Versicherungsrechtliche Medizin. Gewerbepathologie. (Gewerbliche Vergiftungen)

International Journal of Legal Medicine -     

Microstructure of veneered zirconia after surface treatments: A TEM study

Objective

Clinical studies reveal that veneer chipping is one major problem associated with zirconia based dental restorations, the underlying mechanisms being still investigated. We semi-quantitatively analyzed the effects of different surface treatments (thermal etching, 35/105 μm sandblasting and coarse bur drilling (150 μm)) on the microstructure of a zirconia veneered dental ceramic.

Methods

The relative monoclinic content on zirconia surfaces was determined using X-ray diffraction (XRD). The microstructure at the zirconia–veneer interface has thereafter been investigated using transmission electron microscopy (TEM). Selected area electron diffraction (SAED) was used to qualitatively assess the depth of the stress-induced phase transformation.

Results

Sandblasting or bur drilling significantly roughened the zirconia surface. A reverse transformation of already transformed monoclinic zirconia grains back into the tetragonal polymorph has been observed after thermal veneering treatment. In TEM, the mechanically treated samples revealed a highly damaged area of 1–3 μm from the interface. The presence of monoclinic phase in veneered zirconia samples has been observed in SAED up to depths of 4 μm (35 μm sandblasted), 11 μm (105 μm sandblasted) and 9 μm (150 μm diamond drilled) below the interface.

Significance

Regardless of the treatment protocol and produced roughness, the veneering ceramic perfectly sealed the zirconia surface. XRD showed an increased amount of monoclinic phase on the surface treated zirconia. However after thermal treatment, the monoclinic phase was re-transformed into the tetragonal polymorph. TEM/SAED analysis has found indication for a greater extend of the monoclinic transformation into the bulk zirconia compared to the treatment related defective zone depth.     

NO reduces PMN adhesion to human vascular endothelial cells due to downregulation of ICAM-1 mRNA and surface expression

Reperfusion damage is largely due to the adherence of polymorphonuclear leukocytes to the endothelium initiated by adhesion molecule upregulation. The reduced endothelial nitric oxide release during ischemia may be involved in the upregulation of intercellular adhesion molecule 1. In this study, we tested if nitric oxide donors suppress polymorphonuclear leukocyte adherence to activated endothelial cells by inhibition of the intercellular adhesion molecule 1 surface expression. Confluent human umbilical vein endothelial cells were stimulated with tumor necrosis factor alpha (300 U/mL) after preincubation with increasing concentrations of the nitric oxide donors CAS 1609 (0.005-5 mM/L) and 3-(4-morpholinyl)-sydnonimine (0.01-1 mM/L). Intercellular adhesion molecule 1 surface expression was measured in a cell surface enzyme-linked immunosorbent assay, intercellular adhesion molecule 1 mRNA by Northern analysis. Human saphenous vein endothelial cells were transfected with the inducible nitric oxide synthase gene and stimulated with tumor necrosis factor alpha (300 U/mL). Fluorescein green-labeled polymorphonuclear leukocytes adhering to activated human umbilical vein endothelial cells/human saphenous vein endothelial cells were quantified by epifluorescent microscopy. The intercellular adhesion molecule 1 surface expression of activated human umbilical vein endothelial cells/human saphenous vein endothelial cells was significantly diminished to 40 to 60% of the maximum after treatment with CAS 1609, 3-(4-morpholinyl)-sydnonimine, or transfection with the inducible nitric oxide synthase gene. Intercellular adhesion molecule 1 mRNA was diminished by CAS 1609 and 3-(4-morpholinyl)-sydnonimine in the same manner. The functional relevance of our data was shown by reduction of polymorphonuclear leukocyte adherence to activated human umbilical vein endothelial cells/human saphenous vein endothelial cells following treatment with CAS 1609 and 3-(4-morpholinyl)-sydnonimine or transfection with inducible nitric oxide synthase. Tumor necrosis factor-induced polymorphonuclear leukocyte adherence was abolished by blocking antibody against intercellular adhesion molecule 1. Thus, exogenous or endogenous substitution of nitric oxide diminishes the expression of endothelial intercellular adhesion molecule 1 and its mRNA following tumor necrosis factor alpha stimulation. This results in a reduced polymorphonuclear leukocyte adherence to activated endothelium.     

Leichenerscheinungen

International Journal of Legal Medicine -     

Endothelial function in the forearm circulation of patients with the metabolic syndrome--effect of different lipid-lowering regimens

We compared the effect of statin therapy (either alone or combined with ezetimibe) on the inhibition of cholesterol resorption and endothelial function by measuring forearm blood flow in male patients with the metabolic syndrome. Compared to 40 mg atorvastatin alone, combination therapy with 10 mg ezetimibe and 10 mg atorvastatin for 8 weeks resulted in significantly decreased total serum cholesterol and triglycerides levels (n = 14). Endothelium-dependent, acetylcholine-mediated vasodilation was significantly better with combination therapy (p < 0.05). In contrast, endothelium-independent forearm blood flow response to sodium nitroprusside was comparable in both groups. Our data suggest a more effective restoration of endothelial function with the statin/ezetimibe combination compared to statin monotherapy in patients with the metabolic syndrome.     

Plötzlicher Tod aus natrlicher Ursache

Ohne Zusammenfassung     

Sonstige Körperverletzungen. Gewaltsamer Tod

International Journal of Legal Medicine -     

Verletzungen. Gewaltsamer Tod aus physikalischer Ursache

International Journal of Legal Medicine -