Objective:To compare the osteogenic differentiation of dental pulp stem cells(DPSCs)induced by osteopontin(OPN)and mineralizing culture medium(MCM).Methods:DPSCs were cultured with OPN(OPN group)and MCM(MCM group)respectively. The morphology of the DPSCs were observed under inverted microscope.The mineralize nodules were observed by alizarin red staining. RT-RCR was used to detect the mRNA expression of bone sialoprotein (BSP),Runt-related transcription factor 2(Runx-2),osteocal-cin(OCN)and collagen-1(Col-1).Results:Similar number of mineralized nodules was found in the 2 groups(P >0.05)after 28 day culture.The mRNA expression level of BSP gene in OPN group was higher than that in MCMgroup(0.864 ±0.112 and 0.514 ±0.068, P <0.05),while the expression level of Runx-2 gene in OPN group is lower than that in MCMgroup(0.186 ±0.017 and 0.324 ±0. 058,P <0.05).The expression level of Col-1 and OCN genes in both groups were similar(P >0.05).Conclusion:The capabilities of OPN and MCMin inducing osteogenic differentiation of DPSCs are similar.

Objective:To explore the causes of self-management dilemma in young and middle-aged patients with recurrent acute pancreatitis from the perspectives of nurses, patients and patient caregivers, in order to provide reference for developing self-management intervention plans that meet the needs of patients.Methods:Using the descriptive phenomenological methods from qualitative research, 15 patients with recurrent acute pancreatitis, six nurses and nine caregivers from the Hepatobiliary Pancreatic Surgery Ward of the Second Norman Bethune Hospital of Jilin University from November 2021 to December 2022 were selected for semi-structured in-depth interviews. The Colaizzi 7-step method was used to analyze and refine the theme.Results:Two main themes were extracted to explain the difficulties in self-management of young and middle-aged patients with recurrent acute pancreatitis. The internal reasons for the self-management dilemma included cognitive biases in the importance of self-management, limited access to self-management knowledge and negative attitudes towards self-behavior management, and the external reasons for self-management dilemma included insufficient inclusiveness of the external environment towards diseases, fear of disease progression, multiple burdens caused by diseases and busy work.Conclusions:Young and middle-aged patients with recurrent acute pancreatitis experience multiple difficulties in the process of self-management. Clinical medical staff should explore self-management models with contemporary characteristics, enhance patient self-management ability and quality of life, reduce disease recurrence rate.

Background::Alterations in the placental expression of glucose transporters (GLUTs), the crucial maternal-fetal nutrient transporters, have been found in women with hyperglycemia in pregnancy (HIP). However, there is still uncertainty about the underlying effect of the high-glucose environment on placental GLUTs expression in HIP.Methods::We quantitatively evaluated the activity of mammalian target of rapamycin (mTOR) and expression of GLUTs (GLUT1, GLUT3, and GLUT4) in the placenta of women with normal pregnancies (CTRL, n = 12) and pregnant women complicated with poorly controlled type 2 diabetes mellitus (T2DM, n = 12) by immunohistochemistry. In addition, BeWo cells were treated with different glucose concentrations to verify the regulation of hyperglycemia. Then, changes in the expression of GLUTs following the activation or suppression of the mTOR pathway were also assessed using MHY1485/rapamycin (RAPA) treatment or small interfering RNA (siRNA)-mediated silencing approaches. Moreover, we further explored the alteration and potential upstream regulatory role of methyltransferase-like 3 (METTL3) when exposed to hyperglycemia. Results::mTOR, phosphorylated mTOR (p-mTOR), and GLUT1 protein levels were upregulated in the placenta of women with T2DM compared with those CTRL. In BeWo cells, mTOR activity increased with increasing glucose concentration, and the expression of GLUT1, GLUT3, and GLUT4 as well as GLUT1 cell membrane translocation were upregulated by hyperglycemia to varying degrees. Both the drug-mediated and genetic depletion of mTOR signaling in BeWo cells suppressed GLUTs expression, whereas MHY1485-induced mTOR activation upregulated GLUTs expression. Additionally, high glucose levels upregulated METTL3 expression and nuclear translocation, and decreasing METTL3 levels suppressed GLUTs expression and mTOR activity and vice versa. Furthermore, in METTL3 knockdown BeWo cells, the inhibitory effect on GLUTs expression was eliminated by activating the mTOR signaling pathway using MHY1485. Conclusion::High-glucose environment-induced upregulation of METTL3 in trophoblasts regulates the expression of GLUTs through mTOR signaling, contributing to disordered nutrient transport in women with HIP.