Binocular rivalry (BR) is an intriguing phenomenon that occurs when two different images are presented, one to each eye, resulting in alternation or rivalry between the percepts. The phenomenon has been studied for nearly 200 years, with renewed and intensive investigation over recent decades. The rate of perceptual switching has long been known to vary widely between individuals but to be relatively stable within individuals. A recent twin study demonstrated that individual variation in BR rate is under substantial genetic control, a finding that also represented the first report, using a large study, of genetic contribution for any post-retinal visual processing phenomenon. The twin study had been prompted by earlier work showing BR rate was slow in the heritable psychiatric condition, bipolar disorder (BD). Together, these studies suggested that slow BR may represent an endophenotype for BD, and heralded the advent of modern clinical and genetic studies of rivalry. This new focus has coincided with rapid advances in 3D display technology, but despite such progress, specific development of technology for rivalry research has been lacking. This review therefore compares different display methods for BR research across several factors, including viewing parameters, image quality, equipment cost, compatibility with other investigative methods, subject group, and sample size, with a focus on requirements specific to large-scale clinical and genetic studies. It is intended to be a resource for investigators new to BR research, such as clinicians and geneticists, and to stimulate the development of 3D display technology for advancing interdisciplinary studies of rivalry.

The Chato Murciano is the only surviving breed of pig of those historically farmed in the region of Murcia for their quality meat. At present, it is on the verge of extinction, having a population of only 260 reproductive animals. This paper describes the genetic studies made in the conservation and recovery programme of this breed of pig. A study of the morphological characterization of these animals was carried out first, measuring thirteen quantitative and six qualitative variables in a sample of 24 adult animals, 8 males and 16 females.

Subsequently, investigation was made of the consanguinity of the individuals and of the population as well as the future influence of inbreeding in each generation. Finally, the accuracy and precision of the heterozygote-excess method was evaluated using two data sets from the Chato Murciano pig. One data set is an original population and the other is a F3+F4+F5 generation of a line created from mating a Chato Murciano female with a Large White boar as part of an absorption programme based on backcrosses with Chato Murciano boars.

Androgenetic alopecia occurs in men and women, and is characterised by the loss of hair from the scalp in a defined pattern. Determining factors appear to be genetic predisposition coupled with the presence of sufficient circulating androgens. The prevalence of this condition is high (up to 50% of white males are affected by 50 years of age) and, although there are no serious direct health consequences, the loss of scalp hair can be distressing. Knowledge of the pathogenesis of androgenetic alopecia has increased markedly in recent years. Pre-programmed follicles on the scalp undergo a transformation from long growth (anagen) and short rest (telogen) cycles, to long rest and short growth cycles. This process is coupled with progressive miniaturisation of the follicle. These changes are androgen dependent, and require the inheritance of several genes. To date, only one of these genes, which encodes the androgen receptor (AR), has been identified. Of the many treatments available for androgenetic alopecia, only two (finasteride and minoxidil) have been scientifically shown to be useful in the treatment of hair loss. However, these therapies are variable in their effectiveness. Discovery of the involvement of the AR gene, and the identification of other genes contributing to the condition, might lead to the development of new and more effective therapies that target the condition at a more fundamental level.

The question of the nosological status of schizoaffective disorders remains one of the most controversial issues of clinical psychiatry. There are, in fact, at least five different hypotheses about the nature of these disorders: • that they are always variants of schizophrenia, • that they are always variants of major affective disorders, • that they represent a “third psychosis” distinct from both schizophrenia and manic-depressive illness, • that they find their place in the intermediate position of a “continuum” whose poles are represented by the typical forms of schizophrenia and manic-depressive illness, • that they result from the simultaneous occurrence of a true schizophrenia and a true manic-depressive illness in the same patient. The last of these hypotheses can hardly be accepted, since it would predict an annual frequency of schizoaffective disorders of about 2 per 108, compared to the actual frequency of 2 per 105. Of the remaining four hypotheses, the first two are consistent with the Kraepelinian “dichotomic” paradigm, whereas the third and the fourth contradict this paradigm. The results of empirical investigations (that is, of family studies, outcome studies and studies on response to drug treatments in schizoaffective patients) do not provide a full support to any of the above hypotheses. What empirical evidence seems to show, instead, is that schizoaffective disorders represent a heterogeneous group of syndromes. Part of these disorders can be interpreted, upon close scrutiny, as variants of either of the major psychoses (for instance, bipolar schizoaffective States appear to be closely allied to major affective disorders). There seems to be, however, a subpopulation of schizoaffective patients which escapes the Kraepelinian dichotomic model.

The author has reviewed evidence generated during the past decade at the University of Tennessee and other affective disorders research units in support of a psychobiologic understanding of affective disorders as the final common pathway of various psychologic and biologic factors that impinge on midbrain centers of reward, circadian rhythms, and psychomotor function. In this model, inherited temperamental instability, based on a persistent diencephalic abnormality, provides the fertile soil for the development of major affective episodes. The pathogenesis of full-blown affective episodes is then the product of multiple factors, none of which alone is a necessary or sufficient cause. It is submitted that this unified theory, in bridging psychosocial and biologic factors, provides the most comprehensive etiologic understanding of depressive illness permitted by current data. Clinical implications of the theory are discussed.