Annals of medicine最新文献

Background: Acute Ischemic Stroke (AIS) remains a critical global health challenge that requires continuous improvement in diagnostic strategies. Timely and accurate diagnosis is essential for effective reperfusion therapies such as intravenous thrombolysis and mechanical thrombectomy, whose clinical benefits rapidly diminish with treatment delays. Artificial Intelligence (AI) offers promising potential to enhance diagnostic accuracy and clinical decision-making in AIS. However, data fragmentation and strict privacy regulations limit the development of robust AI systems. Objectives: We aim to provide a perspective-style review that explores how collaborative AI can reshape AIS diagnostics by overcoming data access barriers, fostering cross-institutional model development, and improving diagnostic equity.

Methods: We analysed current challenges in developing AIS-related AI tools, particularly the limitations caused by restricted data sharing across healthcare institutions. The study highlights collaborative AI approaches, such as federated learning and privacy-preserving computation, which enable decentralised model training while maintaining patient confidentiality. Relevant literature and recent developments in clinical AI collaboration were reviewed.

Results: Collaborative AI enables multiple institutions to contribute to model training without exposing raw patient data. This approach improves data diversity, model generalizability, and fairness across healthcare settings. Evidence from multi-centre studies suggests that collaborative AI frameworks can produce more accurate and ethically compliant diagnostic models compared to isolated development efforts.

Conclusions: Collaborative AI presents a transformative pathway for AIS management by balancing data utility and privacy protection. It supports the creation of trustworthy, scalable, and inclusive diagnostic systems. As healthcare systems increasingly adopt digital solutions, collaborative AI provides a foundation for equitable and privacy-conscious innovation in stroke care.

Purpose: Behçet's disease (BD) is a multisystem autoinflammatory disorder that may present during childhood. Pediatric BD is challenging to diagnose due to heterogeneous clinical manifestations and the lack of standardised pediatric classification criteria. This study aimed to evaluate the association between systemic inflammatory biomarkers-including the neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), pan-immune-inflammation value (PIV), and C-reactive protein (CRP)/albumin ratio-and systemic organ involvement in children with BD. To our knowledge, no prior study has investigated these markers in pediatric BD.

Methods: In this retrospective study, 41 pediatric patients diagnosed with BD according to the 2015 PEDBD criteria and followed jointly by dermatology and rheumatology departments were included. Age- and sex-matched healthy controls (n = 41) undergoing elective surgery were also enrolled. Inflammatory indices (NLR, SII, PIV, CRP/albumin) were calculated from pre-treatment blood samples. Cut-off values for systemic involvement were determined via ROC analysis. Statistical analyses included the Kolmogorov-Smirnov test, independent t-test or Wilcoxon test, Chi-square and McNemar tests, correlation analysis, logistic regression, and ROC analysis.

Results: Systemic involvement was observed in 28 (68.3%) patients, including neurological involvement in 4 (9.8%), vascular involvement in 5 (12.2%), and other major organ involvement in 19 (46.3%). Inflammatory indices-PIV, SII, NLR, and CRP/albumin-were significantly higher in patients with systemic, neurological, and vascular involvement (all p < 0.05). Optimal cut-off values for each index were established based on systemic involvement.

Conclusion: Systemic inflammatory biomarkers such as NLR, SII, PIV, and CRP/albumin ratio may serve as useful indicators of systemic organ involvement in pediatric BD. Routine assessment of these markers could facilitate earlier recognition and more targeted management of systemic manifestations in this population.

Background: The triglyceride-glucose index (TyG) has gained attention as an alternative indicator for assessing insulin resistance (IR). The purpose of this study was to comprehensively summarize the correlation between the TyG index and cardiovascular events in patients with coronary revascularization.

Methods: PubMed, Web of Science, Embase, and The Cochrane Library databases were searched to find relevant literature on the prognostic assessment of TyG index in patients undergoing coronary artery revascularization. Utilize the risk ratio (RR) and its 95% confidence interval (CI) as the standard for assessing the correlation between TyG and major adverse cardiovascular events (MACEs) in patients undergoing coronary artery revascularization. Conduct sensitivity analysis and subgroup analysis to detect the sources of heterogeneity and assess the stability of the results.

Results: A total of 12 studies involving 9,973 participants were included. The results of the study indicate that a high TyG index was related to the major adverse cardiovascular event in patients undergoing coronary artery revascularization (RR:2.0,95%CI: 1.71-2.35, I²=76.2%, p < 0.0001). Subgroup analysis reveals that the probability of MACEs occurring in patients with high TyG index is higher than in those with low TyG index after two different coronary artery revascularization procedures: CABG group (RR:2.10, 95%CI:1.80-2.45, I2 = 20.9%, p = 0.0001). PCI group: (RR:1.94, 95%CI:1.54-2.46, I2 = 84.2%, p < 0.00001). Additionally, we also demonstrated the prognostic value of the TyG index in all-cause mortality(p = 0.003), non-fatal myocardial infarction(p = 0.003), non-fatal stroke(p < 0.0001) and repeat revascularization(p < 0.0001).

Conclusions: Higher TyG index may be independently associated with higher incidence of MACEs in patients with coronary revascularization.

Background: Tumour microenvironment and cancer cells have constant interaction affecting cancer progression. Tumour-stroma ratio (TSR) in the tumour centre and desmoplastic reaction (DR) classification at the invasive margin are prognostic factors based on stroma evaluation on H&E slides. However, their combined value and immunological associations remain poorly defined. This study examines the prognostic and immunological value of TSR, DR, and their combination in two large colorectal cancer cohorts.

Methods: Two colorectal cancer cohorts (N = 1,876) were analyzed. We introduced a three-tiered Stromal Maturity and Proportion Score (SMAPS) based on the presence of high (>50%) TSR and myxoid stroma (immature DR classification). Alcian blue staining was used to further quantify myxoid stroma. Multiplex immunohistochemistry combined with digital image analyses, was utilized to study immune cell densities associated with SMAPS, TSR, DR, and Alcian blue intensity.

Results: In the study cohort (N = 1,100), SMAPS was a stronger predictor of cancer-specific mortality [HR for high (vs. low) SMAPS 2.01 (95% CI 1.47-2.75), p < 0.0001] compared to TSR [HR for stroma-high (vs. stroma-low) 1.49 (95% CI 1.15-1.93), p = 0.003] and DR classification [HR for immature (vs. mature) 1.84 (95% CI 1.39-2.45), p < 0.0001]. High SMAPS, stroma-high TSR, and immature DR correlated with lower densities of CD3⁺ T cells, B cells, M1-like macrophages, CD66B⁺ granulocytes, and mast cells. Alcian blue staining was associated with immature DR and corresponding immune cells. The validation cohort (N = 776) confirmed the association of SMAPS with survival and T cell densities.

Conclusions: TSR and DR are independent prognostic factors for cancer-specific survival. SMAPS is a promising prognostic tool that integrates stromal maturity at the invasive margin and stromal proportion in the tumour centre. SMAPS has stronger prognostic value compared to TSR and DR classifications alone. A high stromal proportion and myxoid content are associated with an immunosuppressive microenvironment characterized by lower densities of antitumourigenic immune cells.

Patients with the most common chronic inflammatory dermatoses, namely psoriasis and atopic dermatitis, gained access to state-of-the-art therapeutic options providing spectacular improvement of skin lesions. Although generally safe, biological agents and small molecular drugs have also side effects which may be mild and irrelevant to the therapy course, but sometimes, of a greater extent and influencing further therapeutic decisions. In this review, we summarize the molecular explanation for the most common adverse effects of drugs used in the treatment of psoriasis and atopic dermatitis. Biologics used in psoriasis predominantly target TNFα, IL-17, 23, while in AD inhibit IL-4,13,31. Janus kinase (JAK) inhibitors represent small-molecule therapies effective in both conditions, although more prominently in AD. TNFα inhibitors are associated with increased susceptibility to infections, paradoxical psoriasis, eczematoid lesions, and reactivation of tuberculosis. IL-17 inhibitors may cause fungal infections and possibly trigger inflammatory bowel disease. IL-4/13 blockade in AD treatment has been linked to eosinophilia, conjunctivitis, arthritis, and facial erythema, likely due to a shift toward IL-17-driven inflammation. JAK inhibitors may cause infections, acne, dyslipidemia, and, in selected cases, cardiovascular events. This review emphasizes the importance of understanding the pathogenetic background of drug-related complications to introduce appropriate clinical management and patient selection.

Purpose: To investigate the relationship between first-trimester maternal serum iodine concentration (SIC) and foetal ultrasound biometric parameters as well as neonatal size at birth in Chinese pregnant women.

Materials and methods: A birth cohort study of 1881 women from 2022 to 2024 in Zhejiang Province, China, was conducted. SIC in the first trimester was measured using inductively coupled plasma mass spectrometry. Foetal biometric parameters in mid-pregnancy were measured using ultrasound scanning techniques. Neonatal anthropometric measurements were obtained immediately after delivery. Linear regression models were used to explore the association between maternal SIC and both foetal ultrasound biometric parameters as well as birth size indicators.

Results: Log-transformed maternal SIC showed a significant positive association with biparietal diameter (BPD) (β = 0.102, 95% CI: 0.029, 0.174), but significant negative associations with birth length (β = -0.337, 95% CI: -0.608, -0.066) and birth weight (β = -0.091, 95% CI: -0.171, -0.012). Further sex-stratified analysis revealed that among male foetuses, SIC was significantly positively associated with BPD (β = 0.158, 95% CI: 0.053, 0.263), head circumference (HC) (β = 0.414, 95% CI: 0.074, 0.754) and abdominal circumference (AC) (β = 0.490, 95% CI: 0.111, 0.870). but negatively associated with neonatal length (β = -0.402, 95% CI: -0.742, -0.062) and birth weight (β = -0.120, 95% CI: -0.234, -0.005). These associations were attenuated and non-significant in female foetuses. Maternal age stratification showed significantly stronger positive associations between SIC and foetal BPD in women aged <29 years (β = 0.150, 95% CI: 0.036, 0.265) compared to those ≥29 years.

Conclusions: Our findings suggest that first-trimester maternal SIC shows a positive association with foetal BPD but a potential negative association with neonatal anthropometric measures, with these relationships appearing stronger in male foetuses and younger mothers.

Background: This study aimed to profile the molecular signatures of post-traumatic elbow heterotopic ossification (HO) to identify key regulators and potential therapeutic targets.

Methods: Total RNA from post-traumatic elbow HO tissues (n=4) and normal bone tissues (n=6) was subjected to high-throughput sequencing to identify differentially expressed mRNAs (DEGs), microRNAs (DEMs), and lncRNAs (DELs). Bioinformatics analyses included Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein-protein interaction network construction, and transcription factor (TF)-microRNA-mRNA network analysis. The expression trends of four most upregulated and four most downregulated DEGs were validated by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR).

Results: We identified 2,138 DEGs, 40 DEMs, and 905 DELs. DEGs were significantly enriched in biological process "bone mineralization," cellular component "plasma membrane," molecular function "integrin binding," and pathways including PI3K-Akt, NF-κB, JAK-STAT, and TNF signaling pathways. Hub genes with high connectivity included MMP9, IL6, MMP3, CTSK, and BGLAP. Integrated network analysis highlighted the transcription factor JUN and key microRNAs (hsa-miR-124-3p, hsa-miR-548c-3p, and hsa-miR-135b). The qRT-PCR results confirmed the expression trends of selected DEGs.

Conclusions: This study, for the first time, profiled the differentially expressed mRNAs, microRNAs, and lncRNAs in post-traumatic elbow HO using high-throughput RNA sequencing. These findings provide valuable insights into the molecular mechanisms of HO following elbow trauma. The identified hub genes (MMP9, IL6, MMP3, CTSK, and BGLAP), key TF (JUN), and key microRNAs (hsa-miR-124-3p, hsa-miR-548c-3p, and hsa-miR-135b) may serve as potential therapeutic targets for preventing and treating post-traumatic elbow HO.

Objectives: To examine whether the JAK inhibitor tofacitinib alleviates secretory dysfunction and modulates Th17/Treg balance in a Sjögren's disease (SjD) murine model.

Methods: Integrated analysis of SjD transcriptome sequencing (GSE159574, GSE247662) identified key signalling pathways, potential therapeutic agents, and immune cell infiltration. NOD/ShiLtj mice were administered with or without tofacitinib. Secretory function and inflammation were assessed via fluorescein ocular surface staining, tear flow rate, histopathology (HE, Masson, Sirius Red), saliva flow rate, immunohistochemistry, immunofluorescence, flow cytometry, and cytokine measurement. Pearson's linear regression evaluated the correlation between Th17/Treg balance and secretory function.

Results: Bioinformatics analysis showed the JAK-STAT pathway and CD4+ T cells contribute to SjD pathogenesis. Tofacitinib reduced corneal fluorescein staining, increased tear break-up time and secretion, diminished salivary gland lymphocytic inflammation, improved saliva flow rate, and altered phospho-JAK3-STAT1 expression. It also reduced Th17 cell proportion, increased Treg cell proportion in salivary glands and spleens, decreased IL-17, and increased IL-10 and TGF-β in blood. A strong negative correlation existed between secretory function and Th17/Treg balance.

Conclusions: Tofacitinib potently attenuated secretory dysfunction and inflammation in SjD mice, possibly by modulating Th17/Treg balance, suggesting it may be a therapeutic agent for SjD.

Background: Neuropathic pain (NP), resulting from damage or disease affecting the somatosensory nervous system, severely impairs patients' quality of life and constitutes a substantial global disease burden. Recent evidence highlights the critical involvement of mechanosensitive ion channels in peripheral nociception.

Discussion: This review systematically examines the roles of key mechanosensitive channels in NP pathophysiology. TRPV4 mediates mechanical allodynia via ion flux modulation and neuroinflammation; TRPC6 enhances neuronal excitability through calcium dynamics and MAPK/mTOR signaling; TRPA1 regulates pain through neuronal and Schwann cell mechanisms involving the NOX1-oxidative stress-CXCL1 axis and myelin disruption; TREK channels attenuate pain by stabilizing resting membrane potential; TMEM family members modulate neuroimmune signaling; and Piezo2 critically contributes to mechanical and inflammatory hypersensitivity. These mechanisms reveal significant translational potential for analgesic development.

Conclusions: Targeted modulation of mechanosensitive ion channels represents a promising strategy for developing effective, non-addictive analgesics. This review establishes a theoretical foundation for understanding NP pathophysiology and identifies actionable therapeutic targets with substantial clinical relevance.