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Biomedical subjects

G C Astaldi

Publications and source records attributed to G C Astaldi.

25 records · Page 2Linked to original sources
PubMed1977

Effect of a human serum thymic factor on hydrocortisone-treated thymocytes.

A human serum thymic factors (SF) stimulated cyclic adenosine-3' ,5'-monophosphate (cAMP) synthesis in normal mouse thymocytes. Such stimulation was no longer observed when thymocytes were depleted of hydrocortisone (HC)-sensitive cells. It was concluded that SF selectively stimulate cAMP in HC-sensitive cells. Furthermore, incubation of thymocytes with SF enlarged the population of HC-resistant thymocytes. These results suggest that SF might act on HC-sensitive thymocytes increasing their cellular cAMP level and inducing their transformation in HC-resistant cells.

Animals↗
PubMed1977

Thymosin-induced human serum factor increasing cyclic AMP.

Thymosin has virtually no in vitro effect on cyclic AMP levels in thymocytes and seems not to react with either the beta-adrenergic receptor or with the putative human serum thymic factor (SF) receptor. However, when thymosin is injected into patients lacking SF activity, it induces the appearance of a serum factor which increases cellular cyclic AMP levels in thymocytes in vitro. This factor appears to act on a membrane site distinct from the beta-adrenergic receptors.

Animals↗
PubMed1975

Immunologic cell features in lymphocytic leukemias: a review.

Since four years, it has been possible to classify most cases of Chronic Lymphocytic Leukemia (CLL) as given to the expansion of abnormal B-lymphocytes. On the contrary, the T-cell class is apparently normal and the T cell extent in CLL-peripheral blood can be even greater than normal when taken as absolute value. The clonal nature theory of B-lymphocytes in CLL is substantiated by the fact that, in general, in every patient only one Ig light chain determinant is present. Again, when serum Ig monoclonality is present in CLL, it appears idiotypically identical to the Ig shown by the lymphocytes of the same patient. Among the most important B-lymphocyte abnormalities in CLL, there are: (a) fluorescence of surface Ig is usually less intense than that in normal subjects, and fluorescence intensity may vary not only from patient to patient, but also from cell to cell in the same patient; (b) the Fc-receptor can be lacking; (c) the C3b-receptor is not always present, or it is from 2 to 20 folds less frequent than the C3d-receptor, whereas normal human lymphocytes do not show any outstanding differences between the number of EAC rosette-forming cells either when tested with mouse complement (C3d-receptor) or with human complement (C3b-receptor); (d) the traffic capacity of peripheral-blood B-lymphocytes in CLL is quite defective. All the above-mentioned data, taken as a whole, suggest that CLL is in general given by the expansion of an abnormal clone of cells of B origin, arrested in their maturative development, non-responsive to the mitogen stimulation, accumulating in the peripheral-blood for a traffic deficiency.

Animals↗
PubMed1975

Lymphocyte immunological patterns in leukaemia: a review.

Investigation of the cell S--Ig in acute lymphocytic leukaemia (ALL), at the onset of relapse of the disease, shows quite marked differences from patient to patient according to the extent of the immunofluorescent-positive cells. They may vary from 0.5 to 25% or more. When these Ig-positive cells are treated with trypsin and then incubated "in vitro" for six hours, many of them are no longer Ig-positive, i.e. they do not synthesize Ig. It might be possible, that the membrane-Ig observed before trypsinization does not represent true Ig-determinants of mature B-cells (antibodies attached to leukaemia-specific determinants?). The extent of these features decrease in remission until their disappearance. Relationship between the cell immunological patterns and the treatment response in ALL could exist. In a group of ALL-patients under the same treatment, that is, vincristine and prednisone, the correlation between the course of the disease after the above-mentioned therapy showed quick and complete remission in patients with low percentage of Ig-positive cells (below 10%) and poor improvement (often without complete remission) in patients with higher percentage of Ig-positive cells. Among the most important B-lymphocyte abnormalities in chronic lymphocytic leukaemia (CLL) are the following: (a) fluorescence intensity may vary not only from patient to patient, but also from cell to cell in the same patient; (b) the Fc-receptor can be lacking; (c) the C3b-receptor is not always present, or it is from 2 to 20-folds less frequent than the C3d-receptor, whereas normal human lymphocytes do not show any outstanding differences between the number of EAC rosette-forming cells either when tested with mouse complement (C3d-receptor) or with human complement C3b-receptor); (d) the traffic capacity of peripheral-blood B-lymphocytes in CLL is quite defective. Results of the observations on lymphocytes in CLL, taken as a whole, suggest that CLL is in general given by the expansion of an abnormal clone of cells of B origin, arrested in their maturative development, non-responsive to the mitogen stimulation, accumulating in the peripheral-blood for a traffic deficiency. On the contrary, the T-cells class is apparently normal, and the T-cell extent in CLL-peripheral blood can be even greater than normal when taken as absolute value.

B-Lymphocytes↗