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At least 487 records · Page 27Linked to original sources
PubMed1988

Kinetics of human cone photopigments explained with a Rushton-Henry model.

Densitrometric measurements of the regeneration of cone visual photopigments have shown effects that cannot be explained by the existing quantitative models. Regeneration from a fully bleached state seems to depend on how this state has been reached and the shape of the regeneration curve cannot be produced by a first order reaction. Rushton and Henry (1968) proposed a store of 11-cis-retinal to explain rapid regeneration after a short bleach. We elaborated this idea into a quantitative model. Regeneration after three different bleach histories and steady state behaviour of the pigments was measured using the Utrecht densitometer. The Rushton-Henry model gives a good fit to the data and is clearly superior to the classical Rushton model in describing densitometric measurements.

Animals↗
PubMed1990

A quantitative animal model of traumatic iridodialysis.

The impact velocities and kinetic energies necessary to create a particular form of ocular injury, traumatic iridodialysis, were quantitatively studied by experimentally traumatizing enucleate porcine eyes. Thicknesses and tensile strengths of porcine and human iris tissue were measured in order to allow for predictions of human results to be made from the animal model. Application of blunt trauma at an impact angle of 30-35 degrees with respect to the iris plane with striking of the eye at the corneolimbal junction was found to optimize tearing of the iris from the root. Using this vector, the minimum velocity for the creation of an iridodialysis at least 6 mm in length in the human eye is predicted to be 14 m/sec for impact with a projectile of 13.4 g with a 6 mm diameter tip.

Animals↗
PubMedDate not supplied

Care quality and implementation of the chronic care model: a quantitative study.

PURPOSE: We wanted to test whether improvements in care quality were correlated with changes in the Chronic Care Model (CCM) in a large medical group that attempted to implement the CCM. METHODS: The leaders of 17 primary care clinics in this medical group completed the Assessing Chronic Illness Care (ACIC) survey measure of CCM implementation before and after care system changes were made. We used administrative data to measure care quality changes for yearly samples of patients with diabetes, coronary heart disease, or depression. RESULTS: The total ACIC score for the CCM increased by an overall average of 1.4 points (from 5.8 to 7.2 on a scale of 1 to 11, P = .02) and significant increases occurred for 3 of the 6 components of the CCM. During this time, patients experienced a significant increase in the proportion meeting a composite outcome measure for low-density lipoprotein (LDL) and glycated hemoglobin levels (from 15.7% to 25.5%, P = .001). Heart disease patients meeting a composite measure for LDL values increased from 46.8% to 57.8%, and the percentage of patients with 1 or more cardiac events dropped from 17.2% to 11.4% (P = .001 for each). Persistent use of new antidepressants did not change, but more of these patients had follow-up visits (P = .02). Only the diabetes measure was significantly correlated with 2 CCM elements-clinical information systems and decision support. CONCLUSION: Despite implementation of the CCM and improvements in quality measures for 3 chronic diseases, there were few significant correlations between these changes. Showing such a relationship may require larger changes, a larger number of clinics, changes in other CCM elements, or a more-sensitive measurement tool.

Ambulatory Care Facilities↗
PubMed2002

Modeling epistasis of quantitative trait loci using Cockerham's model.

We use the orthogonal contrast scales proposed by Cockerham to construct a genetic model, called Cockerham's model, for studying epistasis between genes. The properties of Cockerham's model in modeling and mapping epistatic genes under linkage equilibrium and disequilibrium are investigated and discussed. Because of its orthogonal property, Cockerham's model has several advantages in partitioning genetic variance into components, interpreting and estimating gene effects, and application to quantitative trait loci (QTL) mapping when compared to other models, and thus it can facilitate the study of epistasis between genes and be readily used in QTL mapping. The issues of QTL mapping with epistasis are also addressed. Real and simulated examples are used to illustrate Cockerham's model, compare different models, and map for epistatic QTL. Finally, we extend Cockerham's model to multiple loci and discuss its applications to QTL mapping.

Analysis of Variance↗
PubMed2006

An empirical approach to the bond additivity model in quantitative interpretation of sum frequency generation vibrational spectra.

Knowledge of the ratios between different polarizability betai'j'k' tensor elements of a chemical group in a molecule is crucial for quantitative interpretation and polarization analysis of its sum frequency generation vibrational spectroscopy (SFG-VS) spectrum at interface. The bond additivity model (BAM) or the hyperpolarizability derivative model along with experimentally obtained Raman depolarization ratios has been widely used to obtain such tensor ratios for the CH3, CH2, and CH groups. Successfully, such treatment can quantitatively reproduce the intensity polarization dependence in SFG-VS spectra for the symmetric (SS) and asymmetric (AS) stretching modes of CH3 and CH2 groups, respectively. However, the relative intensities between the SS and AS modes usually do not agree with each other within this model even for some of the simplest molecular systems, such as the air/methanol interface. This fact certainly has cast uncertainties on the effectiveness and conclusions based on the BAM. One of such examples is that the AS mode of CH3 group has never been observed in SFG-VS spectra from the air/methanol interface, while this AS mode is usually very strong for SFG-VS spectra from the air/ethanol interface, other short chain alcohol, as well as long chain surfactants. In order to answer these questions, an empirical approach from known Raman and IR spectra is used to make corrections to the BAM. With the corrected ratios between the betai'j'k' tensor elements of the SS and AS modes, all features in the SFG-VS spectra of the air/methanol and air/ethanol interfaces can be quantitatively interpreted. This empirical approach not only provides new understandings of the effectiveness and limitations of the bond additivity model but also provides a practical way for its application in SFG-VS studies of molecular interfaces.

Journal Article↗
PubMed1993

Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy.

OBJECTIVES: This study was designed to extend the results of a quantitative model originally developed for restenosis after stenting or atherectomy to include restenosis after conventional balloon angioplasty. BACKGROUND: We have previously described a continuous regression model that explains late (6-month) lumen narrowing as the difference between the immediate gain and the subsequent normally distributed late loss in lumen diameter after Palmaz-Schatz stenting or directional atherectomy. METHODS: Lumen diameter was measured immediately before and after coronary intervention on 524 consecutive lesions including those treated by Palmaz-Schatz stenting (102), directional atherectomy (134) and conventional balloon angioplasty (288). Of these lesions, 475 (91%) underwent follow-up angiography 3 to 6 months after treatment. The immediate increase in lumen diameter produced by the intervention (immediate gain) and the subsequent reduction in lumen diameter between the time of intervention to follow-up angiography (late loss) were examined. Association between demographic or angiographic variables and continuous measures of restenosis (late lumen diameter or late percent stenosis) was tested with linear regression techniques; a traditional binary measure of restenosis (late diameter stenosis > or = 50%) was evaluated with logistic regression analysis. RESULTS: Regression models relating late lumen diameter to the immediate lumen result were successfully fitted to all segments studied. According to these models, three indexes of restenosis (late lumen diameter, late percent stenosis and binary restenosis) were found to depend solely on the immediate lumen diameter after the procedure and the immediate residual percent stenosis, but not on the specific intervention used. Moreover, the late loss in lumen diameter was found to vary directly with the immediate gain provided by an intervention, and the "loss index" (a measure that corrects for differences in immediate gain) was uniform among all three interventions. CONCLUSIONS: The quantitative model originally developed for restenosis after stenting or atherectomy may thus be generalized to include conventional balloon angioplasty. It shows that the apparent differences in restenosis among the three interventions studied are due solely to differences in the immediate result provided and not to differences in the behavior of subsequent late loss. Moreover, although the late loss in lumen diameter was found to correlate with differences in the immediate gain provided by an intervention, the "loss index" (a measure that corrects for differences in acute gain) was uniform across all three interventions. It is thus the immediate result (and not the procedure used to obtain that result) that determines late outcome after coronary intervention.

Aged↗
PubMed2005

Pharmacogenomics and drug development.

It is generally anticipated that pharmacogenomic information will have a large impact on drug development and will facilitate individualized drug treatment. However, there has been relatively little quantitative modeling to assess how pharmacogenomic information could be best utilized in clinical practice. Using a quantitative model, this review demonstrates that efficacy is increased and toxicity is reduced when a genetically-guided dose adjustment strategy is utilized in a clinical trial. However, there is limited information available regarding the genetic variables affecting the disposition or mechanism of action of most commonly used medications. These genetic factors must be identified to enable pharmacogenomic testing to be routinely used in the clinic. A recently described murine haplotype-based computational genetic analysis method provides one strategy for identifying genetic factors regulating the pharmacokinetics and pharmacodynamics of commonly used medications.

Animals↗
PubMed2002

Detection of quantitative trait loci influencing dairy traits using a model for longitudinal data.

A longitudinal-linkage analysis approach was developed and applied to an outbred population. Nonlinear mixed-effects models were used to describe the lactation patterns and were extended to include marker information following single-marker and interval mapping models. Quantitative trait loci (QTL) affecting the shape and scale of lactation curves for production and health traits in dairy cattle were mapped in three U.S. Holstein families (Dairy Bull DNA Repository families one, four, and five) using the granddaughter design. Information on 81 informative markers on six Bos taurus autosomes (BTA) was combined with milk yield, fat, and protein percentage and somatic cell score (SCS) test-day records. Six percent of the single-marker tests surpassed the experiment-wise significance threshold. Marker BL41 on BTA3 was associated with decrease in milk yield during mid-lactation in family one. The scale and shape of the protein percentage lactation curve in family four varied with BMC4203 (BTA6) allele that the son received from the grandsire. Some map locations were associated with variation in the lactation pattern of multiple traits. In family four, the marker HUJI177 (BTA3) was associated with changes in the milk yield and protein percentage curves suggesting a QTL with pleiotropic effects or multiple QTL in the region. The interval mapping model uncovered a QTL on BTA7 associated with variation in milk-yield pattern in family four and a QTL on BTA21 affecting SCS in family five. The developed approach can be extended to random regressions, covariance functions, spline, gametic and variance component models. The results from the longitudinal-QTL approach will help to understand the genetic factors acting at different stages of lactation and will assist in positional candidate gene research. Identified positions can be incorporated into marker-assisted selection decisions to alter the persistency and peak production or the fluctuation of SCS during a lactation.

Animals↗
PubMed1988

The effects of force magnitude on a sutural model: a quantitative approach.

In an effort to quantify the biologic effects of an orthodontic tensile force, the rat interpremaxillary suture was investigated as a model for the periodontal ligament and expanded in vivo with a helical spring across the maxillary incisors. Three levels of force were used: light (50 to 75 g), medium (150 to 175 g), and heavy (250 to 300 g). Thymidine labeling and histologic studies after 12 hours and 1, 2, and 4 days of force delivery are described (n = 48 rats), as are biochemical studies after 2 and 4 days including a 6-hour organ culture (n = 32). The percentage of labeled cells increased significantly in all force groups at 1 day, followed by a rapid decline at 2 days, to a value at 4 days not significantly different from the controls. Biochemical studies showed significant increases in proline incorporation and alkaline phosphatase activity after 2 days of heavy force application. Histologic examinations showed obvious tissue changes beginning by day 1 and involving increases in suture width, vascularity, size and number of cells, amount of osteoid production, and changes in suture morphology. The experimental system was convenient, inflammation-free, and appeared to be reliable as evidenced by characteristic, synchronous tissue and autoradiographic changes in all experimental sutures through 4 days.

Alkaline Phosphatase↗
PubMed2003

Investigations into the analysis and modeling of the TNF alpha-mediated NF-kappa B-signaling pathway.

In this study, we propose a system-theoretic approach to the analysis and quantitative modeling of the TNFalpha-mediated NF-kappaB-signaling pathway. Tumor necrosis factor alpha (TNFalpha) is a potent proinflammatory cytokine that plays an important role in immunity and inflammation, in the control of cell proliferation, differentiation, and apoptosis. To date, there have been numerous approaches to model cellular dynamics. The most prominent uses ordinary differential equations (ODEs) to describe biochemical reactions. This approach can provide us with mathematically well-founded and tractable interpretations regarding pathways, especially those best described by enzyme reactions. This work first introduces a graphical method to intuitively represent the TNFalpha-mediated NF-kappaB-signaling pathway and then utilizes ODEs to quantitatively model the pathway. The simulation study shows qualitative validation of the proposed model compared with experimental results for this pathway. The proposed system-theoretic approach is expected to be further applicable to predict the signaling behavior of NF-kappaB in a quantitative manner for any variation of the ligand, TNFalpha.

Computer Simulation↗
PubMed1993

Evolutionary models of quantitative disease risk factors.

Numerous mutations are now known that have significant effects on various phenotypes; many of these mutations are of interest because they influence quantitative risk factors for major diseases. Such diversity raises the question of how much genetic heterogeneity we should expect to find in the effects of alleles, that is, the size of the effects, the number of severe alleles, and their frequency in the population. Can evolutionary models suggest a general pattern? In this article we examine what is currently known about several basic aspects of the problem. These include the distribution of quantitative effects of new mutations on a phenotype, the distribution of allelic effects that would be found in a natural population, and the relationship between these effects and Darwinian fitness. We discuss these issues in light of various models that have been proposed and the existing relevant data. Then we consider how these points relate to the distribution of genetic effects on an important human trait, the cholesterol ratio, an important risk factor for coronary heart disease. The complexities of quantitative traits and inadequacies in the available data prevent definitive models that can directly connect the mutational effects, allelic effects, and fitness distributions from being developed, and we consider how sample limitations and the nonequilibrium of human populations caused by our demographic history make rigorous solutions difficult. However, based on what is currently known, we argue that for human quantitative chronic disease risk factors the nearly neutral models of allelic evolution at single loci probably apply reasonably well. In general, and although much is still speculative, the data available for such risk factors are consistent with these expectations and may enable us to predict many aspects of etiologic heterogeneity for human disease.

Adolescent↗
PubMed2005

A simple thermodynamic model for quantitatively addressing cooperativity in multicomponent self-assembly processes--Part 2: Extension to multimetallic helicates possessing different binding sites.

The extended site-binding model, which explicitly separates intramolecular interactions (i.e., intermetallic and interligand) from the successive binding of metal ions to polytopic receptors, is used for unravelling the self-assembly of trimetallic double-stranded Cu(I) and triple-stranded Eu(III) helicates. A thorough analysis of the available stability constants systematically shows that negatively cooperative processes operate, in strong contrast with previous reports invoking either statistical behaviours or positive cooperativity. Our results also highlight the need for combining successive generations of complexes with common binding units, but with increasing metallic nuclearities, for rationalizing and programming multicomponent supramolecular assemblies.

Journal Article↗
PubMed1999

Empirical versus mechanistic modelling: comparison of an artificial neural network to a mechanistically based model for quantitative structure pharmacokinetic relationships of a homologous series of barbiturates.

The aim of the current study was to compare the predictive performance of a mechanistically based model and an empirical artificial neural network (ANN) model to describe the relationship between the tissue-to-unbound plasma concentration ratios (Kpu's) of 14 rat tissues and the lipophilicity (LogP) of a series of nine 5-n-alkyl-5-ethyl barbituric acids. The mechanistic model comprised the water content, binding capacity, number of the binding sites, and binding association constant of each tissue. A backpropagation ANN with 2 hidden layers (33 neurons in the first layer, 9 neurons in the second) was used for the comparison. The network was trained by an algorithm with adaptive momentum and learning rate, programmed using the ANN Toolbox of MATLAB. The predictive performance of both models was evaluated using a leave-one-out procedure and computation of both the mean prediction error (ME, showing the prediction bias) and the mean squared prediction error (MSE, showing the prediction accuracy). The ME of the mechanistic model was 18% (range, 20 to 57%), indicating a tendency for overprediction; the MSE is 32% (range, 6 to 104%). The ANN had almost no bias: the ME was 2% (range, 36 to 64%) and had greater precision than the mechanistic model, MSE 18% (range, 4 to 70%). Generally, neither model appeared to be a significantly better predictor of the Kpu's in the rat.

Algorithms↗