It is immediately apparent, that the difficulties encountered in studies of the genetics of the mind are formidable, for several reasons. In the first place, the traits concerned are difficult or impossible to classify or to measure with accuracy. In the second place, they may be unstable towards environmental influence; and they vary with age, or exhibit periodic changes.

It is therefore not surprising that our understanding of genetic mechanisms is limited in those conditions where analysis has been carried out merely on the basis of the mental traits.

The situation is strikingly different in the conditions where an association has been found between a mental trait and some clearly recognisable physical or biochemical trait. As we all know, in several such cases an exact genetic analysis in Mendelian terms has been found possible, for instance in the amaurotic idiocies and phenylketonuria.

After having examined the literature on the subject, the Author explains his research study, according to which insulin treatment in pregnant rats, during the first months of pregnancy, has given rise to fetal alterations in the fourth ventricle and the spinal cord. Accordingly, it could be possible that fetal malformations in diabetic women are somehow related to irrational treatments of insulin.

Data on the occurrence of poly- and syndactylies among 64793 newborn children were collected from the hospital records of two different Swedish hospitals, one being located in the North and the other in South Sweden. Frequency estimates are given for the different types of anomalies and the families of 35 probands were studied.

Some pedigrees were compatible with dominant transmission of the traits, while in others the mode of inheritance is irregular. There was no evidence for Y-linked syndactyly. In several cases it was found that a proband with Polydactyly had relatives with syndactyly and vice versa. Some pedigrees included also individuals with reductions of phalanges and fingers.

A statistical analysis has been made on the clinico-anamnestic information concerning 432 mongol propositi, taking into particular consideration the age of parents, the order of birth and the reproductive features observed in the families of the propositi. The Authors furthermore examine the possibility of making an eugenical counseling concerning the probability of a new occurrence of the syndrome.

May I begin by recalling that at the Copenhagen Conference five years ago, Tjio and Levan had just published their almost apologetic announcement that they could only find 46 chromosomes in cultured human somatic cells, and Hamerton and I presented evidence that there were 23 bivalents in spermatocytes, not 24.

Since that time there has been a very marked expansion of work in human cytogenetics. The reason is not hard to seek: the findings have been of significance in so many fields of medicine ranging from endocrinology, through paediatrics, gynaecology and mental diseases to haematology and cancer.

To the biologist, this outpouring of interest may seem at times to have bordered on the hysterical. For him the developments may have done little more than illustrate in our own species the principles that were established in the twenties and thirties with other material. On second throughts he will realize that man offers unique advantages for cytogenetic study in virtue of the enormous numbers of individuals who are subjected to medical scrutiny and thereby become candidates for chromosomal examination. But he will also remember the serious disadvantages, (some shared with human Mendelian genetics) of long generation time, small family size, impossibility of experimental mating and lack of opportunity (except perhaps rarely in males) to study the meiotic pairing which can be so revealing of homology.

If opportunities for direct test of an interpretation are few, reliance on general hypotheses must be the greater. I make it a rule to doubt an observation if it is not in accord with hypothesis. This is not to reject Bateson's exhortation to “treasure your exceptions”; but one must first make quite sure that they are exceptions. Perhaps one does not make so many new discoveries this way, but fewer may later be shown not to be discoveries after all.

A description is made of a large Brazilian family of white ancestry in which some individuals presented polydactyly, other spherocytosis, and some both anomalies together. The information obtained involves five generations totaling 117 related members. Seventy eight of them were examined by the authors through clinical and laboratory methods. Both anomalies were found to be inherited by means of autosomic dominant genes; their joint occurrence seems to be casual. No genetic linkage was apparent between the genes which conditioned spherocytosis and those responsible for the ABO, MN and Rh blood group systems.

The AA. report 2 cases which are very similar to the Cooley disease and the careful genetic and haematologic observation of parents and relatives has pointed out an increase in the haemoglobinic fraction A2 in the husbands but no microcytaemic peculiarity at all.

After discussing the possible relationship to the microcytaemic stigmata the A2 try to see the case among the veritable haemoglobinopathies of this rare genetic form.

On 12th December, 1953 a set of conjoined male twins was born to Mr. & Mrs. Cecil Hartley in Petersburg, Indiana (U.S.A.). The mother, aged 28, had previously given birth to four normal children.

Each of the twins had a neck, a pair of shoulders, two arms, one heart and one stomach. One of them had two lungs, while the other had just one. Two nervous systems were found. The genitalia were normal.

Both twins died of acute cardiac dilatation on 12th April, 1954 having survived four months.

The more significant developments in the field of human population genetics during the past decade can for the most part be subsumed under three headings, as follows:

1. The recognition of an increasing number of genetic traits capable of serving as analytic tools in population studies.

2. The recognition that many of these traits attain frequencies, although some only in limited areas, such that they have to be labelled genetic polymorphisms. Table 1 is an attempt to list the presently recognized human polymorphisms for which the genetic basis seems clear.

3. The emergence of at least a few clues as to the factors responsible for the maintenance of some of the plymorphisms, although it must be confessed that for the majority of the traits listed in Table 1, there is as yet no real insight into their role in populations.

As is well known from the contributions of Fisher, Wright, Dobzhansky, Lerner, Crow, Kimura, and others, genetic polymorphisms have the property of acting as stabilizing mechanisms in maintaining certain aspects of the fitness of populations. Consequently, whereas what we may term the “classical model” of the dynamics of a genetic locus in a population looked to mutation pressure as the source of the impairment of population fitness which could be traced to that locus, the “polymorphic model” views that impairment as in part a price a population pays for the maintenance of an optimum level of heterozygosity at that locus. The two models have such profoundly different practical and philosophical consequences that it is small wonder that in recent years the running discussion of their relative merits and roles has generated a degree of heat matched by few other current biological questions.

The behaviour of the ossification in newborn brothers has been radiologically examined. The findings indicate a uniform behaviour with respect to the duration of the pregnancy in the sons of the same mother. The authors pointout the possible interpretations of this fact.

The intimate connection between natural selection and heredity is indicated by Prof. Dobshansky's definition of evolution as essentially just a change in gene frequencies, for natural selection is the agency that causes gene frequencies to change. Just as mutations are the raw material of evolution, selection is the force that preserves good genes, eliminates bad genes, and produces the changes that lead to the formation of races, and eventually species.

The problem of the action of selection on gene frequencies can be treated, with suitable simplifying assumptions, mathematically, and many years ago Prof. J. B. S. Haldane published a series of papers on this subject (tab. I). The rate at which gene frequencies would change under the action of slow selection is shown in fig. 1. It will be seen that selection acts more slowly, at first, on recessive genes than on dominants, but in the long run the frequencies change from nearly zero to nearly one, or vice versa. Deleterious genes are often never completely eliminated, because they are continually recruited by recurring mutations.

That selection is effective in bringing about considerable changes in organisms is shown by the achievements of domestic plant and animal breeders. The results of selecting for long shanks in chickens are shown in fig. 2, and for a larger number of abdominal chaetae in fruit flies in fig. 3. Though it is not shown here, selection for a lower number of chaetae is also effective.

It is to assess the occurrence of symmetrical and asymmetrical combinations of papillary patterns on the Brahmins of Rajasthan (both the sexes) that this paper has been attempted. Symmetrical combinations are those patterns which are of the same type on the corresponding digits of Right and Left hands, while the asymmetrical are those which are of different types on the digits of corresponding Right and Left hands. All the Loops whether Ulnar or Radial are put into one category. The actual frequencies (AF) and chance frequencies (CF) of Various combinations are calculated.

1. The pattern combination W/W preponderate on I, II, & IV digits in both the sexes, while U/U is more often observed on the III and V digits. The pattern combination A/A is more common in males than in females, moreover this combination is more frequently noticed on II and III digits only.

2. Comparing the values of AF/CF ratio for the symmetrical combination of Whorls-Whorls, Loops-Loops and Arches-Arches in Brahmin series it is observed that the combination Loops-Loops exhibit the lowest value, while the Arches-Arches show the highest, indicating thereby that the tendency to symmetrical patterns is highest in Arches, lower in Whorls and lowest in Loops.

3. The least AF-CF value in the various asymmetrical combination shows the tendency to the repulsion of the combination. It is observed that this tendency is highest in Whorl-Arch and lowest in Loop-Arch combination.

4. A strong tendendy to repulsion on the part of asymmetrical patterns is observed and which consequently increases the tendency more towards the symmetrical patterns.

5. The value of AF/CF ratio is inversely proportionate to the value of chance frequency (CF) or in other words the decrease of CF value increases the AF/CF ratio

6. It is possible to calculate the chance frequencies (CF) when the percentile frequencies of various patterns are given.

The concepts of dominance and recessivity as applied to human genetical traits are losing their original connotations. It is better to speak of genes unconditionally deleterious in heterozygote form and those for which such disadvantage is doubtful. The classical dominant traits come into the first category and in the large majority they give rise to grossly pathological conditions and are ipso facto harmful-many in fact are lethal. In the case of these genes it is difficult to conceive that any agency other than recurrent mutation is instrumental in keeping them at their present frequency.

Assuming that such mutation rates are of the same order of magnitude over the entire spectrum, the frequency of these traits will vary inversely with their severity and this is found to be approximately true-from an incidence of 3/million for an almost invariably lethal trait such as acrocephalosyndactyly to 1/1000 for a relatively innocuous trait such as ptosis.

We would not expect genes even at the higher of these frequencies to be often seen and recognised in homozygote form with the low degree of inbreeding prevalent in human populations. This is in fact confirmed in practice and examples of possibly homozygous forms or dominant conditions are very rare. To be recognized as causing a recessive trait, with a few exceptions in inbred communities, a gene must be more common and often cannot therefore be maintained by recurrent mutation alone. Very wide geographical variations in the incidence of such traits also militate against such an interpretation. Phenylketonuria is an excellent example. The abnormal gene reaches a frequency of as much as 1% in some populations and it is unknown in others.