Polyvinylpyrrolidone as a primer for resin-dentin bonding.

OBJECTIVE: This study aimed to investigate the effects of polyvinylpyrrolidone (PVP)-containing primer (PCP) on dentin bonding. METHODS: PVP and anhydrous ethanol were used to prepare the PCPs, which were prepared at concentrations of 0.5%, 1%, and 2% (w/v). These PCPs were subsequently applied to the dentin surface, denoted as E1, E2, and E3, respectively. In the control group, no primer was applied. Following the treatment, the dentin surfaces were subjected to analysis using Fourier-transform infrared spectroscopy (FTIR), and the micro-tensile bond strength (MTBS) was evaluated. The failure mode, nanoleakage, and bonding longitudinal section were observed utilizing scanning electron microscopy (SEM). Additionally, the effect of PCPs on matrix metalloproteinases (MMPs) activity was analyzed through an in situ zymography test. Data were subjected to statistical analysis using ANOVA tests (α = 0.05). RESULTS: Significant alterations in the infrared resonances associated with collagen cross-linking within the collagen matrix were observed across all PCP groups. The application of PCP demonstrated a noteworthy enhancement in micro-tensile bond strength (MTBS) compared to group C (p < 0.05). Notably, group C exhibited the lowest MTBS (41 ± 7.7 MPa), whereas group E2 demonstrated the highest MTBS (66 ± 11.9 MPa). Even after undergoing aging, the MTBS of the PCP groups remained superior to that of group C (p < 0.05). The resin tag length in the PCP groups was found to be greater than that of group C, and the occurrence of nanoleakage was comparatively lower in the PCP groups, both before and after aging. Additionally, PCP exhibited a dose-dependent inhibition of matrix metalloproteinases (MMPs) activity, which was statistically significant (p < 0.05). CONCLUSIONS: The utilization of PCP Primer exhibits notable enhancements in bond strength, mitigates nano-leakage, and suppresses enzyme activity within the hybrid layer.

Prediction of matrix metal proteinases-12 inhibitors by machine learning approaches.

Matrix metal proteinases-12 (MMP-12) is a hot pharmaceutical target on the treatment of many human diseases. There's a crying need for designing and finding new MMP-12 inhibitors. In this work, four machine learning approaches, support vector machine, k-nearest neighbor, C4.5 decision tree, and random forest, were employed to derive statistical models from datasets with well distributed biological activities and predict a compound whether it is a MMP-12 inhibitor. The prediction accuracies of the models are in the range of 96.15-98.08% for sensitivity, 87.23-100.00% for specificity, 91.92-98.99% for the overall prediction accuracy and 0.8401-0.9800 for Matthews correlation coefficient, all producing satisfactory results. By means of diverse feature selection methods, several sets of critical descriptors with key information of inhibitory properties were selected by different models, accelerating the classification for MMP-12 inhibitors and non-inhibitors. Communicated by Ramaswamy H. Sarma.

Studies on proliferation and migration effects and mechanisms of M3 mAChR in NSCLC cells / 中国药理学通报

Aim To investigate the effect of M3 mAChR on the proliferation and migration of NSCLC and the molecular mechanisms. Methods CCK-8 as-say,Wound-healing assay and Transwell invasion as-saywere used to determine the cell proliferation,migra-tion and invasion. Calcium imaging was used to identi-fy the M3 mAChR subtype mediating carbachol-in-duced increase in intracellular calcium. Western blot was used to determine the protein level of proliferation, migration and cell cycle related signaling molecules. Results Following the treatment with M3R antagonists 1. 25 ~ 80 μmol · L - 1 for 48 h,the proliferation of NSCLC cells was inhibited,the inhibitory effect:R2-8018 > Darifenacin,H1299 > H460. After the treat-ment with R2-8018,the migration and invasion of H1299 significantly declined. Western blot showed that the protein level of p-Akt,p-GSK3β,cyclinD1 de-clined significantly with the increase of time and that the protein level of p21 increased. Conclusion M3R antagonists induce cell cycle arrest by suppressing the activation of Akt,down-regulating GSK3β and cy-clinD1,and up-regulating p21,then inhibiting the proliferation of NSCLC cells. It also inhibits the inva-sion and migration by down-regulating MMP-2.