Biomedical subjects
Publications and source records attributed to G Piccoli.
A direct radioassay for the erythrocyte enzyme using U14C-glucose as substrate has been developed. With respect to the indirect spectrophotometric assay this method allows for the determination of true hexokinase activity. The assay proposed is sensitive, rapid and well suited for the determination of hexokinase activity in the erythrocyte lysate where the enzyme level is particularly low.
Sera of patients on peritoneal dialysis and regular hemodialysis were analyzed over a follow-up period of 8 months for the capacity of normal lymphocytes to inhibit E-rosette formation. The percentage of inhibition in sera from peritoneal dialysis patients was significantly reduced (p less than 0.02) only 1 month after treatment was started, whereas in hemodialysis patients the percentage of inhibition remained unchanged. No difference was observed between sera collected before and after the hemodialysis sessions. There was no significant positive correlation between the percentage of E-rosette inhibition and p-urea, p-creatinine, s-albumin, and s-proteins, respectively. Statistical analysis of the E-rosette inhibition test by uremic serum and spontaneous E-rosettes in these patients showed a significant regression coefficient (p less than 0.01) in both groups. The fact that, unlike ultrafiltrate from hemodialysis, peritoneal dialysate significantly (p less than 0.05) inhibits the E-rosette formation capacity of normal lymphocytes, confirms these findings, suggesting an inhibitory activity of serum factors on lymphocyte function.
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The distribution of IgA subclasses in IgA immune complexes (IgA IC) in sera of patients with primary IgA glomerulonephritis and Henoch-Schönlein purpura nephritis was analysed. High levels of IgA IC containing both IgA1 and IgA2 subclasses were present in correlation with the phases of clinical activity. In these nephropathies the finding of IgA subclass distribution in IgA IC similar to that found in secretions may add further support to the hypothesis that IgA IC are of mucosal origin, albeit a primary derangement of the humoral immune system in these patients cannot be disregarded.
The Fc-receptor function of macrophages and monocytes was studied in 10 healthy subjects and 10 patients (5 in phase of clinical activity) affected by systemic vasculitis with histological evidence of renal involvement. Macrophage function was detected by measuring the clearance in vivo of IgG-sensitized 51Cr-labelled autologous red blood cells (RBC). In vitro immune phagocytosis of monocytes was analysed as a kinetic phenomenon by incubating IgG-coated RBC with nearly pure suspensions of peripheral monocytes. All 5 patients studied in phase of clinical activity showed a defective Fc-receptor function in both the assays, as compared with normal subjects. Since a good correlation was found between the in vitro and the in vivo methods, the use of this non-invasive in vitro procedure is proposed as a substitute for the radioactive in vivo techniques in monitoring the course of the above disease.
Peripheral and peritoneal lymphocytes were assayed by numerical tests in adults on peritoneal dialysis. T lymphocytes were classified by monoclonal antibodies (OKT3, OKT4, OKT8) and B lymphocytes by the presence of surface immunoglobulins, using the immunofluorescence technique. Peripheral T cells showed no significant change from the normal, except for T suppressor cells which increased in patients with 2 or more peritonitis episodes. Examination of peritoneal lymphocytes showed a significant reduction in S-IgA lymphocytes (B cells bearing IgA receptors) and an increase in T-suppressor cells (OKT8+) in patients who developed peritonitis in the follow-up study. The implications of these results are discussed with particular reference to susceptibility to peritonitis.
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Numerical and functional markers of peripheral lymphocytes were adopted to study the influence of cimetidine on the immune response in immunocom-promized patients. Twenty-three patients on regular dialysis treatment, who had been given cimetidine (400 mg daily) for peptic ulcer, were studied during a follow-up of 3 months. Thirty healthy people served as controls for the study of the immunological parameters, i.e. DNCB and PPD skin tests, E-rosetting assays, monoclonal antibodies to T-cells, membrane immunoglobulins for the B-cells, serum immunoglobulins and complement. Before therapy was started CMI was impaired in all patients, with a significant reduction in the E-rosette count (P less than 0.01) and depressed DTH (DNCB, PPD). The number of active E-rosettes and OKT4 subsets increased slightly during the period of treatment, though this finding was not confirmed by functional in vivo tests. No change was observed in the B-lymphocyte count and in serum immunoglobulins or complement. The fact that treatment with cimetidine does not seem to influence the immune response in patients on RDT, may suggest that this therapy does not restore the principal immunopathological disorder of these patients, and further justifies its use in patients awaiting renal transplantation or in those who have been given transplant.
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IgA subclasses in circulating immune complexes (IgA1IC), serum immunoglobulins and mesangial deposits in Berger's and Schönlein-Henoch glomerulonephritis (GN) were studied. Both IgA1IC and IgA2IC were significantly higher in Berger's and Schönlein-Henoch GN than in healthy people. In phases of clinical activity both IgAIC subclasses further increased. The IgA1/IgA2 ratio was found not to differ from controls in either groups of patients. An increase in polymeric IgA was observed in Berger's and in Schönlein-Henoch GN. Both IgA subclasses were found in mesangial deposits.
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