Gastric cancer (GC) occupies the first few places in the world among tumors in terms of incidence and mortality, causing serious harm to human health, and at the same time, its treatment greatly consumes the health care resources of all countries in the world. The diagnosis of GC is usually based on histopathologic examination, and it is very important to be able to detect and identify cancerous lesions at an early stage, but some endoscopists' lack of diagnostic experience and fatigue at work lead to a certain rate of under diagnosis. The rapid and striking development of Artificial intelligence (AI) has helped to enhance the ability to extract abnormal information from endoscopic images to some extent, and more and more researchers are applying AI technology to the diagnosis of GC. This initiative has not only improved the detection rate of early gastric cancer (EGC), but also significantly improved the survival rate of patients after treatment. This article reviews the results of various AI-assisted diagnoses of EGC in recent years, including the identification of EGC, the determination of differentiation type and invasion depth, and the identification of borders. Although AI has a better application prospect in the early diagnosis of ECG, there are still major challenges, and the prospects and limitations of AI application need to be further discussed.

This review aims to summarize the epidemiology, pathogenesis, clinical features, management, prognosis and regression of Neonatal lupus erythematosus (NLE) with a view to providing directions for standardized diagnosis, treatment and further research. We conducted a comprehensive literature review of NLE. NLE-related peer-reviewed papers were searched through PubMed/Medline were searched up to November 2024. NLE is a rare acquired autoimmune disease (AD) linked to organ damage from maternal autoantibodies crossing the placenta to the foetus. However, not all mothers have ADs or associated antibodies. The disease involves autoantibody-induced inflammation, apoptosis, fibrosis, calcium channel dysregulation in cardiomyocytes, and increased interferon expression. NLE incidence shows no sex difference, but there is a differential distribution of clinical features across ethnic groups. The frequency of organ involvement in NLE patients is more common in the cutaneous and cardiac. NLE also affects the haematological and hepatobiliary systems, and some patients may experience neurological and endocrinological involvement. Steroids and immunoglobulins can aid in the recovery of some patients. Proper use of antimalarials during prenatal and gestational periods may prevent or improve the prognosis of patients with congenital heart block (CHB). Implantation of a pacemaker is effective in maintaining cardiac function in children with complete atrioventricular block. Symptoms associated with NLE may improve with antibody depletion, but some patients may experience sequelae such as irreversible CHB, neuropsychiatric disorders and developmental delays. Universal screening for autoantibodies to Sjögren syndrome A or B autoantigens should be offered to women of childbearing age experiencing desiccation syndrome. Antibody-positive individuals require appropriate reproductive counselling and advice, along with close foetal monitoring starting at 16 weeks of gestation and postnatal prognostic follow-up. Epidemiologic investigations and clinical studies on NLE are currently inadequate, and large-scale epidemiologic investigations, prospective clinical studies, and basic research are needed in the future to improve the understanding of the disease and the standardization of its clinical management.

Neonatal necrotizing enterocolitis (NEC) is a devastating intestinal disease that primarily affects preterm infants. Unfortunately, no specific treatment for NEC is currently available, making it crucial to further investigate its underlying mechanisms. In this study, we aimed to identify the key target gene, CHI3L1, which was significantly upregulated in the intestinal tissues of both affected children and model mice from the GEO database. CHI3L1 is known to play important roles in inflammatory and immune responses, as well as in tissue damage and repair, all of which are closely associated with the development of NEC. We conducted validations at both the cellular and animal levels, demonstrating that the inhibition or knockdown of CHI3L1 significantly reduced the severity of NEC. Mechanistic investigations revealed that the knockdown of CHI3L1 inhibited the PI3K-Akt-FoxO1 signalling pathway, alleviating excessive autophagy in intestinal epithelial cells and subsequently reducing injury and inflammatory responses. Clinical studies have revealed that elevated serum CHI3L1 expression in paediatric patients is associated with both the occurrence and severity of necrotising enterocolitis NEC, demonstrating positive correlations with the Duke Abdominal Assessment Scale (DAAS), C-reactive protein (CRP), procalcitonin (PCT), red cell distribution width (RDW), and lactate dehydrogenase (LDH) levels. In conclusion, our findings confirmed a close relationship between CHI3L1 and the occurrence and severity of NEC, suggesting that it may mitigate inflammatory responses and tissue damage by alleviating excessive autophagy in intestinal epithelial cells. Therefore, targeting CHI3L1 may be an effective strategy to combat NEC.

Neonatal lupus erythematosus (NLE) is a rare autoimmune condition triggered by the transplacental transfer of maternal antibodies. Despite its recognized clinical manifestations, the underlying pathogenesis remains incompletely understood. This study seeks to explore the disruption of the gut microbiota-host metabolism-immune axis in anti-Ro/La-positive neonates, and to assess its potential role in the development of NLE. This multicenter, cross-sectional study included 90 neonates, divided into three groups: 30 with neonatal lupus erythematosus (NLE), 30 with positive antibodies but without clinical manifestations (No-NLE), and 30 healthy controls. We performed 16 S rRNA sequencing to analyze gut microbiota composition, untargeted plasma metabolomic profiling, and proteomic analysis to identify alterations associated with the pathogenesis of NLE. We identified significant alterations in the gut microbiota, plasma metabolome, and proteome profiles of anti-Ro/La-positive neonates. NLE infants exhibited marked enrichment of Enterobacteriaceae and depletion of Bifidobacterium and Clostridium butyricum. Metabolomic analysis revealed hyperactivation of β-alanine and purine metabolism, along with impaired α-linolenic acid metabolism and endocannabinoid signaling. Proteomic profiling indicated aberrant protein expression that modulated IFN signaling, particularly within the C-type lectin receptor pathway. Dysregulation of the spleen tyrosine kinase (SYK) and high-affinity immunoglobulin epsilon receptor subunit gamma (FCER1G) decoupling was observed, correlating with elevated IFN-α and NF-κB p65 levels. Integrated correlation analysis revealed significant associations among differential microbial taxa, plasma metabolites, and proteins. Notably, E. coli-associated metabolites and proteins displayed inverse relationships with those associated with C. butyricum. These findings represent comprehensive evidence of dysregulation along the "gut microbiota-host metabolism-immune" axis in neonatal lupus erythematosus (NLE), providing novel insights into the disease's underlying heterogeneity.

Sphingolipid metabolism critically links intestinal barrier integrity to inflammatory responses, and its role in necrotizing enterocolitis (NEC) pathogenesis may inform strategies for prevention and treatment. To investigate this association, metabolomic profiling of serum samples from preterm infants was performed, and the findings were validated in independent cohorts. The effects of sphingosine-1-phosphate (S1P) were evaluated in LPS-induced IEC-6 cells and experimental NEC models. Mechanistic studies were performed using pharmacological inhibitors, and microbiota-dependent effects were assessed through bacterial intervention experiments. Serum S1P levels were reduced prior to NEC diagnosis and correlated with disease severity. Opaganib reduced S1P levels and exacerbated NEC pathology, while S1P supplementation reversed these effects. Mechanistic investigations revealed that S1P exerted a protective effect against NEC by modulating mitochondrial oxidative respiration and redox balance, as well as by reshaping the gut microbiota to attenuate inflammation, apoptosis, and intestinal barrier disruption. The protective effects of S1P were partially attenuated by S1PR1 blockade. In addition, supplementation with Bacteroides thetaiotaomicron improved sphingolipid metabolic profiles in NEC intestinal tissues and upregulated S1P levels. These findings suggest that dysregulation of sphingolipid metabolism is associated with NEC and intestinal barrier dysfunction. S1P may alleviate NEC-related injury in experimental models, potentially involving S1PR1 signaling, mitochondrial redox balance, and interactions with the gut microbiota.

Background: Neonatal necrotizing enterocolitis (NEC) is a life-threatening intestinal disease primarily affecting preterm infants. Although the exact pathophysiology remains unclear, immune responses and redox reactions play crucial roles in its development. Methods: We identified Dual Oxidase 2 (DUOX2) as a significantly upregulated gene in the intestinal tissues of NEC patients. Subsequent analyses included Gene Ontology (GO) enrichment and immune infiltration profiling related to DUOX2. Using a nested case-control design, we then evaluated the clinical relevance of serum DUOX2 protein levels in preterm infants with NEC (gestational age <32 weeks). Results: DUOX2 was significantly highly expressed in NEC intestinal tissues, with an AUC value of 0.844 (0.599-1.000) predicting the occurrence of NEC. GO enrichment analysis revealed that the differentially expressed genes (DEGs) between the NEC and control groups mainly affect redox reactions, including reactive oxygen species (ROS) and superoxide. Immunoinfiltration analysis revealed a positive correlation between DUOX2 expression and plasma cells (R=0.69, P =0.041). Univariate and multivariate analyses identified high levels of serum DUOX2 as a risk factor for developing NEC. Serum DUOX2 levels were negatively correlated with albumin levels and positively correlated with red blood cell distribution width and lactate dehydrogenase levels. The AUC value of serum DUOX2 levels for diagnosing NEC was 0.809 (95% CI: 0.712–0.906), with an optimal cut-off value of 2.483 ng/mL, a sensitivity of 91.30%, and a specificity of 78.26%. Conclusion: This study demonstrates a significant association between elevated DUOX2 expression and the development of NEC in preterm infants.