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C Florio

Publications and source records attributed to C Florio.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effects of divalent cations on adenosine agonist binding to A1 receptors and non-A1/non-A2 sites in rat cerebral cortex.

In the present study results are reported concerning the effects of several divalent cations on the binding characteristics of [3H]-cyclohexyladenosine on A1 adenosine receptors and of [3H]-N-ethylcarboxamidoadenosine on non-A1/non-A2 sites in membranes from cerebral cortex of the rat. The [3H]-cyclohexyladenosine binding to A1 receptors was dose-dependently increased by Mn2+, Co2+, Ca2+. The binding characteristics of the agonist were differently affected by Ca2+/Mn2+ and Mg2+. Ca2+ and Mn2+ increased the Bmax value without any change in Kd, whereas Mg2+ decreased the Kd value without changing the Bmax. In the presence of Ca2+ and Mg2+ the Kd value was similar to that obtained in the presence of Mg2+, whereas the Bmax value was similar to the apparent number of binding sites calculated in the presence of Ca2+. The cations, Cu2+, Cd2+, Zn2+, decreased the A1 binding with IC50 values of 19.6 microM, 39.2 microM and 103.9 microM, respectively. The binding characteristics of [3H]-N-ethylcarboxamidoadenosine to non-A1/non-A2 sites were affected by Ca2+, Mn2+, Co2+ and Mg2+ in the opposite manner to A1 receptors. They decreased the binding with IC50 values of 20.1 mM, 22.8 mM, 93.0 mM and 18.1 mM, respectively. This occurs through an enhancement in Kd values without changes in the number of binding sites. The findings on A1 receptor and non-A1/non-A2 binding site, taken together, suggest that cations could also exert a modulatory action via specific interactions with divalent cation binding sites on the receptor molecule.

Adenosine↗
PubMed1994

Antiproliferative effect of prostaglandin E2 in cultured guinea pig tracheal smooth muscle cells.

The respiratory epithelium plays an important role in modulating airway smooth muscle responsiveness to contractile agonists, and damage of the epithelium may be involved in the pathogenesis of bronchial hyperresponsiveness. This study was undertaken to determine whether prostaglandin E2 (PGE2), a relaxant agent synthesized and released by airway epithelial cells, could exert long-term effects on airway smooth muscle by regulating cell proliferation. Incubation of growth-arrested tracheal smooth muscle cells with serum for 24 h stimulated DNA synthesis in a concentration-dependent manner, as determined by [3H]thymidine incorporation. PGE2 and forskolin, a direct activator of adenylate cyclase, inhibited serum-induced cell proliferation, and the effects were dose dependent. PGE2 and forskolin also stimulated adenosine 3',5'-cyclic monophosphate accumulation. An inhibitor of cyclooxygenase, indomethacin, enhanced DNA synthesis induced by serum. These results indicate that exogenous PGE2 exerts an antiproliferative effect on smooth muscle cells in culture by activation of adenylate cyclase and suggest a role for the epithelium in modulating airway smooth muscle growth.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Circadian rhythm of cortical and striatal adenosine receptors.

In order to investigate diurnal variations in binding parameters of A1 and A2 adenosine receptors, Kd and Bmax were calculated in mice that had been housed under controlled light-dark cycles for 4 weeks (light on from 7.00 to 19.00 h). A1 cortical receptors were labelled by N6-cyclohexyl-[3H]adenosine, and A1 and A2 striatal receptors by 5'-N-ethylcarboxamido[8-3H]adenosine. Significant differences were found for Bmax values measured at 3-h intervals across a 24-h period. Cyclic variations of the number of binding sites were shown, with a minimum number of A1 and A2 receptors during the light period and a maximum during the dark period. The amplitude for cortical A1 receptors, between 03.00 and 18.00 h, was 39%, while for striatal A1 receptors, between 03.00 and 15.00 h, was 92%. The amplitude for the A2 striatal receptors, between 03.00 and 15.00 h, was 147%. No substantial rhythm was found in the Kd values. These differences in the amplitude could suggest a different physiological modulation of the two adenosine receptor subtype moiety which could reflect a physiologically-relevant mechanism by which adenosine exerts its modulatory role in the central nervous system.

Adenosine↗
PubMed1992

Identification of adenylate cyclase-coupled histamine H2 receptors in guinea pig tracheal smooth muscle cells in culture and the effect of dexamethasone.

Histamine acts on airway contractile elements through at least two different receptor subtypes: H1, which mediates Ca(2+)-dependent contraction, and H2, which stimulates cyclic adenosine monophosphate (cAMP) synthesis and possibly relaxation. The aim of this study was to determine the relative contribution of the different receptor subtypes to histamine-stimulated cAMP production by guinea pig tracheal smooth muscle (GPTSM) cells in primary culture. Histamine and N-alpha-methylhistamine induced concentration-dependent cAMP synthesis; these effects were entirely blocked by 10(-4) M cimetidine, an H2-receptor antagonist, whereas 10(-6) M thioperamide, a selective H3 blocker, was ineffective. The H3 agonist, R-(alpha)-methylhistamine, did not stimulate cAMP synthesis. Triprolidine, an H1 antagonist, did not modify histamine (10(-5) M)-stimulated cAMP synthesis. Histamine (10(-5) M) doubled [Ca2+]i in GPTSM. A 24-h pretreatment of GPTSM cells with 10(-6) M dexamethasone enhanced cAMP synthesized in response to 10(-5) M histamine and to 5 x 10(-6) M forskolin but did not significantly alter either the affinity or the binding capacity for [3H]-tiotidine, an H2-receptor antagonist. These results indicate that GPTSM cells in culture express H2 but not H3 receptors, which are linked to adenylate cyclase; their functional expression does not seem to be modulated by the concurrent activation of H1 receptors, whose presence in GPTSM is evidenced by a histamine-stimulated increase in [Ca2+]i. The most likely site of action of dexamethasone in enhancing histamine-stimulated cAMP synthesis is at the level of adenylate cyclase since the steroid had no effect on the H2 receptor itself.

Adenylyl Cyclases↗
PubMed1991

Circadian rhythm in adenosine A1 receptor of mouse cerebral cortex.

In order to investigate diurnal variation in adenosine A1 receptors binding parameters, Bmax and Kd values of specifically bound N6 - cyclohexyl-[3H]adenosine were determined in the cerebral cortex of mice that had been housed under controlled light-dark cycles for 4 weeks (light on from 7.00 to 19.00 h). Significant differences were found for Bmax values measured at 3-hr intervals across a 24-h period, with low Bmax values during the light period and high Bmax values during the dark period. The amplitude between 03.00 and 18.00 hr was 33%. No substantial rhythm was found in the Kd values. It is suggested that the changes in the density of A1 receptors could reflect a physiologically-relevant mechanism by which adenosine exerts its modulatory role in the central nervous system.

Adenosine↗
PubMed1990

Characterization of the receptor for keratinocyte growth factor. Evidence for multiple fibroblast growth factor receptors.

Keratinocyte growth factor (KGF) is a member of the fibroblast growth factor (FGF) family. KGF exhibits potent mitogenic activity for a variety of epithelial cell types but is distinct from other known FGFs in that it is not mitogenic for fibroblasts or endothelial cells. We report saturable specific binding of 125I-KGF to surface receptors on intact Balb/MK mouse epidermal keratinocytes. 125I-KGF binding was completed efficiently by acidic FGF (aFGF) but with 20-fold lower efficiency by basic FGF (bFGF). The pattern of 125I-acidic FGF binding and competition on Balb/MK keratinocytes and NIH/3T3 fibroblasts suggests that these cell types possess related but distinct FGF receptors. Scatchard analysis of 125I-KGF binding suggested major and minor high affinity receptor components (KD = 400 and 25 pM, respectively) as well as a third high capacity/low affinity heparin-like component. Covalent affinity cross-linking of 125I-KGF to its receptor on Balb/MK cells revealed two species of 115 and 140 kDa. KGF also stimulated the rapid tyrosine phosphorylation of a 90-kDa protein in Balb/MK cells but not in NIH/3T3 fibroblasts. Together these results indicate that Balb/MK keratinocytes possess high affinity KGF receptors to which the FGFs may also bind. However, these receptors are distinct from the receptor(s) for aFGF and bFGF on NIH/3T3 fibroblasts, which fail to interact with KGF.

Animals↗
PubMed1990

[Ileal stenosis caused by chronic granulomatous inflammation secondary to a foreign body simulating Crohn disease].

A case of ileal stenosis due to foreign body induced chronic granulomatous inflammation simulating Crohn's disease with onset on an ileo-ileostomy carried out 23 years before due to iatrogenic rupture of ileal loop following clandestine abortion is reported. After noting the problem of attributing to the foreign body alone responsibility for the stenosis, the hypothesis that it might have been an acute occurrence of Crohn's disease or the expression of an association of Crohn's disease and granulomatous inflammation due to surgical material is advanced. This for the moment is the only plausible cause. It is concluded that for accurate nosological classification and, therefore, definitive clinical diagnosis, prolonged clinical control of the patient is indispensable.

Constriction, Pathologic↗
PubMed1990

Adenosine receptors in cortical-derived vesicles of the rat: studies on binding sites and accumulation of cyclic AMP.

A vesicular preparation derived from the cerebral cortex of the rat was used to obtain, under the same experimental condition, binding parameters and stimulation data for cyclic AMP. Two analogues of adenosine were employed in the binding studies: [3H]NECA, a mixed A1/A2 agonist and [3H]CHA, a more selective A1 agonist. The [3H]CHA seemed to bind to a single high affinity site (Kd = 1.31 nM, Bmax = 0.327 pmol bound); saturation data for [3H]NECA were resolved for the presence of a high and a low affinity binding site (Kd1 = 3.08 nM, Bmax1 0.115 pmol bound; Kd2 = 204 nM, Bmax2 1.59 pmol bound), but only when calcium ions were omitted from the incubation medium. At 0 degree C, [3H]NECA bound to a single, low affinity site; the presence of calcium ions (1 mM) significantly reduced the affinity of [3H]NECA (Kd 419 nM), with respect to the absence of calcium (Kd 208 nM), without affecting the Bmax value. The influence of calcium ions was also investigated on the binding of [3H]CHA and a reduction of the Bmax value (36%) was found. Regardless of the presence or the absence of calcium ions, NECA stimulated accumulation of cyclic AMP in a dose-dependent way with an EC50 of 2.79 microM; this value did not correlate with the Kd of the low affinity binding site for [3H]NECA. Thus, the purpose of establishing a correlation between binding sites for analogues of adenosine and the site in the cerebral cortex through which the accumulation of cyclic AMP is induced, was not achieved. It is concluded that the stimulatory effect of analogues of adenosine on adenylate cyclase might not be a receptor-mediated effect. The complex influence of calcium ions on affinity and binding capacity of analogues of adenosine is discussed.

Adenosine↗
PubMed1988

5'-N-ethylcarboxamido[8-3H]adenosine binds to two different adenosine receptors in membranes from the cerebral cortex of the rat.

In the present study it is reported that [3H]NECA binds in a specific and saturable manner to membranes from the cerebral cortex of the rat. Scatchard analysis revealed two binding sites. The high affinity binding site (Kd 10.66 +/- 5 nM, Bmax 0.305 +/- 0.05 pmol/mg prot) was characterized by the following features: maximum binding at 25 degrees C, sensitivity to pretreatment with NEM and regulation by Gpp[NH]p, enhancing of binding in the presence of 1.0 mM MgCl2 and 1.5 mM CaCl2; the rank order of potency of several analogues of adenosine in competing with [3H]NECA for binding, was CHA greater than L-PIA greater than NECA greater than CADO. The low affinity binding site (Kd261.8 +/- 50 nM, Bmax 4.19 +/- 0.33 pmol/mg prot) showed maximum binding at 0 degrees C, insensitivity to pretreatment with NEM up to 1 mM and to regulation by Gpp[NH]p, and inhibition of binding in the presence of MgCl2 and CaCl2. The low affinity site was also present in membranes not pretreated with adenosine deaminase and, even in this condition, an IC50 of 188.5 +/- 36 nM for NECA and an IC50 of 4.35 +/- 0.20 microM for adenosine were found. It is concluded that the high affinity binding site is similar to the A1 adenosine receptors. The low affinity binding site is not classifiable among the A-type adenosine receptors, although it shows peculiar features shared both with the human platelet A2 receptor and the adenosine receptor formerly studied with [3H]adenosine in membranes from the brain of the rat; these results could reflect heterogeneity of adenosine receptors in central nervous system.

Adenosine↗
PubMed1988

Synthesis of 1H-pyrazolo[4,3-d]pyrimidine-7(6H)-ones and pyrazolo-5-carboxamides and interaction with benzodiazepine and adenosine A1 receptors in rat cerebral cortex.

The effects of several newly synthesized pyrazolo [4,3-d] pyrimidine-7-ones and pyrazolo-5-carboxamides on [3H]-flunitrazepam and [3H]-cyclohexyladenosine binding in rat cerebral cortex membranes have been studied. The compounds under examination, displaying affinities in the micromolar range for both benzodiazepine and adenosine A1 receptors, could be of interest in the study of a possible link between the two receptor systems.

Animals↗
PubMed1987

Effects of an atypical barbiturate (valofan) on spontaneous and stimulated locomotor activity and on brain serotonin metabolism in mice.

The effects of an atypical barbiturate, 2-allophanyl-2-allyl-4-valerolactone (valofan), have been studied on spontaneous locomotor activity and amphetamine-induced hypermotility in mice. Some serotonergic agents were employed in order to evaluate the possible involvement of serotonin on its mechanism of action. Valofan (250 and 500 mg/kg) always reduced spontaneous locomotion and amphetamine-induced hypermotility; after the administration of L-tryptophan (10 mg/kg) and tranylcypromine (1 mg/kg) both locomotions decreased; when administered in combination with valofan they resulted in an additive effect. Similar results have been obtained by administration of 5-methoxy-N,N-dimethyltryptamine (1 mg/kg) and pindolol (5 mg/kg) alone or combined with valofan. Valofan affected the serotonin metabolism increasing 5-HT and 5-HIAA concentrations in a dose dependent way in the cortex, in the brainstem or in total brain. No correlation seems to exist between the effects of valofan, on its own or combined with serotonergic agents, on motor activity and its effects on the accumulation of 5-HT and 5-HIAA. We can therefore suggest that valofan manifests its central effects by an unclear mechanism which cannot completely be accounted for its metabolic effects on cerebral serotonin and dopamine.

Animals↗
PubMed1986

Co-activation of protein kinase C and NADPH oxidase in the plasma membrane of neutrophil cytoplasts.

Enucleated, granule-free neutrophil cytoplasts, which in hypotonic media fully release cytosolic components and generate ghosts, have been used to study the cell localization of protein kinase C (PK-C). Treatment of cytoplasts with phorbol myristate acetate, a potent activator of neutrophil functions, triggers translocation of PK-C from the cytosol to the plasma membrane, with an activity recovery of 83 +/- 16%. In the ghost fraction, PK-C catalyzes the phosphorylation of polypeptides with an apparent mol. wt. of 115K, 89K, 79K, 62K, 47K and 19K. From the plasma membrane PK-C can be extracted in an active form by Triton X-100 but not by EGTA. Translocation of PK-C is already evident at 5 sec and plateaus at about 50 sec. Activation of plasmalemmal, O-2 generating NADPH oxidase by the phorbol ester is delayed by about 20 sec with respect to the activation of PK-C. Dose/response experiments show that the pattern of activation of O-2 generation by cytoplasts strictly superimposes with the pattern of PK-C translocation.

Adenosine Triphosphate↗
PubMed1985

Activation of protein kinase C in neutrophil cytoplasts. Localization of protein substrates and possible relationship with stimulus-response coupling.

Treatment of enucleated, granule-free neutrophil cytoplasts with the protein kinase C activator phorbol 12-O-myristate-13-acetate (PMA) causes an increased 32P-incorporation into a variety of polypeptides. Permeabilization of PMA-stimulated, 32P-labeled cytoplasts by 0.01% digitonin fully releases the majority of these phosphorylated proteins. A statistically significant correlation is found between the extent of PMA-induced activation of generation of superoxide anion (O2-) and the phosphorylation of a cytosolic polypeptide with an apparent Mr of 46,000, whose 32P-labeling is also enhanced by the treatment of cytoplasts with 1-oleyl-2-acetylglycerol, the Ca2+ ionophore ionomycin or latex beads. Furthermore, treatment of cytoplasts with the protein kinase C inhibitor trifluoperazine markedly inhibits the 32P-labeling of proteins in the 40 000 Mr range, including the 46 kDa polypeptide, and almost totally abolishes the activation of O2- production by PMA.

Animals↗
PubMed1984

Mobilization of heparan sulfate induced by immunostimulation in a patient with mucopolysaccharidosis IIIA.

Unspecific immunostimulation by bacterial vaccines of a patient with mucopolysaccharidosis IIIA (Sanfilippo A) syndrome induces a marked increase in the urinary excretion of heparan sulfate and of uronate-containing oligosaccharides. This event is presumably linked to an increased vascular permeability and exocytosis of storage material, elicited by mediators of inflammation, as well as to enhanced degradation of stored polymers in activated macrophages and surrounding tissue.

Bacterial Vaccines↗
PubMed1984

C. T. criteria of the differential diagnosis in primary retroperitoneal masses.

This personal series of 44 primary retroperitoneal masses (P.R.P.M.) studied by C. T. is analyzed. The reliability of C. T. in the identification (44/44), characterization (43/44) and origin evaluation (41/44) of P.R.P.M. has been absolutely satisfactory. In particular, those criteria of C. T. diagnosis which may be utilized in the evaluation of the origin of upper abdominal masses are thoroughly described. The evaluation of the involvement (non invasive; invasive) of adjacent viscera has been achieved in 22/38 P.R.P.M. verified at operation. The evaluation of tumour resectability has been less reliable due to the high incidence of under-diagnosis (60% in our personal experience). C. T. may be used in addition as an aid to different diagnostic techniques (percutaneous guided needle biopsy) or to therapy (drainage of retroperitoneal abscesses). C. T. is absolutely necessary in the follow-up of P.R.P.M. after surgery, radiotherapy or chemotherapy.

Adrenal Gland Neoplasms↗
PubMed1980

[DPA and clonazepam activity in febrile convulsions: preliminary results].

A pharmacological trial has been performed for the prophylaxis of febrile convulsions in childhood. The administration of two antiepileptic drugs, Sodium Valproate and Clonazepam, reduces significantly seizures occurrence compared with unmedicated controls. Furthermore, Sodium Valproate has been found to be more effective than Clonazepam. Both anticonvulsants are thought to act by a Gabaergic modulation in CNS.

Benzodiazepinones↗