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Biomedical subjects

F Di Gregorio

Publications and source records attributed to F Di Gregorio.

At least 73 records · Page 4Linked to original sources
PubMed1988

Ganglioside treatment of vincristine-induced neuropathy. An electrophysiologic study.

A 5-week treatment with vincristine (0.20 or 0.25 mg/kg, i.v., once/week) in the rabbit produced a peripheral neuropathy characterized by both morphologic and electrophysiologic alterations. In particular, electrophysiologic recordings demonstrated that the amplitude, area and conduction velocity of compound action potential (CAP) were consistently reduced in a dose-dependent manner. The simultaneous daily administration of 50 mg/kg ganglioside mixture counteracted significantly this functional impairment, area and amplitude of the monophasic CAP being maintained closer to control values. These results suggest that the loss of functional nerve fibers can be reduced, in vincristine-induced neuropathy, by ganglioside treatment.

Action Potentials↗
PubMed1988

Insulin dependent diabetes in thalassaemia.

Diabetes mellitus was observed in 29 of 448 patients with thalassaemia major attending seven Italian centres. Twelve patients, at onset of clinical diabetes, presented with an asymptomatic glycosuria, 13 with ketosis, and four with ketoacidosis. All were diagnosed after 1979, at a mean age of 17 years. Mean age at diagnosis of diabetes was lower in patients born in the last two decades. In these patients transfusions were started at a younger age and pre-transfusion haemoglobin concentration, serum ferritin concentration, incidence of liver disease, and the presence of a family history of diabetes were higher than in patients born previously. Although 27 (93%) cases had iron chelating treatment the mean serum ferritin concentration was 5600 micrograms/l; 25 (92%) of these patients had signs of liver impairment. The determination of C peptide in 10 patients showed a wide variation in pancreatic beta cell function, and insulin requirements ranged between 0.15 and 1.72 U/kg body weight. Metabolic control was generally poor. The onset of diabetes mellitus was followed in most patients by the appearance of other endocrine or cardiac complications, or both. Fourteen patients died within three years of presenting with overt diabetes. Haemosiderosis, liver infections, and genetic factors seemed to be crucial in diabetes development. Thalassaemic patients developing clinical diabetes mellitus are at high risk for other complications and should be strictly monitored, especially for thyroid impairment.

Age Factors↗
PubMed1987

Immunological changes in beta-thalassemia major patients positive for HTLV-III antibodies.

Antibodies to HTLV-III were found in 6 of 206 Sicilian patients with thalassemia major, aged 1 to 30 years. None of the patients showed clinical signs related to immuno-deficiency syndromes. Immunological investigations carried out in all positive patients showed alterations similar to those found in thalassemic patients without antibodies to HTLV-III. These immunological changes could not depend on the HTLV-III infection, but could be related to the thalassemic condition.

Adolescent↗
PubMed1987

Leukocyte alkaline phosphatase (LAP). A useful marker of zinc status in beta-thalassemic patients.

Intensive desferrioxamine treatment may negatively affect zinc stores in thalassemic patients. Two groups of young thalassemic patients, with good and poor compliance to desferrioxamine treatment, and a control group were investigated. Leukocyte alkaline phosphatase (LAP), zinc content in neutrophils, plasma zinc levels, and urinary zinc excretion were determined. LAP score, and neutrophil zinc and plasma zinc levels of the good compliance patients were statistically lower than those seen in the controls and in the poor compliance patients. Urinary zinc excretion was statistically higher in good compliance patients than in controls and poor compliance patients only during high-dose intravenous desferrioxamine. On the contrary, poor compliance patients had LAP scores, neutrophil zinc, plasma zinc, and urinary zinc excretion values within the normal range. We conclude that high-dose desferrioxamine produces a reduction of zinc stores in thalassemic patients. LAP scores determinations, which are a reliable and inexpensive marker of body zinc, could become a routine test for monitoring thalassemic patients undergoing hypertransfusion programs.

Adolescent↗
PubMed1987

[Prevalence of anti-LAV/HTLV III antibodies in groups at risk of infection and in donors blood in the province of Catania].

The prevalence of anti-LAV/HTLV III antibodies in serum samples of individuals at high risk for AIDS and of healthy individuals living in the province of Catania is reported. Serum samples were collected over the period 1983-86 from 220 drug addicts adults, 339 from multitransfused thalassemia patients, 71 from hemophiliacs, 22 from subjects of the hospital staff who had had contacts with positive subjects, 9 from family contacts of positive multitransfused thalassemics and 7270 from blood donors. Prevalence of antibodies among drug addicts was 14% and a positive subject was found as early as 1983. This result suggested that LAV/HTLV III was already present in Catania at that year. Among the thalassemics and the hemophiliacs the prevalence was 2.3% and 21% respectively. No positive subject was found among hospital staff nor among family contacts of positive thalassemic subjects. Three positive cases have been found among the blood donors and even though these are drug addicts, it is important to underline the necessity of a regular screening of the blood units to prevent LAV/HTLV III diffusion.

Adult↗
PubMed1985

The facilitating effect of gangliosides on the electrogenic (Na+/K+) pump and on the resistance of the membrane potential to hypoxia in neuromuscular preparation.

The effects have been investigated of a mixture of gangliosides from beef brain cortex (GM1, GD1a, GD1b and GT1) either added to the bathing medium or injected intraperitoneally on muscle fibres and nerve terminals in mouse diaphragm. The electrogenic (Na+/K+) pump activity of muscle fibres enriched with sodium was increased by 38% after 2-h pretreatment with gangliosides (5 X 10(-8) mol X 1(-1]. Muscles from animals treated with gangliosides did not show the substantial depolarization of the resting membrane potential (RMP) in K+-free solution (6 h) shown by control muscles. Further, treatment with gangliosides slowed the changes in muscle fibre RMP and frequency of the miniature end-plate potentials in oxygen deprived muscles.

Animals↗
PubMed1984

Gangliosides' dual mode of action: a working hypothesis.

Using in vitro preparations, we have tested the hypothesis that gangliosides, and more specifically GM1, may prevent progressive neural damage following a trauma by means of complex intracellular mechanisms that might be triggered originally by ganglioside interaction with neuronal membranes. We have recently shown that 2-hr ganglioside incubation in vitro stimulates the membrane Na/K pump in neuromuscular preparations. However, 5-6-hr incubation or in vivo treatment for 3 days with a daily injection of gangliosides at a dose of 1 or 10 mg/kg prevents the depolarization that normally occurs after several hours of exposure to K+-free solutions. In such undepolarized muscles, the electrogenic Na+/K+ pump does not seem to be activated. Hippocampal slices subjected to hypoxia undergo depolarization, which is reversed after oxygen readmission. The recovery phase is characterized by a huge hyperpolarization, probably reflecting electrogenic pump activity. In control preparations the depolarization occurs after 3.15 +/- 0.4 min and has a value of 48.7 +/- 5.7 mV; GM1 treatment for at least 4-5 hr increases the latency to 7.3 +/- 2.3 min, and the depolarization is reduced to 31.8 +/- 4.5 mV. This protective effect is accompanied by a reduced hyperpolarization in treated preparations. The ionic studies performed on neuromuscular preparations indicate that the protective effect may not be solely dependent on K+ leakage; however, the experiments are not conclusive and must be repeated with more direct methods. The results obtained indicate a dual mode of action for gangliosides. The early one seems characterized by membrane-enzyme activation, perhaps in relationship to their incorporation in the membrane, which could be compatible with previously described effects, such as enhancement of neuronal sprouting and neuritogenesis. The late one, occurring 4-5 hr after ganglioside addition in vitro, might reflect intracellular events and be compatible with the protective action exhibited by gangliosides against neural damage.

Animals↗
PubMed1984

Ganglioside treatment of genetic and alloxan-induced diabetic neuropathy.

Peripheral neuropathy is a common complication of diabetes. Using the mutant diabetic mouse C57BL/ks (db/db) and alloxan-treated rats, 30 days after intoxication, we investigated development and treatment with gangliosides of such a disease. The db/db mouse develops a neuropathy characterized by a loss in conduction velocity shown as early as 80-90 days after birth and maintained throughout life. At later stages (5-6 months of age) there is a drop in slow transport and myelin particle density. These changes are correlated by a lack of response to insulin treatment, which, prior to this stage, is capable of improving nerve conduction velocity (NCV). On the other hand gangliosides became effective, improving NCV, myelin particle density and sensory perception (auditory deficit) at 5 months of age in the db/db mouse. We presume that this differential neuronal response to insulin and gangliosides indicates a change of the neuropathy from a metabolic stage to neuronal. Alloxan induced diabetic neuropathy is treatable with gangliosides even 30 days after intoxication.

Acetylcholinesterase↗
PubMed1984

Effects of vinblastine in the frog neuromuscular junction during repetitive stimulation.

Vinblastine (10(-5) to 10(-4) M) applied in a Mg-blocked sciatic nerve-sartorius muscle preparation of the frog at the beginning of 20 min of repetitive stimulation of the nerve at 10 Hz, markedly inhibited the facilitation period. There was a smaller increase of end-plate potential amplitude, of quantal content, and of miniature end-plate potential (MEPP) frequency in comparison with that found in experiments without the drug. This depressant effect was more evident when the preparation was preincubated in vinblastine: synaptic responses often disappeared after a few minutes, whereas MEPP frequency attained a maximum at the 5th min. The results suggest a multiple site of action for vinblastine. First, an alteration of both vesicle and plasmalemma membrane, as revealed by the increase of MEPP frequency and by the change of the binomial release features. Second, the drug could damage the intracellular transport system, interfering with the mobilization of the vesicles toward the nerve endings, as shown by the very low or absent facilitation.

Animals↗