The implementation of a diversified teaching model can enhance the quality and efficacy of dental materials science.

OBJECTIVE: Dental materials science is one of the fundamental disciplines in stomatology, encompassing clinical areas such as orthodontics, prosthodontics, and endodontics. Due to its extensive knowledge base, strong professional nature, and wide scope, teaching dental materials science presents a challenge. This study aimed to enhance the application of dental materials science in oral teaching by comparing the effectiveness of different teaching methods. METHODS: This research project was evaluated by the Xi'an Jiaotong University Committee on Human Subjects Research and approved as exempt research. A total of 56 clinical stomatology students from the first year and second year cohorts at the Stomatology Hospital of Xi'an Jiaotong University were selected for the study. The first year cohort served as the nonteaching reform class, while the second year cohort formed the teaching reform class. The impact of the teaching reform was assessed through a questionnaire survey and final examination results. RESULTS: The questionnaire survey of students in the teaching reform class indicated a significant improvement in their interest in professional courses and overall satisfaction with the teaching. Additionally, the final examination results revealed a significantly greater rate of excellence among students in the teaching reform class than among those in the nonteaching reform class, with no students failing. CONCLUSION: The use of diverse teaching modes can enhance the quality and effectiveness of dental materials science instruction, offering a new approach for improving teaching in this discipline.

The impact of digitization and conventional techniques on the fit of fixed partial dentures FPDs: systematic review and Meta-analysis.

PURPOSE OF THE STUDY: The goal behind this study is to answer the question "In tooth-supported fixed partial dentures (FPDs), does the digital impression techniques compared to fabrications using conventional impression methods improve the marginal and internal fit? BACKGROUND: The incorporation of digital technology in the fabrication of fixed partial dentures (FPDs) has accelerated over the past decade. This study is directed at evaluating the marginal and internal fit of FPDs manufactured using digital approaches compared to conventional techniques. The need for updated data has encouraged this review. MATERIALS AND METHODS: An electronic search was conducted in PubMed, Scopus, Web of Science, and the Grey Database to identify relevant studies. The Modified Methodological Index for Non-Randomized Studies (MINORS) was used to assess the risk of bias in in vitro experiments. The key results of this meta-analysis were the standard mean differences (SMDs) and 95% confidence intervals (CI) of each main variance, marginal fit, and internal fit between the digital and conventional techniques. Additional analyses were performed to assess the significance of three subgroup parameters: method of digitalization, cement spacer thickness, and span length, and their influence on the fit of the FPDs. RESULTS: Based on predefined criteria, of the seven articles included in this systematic review, only five were selected for the quantitative data analysis. The marginal fit results were (P = 0.06; SMD: -1.88; 95% CI: - 3.88, 0.11) (P > 0.05) and the internal fit results were (P = 0.02; SMD: -0.80; 95% CI: - 1.49, - 0.10) (P < 0.05). Regarding the subgroup analyses, the method of digitalization subgroup results were (P = 0.35; SMD: -1.89; 95% CI: - 3.89, 0.11) and (P = 0.80; SMD: -0.80; 95% CI: - 1.49, - 0.11) for marginal and internal fit, respectively. The span length results were (P = 0.10; SMD: -1.89; 95% CI: - 3.89, 0.11) for marginal fit and (P = 0.02; SMD: -0.80; 95% CI: - 1.49, - 0.11) for internal fit. The cement spacer thickness (P = 0.01; SMD: -1.89; 95% CI: - 3.89, 0.11) and (P = 0.04; SMD: -0.80; 95% CI: - 1.49, - 0.11) for marginal and internal fit, respectively. CONCLUSION: Tooth-retained fixed partial dentures FPDs produced by digital scanning and computer-aided design/computer-aided manufacturing (CAD/CAM) systems can significantly enhance the internal fit compared with those manufactured by traditional methods. Intraoral scanners can replace conventional impressions for the fabrication of FPDs because they minimize the operating time and reduce patient pain. Further clinical studies are required to obtain more conclusive results. SYSTEMATIC REVIEW REGISTRATION: This systematic review and meta-analysis was registered in the International Prospective Register of Systematic Reviews (PROSPERO), registration number CRD42021261397.

Organotin compound DBDCT induces CYP3A suppression through NF-κB-mediated repression of PXR activity.

Organotin anticancer agent di-n-butyl-di-(4-chlorobenzohydroxamato)tin(iv) (DBDCT) exerted an inhibitory effect on its major metabolic enzyme cytochrome CYP3A. But whether hepatic drug-metabolizing enzymes and their regulatory nuclear receptors including pregnane PXR and constitutive androstane CAR binding with retinoid receptor RXR as a heterodimer are involved in the DBDCT-mediated regulation of CYP3A remains unclear. This study was undertaken to determine the mechanisms responsible for the effects of DBDCT on CYP3A suppression, focusing on the PXR-mediated and NF-κB pathways. The results indicated DBDCT suppressed CYP3A expression by inhibiting CAR expression. But what's interesting is, both protein and mRNA of PXR increased with increasing DBDCT. A further exploration, dual luciferase reporter gene analysis, clarified that DBDCT induced CYP3A expression elevation via the PXR-mediated pathway and this induction was countered by activation of NF-κB, which played a pivotal role in suppression of CYP3A through disrupting the association of the PXR-RXRα complex with DNA sequences by EMSA. PXR-mediated CYP3A expression was similarly demonstrated by RNAi. As expected, expression of CYP3A and its mRNA levels were reduced by DBDCT only in NF-κB(+/+) but not in NF-κB(-/-) cells. The inductive effect of DBDCT on CYP3A4 mRNA was enhanced in PXR shRNA-transfected cells but weakened in the ip65 group, which showed both PXR up-regulated CYP3A expression and NF-κB p65 activation directly contributed to CYP3A inhibition. In conclusion, activated NF-κB by DBDCT interacts directly with the DNA-binding domain of PXR, and disrupts the binding between the PXR-RXR dimer, thereby affecting the regulatory process for CYP3A transcription and, therefore, leading to a decrease of the expression of the PXR-regulated CYP3A.

Anticancer Effects of 1,3-Dihydroxy-2-Methylanthraquinone and the Ethyl Acetate Fraction of Hedyotis Diffusa Willd against HepG2 Carcinoma Cells Mediated via Apoptosis.

Hedyotis Diffusa Willd, used in Traditional Chinese Medicine, is a treatment for various diseases including cancer, owing to its mild effectiveness and low toxicity. The aim of this study was to identify the main anticancer components in Hedyotis Diffusa Willd, and explore mechanisms underlying their activity. Hedyotis Diffusa Willd was extracted and fractionated using ethyl acetate to obtain the H-Ethyl acetate fraction, which showed higher anticancer activity than the other fractions obtained against HepG2 cells with sulforhodamine B assays. The active component of the H-Ethyl acetate fraction was identified to be 1,3-dihydroxy-2-methylanthraquinone (DMQ) with much high inhibitory rate up to 48.9 ± 3.3% and selectivity rate up to 9.4 ± 4.5 folds (p<0.01) at 125 µmol/L. HepG2 cells treated with the fraction and DMQ visualized morphologically using light and fluorescence microscopy. Annexin V--fluorescein isothiocyanate / propidium iodide staining flow cytometry, DNA ladder and cell cycle distribution assays. Mechanistic studies showed up-regulation of caspase-3, -8, and -9 proteases activities (p<0.001), indicating involvement of mitochondrial apoptotic and death receptor pathways. Further studies revealed that reactive oxygen species in DMQ and the fraction treated HepG2 cells increased (p<0.01) while mitochondrial membrane potential reduced significantly (p<0.001) compared to the control by flow cytometry assays. Western blot analysis showed that Bax, p53, Fas, FasL, p21 and cytoplasmic cytochrome C were up-regulated (p<0.01), while Bcl-2, mitochondrial cytochrome C, cyclin E and CDK 2 were down-regulated dose-dependently (p<0.01). The reverse transcriptase-polymerase chain reaction showed that mRNA expressions of p53 and Bax increased (p<0.001) while that of Bcl-2 decreased (p<0.001). Pre-treatment with caspase-8 inhibitor Z-IETD-FMK, or caspase-9 inhibitor Z-LEHD-FMK, attenuated the growth-inhibitory and apoptosis-inducing effects of DMQ and the fraction on HepG2 cells. These results suggested that DMQ and the H-Ethyl acetate fraction of Hedyotis Diffusa Willd showed potential anticancer effects. Furthermore, the mechanisms of action may involve mitochondrial apoptotic and death receptor pathways.

Mitogenic effect of arginine vasopressin on adult rat cardiac fibroblast: involvement of PKC-erk1/2 pathway.

Arginine vasopressin (AVP) has been implicated in the pathophysiology of cardiac hypertrophy. We previously demonstrated that AVP is a mitogen for neonatal rat cardiac fibroblasts (CFs). In the present study, we extend our investigation to adult rat CFs to explore whether AVP could induce adult rat CFs proliferation and, if so, to identify the underlying mechanisms. We found that AVP stimulated cell proliferation, an effect abolished by V1 receptor antagonist, d(CH2)5[Tyr2(Me), Arg8]-vasopressin, but not V2 receptor antagonist, desglycinamide-[d(CH2)5, D-Ile2, Ile4, Arg8]-vasopressin. AVP also activated extracellular signal-regulated kinase 1/2 (erk1/2), a response mimicked by protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA), but abolished by depleting cellular PKC through chronic PMA incubation. Calphostin C, an inhibitor of PKC, attenuated and PMA mimicked the effect of AVP on cell proliferation, whereas Ca2+ chelating agent 1,2-bis(2-aminophenoxy)ethane N, N, N', N'-tetraacetic acid (BAPTA) had no effect. Further, AVP downregulated protein expression of p27Kip1, increased cyclins D1, A, and E expressions and induced cell cycle progression through G0/G1 into S stage. Antisense oligonucleotides against cyclins D1, A, and E decreased cell number in the presence of AVP. Whereas antisense treatment against p27Kip1 and overexpression of p27Kip1 exerted a stimulatory and inhibitory effect, respectively. Inhibiting erk1/2 activation by PD98059 abolished the effect of AVP on cell proliferation, cell cycle regulatory proteins, and cell cycle progression. These results suggest that AVP is a mitogen for adult rat CFs via the mediation of V1 receptor and PKC-erk1/2 pathway.