Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEREDITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2004

Characterisation of subjects with early abnormalities of glucose tolerance in the Stockholm Diabetes Prevention Programme: the impact of sex and type 2 diabetes heredity.

AIMS/HYPOTHESIS: We evaluated the impact of sex and type 2 diabetes heredity on the prevalence and pathogenesis of early abnormalities of glucose homeostasis in subjects participating in the Stockholm Diabetes Prevention Programme. METHODS: A sample of 3,128 men and 4,821 women, of whom approximately half had a family history of type 2 diabetes (FHD) was categorised according to an OGTT: NGT, IFG, IGT, combined glucose intolerance and type 2 diabetes. The homeostasis model assessment was used to determine insulin sensitivity and beta cell function. RESULTS: Prevalence of early abnormalities of glucose metabolism was two to three times higher in subjects with FHD and two to three times higher in men compared to women. Both maternal and paternal heredity of type 2 diabetes were associated with an increased risk of having early abnormalities of glucose metabolism. However, in women with type 2 diabetes heredity on the father's side seems to have less impact on an increased risk of having type 2 diabetes. Both waist circumference and systolic blood pressure were increased in subjects with abnormalities of glucose homeostasis, whereas insulin sensitivity and beta cell function were decreased. Subjects with IFG had more pronounced impairment of beta cell function and insulin sensitivity than subjects with IGT. CONCLUSION/INTERPRETATION: An FHD and male sex increased the prevalence of abnormalities of glucose homeostasis. Subjects with IFG had more pronounced defects of insulin secretion and action than subjects with IGT.

Blood Glucose↗
PubMed1986

The cyclic AMP second messenger system in man: the effects of heredity, hormones, drugs, aluminum, age and disease on signal amplification.

The intracellular effects of a number of hormonal signals are mediated by the cyclic AMP second messenger system in man and the ubiquitous distribution of hormone-stimulated adenylate cyclase suggests the importance of this enzyme complex in normal aging and pathophysiological states. Various vectors including heredity, endogenous catecholamines, steroid hormones, and drugs affect the activity of hormone-stimulated adenylate cyclase in man. The effect of heredity was studied using lymphocytes obtained from monozygotic twin pairs and age and sex-matched sib pairs. Only for forskolin-stimulated activity is a significant proportion of individual variance attributable to heredity, suggesting the relative stability of the catalytic subunit. Beta-adrenergic and prostaglandin E-1 activity are "state" characteristics and their activities are controlled by environmental parameters. A significant reduction in isoproterenol-stimulated cyclic AMP accumulation between the menses and luteal phase of the menstrual cycle is observed in lymphocytes obtained from 11 female subjects. The lowest level of beta-adrenergic receptor activity is associated with the highest levels of progesterone and estradiol hormone levels in blood. Lithium at therapeutic concentrations markedly inhibits adenylate cyclase activity in platelet membranes. Moreover, marked individual differences are observed in sensitivity to lithium as determined by Dixon plot derived Ki values for 9 normal, healthy subjects. Human adenylate cyclase obtained from platelets and lymphocytes is activated by micromolar amounts of aluminum in the presence of NaF. Irreversible activation of adenylate cyclase by aluminum is suggested as a possible mechanism of this metal's neurotoxicity. The biochemical basis for the age-associated decline in beta-adrenergic responsiveness in man is discussed. Several investigations suggest a deficit at two levels in the adenylate cyclase complex: an impaired coupling of the receptor/N protein subunits and an additional lesion distal to the receptor at the level of N/C coupling. Perfusion studies with salbutamol suggest that the decline in beta-adrenergic sensitivity is general and not restricted to lymphocytes. Possible abnormalities in cyclic AMP signal amplification and recognition in various disease states is discussed. Increased prostaglandin E-1-stimulated cyclic AMP accumulation is observed in lymphocytes obtained from patients with Alzheimer's disease compared to age-matched controls and correlated with severity of the disease state.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMed2001

Francis Galton on twins, heredity and social class.

In 1875 Francis Galton was the first to study twins as a test of the relative strenght of heredity and environment. This paper examines Galton's work on twins, using his surviving working papers. It shows that his enquiry was larger and more systematic than previously realized. Galton issued several hundred questionnaires to parents of twins, with the aim of establishing how far the similarities and differences between twins were affected by their life experiences. The paper also discusses Galton's study in relation to his understanding of the physiology of twinning and his theory of heredity. The modern concept of monozygotic twins had not yet been established, and the similarity between Galton's work and modern twin studies should not be overstated. While Galton's work was important as a pioneering study, in some respects his conclusions went beyond his evidence. The paper finally examines whether Galton's twin studies influenced his position on the links between social class, heredity and social mobility, and surveys the evidence for his views on these issues.

Genetics↗
PubMed1999

The development of Francis Galton's ideas on the mechanism of heredity.

Galton greeted Darwin's theory of pangenesis with enthusiasm, and tried to test the assumption that the heredity particles circulate in the blood by transfusion experiments on rabbits. The failure of these experiments led him to reject this assumption, and in the 1870s he developed an alternative theory of heredity, which incorporated those parts of Darwin's theory that did not involve the transportation of hereditary particles throughout the system. He supposed that the fertilized ovum contains a large number of hereditary elements, which he collectively called the "stirp," a few of which are patent, developing into particular cell types, while the rest remain latent; the latent elements can be transmitted to the next generation, while the patent elements, with rare exceptions, cannot since they have developed into cells. The problem with this theory is that it does not explain the similarity between parent and child unless there is a high correlation between latent and patent elements. Galton probably came to realize this problem during his subsequent statistical work on heredity, and he quietly dropped the idea that patent elements are not transmitted in Natural Inheritance (1889). Galton thought that brothers and sisters had identical stirps, and he attributed differences between them to variability in the choice of patent elements from the stirp, that is to say to developmental variability. He attributed the likeness of monozygotic twins to the similarity of their developmental environment. Galton's twin method was to track the life history changes of twins to see whether twins who were similar at birth diverged in dissimilar environments or whether twins who were dissimilar at birth converged in similar environments. It is quite different from the modern twin method of comparing the similarities between monozygotic and dizygotic twins, on the assumption that monozygotic twins are genetically identical whereas dizygotic twins are not. It has been argued that Galton foreshadowed Weismann's theory in the continuity of the germ-plasm, but this is only true in a weak sense. They both believed that the inheritance of acquired characters was either rare or impossible, but Galton did not forestall the essential part of Weismann's theory, that the germ-plasm of the zygote is doubled, with one part being reserved for the formation of the germ-cells.

Genetics↗
PubMed1981

An overview of a multifactor-system theory of personality and individual differences: III. Life span development and the heredity-environment issue.

In Part III of this three-part series on multifactor-system theory, multivariate, life-span development is approached from the standpoint of a quantitative and qualitative analysis of the ontogenesis of factors in each of the six systems. The pattern of quantitative development (described via the Gompertz equation and three developmental parameters) involves growth, stability, and decline, and qualitative development involves changes in the organization of factors (e.g., factor differentiation and convergence). Hereditary and environmental sources of variation are analyzed via the factor gene model and the concept of heredity-dominant factors, and the factor-learning model and environment-dominant factors. It is hypothesized that the sensory and motor systems are heredity dominant, that the style and value systems are environment dominant, and that the cognitive and affective systems are partially heredity dominant.

Genotype↗
PubMed2000

Influence of heredity for obesity on adipocyte lipolysis in lean and obese subjects.

OBJECTIVE: To evaluate a possible influence of a hereditary trait for obesity on the regulation of adipocyte metabolism in vitro in subcutaneous fat cells in obese and non-obese subjects. DESIGN: A biopsy from abdominal subcutaneous fat was obtained from consecutive subjects with or without a family trait for obesity. A positive family history of obesity was considered present if one or more of the first degree relatives had a BMI of 27 kg/m2 or more. SUBJECTS: 67 non-obese and 60 obese subjects, age 19-60 y. A family trait for overweight was present in 42 of the lean subjects and in 50 of the obese subjects. MEASUREMENTS: Fat cells were isolated and incubated in vitro with isoprenaline (a non-selective beta-adrenoceptor agonist), forskolin (activates the adenylyl cyclase) and dibutyryl cyclic AMP (stimulates the protein kinase hormone-sensitive lipase complex). Glycerol release was measured and used as lipolytic index. RESULTS: Maximal lipolytic response per g triglycerides was about 50% lower in obese subjects both with and without a positive heredity and in non-obese subjects with a family trait for obesity as compared to non-obese subjects without such trait (P=0.0001). Fat cell volume was twice as high in obese as compared to lean subjects. Drug-induced maximal glycerol release per fat cell in the obese subjects, regardless of family history of obesity, reached a similar level, but did not exceed that of the lean group without heredity. CONCLUSIONS: Obesity is associated with catecholamine resistance with a relatively ineffective lipolysis in fat cells, and presence of a family history of obesity was not associated with a further suppression of lipolysis. In the lean subjects, heredity for obesity significantly influenced lipolysis to similar low levels as in the obese subjects.

Adipocytes↗
PubMed2001

Fetal exposure, heredity and risk indicators for cardiovascular disease in a Swedish welfare cohort.

BACKGROUND: The overall aim was to test whether low birthweight (LBW) in newborns is associated with the risk indicators for cardiovascular disease in early middle age, even in a welfare society. Further, a possible interaction of LBW and heredity for myocardial infarction or stroke was investigated. METHODS: Overall, subjects were identified as newborns in a local birth register, and as adult participants, in the Västerbotten Intervention Program (n = 7876). Outcome measures such as systolic (SBP) and diastolic blood pressures (DBP), body mass index (BMI), cholesterol, triglycerides and anthropometrics were investigated (at age 29-41 years) in relation to LBW. RESULTS: Low birthweight was associated with increased SBP and DBP. Triglycerides were elevated among women with LBW and total cholesterol was elevated in men with LBW. Heredity for myocardial infarction or stroke interacted with LBW, and indicated a synergistic effect on the level of SBP. The BMI did not differ between LBW and normal birthweight subjects. CONCLUSIONS: Our interpretation is that the 'fetal origins' hypothesis' is valid for middle-age subjects who grow up in a welfare society. The population attributable proportions that result from different exposures to LBW were relatively small overall; from a public health perspective, heredity was more important than LBW for elevated SBP.

Adult↗
PubMed1995

Neonatal IgA and IgE levels among infants with paternal heredity for atopic disease.

Serum IgA and IgE levels were studied in the postnatal period in 21 infants having a paternal heredity of atopic disease. Three different sampling techniques were used, aspirated cord blood (CB), gravity-collected cord blood, and capillary collected blood at 4-5 days of age. Significant differences among the three sampling techniques were recorded for IgA (P < 0.01), but not for IgE. The IgA levels decreased from birth to 4-5 days of age in 90% (19/21 of infants (P < 0.01). The corresponding decrease in IgE levels was 20%. This postnatal difference in the frequency of decreasing/increasing IgA and IgE levels was significant (P < 0.05). An analysis of CB IgA to detect maternal contamination of CB was found to be of questionable value, since only 50% (2/4) of the cases with an elevated CB-IgA level could be considered contaminated. The results of this study further emphasize that aspiration of CB and capillary collection of blood at 4-5 days of age are the best sampling techniques to avoid contamination. The general finding that paternal heredity had no significant influence on infant IgE contrasts with the strong influence of maternal heredity. Further studies will show whether the explanation lies in genetic or transplacental factors, or in both kinds of factors.

Fetal Blood↗
PubMed1987

Prolonged exclusive breast feeding and heredity as determinants in infantile atopy.

We followed 183 infants for two years, 31 of whom were breast fed less than three and a half months (median 70 days; short breast feeding group) and a further 31 of whom were exclusively breast fed for more than nine months (long breast feeding group). We assessed heredity for atopy, number of infections, and duration of breast feeding as determinants of atopy. During the first year of life 14 infants has signs of atopy. During the second year parents reported signs of atopy in a further 31. Heredity was the only significant predictor of atopy. Atopy was seen in 33% of infants with a positive heredity and in 16% without family history for atopy. The duration of breast feeding affected the incidence of atopy only among the infants without family history for atopy: fewer in the short breast feeding group (1/18) had atopy than in the long breast feeding group (5/13). Duration of breast feeding did not associate with incidence of respiratory infections. Diarrhoea was more common in the short breast feeding group than in the long breast feeding group during the first year of life. We conclude that prolonging exclusive breast feeding from the median of 70 days to nine months did not contribute to the prevention of infantile atopy and respiratory tract infections.

Breast Feeding↗
PubMedDate not supplied

[The role of heredity in the prevalence of arterial hypertension and its risk factors].

Studied in the rural population both men and women residing in the territories of Chernigov Province was prevalence of aggravated heredity in respect of myocardial infarction, cerebral insult, arterial hypertension, diabetes mellitus, and sudden non-murderous death. More frequently encountered in the above population is aggravated heredity in respect to arterial hypertension, with significant predominance being recordable of maternal-lineage heredity. The prevalence of arterial hypertension in probands with hereditary aggravation is much greater than in the population, especially so among women. Positive correlation was disclosed between arterial hypertension with excess consumption of table salt and overweight in probands with hereditary aggravation.

Adult↗
PubMed2005

[The heredity of flower colors and the discovery of flower color chimera in chrysanthemum species].

The reciprocal crosses of yellow colored chrysanthemum x red colored chrysanthemum and white colored chrysanthemum x red colored chrysanthemum were conducted in order to analyze the heredity of flower colors. The results revealed that the heredity of flower colors was very complicated, and mainly exhibited matroclinous characteristics when red colored materials was used as maternal parent but not in the combinations when the yellow or white colored materials were used as maternal parents. The incomplete dominance and mosaic dominance also existed in the heredity of chrysanthemum flower colors. The flower-color chimeras with two kinds of flower buds were discovered in the cross of 3501 x 3509, i.e. one side of the flower buds was completely in red color, which was same as the parental material of 3509, and another side was generally in yellow color with red spots on them. Cytological analysis showed that two sides were both with 36 chromosomes, indicating that the formation of chimera was not resulted from the changes of chromosome numbers, but from the destruction of pigment synthesis genes by the insert of transposable element.

Chimera↗
PubMed1987

[Role of heredity in the prevalence of ischemic heart disease and its risk factors].

The relationship of heredity with CHD prevalence and the main risk factors (RF) was analyzed on the basis of the results of a primary cardiological screening of the male population aged 40 to 59 in Minsk and Kaunas (10012 persons). The results of the analysis were in favor of hereditary predisposition to CHD. The prevalence of CHD and the main RF in probands with aggravated heredity was much higher than that in probands with favorable heredity. CHD prevalence in the compared groups was 12.4 and 10.7%; SK 3.9 and 0.2%; cerebral stroke 1.6 and 0.6%, respectively. Statistically significant changes were also revealed in RF frequency: AH--32.6 and 27.1%; HCS--27.7 and 24.1%; EBM--16.6 and 13.8%; smoking--43.6 and 47.0%. Over 1/3 of all types of CHD and AH were found in the persons with hereditary predisposition to CHD on the maternal side with a tendency to CS.

Adult↗
PubMed1985

Salt sensitivity in normotensives with and salt resistance in normotensives without heredity of hypertension.

We have studied blood pressure responses to moderate sodium restriction from 200 to 50 mmol/day over 2 weeks in 62 normotensive subjects with and without a family history of hypertension by continuous automatic blood pressure recording. Based on the average of the blood pressure of 1 hour continuous monitoring under basal conditions, we have been able to demonstrate a significant fall of blood pressure in 28 young subjects with a heredity of hypertension after moderate sodium restriction from 200 to 50 mmol over 2 weeks (fall in systolic blood pressure 5.4 +/- 1.1, diastolic 2.5 +/- 0.8, mean blood pressure 2.9 +/- 0.7 mmHg, mean +/- SEM), whereas blood pressure remained unchanged in a group of 34 subjects without heredity of hypertension after moderate sodium restriction (change in systolic blood pressure -1.0 +/- 0.6, diastolic blood pressure -0.6 +/- 0.7 and mean blood pressure -0.93 +/- 0.67 mmHg). 29 of the subjects were studied a third time 2 weeks after having returned to their usual high sodium diet and in those in whom a blood pressure fall was observed during sodium restriction it returned to pre-intervention values. This demonstrates that normotensives with a heredity of hypertension are salt sensitive and adds further evidence that a high sodium intake may be of critical importance for the initiation of essential hypertension.

Adult↗
PubMed2005

Ideas about heredity, genetics, and 'medical genetics' in Britain, 1900-1982.

The aim of this paper is to understand how evolving ideas about heredity and genetics influenced new medical interests and practices and, eventually, the formation of 'medical genetics' as a medical specialism in Britain. I begin the paper by highlighting the social and institutional changes through which these ideas passed. I argue that, with time, there was a decisive convergence in thought that combined ideas about the familial aspects of heredity and the health needs of populations with an omnibus 'genetic' approach to health and illness that focused on the structures and activities of chromosomes and genes in individuals. I show how this convergence in thought was spurred on, first, by innovations in genetic science and technology in the years after 1960, and, second, by negotiated protocols and standards of medical practice worked out by bodies such as the relevant royal colleges, the linked associations and societies for medical professionals, affected training and research authorities, and the state. The notion of 'medical genetics' in Britain consequently gained a semblance of unanimity over its basic reference points and arrived at a meaning directly tributary to current acceptance of the term in the context of a medical specialism.

Eugenics↗
PubMed2003

Parents and children: ideas of heredity in the 19th century.

The concept of heredity played a powerful role in structuring 19th-century debates over sickness, morality, class, race, education, social change and evolution. But there was very little agreement as to which qualities were heritable and how new hereditary variants were acquired. In consequence, notions of heredity existed in a wide variety of forms, expressing anything from extreme determinism and a belief in the incorrigibility of individuals, social and racial groups, to unleavened optimism, and a faith in ultimate human perfectibility. This article explores these rich hereditarian discourses to convey an impression of a century that was at least as preoccupied with the concept of biological inheritance as we are today.

Adult↗
PubMed2002

How theories became knowledge: Morgan's chromosome theory of heredity in America and Britain.

T. H. Morgan, A. H. Sturtevant, H. J. Muller and C. B. Bridges published their comprehensive treatise The Mechanism of Mendelian Heredity in 1915. By 1920 Morgan's "Chromosome Theory of Heredity" was generally accepted by geneticists in the United States, and by British geneticists by 1925. By 1930 it had been incorporated into most general biology, botany, and zoology textbooks as established knowledge. In this paper, I examine the reasons why it was accepted as part of a series of comparative studies of theory-acceptance in the sciences. In this context it is of interest to look at the persuasiveness of confirmed novel predictions, a factor often regarded by philosophers of science as the most important way to justify a theory. Here it turns out to play a role in the decision of some geneticists to accept the theory, but is generally less important than the CTH's ability to explain Mendelian inheritance, sex-linked inheritance, non-disjunction, and the connection between linkage groups and the number of chromosome pairs; in other words, to establish a firm connection between genetics and cytology. It is remarkable that geneticists were willing to accept the CTH as applicable to all organisms at a time when it had been confirmed only for Drosophila. The construction of maps showing the location on the chromosomes of genes for specific characters was especially convincing for non-geneticists.

Chromosomes↗
PubMed2006

Heredity: a prognostic factor for acne.

BACKGROUND: The role of heredity in acne severity and therapeutic response remains unclear. OBJECTIVE: A prospective epidemiologic study was performed to compare clinical and evolutive features of acne and response to treatment in 151 patients with acne with (A+) or without (A-) family history of acne. METHODS: A+ and A- patients were compared on clinical and therapeutic criteria. A+ patients were then distributed into subgroups (M+, F+, M+F+) following the origin of family history (father: F, mother: M). RESULTS: The clinical profile was similar in the A+ and A- populations. Acne occurred earlier and more often before puberty in the A+ population, in which oral treatments and relapse after isotretinoin were more frequent. Retentional lesions (number and extent) were more important in the M+ and M+F+ populations. CONCLUSION: This study confirms the importance of heredity as a prognostic factor for acne. Family history of acne is associated with earlier occurrence of acne, increased number of retentional lesions and therapeutic difficulties.

Acne Vulgaris↗
PubMedDate not supplied

[Natural history and eighteenth-century ideas regarding generation and heredity: Buffon and Bonnet].

The intellectual course of natural history reveals three conceptual approaches. The first was the taxonomic point of view, where naturalists worked to name and classify the living beings created by God. The second approach was provided by the eighteenth century's philosophical doctrine of mechanism, which lent natural history its method of endeavoring to comprehend the workings of organisms, inasmuch as the world "ran". Calling into question the adequacy of prior message, the third approach argued that living things display characteristics quite distinct from those of non-living matter, making it necessary to understand processes rather than simply decompose phenomena to then analyze them. This inadequacy became apparent at the moment when ideas of generation and heredity ascribed a reproductive history to living things, a history where the act of one fellow creature being formed by another plays an important role in coming to understand the workings of life. The paper analyzes these conceptual approaches from the perspective of Buffon's and Bonnet's ideas on reproduction and heredity, which represented opposite schools of thought: epigenesis and preformation.

Biology↗