Zhongguo Fei Ai Za Zhi. 2026 Jul 20;29(7):540-547. doi: 10.3779/j.issn.1009-3419.2026.101.17.

ABSTRACT

Immune checkpoint inhibitors (ICIs) have significantly improved the prognosis of patients with lung cancer. However, checkpoint inhibitor-related pneumonitis (CIP), as one of the most severe immune-related adverse events, lacks well-defined diagnostic criteria and reliable risk stratification tools. Radiomics enables high-throughput feature extraction from computed tomography images and provides a non-invasive technical approach for the early identification and risk stratification of CIP. This article systematically reviews the recent advances in the application of radiomics to risk prediction, diagnosis and differential diagnosis, and prognostic evaluation of CIP in lung cancer immunotherapy. Furthermore, it explores the value of integrating radiomics with multi-omics data in elucidating the pathogenesis of CIP, as well as the role of explainable artificial intelligence (XAI) in enhancing the clinical trustworthiness of models. .

PMID:42705857 | DOI:10.3779/j.issn.1009-3419.2026.101.17

EPMA J. 2026 Aug 21;17(3):665-700. doi: 10.1007/s13167-026-00465-4. eCollection 2026 Sep.

ABSTRACT

Chronic atrophic gastritis (CAG) is a critical precancerous stage in the development of gastric cancer (GC). Circadian rhythm disruption perturbs the core clock gene network, including circadian locomotor output cycles kaput (CLOCK), brain and muscle ARNT-like 1 (BMAL1), period circadian protein homolog (PER), and cryptochrome (CRY). These alterations contribute to a multi-layered pathological cascade involving DNA damage accumulation, epigenetic remodeling, altered epithelial cell plasticity, cellular senescence, microbiota dysbiosis, tumor microenvironment remodeling, metabolic reprogramming, aberrant angiogenesis, and dysregulated cell death, thereby accelerating CAG to GC progression. However, existing studies have predominantly treated the circadian rhythm as a passive risk factor for disease onset and have yet to elevate it to an actionable interventional target within the full-course management of gastric precancerous lesions. Building on a systematic synthesis of the mechanistic evidence outlined above, this review proposes a predictive, preventive and personalised medicine (PPPM/3PM) three-tier management framework grounded in circadian-based individualised protection. At the predictive level, digital biomarkers (sleep-wake rhythms, light exposure, physical activity, and dietary behavior), multi-omics profiles, and circadian-related molecular signatures are integrated to achieve dynamic risk stratification of CAG populations. At the targeted prevention level, pharmacological agents and natural compounds with circadian-regulating potential are deployed to develop proactive protective strategies tailored to distinct pathological stages and circadian phenotypes. At the personalised treatment level, lifestyle interventions, chronotherapy, nano-carrier-based circadian-synchronised delivery, and dynamic biomarker monitoring are combined to formulate precision intervention regimens informed by individual circadian phenotypes. This framework repositions the circadian rhythm from a latent risk factor to a protectable and therapeutically targetable axis, offering new insights into time-optimised intervention strategies for the inflammation to cancer transition in CAG.

PMID:42682657 | PMC:PMC13530114 | DOI:10.1007/s13167-026-00465-4

Exp Ther Med. 2026 Mar 30;31(6):148. doi: 10.3892/etm.2026.13143. eCollection 2026 Jun.

ABSTRACT

Streptococcus pneumoniae (SP) infection often leads to persistent lung injury even after antibiotic treatment. Despite this phenomenon, the mechanisms underlying host cell recovery remain poorly understood. Upon breaching the epithelial barrier, SP primarily targets the pulmonary interstitial cells, which constitute the major mesenchymal component of the lung. These cells serve as essential effectors of tissue repair, extracellular matrix remodeling and epithelial restoration. Therefore, a feline pulmonary interstitial cell (FCA-L2) model of SP infection was established to investigate the protective effects of glutamine (GLU) and fish collagen peptides (FCP) through integrated transcriptomic and metabolomic analyses. Cells were infected with SP (0.05 McFarland units for 4 h) and then treated with doxycycline (7.5 µg/ml for 18 h) followed by GLU (40 mM) or FCP (500 µg/ml). Notably, SP infection increased lactate dehydrogenase (LDH) release by 3.5-fold, induced secretion of IL-1β, TNF-α and IL-8, disrupted tight-junction proteins (claudin, ZO-1 and occludin) and caused oxidative imbalance and apoptosis despite antibiotic (doxycycline) treatment. However, treatment with GLU or FCP significantly reduced LDH release by ~40%, restored junctional proteins, suppressed inflammatory cytokines and enhanced antioxidant enzyme activities. Multi-omics analysis revealed that GLU promoted amino acid biosynthesis and energy metabolism and suppressed aminoacyl-tRNA synthetases and cell-cycle regulators, thereby enhancing metabolic adaptability. By contrast, FCP activated amino and nucleotide sugar metabolism, increased polyunsaturated fatty-acid synthesis and supported glycocalyx repair and membrane reconstruction. GLU and FCP provided complementary metabolic and structural protection, which mitigated post-infectious stress and promoted cellular recovery. The findings of the present study underscore the potential of bioactive food-derived compounds as adjunctive therapies that may accelerate lung tissue repair and enhance the efficacy of conventional antibiotics.

PMID:41988354 | PMC:PMC13077270 | DOI:10.3892/etm.2026.13143