Biomedical subjects

T S Perry

Publications and source records attributed to T S Perry.

9 recordsLinked to original sources

PubMed2002

Observation of a hydrodynamically driven, radiative-precursor shock.

Observations of a radiative-precursor shock that evolves from a purely hydrodynamic system are presented. The radiative precursor is observed in low-density SiO2 aerogel foam using x-ray absorption spectroscopy. A plastic slab, shocked and accelerated by high-intensity laser irradiation, drives the shock which then produces the radiative precursor. The length and temperature profile of the radiative precursor are examined as the intensity of the laser is varied.

Journal Article↗

PubMed2002

Experimental investigation of the three-dimensional interaction of a strong shock with a spherical density inhomogeneity.

Laser-driven experiments are described which probe the interaction of a very strong shock with a spherical density inhomogeneity. The interaction is viewed from two orthogonal directions enabling visualization of both the initial distortion of the sphere into a double vortex ring structure as well as the onset of an azimuthal instability that ultimately results in the three-dimensional breakup of the ring. The experimental results are compared with 3D numerical simulations and are shown to be in remarkable agreement with the incompressible theory of Widnall et al. [J. Fluid Mech. 66, 35 (1974)].

Journal Article↗

PubMed1991

Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Stanford Lipid Research Clinics Family Study.

We examined the familial aggregation of lipids [total cholesterol (CH) and triglyceride (TG)] and lipoproteins [high-density lipoprotein cholesterol (HDL) and low-density lipoprotein cholesterol (LDL)] in families ascertained through random and nonrandom probands in the Stanford Lipid Research Clinics Family Study. Nonrandom probands were selected because their lipid levels at a prior screening visit exceeded a certain prespecified threshold. The statistical method is based on selection through indirect truncation on a correlated trait (in which the likelihood function is conditioned on the actual event that the proband's value is beyond the threshold). This method allows for estimation of the path model parameters in randomly and nonrandomly ascertained families jointly and separately, thus enabling tests of heterogeneity between the two types of samples. The results suggest that the multifactorial transmission is homogeneous in the random and hyperlipidemic samples for CH. However, the evidence for heterogeneity is moderate for LDL, marked HDL, and mixed for TG. The general pattern of observed results is for somewhat higher genetic heritabilities in the random than nonrandom samples, which is compatible with a higher prevalence in the random sample of certain dyslipoproteinemias associated with nonelevated lipids. Substantial genetic heritability is found for CH, HDL, and LDL, with somewhat lower estimates for TG. Cultural heritability is low but significant for all four traits. Little or no spouse resemblance or nontransmitted shared sibship effects are seen. In contrast to the findings from previous studies, little or no parental cultural transmission is seen.

Adult↗

PubMed1991

Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Iowa Lipid Research Clinics family study.

The aggregation of lipids [total cholesterol (CH) and triglyceride (TG)] and lipoproteins [high-density lipoprotein cholesterol (HDL) and low-density lipoprotein cholesterol (LDL)] in families ascertained through random and nonrandom probands in the Iowa Lipid Research Clinics family study was examined. Nonrandom probands were selected because their lipid levels (at a prior screening visit) exceeded a certain pre-specified threshold. The statistical method conditions the likelihood function on the actual event that the proband's value is beyond the threshold. This method allows for estimation of the path model parameters in randomly and nonrandomly ascertained families jointly and separately, thus enabling tests of heterogeneity between the two types of samples. Marked heterogeneity between the random and the hyperlipidemic samples is detected in the multifactorial transmission for TG and HDL, and moderate heterogeneity is detected for CH and LDL, with a pattern of higher genetic heritability estimates in the random than nonrandom samples. The observed pattern of heterogeneity is compatible with a higher prevalence in the random sample of certain dyslipoproteinemias that are associated with nonelevated lipids. For the random samples, genetic heritabilities are higher for CH and HDL (about 60%) than for TG and LDL (about 50%). For the nonrandom samples those estimates are about 45, 40, 35 and 30% for HDL, CH, LDL and TG, respectively. Little to no cultural (familial environmental) heritability is evident for CH and LDL, although 10-20% of the phenotypic variance is due to cultural factors for TG and HDL. These results suggest that the etiologies for lipids and lipoproteins may be quite different in random versus hyperlipidemic samples.

Adult↗

PubMed1991

Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Minnesota Lipid Research Clinic Family Study.

The familial aggregation of lipids [total cholesterol (CH) and triglyceride (TG)] and lipoproteins [high-density lipoprotein cholesterol (HDL) and low-density lipoprotein cholesterol (LDL)] was investigated in families ascertained through both random and nonrandom probands in the Minnesota Lipid Research Clinic Family Study. Nonrandom proband ascertainment was based on single selection through truncation for hyperlipidemia at an earlier screening. A path model was used to investigate the nature of familial resemblance using appropriate adjustments for ascertainment and to determine whether random and hyperlipidemic samples are heterogeneous with regard to the multifactorial model. The results suggest that parameter estimates are consistent with those from previous studies in which only random families were used and that random and nonrandom samples are homogeneous with regard to the path model for CH and LDL. However, for TG and HDL the random and hyperlipidemic samples are significantly heterogeneous. This heterogeneity would be observed if familial hypertriglyceridemia and/or familial hypoalphalipoproteinemia segregates predominantly in the hyperlipidemic rather than in the random sample, as on might expect.

Chromosome Banding↗

PubMed1990

Heterogeneity in the familial aggregation of fasting serum uric acid level in five North American populations: the Lipid Research Clinics Family Study.

This study represents the first formal examination for heterogeneity in the familial aggregation of fasting serum uric acid (UA) levels. Data from 5 clinics (Cincinnati, Stanford, Iowa, Minnesota, and Oklahoma) participating in the Lipid Research Clinics (LRC) family study, which included a total of 685 nuclear families (N = 2,146), were analyzed. Heterogeneity among the clinics in familial resemblance was detected. However, this heterogeneity could not be attributed to differences in distributional properties (such as means and variances) or to path model parameters representing latent genetic or cultural (environmental) components associated with UA levels. Intergenerational differences in genetic heritabilities were found, with higher offspring (h2 = 43%) than parent (h2z2 = 16%) estimates, but no generational differences were detected for cultural heritability (c2 = 0.09). Equal maternal and paternal cultural transmission was found, and effects due to extra sibling environments and to marital resemblance were both significant. These results show no clear indication as to the source of the heterogeneity observed for familial resemblance of UA levels in randomly selected data. This question should be further investigated, especially in clinical samples such as dyslipoproteinemic families.

Adult↗

PubMed1990

Heterogeneity in the familial aggregation of fasting plasma glucose in five North American populations: the Lipid Research Clinics Family Study.

Heterogeneity in the familial aggregation of plasma glucose in five samples of the Lipid Research Clinics Family Study (LRC) was investigated using path analysis. This study was deemed appropriate since recent investigations reported a wide range of estimates for genetic and cultural factors. The path model incorporated a measured index of the familial environment in order to separate the effects of genes and environments in the nuclear family design, genetic and environmental heritabilities, spouse resemblance, sibling environmental effects, and parental cultural transmission. The methodology was completely general in allowing sample-specific, as well as pooled-sample, estimation of all or any subset of the model parameters. Genetic heritability estimates were heterogeneous, ranging from zero to 33% across the clinics. Environmental heritability (7%), spouse resemblance, non-transmitted sibling environmental effects, and parental cultural transmission were homogeneous across samples. No support was found for specific maternal effects, nor for intergenerational differences in cultural or genetic heritability. We conclude that the genetic and environmental heritabilities for plasma glucose in the LRC are consistent with the diverse reports by earlier investigators. In addition, we were able to exclude methodological differences as a cause of this heterogeneity. Furthermore, formal hypothesis tests suggest that the aetiology of this heterogeneity is genetic (and not cultural), taking the form of two distinct homogeneous patterns (one for no genetic effect, and one for a moderate genetic effect). Only formal heterogeneity tests of the type described here can detect these effects, and allow pooling of separate studies in order to obtain more precise estimates of the parameters of interest.

Adult↗

PubMed1989

Heterogeneity in the biological and cultural determinants of high-density lipoprotein cholesterol in five North American populations: the Lipid Research Clinics Family Study.

Heterogeneity in the source of familial resemblance for high-density lipoprotein (HDL) cholesterol in 5 different Lipid Research Clinics (Cincinnati, Iowa, Minnesota, Oklahoma and Stanford) was assessed using a general linear model for cultural and biological inheritance. No evidence of heterogeneity was found in any of the parameters of the model. Under the most parsimonious hypothesis, using data pooled over all clinics, genetic and cultural heritability were both significant and were estimated to be 0.52 +/- 0.04 and 0.09 +/- 0.02, respectively; there was cultural transmission but no maternal effects; marital and nontransmitted sibship environmental resemblance were significant.

Cholesterol, HDL↗

PubMedDate not supplied

Commingling and segregation analysis of serum uric acid in five North American populations: the Lipid Research Clinics family study.

The role of major genes in the expression of serum uric acid (UA) levels was investigated in data collected from five clinics of the Lipid Research Clinics (LRC) family study. Over 2,000 randomly ascertained individuals were analyzed. The UA distributions were homogeneous among the five LRC clinics and between the parental and offspring generations. This result suggested that the data could be pooled across clinics, thereby increasing the statistical power associated with larger sample sizes for testing various null hypotheses. Additionally, a mixture of three normal distributions best characterized the combined-clinics data. Segregation patterns were examined in the untransformed data, as well as in a more conservative (and biologically meaningful) log transformation. Prior to log transformation, both major and multifactorial effects were detected. The major effect was not transmissible, i.e., was not compatible with Mendelian transmission, and accounted for 39% of the variance in UA levels. However, after the log transform was applied to the data and the segregation analysis was repeated, support for the major effect disappeared altogether and only the multifactorial component remained, accounting for 50% of the variation in offspring and 19% in patients.

Adolescent↗