The Author deals with the problem of morbid disposition from the genetic standpoint. He further reports and discusses the results obtained by studying 447 pairs of tuberculous brothers, as far as the age of onset, the clinical form and the localization of the tubercular process are concerned.

Data are also reported concerning the morbidity of silicosis among 683 Sardinian mineworkers, especially concerning its frequency in the families of both affected and healthy propositi, for a total amount of 9,127 individuals examined. The results are also shown of a wide survey carried out on 293 single-born and 2,474 twins, concerning the following allergic diseases: eczema, asthma, urticaria and hay-fever. The possible mechanism of inheritance of morbid disposition is also discussed.

An unusual case is described in which a man was accused of the paternity of a child, and an expert reported him to be type RhzRh1, the mother as type Rh1rh and the child as type Rh2rh, thus excluding paternity. In repeat blood tests, the author confirmed the typing results on the putative father and the mother, but showed the child to be type Rhzrh instead of type Rh2rh, so that paternity was not excluded. Instead, the presence in both putative father and child of the rare gene RZ (or ry) could be considered circumstantial evidence that the accused man actually was the father. It is pointed out that the error could easily have been due to the mistaken use of anti-rhi serum in place of anti-rh′ serum. Such an error would be more apt to occur with a worker using the fallacious C-D-E notations, because the tacit assumption implicit in those notations that each agglutinogen has but a single corresponding antibody (and blood factor) would render unthinkable the concept of more than one kind of anti-rh′ (anti-C) reagent.

The authors briefly describe their old and recent research work on the etiology of leukemia, and discuss the genetic-viral hypothesis of human leukemia. The injection of human leukemic blood in fertilized chicken eggs, before incubation, causes a severe disease in the embryos. This disease is characterized by the fact that the hemoblasts are extremely atypical, and loose the ability to produce intravascular blood cells, while they form perivascular infiltrates. The disease is indefinitely transmitted from egg to egg, also using acellular filtered material. The transmissibility is inactivated by heat. In conclusion, we can say that the observations described strongly support the viral etiology of human leukemia and suggest the hypothesis that the virus might be responsible for a somatic mutation of the blasts.

Duodenal ulcer is a rather common disease, showing a clear family concentration. The aim of this work was to detect, in the etiology of this disease, possible genetic components, and to study their characteristics. The survey has been carried out by analyzing the data collected in 100 families, assembled by starting from a corresponding number of « index cases », and utilizing for comparison and also further analyzing the data by Doll and Buch (1950) and by Doll and Kelloch (1951). The " secondary cases " found, as a whole, were 109 (90 males and 19 females). The results may be summarized as follows:

1) the frequency of the disease in the sibships, independently from sex and corrected for age, is of 32.5% ± 2.5;

2) the frequency is, however, different in the two sexes. The estimate of this difference has been obtained calculating the relative risk (x) to contract the disease in the males, as compared to the females. Considering all the families together, such risk is x =5.8. However, x =16.7 in the 39 families with both healthy parents; x = 4.0 in the 45 families with the father affected; x = 2.9 in the families with the mother affected;

3) though the analysis of segregation ratios would not allow, by itself, definitely excluding the hypothesis of a monofactorial recessive inheritance, many reasons lead to think of a possible case of « simulated mendelism »;

4) the application of the methods of analysis proposed and worked out, in their theoretical basis, by Penrose (1953) and by Edwards (1960) for the genetic study of common diseases, makes much more probable the hypothesis that the genetic basis of duodenal ulcer is multifactorial. This does not exclude, however, that some particular environmental factors may increase the phenotypical correlation among the brothers — at least in the material under consideration.

Therefore, the hypothesis now allowing the best interpretation of the observations is that duodenal ulcer could be controlled by a number of additive genes with a weak effect.

Present status of genetic and anthropological knowledge concerning haptoglobins, and report on the results of a survey carried-out on 141 subjects from Campania: Hp 1-1, 15 (10.6%); Hp 2-2, 60 (42.6%); Hp 2-1, 66 (46.8%); gene Hp1, 34.1%, gene Hp2, 69.1%.

Furthermore, a geographical peculiarity of haptoglobins is stressed, i.e. a rise in the frequency of the Hp2 gene from Westward to Eastward.

Methods have been presented for the determination of main-line index and transversality of the distal plantar ridges. For studying the collective main-line formula, a scheme of ‘modal types’ for the four main lines has been introduced. The computation of the summational main-line index has been made possible by devising a scheme of numerical values for the various terminations of main lines D and A. Cases where the main line D or A is abortive or non-existent should be eliminated from the assessment of main-line index. The degree of transversality should be determined from the percentage proportion of the mean main-line index with the maximum possible index.

A case of puberal goiter in a pair of monozygotic twins is described. The striking similarity in the clinical and laboratory findings, including the histological pattern, is emphasised. The possibility that an hereditary factor plays a part in the pathogenesis of goiter is discussed.

A description is made of a Caucasian family of Lithuanian and Italian ancestry living in Pôrto Alegre, Brazil, in which there is segregation of the gene which conditions the type of thalassemia which does not raise the fraction A2. The information obtained involves four generations in a total of thirty four individuals, eight of which were examined. Tests about the concentration of serum iron and the iron-binding capacity of thalassemic individuals resulted normal.