Genetic determinism or genetic discrimination?
Explore the source record for details and available documents.
Bioethics↗
SEARCH · PubMed Health
Results for “Genetic Determinism”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Polymorphism of Ps (parotid size variant) and detection of a protein (PmS) related to the Pm (parotid middle band) system with genetic linkage of Ps and Pm to Gl, Db, and Pr genetic determinants.
Genetic polymorphism of the Ps (parotid size variant) proteins found in saliva is determined by autosomal inheritance of two expressed and one unexpressed allele. This hypothesis is supported by studies in 43 families including 153 children. Gene frequencies determined for 150 randomly collected salivas from whites and 101 randomly collected salivas from blacks are as follows: for whites, Ps1 = 0.598, Ps2 = 0.101, Ps0 = 0.301; for blacks, Ps1 = 0.185, Ps2 = 0.126, and Ps0 = 0.689. The electrophoretic polymorphism is manifested by apparent differences in molecular weights between Ps proteins. The Ps proteins are glycosylated and have an approximate isoelectric point of pI 8.1 as determined by isoelectric focusing in gels. We have also found in saliva the presence of a protein (PmS) which shows strong positive correlations with the presence of the smaller sized Pm (PmF) salivary protein described by Ikemoto et al. (1977). This suggested that PmS is probably part of the Pm protein polymorphic system. For randomly collected salivas from whites, the gene frequencies are PmF+ = 0.15 (N = 140) and PmS+ = 0.12 (N = 150). For randomly collected salivas from blacks, the gene frequency is PmS+ = 0.24 (N = 101). The gene frequency of PmF+ was not determined. Family studies support autosomal inheritance of PmF and PmS.
Adult↗
Embryo transfer in the rat as a tool to determine genetic components of the gestational environment.
Embryo transfer, with the recipient dam nursing the transferred progeny, was used to study the impact of the gestational environment on adult blood pressure (BP) in three inbred rat strains, the hypertensive Dahl salt-sensitive SS/JrCtr, the normotensive Dahl salt-hypertension resistant SR/Jr, and the normotensive Dark Agouti rat. Rats that had been cross-fostered within 6 h of birth were included as a control for lactational and nurturing factors. Systolic BP was measured by tail-cuff plethysmography twice a week in rats after the age of 7 weeks. Embryo transfer success, measured as the percentage of embryos transferred resulting in pups weaned at 4 weeks, was 27% between the SS/JrCtr and SR/Jr and 53% for the SS/JrCtr and Dark Agouti. This assessment included all failures, some of which probably were not associated with the transfer. If only the number of embryos transferred to dams with successful pregnancies was included, the success rate was 48% between the SS/JrCtr and SR/Jr and 82% between the SS/JrCtr and Dark Agouti strains. Anomalies in pups were not evident. In contrast to the lactational environment, the gestational milieu had a profound effect on basal blood pressure of the hypertensive SS/JrCtr progeny, less of an effect on that of the Dark Agouti, and no effect on that of the SR/Jr. Although the SS/JrCtr strain is significantly larger than the SR/Jr and Dark Agouti strains, neither embryo transfer nor cross-fostering altered body weight of rats at the age of 6 weeks. These data indicate that embryo transfer can be an easy and efficient method of isolating genetically determined factors of the gestational environment.
Animals↗
The genetic determination of left ventricular mass in healthy adults.
AIMS: The extent to which left ventricular (LV) mass, an independent cardiovascular risk factor, is determined by genetic factors is unclear. The aim of this study was to assess the heritability of LV mass and its association with three potential candidate genes. METHODS: A population-based adult twin study model was utilized. Echocardiographic assessment of LV mass was performed in 110 twin pairs (mean age 55.9+/-10.9 years). An estimate of genetic determination, heritability, was calculated for the main echocardiographic parameters. The cohort were genotyped for the G-protein beta-3, aldosterone synthase, and beta-1 adrenoceptor genes. RESULTS: The intra-class correlation coefficients for LV mass were 0.69 for monozygotic (r-MZ) twins and 0.32 for dizygotic (r-DZ) twins, P=0.008 (heritability estimate of 0.69). This pattern persisted following correction for known confounding factors. Within-pair differences in the monozygotic, discordant and concordant dizygotic twins showed no differences for the three genes with respect to left ventricular wall thickness or mass. There was a non-significant trend towards a relationship between LV mass and the beta-1 adrenoceptor genotype. CONCLUSION: Within a normal population left ventricular mass has a significant genetic determination. Further investigation of potential candidate genes is required.
Cohort Studies↗
Genetic determination of the queen caste in an ant hybrid zone.
The question of how reproductives and sterile workers differentiate within eusocial groups has long been a core issue in sociobiology because it requires the loss of individual direct fitness in favor of indirect or group-level fitness gains. The evolution of social behavior requires that differentiation between workers and female reproductives be environmentally determined, because genetically determined sterility would be quickly eliminated. Nevertheless, we report clear evidence of genetic caste determination in populations of two seed harvester ant species common to the southwestern USA, Pogonomyrmex rugosus and Pogonomyrmex barbatus. The genetic differentiation between workers and queens is found only in areas of sympatry of the two species, and thus appears to arisen from hybridization. Our data suggest that this hybridization has had a profound historical effect on the caste determination systems and mating patterns of each of these species.
Animals↗
[Genetic determinants of glomerulonephritis. Genetic aspects and pathophysiology of immune complex diseases of the kidney].
Explore the source record for details and available documents.
Antigen-Antibody Complex↗
Level of an advanced glycated end product is genetically determined: a study of normal twins.
Reducing sugars react with amino groups in proteins, lipids, and nucleic acids to produce advanced glycation end products (AGEs), including N(epsilon)-carboxymethyl lysine (CML), which have been implicated in oxidative stress and vascular damage. The aim of this study was to determine whether genetic factors influence serum CML levels in normal subjects. We performed a classical twin study of CML in healthy nondiabetic female twins, 39 monozygotic and 45 dizygotic pairs, aged 21-74 years. Serum CML levels were estimated by enzyme-linked immunosorbent assay. Twin correlations (r) for serum CML levels were higher in monozygotic (r = 0.71) compared with dizygotic (r = 0.50) twin pairs, suggesting a substantial genetic effect and confirmed by quantitative genetic model fitting. Additive genetic effects (heritability) explained 74% (95% CI 58-84) of population variance in CML. Heritability (%) of fasting glucose (51%) and HbA(1c) (62%) could not explain CML heritability, which was not associated with them. CML levels are, therefore, predominantly genetically determined and independent of genes influencing fasting glucose or HbA(1c). Thus familial, largely genetic factors influence AGE implicating these glycoxidation products in the genetic contribution to macro- and microvascular disease.
Adult↗
Migraine, ataxia and epilepsy: a challenging spectrum of genetically determined calcium channelopathies. Dutch Migraine Genetics Research Group.
Clinical and genetic heterogeneity as well as influence of environmental factors have hampered identification of the genetic factors which are involved in episodic diseases such as migraine, episodic ataxia and epilepsy. The study of rare, but clearly genetically determined subtypes, may help to unravel the pathogenesis of the more common forms. Recently, different types of mutation in the brain-specific P/Q type calcium channel alpha 1A subunit gene (CACNA1A) on chromosome 19p13 were shown to be involved in three human disorders: familial hemiplegic migraine (FHM), episodic ataxia type 2 (EA2), and chronic spinocerebellar ataxia type 6 (SCA6). In addition, evidence is accumulating that the same gene is also involved in the common forms of migraine with and without aura. In the tottering and leaner mouse, which are characterised by epilepsy and ataxia, similar mutations were identified in the mouse homologue of the calcium channel alpha 1A subunit gene. These findings add to the growing list of episodic (and now also chronic) neurological disorders, which are caused by inherited abnormalities of voltage-dependent ion channels. The findings in migraine illustrate that rare, but monogenic variants of a disorder, may be successfully used to identify candidate genes for the more common, but genetically more complex, forms.
Animals↗
HbA(1c) levels are genetically determined even in type 1 diabetes: evidence from healthy and diabetic twins.
HbA(1c), a measure of blood glucose regulation, reflects glucose levels in the preceding months. In diabetes, HbA(1c) levels predict the risk of microvascular complications. The aim of this study was to determine whether genetic factors could influence HbA(1c) levels in normal subjects and type 1 diabetic patients. We performed a classical twin study of HbA(1c) in healthy nondiabetic female twins and 42 monozygotic (MZ) and 47 dizygotic (DZ) pairs. Interclass correlations (r) were higher in MZ (r = 0.77) compared with DZ (r = 0.53) twin pairs, suggesting a substantial genetic effect; this was confirmed by quantitative genetic model fitting. Additive genetic effects (heritability) explained 62% (95% CI 47-75) of population variance in HbA(1c); the remainder was attributable to the influence of unique environment (23% [15-36]) and age (14% [5-28]). Multivariate modeling showed that genetic factors also have a substantial influence on fasting glucose levels (51%). However, HbA(1c) heritability could not be explained by genes in common with fasting glucose. In the patients with type 1 diabetes, HbA(1c) levels were correlated in 33 MZ twins concordant for diabetes (r = 0.68; P < 0.001) but also in 45 MZ twins discordant for the disease (r = 0.52; P < 0.001). These significant correlations for HbA(1c) in both concordant and discordant pairs indicate a diabetes-independent familial effect. Thus, HbA(1c) levels are largely genetically determined and independent of the genes influencing fasting glucose. Even in type 1 diabetes, familial (i.e., diabetes-independent) factors influence protein glycation, implying that familial factors may explain, in part, the risk for microvascular complications, as indicated by high HbA(1c) levels.
Adult↗
[Adrenaline-induced damage to the myocardium in rats with genetically determined arterial hypertension].
Genetically hypertensive and normotensive rats were subjected to acute myocardial injury by a single subcutaneous injection of adrenaline (0.5 mg/100 g bw). The animals were sacrificed one day later. The lesions showed the signs of focal coagulative necrosis and intracellular myocytolysis. The damaged cardiomyocytes with high sarcolemmal permeability for blood plasma proteins were more widespread in the hypertensive versus normotensive rats. Intracellular myocytolysis, which is not associated with alterations in the cell membrane, was found in both experimental groups at an equal rate. The data agree with the concepts of alterations in biological membranes in genetically determined arterial hypertension.
Animals↗
[Sulfalene pharmacogenetics. I. The genetic determination of the pharmacokinetic indices].
Genetic determination of pharmacokinetics of sulfalen, a new antibacterial drug, has been studied in 28 twin pairs of Moscow Russian population. In order to determine the degree of heritability of such pharmacokinetic parameters of sulfalen as t 1/2 (half-life); Vd and delta (apparent and specific volumes of distribution) and Co (apparent initial concentration) Holtsinger H-statistics values have been calculated, which are 0.891, 0.866, 0.766 and 0.797 respectively. Possible causes of discrepancies between these values and the coefficients of genetic determination G, calculated by decomposition of general phenotypical dispercion of the parameters via the main equation of quantitative traits of genetics are given (0.913, 0.762, 0.828, 0.856 in that order). The data obtained make it possible to assume that genetic determination t 1/2 of sulfalen is carried out within the system of monogenous interaction (HD = 0.91, HA = 0), that of Vd and Co--within the system of additive-polygenous interaction, while linear and non-linear effects contribute to delta determination (HD = 0.232, HA = 0.596).
Administration, Oral↗
Platelet function and survival in rats with genetically determined hypercholesterolaemia.
Platelets from rats with genetically determined hypercholesterolaemia are hypersensitive to aggregation induced by thrombin compared with platelets from their genetic controls without hypercholesterolaemia. Aggregation or release induced by thrombin of platelets from hypercholesterolaemic and control rats correlated significantly with plasma cholesterol concentrations. Platelet responses to ADP or collagen were not different between the groups. The hypersensitivity to thrombin-induced aggregation was independent of released ADP or products of arachidonic acid metabolism. The changes in platelet sensitivity occurred with only moderate increases in plasma cholesterol concentration and with no detectable changes in total platelet cholesterol. The hypersensitivity of platelets from hypercholesterolaemic rats was not associated with a reduction in platelet survival or any significant injury to the aortic endothelium in these animals. Platelets from hypercholesterolaemic rats were smaller than platelets from controls. Thus, platelets from rats with genetically determined hypercholesterolaemia have alterations in function similar to those found with platelets from rats with diet-induced hypercholesterolaemia indicating that this strain can be used to study the mechanisms by which cholesterol can change platelet function without the possible complicating effects of dietary factors. Since platelet hypersensitivity occurred in rats with genetically determined hypercholesterolaemia without a reduction in platelet survival, these studies are also consistent with the reduced platelet survival found in animals with diet-induced hypercholesterolaemia being independent of platelet changes.
Animals↗
[The relevance of genetically determined polymorphism CYP2D6 in psychopharmacology; the relationship between genotype and phenotype].
Based on literature review the paper presents some clinical aspects of the genetically determined polymorphism of the CYP2D6. One of the main biotransformation processes of psychotropic drugs is oxidation catalysed by enzymes of cytochrome P-450. CYP2D6 is an isoenzyme of cytochrome P-450. Its activity is determined genetically and is characterised by interindividual variability. Genetically determined polymorphism of CYP2D6 is related to mutated alleles that code enzymatic proteins with different activity. Based on individual ability to oxidize drugs by CYP2D6 in population there are four phenotypically different groups: extensive (EM), ultra-rapid (UM), intermediate (IM) and poor metabolizers (PM). Each phenotype is determined by a given genotype. About 6-10% of the Caucasian population is known as PM phenotype. Drugs used in standard doses in this group may reach a markedly higher level in blood, even a toxic level. Compared to the group with EM phenotype persons with PM or IM phenotype are more likely to suffer from side effects that are related to impaired metabolic pathways that are catalyzed by CYP2D6. In the group with UM phenotype (1-7% of population) metabolism is very rapid, thus they need higher doses of psychotropic drugs to reach therapeutic blood level of drug.
Asian People↗
Thrombin-induced inositol phosphate production by platelets from rats with diet-induced or genetically determined hypercholesterolemia.
Platelets from rats with diet-induced or genetically determined hypercholesterolemia are hypersensitive to thrombin through a pathway that is independent of the effects of released ADP or formation of thromboxane A2. We examined production of inositol phosphates by platelets from these hypercholesterolemic rats to determine whether the enhanced responsiveness to thrombin is associated with increased production of inositol trisphosphate (IP3). The opportunity to study rats with hypercholesterolemia determined genetically or induced by diet makes it possible to determine whether any differences in inositol phosphate production are caused by hypercholesterolemia alone rather than to any other effect of the diet used to induce hypercholesterolemia. Platelets were prelabeled with [3H]inositol so that increases in inositol phosphates (IP, IP2, and IP3) upon stimulation with thrombin could be assessed by measuring the amount of label in these compounds. Platelets were preincubated with CP/CPK, to inhibit effects of released ADP, and aspirin, to inhibit formation of thromboxane A2/endoperoxides. In platelets from rats with either form of hypercholesterolemia, the percentage increase in labeling of IP3 was significantly greater 30 seconds after stimulation with low concentrations of thrombin than in platelets from control rats. Increased IP3 formation in platelets from hypercholesterolemic rats indicates that there is increased activity of a pathway(s) leading to IP3 formation and that this may be a mechanism responsible for the thrombin-induced hypersensitivity of these platelets.
Animals↗
[Evidence of the existence of hemolysin II from Bacillus cereus: cloning the genetic determinant of hemolysin II].
The hemolysin genetic determinant distinct from cereolysin AB genetic determinant (lecithinase and sphingomyelinase genes) has been cloned in Escherichia coli and Bacillus subtilis cells as an EcoRI fragment (2.9 kb) of Bacillus cereus VKM-B771 chromosome DNA. The hemolytic product encoded by the cloned DNA fragment possessed all the properties of hemolysin II known to date: it was not inhibited by cholesterol, exhibited the Arrhenius effect, and had a relatively long (in comparison with cereolysin) lag period in erythrocyte lysis. The cloned DNA fragment was concluded to contain the gene of hemolysin II from B. cereus. In contrast to previous suggestions that hemolitic activity ascribed to hemolysin II is due to the combined action of sphingomyelinase and lecithinase, the results obtained present convincing evidence that hemolysin II is an independent B. cereus hemolytic factor different from cereolysin AB.
Bacillus cereus↗
Heart mass and blood pressure have separate genetic determinants in the New Zealand genetically hypertensive (GH) rat.
OBJECTIVE: To determine associations between cardiovascular parameters and genotype in 205 F2 rats of both sexes and lineages from reciprocal crosses made between rats of the New Zealand genetically hypertensive (GH) and Brown Norway (BN) rat strains. METHODS: Systolic tail blood pressure, mean arterial blood pressure, pulse rate, heart mass, body mass and relative heart mass were determined for each rat in the age range 17-19 weeks, and DNA polymorphisms were examined for the guanylyl cyclase A (GCA), angiotensin converting enzyme (ACE) and renin (REN) genes. RESULTS: The phenotypic data indicated the presence of genes on the X and Y chromosomes that affected blood pressure. The GH GCA allele, in males only, and the GH ACE allele, in females only, both cosegregated with increased blood pressure. The ACE effect was confined to rats of one lineage only, namely those with GH grandfathers. A cosegregation of the GH REN allele with decreased blood pressure was also detected in females with BN grandfathers. In contrast, the GH REN allele cosegregated with a smaller heart in males only, whereas the GH ACE allele cosegregated with a larger heart both in males and in females. In males this was the consequence of a decrease in body mass with no change in absolute heart mass, whereas in females there were changes in both of these parameters. CONCLUSIONS: The results show that cardiac hypertrophy and blood pressure have independent genetic determinants in the GH rat, and indicate the importance of sex in determining the phenotypic expression of genes underlying cardiovascular pathology.
Animals↗
Is poliomyelitis a genetically-determined disease: I: A genetic model.
Explore the source record for details and available documents.
Age Factors↗
[Genetic determination of growth processes in the peripubertal period of human ontogeny].
Chronological peculiarities of genetic determination of three factors of physical development in different phases of peripubertal stage of human ontogenesis were studied. The differences between sexes are explained by the hypothesis of mutual "clearing off" of X-linked genes' effects. This hypothesis is confirmed by the coincident dynamics of two indices--of additive genetic effects in boys and of nonlinear genetic effects in girls. The results point to autonomous nature of genetic determination of head's morphological structures, which is more expressed in boys. The component partitioning of the phenotype variance of the individual scores of linear discriminant functions revealed steady decrease across the peripubertal stage in the level of genetic determination of the variability of children's belonging to the different age periods. In the whole, the results indicate the existence of marked genetic determination of physique's growth and development in a stage under study of human ontogenesis.
Adolescent↗