Search

Orthodontic patients often suffer from mucosal discomfort due to the friction stimulation of orthodontic components on the oral mucosa, and semiconductor laser can treat the oral mucosal discomfort caused by orthodontic treatment, such as redness, swelling, ulcers, etc. This study innovatively created a persistent traumatic environment in the mouth of rats to simulate the intraoral conditions of orthodontic patients, with the aim of using animal models to broaden the understanding of semiconductor laser repair mechanisms of orthodontic traumatic ulcers. 32 male Wistar rats were randomly divided into 6 groups: 1) blank control group; 2) control group; 3) chlorhexidine group; 4) laser group 1; 5) laser group 2; 6) laser group 3. The research contents included ulcer healing degree score, enzyme-linked immunosorbent assay, histological observation of stained sections of ulcer tissue, and analysis of microbial attachment on ulcer surface. The results showed that the continuous traumatic environment significantly prolonged the healing time of ulcer (P<0.05). During the ulcer duration, the proinflammatory factor level was lower, the anti-inflammatory factor level was higher and the healing score was better in the laser group (P<0.05). The antibacterial effect of semiconductor laser is less than 0.12% chlorhexidine solution; Hematoxylin-eosin tissue sections showed lower inflammatory cell infiltration and better epithelial healing in the laser group. This study shows that continuous traumatic environment can delay ulcer healing, and semiconductor laser with appropriate irradiation time is superior to traditional 0.12% chlorhexidine solution in reducing inflammation, relieving pain and promoting ulcer tissue healing. Compared with previous studies, the animal model in this study has made some progress and is closer to the real oral conditions of orthodontic patients. The results further demonstrated the potential of semiconductor laser in the treatment of oral traumatic ulcers during orthodontics. [ABSTRACT FROM AUTHOR]

Silk of maize (Zea mays L.) contains diverse metabolites with complicated structures and functions, making it a great challenge to explore the mechanisms of metabolic regulation. Genome‐wide identification of silk‐preferential genes and investigation of their expression regulation provide an opportunity to reveal the regulatory networks of metabolism. Here, we applied the expression quantitative trait locus (eQTL) mapping on a maize natural population to explore the regulation of gene expression in unpollinated silk of maize. We obtained 3,985 silk‐preferential genes that were specifically or preferentially expressed in silk using our population. Silk‐preferential genes showed more obvious expression variations compared with broadly expressed genes that were ubiquitously expressed in most tissues. We found that trans‐eQTL regulation played a more important role for silk‐preferential genes compared to the broadly expressed genes. The relationship between 38 transcription factors and 85 target genes, including silk‐preferential genes, were detected. Finally, we constructed a transcriptional regulatory network around the silk‐preferential gene Bx10, which was proposed to be associated with response to abiotic stress and biotic stress. Taken together, this study deepened our understanding of transcriptome variation in maize silk and the expression regulation of silk‐preferential genes, enhancing the investigation of regulatory networks on metabolic pathways. [ABSTRACT FROM AUTHOR]

Background: Periodontal ligament cells (PDLCs) are a major component of the periodontal ligament and have an important role in the regeneration of periodontal tissue and maintenance of homeostasis. High glucose can affect the activity and function of PDLCs in a variety of ways; therefore, it is particularly important to find ways to alleviate the effects of high glucose on PDLCs. Annexin A2 (ANXA2) is a calcium- and phospholipid-binding protein involved in a variety of cellular functions and processes, including cellular cytokinesis, cytophagy, migration, and proliferation., Aim: The aim of this study was to exploring whether ANXA2 attenuates the deleterious effects of high glucose on PDLCs and promotes osteogenic differentiation capacity., Methods and Results: Osteogenic differentiation potential, cellular senescence, oxidative stress, and cellular autophagy were detected. Culturing PDLCs with medium containing different glucose concentrations (CTRL, 8 mM, 10 mM, 25 mM, and 40 mM) revealed that high glucose decreased the protein expression of ANXA2 ( p  < 0.0001). In addition, high glucose decreased the osteogenic differentiation potential of PDLCs as evidenced by decreased calcium deposition ( p  = 0.0003), lowered ALP activity ( p  = 0.0010), and a decline in the expression of osteogenesis-related genes ( p  = 0.0008). Moreover, β-Galactosidase staining and expression of p16, p21 and p53 genes showed that it increased cellular senescence in PDLCs ( p  < 0.0001). Meanwhile high glucose increased oxidative stress in PDLCs as shown by ROS ( p  < 0.0001). However, these damages caused by high glucose were inhibited after the addition of 1 µM recombinant ANXA2 (rANXA2), and we found that rANXA2 enhanced autophagy in PDLCs under high glucose conditions., Conclusions and Discussion: Therefore, our present study demonstrates that alterations in ANXA2 under high glucose conditions may be a factor in the decreased osteogenic differentiation potential of PDLCs. Meanwhile, ANXA2 is associated with autophagy, oxidative stress, and cellular senescence under high glucose conditions., Competing Interests: The authors declare there are no competing interests., (©2024 Huang et al.)