The program of genetic-epidemiological study of schizophrenia in five districts of the Tomsk region is presented. According to standardized methods, 610 diagnosed patients (epidemiological register) were examined, 74.1% of them being at random registered as probands (452 families of the epidemiological sample). 229 probands of non-epidemiological sample were registered in psychiatric hospitals. Schizophrenia occurrence parameters among first-degree relatives of probands of the non-epidemiological sample were regularly overestimated, as compared to the epidemiological sample. The methodical sources of contradictions in clinico-genealogical studies are discussed; the conclusion about representativeness+ of the probands' epidemiological sample is made.
This paper reviews how the Emergency Communications Research Unit (ECRU) at Carleton University in Ottawa, Canada, developed its field research techniques with emphasis on some of its approaches to sampling. Then based on ECRU's experience, it discusses the problems that would arise if an attempt were made to research an incident involving not only mass casualties, but also chemically contaminated mass casualties. While ECRU's findings have been published in scores of book chapters, monographs and academic and other articles, this is only the second time since 1977 that its methods have been described [The Development of a Standby Research Capacity at Carleton University. Emergency Planning: Ottawa, Canada; Int. J. Mass Emergencies and Disasters 1977; 2(1):35-41; Methods of Disaster Research. Xlibris Corporation, 26-302], and the very first time its approaches to sampling have been discussed.
Human genetics has long been preoccupied with the study of simple, single locus traits and, indeed, it is still asserted that "the primary goal of human genetic analysis should be the detection and estimation of single gene effects" (102). But there is increased recognition that the greater portion of the human burden of disease and disability stems not from such conditions but rather those in which the appearance of the disorder is only the last stage in a lifelong train of prodromal states. There is almost universal agreement that our living conditions and behavior are major contributory factors to their occurrence. It is equally true that there are inherent differences among us which also contribute. The assessment of the roles of these contributors, intrinsic and extrinsic, and the development of environmental manipulations which cure or prevent disease and disability of this nature have become the new frontiers of genetics and human medicine. We have described briefly four investigative, genetic strategies, two essentially concerned with analysis and two with sampling, which can contribute to the conquest of these frontiers. We have attempted to place these strategies in an epidemiologic context.