Search PubMed⌕ Search

Biomedical subjects

R Ciccarelli

Publications and source records attributed to R Ciccarelli.

At least 55 records · Page 3Linked to original sources
PubMed1989

[Radiological semeiology of the lacunar injuries of the mandible].

The paper discusses the radiological findings in the mandibular cavities on the basis of an anatomopathological classification system and suggests some useful criteria for definitive diagnosis. It concludes by stating that it is not always possible to define the radiological findings which allow us to understand the real nature of the lesion, whereas benign or malignant characteristics are quite easily recognisable.

Diagnosis, Differential↗
PubMed1988

Sodium and calcium dependence of purine release from rat cerebral cortical slices.

Electrically evoked purine release from rat cerebral cortical slices was evaluated, using a HPLC analysis combined with radioactivity measurement of the identified fractions. Two different pools of released purines have been identified: one probably related to cell metabolism and the other strictly linked to the nervous transmission. Since a linear increase, due to the stimulation frequencies, was found for the purines released from this second pool, a possible dependence on sodium and calcium transmembrane fluxes was evaluated. Pretreatment of the slices with TTX (5 x 10(-7) M) caused only a partial inhibitory effect on purine release (50%). This effect was probably related to the drug activity on the neuronal component of slices, since TTX induces an almost complete inhibition of purine release from isolated neurons "in cultures" and does not affect it from glial cells. Verapamil (1 x 10(-4) M), a calcium-channel blocker at glial and neuronal level, and TEA (3 x 10(-2) M), a specific inhibitor of calcium-mediated potassium efflux from glial cells, administered to the slices alone or in combination, showed a partial calcium-dependence of purine release. These results suggest a glial role in modulation of electrically-evoked purine release. These cells could exert a "buffering action" that regulates the calcium-mediated potassium availability, by which neuronal activity might be influenced.

Adenosine↗
PubMed1988

Cultures of glial cells release purines under field electrical stimulation: the possible ionic mechanisms.

Dissociated primary cultures of glial cells released a remarkable amount of purines, at rest and during field electrical stimulation. The HPLC identification of labelled compounds derived from 3H-Adenosine (3H-Ado) (employed to preload the cultures) indicated that nucleotides and nucleosides were represented in the superfusate in equivalent proportions (43.86% and 56.14% respectively). Very much higher amounts of unlabelled purines prevalently constituted by nucleotides compounds (91.10%) were also released and detectable in the superfusate. In all the experimental conditions their evoked release did not result frequency-dependent. Since: a linear increase related to the stimulation frequencies was found for the released labelled compounds; no labelled purines were assayed in 5 x 10-5M Dipyridamole-treated cultures; any significant presence of labelled nucleotides, inosine and hypoxantine was not found in cultures simultaneously treated with 1 x 10-5M 2'-deoxycoformycin and 1 x 10-4M 1-(-5-isoquinolinsulfonyl)-2-methylpiperizine (H7) (3H-Ado amounts resulted more than doubled in these experimental conditions); labelled compounds have been assumed as tracers of a glial purine rate whose release can be connected to electrically-evoked action potentials. Purine outflow from glial cells is not sodium dependent, in fact TTX (5 x 10-7M) did not affect their basal or electrically-evoked release. A remarkable calcium-dependence was also evidentiated by the 1 x 10-4M Verapamil-induced inhibition of basal and evoked release. TEA (1 x 10-2M), a specific inhibitor of potassium efflux throughout calcium-mediated specific channels, strongly reduced the evoked purine outflow and any additive effect of its was not detectable when administered simultaneously to the calcium antagonist. These findings indicate that the frequency-dependent purine release from cultured glial cells is linked to ionic mechanisms, which calcium and potassium are mainly involved in.

Adenosine↗
PubMed1982

Adenosine--norepinephrine interactions on cyclic AMP generating system in human tumoral brain slices.

Many experimental findings suggest that the administration of exogenous Norepinephrine (NE), in cerebral cortical slices surviving in vitro, increases cyclic AMP (cAMP) levels, although the NE receptor turns out to be different for the different animal species. Likewise, in the same experimental model, Adenosine (A) increases the cAMP intracellular levels. Furthermore, A sites seem to be linked with adrenoreceptors related to the cAMP-generating system. In this report we studied the interaction of NE on the cAMP system of human cerebral tissue slices, normal and tumoral. In the normal slices, NE increases cAMP levels in a dose-dependent manner, probably through beta-receptors; in fact, Propranolol counteracts this effect. Also A induces a dose-dependent rise of cAMP levels; Theophylline prevents, while low doses of Dipyridamole potentiate, this effect. The contemporaneous administration of NE and A produces an effect on cAMP levels greater than that displayed by each drug alone. Probably the enhanced cAMP increase is due to the endogenous release, evoked by NE. In fact, Propranolol reduces, but does not completely prevent, the effect of NE. In cortical tumor slices, the effect of NE on the cAMP-generating system is very reduced. This suggests that the membrane damage of neoplastic cells affects the availability of adrenoreceptors. On the other hand, the responsiveness of A sites is deeply altered. The receptor antagonists or the re-uptake inhibitors of this Adenine nucleotided do not exert their effect selectively.

Adenosine↗
PubMed1980

[Myelography with B 15000, a new nonionic water-soluble contrast medium. Technical aspects and preliminary clinical experiences (author's transl)].

This is a report of myelography findings obtained in 50 patients with B 15000 (Iopamidol), a new non ionic water-soluble contrast medium. The procedure was easily carried out with a tilting table wired to a TV image amplifier. The dose of contrast medium injected intrathecally was 10 divided by 15 cm3 of a preconstituted solution containing iodine 200 or 300 mg/cm3. There were no accidents or major complications. The myelograms obtained with the test material afforded accurate diagnosis of intramedullary and extramedullary lesions, and signally of intervertebral disk protrusion and hernia.

Adolescent↗
PubMed1979

Cyclic AMP and cyclic GMP levels in human colonic mucosa before and during chenodeoxycholic acid therapy.

Previous experimental studies suggest that bile salt-induced colonic fluid secretion is mediated by adenosine 3':5'-phosphate (cyclic AMP). Two biopsy specimens of colonic mucosa were obtained endoscopically before and after different periods of therapy (five, 10, or 15 days), from each of 21 patients receiving chenodeoxycholic acid. A rise of cyclic AMP intracellular levels was found, but only after five and 10 days of treatment was the increase statistically significant when compared with basal levels. Similar changes were observed for guanosine 3':5'-phosphate (cyclic GMP), but percentage increases were higher than for cyclic AMP. Initial diarrhoea disappeared spontaneously, and at 15 days the levels of both cyclic nucleotides were not significantly different from basal levels. Our findings suggest that colonic adaptation to increase in luminal bile salt levels is related to changes in intracellular levels of cyclic nucleotides and support the hypothesis that not only cyclic AMP, but also cyclic GMP may play an important role in producing bile salt-induced diarrhoea in man.

Adult↗
PubMed1978

[Positive effects of chenodeoxycholic acid (CDCA) on the biohumoral clinical aspect of cholesterin calculosis of the gallbladder].

The efficacy and possible sideeffects of chenodeoxycholic acid have been studied in 35 patients with biliary calculosis lithiasis. In 53% of the cases treated for six months or more partial or complete gallstone dissolution was observed. The action of this drug on hematic triglyceride level and on severity and frequency of the hypostenic dyspeptic symptoms and biliary colic is interesting from the viewpoint of new therapeutic prospects. Diarrhea has been the only relevant side-effect.

Adult↗
PubMedDate not supplied

Influence of PLA2-PG system on purine release and cAMP content in dissociated primary glial cultures from rat striatum.

Purine release and prostaglandin (PG) outflow were simultaneously evaluated from untreated glial primary cultures of rat striatum, at rest and under field electrical stimulation. Purine release was also assayed from sister cultured cells in which a suitable pharmacological treatment with 1 x 10(-6) M dexamethasone or 1 x 10(-4) M indomethacin had produced a complete inhibition of the phospholipase A2-prostaglandin (PLA2-PG) system. Purine release from untreated cells seems to be regulated by specific receptor sites for released adenosine (Ado); A1 receptors exert an inhibitory control on purine release while A2 receptors facilitate it. PG release appears to be related to A1-mediated Ado activity, since culture treatment with 1 x 10(-10) M 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) or 1 x 10(-4) M N-ethylmaleimide (NEM), A1 receptor inhibitory agents able to increase purine release, induced a significant reduction of the evoked PG outflow. Purine amount, released from glial cells with inhibited PLA2-PG system, was remarkably greater than that one assayed from control cultured cells. In so treated cultures, no additive effect, NEM-induced, was detected, while the addition of a mixture of PGs partially reduced the increased purine outflow. An electrically evoked cAMP accumulation, significantly greater than that found in controls, was even detected in cultured cells with inhibited PLA2-PG system. Since 10 micrograms/ml adenosine deaminase (ADA) reduced while DPCPX enhanced the evoked cAMP accumulation, it seems partially due to released Ado and accounts for a prevalent A2-stimulating rather than an A1-inhibitory control on adenylate cyclase activity. Thus, in cultured glial cells, the PLA2-PG system, likely linked to A1 receptor sites, concurs to control purine release and seems to affect less directly cAMP accumulation.

Animals↗
PubMedDate not supplied

AIT-082 and methylprednisolone singly, but not in combination, enhance functional and histological improvement after acute spinal cord injury in rats.

Extracellular non-adenine based purines are neuroprotective. Preliminary studies indicate that administration of the synthetic purine 4-[[3-(1,6 dihydro-6-oxo-9-purine-9-yl)-1-oxypropyl] amino] benzoic acid (AIT-082, leteprinim potassium) to rats immediately after acute spinal cord injury (SCI), improves functional outcome. The effects of potential new agents are often compared to methylprednisolone (MPSS). We evaluated the effects of AIT-082 and MPSS, separately and in combination, on the functional and morphological outcome of acute SCI in adult rats. After standardized T11-12 spinal cord compression rats were given intraperitoneally one of the following: vehicle (saline); MPSS (30 mg/kg or 60 mg/kg body weight, first dose 15 min after crush); AIT-082 (60 mg/kg body weight daily, first dose 15 min after crush); or AIT-082 plus MPSS. After 1, 3, or 21 days, the rats were perfused for histological analysis. AIT-082 administrations significantly reduced locomotor impairment from 121 days post-operatively. At 1 and 3 days post injury, AIT-082-treatment reduced tissue swelling, tissue loss and astrogliosis at the injured cords but did not alter the extent of hemorrhage and the number of macrophages and/or microglia. MPSS reduced hemorrhage and the number of macrophages and/or microglia, but did not alter astrogliosis. At 21 days, either AIT-082 or MPSS administration improved function and morphology similarly (less tissue loss and astrogliosis). In contrast, administration of AIT-082 and MPSS together abolished the beneficial effects observed when either drug was given individually. These results suggest that MPSS and AIT-082 may exert their beneficial effects through different and potentially antagonistic pathways.

Aminobenzoates↗
PubMedDate not supplied

P2Y1 and cysteinyl leukotriene receptors mediate purine and cysteinyl leukotriene co-release in primary cultures of rat microglia.

Inflammation is widely recognized as contributing to the pathology of acute and chronic neurodegenerative conditions. Microglial cells are pathologic sensors in the brain and activated microglia have been viewed as detrimental. Leukotriene, including cysteinyl leukotrienes (CysLTs) are suggested to be involved in brain inflammation and neurological diseases and ATP, by its receptors is a candidate for microglia activation. A23187 (10 microM) stimulated microglia to co-release CysLTs and [3H] adenine based purines ([3H] ABPs), mainly ATP. The biosynthetic production of CysLTs was abolished by 10 microM MK-886, an inhibitor of 5-lipoxygenase-activating protein activity. RT-PCR analysis showed that microglia expressed both CysLT1 / CysLT2 receptors, P2Y1ATP receptors and several members of the ATP binding cassette (ABC) transporters including MRP1, MRP4 and Pgp. The increase in [Ca2+]i elicited by LTD4 (0.1 microM) and 2MeSATP (100 microM), agonists for CysLT- and P2Y1-receptors, was abolished by the respective antagonists, BAYu9773 (0.5 microM) and suramin (50 microM). The stimulation of both receptor subtypes, induced a concomitant increase in the release of both [3H] ABPs and CysLTs that was blocked by the antagonists and significantly reduced by a cocktail of ABC transporter inhibitors, BAPTA/AM (intracellular Ca2+ chelator) and staurosporine (0.1 microM, PKC blocker). P2Y antagonist was unable to antagonise the effects of LTD4 and BAYu9773 did not reduce the effects of 2MeSATP. These data suggest that: i) the efflux of purines and cysteinyl-leukotrienes is specifically and independently controlled by the two receptor types, ii) calcium, PKC and the ABC transporter system can reasonably be considered common mechanisms underlying the release of ABPs and CysLTs from microglia. The blockade of P2Y1 or CysLT1/CysLT2 receptors by specific antagonists that abolished the raise in [Ca2+]i and drastically reduced the concomitant efflux of both compounds, as well as the effects of BAPTA and staurosporine support this hypothesis. In conclusion, the data of the present study suggest a cross talk between the purine and leukotriene systems in a possible autocrine/paracrine control of the microglia-mediated initiation and progression of an inflammatory response.

ATP-Binding Cassette Transporters↗
PubMedDate not supplied

P2X7 receptor activation in rat brain cultured astrocytes increases the biosynthetic release of cysteinyl leukotrienes.

Astrocytes have been recognized as important elements in controlling inflammatory as well as immune processes in the central nervous system (CNS). Recently, glial cells have been shown to produce cysteinyl leukotrienes (CysLTs) which are known lipid mediators of inflammation and whose extracellular concentrations rise under different pathological conditions in the brain. In the same conditions also extracellular concentrations of ATP dramatically increase reaching levels able to activate P2X7 ionotropic receptors for which an emerging role in neuroinflammation and neurodegeneration has been claimed. RTPCR analysis showed that primary cultures of rat brain astrocytes express P2X7 receptors. Application of the selective P2X7 agonist benzoyl benzoly ATP (BzATP) markedly increased [Ca2+]i which was mediated by a calcium influx from the extracellular milieu. The P2X7 antagonist, oATP, suppressed the BzATP-induced calcium increase. Consistent with the evidence that increased calcium levels activate the leukotriene biosynthetic pathway, challenge of astrocytes with either the calcium ionophore A23187 or BzATP significantly increased CysLT production and the cell pre-treatment with EGTA abolished these effects. Again the P2X7 antagonist prevented the BzATP-mediated CysLT efflux, whereas the astrocyte pretreatment with MK-571, a CysLT1 receptor antagonist, was ineffective. The astrocyte pre-treatment with a cocktail of inhibitors of ATP binding cassette (ABC) proteins reduced the BzATP-mediated CysLT production confirming that ABC transporters are involved in the release of CysLTs. The astrocyte P2X7- evoked rise of CysLT efflux was abolished in the presence of MK-886, an inhibitor of 5-lipoxygenase activating protein (FLAP) whose expression, along with that of 5-lipoxygenase (5-LO) was reported by Northern Blot analysis. The stimulation of P2X7 induced an up-regulation of FLAPmRNA that was reduced by the antagonist oATP. These data suggest that in rat brain cultured astrocytes P2X7ATP receptors may participate in the control of CysLT release thus further supporting a role for extracellular ATP as an integral component of the inflammatory brain response.

5-Lipoxygenase-Activating Proteins↗