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P Preziosi

Publications and source records attributed to P Preziosi.

At least 109 records · Page 6Linked to original sources
PubMed1996

[Iron accumulation in the liver of patients with thalassemia major assessed with low field strength magnetic resonance: correlation with clinico-instrumental parameters].

Eight transfusion dependent patients (3 women and 5 men) with thalassemia major undergoing long-term treatment with Desferoxamine were submitted to MRI, with T2* GE sequences and low field strength. The ratio between liver mean signal intensity and skeletal muscle (L/M) and the ratio between the former and subcutaneous fat (L/F) were calculated in all patients. The results were compared with those of a control group of 7 healthy volunteers (7 men). L/M and L/F ratios were separately correlated with the following parameters: patient's age, transfusion history, serum ferritin, ferritin peak and its onset, transaminases (AST and ALT) and chelation index. The latter is a complex parameter allowing the actual assessment of iron content and of the real efficacy of chelation therapy. In all patients, both the L/M and the L/F ratios decreased significantly (L/M ratio: 0.67 +/- 0.45 vs. 1.2 +/- 0.21, p < 0.02; L/F ratio: 0.39 +/- 0.15 vs. 0.84 +/- 0.11, p < 0.001) relative to the control group. No significant correlation was found between the ratios and any hematochemical parameter, except for r = 0.77 (p < 0.04) between L/F ratio and the chelation index. Our study demonstrates that MRI may play a major role in the examination of thalassemic patients even at low field strength and with GE sequences, which yield good quality images with a relatively short acquisition time. Thus, MRI can be suggested for routine liver studies thanks to its high quality depiction of the liver and to its qualitative and semiquantitative yield. The good correlation between L/F ratio and the chelation index permits MR evaluation of the efficacy of different chelation treatments.

Adolescent↗
PubMed1996

Effect of 6 month supplementation with different combinations of an association of antioxidant nutrients on biochemical parameters and markers of the antioxidant defence system in the elderly. The Geriatrie/Min.Vit.Aox Network.

OBJECTIVES: To study the effect of supplementation with an association of small physiological amounts of antioxidant nutrients upon biochemical parameters and indicators of oxidative stress and antioxidant enzymes. DESIGN: The study included a double-blind placebo-controlled design. SETTING: Nursing homes in different areas in France. SUBJECTS: 575 elderly long term hospitalized subjects aged 65-103 years. INTERVENTION: Four groups were compared. They received daily: (V) vitamins (vitamin E, 15 mg and vitamin C, 120 mg) and beta-carotene, 6 mg; (T) trace elements (zinc, 20 mg, selenium, 100 micrograms); (VT) vitamins associated with trace elements; or (P) a placebo. Biological markers of vitamin and trace element status, and free radical parameters were measured initially and after 6 months of supplementation. RESULTS: An analysis of variance indicated a significant effect of vitamin supplementation on serum alpha-tocopherol, beta-carotene and vitamin C, a significant effect of trace element supplementation on serum zinc and both a significant trace element and a vitamin-trace element interaction on serum selenium. We observed significant effects of both trace element and vitamin supplementation on GPx activity (P < 0.01), an effect of vitamin supplementation on SOD activity (P < 0.05). CONCLUSION: Our results indicate that short-term supplementation with moderate doses of antioxidant vitamins and trace elements in elderly subjects clearly improves both non-enzymatic (alpha-tocopherol, beta-carotene, vitamin C) levels and enzymatic antioxidant (GPx and SOD) activity.

Aged↗
PubMed1996

[Role of computerized tomography in bladder carcinoma treated with simultaneous combined radiotherapy and chemotherapy].

We report on the pneumocystography-CT follow-up of locally aggressive bladder carcinoma patients treated with combined and simultaneous irradiation and chemotherapy. Particular attention was paid to assess residual thickening of the wall involved by the tumor, which is the most critical parameter to discriminate a persistent from a resolved condition. We examined 16 patients (mean age: 66.5 years) with histologically locally advanced urinary bladder cancer staged T2-T3. All patients underwent the first CT exam of the bladder with the pneumocystography technique before therapy, for disease staging, another exam after chemotherapy and a third one after simultaneous irradiation and chemotherapy. The endoluminal mass completely regressed in all cases, with normal endoscopic findings. In 9 of 16 cases, the bladder wall was thickened in the tumor site, with normal mucosal surface. The histology of bioptic specimens obtained during cystoscopy showed a high frequency of phlogistic reactions from foreign bodies, corresponding to the bladder wall thickening seen on CT images. We conclude that, in extensive neoplastic bladder wall involvement, therapy-induced histologic regressive phenomena can cause a granulomatous reaction in the bladder wall, thus thickening it, which is the most frequent sign in these cases but that, in our experience, was never associated with tumor invasion. This should be always considered in the CT studies performed after this kind of combined treatment.

Aged↗
PubMed1996

[Study of prostatic carcinoma with ultrasonography and magnetic resonance with "dedicated" surface coil].

We investigated the role of an experimental surface coil for low field (0.2 T) MRI of prostatic gland carcinoma; the study was performed comparing MRI with US findings and with bioptic and pathologic results. To this purpose, 16 patients with prostatic cancer suspected at US and demonstrated with US-guided biopsy, were examined with low intensity field (0.2 T) MRI performed with a dedicated saddle-shaped coil and a body coil. This experimental surface coil with perineal application is used to study the prostatic gland with low field MR equipment where no transrectal probe is available. We analyzed the results of this study and found that, in all patients but one, the neoplastic lesions exhibited low signal intensity on T2-weighted images, while the normal gland was hyperintense. Six patients underwent radical prostatectomy and diagnostic imaging findings were correlated with pathologic findings obtained with whole mount specimens and serial histologic slides. The number of tumor foci, their site and size, and stromal reaction were studied on T2-weighted images; the typical low signal intensity was absent in one of 16 patients, in which case the microscopic exam of pathologic specimens showed extensive tumor spread with infiltration of perineural lymphatic vessels, with neither nodular patterns nor stromal reactions. The correlation between MR findings and the whole mount specimens (n = 6) demonstrated MR underestimation of tumor spread. In our opinion, this technique is useful for the detection and characterization of prostatic lesions, in spite of the presence of isointense lesions and the risk of underestimating the disease, especially to the prostatic capsule. To conclude, the dedicated surface coil can improve the diagnostic accuracy of low field MRI.

Adenocarcinoma↗
PubMed1995

A possible role for nitric oxide but not for prostaglandin E2 in basal and interleukin-1-beta-induced PRL release in vitro.

In previous experiments we have shown that nitric oxide (NO) was able to modulate CRH and ACTH release from cultured rat hypothalamic and anterior pituitary cells, in vitro. Now, we show experimental evidence of an involvement of NO in basal and interleukin-1 beta-induced prolactin (PRL) release. L-NG-nitro-arginine, an inhibitor of nitric oxide synthetase, and hemoglobin, a NO scavenger, impaired basal and interleukin-1-beta-induced PRL release, while molsidomine, a NO donor, was able to release PRL and to amplify interleukin-1-beta-induced PRL release, confirming a modulatory role for nitric oxide in pituitary hormone secretion. On the other hand, no evidence regarding a possible role of prostaglandin E2 (PGE2) in IL-1beta-induced PRL release came out from our experiments.

Animals↗
PubMed1995

Interleukin-1 receptor antagonist displays intrinsic agonist activity on rat gastric fundus motility in vitro.

It has been shown previously that both forms of interleukin-1, 1 alpha and 1 beta, produce dose-dependent relaxation of the rat gastric fundus in vitro, accompanied by an increased production and release of eicosanoids. This effect appears to be mediated, at least in part, by leukotrienes, since the inhibition of 5-lipoxygenase by specific drugs counteracts interleukin-1-induced gastric relaxation. In the present study, we attempted to antagonize interleukin-1-induced inhibition of gastric fundus motility with a interleukin-1 receptor antagonist. Surprisingly, the interleukin-1 receptor antagonist itself possessed interleukin-1-like agonist activity, since: (a) it produced rapid, dose-dependent relaxation of the rat gastric fundus, with an estimated EC50 of 70 pg/ml and a maximal effect at 10 ng/ml; (b) interleukin-1 receptor antagonist-induced relaxation was dose dependently inhibited by N-(3-phenoxycinnamyl)acetohydroxamic acid (BW A4c), a specific inhibitor of 5-lipoxygenase; (c) in the first 5 min after its addition to the bath solution, interleukin-1 receptor antagonist produced a significant increase in prostaglandin E2 release from the gastric strips. This evidence suggests that, shortly after receptor occupancy, in this experimental model interleukin-1 and interleukin-1 receptor antagonist share the same pattern of mechanical and biochemical activities.

Analysis of Variance↗
PubMed1995

Evidence that the interleukin-1 beta-induced prostaglandin E2 release from rat hypothalamus is mediated by type I and type II interleukin-1 receptors.

Interleukin-1 beta (IL-1 beta) has been shown to specifically increase the release of prostaglandin (PG) E2 from rat hypothalamic explants in short-term experiments. In this study we attempted to characterize the receptor subtype(s) involved in this response. Rat hypothalamic explants were incubated with mouse monoclonal antibodies (mAbs) raised against human IL-1 type I or type II receptors, IL-1 receptor antagonist (IL-1ra) and alpha-melanocyte-stimulating hormone (alpha-MSH) (which appears to antagonize certain IL-1 induced inflammatory effects in vivo), alone and in the presence of IL-1 beta. PGE2 released into the incubation medium was measured by radioimmunoassay. The anti-type I mAb reduced both basal and IL-1 beta-stimulated PGE2 release at 10 micrograms/ml, but not at lower concentrations. The anti-type II mAb also produced a significant decrease in stimulated release but had no effect on basal release. IL-1ra mimicked the effects of the anti-type I mAb, while alpha-MSH failed to alter either basal or stimulated PGE2 release. These findings suggest that IL-1 beta controls production and release of PGE2 by the rat hypothalamus via both type I and type II receptors, although the latter appear to be involved only in the response to high levels of IL-1.

Animals↗
PubMed1995

Effects of vindesine on hypothalamic-pituitary-adrenal axis.

Vindesine, a cell-cycle-specific agent currently employed in the treatment of some neoplasias, was able to produce a remarkable dose-dependent adrenocortical activation, but it was unable to increase plasma corticosterone in hypophysectomized rats in vivo. In addition, vindesine was able to increase ACTH release in vitro when tested on isolated pituitary cells in culture suggesting a direct involvement of the pituitary gland in the increase of adrenal secretion in vivo.

Adrenocorticotropic Hormone↗
PubMed1995

Anticancer drug toxicity via cytokine production: the hydroxyurea paradigm.

Our previous observations on the toxic effects of hydroxyurea (HU) in adrenalectomized (ADX) rats prompted us to suggest that these effects might be mediated by an increased synthesis of proinflammatory cytokines. This study was conducted to determine whether HU stimulates cytokine gene expression in vivo. The polymerase chain reaction (PCR) technique was used to assess levels of mRNA for interleukin-1 alpha (IL-1 alpha), tumor necrosis factor (TNF) and interleukin-4 (IL-4) in spleen cells from intact and ADX rats treated with HU or vehicle. In ADX rats, expression of proinflammatory-cytokine mRNA was markedly increased by HU, but no expression of these genes was seen in intact animals after treatment. In the latter rats, cytokine-gene expression seemed to be down-regulated by HU-induced elevations in plasma corticosterone levels, since IL-1 alpha and TNF transcripts could be detected only after corticosterone levels had returned to normal (24 h after treatment). Interestingly, IL-4 mRNA could not be detected in either treated or untreated ADX rats, indicating that expression of this gene is closely related to circulating levels of corticosterone. These findings strongly suggest that the increased toxicity displayed by HU in ADX animals is mediated by stimulation of cytokine synthesis in vivo.

Adrenalectomy↗
PubMed1995

[Motivations of volunteers for participation in an interventional study in the field of nutritional prevention: results of a pilot study of the SU.VI.MAX project].

In this paper, we try to understand the motivations and characteristics of people susceptible to be volunteers for the SU.VI.MAX study. The objective of this study will be to recruit and to follow during 8 years, a cohort of 15,000 subjects at a national level, for an intervention trial in the field of nutritional prevention. A short media campaign has been organised to recruit "1,000 volunteers to help to test and to validate tools specifically developed for the SU.VI.MAX study". In total, 15,789 subjects matching selection criteria answered to our invitation. All received a short questionnaire; 10,984 sent back correctly filled up questionnaires (70%) and 1005 were selected at random for a complete analysis. A lexical analysis of motivations disclosed 6 different groups organised in two poles. The pole of true altruists with a speech relative to notions such as "volunteers-benevolent" (7% of subjects), wishes to participate to a "humane task" (9% of subjects) or to progress of medical research (27% of subjects). The other pole corresponds to people interested personally by the theme of the project with 3 kinds of speech: personal past history (13% of subjects), interest for foods fortified with vitamins and/or minerals (19% of subjects) or for relationships between food consumption and health (22% of subjects).

Adult↗
PubMed1994

Evidence that interleukin-1 beta and tumor necrosis factor inhibit gastric fundus motility via the 5-lipoxygenase pathway.

In this study, we compared the effects of interleukin-1 beta and tumor necrosis factor (TNF) on in vitro rat gastric fundus motility. Interleukin-1 beta produced rapid, concentration-dependent relaxation of rat gastric fundus strips, similar to that seen with TNF, with a maximal effect at 30 U/ml and an estimated EC50 at 0.9 U/ml. The relaxant effects of interleukin-1 beta and TNF were not influenced by the inhibition of cyclooxygenase or nitric oxide-synthase activities. Interleukin-1 beta- and TNF-induced gastric relaxations were concentration dependently inhibited by BW 755c, which inhibits both cyclooxygenase and lipoxygenase, BW A4, which selectively inhibits the 5-lipoxygenase pathway, and SC 41930, a selective leukotriene B4 receptor antagonist, providing pharmacological evidence that leukotriene B4 is involved in the relaxant effects of both cytokines. The interleukin-1 beta- and TNF-induced activation of 5-lipoxygenase pathway did not appear to be triggered by phospholipase A2. An alternative pathway could involve the following steps: (i) activation of phospholipase C and the formation of diacylglycerol; (ii) diacylglycerol-induced activation of protein kinase C; (iii) formation of free arachidonic acid from diacylglycerol by diacylglycerol-lipase. This mechanism is suggested by the finding that leukotriene B4 is able to mimic cytokine-induced strip relaxation only in the presence of phorbol 12-myristate 13-acetate, which selectively activates protein kinase C.

Animals↗
PubMed1994

Effects of lipopolysaccharide on hypothalamic-pituitary-adrenal axis in vitro.

The possible involvement of lipopolysaccharide (LPS) and interleukin-1 beta (IL-1 beta) and their eventual interplay in CRH and ACTH release from cultured hypothalamic and pituitary cells respectively, have been studied. IL-1 beta was able to activate the hypothalamo-pituitary-adrenal axis at both hypothalamic and pituitary sites; LPS showed no direct action at hypothalamic level but it was able to inhibit basal and IL-1 beta-induced ACTH release: this could be responsible for a blunting of the adrenal cortex response that normally occurs in septic shock syndrome.

Adrenocorticotropic Hormone↗
PubMed1994

Regulation of interleukin 6 production by cAMP-protein kinase-A pathway in rat cortical astrocytes.

In this study we analysed the involvement of the cAMP-protein kinase-A system in the regulation of interleukin 6 production by cultured cortical astrocytes. Vasoactive intestinal peptide strongly increased, in a dose-dependent manner, interleukin 6 production. This effect was reduced when protein kinase A was blocked by KT-5720; it was not affected by calphostin C, a protein kinase C inhibitor. Forskolin caused a concentration-dependent increase in interleukin 6 release, that was also inhibited by KT-5720. Since prostaglandins are believed to play a role in interleukin 6 production, we tried to determine whether the stimulatory effects of vasoactive intestinal peptide and forskolin on cytokine release might be mediated by stimulation of prostaglandin production in cortical astrocytes. Vasoactive intestinal peptide did not increase the production of either prostaglandin E2 or F2 alpha. Conversely, forskolin concentration-dependently stimulated the production of both prostaglandins, an effect that was blocked by indomethacin. Indomethacin did not affect either vasoactive intestinal peptide- or forskolin-stimulated interleukin 6 production. To exclude the possibility that prostaglandins participate in interleukin 6 production induced by forskolin, we tested the effect of prostaglandins E2 and F2 alpha on the cytokine production. The former was completely ineffective in eliciting the cytokine production, while prostaglandin F2 alpha slightly increase interleukin 6 only at the highest concentration. 8-Br-cAMP and (BU)2- cAMP stimulated interleukin 6 production to a lesser extent than vasoactive intestinal peptide and forskolin. In conclusion, we provide evidence that vasoactive intestinal peptide increases interleukin 6 production by astrocytes through the stimulation of the cAMP-protein kinase-A pathway, an effect that is reproduced by cAMP analogues. In addition, we point out that prostaglandins are not involved in vasoactive intestinal peptide- and forskolin-mediated induction of interleukin 6 production in cultured astrocytes.

Animals↗
PubMed1994

Interleukin-1 beta- and tumour-necrosis-factor-induced inhibition of rat gastric fundus motility in vitro.

In this study, we compared the effects of interleukin-1 beta (IL-1 beta) and tumour necrosis factor (TNF) on in vitro rat gastric fundus motility. IL-1 beta and TNF produced rapid, concentration-dependent relaxation of the rat gastric fundus strips with maximal effect at 300 pg ml-1 and 10 ng ml-1, and estimated EC50S at 10 and 450 pg ml-1, respectively. The relaxant effects of IL-1 beta and TNF were not influenced by the inhibition of cyclo-oxygenase or NO-synthase activities. IL-1 beta- and TNF-induced gastric relaxations were inhibited by BW 755c, which inhibits both cyclo-oxygenase and lipoxygenase (LO), BW A4c, which selectively inhibits the 5-LO pathway, and SC 41930, a selective leukotriene B4 (LTB4) receptor antagonist, providing pharmacological evidence that LTB4 is involved in the relaxant effects of both cytokines. The IL-1 beta- and TNF-induced activation of 5-LO pathway did not appear to be triggered by phospholipase A2. An alternative pathway could involve the activation of a phospholipase C, specific for phosphatidylcholine, from which, in sequence: the formation of diacylglycerol (DAG), DAG-induced activation of protein kinase C and the formation of free arachidonic acid from DAG would ensue. This mechanism is suggested by the finding that LTB4 is able to mimic cytokine-induced strip relaxation only in the presence of phorbol 12-myristate 13-acetate, which selectively activates protein kinase C.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1994

Vasoactive intestinal peptide and forskolin stimulate interleukin 6 production by rat cortical astrocytes in culture via a cyclic AMP-dependent, prostaglandin-independent mechanism.

In this study we analyzed the involvement of the cyclic AMP (cAMP)-protein kinase A system in the regulation of interleukin 6 production by cultured cortical astrocytes. Vasoactive intestinal peptide strongly increased, in a dose-dependent manner, interleukin 6 production. This effect was reduced when protein kinase A was blocked by KT-5720; it was not affected by calphostin C, a protein kinase C inhibitor. Forskolin caused a concentration-dependent increase in interleukin 6 release that was also inhibited by KT-5720. Because prostaglandins are believed to play a role in interleukin 6 production, we tried to determine whether the stimulatory effects of vasoactive intestinal peptide and forskolin on cytokine release might be mediated by stimulation of prostaglandin production in cortical astrocytes. Vasoactive intestinal peptide did not increase the production of either prostaglandin E2 or F2 alpha. Conversely, forskolin concentration-dependently stimulated the production of both prostaglandins, an effect that was blocked by indomethacin. Indomethacin did not affect either vasoactive intestinal peptide- or forskolin-stimulated interleukin 6 production. To exclude the possibility that prostaglandins participate in interleukin 6 production induced by forskolin, we tested prostaglandins E2 and F2 alpha. The former was completely ineffective in eliciting the cytokine production, whereas prostaglandin F2 alpha slightly increased interleukin 6 production only at the highest concentrations. 8-Bromo-cAMP and dibutyryl-cAMP stimulated interleukin 6 production to a lesser extent than vasoactive intestinal peptide and forskolin. In conclusion, we provide evidence that vasoactive intestinal peptide increases interleukin 6 production by astrocytes through the stimulation of the cAMP-protein kinase A pathway, an effect that is reproduced by cAMP analogues.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Peptide histidine isoleucine-like immunoreactivity release from the rat gastric fundus.

1. Longitudinal muscle strips from the rat gastric fundus were subjected to in vitro electrical field stimulation (EFS) under non-adrenergic non-cholinergic (NANC) conditions to study the release of peptide histidine isoleucine-like immunoreactivity (PHI-LI) and the correlation between PHI-LI release and NANC relaxation. 2. Different radioimmunoassay (RIA) systems employing C-terminal- and N-terminal-specific anti-PHI sera were used to determine the relative contributions of PHI and its C-terminally extended forms, peptide histidine glycine (PHI-Gly) and peptide histidine valine [PHV(1-42)], to the PHI-LI released by the rat gastric fundus. 3. In the presence of atropine (1 microM) and guanethidine (5 microM), EFS (120 mA, 1 ms, 0.25-32.0 Hz, trains of 2 min) induced frequency-dependent relaxations of 5-hydroxytryptamine (3 microM) pre-contracted strips. 4. EFS at frequencies of 8-32 Hz evoked significant increases in PHI-LI outflow. The increases in PHI-LI outflow evoked by 16-Hz EFS were abolished by tetrodotoxin (3 microM) and by a calcium-free medium, indicating an active release process from intramural nerves. 5. The EFS-induced release of PHI-LI measured with the N-terminal-specific antiserum was significantly greater than that detected with the C-terminal-specific antisera. 6. Sephadex G-25 gel permeation chromatographic analysis was performed on the PHI-LI release in response to 32-Hz EFS. A C-terminal-specific antiserum revealed one peak co-eluting with the rat PHI standard. When PHI-LI was measured with the N-terminal-specific antiserum, two peaks were found that co-eluted with the rat PHV(1-42) and rat PHI-Gly/PHI standards, respectively. 7. The present data suggest that the extended forms of PHI are the primary components of the PHI-LI released by NANC inhibitory neurones in the rat gastric fundus and support a NANC inhibitory neurotransmitter role for PHI and its extended forms in this tissue.

Animals↗
PubMed1994

Release of immunoreactive interleukin-1-alpha from rat hypothalamic explants is increased by bacterial lipopolysaccharide and high KCL concentrations.

It has previously been shown that interleukin (IL)-1-like bioactivity is released from rat hypothalamic explants in short-term incubations. Experiments conducted with antiserum against IL-1 alpha or IL-1 beta showed that IL-1 alpha is released more abundantly under basal conditions. For the present study, we developed a specific radioimmunoassay to investigate the release of immunoreactive (ir) IL-1 alpha from the rat hypothalamus in short-term experiments, and observed that release of irIL-1 alpha increased with time and was significantly increased by high KCL concentrations. The stimulatory effect of 28 mM KCL was significantly inhibited by verapamil. Subsequent investigation of the effects of putative modulators of IL-1 alpha secretion, bacterial lipopolysaccharide (LPS) and the prostaglandins E2 (PGE2) and F2 alpha (PGF2 alpha), showed that irIL-1 alpha release was stimulated by 100 ng/ml LPS, but not by higher concentrations, PGE2 had no effect and PGF2 alpha caused dose-dependent inhibition. However, the latter did not seem to exert a tonic inhibitory influence on irIL-1 alpha release, since blockade of cyclo-oxygenase activity by indomethacin had no effect on cytokine release under basal conditions. We conclude that LPS stimulates and PGF2 alpha inhibits basal release of hypothalamic IL-1 alpha, the characteristics of the secretion of which suggest that it may be, at least in part, of neuronal origin.

Animals↗