Atopic dermatitis is a multifactorial disease that seems both to rise in frequency and to be dependent on a genetic predisposition. In order to clarify these issues we encircled a representative twin series with atopic dermatitis from a total twin population of 592 like-sexed twin pairs. We found (1) that the cumulative incidence rate (0-7 years) of atopic dermatitis in Denmark has increased significantly from 0.03 for the birth cohort 1960-1964 to 0.10 for the birth cohort 1970-1974, (2) that monozygotic twin pairs are more often concordant for atopic dermatitis than dizygotic twin pairs, (3) that monozygotic twins run a risk of 0.86 of having atopic dermatitis if the twin partner has the disease, whereas the disease risk of 0.21 run by dizygotic partners does not differ from the frequency seen in ordinary brothers and sisters. The results indicate (1) that genetic factors play a decisive role in the development of atopic dermatitis and (2) that widespread environmental factors are operating in genetically susceptible individuals.

Atopic dermatitis: A genetic-epidemiologic study in a population-based twin sample

Average mutation frequencies per locus per dose of mutagen — EMS, X-rays and fast neutrons — were estimated from 15 different loci of Arabidopsis thaliana . These loci related to clearly distinguishable phenotypic mutant groups, each affected by a limited number of loci. There were significant differences in mutation rate between individual loci. The proposition of a linear relationship between DNA content and mutation frequency per locus is rejected.

EMS- and radiation-induced mutation frequencies at individual loci in Arabidopsis thaliana (L.) Heynh.

This review presents the cardiac and non-cardiac malformations in 60 cases with asplenia and polysplenia with special reference to distinguishing factors which may be helpful in the clinical recognition of these syndromes. The asplenia cases were predominantly male and presented with cyanosis. They frequently had transposition of the great arteries (72%) with pulmonary stenosis or atresia (88%) and total anomalous pulmonary venous drainage (72%). Deaths were caused by cardiac failure and anoxia in 57 per cent of cases. Most of the patients died in the first year of life (79%), but longer survival is possible in the asplenia syndrome. The polysplenia cases were predominantly female and survived longer. The characteristic clinical findings were the relatively more benign presenting signs and the leftward or superiorly orientated P wave axis on the electrocardiogram. Conotruncal abnormalities were less common and total anomalous pulmonary venous drainage did not occur. On angiography the inferior vena caval drainage via the azygos system was clearly identified and this was present in all cases at surgery. Our study indicated that the cardiac anomalies in polysplenia were less severe than they were in asplenia and therefore the prognosis in the former syndrome is likely to be more favourable. Three families had two affects sibs but no single genetic factor could be identified. The aetiology of these syndromes remains undetermined.

https://heart.bmj.com/content/heartjnl/37/8/840.full.pdf

Syndromes of asplenia and polysplenia. A review of cardiac and non-cardiac malformations in 60 cases withspecial reference to diagnosis and prognosis.

SUMMARY The multiple recapture census for closed populations is reconsidered, assuming an underlying multinomial sampling model. The resulting data can be put in the form of an incomplete 2k contingency table, with one missing cell, that displays the full multiple recapture history of all individuals in the population. Log linear models are fitted to this incomplete contingency table, and the simplest plausible model that fits the observed cells is projected to cover the missing cell, thus yielding an estimate of the total population size. Asymptotic variances for the estimate of the population size are considered, and the techniques are illustrated on a population of children possessing a common congenital anomaly.

The multiple recapture census for closed populations and incomplete 2k contingency tables

AN analysis has been made of the family histories of a survey of 1280 cases of IDDM entering Children's Hospital of Pittsburgh between December 31, 1964 and January 1, 1981, discharged on insulin and initial age of onset under 17 yr. Family histories revealed an increased occurrence of IDDM among relatives in the affected families. The risk to siblings was estimated by age-corrected proband exclusion (3.3%) by age 20 and by the Li-Mantel segregation ratio estimator (6.0%). The comparison of these risk measures is discussed. The occurrence of IDDM among the parents is 2.6% and of NIDDM among the parents is 2.4%. A comparison of risk to relatives (parents, sibs, uncles, half-sibs) observed in the Pittsburgh Study to those of six other studies reveal essentially equivalent rates. There is no increased risk to siblings of a diabetic who had an early age of onset. There is an increased risk to siblings of a diabetic (10.5%) in families where at least one parent has insulin-dependent diabetes mellitus (IDDM) and also an increased risk to siblings of a diabetic (8.8%) when at least one parent has non-insulin-dependent diabetes (NIDDM). The average age of onset for second cases in a family is significantly older than age of onset in single case families.

C C Li

Papers

A simple method of estimating the segregation ratio under complete ascertainment.