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Biomedical subjects

E L Romano

Publications and source records attributed to E L Romano.

36 records · Page 2Linked to original sources
PubMed1984

The effect of desferrioxamine on the proliferative response of rat lymphocytes stimulated with various mitogens in vitro.

This paper reports experiments designed to evaluate the effect of desferrioxamine on lymphocytes obtained from the spleen of Sprague-Dawley rats. The results showed that desferrioxamine inhibits the proliferative response of lymphocytes stimulated by concanavalin A or pokeweed mitogen, the effect being proportional to the dose used, and being maximal at the end of the culture period. To exert its effect, desferrioxamine has to be present from the initiation of the cultures--its addition 24 h later markedly reduced its inhibitory effect. Studies of cell viability indicated that the inhibition was not due to toxicity. Lymphocytes obtained from young animals (4 to 12-week-old) were more sensitive to desferrioxamine than older animals (13 to 18-week-old). Saturation of desferrioxamine with iron abolished its effect, suggesting a direct relationship between chelating properties and inhibition, and reinforcing the hypothesis that iron plays an important role in the process of cell division.

Animals↗
PubMed1984

Destruction of IgG anti-A sensitized erythrocytes by mononuclear leucocytes from normal and ABO haemolytic disease affected infants.

Studies were undertaken to investigate the antibody-dependent cell-mediated cytotoxicity (ADCC) activity of mononuclear leucocytes (MNL) from cord and healthy adult blood and that from infants with ABO haemolytic disease. The ADCC levels of MNL from both types of newborn blood were found to be higher than that of MNL from adult blood. The extent of ADCC was positively related to the degree of antibody sensitization of the red cells and to the effector cell target cell ratio. The ADCC activity was effected mainly by the adherent cell fraction and could be inhibited by cytochalasin B, hydrocortisone and also by high concentrations (more than 0.5 mg/ml) of non-specific free human IgG. Phagocytosis was also demonstrated to be an important mechanism in the destruction of IgG anti-A coated red cells by the MNL.

ABO Blood-Group System↗
PubMed1983

Studies on the binding of IgG and F(ab) anti-A to adult and newborn group A red cells.

The values of the functional affinity constants for the binding of human IgG anti-A and its F(ab) derivative with adult and newborn group-A red cells have been determined. The values obtained for both monovalent and bivalent antibody with both types of cells were of the same order (about 1 X 10(8) M-1), indicating that IgG anti-A binds to red cells only by one of its F(ab) arms.

ABO Blood-Group System↗
PubMed1982

Plasma fibrinogen concentration in ABO-hemolytic disease of the newborn.

Plasma fibrinogen and total serum proteins were measured in infants affected by ABO-hemolytic disease and in normal infants' cord blood and blood taken 48 h after birth. The average plasma fibrinogen concentrations in the blood of infants with ABO-hemolytic disease was 447.36 mg/dl as compared with 267.09 mg/dl (p less than 0.005) in cord blood and 313.82 mg/dl (p less than 0.005) in blood samples taken 48 h after birth. A simple 'autoagglutination' test is found to be helpful when establishing the diagnosis of ABO-hemolytic disease.

ABO Blood-Group System↗
PubMed1979

Fe(III)-EDTA complex as iron fortification. Further studies.

The data presented confirm the advantages of Fe(III)-EDTA as a salt for iron fortification. This iron compound exchanges completely with intrinsic wheat iron in the lumen of the gut. The iron absorption data from this salt tested with six different food vehicles compared with the absorption of ferrous sulfate administered with the same vehicles indicate that while the mean absorption from ferrous sulfate varies from 2 to 30% according to the food vehicle mixed with the salt, the absorption from Fe(III)-EDTA remains practically the same. Apparently, the iron absorption from Fe(III)-EDTA complex is slightly or not affected by the presence of vegetable foods or milk. All these data suggest that only a small amount of iron from this salt, about 10 mg/day, would be necessary to prevent iron deficiency anemia even in those populations relying for their subsistence on vegetable food only.

Absorption↗
PubMed1978

Number of B sites generated on group O red cells from adults and newborn infants.

When red cells from the group O blood of adults and newborn infants (cord blood) were incubated with UDP-galactose and group B serum, over 200,000 B sites per cell were generated on adult O cells but only 40,000--70,000 sites per cell on cord cells. It is concluded that smaller amounts of substrate for the B transferase are present on cord cells.

ABO Blood-Group System↗
PubMed1976

Direct observation of immunoglobulins on the erythrocyte membrane.

A modification of the sublimation procedure for observation of cell membrane exteriors is described. By retaining basic advantages of the freeze-fracture technique, without actual fracturing of the sample, high quality replicas can be produced on which molecules such as immunoglobulins can be identified and mapped on extensive areas of the erythrocyte membrane surfaces. The method can be used for direct observation of antibodies without recourse to labelling with other marker molecules, such as for example ferritin. In addition, direct visualization of clumping of red cells, as induced by such antibodies, is feasible.

Cell Membrane↗
PubMed1975

Red cell destruction in vivo by low concentrations of IgG anti-A.

Red cells coated with as little as 0.3-0.5 mug anti-A/ML cells were found to agglutinate if mixed with plasma and rocked on a tile, whereas the minimum amount of IgG anti-Rh required for agglutination under these conditions was about 50 mug antibody/ml cells. Complement-binding by red cells coated with IgG anti-A could be demonstrated only when the amount of antibody on the cells was at least 14 mug antibody/ml cells. Since in ABO haemolytic disease the amount of antibody on the cells is frequently less than 0.6 mug/ml cells, it seems that red cell destruction in this syndrome is not due to the activation of complement but may be due to the sequestration of agglutinated cells. A few experiments are described in which the survival in vivo of small amounts of agglutinated cells was studied. Reasons are given for considering that such experiments fail to mimic the conditions prevailing in ABO haemolytic disease.

ABO Blood-Group System↗
PubMed1975

Distribution and mobility of the A, D and c antigens on human red cell membranes: studies with a gold-labelled antiglobulin reagent.

Studies are presented in which a gold-labelled anti-IgG reagent has been used to map the distribution of A, D and c antigen sites on the human red cell membrane. Red cells were combined with IgG antibodies; ghosts were produced which were then labelled with gold-anti-IgG. D antigen sites were found to be single entities dispersed on the red cell membrane of lysed but otherwise untreated Rh positive cells. Following papain treatment prior to lysis, a clustered distribution was observed. Clustering of D sites was also observed on non-enzyme-treated red cells of the -D- phenotype. Further studies indicated that D and c antigen sites are closely associated on ccDEE red cells. The distribution of A antigen sites was found to be clustered in proportion to the amount of IgG anti-A combined with the cells. Reasons are given for considering such distribution as indirect evidence of mobility of A sites. There was an association between agglutinability of red cells by IgG antibodies and the extent of the clustering of the antigen sites.

ABO Blood-Group System↗
PubMed1973

Direct antiglobulin reaction in ABO-haemolytic disease of the newborn.

The minimum number of IgG anti-A (or anti-B) molecules detectable on A or B red cells by the antiglobulin reaction was found to be the same-that is, about 150 molecules per red cell-with newborn as with adult cells. Furthermore, the ratio of anti-IgG bound to IgG anti-A (or anti-B) molecules was the same whether the anti-A (or anti-B) molecules were present on newborn or on adult cells and was similar to that found for anti-IgG bound to IgG anti-Rh.In 15 infants (11 group A, 4 group B) with haemolytic disease of the newborn due to ABO-incompatibility the amount of anti-A or anti-B on the red cells ranged from 0.25 to 3.5 mug antibody per ml red cells, corresponding to 90-1,320 antibody molecules per cell; only five infants had more than 0.55 mug antibody per ml of red cells. These amounts are far smaller than those found in most moderate or severe cases of Rh-haemolytic disease.It is concluded that the weak direct antiglobulin reactions observed in ABO-haemolytic disease are due simply to the fact that the number of anti-A (or anti-B) molecules on the infant's red cells is at the lower limit of sensitivity of the test. Since ABO-haemolytic disease can be quite a severe process it seems probable that IgG anti-A and anti-B molecules are more effective than anti-Rh molecules in bringing about red cell destruction.

ABO Blood-Group System↗
PubMedDate not supplied

Complement fixation by Rh blood group antibodies.

Rh blood group antibodies normally do not fix complement. Rh positive intact red blood cells treated with papain do not lyse when incubated with corresponding antibody and complement. This study was done to determine if complement fixation occurs when antibodies were combined with Rh positive red blood cell ghosts untreated or treated with papain. Complement fixation was observed with IgG anti-D, anti-DC and anti-c when papain treated ghosts were used. No complement fixation or a smaller degree of it was observed in the case of untreated Rh positive red blood cell ghosts when incubated with similar anti-Rh antibodies. It is concluded that the papain treatment of Rh positive red blood cell ghosts, possibly by inducing aggregation of antigen sites, allowed complement binding by Rh antibodies.

Animals↗