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Biomedical subjects

A Antonelli

Publications and source records attributed to A Antonelli.

At least 127 records · Page 7Linked to original sources
PubMed1992

[The combined therapy of Basedow's ophthalmopathy with retrobulbar radiotherapy and i.v. immunoglobulins. The preliminary results].

The most frequently used medical treatment of Graves' ophthalmopathy is the combination of orbital irradiation and systemic corticosteroid. In this study the effectiveness of "high dose intravenous immunoglobulin" (IVIG) in Graves' ophthalmopathy treatment is explored. 11 patients were treated with orbital radiotherapy combined with systemic corticosteroid (Group 1), while 10 patients were treated with the combination of orbital irradiation and IVIG (Group 2). The therapeutic effect was assessed by an ophthalmopathy index based on the American Thyroid Association, classification of ocular changes of Graves' ophthalmopathy. All signs and symptoms of endocrine ophthalmopathy improved significantly in both groups. The mean ophthalmopathy index decreased from 7.0 +/- 1.3 to 3.4 +/- 1.5 in Group 1, and from 7.0 +/- 1.8 to 3.0 +/- 2.1 in Group 2. Statistical analysis showed no significant difference between Group 1 and 2 mean initial and final ophthalmopathy index, and a significant difference between initial and final ophthalmopathy index both in Group 1 and 2. While side effects were present in Group 1 treated with systemic corticosteroid, no side effect was observed in patients treated with IVIG. These preliminary results suggest that IVIG is safe and effective in the treatment of Graves' ophthalmopathy.

Adult↗
PubMed1992

Mucolytic effects of domiodol in tracheostomized patients after total laryngectomy. Double-blind, placebo-controlled, randomized pilot study with four-month follow-up.

The results obtained in a controlled clinical trial aimed at evaluating the efficacy and tolerability of a mucolytic treatment in laryngectomized patients are described. Domiodol (Mucolitico Maggioni, CAS 61869-07-6), an organic iodinated mucolytic agent, was given at the dosage of 60 mg t.i.d. to 20 patients in the post-operative period after laryngectomy (average 2 weeks in hospital and 4 months follow-up at home). A matched series of patients received a placebo during the hospital period and no treatment after discharge. The patients receiving the active treatment showed a statistically and clinically significant improvement of respiratory parameters (cough intensity, sputum quantity, sputum quality, expectoration difficulty). Such improvement was earlier and greater than that observed in the placebo-treated patients. It is concluded that a mucolytic treatment may be helpful in the post-operative treatment of laryngectomized patients with permanent tracheostomy.

Aged↗
PubMed1991

Evidence for a particulate location of ubiquitin conjugates and ubiquitin-conjugating enzymes in rabbit brain.

Conjugate ubiquitin was previously found in the nucleus, cytoplasm, and membranes of eukaryotic cells while the enzymes of the ubiquitin-conjugating system appear to be cytoplasmic. We have prepared the mitochondrial fraction from rabbit brain by discontinuous density gradient ultracentrifugation and by Western blotting, using a specific antibody against conjugate ubiquitin, showing that it contains ubiquitin conjugates in a very wide molecular weight range. Electron microscopy and measurement of specific enzyme markers show that this fraction not only contains mitochondria but also some endoplasmic reticulum vesicles. Immunostaining with anti-ubiquitin IgG followed by immunodecoration with colloidal gold particles provides evidence for the presence of conjugate ubiquitin both in mitochondria and in the endoplasmic reticulum. Furthermore, this "mitochondrial fraction" shows a pronounced ATP-dependent ability to conjugate 125I-ubiquitin into a number of endogenous proteins as evidenced by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Addition of E1, E2, and E3, the enzymes of the ubiquitin conjugating system purified from rabbit reticulocytes, does not further increase this ubiquitination nor incorporate 125I-ubiquitin into additional protein bands. The same mitochondrial fraction is not able to carry out any ATP-dependent degradation of 125I-albumin; however, it contains an isopeptidase activity able to release the covalently incorporated 125I-ubiquitin and is also able to conjugate 125I-ubiquitin to exogenous proteins as oxidized RNase. By affinity chromatography on ubiquitin-agarose of fraction II of a crude Triton X-100 extract of the mitochondrial fraction, several proteins corresponding in Mr to the E1 and E2s enzymes were obtained. These proteins were also able to form specific ubiquitin-thiol ester bounds on sodium dodecyl sulfate-polyacrylamide gels and to support 125I-ubiquitin conjugation to oxidized RNase. Detergent fractionation of the mitochondrial fraction provided evidence for a possible localization of the ubiquitin conjugating activity in the mitochondrial external membrane and endoplasmic reticulum. The presence of an active ubiquitin protein conjugating system in mitochondria and endoplasmic reticulum may be related to the turnover of organelle proteins as well as to specific cell functions such as import of proteins into mitochondria and ubiquitination of externally oriented membrane-bound proteins.

Animals↗
PubMed1991

Density-dependent expression of hyaluronic acid binding to vascular cells in vitro.

Alterations in glycosaminoglycans and their receptors have been associated with changes in cell proliferation during development, wound healing, regeneration, and remodeling. We have previously found a differential effect of hyaluronic acid on the attachment of vascular cells in vitro; endothelial cell (EC) attachment was improved on hyaluronic acid-coated substrates, whereas that of smooth muscle cells (SMC) was reduced (Orlidge and D'Amore, 1986). To determine if hyaluronic acid binding sites are involved in these different substrate preferences, we have studied specific hyaluronic acid binding to cultured bovine aortic EC and SMC. Since very large numbers of cells are required for these binding assays (3 x 10(6)/data point), and since the level of hyaluronate binding to fixed and native SMC and EC was similar, fixed cells were used throughout this study. The effect of cell density on hyaluronic acid binding was investigated. No significant difference was observed between hyaluronic acid binding to sparse and high density SMC. On the other hand, a more than threefold elevation in specific hyaluronic acid binding was observed on low density EC when compared to binding on high density EC. Hyaluronic acid binding was found to be specific; excesses of heparan sulfate and chondroitin sulfate had no effect on the levels of specific binding. Finally, the effect of cell passage on SMC binding of hyaluronic acid was measured. Specific binding was measured from 1st to 12th passage cells and was found to increase with passage number so that by passage 12, hyaluronic acid binding was fourfold that of 1st passage cells. These data support the concept that SMC may become less differentiated upon continuous culture. Our results indicate quantitative changes in the level of hyaluronic acid binding to vascular cells as a function of their growth state. Further, these data correlate well with in vivo observations which suggest a role for hyaluronic acid in vascular development.

Animals↗
PubMed1991

Human cells (normal and ataxia telangiectasia) transfected with pR plasmid are hypersensitive to DNA strand-breaking agents.

Ataxia telangiectasia (AT) cells are known to be hypersensitive to ionizing radiations and to drugs such as bleomycin and epipodophyllotoxin VP16, a topoisomerase II poison. Both of these produce DNA double-strand breaks even if through different mechanisms. In this work we analyzed the sensitivity to bleomycin and to epipodophyllotoxin of AT cells after transfection with pR plasmid. This plasmid, interacting with bacterial SOS repair pathways, expresses itself in mammalian cells conferring cell resistance to the SOS inducers UV and 4NQO and cell sensitivity to different drugs such as bleomycin. This effect is presumably due to the interaction of pR products with double-strand breaks. Our findings indicate that pR plasmid, in both AT lines tested (AT5BIVA fibroblasts and ATL6 lymphoblasts), expresses itself (increasing UV protection) and amplifies the already enhanced AT cell sensitivity to both bleomycin and VP16.

Ataxia Telangiectasia↗
PubMed1990

Regional localization by in situ hybridization of a human chromosome 9 marker tightly linked to the Friedreich's ataxia locus.

In order to determine the regional localization of the Friedreich's ataxia (FA) gene on chromosome 9, the DNA probe DR47 (D9S5), which detects a restriction fragment length polymorphism (RFLP) in tight linkage with the disease, was hybridized in situ to metaphase chromosomes. Our results enable the D9S5 locus to be assigned to the 9q12-q13 region, thus indicating that this is also the localization of the FA gene.

Autoradiography↗
PubMed1990

Friedreich ataxia in Italian families: genetic homogeneity and linkage disequilibrium with the marker loci D9S5 and D9S15.

Friedreich ataxia (FA) is an autosomal recessive degenerative disease of the nervous system of unknown biochemical cause. The FA gene has been shown to be in close linkage with the two chromosome 9 markers D9S5 and D9S15, and linkage disequilibrium between FA and D9S15 has been detected in French families by Hanauer et al. We used new highly informative markers at the above loci to analyze Italian FA families for linkage and linkage disequilibrium. The new markers were a three-allele BstXI RFLP at D9S5 (PIC = .55) and a six-allele microsatellite, typed by polymerase chain reaction, at D9S15 (PIC = .75). We obtained maximum lod scores of 8.25 between FA and D9S5, 10.55 between FA and D9S15, and 9.52 between D9S5 and D9S15, all at zero recombination. Our results, combined with those reported by other authors, reduce maxlod-1 (maximum lod score minus 1) confidence limits to less than 1.1 cM between FA and D9S5, 1.2 cM between FA and D9S15, and 1.4 cM between D9S5 and D9S15. Linkage disequilibrium with FA was found only for D9S15 when all families were evaluated but was also found for a D9S5/D9S15 haplotype in a subgroup of southern Italian families. We conclude that FA, D9S5, and D9S15 are tightly clustered and that studies of geographically restricted groups may reveal a limited number of mutations responsible for the disease in the Italian population. We present preliminary evidence from pulsed-field gel electrophoresis that D9S5 and D9S15 may be less than 450 kb apart. Linkage disequilibrium between FA and D9S15 suggests that the disease gene may be at an even shorter distance from this marker locus, which therefore represents a very good starting point for cloning attempts.

Alleles↗
PubMed1989

Normalization of short-chain acylcoenzyme A dehydrogenase after riboflavin treatment in a girl with multiple acylcoenzyme A dehydrogenase-deficient myopathy.

A 12-year-old girl was shown to have carnitine-deficient lipid storage myopathy and organic aciduria compatible with multiple acylcoenzyme A (acyl-CoA) dehydrogenase deficiency. In muscle mitochondria, activities of both short-chain acyl-CoA dehydrogenase (SCAD) and medium-chain acyl-CoA dehydrogenase (MCAD) were 35% of normal. Antibodies against purified SCAD, MCAD, and electron-transfer flavoprotein were used for detection of cross-reacting material (CRM) in the patient's mitochondria. Western blot analysis showed absence of SCAD-CRM, reduced amounts of MCAD-CRM, and normal amounts of electron-transfer flavoprotein-CRM. The patient, who was unresponsive to treatment with oral carnitine, improved dramatically with daily administration of 100 mg oral riboflavin. Increase in muscle bulk and strength and resolution of the organic aciduria were associated with normalization of SCAD activity and "reappearance" of SCAD-CRM. In contrast, both MCAD activity and MCAD-CRM remained lower than normal. These results suggest that in some patients with multiple acyl-CoA dehydrogenase deficiency riboflavin supplementation may be effective in restoring the activity of SCAD, and possibly of other mitochondrial flavin-dependent enzymes.

Acyl-CoA Dehydrogenases↗
PubMed1989

A case of Refsum disease with atypical clinical picture in family members.

A typical case of Refsum disease with high phytanic acid plasma levels is described. Two siblings showed some features but not the entire clinical spectrum of the disease. The unusual condition of the patient's father, a presumed heterozygotic carrier with characteristic bone abnormalities and a delayed onset retinopathy, is discussed.

Adult↗
PubMed1989

Somatostatin effect in postprandial hypoglycemia.

The effect of the administration of oral glucose with or without a simultaneous intravenous somatostatin infusion on blood glucose, immunoreactive insulin, C-peptide, and glucagon levels in seven patients with idiopathic postprandial hypoglycemia was studied. Oral glucose alone induced an excessive insulin response and hypoglycemia, whereas a slight suppression in glucagon levels without any increase at the hypoglycemic nadir was observed. The simultaneous administration of somatostatin significantly reduced the insulin response and induced a slower rise of blood glucose; no hypoglycemia developed. Only minor variations in glucagon were observed with respect to the basal test. A rebound in insulin, C-peptide, and glucagon levels was observed at the end of the somatostatin infusion. These data show that somatostatin can suppress glucose-induced hypoglycemia in these subjects, thus suggesting that its long-acting analogues might be worth a therapeutic trial in severe idiopathic postprandial hypoglycemia.

Adult↗
PubMed1989

Distribution of calcitonin- and somatostatin-containing cells in thyroid lymphoma and in Hashimoto's thyroiditis.

Eleven cases of thyroid lymphoma were studied by the immunoperoxidase avidin-biotin technique with calcitonin and somatostatin rabbit antisera. In 6 cases of non-Hodgkin lymphoma, in thyroid tissue residual to the lymphomatous infiltration, the C cell density was markedly increased and clustering was often observed; the C cells often took part in the follicular lining, frequently with polar distribution; these elements displayed a strong positivity for calcitonin, while the number of somatostatin-containing cells was lower and the staining less intense. In the only case of Hodgkin's lymphoma of the thyroid gland the staining was negative; in other 4 cases of non-Hodgkin lymphoma no residual thyroid tissue was found and the staining was also negative. As Hashimoto's thyroiditis is often associated with thyroid lymphoma, 13 cases of Hashimoto's thyroiditis were also studied; no C cells were observed and both stainings were negative. These data show that an increase in the C cell number may be a hallmark of thyroid lymphoma and that hyperplastic C cells show an intensive positivity for calcitonin. On the other hand, C cell hyperplasia is not present in Hashimoto's thyroiditis, in spite of the close association with thyroid lymphoma. Furthermore, we provide evidence that somatostatin-containing cells are present both in normal thyroid glands and in thyroid lymphoma.

Calcitonin↗
PubMed1988

Establishment of a new Epstein-Barr virus-immortalized cell line from chronic lymphocytic leukemia with trisomy of chromosome 12 that produces monoclonal IgM against a sheep RBC antigen.

Leukemia cells from a patient with chronic lymphocytic leukemia (CLL) were found to bind sheep RBC (SRBC) through their monoclonal surface IgM. A lymphoblastoid cell line was obtained by immortalization of leukemic cells with Epstein-Barr virus (EBV). Cultured leukemic cells were found to have a supernumerary chromosome 12, an abnormality typical of CLL of the B cell type. To our knowledge, this is the first EBV-immortalized cell line from B-CLL cells of known SRBC specificity and the third reported CLL cell line carrying trisomy of chromosome 12.

Animals↗