Search

Background: Diabetes is accompanied by a high prevalence of hyposalivation, causing severe damage to oral and systemic health. Mitochondrial dynamics play important roles in the pathogenesis of various diabetic complications; however, little is known about their roles in diabetic hyposalivation. Materials and Methods: A diabetic mouse model and a high glucose (HG)‐induced diabetic submandibular gland (SMG) cell model were employed. Results: More mitochondria surrounded by autophagosomes and higher expression of mitophagy‐related proteins were detected in the SMGs of diabetic mice and HG‐treated SMG cells. In diabetic SMGs, dynamin‐related protein 1 (DRP1) was upregulated, whereas mitofusin‐2 was downregulated both in vivo and in vitro. Shortened mitochondria and impaired mitochondrial functions were observed in the HG group. A DRP1‐specific inhibitor, mdivi‐1, suppressed mitochondrial fission and mitophagy, as well as restored mitochondrial functions in the HG condition. Moreover, the interaction of F‐actin and DRP1 was enhanced in the diabetic group. Inhibiting F‐actin with cytochalasin D repaired the injured effects of HG on mitochondrial dynamics and functions. Conversely, the F‐actin‐polymerization‐inducer jasplakinolide aggravated mitochondrial fission and dysfunction. Conclusions: F‐actin contributes to HG‐evoked mitochondrial fission by interacting with DRP1, which induces mitophagy and impairs mitochondrial function in SMG cells, ultimately damaging the SMG. [ABSTRACT FROM AUTHOR]

Current interdisciplinary medical training calls for reforms and innovations in the assessment of pathophysiology education. Formative assessment is used to monitor student learning to provide ongoing feedback that can improve both learning and teaching. Beginning in 2016, we implemented a formative assessment composed of case-based multiple-choice questions (MCQs) for all students in all majors. In 2017, case study questions began to be employed in the formative assessment, and student-set, case-based questions were further introduced. Aiming to gather the students' suggestions and feedback on the mixed-method assessment, we conducted a survey on aspects such as the effectiveness of the assessment, assessment content and completion, opinions on student-set questions, and the impact on pathophysiology learning for students from 2017 to 2019. In addition, we compared students' semesterly final scores with those of previous students and evaluated the relationship between formative and summative assessment scores. The results for 1,277 students clearly showed that the reformed formative assessment system was well received by the students. The students thought that the formative assessment not only allowed for the provision of real-time feedback on the effectiveness of teaching and learning but also nurtured self-motivation, the development of analytical and problem-solving skills, and collaborative efforts. Both the semesterly final scores and the proportions of students scoring in higher score ranges increased after the implementation of the formative assessment, and the summative assessment scores were positively related to the formative assessment scores. Consequently, the reformed formative assessment system significantly improved the quality of pathophysiology education.

Objectives: Tight junctions (TJs) are involved in the regulation of salivary secretion via paracellular pathway. Botulinum toxin type A (BTXA) is widely used for the treatment of hypersecretion diseases such as sialorrhea. This study aimed to investigate the role of TJs in BTXA‐inhibited secretion of the submandibular gland (SMG). Materials and Methods: BTXA was injected into the SMGs of rats, and the same amount of saline was injected as a control. Western blot, real‐time PCR, and immunofluorescence staining were used to detect the expression and distribution of TJ proteins. Paracellular permeability was evaluated using the transepithelial electrical resistance (TER) measurements and fluorescent tracer detection in BTXA‐stimulated SMG‐C6 cells. Results: BTXA injection into the SMGs of rats led to increased expression of claudin (Cldn) −1 and Cldn3. Immunofluorescence staining showed no significant changes in the distribution of TJ proteins. In vitro, BTXA increased the TER values and significantly reduced the permeability of fluorescent tracer, suggesting that BTXA decreased the paracellular permeability. The expression levels of Cldn1, Cldn3, and Cldn4 were upregulated after BTXA treatment. Conclusion: The expression of TJ proteins changed in both animal models and SMG‐C6 cells after BTXA treatment, which may contribute to the inhibition of salivary secretion. [ABSTRACT FROM AUTHOR]

Objective: Obesity contributes to the dysfunction of salivary gland. To explore the specific underlying mechanism for obesity‐induced hyposalivation, a model for high‐fat diet‐induced obese (DIO) mice were constructed to analyze long non‐coding RNAs (lncRNAs) and messenger RNAs (mRNAs) expression profiles. Methods: The DIO group and control group were fed a diet containing 60 kcal% fat and a normal chow diet for 16 weeks respectively. Microarray analyses were performed to detect the expression profiles of lncRNA and mRNA in submandibular gland tissues from control group mice and DIO mice. Gene ontology, kyoto encyclopedia of genes and genomes, protein–protein interaction, coding‐non‐coding gene co‐expression, transcription factors and competing endogenous RNA analyses were performed to examine the function of differentially expressed genes. Results: Microarray analyses identified that 624 lncRNAs, along with 297 mRNAs were differentially expressed. Bioinformatic analyses revealed that "complement and coagulation cascades," "glutathione metabolism," "cysteine and methionine metabolism," and "estrogen signaling pathway" were significantly associated with candidate lncRNAs. Transcription factors analysis on candidate lncRNAs revealed several genes such as tribbles pseudokinase 3 may play regulatory roles. Conclusions: Our results revealed the expression profiles of lncRNAs and mRNAs and provided new insights into the mechanism of obesity‐induced hyposalivation using bioinformatic analyses. [ABSTRACT FROM AUTHOR]