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Biomedical subjects

J M Ross

Publications and source records attributed to J M Ross.

At least 73 records · Page 4Linked to original sources
PubMed1979

Fathering: a review of some psychoanalytic contributions on paternity.

The paper has traced psychoanalysis' gradual appreciation of a father's facilitative impact on his children's psychosexual and psychosocial growth. Freud's initial notions accentuated the inhibiting, punitive aspects of the paternal representation, highlighting, as they did, the oedipal father of the primal horde. Save for a few significant glimmers here and there, he pretty much failed to consider a son's or daughter's search for a father with whom to identify and, with this, underplayed some of the crucial preconditions for the oedipal complex itself. In recent years, an ego-psychological focus on the 'dual unity' of mother and child, in Mahler's words, has tended to relegate the father to a secondary role in pre-oedipal development. And yet, influenced by this overview, Loewald, Greenacre, Abelin and others have underlined the ways in which a father helps extricate a child from the maternal orbit, facilitating a sense of reality, self-constancy, sexual identify and other epigenetic achievements which help secure object constancy and self-identity. What remains is a fuller elucidation of the reciprocal and complex affective interchanges that take place within the father-child dyad throughout childhood.

Child↗
PubMed1973

Association of white cell and red cell antibodies in human sera.

Five hundred and eighteen human sera containing known red cell antibodies were tested for lymphocytotoxic antibodies and 81 sera were found to contain them. Thirty-nine antibodies were fully characterized. The frequencies of anti-I, K, V(w), and Wr(a) were significantly greater in those of the 518 sera which also contained white cell antibodies.Four hundred and ninety-four of the 518 sera containing red cell antibodies contained anti-Rh and anti-Kell. The frequency of white cell antibodies in this group was 15% compared with a frequency of 12% in a series of 923 antenatal samples not containing anti-Rh or anti-Kell. The frequencies of different anti-HL-A specificities were compared in the two groups with or without anti-Rh and anti-Kell antibodies. Anti-HL-A 1, 7, and 8 occurred more frequently in the absence of these red cell antibodies and anti-HL-A 12 occurred more frequently in their presence. No correlation was found between particular red cell and white cell antibodies.

Antibodies↗
PubMed1972

Unstable variant of NADH methemoglobin reductase in Puerto Ricans with hereditary methemoglobinemia.

The electrophoretic mobility of erythrocyte NADH methemoglobin reductase in five hereditary methemoglobinemia patients from three Puerto Rican kindreds was 118% of normal at pH 8.6. The methemoglobin ferrocyanide reductase activity of the enzyme in erythrocyte hemolysates was 3.2-6.4% of normal. Electrophoresis of hemolysates prepared from the blood of patients from two different families at six pH values between 4.6 and 9.3 did not differentiate between the variant enzymes. Examination of the deficient enzymes extracted from the erythrocytes of one patient from each kindred revealed altered affinity for NADH and dichloroindophenol dye and decreased thermal stability. The quantitative similarity of the abnormal findings, together with the Puerto Rican origin of the kindreds, suggested that the cyanotic patients possessed the same abnormal enzyme and were thus homozygous for the same rare mutant gene. Consanguinity of the kindreds could not be established. The rates of decline of the normal and variant NADH methemoglobin reductase enzymes in vivo were measured in erythrocyte fractions of increasing cell age. The rate of decline of the variant enzyme was increased 20-fold by comparison with the normal enzyme. The methemoglobin percentage in erythrocyte fractions of increasing cell age correlated inversely with the activity of the variant. The variant enzyme averaged 37% of normal mean activity in young cells and 1% in old cells. The normal enzyme, on the other hand, lost only one-sixth of its activity as the cells aged, and the methemoglobin content in old normal cells did not rise. These observations support the hypothesis that the deficient activity and the heterogeneous pattern of methemoglobin accumulation in vivo arise principally from the accelerated inactivation of variant NADH methemoglobin reductase during the life-span of the red blood cell.

Adolescent↗