Influence of microcapsule parameters and initiator concentration on the self-healing capacity of resin-based dental composites

ObjectiveFracture is one of the main causes for failure of resin-based composite restorations. To overcome this drawback, self-healing resin-based composites have been designed by incorporation of microcapsules. However, the relationship between their self-healing capacity and microcapsule and resin parameters is still poorly understood. Therefore, the objective of this study was to systematically investigate the effect of initiator concentration (in the resin) and microcapsule size and concentration on the self-healing performance of commercially available flowable resin-based composites.MethodsPoly(urea-formaldehyde) (PUF) microcapsules containing acrylic healing liquid were synthesized in small (33 ± 8 μm), medium (68 ± 21 μm) and large sizes (198 ± 43 μm) and characterized. Subsequently, these microcapsules were incorporated into a conventional flowable resin-based composite (Majesty Flow ES2, Kuraray) at different contents (5–15 wt%) and benzoyl peroxide (BPO) initiator concentrations (0.5–2.0 wt%). Fracture toughness (K_IC) of test specimens was tested using a single edge V-notched beam method. Immediately after complete fracture (K_IC-initial), the two fractured parts were held together for 72 h to allow for healing. Subsequently, fracture toughness of the healed resin-based composites (K_IC-healed) was tested as well.ResultsThe fracture toughness of healed dental composites significantly increased with increasing microcapsule size and concentration (2 wt% BPO, p < 0.05). The highest self-healing efficiencies (up to 76%) were obtained with microcapsules sized 198 ± 43 um.Significancecommercially available resin-based composites can be rendered self-healing most efficiently by incorporation of large microcapsules (198 ± 43 μm). However, long-term tests on fatigue and wear behavior are needed to confirm the clinical efficacy.     

Rapid Increase in Marrow Fat Content and Decrease in Marrow Perfusion in Lumbar Vertebra Following Bilateral Oophorectomy: An MR Imaging-Based Prospective Longitudinal Study

ObjectiveBilateral oophorectomy leads to reduced bone mineral density (BMD), and reduced BMD is associated with increased marrow fat and reduced marrow perfusion. Purpose of this study was to investigate how soon these changes occur following surgical oophorectomy.ResultsReduced BMD, increased marrow FF, and reduced marrow perfusion occurred synchronously post-oophorectomy. There was a sharp decrease of 12.5 ± 7.2% in BMD (n = 6), a sharp increase of 92.2 ± 46.3% (n = 6) in FF, a sharp decrease of 23.6 ± 3.9% in maximum contrast enhancement (n = 5), and of 45.4 ± 7.7% for enhancement slope (n = 5) during the initial 3 months post surgery. BMD and marrow perfusion continued to decrease, and marrow FF continued to increase at a slower rate during the following 18 months. Friedman test showed a significant trend for these changes (p < 0.05).ConclusionBilateral oophorectomy leads to a rapid decrease in lumbar BMD, an increase in marrow fat content, and a decrease in marrow blood perfusion.     

Calculation of aortic regurgitation orifice area by Doppler echocardiography: an application of the continuity equation.

The evaluation of aortic regurgitation by current echocardiographic techniques has been qualitative and load-dependent. The area of the regurgitant orifice, which is theoretically independent of haemodynamic conditions, has not been determined non-invasively. In 20 patients with various degrees of aortic regurgitation, this area was determined by use of the continuity equation applied during diastole. The velocity-time integrals were determined at the supravalvar (VTIs) and regurgitant orifice (VTIj) levels by pulsed and continuous wave Doppler respectively. The cross sectional area at the supravalvar level (As) was also measured by cross sectional echocardiography. The regurgitant orifice is given by: (As x VTIs)/VTIj. Other non-invasive measurements of the aortic regurgitation severity were also recorded: (a) an overall echo score (1-5+) given blindly by two echocardiographers, (b) the maximal proximal jet width by colour Doppler, (c) left ventricular end systolic and end diastolic volumes and left ventricular mass. The regurgitant area ranged from 0.25 to 1.7 cm2 and this area accorded with the overall echo score and the maximal proximal jet width measured by colour Doppler. The aortic regurgitation orifice area can be calculated non-invasively and it may be a quantitative measure of the severity of aortic regurgitation.     

Suppression of DNA synthesis in hepatoma cells exposed to glucocorticoid hormone in vitro

Glucocorticoid hormone is shown to markedly suppress DNA synthesis in a line of rat hepatoma cells in vitro. In the presence of 300 nM hydrocortisone or 30 nM dexamethasone the incorporation of radioactive thymidine falls to 50% of control levels by 36 hr, and at higher concentrations of hormone inhibition can be noted as early as 12 hr and is nearly complete by 24 hr. This inhibition of radioactive thymidine incorporation reflects a true suppression of DNA synthesis, is accompanied by a corresponding inhibition of cell proliferation, and is readily reversible upon subsequent removal of hormone. In contrast to previously described effects of the glucocorticoid hormones on various cells of lymphoid origin, the inhibition of DNA synthesis in these hepatoma cells is not accompanied by appreciable cell lysis or by degradation of preformed DNA, and even when [(3)H]thymidine incorporation into DNA is inhibited by 90% or more, incorporation of [(14)C]uridine into RNA proceeds with little change. These findings all parallel previous observations on the effects of glucocorticoid hormone on the livers of intact animals and suggest that studies on the mechanism of the inhibition of DNA synthesis in the present more isolated system may lead to a better understanding of the means by which these compounds inhibit liver growth in vivo.Despite the ready suppressibility of DNA synthesis in these hepatoma cells and in two other cell lines of liver origin, none of these cell lines was found to be inducible for tyrosine aminotransferase. The apparent dissociation between two "steroid-sensitive" phenomena is of interest and warrants further investigation.