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E Gilardi

Publications and source records attributed to E Gilardi.

At least 19 recordsLinked to original sources
PubMed2003

Postpartum thyroiditis is associated with fluctuations in transforming growth factor-beta1 serum levels.

Postpartum thyroiditis (PPT) is characterized by a rapid evolution and recovery of euthyroidism. Therefore, it can represent a good model to study early cytokine fluctuations in autoimmune thyroid diseases. TGFbeta1 is an immunosuppressive cytokine, as it inhibits T and B cell proliferation, natural killer cell cytotoxic activity, and the generation of T cell cytotoxicity. The aim of this study was to assess serum concentrations of TGFbeta1 during pregnancy and to study possible serum fluctuations of this cytokine during the different phases of PPT. Thyroid biochemical pattern, antithyroid autoantibodies (ATA), and total and active TGFbeta1 (aTGFbeta1) serum concentrations were evaluated in 63 pregnant women. Thirty-four of them were ATA(+), and 29 were ATA(-). Twenty of the 34 ATA(+) women were followed in the postpartum year. Nine of these 20 women developed PPT; 11 remained euthyroid. All of the PPT women became euthyroid during the follow-up. Our results showed 1) detectable serum levels of aTGFbeta1 in 50% of ATA(+) pregnant women, suggesting that the presence of autoantibodies may characterize a favorable condition for TGFbeta1 activation; and 2) decreased total TGFbeta1 and increased aTGFbeta1 serum levels during the active phase of PPT in ATA(+) women. This seems to suggest that inflammation may be responsible for TGFbeta1 activation and autoantibody increase because of antigen release. Although further studies of women with persistent hypothyroidism after the postpartum year are needed, the possibility that the enhanced activation of TGFbeta1 may contribute to resolution of thyroid inflammation postpartum cannot be excluded.

Adult↗
PubMed1998

[Goiter prevalence and urinary excretion of iodine in a sample of school age children in the city of Rome].

The aim of the study was the assessment of the urinary iodine excretion and the evaluation of thyroid volume compared with clinical examination in 1040 schoolchildren (6-14 years old), living in Rome. Mean urinary iodine excretion was 98.52 +/- 49.81 micrograms/l (median 92 micrograms/l). Thyroid enlargement, as assessed by palpation, was found to be grade 1A in 35.4% of the children, grade 1B in 9.6% and grade 2 in 0.2%. Thyroid volume, determined by ultrasound, increased with age, was significantly correlated with body surface area and was significantly higher in females, as compared to males, in the 11 and 12 years old group. Eleven children (1.9%) were negative at palpation (grade 0) but showed thyroid enlargement by ultrasound. The prevalence of goiter determined by ultrasound resulted to be 4.7%.

Adolescent↗
PubMed1996

Specificity of proteolysis inhibitors in rabbit plasma.

Hydrolysis and inhibition of hydrolysis of leucine enkephalin in Oryctolagus plasma were studied by kinetics and chromatographic techniques. By data obtained, in this species, enkephalins are degraded by the same enzymes active in other mammals: aminopeptidases, dipeptidylaminopeptidases, and dipeptidylcarboxypeptidases. At variance with data obtained in other species, where enkephalins are hydrolyzed mostly by aminopeptidases, in Oryctolagus Leu-enkephalin hydrolysis is mainly due to dipeptidylcarboxypeptidases, whereas aminopeptidases contribution is the minimum of all three enzyme groups. Comparative analyses performed in the presence and in the absence of plasma inhibitors indicate that the ability of these substances to reduce substratum hydrolysis is very limited. On the contrary, the specific hydrolysis pattern evidenced appears to originate primarily from selective inhibition of the three groups of enzymes. Results obtained appear consistent with a role of plasma inhibitors in tuning hydrolysis to specific substrata, without appreciably modifying the amount of the substratum degraded.

Aminopeptidases↗
PubMed1994

Early detection of nephrotoxic effects in thalassemic patients receiving desferrioxamine therapy.

Nineteen transfusion-dependent beta-thalassemia major patients were included in the study. Six of these patients underwent chelation therapy with desferrioxamine by subcutaneous infusion (50 mg/kg/12 hr) and 13 received intravenous infusion (50 mg/kg/6 hr or 100 mg/kg/24 hr). BUN, creatinine, creatinine clearance, beta 2-microglobulin, urinary beta 2-microglobulin and urinary growth hormone excretion were evaluated during desferrioxamine treatment. Thirteen out of nineteen patients presented tubular damage indicated by increased excretion of urinary beta 2-microglobulin. 85% (11 of 13) of these patients showed more serious tubular damage, as demonstrated by concurrent increased urinary growth hormone excretion. Moreover, a positive correlation between urinary growth hormone excretion and urinary beta 2-microglobulin was observed (P < 0.05).

Administration, Cutaneous↗
PubMed1993

Thyroid hypofunction related with the progression of human immunodeficiency virus infection.

Thyroid function was evaluated in 119 human immunodeficiency virus (HIV) infected patients at different stages of infection, compared with euthyroid normal subjects and hepatitis C virus infected blood donors as control groups. The low T3 state, well documented in severe nonthyroidal illnesses, was not found in these HIV infected patients. They showed lower FT4 levels and higher TSH and TBG values than euthyroid normal controls. These findings suggested a thyroid hypofunction becoming more evident with the progression of the infection as also supported by the presence of antithyroid autoantibodies mainly found in the symptomatic stages of the infection.

Adult↗
PubMed1993

Enkephalin-degrading dipeptidylcarboxypeptidases in human and Cavia porcellus plasma.

1. The dipeptidylcarboxypeptidases that degrade leucine enkephalin in human and guinea pig plasma were studied by kinetic and chromatographic techniques. 2. The extremely rapid degradation of enkephalins in Cavia plasma seems to be caused by both increased activity of enzymes and reduced role of inhibitors. 3. The increased role of dipeptidylcarboxypeptidases in Cavia as compared to Homo appears prevalently caused by the presence in the former species of a considerable number of very active enzymes. 4. The sum of these data indicates the existence of noticeable intraspecific differences either in peptide-degrading enzymes present in plasma, or in plasma peptides, or in both.

Amino Acid Sequence↗
PubMed1992

Hydrolysis and association of leucine enkephalin to lymphomic and erythroleukaemic cell lines--II.

The relationship between the hydrolysis of labelled leucine enkephalin and the association of its radioactive label to the cells of lymphomic and erythroleukaemic cell lines have been studied using intact cells and resealed membranes obtained from these cells as models. Hydrolysis by cell enzymes and its effect on association have been analysed using protease inhibitors and non-hydrolysable enkephalin analogues. Results obtained confirm that hydrolysis of the pentapeptide is a prerequisite for association of the radiolabel to cells. The same results provide evidence of marked differences between enkephalin hydrolysis by whole cells and hydrolysis measured in the presence of resealed membranes, suggesting the existence in intact cells of proteolytic enzymes other than those bound to the membranes. The lack of reversibility of association and the intracellular localization of the radioactive label suggest that the association measured is prevailingly caused by internalization of a hydrolysis fragment, and not by binding to receptors. In order to determine the nature of the active fragment, association was measured in the presence of all four labelled N-terminal hydrolysis fragments of leu-enkephalin under conditions of nearly-total inhibition of proteolytic enzymes. Under these conditions, the label carried by Tyr, but not that carried by the other N-terminal fragments, was associated with cells. Free Tyr, furthermore, inhibits the association to cells of both labelled Tyr and leu-enkephalin. Data summarized above are consistent with the hypothesis that the radioactive label is taken up by the cells as Tyr, freed from the parent peptide by cell-related enzymes. The same data tend to exclude that a relevant fraction of the intact pentapeptide is bound to membrane receptors or that the radioactive label is carried into the cell by a N-terminal fragment other than Tyr.

Chromatography, Thin Layer↗
PubMed1991

Isoelectric focusing and immunoblotting analysis of thyroglobulin from different thyroid diseases.

Thyroglobulins (Tgs) have been obtained from macro-microfollicular goiter, toxic adenomas, papillary carcinomas and metastatic lympho-node and chromatographed by gel filtration. The 19S Tgs so obtained have been characterized by isoelectric focusing (IEF) and immunoblotting. IEF showed microheterogeneity pattern of Tgs from normal tissue, macro-microfollicular goiter and toxic adenomas to be within pH range from 4.2 to 4.5, while that from papillary carcinomas and metastatic lympho-node showed a wider microheterogeneity. Passive blotting of focused Tgs and immunoreaction with rabbit anti-Tg peroxidase conjugated antibody have been carried out and a positive reaction for all examined samples have been evidenced. Also two bands, focused at more cathodic pH value (pH 4.7), observed in IEF patterns of Tgs from carcinomas and metastatic lympho-node, gave a positive reaction with anti-Tg conjugated antibody. These differences observed in IEF and immunoblotting patterns of Tgs from papillary carcinomas and metastatic lympho-node are discussed in this report.

Adenoma↗
PubMed1986

Control mechanisms of peripheral enkephalin hydrolysis in mammalian plasma.

The protection of the adrenal-released enkephalins from enzyme hydrolysis by endogenous plasma components was studied in laboratory animals and in man. The results indicate that mechanisms active in protecting leu-enkephalin from hydrolysis are present in the plasma of all species examined. The protection seems to be due to two groups of substances, possibly of peptidic nature. The amount of protection given by these substances seems to be sufficient to play a significant role in controlling the physiological levels of leu-enkephalin released into the bloodstream.

Amino Acids↗
PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. III. Current pathogenetic and nosographic aspects].

There is much evidence to suggest that temporal arteritis and rhizomelic polymyalgia are both immunological diseases. The classic results of experimental pathology are discussed, together with the relations between rhizomelic polymyalgia and both virus hepatitis B and the HLA system. From the clinical standpoint, it is now agreed that differences in individual response may lead to either a synovial or an arteritic response in both forms. Their association in what Hamrin has called "polymyalgia arteritica" is also common.

Antigen-Antibody Complex↗
PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. II. Rhizomelic polymyalgia. Arteritic polymyalgia].

Rhizomelic polymyalgia is an inflammatory form. Its site of choice is the shoulder girdle and it is almost solely observed in elderly subjects. An account is given of its epidemiological, clinical and anatomopathological aspects. Its aetiology is also discussed with particular reference to its possible immunological or vascular origin. The rheumatic symptoms of rhizomelic polymyalgia are similar to those observed in temporal arteritis. Since artery lesions are found in most cases, the name "polymyalgia arteritica" has been suggested as an alternative clinical description by Hamrin .

Adrenal Cortex Hormones↗
PubMed1984

[Hutchinson-Horton giant cell arteritis and rhizomelic polymyalgia. I. Hutchinson-Horton arteritis].

Temporal arteritis (also known as Horton's or giant cell arteritis) is a panarteritis of the large and medium-calibre cranial vessels. An account is given of its epidemiological, clinical and anatomopathological aspects and its involvement of the locomotor apparatus (Horton's rheumatism). Reference is also made to the close relationship between temporal arteritis and pulseless disease. Some workers are of the opinion that they share the same aetiology, and that their clinical expression in different areas is dictated by age and constitutional factors.

5'-Nucleotidase↗
PubMed1982

Serial blood T4 and TSH determinations in low birth weight infants. Influence of gestational age, birth weight and neonatal pathology on thyroid function.

Serial blood T4 and TSH determinations were performed on a total number of 352 low birth weight (LBW) infants: 210 healthy newborns and 142 infants affected by respiratory distress syndrome (RDS), sepsis, hyperbilirubinaemia, hypocalcemia, or hypoglycemia. The healthy infants have been divided into three groups in relation to gestational age (less than or equal to 33 wk, 34-36 wk, greater than or equal to 37 wk). Statistical evaluation among groups shows that reduced T4 concentration in LBW infants is strictly related to gestational age, while TSH failed to demonstrate any significant correlation. No significant influence of birth weight on T4 and TSH has been observed. The preterm newborns affected by RDS or sepsis showed a significant reduction of mean T4 concentrations up to 20th day of life when compared with healthy controls similar for gestational age and birth weight. TSH levels are not significantly different. No significant modifications of T4 and TSH have been found related to the other pathological conditions. The significant reduction of T4 and the high incidence of subjects with low T4 values observed in healthy and sick preterm population lend further support to the use of TSH determination for optimum screening of congenital hypothyroidism.

Birth Weight↗
PubMed1980

[Amyloidosis. II. Current pathogenetic and clinico-nosographic aspects].

Amyloidosis is due to the overproduction of a precursor protein and its conversion into products capable of polymerisation into fibrils. The primary form, or that associated with multiple myeloma or Waldenström's macroglobulinaemia, marked by the presence of protein AL, includes the overproduction of Ig light chains followed by conversion on the part of lysosome enzymes. The forms can thus be classified as immunoproliferative diseases (plasma-cell dyscrasias). Secondary amyloidosis is primarily associated with neoplasia or chronic inflammation. Its biochemical label is the AA protein. Initially, there is overproduction of protein SAA, while the formation of AA-amyloid fibrils may theoretically be attributed to a variety of factors: changes in the amount of circulating SAA, the presence of amyloidogenetic SAA, variations in the activity of SAA catabolic systems, insufficient removal of acculated fibrils. The way in which the immunocompetent system intervenes is a controversial subject. Lesser froms of amyloidosis are known in which there are local deposits of amyloid: APUD-amyloidosis, amyloidomas. In some forms, the features of systemic accumulation are maintained, but only one organ is primarily involved. They are rarely of clinical significance (e.g. senile amyloidosis). Current biochemical techniques enable a clinical and nosographic distinction to be drawn between an Ig (AL)-amyloidosis and non-Ig (AA, APUD and AS) forms.

Amyloid↗
PubMed1980

[Amyloidosis. I. Recent findings concerning amyloid substance].

The considerable progress made recently in the study of amyloid substance have led to the identification of numerous organised protein components in typical microfibrillar structures. In spite of the biochemical heterogeneity of fibril proteins, it is still possible to find similar chemicophysical and tintorial features in the various types of amyloid, probably due, at least in part, to the common Beta type molecular configuration, a structure proper to fibril proteins. In so-called primary amyloidosis and in that associated with myelomatous diseases, the principal protein component consists of AL protein, correlated with the light immunoglobulin chains, with which analogies have been observed both in the amino acid sequence and in antigenic characteristics. In secondary amyloidosis, AA protein, which is unrelated to immunoglobulins or other known human proteins, is prevalent. AA protein probably derives from a serum globulin, SAA, whose blood levels increase during numerous pathological processes, particularly in those of neoplastic or inflammatory type. The origin of serum protein, which might be either a normal tissue component released under stimulus or a reagent of the acute phase synthesised ex novo, and its function, which is probably of immunomodulator or more specifically immunosuppressive type, are still to be defined. In all forms of amyloidosis studied, a common observation is the presence of AP protein, organised in pentagonal structures. This protein would appear to derive from a serum component defined as SAP, with a marked affinity for amyloid fibrils. Also identifiable are other forms of amyloid such as APUD-amyloid, which probably derives from polypeptide hormones, and AS amyloid, which is present in some organs of elderly patients and is biochemically identifiable at cardiac level with A(SCA) protein. Still awaiting definition in amyloid tumours or amyloidomas is the precise chemical composition of deposited proteins.

Amyloid↗
PubMedDate not supplied

Familial thyroxine-binding globulin deficiency detected in a pilot screening program for congenital hypothyroidism.

During a pilot screening program for congenital hypothyroidism, performed in Italy over a three years period on 38,000 newborns, seven cases (1/5,400) of thyroxine-binding globulin (TBG) deficiency, have been detected. None of these infants was affected by any pathology or had been treated with drugs which could explain TBG deficiency as an acquired condition. Familial studies pointed out that the transmission of the defect is consistent or compatible with X-chromosome linkage.

Congenital Hypothyroidism↗