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Biomedical subjects

R Bellazzi

Publications and source records attributed to R Bellazzi.

12 recordsLinked to original sources
PubMed1992

Drug delivery optimization through Bayesian networks.

This paper describes how Bayesian Networks can be used in combination with compartmental models to plan Recombinant Human Erythropoietin (r-HuEPO) delivery in the treatment of anemia of chronic uremic patients. Past measurements of hematocrit or hemoglobin concentration in a patient during the therapy can be exploited to adjust the parameters of a compartmental model of the erythropoiesis. This adaptive process allows more accurate patient-specific predictions, and hence a more rational dosage planning. We describe a drug delivery optimization protocol, based on our approach. Some results obtained on real data are presented.

Anemia↗
PubMed1991

GAMEES: a probabilistic environment for expert systems.

This paper describes GAMEES (Graphical Modelling Environment for Expert Systems), an interactive graphical environment for building and processing Belief Networks and Influence Diagrams. We review the existing systems designed for analogous purposes, and, after a brief introduction to Belief Networks and Influence Diagrams, we describe the graphical interface, discuss algorithms for probabilistic inference on these networks and illustrate the current implementation of GAMEES. The system has been designed for being integrated within wider expert systems and actually it is part of the Therapy Advisor module within an expert system for the management of anemic patients.

Algorithms↗
PubMed1991

Acute effects of repetitive hemodialysis on circulating immunoreactive parathyroid hormone levels in uremic patients undergoing vitamin D (calcitriol) therapy.

The acute effects on parathyroid gland activity of repetitive hemodialysis with a dialysate calcium concentration of between 3.5 and 4 mEq/l were evaluated in 21 hemodialysis patients on calcitriol therapy for 1 year or more. In this study circulating immunoreactive parathyroid hormone (iPTH) levels were measured using radioimmunoassay specific for C-terminal iPTH (C-PTH), middle molecule iPTH (MM-PTH) and intact iPTH (I-PTH), before the dialysis session at the end of the week (I), after 4 h regular hemodialysis (II) and after a further 72 h (III). C-PTH was abnormally high (202 +/- 64 pmol/l) (I) in 18 patients with no documented parathyroid hyperplasia and showed no significant difference in subsequent controls. MM-PTH was also high (379 +/- 125.5 pmol/l) (I), but decreased to 348 +/- 136.7 (II) (p less than 0.05) and returned to predialysis levels (III). I-PTH (I) was 8.2 +/- 5.3 pmol/l (normal levels in 8 patients), fell to 3.4 +/- 2.6 pmol/l (II) (p less than 0.01), and increased (p less than 0.01) with respect to the basal levels of 11.1 +/- 7.5 pmol/l (III). Three patients presented echographically documentable parathyroid hyperplasia and, despite constantly high iPTH levels, showed a similar I-PTH behavior while MM-PTH and C-PTH revealed no constant pattern. The decrease in iPTH levels was accompanied by a significant increase in total calcium and ionized calcium during the hemodialysis session. No significant changes in iCa and Ca together with I-PTH levels were found in 4 volunteers before and after the hemodialysis session with dialysate calcium 2.75 mEq/l. We conclude that I-PTH assay has been shown to capture acute changes in parathyroid gland activity in hemodialyzed patients for both low and high iPTH levels. High calcium dialysate hemodialysis inhibits acutely intradialytic PTH secretion but the effect is just temporary and the 72-hour interdialytic period, despite vitamin D therapy, stimulates parathyroid secretion significantly. Nevertheless, I-PTH fluctuations occur in some patients within the normal range, and high dialysate and calcitriol therapy seem to be capable of controlling parathyroid activity; as regards the remaining population, we suggest that a personalized therapeutic approach should be studied with a view to achieving a better control of interdialytic calcium homeostasis.

Adult↗
PubMed1982

Insulin receptors in myotonic dystrophy: a study with mononuclear leucocytes and erythrocytes.

We evaluated insulin receptor activity on mononuclear leucocytes and erythrocytes in 9 patients with myotonic dystrophy and in 9 controls. The results demonstrated that in myotonic dystrophy: 1. insulin binding to specific receptors was significantly impaired (P less than 0.01) because of a reduction in the number of high and low affinity receptors. 2. the affinity constants were not significantly affected 3. there was no correlation between receptor activity, insulin behaviour and glucose tolerance. These data obtained in two different cellular systems suggest that the constant numerical reduction of insulin receptors was probably due to a systemic membrane defect, typical of myotonic dystrophy.

Adult↗
PubMed1979

Insulin receptors in human mononuclear leucocytes. II. Binding and degradation of insulin in obese subjects.

The binding of insulin to the receptors on circulating mononuclear cells of obese subjects is significantly decreased when compared to the binding in normal subjects. This fenomenon is due to the reduction of the number of insulin receptors rather than reduction in affinity. The insulin degradation is also reduced, but a very strong correlation, similar to that demonstrated in normal subjects exist between insulin binding to its receptors and insulin degradation.

Adult↗
PubMed1979

Insulin receptors in psoriasis.

We have demonstrated how in psoriasis, irrespective of any diabetic family history, there exists a state of hyperinsulinism with a decreased resistance to insulin, which is aggravated by obesity. Since reviewing the latest studies concerning diabetes at the receptor level, we have carried out a comparative study dealing with insulin receptors in lymphocytes in homogeneous groups of normal, obese, and psoriatics of normal weight and overweight. We have also made a comparison regarding the behaviour of the receptors in these various metabolic states.

Blood Glucose↗
PubMedDate not supplied

Binding and degradation of 125I-insulin in human erythrocytes. Comparative studies with hemolysate and membranes.

Insulin degradation in human erythrocytes obtained from normal subjects is studied. Under the experimental conditions used, insulin binding and insulin degradation are strictly correlated, and no degrading activity is released in incubation medium. Comparative analysis of hemolysate and membranes shows that hemolysate possesses a definite insulin-degrading activity which is not linked to the hemoglobin molecule; the km of this enzymatic activity is of the same order of magnitude as that reported in other cells. At the concentration and in the condition used in this study, membranes degrade insulin at a lower rate than hemolysate.

Erythrocyte Membrane↗