Search

Objective: To analyze the impact of the translucency/opacity of two commercial brands of resin cements and different translucency of lithium disilicate on the masking ability of saturated substrates., Methods: 120 samples (n = 5) were prepared using 0.5 mm lithium disilicate (IPS e.max CAD) in three translucencies (HT, MT, LT). These were cemented onto A1 and A4 resin substrates using two brands of resin cements: Allcem Veneer (FGM) in Trans (T) and Opaque White (OW), and Variolink Esthetic LC (Ivoclar Vivadent) in Neutral (N) and Light+ (L+), with a thickness of 100 µm. Color analysis was performed using reflectance measurements with a CM-3700d spectrophotometer (Konica Minolta). The Relative Translucency Parameter (RTP) and the Color Difference (∆E00) were calculated using the CIEDE2000 formula, with Perceptibility Threshold (PT) of ∆E00 = 0.8 and Acceptability Threshold (AT) of ∆E00 = 1.8. Statistical analyses were conducted using three-way ANOVA followed by Tukey's tests (α=0.05)., Results: For ∆E00 between substrates saturation (A1 VS A4), the isolated fixed factors and their interaction were statistically significant (p < .001) and showed ∆E00 > 1.8 for all groups. ∆E00 between resin cements colors of the same brand reveals significant factors (p < .001) but a non-significant statistical interaction (p = 0.072). The RTP of the resin cement were N(47.64) > T(47.47) > Ow(42.02)>L+ (23.39). For restorative set RTP, a non-significant interaction (p > 0.05) and groups cemented with L+ reveal lower RTP values than those cemented with OW., Significance: The ceramic translucency, the resin cement brand and color were influential on ability to mask substrates of different saturations. The opaquest resin cement contributes to reduce the influence of the ceramic on restoration final color. Resin cement brand and color influences restoration esthetics., Competing Interests: Declaration of Competing Interest The authors declare do not have any conflict of interest., (Copyright © 2025 Elsevier Inc. All rights reserved.)

The aim of this study was to test whether combined physical exercise training of moderate intensity executed during the development of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) hinders the progression of pulmonary and right heart harmful functional and structural remodeling in rats. Wistar rats were injected with MCT (60 mg/kg) and after 24 h were exposed to a combined exercise training program: aerobic exercise (treadmill running-60 min/day; 60% of maximum running speed); and resistance exercise (vertical ladder climbing-15 climbs; 60% of maximum carrying load), on alternate days, 5 days/wk, for ∼3 wk. After euthanasia, the lung and right ventricle (RV) were excised and processed for histological, single myocyte, and biochemical analyses. Combined exercise increased the tolerance to physical effort (time until fatigue and relative maximum load) and prevented increases in pulmonary artery resistance (acceleration time (TA)/ejection time (TE)] and reductions in RV function [tricuspid annular plane systolic excursion (TAPSE)]. Moreover, in myocytes isolated from the RV, combined exercise preserved contraction amplitude, as well as contraction and relaxation velocities, and inhibited reductions in the amplitude and maximum speeds to peak and to decay of the intracellular Ca 2+ transient. Furthermore, combined exercise avoided RV (RV weight, cardiomyocyte, extracellular matrix, collagen, inflammatory infiltrate, and extracellular matrix) and lung (pulmonary alveoli and alveolar septum) harmful structural remodeling. In addition, combined exercise restricted RV [nitric oxide (NO) and carbonyl protein (CP)] and lung [catalase (CAT), glutathione S-transferase (GST), and NO] oxidative stress. In conclusion, the applied combined exercise regime hinders the progression of pulmonary and right heart functional and structural harmful remodeling in rats with MCT-induced PAH. NEW & NOTEWORTHY This study reveals that combined exercise improves tolerance to physical effort, prevents increases in pulmonary artery resistance, and conserves the right heart function during the progression of pulmonary arterial hypertension. Our analyses show that combined exercise hinders harmful right ventricular and lung structural remodeling and oxidative stress, which reflects in the maintenance of right ventricular myocytes' contractile function by preserving the intracellular calcium cycling. An attenuated progression of the disease impacts positively on its prognosis.