Perioperative anaphylaxis is a rare, life-threatening, iatrogenic condition that predominantly arises following anesthesia. The unique context of this condition, characterized by the concurrent administration of multiple drugs, patient draping, and altered physiological states, presents significant diagnostic and therapeutic challenges, contributing to a higher mortality rate compared to anaphylaxis in other settings. This narrative review synthesizes the evidence to delineate the evolving etiology, pathophysiology, atypical clinical presentation, evidence-based immediate management, and strategic prevention of perioperative anaphylactic reactions. The primary causative agents include neuromuscular blocking agents, antibiotics, and latex, with emerging culprits such as chlorhexidine, dyes, and novel agents like remimazolam. Diagnosis is complicated by the paucity of cutaneous signs; thus, cardiovascular collapse combined with a low end-tidal carbon dioxide level has emerged as a useful supportive diagnostic indicator that requires integration with the clinical context. Immediate management prioritizes the prompt administration of epinephrine and aggressive fluid resuscitation. Subsequent allergological investigations, primarily via skin testing and serum tryptase/histamine measurement, are paramount for identifying the causative agent and preventing its recurrence. Prevention strategies emphasize meticulous history-taking, risk stratification, and the creation of latex-free environments. Future directions must focus on establishing global surveillance networks, exploring novel biomarkers and risk factors such as the circulating microbiome—a preliminary but promising area of research—and enhancing team preparedness through simulation training to improve patient safety outcomes.

Comparative data on sequential transarterial chemoembolization (TACE) after stereotactic body radiation therapy (SBRT) in recurrent hepatocellular carcinoma (HCC) remain limited. This study aimed to evaluate the efficacy of this combination.

We retrospectively reviewed 152 patients with recurrent HCC who met predefined eligibility criteria; 109 received SBRT alone and 43 received SBRT plus TACE. To minimize selection bias, a 2:1 propensity score matching was performed, resulting in 68 patients in the SBRT-alone group and 36 in the SBRT plus TACE group for the final comparative analysis. Overall survival, progression-free survival, and local control were assessed using the Kaplan-Meier method.

The SBRT plus TACE group was associated with numerically higher survival rates, although this difference did not reach statistical significance. The cumulative one-, three-, and five-year overall survival rates were 91.2%, 76.3%, and 61.8% for SBRT alone, compared to 100.0%, 86.1%, and 77.5% for the combination therapy ( p = 0.069). The corresponding progression-free survival rates were 73.1%, 51.1%, and 32.3% versus 88.9%, 58.1%, and 52.3% ( p = 0.091). No acute grade ≥3 toxicities were observed in either group.

In this exploratory analysis of recurrent HCC, the combination of SBRT and TACE demonstrated a favorable trend toward improved survival compared with SBRT alone, without an increase in severe toxicity. While these findings did not reach statistical significance, they establish the safety profile of the combined approach and provide preliminary evidence supporting its potential therapeutic role. This hypothesis-generating study justifies and informs the design of larger, prospective trials to definitively evaluate the efficacy of this regimen.

Predicting the malignant transformation of rectal precancerous lesions remains challenging because conventional Whole Slide Images (WSIs) capture morphological information but lack molecular insight. Multiomics data provide complementary biological signals that often precede visible morphological changes. This study aimed to develop an artificial intelligence (AI)-based multimodal framework integrating WSI and multiomics data for accurate early prediction of malignant transformation.

WSI patches (512×512 px at 20× magnification) and matched multiomics profiles were used for 450 rectal tissue samples from the publicly available The Cancer Genome Atlas dataset. A multimodal architecture was designed, employing a Vision Transformer (ViT-B/16) for WSI feature extraction and a Variational Autoencoder for multiomics representation learning. Features were fused via a cross-attention mechanism to capture inter-modality dependencies. Baseline models, including a convolutional neural network-only image model and an omics-only multilayer perceptron, were trained for comparison. Five-fold cross-validation was applied, with binary cross-entropy loss, the AdamW optimizer, early stopping, and hyperparameter tuning to ensure reproducibility.

The multimodal Vision Transformer–Variational Autoencoder fusion model outperformed unimodal baselines, achieving an accuracy of 0.892 ± 0.012 and an area under the receiver operating characteristic curve of 0.927 ± 0.009, corresponding to a 7–10% improvement over WSI-only and omics-only models. Cross-attention–based fusion improved prediction stability and classification performance, while interpretability analyses (Grad-CAM and SHAP) highlighted biologically meaningful histopathological regions and molecular feature contributions.

This study presents a robust and scalable AI-based framework for integrating WSI and multiomics data in rectal precancerous lesions. The model improves predictive precision compared with unimodal baselines and offers preliminary interpretability insights through attention mechanisms. These findings support the potential of multimodal AI for early cancer risk assessment and precision pathology.

Obstructive sleep apnea (OSA) is a prevalent sleep disorder characterized by intermittent hypoxia and sleep fragmentation, which may contribute to lung cancer development and progression. This review synthesizes epidemiological evidence on the association between OSA and lung cancer incidence and mortality, highlighting inconsistencies due to study design, population differences, and confounding factors such as smoking and obesity. While some studies report an increased lung cancer risk, particularly with severe nocturnal hypoxemia, others suggest no significant association or a potential protective effect. Pathophysiologically, OSA promotes oncogenesis through hypoxia-inducible factor activation, tumor immune microenvironment remodeling, exosome-mediated signaling, nuclear factor κB pathway activation, and enhanced cancer stem cell properties. Continuous positive airway pressure therapy may mitigate these effects, with evidence suggesting reduced lung cancer incidence and improved prognosis in adherent patients. This review underscores the need for standardized studies using objective diagnostics and robust confounder adjustment to clarify the OSA–lung cancer link and optimize clinical management.

Diabetic cardiomyopathy (DCM), a diabetes-specific cardiovascular complication, is pathologically characterized by cardiomyocyte apoptosis, oxidative stress, inflammatory responses, and myocardial fibrosis, distinguishing it from other cardiac disorders, such as hypertension and coronary artery disease. Challenges in early diagnosis, coupled with the limited efficacy and adverse effects of current treatments, have made DCM a significant contributor to heart failure and mortality in patients with diabetes. Natural products, recognized for their diverse sources, structural variety, and multitarget therapeutic potential, have shown promise in preventing and treating DCM. Drawing on advances over the past five years, this review systematically summarizes the pharmacological effects and molecular mechanisms of natural products (e.g., flavonoids, terpenoids, phenylpropanoids, alkaloids, and polysaccharides) in the treatment of DCM, with the aim of providing a theoretical foundation for further research and drug development.

Micro- and nanoplastics (MNPs) are pervasive environmental contaminants with growing recognition as potential contributors to human disease. Widespread human exposure occurs primarily through ingestion of contaminated food and water, and MNPs have been detected in multiple human tissues, including the gastrointestinal tract. Experimental evidence provides a plausible biological basis for disease associations, including impairment of intestinal barrier integrity, activation of mucosal immune pathways, and alteration of gut microbial communities caused by MNP exposure. Although human data remain limited, early studies demonstrate MNP detection in stool and suggest potential correlations with inflammatory biomarkers such as fecal calprotectin. These findings, together with mechanistic data from in vitro and animal models, raise concern that MNP exposure represents a paradigm shift in the pathogenesis or modulation of inflammatory bowel disease (IBD); however, methodological variability, small sample sizes, and contamination challenges currently limit definitive conclusions. The aim of this review is to evaluate the current understanding of MNP exposure and its impact on intestinal health, particularly in relation to IBD. We synthesize mechanistic and early clinical evidence linking MNPs to IBD and highlight critical research gaps. Future standardized exposure assessment, mechanistic validation in human systems, and longitudinal studies are essential to clarify causal relationships. Given the modifiable nature of environmental plastic exposure, advancing this field may offer new opportunities for IBD prevention and intervention.