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Biomedical subjects

G Goracci

Publications and source records attributed to G Goracci.

At least 19 recordsLinked to original sources
PubMed2000

Detubularized rectosigmoid neobladder in women after cystectomy for bladder cancer.

BACKGROUND AND OBJECTIVES: We present the long-term functional results of a new technique for bladder substitution after cystectomy for bladder cancer in women. METHODS: Between 1991 and 1995, 10 women underwent radical cystectomy for bladder cancer with a new technique. We created a detubularized rectosigmoid neobladder associated with either a terminal colostomy or intrasphincteric perineal colostomy section (Heitz-Boyer-Hovelacque). We evaluated neobladder functioning over almost 5 years by means of urodynamic studies, ultrasound scans, urograms and pouchgrams, and renal function tests. RESULTS: Neobladder function was excellent in all patients, with good diurnal and nocturnal urinary continence, voiding patterns, and preservation of the upper urinary tract. CONCLUSIONS: This new technique, which is a modification of the standard rectal or rectosigmoid neobladder technique, is a valid alternative to the ortothopic neobladder in women, with good functional results.

Colon, Sigmoid↗
PubMed2000

Properties and regulation of microsomal PAF-synthesizing enzymes in rat brain cortex.

Platelet-activating factor (PAF) is a phospholipid mediator of long-term potentiation, synaptic plasticity and memory formation as well as of the development of brain damage. In brain, PAF is synthesized by two distinct pathways but their relative contribution to its productions, in various physiological and pathological conditions, is not established. We have further investigated on the properties of the two enzymes that catalyze the last step of the de novo or remodeling pathways in rat brain microsomes, PAF-synthesizing phosphocholinetransferase (PAF-PCT) and lysoPAF acetyltransferase (lysoPAF-AT), respectively. The latter enzyme is fully active at microM Ca2+ concentration, inhibited by MgATP and activated by phosphorylation. Because the reversibility of the reaction catalyzed by PAF-PCT, its direction depends on the ratio [CDP-choline]/[CMP], which is related to the energy charge of the cell. These and other properties indicate that the de novo pathway should mainly contribute to PAF synthesis for maintaining its basal levels under physiological conditions. The remodeling pathway should be more involved in the production of PAF during ischemia. During reperfusion, the overproduction of PAF should be the result of the concomitant activation of both pathways.

Acetyltransferases↗
PubMed1999

Evidence that cytosolic phospholipase A2 is down-regulated by protein kinase C in intact human platelets stimulated with fluoroaluminate.

We reported that protein kinase C (PKC) inhibitors increase the release of arachidonic acid induced by fluoroaluminate (AlF4-), an unspecific G-protein activator, in intact human platelets. Now we demonstrate that this effect is independent of the extracellular Ca2+ concentration and that AlF4(-)-induced release of AA is abolished by BAPTA, an intracellular Ca2+ chelator, even in the presence of GF 109203X, a specific and potent PKC inhibitor. This compound also blocks the liberation of the secretory phospholipase A2 in the extracellular medium, indicating that this enzyme is not involved in the potentiation of arachidonic acid by PKC inhibitors. On the other hand, the latter effect is completely abolished by treatment of platelets with AACOCF3, a specific inhibitor of cytosolic phospholipase A2 (cPLA2). These observations indicate that cPLA2 is responsible for the AlF4(-)-induced release of arachidonic acid by a mechanism that is down-regulated by PKC.

Aluminum↗
PubMed1999

Terminal end of the human odontoblast process: a study using SEM and confocal microscopy.

Towards the middle of the eighteenth century, Tomes described the presence of membranous structures of cellular origin inside the dentinal tubules. Subsequent studies have been controversial regarding the terminal end of the odontoblasts. According to Fusayama, this cellular process reaches even the dentinal-enamel junction; others, such as Brännström, believed that this cellular process is present only in the inner third of the dentin. The aim of the present study was to determine the exact area up to which the terminal ends of the odontoblasts extend. With the aid of advanced confocal laser scanning microscopy (CLSM) cylindrical structures were demonstrated inside the tubules even in the absence of odontoblasts. This would confirm that the structures previously described as cellular processes can be identified with the lamina limitans of the peritubular dentin. High resolution field-emission scanning electron microscopy (FE-SEM) provided further evidence that tubular structures are only seen in the inner third of the dentin, towards the pulp.

Adult↗
PubMed1999

Platelet-activating factor and group I metabotropic glutamate receptors interact for full development and maintenance of long-term potentiation in the rat medial vestibular nuclei.

In rat brainstem slices, we investigated the interaction between platelet-activating factor and group I metabotropic glutamate receptors in mediating long-term potentiation within the medial vestibular nuclei. We analysed the N1 field potential wave evoked in the ventral portion of the medial vestibular nuclei by primary vestibular afferent stimulation. The group I metabotropic glutamate receptor antagonist, (R,S)-1-aminoindan-1,5-dicarboxylic acid, prevented long-term potentiation induced by a platelet-activating factor analogue [1-O-hexadecyl-2-O-(methylcarbamyl)-sn-glycero-3-phosphocholine], as well as the full development of potentiation, induced by high-frequency stimulation under the blocking agent for synaptosomal platelet-activating factor receptors (ginkolide B), at drug washout. However, potentiation directly induced by the group I glutamate metabotropic receptor agonist, (R,S)-3,5-dihydroxyphenylglycine, was reduced by ginkolide B. These findings suggest that platelet-activating factor, whether exogenous or released following potentiation induction, exerts its effect through presynaptic group I metabotropic glutamate receptors, mediating the increase of glutamate release. In addition, we found that this mechanism, which led to full potentiation through presynaptic group I metabotropic glutamate receptor activation, was inactivated soon after application of potentiation-inducing stimulus. In fact, the long-lasting block of the platelet-activating factor and metabotropic glutamate receptors prevented the full potentiation development and the induced potentiation progressively declined to null. Moreover, ginkolide B, given when high-frequency-dependent potentiation was established, only reduced it within 5 min after potentiation induction. We conclude that to fully develop vestibular long-term potentiation requires presynaptic events. Platelet-activating factor, released after the activation of postsynaptic mechanisms which induce potentiation, is necessary for coupling postsynaptic and presynaptic phenomena, through the activation of group I metabotropic glutamate receptors, and its action lasts only for a short period. If this coupling does not occur, a full and long-lasting potentiation cannot develop.

Afferent Pathways↗
PubMed1999

[Splenic pseudoaneurysms following acute pancreatitis].

Splenic artery pseudoaneurysms are the most common of visceral artery pseudoaneurysms. Splenic pseudoaneurysms appear to have developed as a consequence of inflammatory processes adjacent to the splenic artery, particularly acute pancreatitis and chronic pancreatitis with associated pseudocysts. They are often asymptomatic and picked up on abdominal examination for ultrasound or CT scanning for other conditions. Complications include rupture with retroperitoneal hemorrhage or intraperitoneal hemorrhage. Two cases of splenic pseudoaneurysms, following acute pancreatitis, are reported between the years 1987 and 1996.

Adult↗
PubMed1999

[Treatment of parastomal colostomy hernia].

BACKGROUND: Parastomal hernias are the most common cause of in patients surgically with stomy reoperation treated. METHODS: Treatment of parastomal hernias has been faced through two kind of technics: the first one consisted in the translocation of colostomy, the second one was placing around the colostomic hole a marlex mesh which was inserted at muscular structure level. From January 1993 to May 1997 we treated 8 patients affected by paracolostomic hernia associated to laparocele. The laparocele was treated according Rives' technique with the prosthesis positioned in the properitoneal site. The parastomal hernia was treated with translocation of the colostomy in 3 cases; in the other patients a plastic surgery of the colostomic orifice was made using polypropylene little bandages in properitoneal site. RESULTS: In the postoperative period the complications concerned a single case of skin parcellar necrosis, that healed spontaneously with medications and a case of prolonged serous secretion the mean follow-up was 2 years from the wound. CONCLUSIONS: In our experience the use of marlex mesh may be effective in treatment of parastomal hernia only a patient treated with translocation of the stoma showed a recurrence of parastomal hernia. The positioning of the prosthesis at properitoneal level is subject to a lower incidence of recurrent parastomal hernia.

Aged↗
PubMed1999

Esthetic and functional reproduction of occlusal morphology with composite resins.

The increasing use of composite resin restorations in posterior sectors produces some difficulties in the exact reproduction of occlusal morphology. In this article we present a new operative method that allows a quick and precise reproduction of occlusal morphology with minimal carious destruction of the occlusal enamel of posterior dental elements in the case of initial carious lesions. This method is indicated for class I and II carious lesions and is based on a preoperative record of the occlusal morphology made with a transparent silicone mold. This mold is placed on the tooth after the application of the last layer of composite resin, which is then polymerized through the silicone. Illustrated as a clinical case, the method is particularly rapid, easy to perform, and contributes to the improved quality and subsequent success of composite restorations in posterior sectors.

Adult↗
PubMed1999

Hepatoid carcinoma of the stomach: is it still an unusual anatomo-clinical entity? Six cases-report.

Hepatoid carcinoma of the stomach is a rare neoplasm (especially in western countries) characterized by high levels of serum alpha-fetoprotein (AFP), the presence of "hepatoid foci" inside the gastric tumor and poor prognosis, due to the earlier onset of liver metastases. We treated six patients for hepatoid carcinoma of the stomach between 1990 and 1997. The female to male ratio was 1:1, the average age was 71 (54-81) and the average AFP-level was 1160 ng/ml (603-1531). We performed 2 total gastrectomies, 2 subtotal gastrectomies and 2 gastro-jejunostomies (due to presence of liver metastases): in one case, the patient underwent a splenectomy as well. All the tumors showed the presence of "hepatoid foci" (the morphological feature is close to the hepatocellular carcinoma) and a positive immunoreactivity to AFP. The mean survival was 3 months: only one patient is still alive and disease-free (with a 52 months follow-up). After radical surgery, she underwent a chemotherapic treatment with cisplatin, epirubicin, 5-fluorouracil and l-leucovorin. We conclude that our series (the widest in Italy and one of most impressive in Europe) confirm the poor prognosis of this neoplasm, but we also want to underline that this tumor is not so "unusual" any more and it requires new types of treatment, like postoperative chemotherapy, besides surgery, to be fighted properly.

Aged↗
PubMed1998

PAF levels in saliva are regulated by inflammatory cells.

Platelet activating factor (PAF), a powerful inflammatory phospholipid mediator, has been detected in normal human saliva and found to be increased in periodontitis. The cellular source of PAF in saliva is controversial although several data suggest an origin related to the presence of inflammatory cells. PAF levels in biological fluids are regulated by PAF-producing cells and by the PAF-degrading acetylhydrolase. Although in normal human saliva acetylhydrolase activity is very low, no information is available on the levels of this enzyme in inflammatory conditions of the mouth. The aim of our study was to assess the contribution of inflammatory cells to the levels of PAF in saliva in normal subjects and in patients with periodontitis. PAF was measured by radioimmunoassay (RIA) in mixed uncentrifuged saliva and in cell-free saliva from healthy subjects, before and after tooth brushing, and in patients with periodontitis. In healthy subjects PAF levels were significantly higher in whole saliva than in centifuged saliva (1.51 +/- 0.22 vs. 0.92 +/- 0.04 ng/ml, p < 0.0039). A significant increase in the amount of PAF was detected in whole saliva, but not in centifuged saliva, 2 h after tooth brushing. In patients with periodontitis PAF levels were not different from those of healthy individuals when using centrifuged saliva but were significantly higher when using whole, uncentrifuged saliva. Exogenous radiolabelled PAF was degraded much more rapidly by the saliva of periodontitis patients than by that of normal subjects. In conclusion, our study shows that inflammatory cells regulate the levels of PAF in saliva contributing to its production and degradation. The differential degradation of PAF in normal and inflammatory saliva highlights the absolute need of a series of methodological precautions when performing studies on salivary PAF.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1998

Role of platelet-activating factor in long-term potentiation of the rat medial vestibular nuclei.

In rat brain stem slices, we investigated the role of platelet activating factor (PAF) in long-term potentiation (LTP) induced in the ventral part of the medial vestibular nuclei (MVN) by high-frequency stimulation (HFS) of the primary vestibular afferent. The synaptosomal PAF receptor antagonist, BN-52021 was administered before and after HFS. BN-52021 did not modify the vestibular potentials under basal conditions, but it reduced the magnitude of potentiation induced by HFS, which completely developed after the drug wash-out. The same effect was obtained by using CV-62091, a more potent PAF antagonist at microsomal binding sites, but with concentrations higher than those of BN-52021. By contrast both BN-52021 and CV-6209 had no effect on the potentiation once induced. This demonstrates that PAF is involved in the induction but not in the maintenance of vestibular long-term effect through activation of synaptosomal PAF receptors. In addition, we analyzed the effect of the PAF analogue, 1-O-hexadecyl-2-O- (methylcarbamyl)-sn-glycero-3-phosphocoline (MC-PAF) and the inactive PAF metabolite, 1-O-hexadecyl-sn-glycero-3-phosphocoline (Lyso-PAF) on vestibular responses. Our results show that MC-PAF, but not Lyso-PAF induced potentiation. This potentiation was prevented by D,L-2-amino 5-phosphonopentanoic acid, suggesting an involvement of N-methyl-D-aspartate receptors. Furthermore, under BN-52021 and CV-6209, the MC-PAF potentiation was reduced or abolished. The dose-effect curve of MC-PAF showed a shift to the right greater under BN-52021 than under CV-6209, confirming the main dependence of MC-PAF potentiation on the activation of synaptosomal PAF receptors. Our results suggest that PAF can be released in the MVN after the activation of postsynaptic mechanisms triggering LTP, and it may act as a retrograde messenger which activates the presynaptic mechanisms facilitating synaptic plasticity.

Animals↗
PubMed1997

Activities of enzymes involved in the metabolism of platelet-activating factor in neural cell cultures during proliferation and differentiation.

Platelet-Activating Factor (PAF) is a potent lipid mediator involved in physiological and pathological events in the nervous tissue where it can be synthesized by two distinct pathways. The last reaction of the de novo pathway utilizes CDPcholine and alkylacetylglycerol and is catalyzed by a specific phosphocholinetransferase (PAF-PCT) whereas the remodelling pathway ends with the reaction catalyzed by lyso-PAF acetyltransferase (lyso-PAF AcT) utilizing lyso-PAF, a product of phospholipase A2 activity, and acetyl-CoA. The levels of PAF in the nervous tissue are also regulated by PAF acetylhydrolase that inactivates this mediator. We have studied the activities of these enzymes during cell proliferation and differentiation in two experimental models: 1) neuronal and glial primary cell cultures from chick embryo and 2) LA-N-1 neuroblastoma cells induced to differentiate by retinoic acid (RA). In undifferentiated neuronal cells from 8-days chick embryos the activity of PAF-PCT was much higher than that of lyso-PAF AcT but it decreased during the period of cellular proliferation up to the arrest of mitosis (day 1-3). During this period no significant changes of lyso-PAF AcT activity was observed. Both enzyme activities increased during the period of neuronal maturation and the formation of cellular contacts and synaptic-like junctions. The activity of PAF acetylhydrolase was unchanged during the development of the neuronal cultures. PAF-PCT activity did not change during the development of chick embryo glial cultures but lyso-PAF AcT activity increased up to the 12th day. RA treatment of LA-N-1 cell culture in proliferation decreased PAF-PCT activity and had no significant effect on lyso-PAF AcT and PAF acetylhydrolase indicating that the synthesis of PAF by the enzyme catalyzing the last step of the de novo pathway is inhibited when the LA-N-1 cells are induced to differentiate. These data suggest that: 1) in chick embryo primary cultures, both pathways are potentially able to contribute to PAF synthesis during development of neuronal cells particularly when they form synaptic-like junctions whereas, during development of glial cells, only the remodelling pathway might be particularly active on synthesizing PAF; 2) in LA-N-1 neuroblastoma cells PAF-synthesizing enzymes coexist and, when cells start to differentiate the contribution of the de novo pathway to PAF biosynthesis might be reduced.

Acetyltransferases↗
PubMed1997

Bonding mechanism of three "one-bottle" systems to conditioned and unconditioned enamel and dentin.

PURPOSE: This in vivo study investigated the formation of hybrid layer, resin tags and adhesive lateral branches, by use of the latest generation of enamel-dentin bonding systems ("one-bottle" systems) on conditioned and unconditioned enamel and dentin. MATERIALS AND METHODS: The dentin adhesives were tested on 24 flat dentin preparations made on facial surfaces of vital, periodontally compromised teeth. The experimental teeth were randomly divided in six groups of four samples each. Group 1: Prime & Bond 2.1 (conditioned dentin, CD); Group 2: Single Bond (CD); Group 3: Syntac Sprint (CD); Group 4: Prime & Bond 2.1 (unconditioned dentin, UD); Group 5: Single Bond (UD); Group 6: Syntac Sprint (UD). In the first three groups, the "one-bottle" systems were applied following the manufacturers' instructions, while in the other three groups the dentin and the enamel were not treated with phosphoric acid and the primer was applied directly on the prepared surfaces. On top of the primer-adhesive, a thin layer of resin was applied and light-cured for 20 seconds. The sample teeth were extracted immediately after the adhesive material was light-cured. All the samples were split-fractured along their long axis. Half of the samples were deproteinized and decalcified at the interface in order to visualize the hybrid layer and the other halves were completely dissolved in order to observe the morphology of resin tags by use of scanning electron microscopy. RESULTS: Groups 1-3: All the tested products showed the same micromechanical bonding mechanism to conditioned dentin with phosphoric acid: they formed hybrid layer, resin tags and adhesive lateral branches. In the samples of the first three groups, characteristic reverse cone-shaped tags with their corresponding adhesive lateral branches were evident. At the enamel site, traditional pattern of etch enamel was always observed. Groups 4-6: When the bonding systems were applied on unconditioned dentin, hybrid layer was not formed, resin tags were rarely noted and their shape was narrow and they did not completely seal the tubular orifices. The tubules remained mainly closed by smear plugs. At the enamel site, the unetched surface showed absence of characteristic etch pattern and of resin tags.

Acid Etching, Dental↗
PubMed1997

["Hepatoid" gastric tumor].

In this study the Authors describe two cases of hepatoid adenocarcinoma of the stomach: one is characterized by the presence of alpha-fetoprotein (AFP) high levels of the serum both pre and post-operating and by the very positive response to the adjuvant chemotherapy (how the return to the normality of such values demonstrates). The other is instead characterized by the presence of post operating hepatic metastasis, event which is very frequent in this kind of neoplasm, but presents many problems concerning the differential histological diagnostics with the primitive hepatocarcinoma (problems which are nowadays not completely solved). Moreover the Authors relate to this study the revision of the international literature of the main characteristics and of prognosis of this particular and rare neoplasm.

Adenocarcinoma↗
PubMed1996

Protein kinase C inhibitors enhance G-protein induced phospholipase A2 activation in intact human platelets.

Washed intact human platelets were prelabelled with [3H]arachidonic acid ([3H]AA) and stimulated with thrombin or with AlF4-, a known unspecific activator of G-proteins. Both stimuli induced the liberation of [3H]AA, the release of beta-thromboglobulin (beta-TG) and platelet aggregation. PMA did not induce liberation of [3H]AA although it induced beta-TG release and aggregation; preincubation with PMA did not modify significantly the amounts of [3H]AA and beta-TG released by thrombin or AlF4-. Different inhibitors of PKC (staurosporine, H-7 and calphostin C) increased the release of [3H]AA and inhibited beta-TG release and aggregation induced by AlF4- but they had no effect when platelets were stimulated with thrombin (0.5 U/ml). Calphostin C was able to release [3H]AA by itself without inducing aggregation of beta-TG release. Okadaic acid (a serine/threonine phosphoprotein phosphatase inhibitor) greatly inhibited the release of [3H]AA, beta-TG and aggregation in AlF4--stimulated platelets. These results indicate the presence of a G-protein mediated mechanism for the activation of a platelet phospholipase A2 which is negatively affected by a protein kinase, sensible to putative inhibitors of protein kinase C, and it is activated by a protein phosphatase, sensible to okadaic acid.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Production and function of lipid second messengers in proliferating and differentiated neuroblastoma cells.

Multiple cellular responses are regulated through the generation of lipid second messengers upon activation of phospholipases. One such response concerns the activity of a class of kinase constituting the protein kinase C family. The production of specific molecular species of lipid second messengers may be therefore of prime importance in the activation of a member of the PKC isoforms. Prompted by this possibility we investigated the production of 1,2 diacyl-sn-glycerol (DAG) and phosphatidic acid (PtdOH) in LA-N-1 neuroblastoma cells under various physiological states. 12-0-Tetradecanoylphorbol 13-acetate (TPA) stimulation activated a phospholipase D (PLD) specific for phosphatidylcholine (PtdCho) in proliferating cells and a phospholipase C (PLC) specific for phosphatidylethanolamine (PtdEtn) in retinoic acid (RA) differentiated cells. These separate activations produced different molecular species of DAG or PtdOH. PtdOH was able to stimulate the Ca2+ dependent protein kinase C (PKC) by a mechanism which differed from the action of DAG. PtdOH did not induce the translocation of the PKC to the membrane. Moreover PtdOH, in contrast to DAG, prevented PKC degradation by inhibiting the enzymatic hydrolysis by m-calpain. These observations suggest that the stimulation of cells by agonists elicited the production of specific molecular species of lipid second messengers depending on the physiological status of the cells, and probably on the nature of the stimulus. It seems therefore likely that the generation of specific lipid second messengers may activate specific PKC isoforms resulting in a specific cellular response.

Animals↗