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Objective To study the effect of artificial intelligence in the pathological diagnosis of periapical cysts and to explore the application of artificial intelligence in the field of oral pathology. Methods Pathological images of eighty-seven periapical cysts were selected as subjects to read, and a neural network with a U-net structure was constructed. The 87 HE images and labeled images of periapical cysts were divided into a training set (72 images) and a test set (15 images), which were used in the training model and test model, respectively. Finally, the target level index F1 score, pixel level index Dice coefficient and receiver operating characteristic (ROC) curve were used to evaluate the ability of the U-net model to recognize periapical cyst epithelium. Results The F1 score of the U-net network model for recognizing periapical cyst epithelium was 0.75, and the Dice index and the areas under the ROC curve were 0.685 and 0.878, respectively. Conclusion The U-net network model constructed by artificial intelligence has a good segmentation result in identifying periapical cyst epithelium, which can be preliminarily applied in the pathological diagnosis of periapical cysts and is expected to be gradually popularized in clinical practice after further verification with large samples.

Background: Gastric intestinal metaplasia is a common pathological feature in patients with Helicobacter pylori (H. pylori) infection. Rabeprazole was widely used as the first-line regimen for H. pylori infectious treatment. The objective of this study is to explore the mechanism of rabeprazole in gastric intestinal metaplasia treatment. Methods: Real-time PCR, Western blotting (WB) and ROS analysis were conducted to confirm that rabeprazole could induce ferroptosis to suppress gastric intestinal metaplasia. Cellular fraction, luciferase and chromatin immunoprecipitation (ChIP) were used to identify the mechanism underlying rabeprazole modulated ferroptosis. Results: Herein, we found rabeprazole treatment led to inhibit CDX2 and MUC2 expression, alleviating gastric intestinal metaplasia, which was attributed to enhanced ferroptosis characterized by decreased GPX4 expression. Inhibition of ferroptosis by ferrostatin-1 (Fer-1) could reverse decreased CDX2 and MUC2 expression caused by rabeprazole. Mechanically, Rabeprazole could inhibit CREB phosphorylation and nuclear translocation, which further decreased the binding of CREB to GPX4 promoter, reducing GPX4 transactivity. Moreover, endogenous PKA interacted with CREB, and this interaction was drastically destroyed in response to rabeprazole treatment. Most importantly, enhanced ferroptosis was observed in H. pylori- infected gastric intestinal metaplasia in comparison to HC control. Conclusion: These findings suggested that rabeprazole induced ferroptosis to reduce CDX2 expression in gastric epithelial cells through PKA/CREB cascade signaling, implying that targeting ferroptosis could be a promising strategy in improving gastric intestinal metaplasia during H. pylori -infected patients. [ABSTRACT FROM AUTHOR]

Vascular calcification is quite common in patients with end-stage chronic kidney disease and is a major trigger for cardiovascular complications in these patients. These complications significantly impact the survival rate and long-term prognosis of individuals with chronic kidney disease. Numerous studies have demonstrated that the development of vascular calcification involves various pathophysiological mechanisms, with the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) being of utmost importance. High phosphate levels, bone morphogenetic protein 2 (BMP2), and runt-related transcription factor 2 (RUNX2) play crucial roles in the osteogenic transdifferentiation process of VSMCs. This article primarily reviews the molecular mechanisms by which high phosphate, BMP2, and RUNX2 regulate vascular calcification secondary to chronic kidney disease, and discusses the complex interactions among these factors and their impact on the progression of vascular calcification. The insights provided here aim to offer new perspectives for future research on the phenotypic switching and osteogenic transdifferentiation of VSMCs, as well as to aid in optimizing clinical treatment strategies for this condition, bearing significant clinical and scientific implications. [ABSTRACT FROM AUTHOR]

Clinical trials are the key step in verifying the effectiveness, safety and usability of novel oral medical devices. With improvements in invention capability, the number of clinical trials of medical devices has steadily increased domestically, indicating the need for new requirements for quality management. Here, on the basis of summarizing the characteristics of clinical trials for oral medical devices in China, we proposed a whole-process quality-control model for good clinical practice (WQGCP). This model clarified the management specifications for oral medical device clinical trials in the new era. It indicates that the clinical trial design is the breakthrough point, while whole-process risk control is the key point. This suggests the need for the establishment of a quality management cooperation system, evaluation and postevaluation systems and the training of high-level personnel who conduct clinical trials. It also provides suggestions to promote the participation of oral clinicians in high-quality research and invention of novel clinical medical devices with the aim of accelerating the development of oral medical devices in China.

Objective. Microfold cells (M cells) are specific intestinal epithelial cells for monitoring and transcytosis of antigens, microorganisms, and pathogens in the intestine. However, the mechanism for M-cell development remained elusive. Materials and Methods. Real-time polymerase chain reaction, immunofluorescence, and western blotting were performed to analyze the effect of sorbitol-regulated M-cell differentiation in vivo and in vitro, and luciferase and chromatin Immunoprecipitation were used to reveal the mechanism through which sorbitol-modulated M-cell differentiation. Results. Herein, in comparison to the mannitol group (control group), we found that intestinal M-cell development was inhibited in response to sorbitol treatment as evidenced by impaired enteroids accompanying with decreased early differentiation marker Annexin 5, Marcksl1, Spib, sox8, and mature M-cell marker glycoprotein 2 expression, which was attributed to downregulation of receptor activator of nuclear factor kappa-В ligand (RANKL) expression in vivo and in vitro. Mechanically, in the M-cell model, sorbitol stimulation caused a significant upregulation of phosphodiesterase 4 (PDE4) phosphorylation, leading to decreased protein kinase A (PKA)/cAMP-response element binding protein (CREB) activation, which further resulted in CREB retention in cytosolic and attenuated CREB binds to RANKL promoter to inhibit RANKL expression. Interestingly, endogenous PKA interacted with CREB, and this interaction was destroyed by sorbitol stimulation. Most importantly, inhibition of PDE4 by dipyridamole could rescue the inhibitory effect of sorbitol on intestinal enteroids and M-cell differentiation and mature in vivo and in vitro. Conclusion. These findings suggested that sorbitol suppressed intestinal enteroids and M-cell differentiation and matured through PDE4-mediated RANKL expression; targeting to inhibit PDE4 was sufficient to induce M-cell development. [ABSTRACT FROM AUTHOR]