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At least 235 records · Page 13Linked to original sources
PubMed2006

Evidence that trait-anxiety and trait-depression differentially moderate cortical processing of pain.

OBJECTIVES: The purpose of this study was to examine the influence of neuroticism (N) and its different subfacets anxiety (N-anx) and depression (N-dep) on cortical pain processing expressed as event-related potentials (ERPs). METHODS: Seventy-five healthy participants received electrical pain stimuli under condition of simultaneous electroencephalogram registration. Multiple regression analyses were conducted to study the amount of pain-ERP variance. ERP variance was explained by N and its subfacets. RESULTS: N moderated the way pain was processed cortically. Higher levels of N were associated with higher pain-ERP amplitudes. Within this association, differential subfacet effects were observed: N-anx reduced, whereas N-dep augmented pain-ERP amplitudes. DISCUSSION: A personality trait reflecting bias toward negative emotions may moderate the way pain is processed cortically, with directionally different effects depending on whether the trait is expressed predominantly in the realm of anxiety or depression.

Adaptation, Physiological↗
PubMed1987

The trait and method components of ratings of conduct disorder--Part II. Factors related to the trait component of conduct disorder scores.

A theoretical model designed to estimate the associations of variables of interest with the trait component of maternal and teacher ratings of conduct disorder is outlined. This model was applied to data collected in a birth cohort of New Zealand children. The analysis showed marked differences between the correlations for various measures and observed conduct disorder scores and the corresponding correlations with the estimated trait components of these scores. In some cases correlations increased as a result of correction for measurement error whereas in other cases correlations declined as a result of correction for the effects of method factors.

Child↗
PubMedDate not supplied

Prediction error variance and expected response to selection, when selection is based on the best predictor - for Gaussian and threshold characters, traits following a Poisson mixed model and survival traits.

In this paper, we consider selection based on the best predictor of animal additive genetic values in Gaussian linear mixed models, threshold models, Poisson mixed models, and log normal frailty models for survival data (including models with time-dependent covariates with associated fixed or random effects). In the different models, expressions are given (when these can be found - otherwise unbiased estimates are given) for prediction error variance, accuracy of selection and expected response to selection on the additive genetic scale and on the observed scale. The expressions given for non Gaussian traits are generalisations of the well-known formulas for Gaussian traits - and reflect, for Poisson mixed models and frailty models for survival data, the hierarchal structure of the models. In general the ratio of the additive genetic variance to the total variance in the Gaussian part of the model (heritability on the normally distributed level of the model) or a generalised version of heritability plays a central role in these formulas.

Analysis of Variance↗
PubMed1998

Effects of sickle cell trait and hemoglobin C trait on determinations of HbA1c by an immunoassay method.

OBJECTIVE: A number of studies, including the Diabetes Control and Complications Trial (DCCT), have shown that good glycemic control, as assessed by GHb measurements, can reduce the chronic complications of diabetes. The National Glycohemoglobin Standardization Program (NGSP) was established to insure that GHb measurements by different methods were comparable and could be related to the candidate reference method used in the DCCT. The measurement of HbA1c in patients with Hb variants is one area not directly addressed by the NGSP. Therefore, we assessed the comparability of two DCCT-traceable methods in samples with Hb variants. RESEARCH DESIGN AND METHODS: Samples containing HbAA, HbAC, and HbAS were collected from diabetic and nondiabetic patients. HbA1c concentrations were measured by a high-performance liquid chromatography method (Bio-Rad Diamat) and an immunoassay that is suitable for use in a physician's office (Bayer DCA 2000). RESULTS: The two methods compared well for samples with HbAA and HbAS. However, for samples containing HbAC the immunoassay method showed relative positive biases of 8.4 and 10.4% at HbA1c levels of 7 and 9%, respectively, such that the two methods would not be judged comparable according to NGSP guidelines. CONCLUSIONS: The DCA 2000 HbA1c immunoassay method showed significant positive bias in patients with HbC trait. One possible clinical implication of this overestimation is overly rigorous glycemic control with a concomitant increase in hypoglycemia. This may be especially important in certain ethnic populations, such as African-Americans, who have a relatively high prevalence of HbC trait.

Black People↗
PubMed1997

Benefit of multiple trait selection to increase reproductive traits: experimental evidence from golden hamsters.

Fifteen generations of selection were conducted to study responses for litter size at birth (LSB), weight at weaning of standardized litter (LWW), and individual body weight at 8 wk of age (BW8) using golden hamsters as an experimental model for pigs. The experiment involved three lines: selection on an aggregate breeding value of LSB, LWW, and BW8 (line W); selection on an aggregate breeding value of LSB and LWW (line R); and a randomly selected control (line C). Selection in W and R was based on breeding values from a multiple trait animal model. Restricted maximum likelihood with an animal model was used to estimate genetic parameters and genetic trends. Heritability estimates for LSB, LWW, and BW8 were .10, .47, and .52, respectively, and genetic correlations between traits were all positive. The mean estimated breeding value (EBV) for LSB in generation 15 was +2.2 pups in W and R. The mean EBV for LWW in generation 15 was +318 g for W and +174 g for R, and for BW8 means were +64 g and +24 g, respectively. Average inbreeding at generation 16 was 13.4, 19.5, and 8.0% for W, R, and C, respectively. Including BW8 in the selection criterion reduced inbreeding and had a beneficial effect on selection responses in LSB, LWW, and BW8.

Animals↗
PubMed1979

The State-Trait Anxiety Inventory A-Trait Scale: dimensions and their generalization.

The State-Trait Anxiety Inventory A-Trait scale was administered to 152 female and 158 male students. Principal-components factor analyses yielded four orthogonal factors for each sex. The findings indicated that factor pattern comparisons should be made prior to pooling data across sex for psychometric investigations. Also, limited support was found for the generalization of dimensions across sex and samples both within and between cultures.

Adjustment Disorders↗
PubMed1983

Hemoglobin G trait and S trait in the same patient.

We describe a subject who had a positive sickle solubility test and a routine alkaline electrophoretic pattern showing three major hemoglobulin bands migrating to the A, S, and A2 positions. In addition, the non-heme protein carbonic anhydrase appeared to be increased, suggesting the presence of a split A2. Two major hemoglobin bands separated on agar gel electrophoresis using a citrate buffer, pH 6.2. A non-S hemoglobin migrating to the position of Hb S was identified as GPhiladelphia. The electrophoretic pattern of GPhil/S trait most closely resembles S/beta+ thalassemia or sickle cell trait. Careful study is essential to avoid misdiagnosis and unfairly stigmatizing patients whose benign abnormality may be confused with more severe disease entities.

Adult↗
PubMed1980

[Analysis of phenotypic correlations between qualitative traits. I. Genetic analysis of the structure of relations between multifactorial traits].

The methods are presented by which the coefficients of phenotypical correlations between multifactorial characters and coefficients of criss-cross correlations for qualitative characters between relatives can be estimated. These coefficients can be calculated from the known incidences of the traits X and Y (qgx and qgy) in general population, the incidence of Y among X bearing persons, the opposite incidence of X among Y bearing persons, the incidence of Y among the relatives of X bearing probands and the incidence of X among the relatives of Y bearing probands. All these correlations can be used to estimate the genetic correlation between qualitative traits and thereby for the genetic analysis of the structure of phenotypical correlations between multifactorial diseases. The validity of the estimations in connection with the sampling procedures is discussed.

Genetic Diseases, Inborn↗
PubMed2006

Replication of small effect quantitative trait loci for behavioral traits facilitated by estimation of effect size from independent cohorts.

Quantitative trait locus (QTL) mapping is often done in a single segregating population, such as a backcross or an intercross. Both QTL location and effect size are then estimated from the same dataset. This approach results in an over-estimate of effect size for two reasons: (1) LOD scores, which are maximized over numerous point-wise tests, are correlated with estimated effect size and (2) small effect QTLs are often undetected in underpowered experiments, yielding inflated effect sizes for detected QTLs (the Beavis effect). When it is impractical to maintain or generate large population sizes, an alternative is to use two populations, one for initial detection and localization and a second for a locus-matched estimate of effect size, not conditioned on significance. Recombinant inbred (RI) panels are eminently suitable for this approach, as each strain genotype can be sampled repeatedly. We present mapping results from the LXS RI panel for two behavioral phenotypes relating to ethanol response: low-dose ethanol activation and loss of righting following high-dose injection. Both the phenotypes were measured in two or three independent cohorts, which were then used to re-estimate effect size. Many small-effect QTLs replicated using this approach, but in all cases, effect size, in the replicate cohorts, was reduced from the initial estimate, often substantially. Such a reduction will have important consequences for power analyses in which sample sizes are determined for subsequent confirmation studies.

Alcoholism↗
PubMed2004

Identification and fine mapping of quantitative trait loci for growth traits on bovine chromosomes 2, 6, 14, 19, 21, and 23 within one commercial line of Bos taurus.

We report the identification and fine mapping of QTL for birth weight (BWT), preweaning ADG (PWADG), and postweaning ADG on feed (ADGF) in a commercial line of Bos taurus using an identical-by-descent haplotype sharing method. One hundred seventy-six calves of 12 bulls (9 to 30 male calves from each sire) of the Beefbooster, Inc., M1 line were typed using 71 genetic markers from bovine chromosomes (BTA) 2, 6, 14, 19, 21, and 23 (8 to 16 markers from each chromosome). Sixteen haplotypes were found to have significant (P <0.05) associations with BWT at the comparison-wise threshold. The 16 haplotypes span 13 chromosomal regions, two on BTA 2 (9.1 to 22.5 cM and 95.0 to 100.3 cM), three on BTA 6 (8.2 to 11.8 cM, 35.5 to 49.7 cM, and 83.0 to 86.2 cM), three on BTA 14 (26.0 to 26.7 cM, 36.2 to 46.2 cM, and 52.0 to 67.7 cM), one on BTA 19 (52.0 to 52.7 cM), two on BTA 21 (9.9 to 20.4 cM and 28.2 to 46.1 cM), and two on BTA 23 (23.9 to 36.0 cM and 45.1 to 50.9 cM). Thirteen haplotypes spanning seven chromosomal regions significantly affected (P <0.05) PWADG at the comparison-wise threshold. The seven chromosomal regions include two regions on BTA 6 (11.8 to 44.2 cM and 83.0 to 86.2 cM), one on BTA 14 (26.7 to 50.8 cM), one on BTA 19 (4.8 to 15.9 cM), one on BTA 21 (9.9 to 20.4 cM), and two on BTA 23 (17.3 to 36.0 cM and 45.1 to 50.9 cM). For ADGF, 11 haplotypes were identified to have significant associations (P <0.05) at the comparison-wise threshold. The 11 haplotypes represented eight chromosomal regions, one on BTA 2 (9.1 to 22.5 cM), two on BTA 6 (49.7 to 50.1 cM and 59.6 to 63.6 cM), two on BTA 14 (17.0 to 24.0 cM and 36.2 to 46.2 cM), two on BTA 19 (52.0 to 52.7 cM and 65.1 to 65.7 cM), and one on BTA 21 (46.1 to 53.1 cM). The QTL regions identified and fine mapped in this study will provide a reference for future positional candidate gene research and marker-assisted selection of various growth traits.

Alleles↗
PubMed2000

Identification of four new quantitative trait loci regulating arthritis severity and one new quantitative trait locus regulating autoantibody production in rats with collagen-induced arthritis.

OBJECTIVE: Collagen-induced arthritis (CIA) is a polygenic model of experimentally induced autoimmunity and chronic joint inflammation. This study maps genetic loci that regulate CIA susceptibility in DA/Bkl (DA) and BN/SsNHsd (BN) rats. METHODS: Genome scans covering chromosomes 1-20 and interval mapping techniques using 159 simple sequence-length polymorphism markers were used to identify quantitative trait loci (QTLs) that regulate CIA in (DA x BN)F2 hybrids. Serum antibody titers to type II collagen were determined by enzyme-linked immunosorbent assay. RESULTS: DA rats were high responders to porcine type II collagen (PII) and developed severe CIA (100%). BN rats were low responders to PII and resistant to CIA (0%). BN genes strongly repressed PII-induced CIA. Only 12% of (DA x BN)F1 rats (7 of 60) and 31% of (DA x BN)F2 rats (307 of 1,004) developed CIA. Three new QTLs (Cia11, Cia12, and Cia13) with significant logarithm of odds (LOD) scores of 5.6, 4.6, and 4.5, respectively, plus a suggestive QTL (Cia14*, LOD 3.0) regulating arthritis severity were identified on chromosomes 3, 12, 4, and 19. A new QTL, Ciaa3, associating with anticollagen antibody titer (antibody to PII LOD 6.5; antibody to rat type II collagen LOD 5.2) mapped to chromosome 9. Of 10 CIA QTLs previously identified in (DA x F344) and (DA x ACI) rats, only Cia1 in the major histocompatibility complex and a region coincident to Cia5 on chromosome 10 (LOD >8.0) influenced CIA severity in (DA x BN)F2 rats. CONCLUSION: Since CIA exhibits many of the pathologic features of rheumatoid arthritis, the data indicate that the variety of genetic elements regulating human autoimmune and rheumatic diseases may be much larger and more varied than originally envisioned.

Animals↗
PubMed2002

Modulation of multiple experimental arthritis models by collagen-induced arthritis quantitative trait loci isolated in congenic rat lines: different effects of non-major histocompatibility complex quantitative trait loci in males and females.

OBJECTIVE: Collagen-induced arthritis (CIA) is a model of inflammatory arthritis with many similarities to rheumatoid arthritis (RA). We previously mapped in F(2) offspring of CIA-susceptible DA and CIA-resistant F344 rats, 5 quantitative trait loci (QTLs) for which F344 alleles were associated with reduced CIA severity. In the present study, we sought to characterize the independent arthritis-modulating effects of these 5 QTLs. METHODS: CIA-regulatory regions were transferred from the F344 genome to the DA background or vice versa by repeated backcrossing. The arthritis-modulating effects of the transferred alleles were determined by comparing the severity of experimentally induced arthritis in congenic rats with that in DA rats. RESULTS: Congenic lines with either the F344 major histocompatibility complex (MHC) on the DA background or the DA MHC on the F344 background were resistant to CIA, confirming both MHC and non-MHC contributions to the genetic regulation of CIA. F344 alleles at the Cia3 and Cia5 regions of chromosomes 4 and 10 reduced CIA severity relative to that observed in DA rats. F344 Cia4 and Cia6 regions of chromosomes 7 and 8 failed to significantly alter CIA severity. Arthritis-modifying effects of Cia4 and Cia6 were, however, detected in pristane-induced and/or Freund's incomplete adjuvant oil-induced arthritis. The arthritis-modifying effects of the non-MHC CIA-regulatory loci differed in males and females. CONCLUSION: These congenic lines confirmed the existence and location of genes that regulate the severity of experimental arthritis in rats. Mechanisms responsible for the sex-specificity of individual arthritis-regulatory loci may explain some of the sex differences observed in RA and other autoimmune diseases in humans.

Animals↗
PubMed2002

Detection of quantitative trait loci for carcass traits in the pig by using AFLP.

For evaluation of the suitability of Amplified Fragment Length Polymorphism (AFLP) for detection of quantitative trait loci in farm animals, a combination of AFLP and selective genotyping has been applied as a rapid screening method for marker-QTL associations. Focusing on loci affecting eye muscle area, six extreme discordant sib pairs were selected from a Duroc x Berlin Miniature Pig F2 experimental cross and examined by using 48 AFLP primer combinations. Two prominent AFLP markers were converted into simple codominant PCR markers ( STS-Bo1 and STS-Bo3) and assigned to Sscr4 by physical and linkage mapping. Single marker analysis indicated association of the STS markers with a putative QTL influencing eye muscle area. Interval mapping confirmed the presence of a significant QTL for eye muscle area (Pgenomewide < 0.01) on the Sscr4, with STS-Bo1 being the closer marker. At the same location, significant effects (Pgenomewide < 0.01) on carcass length and backfat thickness were also detected. Our results demonstrate the capability of the combination of AFLP analysis and selective genotyping as a method for detection of genome regions containing QTL in livestock.

Animals↗
PubMed1999

Complete genome searches for quantitative trait loci controlling blood pressure and related traits in four segregating populations derived from Dahl hypertensive rats.

The Dahl salt-sensitive rat is one of the principal animal models of hereditary hypertension. Genome-wide searches were undertaken to detect quantitative trait loci (QTLs) that influence blood pressure, cardiac mass, and body weight in four F2 populations derived from Dahl salt-sensitive rats and different inbred normotensive control strains of rat. We detected three QTLs associated with one or more of the phenotypes, using a stringent statistical criterion for linkage (p < 0.00003). These included a novel QTL linked to blood pressure on rat Chromosome (Chr) 12, and another QTL on rat Chr 3 linked to body weight. A QTL on rat Chr 10 for which linkage to blood pressure has been described in other crosses was found to be a principal determinant of blood pressure and cardiac mass in some but not all of the crosses examined here. Three other regions showed evidence of linkage to these phenotypes with a less stringent statistical criterion of linkage at QTLs previously reported in other studies. As part of our study, microsatellite markers have been developed for three candidate genes for investigation in hypertension, and the genes have been localized by linkage mapping. These are: the rat Gs alpha subunit (Gnas) gene, the alpha-1B adrenergic receptor (Adra1b), and the Na+, K+-ATPase beta2 subunit (Atp1b2) gene.

Animals↗
PubMed2001

Quantitative trait loci for the monoamine-related traits heart rate and headless behavior in Drosophila melanogaster.

Drosophila melanogaster appears to be well suited as a model organism for quantitative pharmacogenetic analysis. A genome-wide deficiency screen for haploinsufficient effects on prepupal heart rate identified nine regions of the genome that significantly reduce (five deficiencies) or increase (four deficiencies) heart rate across a range of genetic backgrounds. Candidate genes include several neurotransmitter receptor loci, particularly monoamine receptors, consistent with results of prior pharmacological manipulations of heart rate, as well as genes associated with paralytic phenotypes. Significant genetic variation is also shown to exist for a suite of four autonomic behaviors that are exhibited spontaneously upon decapitation, namely, grooming, grasping, righting, and quivering. Overall activity levels are increased by application of particular concentrations of the drugs octopamine and nicotine, but due to high environmental variance both within and among replicate vials, the significance of genetic variation among wild-type lines for response to the drugs is difficult to establish. An interval mapping design was also used to map two or three QTL for each behavioral trait in a set of recombinant inbred lines derived from the laboratory stocks Oregon-R and 2b.

Animals↗
PubMed2003

Interaction between blood pressure quantitative trait loci in rats in which trait variation at chromosome 1 is conditional upon a specific allele at chromosome 10.

We have used inbred and congenic rat strains in F(2) segregation studies to discover epistasis in a polygenic model of hypertension. Previously, we have found evidence that the presence of a blood pressure quantitative trait locus (QTL) on chromosome 1 is conditional upon the allele status of chromosome 10. To prove the existence of an epistatic interaction we have analyzed congenic strains for chromosome 1 and 10 carrying high blood pressure QTL alleles from the spontaneously hypertensive rat on a normotensive background of the Wistar-Kyoto (WKY) rat. Additionally, a double congenic strain was developed with both chromosome 1 and 10 high blood pressure QTL alleles on the WKY background. Analysis of variance for blood pressure phenotypes as determined by radiotelemetry showed a significant effect for chromosome 10 but not chromosome 1 QTL alleles and demonstrated a significant interaction between the two loci (P<0.05). The interaction accounted for 5 mmHg of blood pressure. Thus, the identification of epistasis is critical to the understanding of the quantitative nature of blood pressure genetics.

Alleles↗
PubMed2004

Quantitative trait loci for body weight in layers differ from quantitative trait loci specific for antibody responses to sheep red blood cells.

Quantitative trait loci for BW at 4, 6, 8, 12, and 18 wk of age were detected in an experimental F2 cross of layers divergently selected for primary antibody response to SRBC. A negative phenotypic correlation between levels of antibody titers and BW, was reported earlier within founder lines. The entire experimental population was genotyped with 174 microsatellite markers equally distributed over the genome. Two genetic models were applied in the QTL analysis: a half-sib model and a line-cross model, both using the regression interval method. In the half-sib model, 3 QTL for BW at 4 wk of age on chromosomes GGA2, GGA3, and GGA9 were detected. For BW at 6 wk of age, 3 QTL were detected on GGA2, GGA3, and GGA6. For BW at 8 wk of age, a QTL was detected on GGA7, and for BW at 12 and 18 wk of age, a QTL was detected on GGAZ. With the line-cross analysis model, one QTL on GGA7 for BW at 4 wk of age was detected. Two QTL were detected on GGA3 and GGA7 for BW at 6 wk of age, and one on GGA3 was detected for BW for 8 and 12 wk of age. For BW at 18 wk of age, there were no QTL under the line-cross analysis model. The present data suggest that 1) a different set of genes affects the early and the late growth, and 2) genes selected to humoral immune responsiveness are different from genes underlying growth.

Aging↗