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PubMed2006

Aggressive fibromatosis (desmoid tumors): definition, occurrence, pathology, diagnostic problems, clinical behavior, genetic background.

Aggressive fibromatosis, usually called desmoid tumor develops from muscle connective tissue, fasciae and aponeuroses. This neoplasm is composed of spindle (fibrocyte-like) cells. As regards the site, aggressive fibromatoses can be divided into: extra-abdominal in the area of the shoulder and pelvic girdle or chest and neck wall; abdominal in abdominal wall muscles; intra-abdominal concerning pelvis, mesentery connective tissue or retroperitoneal space. Desmoid tumor is a neoplasm which rarely turns malignant and is non-metastasizing but demonstrates ability to local infiltration into tissue and is characterized by high risk of recurrence (25-65%) after surgical treatment. Desmoid tumor etiology is uncertain. This neoplasm occurs in sporadic (idiopathic) form and is also associated with some familial neoplastic syndromes. Most sporadic cases of aggressive fibromatosis contain a somatic mutation in either the adenomatous polyposis coli (APC) or beta-catenin genes. Sporadic tumors are more frequent in women than in men from 2 : 1 to 5 : 1. In about 10-15 per cent of patients with familial adenomatous polyposis (FAP), aggressive fibromatosis is a parenteral manifestation of this familial syndrome conditioned by APC gene mutation. Abdomen injury--most frequently due to surgery is said to play an important role in the initiation of fibrous tissue proliferative process in the cases of abdominal and intra abdominal forms. High cells growth potential with relatively high local malignancy is observed in about 10% of cases with sporadic tumors as well as in those FAP-associated.

Desmoid Tumors↗
PubMed2005

Genotype-environment interactions in mouse behavior: a way out of the problem.

In behavior genetics, behavioral patterns of mouse genotypes, such as inbred strains, crosses, and knockouts, are characterized and compared to associate them with particular gene loci. Such genotype differences, however, are usually established in single-laboratory experiments, and questions have been raised regarding the replicability of the results in other laboratories. A recent multilaboratory experiment found significant laboratory effects and genotype x laboratory interactions even after rigorous standardization, raising the concern that results are idiosyncratic to a particular laboratory. This finding may be regarded by some critics as a serious shortcoming in behavior genetics. A different strategy is offered here: (i) recognize that even after investing much effort in identifying and eliminating causes for laboratory differences, genotype x laboratory interaction is an unavoidable fact of life. (ii) Incorporate this understanding into the statistical analysis of multilaboratory experiments using the mixed model. Such a statistical approach sets a higher benchmark for finding significant genotype differences. (iii) Develop behavioral assays and endpoints that are able to discriminate genetic differences even over the background of the interaction. (iv) Use the publicly available multilaboratory results in single-laboratory experiments. We use software-based strategy for exploring exploration (see) to analyze the open-field behavior in eight genotypes across three laboratories. Our results demonstrate that replicable behavioral measures can be practically established. Even though we address the replicability problem in behavioral genetics, our strategy is also applicable in other areas where concern about replicability has been raised.

Analysis of Variance↗
PubMed1983

Human behavioral development and genetics.

Behavioral development during childhood is examined in relation to recent concepts and data from evolutionary theory and developmental genetics. The epigenetic framework of Waddington is proposed as a powerful tool for analyzing the progressions in behavior, particularly for recognizing that development involves coordinated pathways of change over time. Many of these pathways appear to depend upon the activity of timed gene-action systems that switch off and on according to a predetermined plan. Behavioral development thus gives expression to the dynamics of preprogrammed change; and in this perspective, behavioral discontinuities may be as strongly rooted in the epigenetic ground plan as the continuities are. The present paper aims to pull together some common themes from different areas that bear on the central issues of behavioral development--the neural foundations, the time course followed, the interplay of maturation and experience, the extent of preorganization furnished by the genetic program, and the adaptive significance of such behaviors in an evolutionary perspective. The final section touches on some hypotheses drawn from developmental neurobiology and developmental genetics that may enrich the analyses of human behavioral development.

Biological Evolution↗
PubMed1996

Genetics and behavioral medicine.

Genetics has substantial relevance to behavioral medicine. A rapidly growing body of evidence indicates the influence of genetics on health and disease and on the behavioral factors related to them. The model of quantitative genetics provides a general interpretational scheme for this burgeoning field. The model focuses on variability, and a major research objective is the decomposition of observed individual differences into portions attributable to various types of genetic and environmental sources of variability. This approach emphasizes the coaction of genes and environments and stands in sharp contrast to the archaic view that places nature and nurture in opposition. Some relevant examples are given in this first article to illustrate the general analytic process. A detailed application to cardiovascular health and disease is provided in the second article, and some policy implications are briefly considered in the third article.

Alleles↗
PubMed1995

Dissection of memory formation: from behavioral pharmacology to molecular genetics.

Behavioral pharmacology has suggested an intricate, multiphasic pathway of memory consolidation. An integrated molecular pharmacological approach in Drosophila has lent support to this theory recently by dissecting consolidated memory into two genetically distinct components: a cycloheximide-insensitive, anesthesia-resistant memory and a cycloheximide-sensitive long-term memory. In addition, experiments using inducible dominant-negative transgenes in Drosophila or gene knockouts in mice demonstrate a role for cAMP-responsive transcription factors in formation of long-term memory. These studies support the application of reverse-genetic strategies, including the use of temporally specific agonists and antagonists, to advance the functional dissection of memory formation.

Animals↗
PubMed1997

Conceptualizing genetic influences on early behavioral development.

The overarching goal of human behavioral genetics is to understand genetic influences on behavior while also considering the complementary influence of the environment. This paper highlights the explicit goals of behavioral genetics, including some that are particularly relevant to the study of human development, and some common misunderstandings concerning the field. Examples are given to illustrate specifically the degree of genetic influence in behaviors representing physical, cognitive and emotional development during infancy using the methodology of twin, adoption and parent-offspring designs. The effect sizes in the prediction of complex behaviors are typically modest, and thus there is ample room for multiple predictors from different domains. Moreover, there is a fundamental recognition that distal and proximal causes can be different in kind, and that factors that play a role in the origins of behavioral dispositions are different from those that elicit or maintain actual behavior.

Child Development↗
PubMed1976

[The pre-morbid personality of schizophrenics in the literature of the last hundred years (author's transl)].

A survey of the literature on the primary personality of schizophrenics shows that the essential concepts derive from Kraepelin (1893), E. Bleuler (who also introduced the technical term "schizoid", 1911) and C.G. Jung introversion; 1913). E Kretschmer (1921) adopted these preliminary findings and integrated them into his system of "Constitution" which greatly stimulated research in this field. Most of the following investigations confirmed his hypotheses on the basis of clinical impressions. A few only criticised his teaching, particularly as a theoretical concept. The musculo-somatotonic type apart, Sheldon's (1940) research agrees with Kretschmer to a large degree. Later investigators, however, could not sufficiently support Sheldon's constitutional biology on empirical grounds. No further pre-morbid types were developed in the following years, if one discards the somewhat rare "stormy" character (Arieti, 1955). All attempts to discover differences between the pre-morbid development of personality and the subheadings of schizophrenia failed. Pre-morbid sexual development is not typical, but the disturbances of contact are in the foreground. Whether schizophrenics differ later in their intelligence is still undecided. But it appears certain that, even before the start of their illness, they achieve a lower social status than their siblings. There exists a large experimental psychologic literature on relationships between the original personality, symptoms and psychophysiologic correlates in which it is confirmed again and again that bad pre-morbid adaptation corresponds closely with the severity of symptoms and loss of achievement. There are no consonant result of investigations into the frequency of schizoid structures in schizophrenics, in psychiatric control groups and in the normal population. Psychometric techniques have been used only rarely, but existing publications confirm in principle that schizophrenics are markedly more schizoid than control groups. As with schizophrenia, there are contrasting ideas as to the cause and pathogenesis of the pre-morbid personality. Psycho- and socio-genetic, behavioral, genetic and neurochemical hypotheses have their adherents. According to recent studies of adoption the genetic factor appears to predominate. The clinician relies on pre-morbid development of the personality in his search for a "kink in the life line" or in his assessment of the quality of remissions. There is general agreement that a schizoid primary personality has an unfavorable influence on the long-term prognosis. This is still true today, in spite of modern possibilities of treatment and rehabilitation. Prophylactic aspects have been discussed for a long time but have remained unhelpful clinically. Often it may be difficult to distinguish between schizoids and mild hebephrenias. In spite of this the clinical concept "schizoid" should never be used for "mild schizophrenia"...

Adoption↗
PubMed1991

Psychology research and NIMH. Opportunities and challenges.

As an essential contributor to the scientific understanding of mental health and illness, psychology continues to be the leading discipline receiving National Institute of Mental Health (NIMH) research support. Future behavioral science research initiatives at NIMH are likely to emphasize cognitive science, behavioral genetics, behavioral patterns and physiological systems, and personality, motivation, emotion, and interpersonal processes. Although prognostication is particularly risky in times of transition such as the present, advocacy efforts focused on mental-illness-related research are most likely to help the NIMH and the field if they avoid polarization and factionalization by providing equal encouragement for studies of biological aspects, of behavioral aspects, and of their interaction.

Animals↗
PubMed2004

E pluribus unum, ex uno plura: quantitative and single-gene perspectives on the study of behavior.

Genetic studies of behavior have traditionally come in two flavors: quantitative genetic studies of natural variants and single-gene studies of induced mutants. Each employed different techniques and methods of analysis toward the common, ultimate goal of understanding how genes influence behavior. With the advent of new genomic technologies, and also the realization that mechanisms underlying behavior involve a considerable degree of complex gene interaction, the traditionally separate strands of behavior genetics are merging into a single, synthetic strategy.

Animals↗
PubMed1998

A multivariate quantitative-genetic analysis of behavioral development in mice.

The present experiment attempted a behavior-genetic dissection of early behavioral development in laboratory mice. To this end, we used a full, replicated diallel cross to uncover the genetical architecture as well as the multivariate genetic structure underlying early behavioral ontogeny. A number of standard sensorimotor tests were administered on postnatal Days 3, 5, 8, 10, 13, 17, and 22 to a total of 622 pups from 120 litters (4-6 pups per litter) from a four times replicated complete diallel cross between five inbred mouse strains. The first day on which an animal showed adult performance was taken as its score on that test. MANOVA did not show any effects of the pup's sex on the speed of development. Hayman's analysis of variance for diallel tables indicated no or only weak additive-genetic effects. Dominance was absent in almost all cases, except for the auricular startle response, where weak directional dominance for fast development was found. These results are in accordance with an evolutionary past of directional selection for well-canalized development. Factor analyses of the phenotypic and additive-genetic correlation matrices indicate that at least two factors are necessary to describe the behavioral variation.

Adaptation, Psychological↗
PubMed1992

The genetic analysis of human behavior: a new era?

Recent developments in DNA-based techniques may revolutionize the study of human behavioral genetics. However, unless these methods are used with great care, many of the same mistakes which have plagued non-molecular genetic analyses of behavior will reoccur. Errors in the application of genetic approaches and in the interpretation of results have been a common feature of published studies in this field. We review studies in human behavioral genetics, focusing on those using identical twins and DNA-based linkage techniques in order to draw attention to recurrent problems in molecular and non-molecular studies. We suggest possible guidelines for future research in the area of the biological basis of human behavior.

Adoption↗
PubMed1990

Genetics of olfactory behavior in Drosophila melanogaster.

We have used a behavioral genetic approach to identify six X-linked loci which specify olfaction in Drosophila melanogaster. Mutations in five of these genes lead to partial anosmias affecting responses either to aldehydes (olfA, olfB, olfE and olfF) or to acetate esters (olfC). Only one of the mutants obtained in our screening (olfD) resulted in a insensitivity to several different odorants. olfA, olfE and olfC map close together in a small region of the chromosome between 7C and 7D. The alleles at the olfC locus fall into two phenotypic classes according to their responses to different acetate esters. The two groups of olfC alleles interact in-trans.

Animals↗
PubMedDate not supplied

Genetics of the serotonergic system in suicidal behavior.

Genetic factors contribute to the risk of psychopathology in many psychiatric conditions, but the specific genes are yet to be identified. Neurotransmitter alterations are implicated in the etiology of psychopathology based, in part, on studies of neurotransmitter receptors and their biosynthetic or degradative enzymes in postmortem tissue. Identification of the altered receptors and enzymes serves to identify candidate genes of potential etiological significance. Polymorphisms in these genes can contribute to alterations in protein function in vivo that are part of the neurochemical underpinnings of psychopathologies such as major depressive disorder, psychoses, alcoholism, personality disorders, aggressive-impulsive traits, or suicidal behavior. Altered serotonergic function is implicated in the etiology and pathogenesis of several major psychiatric conditions. In particular, there is much evidence for an association of lower serotonergic function and suicidal behavior. Thus genes related to the serotonergic system are candidate genes worthy of study as part of the genetic diathesis for suicidal behavior. This review examines the following polymorphisms in the serotonin biosynthetic enzyme tryptophan hydroxylase (TPH; A779C substitution), the serotonin transporter (5-HTT, 5-HTTLPR allele), the 5-HT(1B) receptor (G861C, C129T substitution) and the 5-HT(2A) receptor (T102C) for their relationship to suicidal behavior. For the TPH gene, we found the less common U or A allele variant of the A779C polymorphism was associated with suicide attempt. Other studies have found the U allele to be associated with aggression and lower serotonergic function in vivo. A 44 base pair insertion/deletion in the 5' flanking promoter region of the 5-HTT gene may result in less 5-HTT expression and 5-HTT binding. We examined 220 cases postmortem and found no association between the promoter genotype and 5-HTT binding. We also found no association with major depressive disorder (MDD), suicide or pathological aggression, despite finding significantly fewer 5-HTT sites in the prefrontal cortex of depressed and/or suicide cases. In genomic DNA samples from 178 unrelated subjects, we detected two polymorphisms for the 5-HT(1B) receptor at nucleotides 861 and 129. However, no association between either polymorphism and depression, suicide, aggression, or alcoholism was observed. There are two common polymorphisms for the 5-HT(2A) receptor gene in humans. The results of studies of 5-HT(2A) receptor gene polymorphisms do not indicate significant major associations with suicidal behavior. In contrast, the 5-HT(2A) receptor itself is reported to be increased in suicide. Functional polymorphisms involving the promoter region that affect gene expression may explain this finding. Studies of candidate genes related to serotonergic function in brain are increasingly used to establish genetic alterations contributing to psychiatric illness. The most meaningful studies combine the study of candidate genes with direct measures of related proteins as well as psychopathology.

Brain↗
PubMed1976

Issues in the genetics of social behavior.

The genetics of social behavior presents special difficulties because the phenotype is the product of an interaction between two or more individuals. Social interactions are of two kinds: (1) cooperative, in which the probabilities of transmission of the genes of all participants are similarly affected by the outcome, and (2) agonistic, in which the probabilities for the participants are affected in opposite directions. The latter are of particular interest for evolutionary theory. Three major types of designs for measuring social behavior in genetic experiments are available: (1) homogeneous sets, (2) standard tester, and (3) tester panel representing a reference population. The advantages and limitations of each method are discussed. Important areas for future development include the relationship of genetic and experiential factors in early life to social status as an adult and the extension of the genetic analysis of social behavior to natural populations.

Animals↗