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Biomedical subjects

R Giugliano

Publications and source records attributed to R Giugliano.

17 recordsLinked to original sources
PubMed2000

Effects of tirofiban plus heparin versus heparin alone on troponin I levels in patients with acute coronary syndromes.

Elevated serum troponins following an acute coronary syndrome (ACS) predict a poor clinical outcome. Glycoprotein (GP) IIb/IIIa inhibitors reduce adverse clinical outcomes in patients with ACS, although their effect on serum troponin I (TnI) in this setting has not been described. We therefore studied the effects of the GP IIb/IIIa inhibitor tirofiban on serum TnI levels in a group of patients in the Platelet Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms trial. Serial blood samples were obtained in 53 patients receiving the combination therapy of tirofiban/heparin and in 52 receiving heparin alone, and were analyzed for baseline, peak, and mean concentrations of TnI. Baseline TnI levels were not different between the combination therapy and heparin-only groups (1.6 +/- 3.0 vs 3.1 +/- 6.7 ng/ml, p = 0.15). The peak TnI level was significantly lower in the combination therapy group than in the heparin group (5.2 +/- 8.3 vs 15.5 +/- 29.1 ng/ml, p = 0.017), and mean levels over the initial 24-hour period were also significantly lower in the combination therapy group (3.2 +/- 5.0 vs 8.5 +/- 14.8 ng/ml, p = 0.016). In univariate analysis, combination therapy was associated with lower TnI levels, whereas in a multivariate model, the lower peak and mean TnI levels as a consequence of tirofiban/heparin compared with heparin monotherapy remained significant (peak, p = 0.029; mean, p = 0.035). Among patients with negative TnI at baseline, treatment with the combination of tirofiban/heparin compared with heparin monotherapy still resulted in significantly lower peak (2.5 +/- 5.4 vs 14.6 +/- 32.8 ng/ml, p = 0.024) and mean (1.2 +/- 2.6 vs 6.9 +/- 15.8 ng/ml, p = 0.029) TnI levels. In patients with ACS, therapy with the combination of tirofiban and heparin (compared with heparin treatment alone) resulted in lower serum TnI levels, suggesting reduced myocardial injury.

Angina, Unstable↗
PubMed2000

A new de novo mutation of the connexin-32 gene in a patient with X-linked Charcot-Marie-Tooth type 1 disease.

We report a 26-year-old Italian man with X-linked Charcot-Marie-Tooth (CMT) disease type 1 (CMT-X1) and a negative family history for neuromuscular diseases. Clinical and electrophysiological examinations of the patient's mother and siblings were normal. Molecular analysis by polymerase chain reaction--single-strand conformation polymorphism (PCR-SSCP) on genomic DNA from the patient and all members of his family revealed a C-to-T transition in codon 8 of exon 2 of the connexin-32 (Cx32) gene on the X chromosome only in the patient. This transition in the 5'-coding region, resulting in a Thr-Ile substitution, is likely to be the cause of CMT phenotype in our patient, and it represents a new de novo mutation of the Cx32 gene.

Adult↗
PubMed1993

Mannose-resistant haemagglutination (MRHA) and haemolysin (Hly) production of strains of Escherichia coli isolated from children with diarrhoea: effect of breastfeeding.

Haemolysin production (Hly) and mannose-resistant haemagglutination induction (MRHA) of human (H), bovine (B), and both (HB) erythrocytes was investigated in strains of E. coli isolated from 142 cases of children with diarrhoea aged 0-36 months. Haemolysin production was more frequent in strains isolated from children under 1 year and this characteristic was strongly associated with HB+ haemagglutination (P < 0.005). Isolation frequency of MRHA strains was compared in 53 breastfed and 50 non-breastfed children under 1 year of age. HB+ strains were significantly more frequent in non-breastfed infants (P < 0.025). Severity of diarrhoea evaluated by the number of watery stools per day, was significantly reduced in the breastfed group (P < 0.05). The results suggests that breastfeeding may protect infants against the establishment of HB+ strains which might be acting either as a main pathogen or as an opportunistic strain.

Antigens, Bacterial↗
PubMed1991

Influence of enteral parasites on the blood vitamin A levels in preschool children orally supplemented with retinol and/or zinc.

A sample of 471 pre-school children who frequented schools and crêches in a poor district of Manaus (Amazonas), Brazil, were randomly submitted to faecal parasitological tests. Two-hundred-and-forty children from both sexes between the ages of 3 and 7 years with Ascaris lumbricoides and/or Giardia lamblia were selected. The objective of the study was to determine the possible influence of these two intestinal parasites and vitamin A and/or zinc supplementation on the serum retinol levels of primary school children. The children were submitted to clinical and anthropometric examinations, dietary interviews and biochemical examinations of retinol and carotene in the serum and of zinc in the hair. The parasitic incidence was 85.0% and about 54% of the children were polyparasitic. During the pretreatment phase, the retinol and carotene serum levels were 36% and 57%, respectively, below the normal levels. Using the Waterlow classification, the anthropometric analyses revealed that 88% of the children showed normal growth. A significant effect was observed of the anti-parasitic medicine on the serum retinol levels.

Brazil↗
PubMed1988

Stable isotope metabolic studies of zinc nutrition in slum-dwelling lactating women in the Amazon valley.

1. Zinc metabolism has been studied in a group of undernourished, slum-dwelling, lactating women in Manaus, Brazil, by means of modified metabolic balance techniques and the stable isotope 67Zn. 2. The subjects were found to be consuming a diet which provided an average of 34% of the recommended dietary allowance for lactating women, but six of the seven appeared to achieve Zn balance. In five of the subjects use of 67Zn in a stable isotope dilution manner demonstrated that they were absorbing a high proportion of the dietary Zn (proportional absorption ranged from 0.59 to 0.84), suggesting an adaptation to the chronically low intake. 3. Two subjects had marginally low plasma Zn concentrations, although hair, urine and milk Zn contents were all within accepted normal values. 4. Preliminary findings on the rate of plasma Zn turnover and the size of the exchangeable body Zn pool obtained using 67Zn suggest that these subjects may have a reduction in both.

Brazil↗
PubMed1987

The effects of severe zinc deficiency on protein turnover in muscle and thymus.

Measurements have been made of protein turnover, RNA and DNA in thymus and skeletal muscle from rats fed on a zinc-deficient diet (ZD) for 10 and 17 d, in pair-fed controls (CI) and in muscle from rats fed on the ZD diet for 24 d and then fed on restricted amounts of the deficient diet with (RIZS) or without (RIZD) Zn supplementation, for 8 d. In thymus the ZD diet induced a loss of DNA and protein which was not observed with the CI rats. Accumulation of RNA was less affected but protein synthesis was reduced. In muscle the accumulation of DNA and protein was slowed by the ZD diet, particularly in glycolytic muscles compared with oxidative muscles, and Zn supplementation increased DNA and protein. Protein synthesis and RNA concentrations were reduced in the ZD rats compared with the CI rats, but Zn supplementation at constant restricted food intake did not increase protein synthesis. Muscle protein synthesis per unit RNA varied markedly in the ZD rats after 10 d when the characteristic cycling of the food intakes and body-weight was most pronounced, the highest values being observed in the anabolic phase of the cycle although these were less than values for well-fed controls. The variability was inversely correlated with the plasma Zn levels. The extent of the variability was much less after 17 d and was not apparent in the food-restricted ZD animals. Protein degradation in muscle, assessed as the difference between overall and net protein synthesis, was faster in the ZD rats compared with the CI rats and fluctuated considerably, partly accounting for the cyclic changes in muscle after 10 d, and was entirely responsible after 17 d. The concentration of muscle-free 3-methylhistidine and its urinary excretion rate indicated inconsistent results which could not be satisfactorily interpreted. Plasma insulin was reduced in the ZD rats compared with the CI rats and was insensitive to food intake in contrast to urinary corticosterone excretion which was inversely correlated with the cyclic changes in body-weight and food intake. Furthermore, adrenalectomized rats exhibited increased mortality and reduced cycling of body-weight and food intake. Thus Zn deficiency impairs growth by a combination of reduced food intake, a reduced anabolic response to food due to a reduced capacity for protein synthesis and reduced activation of protein synthesis, possibly reflecting impaired insulin secretion, and an increased catabolic response to the reduced intake in which corticosterone may play a role.

Adrenalectomy↗
PubMed1986

Possible role of calmodulin in the control of histamine release from human basophil leukocytes.

We investigated the possible role of calmodulin (CaM) in the control of histamine release from human basophil leukocytes using several CaM antagonists. Trifluoperazine (TFP) (10(-6)-2 X 10(-5) M), pimozide (10(-6)-1.5 X 10(-5) M), chlorpromazine (CPZ) (10(-5)-10(-4) M) and promethazine (PMZ) (2 X 10(-5)-10(-4) M) inhibited in vitro histamine secretion from human basophils induced by several immunological (antigen, anti-IgE, and formyl-L-methionyl-L-leucyl-L-phenylalanine: f-met peptide) and nonimmunological (Ca2+ ionophore A23187 and the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate: TPA) stimuli. Trifluoperazine sulfoxide (TFP-S) and chlorpromazine sulfoxide (CPZ-S), which have very low affinity to CaM, had practically no inhibitory effect on histamine release from human basophils. The inhibitory effect of TFP could be made irreversible by irradiating the cells with UV light. A sulfonamide derivative, the compound N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) (2.5 X 10(-5)-2 X 10(-4) M), which selectively binds to CaM, inhibited the release of histamine from basophils. In contrast, the chloride deficient analogue, W-5, which interacts only weakly with CaM, had practically no inhibiting effect. The IC50 for enzyme release by a series of eight CaM antagonists was closely correlated (r = 0.91; p less than 0.001) with the CaM specific binding, supporting the concept that these agents act by binding to CaM and thereby inhibiting histamine release. TFP and W-7 inhibited histamine release in the absence and in the presence of increasing concentrations of extracellular Ca2+. These results emphasize the possible role of CaM in the control of histamine secretion from human basophils.

Basophils↗
PubMed1986

Physiological concentrations of zinc inhibit the release of histamine from human basophils and lung mast cells.

We have previously shown that physiological concentrations of zinc (congruent to 7 X 10(-6) M) inhibit the release of histamine from human basophil leukocytes (Marone et al., J. Pharmacol. Exp. Ther. 217: 292, 1981). In these experiments we compared the effect of zinc chloride on the release of chemical mediators from human basophils and mast cells isolated from human lung. Preincubation (5 min, 37 degrees C) of human basophils and lung mast cells with zinc chloride (10(-6)-3 X 10(-5) M) caused dose-related inhibition of histamine and peptide leukotriene C4 (LTC4) release induced by anti-IgE. Increase Ca2+ concentrations (0.3 to 6 mM) in the extracellular medium completely reversed the inhibitory effect of zinc on anti-IgE-mediated histamine secretion. Zinc chloride was a competitive antagonist of the action of Ca2+ in histamine secretion induced by anti-IgE with a dissociation constant (Kd) of about 10(-5) M in both the basophil and mast cell systems. Thus physiological concentrations of zinc inhibit the release of histamine from human basophils and lung mast cells, presumably by blocking Ca2+ uptake induced by anti-IgE activation.

Basophils↗
PubMed1986

Longitudinal study of diarrhoeal disease in a peri-urban community in Manaus (Amazon-Brazil).

A 20-month longitudinal study of diarrhoeal disease was carried out in a poor peri-urban community of Manaus (Amazon-Brazil), and the attack rate of this disease ranged from 0.2 to 4.8 episodes of diarrhoea per person per year. The age group most affected was 0 to 35 months old. A probable aetiological agent was identified in 68 of the 110 faecal samples collected. The most frequent enteropathogens isolated were enterotoxigenic Escherichia coli and Giardia lamblia. Enterotoxigenic Escherichia coli was also isolated from stream-water and from flies collected inside a household.

Adolescent↗
PubMed1986

Human basophil releasability. II. Changes in basophil releasability in patients with atopic dermatitis.

"Releasability" is the theory whereby biochemical events in basophils influence the capacity to release chemical mediators in response to activating stimuli. We have compared the releasability of basophils from 21 young patients with atopic dermatitis (AD) with that from 17 normal donors of matched ages. Basophils were challenged with several different stimuli: rabbit antihuman Fc epsilon (anti-IgE), N-formyl-methionyl-leucyl-phenylalanine (f-met-peptide), Ca++ ionophore A23187, and D2O. Basophils from patients with AD released significantly more histamine both "spontaneously" and in response to D2O than did controls. The basophils of patients with AD were significantly more responsive to anti-IgE and to A23187. There was no difference between the percent f-met-peptide-induced histamine release in patients with AD vs controls. No significant correlation between percent histamine release with optimal or suboptimal concentrations of the stimuli and serum IgE level was found. There was a significant correlation between the sensitivity of the cells to release with f-met-peptide and the response to A23187 both in control and in AD patients. Since basophils are thought to play some role at the site of inflammation in AD, their increased releasability might contribute to the symptoms of these patients.

Adolescent↗
PubMed1985

Studies on human basophil releasability.

Basophil releasability is an important parameter in several pathophysiological conditions. In normal donors, the maximum percent histamine release and cell sensitivity to rabbit anti-Fc epsilon (anti-IgE) is correlated with the age of cell donors. A positive correlation between serum IgE level and anti-IgE-induced histamine release was found in subjects below 20 years old. The response to formyl-Met-Leu-Phe (f-met peptide) was significantly reduced in subjects above 60 years old. In twins, IgE-mediated releasability and serum IgE levels appear to be controlled by two different genetic mechanisms. Basophils of patients with atopic dermatitis were more responsive than those of control subjects of matched ages to anti-IgE.

Adolescent↗
PubMed1984

Growth and zinc homeostasis in the severely Zn-deficient rat.

Male weanling rats were fed on diets either adequate (55 mg/kg), or severely deficient (0.4 mg/kg) in zinc, either ad lib. or in restricted amounts in four experiments. Measurements were made of growth rates and Zn contents of muscle and several individual tissues. Zn-deficient rats exhibited the expected symptoms of deficiency including growth retardation, cyclic changes in food intake and body-weight. Zn deficiency specifically reduced whole body and muscle growth rates as indicated by the fact that (a) growth rates were lower in ad lib.-fed Zn-deficient rats compared with rats pair-fed on the control diet in two experiments, (b) Zn supplementation increased body-weights of Zn-deficient rats given a restricted amount of diet at a level at which they maintained weight if unsupplemented, (c) Zn supplementation maintained body-weights of Zn-deficient rats fed a restricted amount of diet at a level at which they lost weight if unsupplemented (d) since the ratio, muscle mass: body-weight was lower in the Zn-deficient rats than in the pair-fed control groups, the reduction in muscle mass was greater than the reduction in body-weight. Zn concentrations were maintained in muscle, spleen and thymus, reduced in comparison to some but not all control groups in liver, kidney, testis and intestine, and markedly reduced in plasma and bone. In plasma, Zn concentrations varied inversely with the rate of change of body-weight during the cyclic changes in body-weight. Calculation of the total Zn in the tissues examined showed a marked increase in muscle Zn with a similar loss from bone, indicating that Zn can be redistributed from bone to allow the growth of other tissues. The magnitude of the increase in muscle Zn in the severely Zn-deficient rat, together with the magnitude of the total losses of muscle tissue during the catabolic phases of the cycling, indicate that in the Zn-deficient rat Zn may be highly conserved in catabolic states.

Animals↗
PubMed1984

Possible role of calmodulin in the control of lysosomal enzyme release from human polymorphonuclear leukocytes.

Human polymorphonuclear leukocytes (PMNs) were found to contain a mean +/- S.E.M. of 21.7 +/- 7.9 ng of immunoreactive calmodulin (CaM)/10(6) PMNs, which represents 0.032 +/- 0.001% of the total cellular protein. The functional role of CaM in the control of lysosomal enzyme release from human PMNs was investigated using several CaM antagonists. Trifluoperazine (TFP) (10(-6)-2 X 10(-5) M), pimozide (10(-6)-1.5 X 10(-5) M), chlorpromazine (CPZ) (10(-5)-10(-4) M) and promethazine (2 X 10(-5)-10(-4) M) inhibited in vitro lysosomal enzyme release from human PMNs induced by immunological (serum-treated zymosan, concanavalin A and formyl-L-methionyl-L-leucyl-L-phenylalanine) and nonimmunological (Ca++ ionophore A23187) stimuli. Trifluoperazine sulfoxide (TFP-S) and chlorpromazine sulfoxide (CPZ-S), which have very low affinity for CaM, had practically no inhibitory effect on lysosomal enzyme release. The inhibitory effect of TFP could be made irreversible by irradiating the cells with UV light. A sulfonamide derivative, W-7, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (10(-5)-2 X 10(-4) M), which selectively binds to CaM, inhibited the release of lysosomal enzymes from PMNs. In contrast, the chloride-deficient analog, W-5, N-(6-aminohexyl)-1-naphthalenesulfonamide hydrochloride, which interacts only weakly with CaM, had practically no inhibiting effect. The IC50 for enzyme release by a series of eight CaM antagonists was closely correlated (r = 0.89; P less than .001) with their affinity for binding to CaM, supporting the concept that these agents act by binding to CaM and thereby inhibiting lysosomal enzyme release.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗