Relationship between the strength of glass ionomers and their adhesive strength to metals.

OBJECTIVES: The objective of this study was to examine the possible correlation between the strength of glass ionomers and their adhesive strength to metals. METHODS: Three different brands of glass ionomers mixed at four different P/L ratios were evaluated. The compressive and diametral tensile strengths of the cements were determined. The shear bond strengths were determined between four different types of dental casting alloys and the cement made with the different P/L ratios. RESULTS: Significant (p < 0.05) increases in the bond strength to any of the metal surfaces were found in the cement specimens mixed at the highest P/L ratio compared to those mixed at the lowest P/L ratio. For two glass ionomers (FI and DNT), the specimens prepared at the highest P/L ratio showed significantly greater diametral tensile strength than those prepared at the lowest P/L ratio (p < 0.05). SIGNIFICANCE: The present study showed a significant correlation between diametral tensile strengths and bond strengths. It is suggested that the use of glass ionomers with high mechanical strength is an important factor of enhancing the adhesion to metal surfaces.     

Mortality outcomes and clinical background of children on maintenance dialysis without receiving kidney transplantation

Clinical and Experimental Nephrology - Some pediatric patients on maintenance dialysis may need end-of-life care in the future because of being excluded from the indication of kidney...     

Orally Administrated Ascorbic Acid Suppresses Neuronal Damage and Modifies Expression of SVCT2 and GLUT1 in the Brain of Diabetic Rats with Cerebral Ischemia-Reperfusion

Diabetes mellitus is known to exacerbate cerebral ischemic injury. In the present study, we investigated antiapoptotic and anti-inflammatory effects of oral supplementation of ascorbic acid (AA) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. We also evaluated the effects of AA on expression of sodium-dependent vitamin C transporter 2 (SVCT2) and glucose transporter 1 (GLUT1) after MCAO/Re in the brain. The diabetic state markedly aggravated MCAO/Re-induced cerebral damage, as assessed by infarct volume and edema. Pretreatment with AA (100 mg/kg, p.o.) for two weeks significantly suppressed the exacerbation of damage in the brain of diabetic rats. AA also suppressed the production of superoxide radical, activation of caspase-3, and expression of proinflammatory cytokines (tumor necrosis factor-α and interleukin-1β) in the ischemic penumbra. Immunohistochemical staining revealed that expression of SVCT2 was upregulated primarily in neurons and capillary endothelial cells after MCAO/Re in the nondiabetic cortex, accompanied by an increase in total AA (AA + dehydroascorbic acid) in the tissue, and that these responses were suppressed in the diabetic rats. AA supplementation to the diabetic rats restored these responses to the levels of the nondiabetic rats. Furthermore, AA markedly upregulated the basal expression of GLUT1 in endothelial cells of nondiabetic and diabetic cortex, which did not affect total AA levels in the cortex. These results suggest that daily intake of AA attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. AA supplementation may protect endothelial function against the exacerbated ischemic oxidative injury in the diabetic state and improve AA transport through SVCT2 in the cortex.