The genetic study of sterility, although rather complex, may be carried out, as far as the parents are concerned, on the basis of existing detection methods. A number of forms of individual sterility may be detected on the basis of the caryotype (ovarian and testicular dysgenesis, hermaphroditism), while a chromosomal pathologic phenotype is missing for others, and the corresponding genotypes must be detected through clinico-genealogical methods (pseudohermaphroditism, adrenogenital syndrome, Laurence-Moon-Bardet-Biedl syndrome, hereditary malformations). It is noted that the problem of immunitary incompatibility is not sufficiently clear. Examples are presented of others forms of sterility depending on a lethal load of the conceptus, for which consanguineous marriages may be held largely responsible. Cases of sterility may also be found in relation to mental diseases. The importance of eugenic counseling is stressed.

Essential hypertension was first recognized as morbid entity in 1911 and the word “essential” was substituted by “constitutional” in 1933. Diastolic hypertension may be constitutional or “symptomatic” if it belongs to the symptoms of a disease of specific organs (kidneys, endocrine, metabolic disease, cerebral or vascular disease). It is futile to search for such a diseased specific organ in constitutional hypertension (1933). Constitutional hypertension is a constitutional variant due to insufficient perfection of the homeostatic (feed-back) system maintaining the habitual blood pressure at a constant normal level. It is of multifactorial (polygenic) etiology (1960). It is a definite predisposition to actual diseases. It is a matter of semantics whether or not it should be called a disease of its own. The syntropy of constitutional hypertension and diabetes, obesity and arteriosclerosis is best explained by sharing various parts of polygenomes that are the common genetic basis of each of these morbid states.

The mechanism and the familial pattern of the late lepromin reaction (Mitsuda reaction) have been discussed. The interpretation of the familial correlation as mainly depending on a pair of allelic genes has been analysed thoroughly. A new technique has been described for identifying constitutional resistance or susceptibility to leprosy at an in vitro tissular level. The possibilities of this technique have been stressed.

Studies on the glucose-6-phosphate dehydrogenase activity of erythrocytes from 416 males and 820 females are reported. The total number of deficient males (intermediate + complete) varied from 3.9% among the whites (102 persons) to 15.1% among Dark Mulattoes (99 individuals); the incidence in the Negroid sample in general (316 persons) was 12.4%. The data obtained among the women were utilized to study problems of penetrance of the G-6-PDD genes. Results obtained in both sexes were employed to verify, unsuccessfully, possible selection differentials through age analysis and the comparison of the gene incidences of people affected with minor ailments and controls. Problems of gene flow analysis in populations like this one in which the “Negro” and “White” forms of the deficiency are present were stressed.

Data are reported about the occurrence of glucose-6-phosphate dehydrogenase deficiency (G-6-PDD) and abnormal hemoglobins in a sample (316 males and 679 females) of the Negroid population of Porto Alegre, Brazil. The prevalence of double carriers (AS/G-6-PDD) was that expected from the isolated incidence of both anomalies. A review of the literature shows similar results for 3491 males and 289 females from African and American Negroid groups both from areas with and without malaria. Therefore there seem to exist no grounds for postulating an adaptive interaction between these two polymorphisms.

Nineteen variants of the iron-binding protein, transferrin, have been described in human serum. The world literature on the distribution of these variants in human populations is surveyed in comprehensive tables and attention is drawn to some of the outstanding deficiencies in our present knowledge of this distribution. It is pointed out that transferrin variants are important markers in anthropological studies.

It was on June 25, 1943 that the world lost a great mind and a great medical scientist, when Dr. Karl Landsteiner succumbed to the effects of a heart attack that had overtaken him two days before while he was actively at work in his laboratory. He had just passed his seventy-fifth birthday of a lifetime devoted to fundamental research. Shortly before his death he had completed the second edition of his classic book, “The Specificity of Serological Reactions”, and he had also published almost 350 scientific papers describing the results of his pioneering investigations. This year is the centenary of the birth of Karl Landsteiner, and it seems fitting at this time to pay tribute to this genius and benefactor of mankind by reviewing some of his great discoveries.

Of Dr. Landsteiner's discoveries, the one that has captivated the popular imagination the most is his discovery of the A-B-O blood groups, frequently called the Landsteiner blood groups in his honor. At the beginning of the present century, it was recognized that bloods from animals of different species could be distinguished from one another by their serological reactions. For this reason, the use of animal blood for transfusions to human beings was abandoned, but the frequent serious reactions that followed transfusions of blood from one human being to another still remained unexplained. Landsteiner then tested the blood of workers in his laboratory by mixing serum taken from one individual with the red cells of others. He found that instead of the weak or negative reactions that might have been expected, in some combinations strong agglutination of the red cells occurred, while in other combinations no effect was apparent.