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Biomedical subjects

J L Scaro

Publications and source records attributed to J L Scaro.

At least 19 recordsLinked to original sources
PubMed1998

Urinary elimination of erythropoietin in patients under treatment with cytostatics drugs.

Reductions in the hemoglobin (Hb) mass are followed by increases in the level of plasma erythropoietin (EPO) concentrations which are directly proportional to the level of the hormone required to bring the hemoglobin values back to normalcy. Hypoplastic anemias (AHC) on the other hand, are accompanied by significantly larger increases in the erythropoietin concentration. In this study we have measured the relationship between the severity of the anemia and the levels of erythropoietin elimination in the urine patients (EpoU) under treatment with cytostatic drugs. Simultaneously other parameters used as indicators of bone marrow activity were determined. These observations suggest that the levels of erythropoietin depends not only by the tissue oxygen availability but by others factors related to the marrow cellularity.

Anemia↗
PubMed1993

A new approach to the etiopathogenesis of AIDS.

This hypothesis proposes as an explanation for the origin of the Acquired Immuno-Deficiency Syndrome (AIDS), the homosexual transmission of spermatozoons. The male gamete may possess a depressing action on the immuno-competence of the egg aimed to prevent the rejection of the spermatozoon material. The female organism may be able to inactivate this action, an ability that might be absent in the male organism. As a consequence of the loss of its immunological competence, the body is invaded by a variety of microorganisms, among which certain elemental classes of viruses would strive successfully for long periods of time. Their permanence in the depressed organism would enable them to overcome the immune barriers present in normal subjects, becoming thus, transmissible and in some cases even pathogenic for the new host.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Ability of the Fe-transferring complex to transfer Fe to reticulocytes in nutritional anemia].

Using an in vitro technique the ability of the Fe/Transferrin complex in the serum of calories and proteins in chronically deprived adult males was investigated. The study included the behavior of the same function in the sera of other types of anemias. A significant reduction of the Fe donating capacity was found in the sera of patients suffering from nutritional anemia (NA), whereas this change was absent in the sera of other type of anemias. A deterioration of the iron donating function of the Fe/Transferrin complex caused by malnutrition, is postulated. The participation of this alteration in the production of NA is considered.

Adult↗
PubMed1992

Relationship between erythropoietic rate and iron donating capacity of the Fe/transferrin complex in mouse.

The transfer of iron from the Fe/transferrin complex to the erythroid cells was studied in in vitro system in mice in which a drastic and opposite change in their erythropoietic activity was produced by bleeding or actinomycin D administration. A reduction of iron donation in the serum of bled animals was found, whereas the aplastic condition induce in the donors of the serum by actinomycin D did not produce any change in the transfer process. It was also found that in spite of the normalization of the saturation in the serum of bled animals, the diminished donation remained unchanged. The possibility that conditions other than quantitative could produce this behavior is discussed.

Animals↗
PubMed1990

[Trophic effect of testosterone on erythropoiesis in the mouse].

Some differences between erythropoietin biogenesis under the action of natural stimuli and that resulting from testosterone administration are commented. Evidences are presented suggesting that androgens, apart from amplifying erythropoietin production, might exert some action on the stroma as specific erythrocytic tissue. This action could be anabolic or trophic and not erythropoietin dependent, at least to some extent, its effect being applied on the quantitative erythropoietic homeostasis.

Animals↗
PubMed1988

A simple method for concentrating erythropoietin activity in plasma and in other body fluids.

The method here described is based on the property of erythropoietin to remain in water solution in the presence of up to 60% ethanol. More than 90% of inert proteins precipitate in the process and can be eliminated without significant loss of the activity. The addition of sulfuric ether produces the separation of the water phase and of its solutes which can be recovered in the solid material obtained by lyophilization. Using this method a marked erythropoietin activity can be demonstrated in extracts of the plasma from mice with a moderate reduction of the hematocrit.

Erythropoietin↗
PubMed1985

A bioassay method for studying factors stimulating erythropoiesis using as recipient the mouse with a functionally active erythron.

This novel bioassay method basically differs from the conventional plethoric mouse assay in the timing of the onset of induced polycythemia relative to the administration of the substances that are being tested. While the latter measures the regenerating action of erythropoietin at a time when erythropoiesis is virtually absent, the method here described evaluates the stimulatory action(s) required to maintain the normality of the process. This fact opens new approaches for studying factors involved in the quantitative govern of erythropoiesis in the steady state.

Animals↗
PubMed1984

Systemic oxygen transport and erythropoiesis in the mouse.

Removal of 15% of blood volume in the mouse increases erythropoiesis by a factor of 2.2 when measured 12 h after bleeding. Exposure of normal mice to 40% reduced barometric pressure for the same period of time increases erythropoiesis only by a factor of 1.6. The response to hypoxia takes place in the presence of a 40% reduction of oxygen consumption and tissue-venous PO2, changes which are concomitant with a 5-fold increase in plasma erythropoietin activity. The larger response in anemic animals on the other hand occurs without any detectable change in these parameters. These results cast serious doubts about the interpretation of the quantitative homeostatic control of erythropoiesis based solely on the action of erythropoietin.

Anemia↗
PubMed1982

Effects of sphingolipids on erythroblastic maturation in the mouse.

The changes effected by injection of an extract of phospholipids obtained from the plasma of normal human donors (PLE) or an emulsion of commercially available sphingolipids on erythropoiesis in the mouse were studied. The parameters followed were 59Fe uptake by the erythroid tissue and the number of circulating reticulocytes. It was found that in the 12--24-h period following administration of PLE or purified sphingomyelin a significant increase in 59Fe uptake by circulating RBC an by their hemic fraction takes place. This change was associated with a higher 59Fe utilization by the bone marrow and with an increase in the number of circulating reticulocytes.

Animals↗
PubMed1980

Erythropoietic changes effected by foreign serum in the mouse.

Injection of foreign serum into mice increases erythrocyte formation as evaluated by ferrokinetics studies. When erythropoiesis is depressed either by fasting or plethora, the wave of erythropoiesis that follows a transient increase of endogenous erythropoietin is clearly enhanced by pretreatment of the recipients with foreign serum. The response includes a restoration of the responsiveness of the spleen of fasted mice to endogenous erythropoietin stimulation. These changes seem related to an effect of foreign serum on the transition of primitive hematopoietic progenitors into erythroid-committed progenitors.

Animals↗
PubMed1980

Acute hypocalcemia and erythropoiesis in the mouse.

Mice were made acutely hypocalcemic by injection of sodium oxalate. After the transient drop of plasma calcium marked changes in erythroblastic proliferation, number of erythroblasts and 59Fe kinetics were observed. The probable mechanism of this response that may reflect increased erythropoiesis is discussed.

Acute Disease↗