Biomedical subjects
Publications and source records attributed to G Goracci.
Teeth with small interproximal lesions can be treated with reduced cavities for amalgam. This kind of reconstruction produces a good retention while removing less healthy dental tissue and safeguarding the aesthetic appearance with the advantages of amalgam, which is better compared with composite resins, especially for proximal contact and marginal adaptation.
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A review was made of the literature concerning intermediate materials for composite resin fillings and the possibilities of ortho-phosphoric acid infiltration. An experimental study was aimed at evaluating the damages caused by the acid action of the etching material on various type of base materials used. In conclusion, various procedures are suggested for composite resin restoration in order to avoid the risks of lesions of the pulp-dentin organ.
The activity of phospholipase C acting against [3H]-inositol-phosphatidylinositol (PI) and the activity of arachidonic acid (AA) release from [1-14C]arachidonoyl-phosphatidylinositol by enzyme(s) located in synaptic vesicles (SV) isolated from normoxic and ischemic brains was investigated. Brain ischemia significantly activated phospholipase C (PhLC) by about 90% and AA release by about 50%. PhLC and AA release in SV isolated from brain submitted to ischemia were not further activated by 2 mM CaCl2 contrary to the enzymes from normoxic brain. The activation of PhLC and PhLA2 may produce conformational changes and rearrangement of the SV membranes leading to vesicle-membrane fusion and subsequently to massive neurotransmitter release known to occur during ischemia.
The Authors want to repropose a technique which is one of the earliest used in conservative dentistry: the fused-gold reconstruction. A method of easy application is explained by the Authors and will undoubtedly stimulate the dentists' interest towards this kind of reconstruction which still today represents one of the most efficient solutions, in conservative dentistry, of the first and second class cavities.
AD6 is a coumarin derivative which is able to inhibit platelet aggregation and release due to various agonists as adrenaline, PAF, Ca++ ionophore and others. It has been demonstrated that this compound reduces the production of free arachidonate and diglyceride from human platelets pulse-labeled with radioactive arachidonic acid thus suggesting a possible interference with the activity of phospholipase A2 and/or phospholipase C. The present report indicates that the drug has no effect on the increase of the labeling of phosphatidic acid which takes place when platelets pulse-labeled with arachidonic acid are stimulated with thrombin. Furthermore, AD6 is not able to cause changes on the metabolism of phosphoinositides monitored using platelets pre-labeled with [3H] inositol. These observations exclude the possibility that AD6 interferes with phospholipase C activity. Experiments with platelets pulse-labeled with arachidonate suggest that AD6 inhibits phospholipase(s) A2 activity or modulate negatively one or more processes involved in its activation.
Endodontic practice is not risk-free; a variety of technical accidents can complicate root canal treatment, influencing the prognosis and prejudicing the chances of the success. Although such events are infrequent, the author presents a review of the various types of accidents, which he examines in the light of correct diagnosis, prognosis and treatment on the basis of material collected in hospitals and private surgeries.
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Platelet-Activating Factor (PAF, 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is present in nervous tissue and its function is still unknown. We have demonstrated that rat brain is able to synthesize PAF from 1-alkyl-2-acetyl-sn-glycerol and CDP-choline by a "DTT-insensitive" phosphocholine transferase. This represents the last step of the de novo pathway which apparently is the only one existing in the brain for PAF biosynthesis. The enzyme has a microsomal localization, requires Mg++ and is inhibited by Ca++ as reported for phosphocholine transferase utilizing long-chain diradylglycerols as substrates. However, other properties of PAF-synthesizing enzyme (sensitivity to DTT and dependence on pH) are different from those of phosphocholine transferase responsible for the synthesis of diacyl and long-chain alkylacyl glycerophosphocholines. These observations indicate that a specific enzyme for PAF biosynthesis might exist in rat brain.
There are increasingly reports on sensitivity to pressure on teeth filled with composite resins in the days following the filling, a fact that has induced the Authors to carry out a research "in vitro" and "in vivo" in order to study variations of the electrical potential of teeth filled with composite materials. The study has shown that this potential varies considerably in intensity according to the product used for tests in vitro and in vivo, probably due to polimerization defects of the material. These are the first results of a study which will be further extended and which highlights new and so far unknown aspects of widely used filling materials.
The phosphatidylethanolamine fraction isolated from lung surfactant consisted of 33% of the alkylacyl, 39% of the alkenylacyl and 25% of the diacyl subclass. Palmitic acid was the major fatty acid of the alkyl acyl and alkenylacyl subclasses. In diacylphosphatidylethanolamine, saturated and unsaturated fatty acids revealed a ratio of nearly 1.
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The coumarin derivative AD6 is known to inhibit platelet aggregation and release and it possesses vasodilatory properties on coronary arteries of laboratory animals. Furthermore, the inhibition of the production of TxB2 from endogenous substrates after stimulation of human platelets with collagen has been demonstrated. The present report demonstrates that AD6 inhibits the production of labeled arachidonic acid and diglycerides from phospholipids of platelets stimulated with thrombin. This effect is dose-dependent and is already evident at a concentration of the drug (25 microM) which is unable to prevent the aggregation. Apparently, AD6 inhibits the release of arachidonic acid from phosphatidylinositol and choline phosphoglycerides which are the main sources of the substrate for the synthesis of prostaglandins and thromboxanes.
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