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Biomedical subjects

A Tedeschi

Publications and source records attributed to A Tedeschi.

At least 73 records · Page 4Linked to original sources
PubMed1996

Impairment of the inhibitory effect of sodium on basophil histamine release in patients with systemic sclerosis.

It has been demonstrated that Na+ down-regulates IgE-dependent and IgE-independent histamine release from basophils of normal subjects. The aim of this study was to evaluate whether Na+ exerts its inhibitory effect on basophil histamine release in patients with systemic sclerosis (SSc). Peripheral blood leucocytes were stimulated with anti-IgE, n-formyl-methionyl-leucyl-phenylalanine (fMLP) and IL-3 in the presence of high and low Na+ concentrations, and histamine release was measured by a fluorometric method. The dose-response curves of histamine release induced by the above stimuli were similar in SSc patients (n=15) and in normal subjects (n=39). Na+ removal from the extracellular medium and its isosmotic replacement with choline chloride led to a significant increase of anti-IgE-and fMLP-induced histamine release in normal subjects, but not in SSc patients. In the former population, histamine release induced by an optimal dose of anti-IgE (1/5000) was 26.4+/-3.1% in high Na+ and 59.3+/-3.5% in low Na+ (mean+/-s.e.m., P<0.0001), whereas in the latter population mean histamine release was 20.4+/-5.1% in high Na+ and 15.8+or-2.9% in low Na+ (p NS). A similar trend was observed when basophils were stimulated with fMLP. Na+ exerted a dose-dependent inhibitory effect on anti-IgE- and fMLP-induced histamine release in normal subjects, but not in SSc patients. IL-3-induced histamine release from basophils of SSc patients was increased in a low-Na+ solution, but to a lesser extent when compared with normal controls. Therefore basophils from normal subjects and SSc patients behave in a different way when stimulated in a low-Na+ medium. The inhibitory effect of Na+ on basophil histamine release is impaired in SSc patients, and this abnormality could contribute to basophil dysfunction.

Aged↗
PubMed1996

Enhancement of basophil histamine release by interleukin-3: reduced effect in atopic subjects.

The inducing and enhancing effects of interleukin-3 (IL-3) on basophil histamine release in patients with respiratory allergy (n = 28) and in normal subjects (n = 22) were compared. Leukocyte suspensions, prepared by dextran sedimentation, were stimulated with anti-IgE (1/5000), N-formyl-methionyl-leucyl-phenylalanine (FMLP, 1 microM), and IL-3 (0.1-10 ng/ml), and histamine concentration was measured by an automated fluorometric method. A trend toward higher histamine release after challenge with anti-IgE, FMLP, and IL-3 was found in atopic subjects. Preincubation of basophils with IL-3 resulted in a dose-dependent increase of anti-IgE- and FMLP-induced histamine release, with a more marked effect in nonatopic than in atopic subjects. Mean net enhancement of anti-IgE-induced histamine release by 10 ng/ml IL-3 was 2.5 +/- 5% in atopic subjects and 29.6 +/- 4.2% in nonatopic subjects (P < 0.001). The enhancement of FMLP-induced histamine release by IL-3 was 10.3 +/- 3.9% in atopic patients and 29 +/- 2.4% in nonatopic subjects (P < 0.01). In atopic subjects, a negative correlation was found between anti-IgE- or FMLP-induced histamine release and net enhancement by IL-3 (r = -0.45, P < 0.02; r = -0.48, P < 0.01, respectively). The results of this study indicate that in atopic subjects IgE-mediated histamine release can scarcely be enhanced by a basophil response modifier such as IL-3. It is conceivable that the frequent basophil stimulation in atopic patients leads to a reduced sensitivity to the enhancing effect of IL-3.

Adult↗
PubMed1996

Defective inhibition of sodium on basophil histamine release in patients with allergic rhinitis and bronchial asthma.

The aim of this study was to evaluate whether Na+ exerts its inhibitory effect on basophil histamine release induced by immunoglobulin E (IgE)-dependent (anti-IgE) and IgE-independent (N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-3 (IL-3)) stimuli in patients with allergic rhinitis (n = 24) and allergic bronchial asthma (n = 10). Peripheral blood leucocytes were stimulated with anti-IgE, FMLP and IL-3 in the presence of high and low Na+ concentrations, and histamine release was measured using a fluorometric method. In standard Na(+)-containing medium, spontaneous and stimulated histamine release was higher in allergic patients (n = 34) (both rhinitic and asthmatic) than in healthy subjects (n = 41). Na+ removal from extracellular medium and its isosmotic substitution with choline chloride or with N-methyl-D-glucamine led to a significant increase of anti-IgE-, FMLP- and IL-3-induced histamine release in normal subjects, but not in allergic patients. The increase in Na+ concentration in the extra-cellular medium was accompanied by a dose-dependent decrease of anti-IgE- and FMLP-induced histamine release in normal subjects, but not in allergic patients. The behaviour of atopics and healthy subjects was different and not related to the basophil responsiveness to activating signals. The incubation of basophils from healthy subjects with sera from allergic patients did not have a significant influence on the inhibitory effect of Na+. Basophils from healthy subjects and atopic patients respond differently when stimulated in a low Na+ medium. The reduced sensitivity to the inhibitory effect of Na+ may contribute to basophil dysfunction in patients with respiratory allergy.

Adult↗
PubMed1996

[Prognostic factors in acute nonlymphoid leukemias].

Our retrospective study was aimed at assessing parameters affecting the prognosis of acute non lymphoid leukemia (ANLL). Since 1988 to 1994 we observed 84 patients: 52 males, 32 females. For each patient we considered at diagnosis: age, fever, performance status, platelets, hemoglobin and white blood cell count, extramidollary disease, bone marrow blastosis, phenotype and cytogenetic abnormalities of blasts cells. All the parameters listed above were correlated with the time to achieve the complete remission (CR), CR duration and the overall survival. Statistical tests as t-student and chi square test were used. Statistical analysis of the parameters considered revealed that the only value affecting the achievement of a CR was the age. The prognostic significance of immunophenotyping in ANLL has been a controversial issue, with a number of conflicting reports. In our study only the terminal deoxynucleotidyl transferase was significantly associated with prognosis. Our study, as data reported in literature, confirms that the prognostic impact of the various parameters in ANLL is controversial. The study of prognostic factors and of the immunophenotype is important to identify the clinical and the biologic profile of the disease and to evaluate the optimal post-remission treatment.

Adult↗
PubMed1995

IL-3-induced histamine release from human basophils. Dissociation from cationic dye binding and down-regulation by Na+ and K+.

The effect of recombinant human IL-3 on human basophils from normal subjects was evaluated by the decrease of toluidine blue-positive basophils (TB+) and by histamine release. IL-3 (0.001 to 100 ng) caused the decrease of TB+ without concomitant histamine release, whereas anti-IgE-induced TB+ decrease was accompanied by histamine release. IL-3 enhanced both anti-IgE-induced TB+ decrease and histamine release. IL-3-induced TB+ decrease was dose- and Ca2+-dependent and related to the time of incubation (detectable after an incubation of 5 min and maximal after incubation of 2 h). When extracellular Na+ was replaced isosmotically with choline, N-methyl-D-glucamine, or glucose, histamine release also was observed after direct stimulation with IL-3. The effect was dose dependent, related to the time of incubation (detectable after 30 min and maximal after 60 min), and required extracellular Ca2+. The increase in extracellular Na+ or K+ concentrations was accompanied by a reduction of histamine release, with a more marked effect on IL-3- than on anti-IgE-induced histamine release. In line with these results, the Na+ ionophore gramicidin D, which increases Na+ influx, and the K+ channel blocker 4-aminopyridine, which decreases K+ efflux, dose-dependently inhibited anti-IgE- and IL-3-induced histamine release. The inhibitory effects on Na+ and K+ were slightly additive, suggesting an action via the same pathway, which most probably is membrane potential. These results indicate that: 1) IL-3 can induce TB+ decrease without concomitant histamine release, 2) basophils from normal subjects can release histamine on challenge with IL-3 once the inhibitory effect of Na+ is removed, and 3) Na+ and K+ down-regulate IL-3 as well as anti-IgE-induced histamine release.

4-Aminopyridine↗
PubMed1995

Antiallergic activity of loratadine: inhibition of leukotriene C4 release from human leucocytes.

The H1 antagonist loratadine has the capacity to inhibit histamine release from human basophils. The aim of this study was to investigate whether loratadine can also inhibit leukotriene C4 (LTC4) release from human leucocytes. Basophil-enriched mononuclear cell suspensions were prepared by centrifugation of peripheral venous blood (n = 10) on discontinuous Percoll gradients. Leucocytes were stimulated with anti-IgE, N-formylmethionyl-leucyl-phenylalanine (FMLP) and Ca2+ ionophore A23187; immunoreactive (i) LTC4 release in the cell supernatant was measured by a competitive radioimmunoassay and histamine release was evaluated by an automated fluorometric technique. Loratadine, in the concentration range of 1-50 microM, exerted a dose-dependent inhibitory effect on IgE-mediated and IgE-independent histamine and iLTC4 release. The concentrations inhibiting 50% of histamine release were 30 microM (anti-IgE), 27 microM (FMLP) and 19 microM (Ca2+ ionophore A23187). The concentrations inhibiting 50% of iLTC4 release were 2.3 microM (anti-IgE). 11 microM (FMLP) and 1.7 microM (Ca2+ ionophore A23187). The inhibitory activity on iLTC4 release was optimal after preincubation for 2 h at 37 degrees C, and was no longer evident when leucocytes were stimulated 2 h after cell washing. Increased extracellular Ca2+ concentrations reduced the inhibitory activity of loratadine. These results indicate that loratadine has the capacity to inhibit the release of preformed and newly generated mediators from human basophil-enriched mononuclear cell suspensions.

Basophils↗
PubMed1995

Four-year follow-up of glucose tolerance and beta-cell function in nondiabetic cystic fibrosis patients.

Plasma glucose and insulin responses to oral glucose load were investigated and reinvestigated approximately 4 years later in 29 cystic fibrosis children and adolescents with initially normal fasting blood glucose levels. Patients' clinical status was evaluated at the time of both oral glucose tolerance tests. With respect to the basal test, the second one elicited blunted insulin responses and enhanced glycemic levels. Moreover, the prevalence of patients with diabetic glucose tolerance was significantly increased at the second evaluation and insulin secretion was markedly reduced in these patients. Deterioration of glucose tolerance and/or of insulin secretion over time was never accompanied by a significant worsening of clinical and/or nutritional status. In conclusion, in cystic fibrosis subjects with fasting euglycemia (a) both insulin secretion and glucose tolerance deteriorate during a 4-year follow-up, (b) an insulin secretion decrease is more evident in patients who develop diabetic glucose tolerance and (c) these metabolic changes are not significantly linked to a worsening of either nutritional or clinical parameters, even in the patients who develop diabetic glucose tolerance.

Adolescent↗
PubMed1995

[The study of factors affecting ABR in high risk newborn infants].

A.B.R. was employed to examine auditory pathways in a group of 78 newborn infants at risk and one of 20 normal infants. The impaired newborn group suffered of various risk factors or pathologies: 20 premature infants, 12 undersize (small for date), 12 with breathing distress, 11 hiv positive, 5 with neonatal jaundice, 4 suffered of convulsion, 4 at risk for hereditary deafness, 4 born by mothers with mellitus diabetes, 2 with dolichocefalia, 1 with the Albers-Schomberg syndrome, 1 with congenital heart disease and 1 with congenital glycogenosis. The results of A.B.R. of the risk group were compared statistically employing the "t Student's test" with those of the group of normal infants. The influence of risk factors in the first group on alterated A.B.R. parameters was then examined using a step-by-step logistic regression analysis method. The result showed a significant increase in a latency of waves V and III and inter-waves I-V and III-V in risk infants, while wave I and I-III internals were normal. These findings appear to demonstrate that in infants at risk, brainstem acoustic pathways are more sensitive to damage than the cochlea and acoustic nerve. This could be explained by the different degree of maturation that exists between the central acoustic pathways and the coclea and acoustic nerve. Analysis of the influence of pathologies and risk factors on A.B.R. indicate that birth weight followed by chronological age and length of the gestation period are significant in the development of A.B.R. alterations. The Albers-Schomberg syndrome, dolicocephalia, microcephalia, congenital glicogenosys, hiv infection, breathing difficulty and neonatal jaundice proved to be the main pathologies responsible for bringing about A.B.R. alterations.

Auditory Pathways↗
PubMed1994

Modulation of allergen-induced nasal symptoms and mediator release by treatment with N-acetyl-aspartyl-glutamate (ZY15106).

The aim of this study was to evaluate the effects of the new anti-allergic drug, N-acetyl-aspartyl-glutamate (ZY15106), on allergen-induced nasal symptoms and mediator release. Fifteen outpatients suffering from seasonal allergic rhinitis due to grass pollen were included in the study. A nasal antigen challenge followed by evaluation of symptoms was performed in basal conditions. Ten of the 15 patients underwent sequential nasal lavages in order to evaluate allergen-induced mediator release. The study was performed in winter, when the patients were symptom free, and was a randomized single-blind crossover trial of a 6% solution of ZY15106 (daily dosage: 48 mg) versus placebo (lactose). The drug and the placebo were administered intranasally q.i.d. for 1 week, with a 2-week interval between the two treatments. Treatment with ZY15106, but not with placebo, caused a significant reduction in nasal obstruction in the first 30 min after challenge and at 60 min and itching in the first 10 min after challenge, but did not reduce sneezing and rhinorrhoea. Moreover, ZY15106 significantly reduced the histamine release in 5 min postchallenge lavage (4.5 ng.ml-1 after placebo administration vs 2.5 ng.ml-1, after treatment with ZY15106). A reduction in immunoreactive LTC4 release in the 5 and 10 min post-challenge lavages was observed after ZY15106 administration (placebo vs active treatment: at 5 min 2.9 ng.ml-1 vs 1.4 ng.ml-1; at 10 min: 2.25 ng.ml-1 vs 0.9 ng.ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Nasal neutrophilia and eosinophilia induced by challenge with platelet activating factor.

BACKGROUND: It has been demonstrated that in vitro platelet activating factor-acether (1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphorylcholine; PAF) has the capacity to attract eosinophils and neutrophils. We investigated whether the same applies when human nasal airways are stimulated with PAF. METHODS: Symptom scores and cytologic changes in nasal lavage fluids were evaluated in 10 atopic and 10 nonatopic subjects after nasal challenge with PAF, its precursor and metabolite, 1-O-hexadecyl-sn-glycero-3-phosphorylcholine (lyso-PAF), or saline solution. RESULTS: Nasal obstruction was reported by all the atopic subjects and seven of the 10 nonatopic subjects after nasal challenge with PAF; other symptoms such as rhinorrhea, itching, and sneezing were generally mild. PAF induced neutrophilia, which appeared after 30 minutes in atopic subjects and after 1 hour in nonatopic subjects, and peaked at 3 hours in both. Less neutrophilia was found 3 hours after stimulation with lyso-PAF in both groups of subjects. PAF also induced eosinophilia, which appeared after 30 minutes in atopic subjects and only after 3 hours in nonatopic subjects. An increase in eosinophil counts was observed 3 hours after lyso-PAF stimulation in atopic but not in nonatopic subjects. CONCLUSION: PAF can attract neutrophils and eosinophils into human nasal airways; however, the recruitment of inflammatory cells is more rapid in atopic than in nonatopic subjects, suggesting a different degree of responsiveness to PAF challenge in the two groups of subjects.

Adult↗
PubMed1994

Ionic regulation of human basophil releasability. II. Non-releasing basophils are converted into releasing basophils in a low-Na+ medium.

The effects of different extracellular Na+ and Ca2+ concentrations on histamine release from human basophils were investigated. Isosmotic replacement of extracellular Na+ either with choline+, a non-permeant Na+ analogue, or glucose significantly increased spontaneous and anti-IgE-induced histamine release. Basophils from 12 of 49 normal subjects, which were found not to release histamine upon challenge with an optimal dose of anti-IgE in a 135 mM NaCl buffer, were converted into releasing basophils when stimulation with anti-IgE was performed in a low-Na+ medium. The increase in Na+ concentration in the extracellular medium was accompanied by a reduction in the magnitude of basophil response to anti-IgE, which was significantly more pronounced in non-releasers than in releasers (per cent inhibition by 70 mM NaCl 75.5 +/- 3.2 vs 43.5 +/- 9.0, P < 0.01). At higher Na+ concentrations a progressive and almost complete abrogation of histamine release was observed in non-releasers, but not in releasers (maximal per cent inhibition at 140 mM NaCl 97.3 +/- 1.3 vs 50.4 +/- 8.6). The Na+/H+ exchanger monensin had a dose-dependent inhibitory effect on anti-IgE-induced histamine release, and the concentration inhibiting 50% of histamine release was 1.5 x 10(-7) M. When basophils were challenged in the presence of different Na+ and Ca2+ concentrations, it was shown that the two cations have antagonistic effects, which is to say that they down-regulate and upregulate histamine release, respectively. Moreover, the requirement of extracellular Ca2+ was lowered in a low-Na+ medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Inhibitory effect of the H1 antagonist loratadine on histamine release from human basophils.

Loratadine is a powerful H1 antagonist commonly employed in the treatment of allergic disorders. The present study was performed to investigate whether loratadine, in addition to anti-H1 activity, is able to modulate histamine release from human basophils. Leukocyte suspensions were prepared by dextran sedimentation of peripheral venous blood drawn from 10 normal subjects. Leukocytes were stimulated with anti-IgE (1/5,000), N-formyl-methionyl-leucyl-phenylalanine (FMLP; 10 microM) and the Ca2+ ionophore A23187 (1 microM), and histamine release in the cell supernatants was measured by an automated fluorometric method. Loratadine, at concentrations ranging from 1 to 50 microM, exerted a dose-dependent inhibitory effect on IgE-mediated and IgE-independent histamine release. The concentrations inhibiting 50% of histamine release were 30 microM (anti-IgE), 29 microM (FMLP) and 24 microM (Ca2+ ionophore A23187). The inhibitory activity of loratadine was optimal after incubation for 2 h at 37 degrees C and the effect of the drug was no longer evident when leukocytes were stimulated 2 h after cell washing. Increased extracellular Ca2+ concentrations reduced the inhibitory activity of loratadine, indicating that external Ca2+ and loratadine have antagonistic effects on basophil histamine release. These results indicate that loratadine, in addition to H1 receptor blocking activity, has the capacity to inhibit histamine release from human basophils.

Adult↗
PubMed1994

Nasal eosinophilia induced by PAF-acether is accompanied by the release of eosinophil cationic protein.

It has been demonstrated that platelet-activating factor (PAF)-acether can induce nasal neutrophilia and eosinophilia, with a different degree of responsiveness in atopic and in nonatopic subjects. The aim of this study was to evaluate whether PAF can also induce the release of secondary mediators in the human nose. Ten patients with allergic rhinitis and 10 normal subjects underwent nasal challenge with PAF (500 nmol), lyso-PAF (500 nmol) and saline solution. Nasal lavages were performed before and after challenge to evaluate changes in nasal cytology and release of histamine, immunoreactive leukotriene (iLT) C4 and eosinophil cationic protein (ECP). PAF caused neutrophilia and eosinophilia, which appeared earlier in atopic than in nonatopic subjects (30 min vs 1 h), and peaked 3 h after challenge in both groups. Lyso-PAF caused mild neutrophilia, which appeared 3 h after challenge in both groups; an increase in eosinophil counts was observed 3 h after challenge in atopic subjects, but not in nonatopic subjects. PAF insufflation caused a significant release of ECP in nasal lavage fluids 30 min and 3 h after challenge in atopic subjects, and 3 h after challenge in nonatopic subjects. ECP levels in the nasal lavages collected 30 min and 3 h after challenge with PAF were higher in atopic than in nonatopic subjects. Eosinophil counts correlated with ECP levels in the nasal lavages collected 30 min after PAF challenge in atopic subjects. Nasal challenge with lyso-PAF did not provoke any release of ECP. No significant increase of histamine and iLTC4 levels in nasal lavages was found after challenge with either PAF or lyso-PAF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Mast cell and histamine involvement in farmer's lung disease.

The aim of this study was to evaluate the cellular and biochemical characteristics of the bronchoalveolar lavage (BAL) fluid in patients with farmer's lung disease (FLD). Total cell numbers in BAL fluids from patients with FLD (n = 30) were significantly higher than in normal subjects (n = 7; p < 0.01), and differential cell counts were significantly different. Lymphocytes were the most numerous cell type in BAL fluids from patients with FLD (65.4 +/- 2.5 percent vs 6.8 +/- 0.5 percent), and analysis of lymphocyte subsets revealed increased percentages of CD3+ and CD8+ cells (91.8 +/- 0.9 percent vs 68.8 +/- 3 percent, p < 0.01, and 54.3 +/- 3.1 percent vs 30.1 +/- 3.2 percent, p < 0.01, respectively). A marked increase in mast cell numbers, as revealed by the specific alcian blue/safranin staining, was observed in patients with FLD (4.2 +/- 0.57 percent, n = 12, vs 0.18 +/- 0.04 percent, n = 7, p < 0.001). Histamine levels in BAL supernatants were increased in patients with FLD (mean = SEM, 4.4 +/- 0.8 ng/ml vs 0.9 +/- 0.1 ng/ml; median, 2.4 ng/ml vs 0.9 ng/ml, p < 0.01), and correlated positively with mast cell numbers and percentages (r = +0.63, p < 0.03, and r = +0.69, p < 0.02, respectively); conversely, a negative correlation was found between histamine levels and CD8+ lymphocyte percentages (r = -0.48, p < 0.01). Raised neutrophil percentages (5.1 +/- 0.8 vs 0.5 +/- 0.18, p < 0.05) and albumin concentrations (29.2 +/- 3.9 mg/dl vs 3.4 +/- 1.3 mg/dl, p < 0.01) were also found in patients with FLD. These findings show that increased numbers of mast cells, lymphocytes, and neutrophils can be found in BAL fluids of patients with FLD. The increased histamine levels in the supernatants of BAL fluids indicate that mast cells are activated. These data allow us to postulate a role for mast cell accumulation and histamine release in the inflammatory process of FLD.

Adult↗
PubMed1994

No changes of insulin sensitivity in cystic fibrosis patients with different degrees of glucose tolerance: an epidemiological and longitudinal study.

Plasma glucose and insulin responses to oral glucose and insulin sensitivity by the euglycemic hyperinsulinemic clamp technique were investigated in 30 cystic fibrosis patients with normal fasting blood glucose levels and normal (N = 12), impaired (N = 12) or diabetic (N = 6) glucose tolerance, and in 12 control subjects. In a subgroup of 10 cystic fibrosis patients with non-diabetic glucose tolerance both oral glucose tolerance test and clamp were performed again 48-52 months later. Following oral glucose, glycemic responses were higher in cystic fibrosis patients than in controls, whereas insulin responses were reduced significantly only in the patients with diabetic glucose tolerance. Insulin sensitivity did not differ significantly in the patient subgroups with different degrees of glucose tolerance and in controls. In the 10 patients who underwent a 4-year follow-up, insulin responses to oral glucose decreased significantly, whilst insulin sensitivity did not change substantially. Insulin sensitivity persisted unmodified even in the patients with deteriorating glucose tolerance. No correlation were observed between metabolic data and clinical status of patients. In conclusion, in cystic fibrosis subjects with fasting euglycemia and different degrees of glucose tolerance: (i) insulin sensitivity is not impaired; (ii) eventually changes of glucose tolerance over time are not associated with modifications of insulin sensitivity; (iii) insulin secretion deteriorates over time even in the patients with stable glucose tolerance; (iv) eventual deterioration of both glucose tolerance and insulin secretion is not linked to a worsening of either nutritional or clinical parameters.

Administration, Oral↗