Circ_0061140 Facilitates Adenomyosis Progression by Upregulating LIN28B in vitro.

OBJECTIVES: The aim of our study was to explore the role of circular RNA_0061140 (circ_0061140) in adenomyosis progression and its associated mechanism. DESIGN: We first analyzed the expression pattern of circ_0061140 in endometrial tissues of adenomyosis patients (n = 27) and uterine fibroid patients (n = 15). Loss-of-function experiments were conducted to analyze the biological roles of circ_0061140 in regulating the viability, apoptosis, proliferation, migration, and invasion of endometrial epithelial cells. The downstream microRNA (miRNA)/messenger RNA (mRNA) axis of circ_0061140 was predicted by bioinformatics tool Starbase, and its working mechanism was verified by rescue experiments. METHODS: Cell viability, apoptosis, proliferation, invasion, and migration were assessed by cell counting kit-8 assay, flow cytometry analysis, 5-ethynyl-2'-deoxyuridine assay, transwell assay, and scratch test. The binding relationship between miR-141-3p and circ_0061140 or lin-28 homolog B (LIN28B) was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Circ_0061140 expression was upregulated in adenomyosis patients. Circ_0061140 knockdown suppressed the viability, proliferation, invasion, and migration and triggered the apoptosis of endometrial epithelial cells. Circ_0061140 served as a miRNA sponge for miR-141-3p, and miR-141-3p silencing partly reversed circ_0061140 knockdown-induced effects in endometrial epithelial cells. miR-141-3p directly interacted with LIN28B mRNA. LIN28B overexpression partly diminished miR-141-3p overexpression-mediated influences in endometrial epithelial cells. Circ_0061140 knockdown downregulated LIN28B expression by elevating miR-141-3p level in endometrial epithelial cells. LIMITATIONS: The functional verification of circ_0061140/miR-141-3p/LIN28B axis was merely conducted in vitro. CONCLUSION: Circ_0061140 contributed to adenomyosis progression by binding to miR-141-3p to induce LIN28B expression in vitro.

Accuracy of Cone-beam Computed Tomography in Measuring Dentin Thickness and Its Potential of Predicting the Remaining Dentin Thickness after Removing Fractured Instruments.

INTRODUCTION: The purpose of this study was to evaluate the accuracy of cone-beam computed tomographic (CBCT) to measure dentin thickness and its potential of predicting the remaining dentin thickness after the removal of fractured instrument fragments. METHODS: Twenty-three human mandibular molars were selected, and 4-mm portions of #25/.06 taper K3 files (SybronEndo, Orange, CA) were fractured in mesial canals. The teeth were then scanned using a micro-computed tomographic (micro-CT) system and a CBCT unit. Dentin thickness was measured and compared between both micro-CT and CBCT images to study the accuracy of CBCT readings. Then, the process of removing the fragments was simulated in CBCT images using the MeVisLab package (MeVis Research, Bremen, Germany); the predicted minimal remaining dentin thickness after removal was measured in different layers using VGStudio MAX software (Volume Graphics, Heidelberg, Germany). Data were compared with the actual minimal remaining dentin thickness acquired from micro-CT images, which were scanned after removing fractured instruments using the microtrepan technique. The results were analyzed statistically using intraclass correlation coefficients (ICCs) and a forecasting regression model analysis. RESULTS: The ICC for the dentin thickness was 0.988. The forecasting regression model of CBCT imaging estimating dentin thickness was micro-CT imaging = 15.835 + 1.080*CBCT, R2 = 0.963. The ICC for the remaining dentin thickness was 0.975 (P < .001). The forecasting regression model of CBCT imaging forecasting remaining dentin thickness was micro-CT imaging = 147.999 + 0.879*adjusted CBCT, R2 = 0.906. CONCLUSIONS: The study showed that CBCT imaging could measure dentin thickness accurately. Furthermore, using CBCT images, it is reliable and feasible to forecast the remaining dentin thickness after simulated instrument removal.

Oral microbiota distinguishes acute lymphoblastic leukemia pediatric hosts from healthy populations.

In leukemia, oral manifestations indicate aberrations in oral microbiota. Microbiota structure is determined by both host and environmental factors. In human hosts, how health status shapes the composition of oral microbiota is largely unknown. Taking advantage of advances in high-throughput sequencing, we compared the composition of supragingival plaque microbiota of acute lymphoblastic leukemia (ALL) pediatric patients with healthy controls. The oral microbiota of leukemia patients had lower richness and less diversity compared to healthy controls. Microbial samples clustered into two major groups, one of ALL patients and another of healthy children, with different structure and composition. Abundance changes of certain taxa including the Phylum Firmicutes, the Class Bacilli, the Order Lactobacillales, the Family Aerococcaceae and Carnobacteriaceae, as well as the Genus Abiotrophia and Granulicatella were associated with leukemia status. ALL patients demonstrated a structural imbalance of the oral microbiota, characterized by reduced diversity and abundance alterations, possibly involved in systemic infections, indicating the importance of immune status in shaping the structure of oral microbiota.