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PubMed2000

Heredity and risk of cancer of the esophagus and gastric cardia.

The importance of genetic factors in the etiology of esophageal cancer is uncertain. We addressed the question of heredity in a population-based, nationwide case-control study conducted in Sweden during 1995 through 1997. The study involved 189 patients with esophageal adenocarcinoma, 262 with cardia adenocarcinoma, 167 with esophageal squamous cell carcinoma, and, for comparison, 820 control subjects. Familial occurrence of cancer was explored at face-to-face interviews. Logistic regression, with multivariate adjustment for potential confounders, was used to calculate odds ratios (ORs), which estimated relative risk. Occurrence of esophageal cancer among first-degree relatives did not increase the risk of adenocarcinoma or squamous cell carcinoma of the esophagus. Neither were there any significant associations with familial occurrence of gastric cancer or other gastrointestinal tumors. The risk of cardia adenocarcinoma was moderately increased among persons with first-degree relatives with gastric cancer (OR, 1.6; 95% confidence interval, 1.0-2.6). Familial occurrence of any cancer was not associated with increased risks of any of the three studied tumors. In conclusion, heredity does not seem to contribute importantly to the occurrence of esophageal cancer of any histological type. A weak association between familial gastric cancer and the risk of cardia cancer may represent a genetic link.

Adenocarcinoma↗
PubMedDate not supplied

[Populations and heredity: at an intersection].

A population can be defined using different criteria, for example criteria of a geographical or medical nature. Researchers, or even patients and journalists, have complementary or contradictory views of this notion. Heredity is not only a biological fact; it is also a social fact. A systematic study of the genealogical corpus of a group of patients makes it possible to evaluate the soundness of the phenotypic criterion used to define a subpopulation that shares a common pathological heredity.

Genetics↗
PubMed1991

[Changes in central hemodynamics as a risk factor of the development of ischemic heart disease in adolescents with aggravated heredity of atherosclerosis].

The authors provide the data on the central hemodynamics, blood plasma lipoproteins and apoproteins in 101 adolescents with aggravated heredity as regards coronary heart disease and in healthy adolescents of the same age serving as control. The hypokinetic variant of circulation is demonstrated to be coupled with the atherogenic nature of the lipoprotein and apoprotein spectra and heredity to contribute greatly to the traits under study. Criteria for the adolescents' inclusion into the group at the highest risk for early development of atherosclerosis are described.

Adolescent↗
PubMed1989

Type 2 diabetes heredity and nutrient intake. A dietary history assessment in non-obese normoglycaemic men.

The impact of type 2 diabetes heredity on nutrient intake was studied, by means of dietary histories, in 51 normoglycaemic, non-obese men, aged 54-59 years; 29 with familial aggregation of type 2 diabetes, and 22 with no such family history. The average daily intake of energy, macronutrients and minerals was almost identical in the two groups. Mean energy intake was approximately 2400 kcal/d, about 15 per cent of the energy deriving from protein, 35 per cent from fat, 45 per cent from carbohydrate and 5 per cent from alcohol. The average daily intake or dietary fibre was approximately 17 g, or 7 g/1000 kcal. Mean daily sodium and potassium intake, estimated from food sources, was about 3000 and 4000 mg, respectively. The findings provide no support for the existence of any relationship between type 2 diabetes heredity and dietary habits or nutrient intake.

Diabetes Mellitus, Type 2↗
PubMed1989

[Morphological correlates and heredity in functional asymmetry of the cerebral hemispheres].

Morphological findings which may be associated with asymmetric functions of the hemispheres have mostly appeared over the last two decades. They concern the leftsided dominance of the temporal plane and of the cytoarchitectonic region TpT, as well as of the regions which have connections with them. The posterior horn of the left lateral ventricule is usually longer and the left occipital lobe larger. The findings are associated with the leftsided location of speech functions rather than with motor dominance. Several hypotheses have been put forward attempting to explain the mode of heredity of handedness: the hypothesis of biological left--right maturation gradient, the polygenic hypothesis, further the hypothesis suggesting that one pair of genes determines the hemisphere dominant for motor and speech functions and another pair determines whether the dominant hand will be controlled by the ipsilateral or contralateral hemisphere. The hypothesis of Annette offers a plausible explanation of the heredity of handedness. It proposes that the development of a right-handed or left-handed individual is accounted for by the presence or absence of the gene which determines the dominance of the left hemisphere for speech and facilitates the development of right-handed motor dominance.

Animals↗
PubMed1989

[Heredity and diseases of the organs of the urinary system: results and prospects of research].

The paper deals with current ideas of the role played by heredity in the development of diseases of the urinary system organs (USO). Hereditary nephropathies are divided into groups of disorders associated with chromosome aberrations (0.28 percent), monogen-inherited pathology (13 percent), multifactorial or polygen-inherited pathology (86.72 percent). Hereditary predisposition associated with antigenic determinants of the HIA system, immune, metabolic, histological defects and other factors are implicated in the development of multifactorial diseases. The pathways by which the disease predisposition is realized are nonuniform. There prospect well novel biotechnological approaches, virologic, pharmacogenetic studies aimed at understanding of the role of heredity in the development of USO disorders, at diagnosing borderline illnesses, and at preventing the disease manifestations.

Child↗
PubMed1986

[Emery-Dreifuss disease or syndrome of amyotrophy with early contractures and secondary disorders of cardiac conduction with variable heredity].

Emery-Dreifuss myopathy is characterized by the association of early muscle contractures, atrophy predominant on the scapulohumeroperoneal muscles, secondary cardiac conduction anomalies and an X-linked heredity. The case presented here had features corresponding to these criteria except in two respects: the patient was a female, and transmission was of the dominant autosomal type. Three similar families have been reported. This genetic heterogeneity together with doubt as to the exact nature of muscle anomalies, suggests that the syndrome should be termed amyotrophy syndrome with early contractures and secondary cardiac conduction abnormalities with a variable heredity.

Adult↗
PubMedDate not supplied

Separating heredity and environment.

The problems of separating highly confounded heredity and environmental factors are reviewed from an epidemiological point of view. Once the fact rather than the appearance of familial aggregation is established, one can search for and analyze strong indicators of either genetic or environmental effects, and ultimately attempt their separation by strong design. Indicators of genetic effects are classified according to the presence or absence of family recurrence. In the presence of family recurrence, three analytic approaches are available: segregation analysis, linkage, and heritability estimates. In the absence of family recurrence, biological markers and endogamous groups can be used. Indicators of environmental effects are also classified according to the presence or absence of family recurrence of a disorder. In the presence of family recurrence, three environmental indicators are considered: non-Mendelian clustering, such as time of onset versus age in family clusters, and sex clusters; cohabitational effects; and maternal transmission. In the absence of family recurrence, environmental indicators include secular trends, migration, time and place clusters, family size, and birth order. Designs that aim to separate heredity and environment include twin studies, fixed clusters that include a variety of degrees of relatedness (particularly the family set-design), and comparisons of separately reared relatives. The strengths and weaknesses of twin studies and family set designs are reviewed. Separately reared relatives provide the most cogent tests of genetic and environmental hypotheses. Among these, separated twin pairs, half-sibs, and relatives separated through institutional placement or adoption are considered. Adoption strategies are illustrated by the Danish adoption studies of schizophrenia, criminality, and alcoholism, and these studies are reanalyzed from the perspective of epidemiological case-control and cohort studies. Finally, the potential uses of multiple family settings as they occur in the general population are briefly considered.

Diseases in Twins↗
PubMed1974

[Cellular heredity, its alteration and organ restoration].

Patterns of cell heredity in vertebrates and possibility of its alteration, i. e. artificial tissue metaplasia, are considered. These problems are compared with the well studied phenomenon of metaplasia in eyes of the newt in which the removal of some parts of the eye leads to natural metaplasia, an initial step for restoration of eye parts. A brief analysis of sequence of inductive processes in development shows that by the end of the period of induction and the onset of terminal differentiation the maximum concentration of specific inducing agents in induced rudiments can be expected. This suggestion was confirmed by the experiments of specific assimilatory induction in gastrula ectoderm and artificial conversion of pigmented epithelium in retina and lens tissues. On the basis of the data reported and in comparison with the theories of intragenomic regulation, a new hypothesis of cell heredity is put forward. The basic idea of this hypothesis is that the regulatory genes can switch on the genes responsible for the synthesis of terminal proteins via inducing proteins; the latter can simultaneously programm the function of regulatory genes, initiating their own synthesis. Due to such a feedback mechanism forming during development, stable cell types arise. Their inheritance can be altered by the introduction of new inducing agents in parallel with the elimination of conditions stabilizing cell differentiation. Possible ways for application of artificial metaplasia for restoration of eye defects in medical practice are considered.

Animals↗
PubMed1983

[Heredity and coronary artery lesions in patients with ischemic heart disease (clinico-coronarographic comparisons)].

The effect of aggravated heredity for coronary heart disease on the extent of coronary arterial damage and the course of the disease was studied in 575 coronary patients. An information system based on the findings was treated on a third-generation computer M-4030. Coronary patients with aggravated heredity showed high rates of coronary arteries narrowing, more severe course of the disease and frequent large-focal myocardial infarctions with aneurysms of the heart.

Adult↗
PubMed1981

[The influence of diabetes heredity on cardiovasculary risk profile in patients with high age diabetes (author's transl)].

The cardiovasculary risk profile of 105 newly detected, but still untreated, high age diabetics with an average of 69,1 years showing diabetes heredity in relatives of first degree was compared with a corresponding group (same age and same number of patients) without diabetes heredity. Taking into consideration exclusively the danger magnitudes overweight, hypertension, hypertriglyceridaemia, hypercholesterolaemia and hyperuricaemia, one sees an identical risk profile for both groups (the groups of patients were chosen according the principle of biostatistical gemini forming). For the showing of pathogenic magnitudes of influence within the metabolic syndrome the environmental factors seem to have a far greater importance than hereditary diabetogenic ones.

Aged↗
PubMed1995

Cortical memory in Paramecium: a theoretical approach to the structural heredity.

Structural heredity is frequently encountered in ciliates. In particular, during division of Paramecium the cortical characteristics of the 2 daughter cells are inherited from those of the mother cell. Genesis of new structures is therefore only possible if there are pre-existing older structures. We attempted to simulate this phenomenon with a model already used to describe the structure and morphogenesis of the cortex of Paramecium. We show that to initiate spatial organization it is enough to choose special starting conditions which comprise the primer of the structure, even if highly localized and at a low concentration of morphogens. This property does not question the basic concepts of genomic heredity.

Animals↗
PubMed1993

[Summary of results of a study of heredity of intelligence in a sample of the Czech population. III. Longitudinal and genealogic study of twins and their families].

The author presents further results of the longitudinal study of inheritance of intelligence, its components and structure in twins. Summarized results are presented for the age period from 0-15 years as well as detailed results of individual components and the global IQ in the age group of 8-15 years. The paper follows after two previous ones published in 1988 where the applied methods and statistical evaluation were described. Evidence was provided that heredity of intelligence is involved in children from a very early age, i.e. 0-3 years. After the age of 4 heredity predominates markedly over environmental influences up to the age of 15 years investigated so far by the author. (A slight decline occurs during the prepubertal period-age 13 and 14 years.) The author found that in particular the following components of intellect are inborn: abstract thinking, logic, talent for mathematics, concentration, inquisitiveness. Very detailed tables are presented for possible comparison with data in the literature and data from adults. The author found that the development of intelligence from childhood to adult age is very irregular. This uneven character is also mostly inborn. Statistical evaluation revealed several basic types of developmental curves and extreme variants. This will, however, be discussed in another paper. The theoretical results can be used also in practice in school education, counselling psychologic and psychiatric out-patient departments.

Adolescent↗
PubMedDate not supplied

[The nature of the genotype and heredity].

The term "genotype" is used for both hereditary information and its substantial bearer. The most important property of the information is relatively of its content which means very weak dependence on properties of the information substantial bearer (genotype of the second meaning) and very strong dependence on properties of the information recipient. Hereditary information (genotype in the first meaning) is addressed to the ontogenesis system, that is, to phenotype. From this it follows: 1) The genotype content is determined not so much by properties of its substantial bearer as by properties of the phenotype to which it is addressed; 2) Certainty of the genotype content depends not so much on stability of its elements, genes, as on stability of the phenotype of adaptive norm; 3) Genotype possess certain content only for a phenotype inherited from the ontogeny of other (maternal) organism or from a previous ontogenetic stage of the same organism; 4) Genotype (and this is true for any hereditary information of an organism) can not be localized in the primary structures of the nucleic acids. It is an aspect of phenotype and not a part thereof and, in this sense, does not possess independent being; 5) Each element of the phenotype, including genotype, relative to its other elements, is both recipient and bearer of hereditary information; 6) Genotype, as genetic code, is specialized but, not the only, "organ" of storing and transferring of hereditary information; 7) There is no two identical genotypes existing in nature; 8) The only operational definition of the genotype is its treating as genetic information localized in one or several loci; 9) Rather strong relation between certain symbols of genetic code (genes) and certain phenotypic characters reflects stability of reactional system of adaptive norm; 10) High semantic university of some symbols of genetic code indicates deep phylogenetic unity of all existing organisms; 11) Biological sense of structural separateness of the genotype within phenotype is creating and supporting of an information pool undestroyable during ontogenetic development; 12) All and only living systems possess reciprocally determining processes of individual and historic development; 13) Heredity, as an ability of descendants to reproduce safely in their ontogeneses the properties of their ancestors is an integral undecomposable (more exactly, decomposable but for operational purposes) property of the life. There is no and could not be any "heredity substance, as there is no and could not be an "information substance".

Animals↗
PubMedDate not supplied

[Heredity and environment in the genesis, epigenesis and evolution of the orofacial area].

Genetic and evolutionary aspects of the dento-facial complex are described according to the concept of heredity as a force of preservation for the human species, though ruled by natural selection and by mutational changes. Ontogenesis and growth of the oral structures reflect mutual regulations between genes and environmental factors. Therefore, the authors carry out an analysis of environmental and constitutional factors affecting dental and facial development. Three levels are identified: individual morphogenesis and growth; actual heredity of parietal dento-facial traits; role and meaning of teeth, jaws and temporo-mandibular joint during evolution leading to Homo sapiens sapiens. As far as individual development is concerned, genes provide only the input for initial cell proliferation and/or differentiation. Further on, growth and morphogenesis of oro-facial structures takes place by means of cell-to-cell and cell-to-substrate interactions. The final, structural result is due to reciprocal interactions among developing structures: muscles modify bone, teeth alignment influences bony bases alignment, ecc. Each structure is genetically determined (teeth, bones, muscles) and each structure carries out epigenetic regulations on other structures: no structure is secluded from biological function of the organism. The inheritance of oro-facial "traits", then, is hardly valuable. First of all, "traits" actually do not exist: they are the product of complex, multifactorial biological mechanisms. Moreover, facial characteristics are affected by polygenic regulation, each gene often showing pleiotropic effects. It has been calculated that 85-90% of facial dimensions in due to epigenetic modifications. Evolution and phylogenesis give evidence about the deep environmental influence on oro-facial morphology. Apart from certain molecular features regarding tooth structure (several dental proteins are today the same as those of the first Vertebrates who lived 500 millions of years ago), tooth number, form, and size depend upon environmental factors. Therefore, dentistry has the important task to preserve fundamental characteristics of dentition, and to intercept environmental pathogenetic factors, as dentition represents a precious instrument for the survival of the human species.

Biological Evolution↗
PubMed1997

The spectre of inbreeding in the early investigation of heredity.

Inbreeding introduced by R. Bakewell (1725-1795) in England for creating new animal races, was opposed by animal breeders on the Continent on religious grounds, and was soon introduced in sheep breeding for wool production in Moravia. In 1790-1840 the protagonists repeatedly rejected 'the spectre of inbreeding' and included consanguineous matching in scientific breeding. In 1836 they even formulated the research question of heredity and next year proposed the inductive method for its investigation. The achievements of sheep breeders instigated German breeders to reject the dogma of the constancy of race and to elaborate the theory of individual potency. Treating heredity as the force under the influence of environment they could not solve the enigma. The question formulated in 1836 was explained in 1865 by Gregor Mendel. His theory was not perceived by animal breeders as well as by biologists up to the end of the century.

Animals↗
PubMed2005

Telomere length and heredity: Indications of paternal inheritance.

Cellular telomere length is linked to replicative life span. Telomere repeats are lost in peripheral blood cells in vivo by age, and women show less telomere attrition than men. Previous reports have indicated that telomere length and chromosome-specific telomere-length patterns partly are inherited. The mode of heredity has not been clarified, but a link to the X chromosome was recently suggested. We analyzed peripheral mononuclear cells from 49 unrelated families for telomere length using a real-time PCR method. Short-term cultured Epstein-Barr virus-transformed lymphoblasts from the same individuals (n = 130) were analyzed for ability to maintain telomere length and possible gender-linked inheritance. A statistically significant association between telomere lengths comparing father-son (P = 0.011, n = 20) and father-daughter (P = 0.005, n = 22) pairs was found. However, no correlation was observed between mother-daughter (P = 0.463, n = 23) or mother-son (P = 0.577, n = 18). The father-offspring correlation was highly significant (P < 0.0001), in contrast to mother-offspring (P = 0.361). Epstein-Barr virus cultures demonstrated in most cases telomere preservation inversely related to initial mononuclear cell telomere length with short telomeres displaying the most pronounced elongation. Telomere length is inherited, and evidence for a father-to-offspring heritage of this trait was obtained, whereas in vitro telomere length maintenance was found to be dependent on the initial telomere length.

Adult↗
PubMed2006

Discovering DNA encodes heredity and prions are infectious proteins.

The resemblance between the discoveries that DNA is the basis of heredity and that prions are infectious proteins is remarkable. Though four decades separated these two discoveries, the biochemical methodologies and scientific philosophies that were employed are surprisingly similar. In both cases, bioassays available at the time that the projects were initiated proved to be inadequate to support purification studies. Improved bioassays allowed the transforming principle (TP) to be purified from pneumococci and prions from scrapie-infected hamster brains. Publications describing TP as composed of DNA prompted some scientists to contend that undetected proteins must contaminate TP enriched fractions. The simplicity of DNA was thought to prevent it from encoding genetic information. By the time prions were discovered, the genomes of all infectious pathogens including viruses, bacteria, fungi and parasites had been shown to be comprised of nucleic acids and so an antithetical refrain became widely echoed: DNA or RNA molecules must be hiding among the proteins of prions. Finding the unexpected and being asked to demonstrate unequivocally the absence of a possible contaminant represent uncanny parallels between the discoveries that DNA encodes the genotype and that prions are infectious proteins.

Animals↗