bluuebunny/crossref_metadata_2025_split huggingface dataset:
Developmental perspective on size change and allometry in evolution
Authors: Shea Brian T. 
Published: June 2005

AbstractThe evolution of changes in body size is one of the most important patterns in the history of life. Its importance arises from both the frequency of the pattern and the biological implications of size change itself, which affects myriad aspects of an organism's structure and function through well‐known scaling relationships. Yet relatively little attention has been focused on the underlying genetic and developmental controls of size change or their implications with regard to other morphological changes. Here, I review the endocrine growth axis and show that variation in several key growth‐control substances, particularly growth hormone (GH) and insulin‐like growth factor I (IGF I), is clearly linked to intraspecific differences in postnatal growth rates and terminal body size. I intentionally review a considerable amount of literature on nonprimate mammals because this research is vital to an understanding of the general topic. Research on human pygmies, giant transgenic mice, and other models of growth disturbances indicates that shifts in GH and/or IGF I levels not only yield the expected changes in terminal body size, but also result in simple truncations or extensions of underlying allometric patterns. These data provide a possible developmental basis for the common finding of ontogenetic scaling and coordinated transformations in series of closely related fossil or living species that differ in body size. At present, however, this must be viewed as a hypothesis that requires testing through interspecific analyses. A consideration of previous interpretations of the morphological distinctions of human pygmies and some other organisms demonstrates the novel information that a developmental perspective brings to morphological comparisons. Clearly, knowledge of the genetic and developmental controls of morphogenesis will greatly enhance our understanding of a multitude of evolutionary patterns, processes and mechanisms, for it is perturbations in these these controls that ultimately produce the raw material for evolutionary transformations.
The evolution of primate communities and societies in Madagascar
Authors: Kappeler Peter M. , Ganzhorn Jörg U. 
Published: June 2005

AbstractDuring their 120 to 165 million years of isolation, the flora and fauna of Madagascar evolved, to a large extent, independently of the African mainland.1 In contrast to other oceanic islands, Madagascar is large enough to house the major components of tropical ecosystems, allowing tests of evolutionary hypotheses on the level of complete communities. Taking lemurs, the primates of Madagascar, as an example, evolutionary hypotheses correctly predict the organization of their community structure with respect to ecological correlates. Lemur social systems and their morphological correlates, on the other hand, deviate in some respects from those of other primates. Apparently, lemur social systems are influenced by several selection pressures that are weak or rare in other primates. These include variable activity patterns and avoidance of infanticide. The interspecific variation in lemur social systems therefore offers a unique opportunity for a comprehensive study of the determinants of primate social systems.
Predation on primates: Ecological patterns and evolutionary consequences
Authors: Isbell Lynne A. 
Published: June 2005

AbstractIt has long been thought that predation has had important ecological and evolutionary effects on primates as prey. Predation has been theorized to have been a major selective force in the evolution of hominids.1In modern primates, behaviors such as active defense, concealment, vigilance, flight, and alarm calls have been attributed to the selective pressures of predation, as has group living itself. It is clear that primates, like other animals, have evolved ways to minimize their risk of predation. However, the extent to which they have been able to do so, given other constraints of living such as their own need to acquire food, has not yet been resolved. Perhaps most hotly debated is whether predation has been the primary selective force favoring the evolution of group living in primates. Part of the difficulty in resolving the debate lies in a paucity of direct evidence of predation. This is regrettable yet understandable since primatologists, by definition, focus on the study of primates, not predators of primates (unless these are also primates). Systematic direct evidence of the effects of predation can best be obtained by studying predators that are as habituated to observers as are their primate prey. Until this is done, we must continue to rely on opportunistic accounts of predation and predation attempts, and on systematically obtained indirect evidence. Such data reveal several interesting patterns: (1) although smaller primates may have greater predation rates than larger primates, even the largest primates are not invulnerable to predation; (2) the use by primates of unfamiliar areas can result in higher predation rates, which might be one pressure favoring philopatry, or site fidelity; (3) arboreal primates are at greater risk of predation when they are more exposed (at forest edges and tops of canopies) than in more concealed locations; (4) predation by mammalian carnivores may often be episodic; and (5) terrestrial primates may not experience greater predation than arboreal primates.
Rethinking genes
Authors: Marks Jonathan , Lyles R. Brent 
Published: June 2005

AbstractThe gene is the central construct of twentieth‐century biology and evolution. It is a construct because, like “culture” in anthropology, “gene” is widely used and is central to the discipline's discourse, but eludes rigorous definition. Although the gene is acknowledged as a material entity, its membership criteria are unclear and its boundaries are fuzzy—indeed, more than one can occupy the same space at the same time. The purpose of this essay is to bring to light recent refinements in our conception of the gene and their implications for its use in biological anthropology.
Skeletal biology and behavior in ancient humans
Authors: Bridges Patricia S. 
Published: June 2005

AbstractFor many years, it has been known that archaic hominids had more robust long bones than do living populations, a fact that has been linked to their more physically strenuous lives. But many questions remain. How much stronger, for example, were Neanderthals than living humans? And what does this difference in strength tell us about the behavior of our ancestors?Recent research has shown that some of our earlier assumptions about robusticity and behavior in earlier humans are either simplistic or untrue. For example, it is now clear that although earlier humans were, on the average, stronger than living peoples, this is not invariably the case. Some modern human groups have even stronger humeri than those of Neanderthals. The fact that changes in robusticity do not always neatly coincide with subsistence or technological change suggests that interpretations derived in large measure from stone‐tool technology and other artifactual evidence may be misleading. This new information on physical strength in earlier humans necessitates a reassessment of traditional ideas about earlier human behavior.
Historical perspectives on human‐assisted biological invasions
Authors: Burney David A. 
Published: June 2005

AbstractOf all the things we have done to the Earth so far, which one is likely to make the most indelible mark? I have been posing this question to students and colleagues for some time, and usually receive one of three reasonable replies: habitat destruction, human overpopulation, or global climate change. Yet as bad as all these maladies are, they are, to some extent, reversible on time scales to which we can relate. The remedies for these problems, despite mammoth cultural and economic obstacles, can be visualized generally in terms of technology and scientific theory. Only the will is lacking. On longer geological and evolutionary time scales, most such human impacts, if corrected soon, would be mere blips, perturbations of the ecosphere that would leave only a few detectable traces in the fossil record a million years hence.
An application of a model for a genotype‐dependent relationship between a concomitant (age) and a quantitative trait(LDL cholesterol)in pedigree data
Authors: Moll Patricia P. , Sing Charles F. , Lussier‐Cacan Suzanne , Davignon Jean , Rao D. C. 
Published: June 2005

AbstractIn most genetic studies in humans the variability in a quantitative trait is adjusted for variability in concomitants (age, sex, etc) using a single regression equation prior to analyses of pedigree data. To illustrate an alternative approach, a single locus genetic model was tested. This model incorporates genotypic effects on the level of the trait, the variability in the trait, and the relationship between a concomitant and the trait. In this study, the model was applied to measures of age and low‐density lipoprotein (LDL) cholesterol in a large kindred with familial hypercholesterolemia. The application of this model to 322 individuals in four generations provided evidence that genotypic variation at a single locus influences LDL levels early in life, the rate of increase of LDL with age and the phenotypic variance. A model with genotype‐dependent slope and variance fit the data signifcantly better than a model with slope and variance independent of genotype. The inclusion of age‐specific genotypic differences contributed to identification of high‐risk individuals, to statistical support for a major locus, and to evidence for genetic determination of the tracking of LDL levels. Models that incorporate genotype‐specific concomitant effects have the potential to represent more realiscally the relationship between genotypic variability and quantitative phenotypic variation than models that assume that these effects do not exist.
Glucose tolerance and ancestral genetic admixture in six semitraditional pacific populations
Authors: King H. , Zimmet P. , Bennett P. , Taylor R. , Raper L. R. , Rao D. C. 
Published: June 2005

AbstractPopulation‐based data on 1,842 subjects from six semitraditional Pacific communities, collected in the years 1978–1983, have been compared in order to examine the hypotheses that differences in the distribution of plasma glucose concentration between populations are to some extent genetically determined, and that non‐Austronesian (NAN) Melanesians are relatively resistant to glucose intolerance. Semitraditional communities were chosen for study so that the comparison would be minimally confounded by either known or as yet undetermined environmental factors associated with nontraditional living, the effects of which may vary between populations. The samples were also selected so as to provide a gradient of proportional NAN and AN admixture. They were drawn from the following regions: the highlands of Papua New Guinea, New Caledonia, Fiji, the Wallis Islands, Western Samoa, and Kiribati (formerly the Gilbert Islands). The Papua New Guinea highlanders, of entirely NAN ancestry, were regarded as the baseline population.A gradient of increasing mean 2‐hr plasma glucose concentration was observed across the six populations and differences persisted between populations, after controlling for age and obesity. Variations in diet, physical activity, and degree of sociocultural modernization were not considered a sufficient or consistent explanation of these findings and they therefore lend tentative support to the hypothesis of a genetic component to variability in glucose tolerance.The relationship between population estimates of glucose tolerance and estimates of the genetic distance from the baseline NAN Melanesian sample was examined. With the notable exception of Fiji, there was evidence of a linear correlation between the two parameters.
Interpretation of LOD scores with a set of marker loci
Authors: Thompson E. A. , Nance Walter E. 
Published: June 2005

AbstractThe problem discussed is that of interpreting LOD scores when multiple markers are tested for linkage with a particular disease locus. Provided the tests are based on independent segregations, both the maximum and the average LOD can be translated into a score that would have the same significance level were it the result of a single test.
Genetic and environmental causes of variation in renal tubular handling of sodium and potassium: A twin study
Authors: Whitfield J. B. , Martin N. G. , Rao D. C. 
Published: June 2005

AbstractWe have conducted a study of renal sodium and potassium reabsorption in 205 pairs of twins on freely chosen diets; 89 of the subjects were studied on more than one occasion. Renal tubular sodium and potassium handling, as measured by the fractional excretions FENa and FEK, show repeatable differences between individuals.Siblings (in this case monozygotic and dizygotic pairs of twins) are more alike in this respect than unrelated individuals. Comparison of monozygotic and dizygotic twin pairs indicates that genetic, rather than shared environmental, factors are probably responsible for this similarity, with heritability estimates of 0.5 for sodium and 0.6 for potassium. There are indications of sex differences in the sizes of the genetic and environmental effects for both variables and indications that the genetic effects may be qualitatively different for FEK. Such findings need further investigation.
Multivariate path analysis of familial resemblance
Authors: Vogler George P. , Cockerham C. C. 
Published: June 2005

AbstractA method is presented for applying path analysis to general multivariate models of familial resemblance. In path models formulated using this approach, variables are defined as column vectors, path coefficients are defined as matrices of path coefficients, and correlations are defined as matrices of correlations. By applying a few simple rules for multivariate path analysis, general multivariate expected correlations can be derived from a path diagram which is essentially as simple as a univariate diagram and which can be used to analyze any number of variables. Multivariate expected correlations for three models of familial resemblance are derived, with particular attention given to the modeling of assortative mating: nuclear families with a phenotypic homogamy model of assortative mating, nuclear families with a social homogamy model of assortative mating, and twins and their parents with phenotypic homogamy. These models are applicable to many of the types of studies commonly undertaken in genetic epidemiology. The simplicity of the technique facilitates analyses of the etiology of variation and covariation among variables measured in such studies.
Studies on vitiligo I. Epidemiological profile in Calcutta, India
Authors: Das S. K. , Majumder Partha P. , Chakrabotry Ranajit , Majumdar T. K. , Haldar B. , Rao D. C. 
Published: June 2005

AbstractAn epidemiological profile of vitiligo in Calcutta is presented. Prevalence data were gathered from 15,685 individuals drawn from the general population; pedigree data were collected through 293 vitiligo patients. The overall prevalence of vitiligo is about 5 per 1,000 individuals. There are no significant sex or age differences in prevalence rates. About a 4.5‐fold increase in prevalence is observed among close biological relatives of affected individuals. There is, however, no clearcut correspondence between relative risks and kinship coefficients. There are no significant differences in the frequencies of various types of vitiligo between probands with and without positive family history. The overall mean and modal ages of onset are about 22 years and 15 years, respectively. The mean ages among males (24.8 years) and females (19.3 years) are significantly different.
A chi‐square test to distinguish allelic association from other causes of phenotypic association between two loci
Authors: Ott Jurg , Rao D. C. 
Published: June 2005

AbstractIn unrelated individuals, their phenotypes at two gene loci may appear correlated. The two major reasons for such a deviation from independence are linkage disequilibrium (allelic association) and an interaction between the phenotypes. In this paper, it is shown how the usual chi‐square test for association of phenotypes can be partitioned into two components, one being due to allelic association and the other being due to other causes of phenotypic association. The test is demonstrated with an example.
Genetic analysis workshop III: Sib pair analyses to determine linkage groups and to order loci
Authors: Elston R. C. , Keats B. J. B. 
Published: June 2005

AbstractThe methods proposed by Haseman and Elston [1972] were used to estimate the proportion of genes identical by descent shared by each sib pair at each locus. These estimates were then used as a basis for obtaining all possible locus‐locus correlations. The 12 significant correlations (P < .01) and their rank order indicated the correct linkage groups and the order of the loci.
Estimation of myriad haplotype frequencies
Authors: Maclean Charles J. , Morton Newton E. , Rao D. C. 
Published: June 2005

AbstractThe present paper demonstrates algorithms for applying gene counting estimation of haplotype frequencies in very large genetic systems. A factor union representation of phenotypes is used which conveniently yields the sets of potential haplotypes and diplotypes for each phenotype. Methods for storing and rapidly retrieving the relevant haplotypes are given. An example with several hundred frequencies is given which required a few seconds computing time for each estimation iteration on a small computer.A computer program employing the methods described has been written in Fortran‐77 and is available to any investigator on request.
Demonstration of a common major gene with pleiotropic effects on immunoglobulin E levels and allergy
Authors: Borecki I. B. , Rao D. C. , Lalouel J. M. , McGue M. , Gerrard J. W. , Conneally P. M. 
Published: June 2005

AbstractAtopic disease is generally recognized to be familial, although specific genetic components have yet to be identified. High levels of a unique class of immunoglobulins, immunoglobulin E (IgE), have been shown to be associated with allergies. Several investigators have reported evidence indicating a recessive regulatory locus where an individual with the homozygous recessive genotype has persistently elevated levels of IgE. Willcox and Marsh [1978] have proposed a hypothesis relating IgE production and liability to become allergic. A test of this hypothesis was carried out in the present study. Bivariate segregation analysis of IgE levels and allergy was performed on 173 nuclear families, and the results indicate that an IgE regulatory locus contributes to the familial transmission of allergy. The results are further discussed in the context of the Willcox and Marsh hypothesis.
A new model for the resolution of cultural and biological inheritance in the presence of temporal trends: Application to systolic blood pressure
Authors: Province M. A. , Rao D. C. , MacCluer J. W. 
Published: June 2005

AbstractA contemporary path model for the resolution of cultural and biological inheritance is extended to incorporate temporal variation in family resemblance. Specifically, the genetic and environmental effects, like all other parameters of the model, are allowed to vary over an individual's age according to some specific mathematical functions. In the computer program BETREND a library of such functions is incorporated. Data on systolic blood pressure in 542 Japanese‐American nuclear families were analyzed. This new methodology detected significant temporal variation in cultural inheritance, a result that was not found previously by using static models which could only distinguish between adult and childhood heritabilities. Cultural heritability, estimated to be 10% at birth, increases to a maximum of 28% at age 36, at which time it declines until it eventually reaches 10% at age 49. Although not statistically significant, there was some evidence for temporal trends in genetic heritability as well. Ignoring trends, the genetic heritability was estimated as .30. On the other hand, trends in sibling environment were clearly nonsignificant. This model provides an objective method of testing the significance of temporal trends in familial resemblance by using multifactorial models, of resolving varying gene expression and transient environmental effects as possible sources of generating the observed temporal variation, and of estimating continuous changes in heritability with age.
Cancer and autoimmune disease in families with common variable immune deficiency
Authors: Morrell Daphne , Chase Charles L. , Swift Michael , Rao D. C. 
Published: June 2005

AbstractTwenty‐five families including 34 individuals with common variable immune deficiency (CVID), with at least one affected female in each family, were studied. The distribution of cases within families was compatible with autosomal recessive inheritance, making it plausible to test hypotheses about the disease risk of heterozygote carriers of putative CVID genes by comparing the frequency of spouse controls. For cancer, observed numbers of cases or deaths were also compared to expected numbers derived from population rates.No single family had an unusual clustering of autoimmune conditions, and, overall, autoimmune disease was not found more frequently in blood relatives than in spouse controls. Blood relatives did have a modest, although not significant, excess of rheumatic heart disease. For cancer analyses, comparisons with general population rates indicated no heterozygote predisposition, while direct comparisons of blood relatives to spouse controls revealed a significantly elevated cancer rate in females (rate ratio = 2.3, P < 0.003). The estimated relative risk of cancer for female CVID heterozygotes was most elevated in the 45–69‐year‐old age group. It is arguable whether comparisons with population or spouse controls are the most appropriate for evaluating the cancer risk of CVID heterozygotes. The hypothesis that the CVID gene predisposes heterozygous female carriers to cancer may be evaluated more easily in the future when the genetic basis for CVID is better understood.
Symptom patterns and causes of somatization in men: I. Differentiation of two discrete disorders
Authors: Sigvardsson Soren , Bohman Michael , von Knorring Anne‐Liis , Cloninger C. Robert , Conneally P. M. 
Published: June 2005

AbstractTwo distinct patterns of somatization were identified in 807 Swedish adopted men, using comprehensive lifetime psychiatric and sick‐leave records. “Diversiform” somatizers had a high frequency of brief sickness occasions for a wide diversity of complaints, particularly pain in the head, joints, and abdomen. “Asthenic” somatizers had a lower frequency and diversity of complaints. They recuperate more slowly, however, and were more often disabled by fatigue, weakness, and minor illnesses such as upper respiratory infections. Both types of somatizers had associated psychosocial maladjustment, but they had discrete clinical patterns, with infrequent overlap. Diversiform somatizers had a higher risk of alcohol abuse, psychiatric hospitalization, and substandard income than either asthenic somatizers or non‐somatizers. Asthenic somatizers had a higher risk of divorce than either diversiform somatizers or non‐somatizers. Men with prominent somatization had an excess of psychiatric treatment for alcoholism or anxiety disorders, but, unlike female somatizers, no excess of criminality. These clinical differences suggest that the psychiatric processes associated with somatization may be qualitatively different in men and women. The method used here is generally applicable in genetic epidemiology to identify natural clinical subtypes within a heterogeneous phenotype.