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C Denniston

Publications and source records attributed to C Denniston.

At least 19 recordsLinked to original sources
PubMed2004

Lattice Boltzmann algorithm for three-dimensional liquid-crystal hydrodynamics.

We describe a lattice Boltzmann algorithm to simulate liquid-crystal hydrodynamics in three dimensions. The equations of motion are written in terms of a tensor order parameter. This allows both the isotropic and the nematic phases to be considered. Backflow effects and the hydrodynamics of topological defects are naturally included in the simulations, as are viscoelastic effects such as shear-thinning and shear-banding. We describe the implementation of velocity boundary conditions and show that the algorithm can be used to describe optical bounce in twisted nematic devices and secondary flow in sheared nematics with an imposed twist.

Journal Article↗
PubMed2001

Flexoelectric surface switching of bistable nematic devices.

We report on a novel method of dynamically controlling the boundary conditions at the surface of a nematic liquid crystal using a surface flexoelectric effect. By moving the surface directors we show that one is able to manipulate defects which lie near the surface. This can be used to produce switching of a nematic liquid-crystal device between two states with very similar free energies. This results in a bistable device that can retain either state with no applied voltage. Switching between the states occurs when the movement of the surface directors rotates those in the bulk which are then able to create or annihilate defects which lie near the surface of the device.

Journal Article↗
PubMed2001

Molecular and continuum boundary conditions for a miscible binary fluid.

We show that molecular-dynamics simulations can furnish useful boundary conditions at a solid surface bounding a two-component fluid. In contrast to some previous reports, convective-diffusive flow is consistent with continuum equations down to atomic scales. However, concentration gradients can produce flow without viscous dissipation that is inconsistent with the commonly used Navier slip condition. Also, differential wetting of the two components coupled to a concentration gradient can drive convective flows that could be used to make nanopumps or motors.

Journal Article↗
PubMed2001

Phase ordering in nematic liquid crystals.

We study the kinetics of the nematic-isotropic transition in a two-dimensional liquid crystal by using a lattice Boltzmann scheme that couples the tensor order parameter and the flow consistently. Unlike in previous studies, we find that the time dependences of the correlation function, energy density, and number of topological defects obey dynamic scaling laws with growth exponents that, within the numerical uncertainties, agree with the value 1/2 expected from simple dimensional analysis. We find that these values are not altered by the hydrodynamic flow. In addition, by examining shallow quenches, we find that the presence of orientational disorder can inhibit amplitude ordering.

Journal Article↗
PubMed2001

Lattice Boltzmann simulations of liquid crystal hydrodynamics.

We describe a lattice Boltzmann algorithm to simulate liquid crystal hydrodynamics. The equations of motion are written in terms of a tensor order parameter. This allows both the isotropic and the nematic phases to be considered. Backflow effects and the hydrodynamics of topological defects are naturally included in the simulations, as are non-Newtonian flow properties such as shear thinning and shear banding.

Journal Article↗
PubMed2000

Equivalence by descent: pedigree analysis with inbreeding and gametic phase disequilibrium.

In the presence of gametic phase disequilibrium and inbreeding, multiple locus genotype frequencies cannot be written solely in terms of identity by descent (IBD) probabilities. Following Cockerham & Weir (1973) we introduce the concept of 'equivalence by descent' (EBD), an extension of the concept of IBD to include non-allelic genes. Two genes are said to be EBD if they derive ultimately from the same founding gamete of a pedigree. Allelic genes that are EBD are also IBD. For two loci 11 EBD probabilities, the 'J-coefficients,' are required and for three loci 117 J-coefficients are required to write genotype probabilities. It is shown how the 117 J-coefficients for three loci can be reduced to a basic set of 37. Computer programs, written in the algebraic programming language, MAPLE, are described which are capable of calculating the two- and three-locus J-coefficients for any pedigree, subject only to size limitations. The MAPLE packages are available from the author upon request.

Chromosome Mapping↗
PubMed1998

Ionizing radiation and genetic risks. VIII. The concept of mutation component and its use in risk estimation for multifactorial diseases.

Multifactorial diseases, which include the common congenital abnormalities (incidence: 6%) and chronic diseases with onset predominantly in adults (population prevalence: 65%), contribute substantially to human morbidity and mortality. Their transmission patterns do not conform to Mendelian expectations. The model most frequently used to explain their inheritance and to estimate risks to relatives is a Multifactorial Threshold Model (MTM) of disease liability. The MTM assumes that: (i) the disease is due to the joint action of a large number of genetic and environmental factors, each of which contributing a small amount of liability, (ii) the distribution of liability in the population is Gaussian and (iii) individuals whose liability exceeds a certain threshold value are affected by the disease. For most of these diseases, the number of genes involved or the environmental factors are not fully known. In the context of radiation exposures of the population, the question of the extent to which induced mutations will cause an increase in the frequencies of these diseases has remained unanswered. In this paper, we address this problem by using a modified version of MTM which incorporates mutation and selection as two additional parameters. The model assumes a finite number of gene loci and threshold of liability (hence, the designation, Finite-Locus Threshold Model or FLTM). The FLTM permits one to examine the relationship between broad-sense heritability of disease liability and mutation component (MC), the responsiveness of the disease to a change in mutation rate. Through the use of a computer program (in which mutation rate, selection, threshold, recombination rate and environmental variance are input parameters and MC and heritability of liability are output estimates), we studied the MC-heritability relationship for (i) a permanent increase in mutation rate (e.g., when the population sustains radiation exposure in every generation) and (ii) a one-time increase in mutation rate. Our investigation shows that, for a permanent increase in mutation rate of 15%, MC in the first few generations is of the order of 1-2%. This conclusion holds over a broad range of heritability values above about 30%. At equilibrium, however, MC reaches 100%. For a one-time increase in mutation rate, MC reaches its maximum value (of 1-2%) in the first generation, followed by a decline to zero in subsequent generations. These conclusions hold for so many combinations of parameter values (i.e., threshold, selection coefficient, number of loci, environmental variance, spontaneous mutation rate, increases in mutation rate, levels of 'interaction' between genes and recombination rates) that it can be considered to be relatively robust. We also investigated the biological validity of the FLTM in terms of the minimum number of loci, their mutation rates and selection coefficients needed to explain the incidence of multifactorial diseases using the theory of genetic loads. We argue that for common multifactorial diseases, selection coefficients are small in present-day human populations. Consequently, with mutation rates of the order known for Mendelian genes, the FLTM with a few loci and weak selection provides a good approximation for studying the responsiveness of multifactorial diseases to radiation exposures.

Adult↗
PubMed1998

Ionizing radiation and genetic risks. VII. The concept of mutation component and its use in risk estimation for Mendelian diseases.

The responsiveness of Mendelian diseases to an increase in the mutation rate is studied by using the concept of the mutation component (MC) of genetic diseases. Algebraic expressions to evaluate MC at any specific generation following either a one-time or a permanent increase in mutation rate are derived and are illustrated with numerical examples. For a one-time increase in mutation rate, the analysis shows that the first generation MC for autosomal dominant diseases is equal to the selection coefficient; this is also true for X-linked diseases (adjusted for the proportion of X-chromosomes in males). For autosomal recessive diseases the first generation MC is substantially smaller than that for autosomal dominants. In subsequent generations MC gradually decays to zero. Under conditions of a permanent increase in the mutation rate, the MC for autosomal dominant, X-linked and completely recessive autosomal disorders progressively increases to reach a value of one at the new equilibrium. For incompletely recessive autosomal disorders, however, the MC at equilibrium can be larger than one. The rates of approach to the new equilibrium are different for the different classes of diseases, dictated by selection and time (in generations) following radiation exposure. The effects of increases in mutation rate on MC are more pronounced for autosomal dominants, followed by X-linked and are far less for autosomal recessives. Even for autosomal dominants, the early generation effects of radiation exposures would not be appreciable unless the heterozygotes have a severely reduced fitness.

Animals↗
PubMed1995

Managing data by phone.

Information collection for home care poses more of a problem than it does for institution-based health care organizations. Many versions of smaller computers have been developed, but these pose their own problems. Another technology, already widely available, may be the answer for some agencies.

Ambulatory Care Information Systems↗
PubMed1990

Alternative fitness models with the same allele frequency dynamics.

For any set of one- or two-locus genotypic fitnesses there are alternative sets, usually frequency-dependent and often with quite different biological meanings, that give rise to the same equations for change of allele or haplotype frequencies. Therefore, it is not possible to distinguish among alternative fitness models from allele or haplotype frequency trajectories or equilibrium distributions. For a single locus and for two loci when linkage equilibrium can be assumed, a simple procedure generates some of the alternative fitness sets.

Alleles↗
PubMed1989

The nonrandom participation of human acrocentric chromosomes in Robertsonian translocations.

The present study explores the origin of human Robertsonian translocations (RT) and the causes of the nonrandom participation of the different acrocentrics in them. Satellite associations have been analysed in 966 cells from 8 persons, and 1266 RT with ascertainment have been collected from the literature. The observation that the chromosomes preferentially taking part in satellite associations vary between individuals is confirmed. However, since a preferred chromosome appears to associate at random with the others, this phenomenon should not add to the nonrandomness of the RT. Most RT presumably arise through adjacent chromatid exchanges corresponding to mitotic chiasmata, in the pericentric regions of the acrocentrics. Our working hypothesis is that there is a basic exchange rate between any two acrocentrics. The surplus of t(14q21q) is presumed to depend on these two chromosomes having a homologous pericentric region. The 10-20 times higher incidence of t(13q14q) as compared with other RT is best explained by crossing-over between homologous, but relatively inverted, segments in these chromosomes. Of the 246 RT ascertained through repeated abortions or infertility, 56 were found through the latter. Of these, chromosome 14 was involved in 51. The infertility may be caused by a small deletion of 14q, as is often the case in 15q in Prader-Willi syndrome. In all RT ascertained through 21 or 13 trisomy, respectively, the relevant chromosome is one of the participants. Our data thus do not give any support to the idea of interchromosomal effects exerted by RT.

Chromosomes, Human, Pair 13↗
PubMed1985

X chromatin, endomitoses, and mitotic abnormalities in human cervical cancer.

The incidence of X chromatin bodies and mitotic modifications and aberrations has been analyzed using Feulgen-squash preparations in 47 cervical cancers from Helsinki and 35 from Madison. Sixteen of the 82 tumors did not display any X chromatin bodies, and some others showed a lower than normal frequency, especially in the large nuclei. Different hypotheses to explain the absence of Barr bodies in female tumors have been reviewed. A new observation is that 44/82 tumors contained endomitoses. The metaphase/prophase ratio (M/P) was higher than 1.5 in all but three cases, reaching values as high as 23.0 (Madison) and 34.2 (Helsinki), and in one exceptional case, 51.8. The different types of cells, mitotic, endomitotic, and those with large to giant nuclei, form their own strands or layers. Cervical cancer is diagnosed earlier in Finland than in Madison due to a Pap mass screening program, and consequently, the survival of the patients after 5 years was 27/47 in Helsinki and 6/35 in Madison. No correlation could be established between the M/P (or other mitotic phenomena) or the stage and grade of the tumor, the age of the patient, or survival time.

Adult↗
PubMed1985

Screening program theory: decision functions and protocols.

A screening program is defined to include a set of tests, a decision function, and a protocol. The major characteristics of a screening program are the error rates of the individual tests, the overall error rates of the program, the costs of the individual tests, and the overall program costs. It is shown how to calculate the program error rates for any given decision function. The concept of a screening protocol is developed and a method for enumerating all protocols of a given decision function is given. A given protocol has two calculable costs: the average cost of testing a mutagen and the average cost of calculating a nonmutagen. A method for calculating these costs for any protocol is given. All decision functions utilizing up to five tests are enumerated.

Costs and Cost Analysis↗