflammatory markers resolved with supportive care.FindingsThis case provides comprehensive clinical and serological evidence of amivantamab-chemotherapy-induced CRS. The temporal association between the robust cytokine surge, characteristic of T-cell activation, and the observed rapid tumor regression suggests that the same immunologic mechanism likely underpinned both the efficacy and the toxicity.ConclusionCRS is an important adverse event associated with amivantamab-based combination therapy in solid tumors. Early recognition, based on clinical suspicion and characteristic cytokine profiles, and differentiation from infection are crucial. The concurrent rapid tumor response indicates that effective immune activation drives both toxicity and efficacy, underscoring the need for optimal management strategies to mitigate CRS without compromising antitumor activity.

Clear cell renal cell carcinoma (ccRCC) arising in the setting of von Hippel–Lindau (VHL) disease is a rare type of kidney cancer and features VHL germline mutation. This type of ccRCC is rarely characterised at the single-cell level. In this work, whole-exome sequencing and single-cell RNA sequencing (scRNA-seq) were conducted on one ccRCC sample with VHL disease. Integrating scRNA-seq and whole-exome sequencing data by the Seurat package, we determined the relationship between single-cell transcriptome features and gene mutations. Immunohistochemistry and immunofluorescence were performed on one VHL germline mutation ccRCC and six non-VHL germline mutation ccRCC samples. We revealed the gene expression characteristics of ccRCC with VHL germline mutation. The frameshift mutations in OBP2A and BCR1, and the elevated expression of COX7A1 were most specific characteristics of ccRCC tumor cells with VHL mutation. And the extensive infiltration of exhausted T cells was the characteristic of tumor microenvironment. In addition, we discovered the relationship between genetic mutations and immune checkpoints. This work highlights the single-cell transcriptome and DNA-level information of this rare ccRCC and will provide more genetic insights and references into this rare disease.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-27699-y.

Psychological problem and physical–psychological multimorbidity is rising among middle-aged and older adults in China. Whether residential greenness, air pollution and systemic inflammation jointly influence psychiatric outcomes remains unclear. Using a retrospective cross-sectional design based on 2015 China Health and Retirement Longitudinal Study (CHARLS) data, we investigated the link between the Normalized Difference Vegetation Index (NDVI) and psychiatric problems/comorbidities, and evaluated the roles of ambient pollutants (PM₂.₅, PM₁₀) and the inflammatory biomarker C-reactive protein (CRP). The final sample included 6900 adults aged ≥ 45 years. Key findings revealed that a 0.1-unit increase in NDVI was associated with an 18% lower risk of psychiatric problems (OR = 0.82, 95% CI 0.68–0.97, P = 0.024) and a 19% lower risk of physical–psychological multimorbidity (OR = 0.81, 95% CI 0.67–0.99, P = 0.035). Conversely, each unit increase in PM₂.₅ and PM₁₀ was linked to a 1% higher risk of psychiatric problems (PM₂.₅: OR = 1.01, 95% CI: 1.00–1.02, P = 0.033; PM₁₀: OR = 1.01, 95% CI 1.00–1.02, P = 0.042) and multimorbidity (PM₂.₅: OR = 1.01, 95% CI 1.00–1.03, P = 0.048; PM₁₀: OR = 1.01, 95% CI 1.00–1.02, P = 0.052). Inflammatory marker analysis showed that a 10-unit increase in CRP was associated with a 20% higher risk of psychiatric problems (OR = 1.20, 95% CI 1.04–1.39, P = 0.013) and a 22% higher risk of comorbidities (OR = 1.22, 95% CI 1.06–1.42, P = 0.007). Pathway analysis confirmed no significant evidence of mediation effects of PM₂.₅, PM₁₀, or CRP on the association between NDVI and physical–psychological multimorbidity. Cross-sectional analyses indicate an inverse association between residential greenness and psychiatric morbidity, yet longitudinal or interventional evidence is required to establish the clinical significance of this relationship and to determine whether air pollution or inflammation represents a causal mediator before findings can guide policy or practice.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-24005-8.

This article reports a case of SAPHO syndrome misdiagnosed as spinal infection, detailing the clinical manifestations, laboratory tests, and imaging features of the patient. Through a review of the literature, common confounding factors and reasons for misdiagnosis in the diagnostic process of this disease are summarized. Comprehensive analysis of multiple related studies reveals that detailed medical history collection, advanced imaging examinations (such as ECT), and multidisciplinary consultations play a decisive role in making a correct diagnosis. Furthermore, the literature shows that the treatment for SAPHO syndrome is fundamentally different from spinal infection, with the former mainly relying on anti-inflammatory regulation, bone protective agents, and immune modulation therapy, rather than the indiscriminate use of antibiotics. This report aims to remind clinicians to maintain a high level of vigilance when facing spinal lesions, and to compare and summarize the latest advances in diagnosis and treatment, providing a reference for improving the level of diagnosis and treatment in the future.

Pulmonary fibrosis (PF) is a refractory disease characterized by inflammation and fibrosis. Shensiqigui Tablets (SSQGT), a combination of Codonopsis pilosula, Astragalus, and Angelica, is a traditional Chinese medicine with anti-inflammatory and antioxidant properties. Therefore, SSQGT may be a potential therapeutic agent for managing PF. This study aimed to investigate the effects of SSQGT on PF and its potential mechanisms. This study established a mouse model of PF through a single intratracheal injection of bleomycin (BLM) and used a TGF-β1-induced HFL-1 cell model. The experiment included control, model (BLM/TGF-β1), and treatment groups (pirfenidone, compound Biejiaruangan tablet (BJRGT), low-dose SSQGT, medium-dose SSQGT, and high-dose SSQGT). Histopathological changes and collagen deposition in lung tissues were observed using Hematoxylin-Eosin (HE) and Masson staining. Inflammatory exudation in bronchoalveolar lavage fluid (BALF) was assessed using ELISA, including TNF-α, IL-1β, IL-6, and NO. Oxidative stress markers SOD, GSH, and Malondialdehyde (MDA) were measured using commercial kits. mRNA and protein expression levels in lung tissues and in vitro models, including α-SMA, vimentin, collagen I, caspase-3, TGF-β, and the Hedgehog/Wnt-β-catenin pathway, were evaluated using qRT-PCR and western blot analysis. SSQGT significantly alleviated BLM-induced weight loss and lung injury in mice and reduced HYP levels and collagen deposition. Additionally, SSQGT improved oxidative stress markers (decreased MDA levels and increased SOD and GSH activity) and mitigated inflammatory responses (reduced TNF-α, IL-1β, IL-6, and NO levels) and (downregulated α-SMA, collagen I, caspase-3, and TGF-β). Further mechanistic analysis showed that SSQGT inhibited the Hedgehog/Wnt-β-catenin pathway. SSQGT alleviates BLM- or TGF-β1-induced PF by reducing oxidative stress and inhibiting inflammation through the suppression of the Hedgehog/Wnt-β-catenin pathway, suggesting its potential as a therapeutic agent for PF.