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At least 1,711 records · Page 95Linked to original sources
PubMed2006

An etiologic model to help explain the pathogenesis of cervical artery dissection: implications for cervical manipulation.

We present a theoretical etiologic model of cervical artery dissection for the purpose of coalescing our present understanding of its pathogenesis. Although the notion of an underlying arteriopathy and a trigger are universally accepted concepts, we propose in our model that dissection is a product of an underlying (genetic) predisposition, triggered specifically by risk factors associated with environmental exposure, with or without trivial trauma. Given the widespread daily occurrence of neck movements and sporting activities, it seems unlikely that trivial trauma, in the absence of other triggers and an underlying arteriopathy, is sufficient to cause dissection. This concept has significant implications for practitioners of spinal manipulation. This may represent a paradigm shift because the model suggests that stroke following manipulation is unlikely in otherwise healthy individuals. Although this model is consistent with current published case-control studies on cervical artery dissection, further research is necessary to accept or refute it as a tenable hypothesis.

Aortic Dissection↗
PubMedDate not supplied

[Model calculation to explain the BSE-incidence in Germany].

The future development of BSE-incidence in Germany is investigated using a simple epidemiological model calculation. Starting point is the development of the incidence of confirmed suspect BSE-cases in Great Britain since 1988, the hitherto known mechanisms of transmission and the measures taken to decrease the risk of transmission as well as the development of the BSE-incidence in Germany obtained from active post mortem laboratory testing of all cattle older then 24 months. The risk of transmission is characterized by the reproduction ratio of the disease. There is a shift in time between the risk of BSE transmission and the BSE incidence caused by the incubation time of more than 4 years. The observed decrease of the incidence in Germany from 2001 to 2003 is not a consequence of the measures taken at the end of 2000 to contain the disease. It can rather be explained by an import of BSE contaminated products from countries with a high BSE incidence in the years 1995/96 being used in calf feeding in Germany. From the future course of the BSE-incidence in Germany after 2003 a quantification of the recycling rate of BSE-infected material within Germany before the end of 2000 will be possible by use of the proposed model if the active surveillance is continued.

Animals↗
PubMed2003

How much variance is explained by ecologists? Additional perspectives.

A recent meta-analysis of meta-analyses by Møller and Jennions suggested that ecologists using statistical models are explaining between 2.5% and 5.42% of the variability in ecological studies. Although we agree that there is considerable variability in ecological systems that is not explained, we disagree with the approach and general conclusions of Møller and Jennions. As an alternate perspective, we explored the question: "How much ecological variation in relationships is not explained?" We did this by examining published studies in five different journals representative of the numerous sub-disciplines of ecology. We quantified the proportion of variance not explained in statistical models as the residual or random error compared to the total variation in the data set. Our results indicate that statistical models explain roughly half of the variation in variables of interest, vastly different from the 2.5%-5.42% reported by Møller and Jennions. This difference resulted largely from a different level of analysis: we considered the original study to be the appropriate level for quantifying variability while Møller and Jennions combined studies at different temporal and spatial scales and attempted to find universal single-factor relationships between ecological variables across study organisms or locations. Therefore, we believe that Møller and Jennions actually measured the universality of single factor effects across multiple ecological systems, not the amount of variability in ecological studies explained by ecologists. This study, combined with Møller and Jennions', illustrates importance of applying statistical models appropriately to assess ecological relationships.

Animals↗
PubMed2005

Explained randomness in proportional hazards models.

A coefficient of explained randomness, analogous to explained variation but for non-linear models, was presented by Kent. The construct hinges upon the notion of Kullback-Leibler information gain. Kent and O'Quigley developed these ideas, obtaining simple, multiple and partial coefficients for the situation of proportional hazards regression. Their approach was based upon the idea of transforming a general proportional hazards model to a specific one of Weibull form. Xu and O'Quigley developed a more direct approach, more in harmony with the semi-parametric nature of the proportional hazards model thereby simplifying inference and allowing, for instance, the use of time dependent covariates. A potential drawback to the coefficient of Xu and O'Quigley is its interpretation as explained randomness in the covariate given time. An investigator might feel that the interpretation of the Kent and O'Quigley coefficient, as a proportion of explained randomness of time given the covariate, is preferable. One purpose of this note is to indicate that, under an independent censoring assumption, the two population coefficients coincide. Thus the simpler inferential setting for Xu and O'Quigley can also be applied to the coefficient of Kent and O'Quigley. Our second purpose is to point out that a sample-based coefficient in common use in the SAS statistical package can be interpreted as an estimate of explained randomness when there is no censoring. When there is censoring the SAS coefficient would not seem satisfactory in that its population counterpart depends on an independent censoring mechanism. However there is a quick fix and we argue in favour of its use.

Antimetabolites, Antineoplastic↗
PubMed2001

A homeostatic model of oxidative damage explains paradoxes observed in earlier aging experiments: a fusion and extension of older theories of aging.

The Rate of Living and the Threshold Theories of Aging are two contradicting approaches used to explain experimental facts about aging in fruit flies. In this paper we suggest an approach that unifies these theories and removes the contradiction. The approach involves quantitative description of the oxidative stress theory of aging, which is presented in the form of a mathematical homeostatic model. The crucial variable in the model is called 'homeostatic capacity', which is analogous to the classical notion of vitality. We model the process of aging as the age-related accumulation of damage produced by oxidative stress, which reduces the homeostatic capacity of the organism. The model is tested with the experimental data obtained in the classical experiments by Maynard Smith in 1958-1963. Our homeostatic model explains the well-known results of these experiments more accurate than any one of the early theories of aging. We form an hypothesis about the mechanisms underlying the results observed in the experiments and analyze a possible interplay of these mechanisms. Our virtual replication of Maynard Smith's classical experiments demonstrates that mathematical modeling can be a powerful tool to reveal and investigate the inherent genetic and physiological processes underlying the data observed in complicated insect experiments.

Aging↗
PubMed2005

Catch-bond model derived from allostery explains force-activated bacterial adhesion.

High shear enhances the adhesion of Escherichia coli bacteria binding to mannose coated surfaces via the adhesin FimH, raising the question as to whether FimH forms catch bonds that are stronger under tensile mechanical force. Here, we study the length of time that E. coli pause on mannosylated surfaces and report a double exponential decay in the duration of the pauses. This double exponential decay is unlike previous single molecule or whole cell data for other catch bonds, and indicates the existence of two distinct conformational states. We present a mathematical model, derived from the common notion of chemical allostery, which describes the lifetime of a catch bond in which mechanical force regulates the transitions between two conformational states that have different unbinding rates. The model explains these characteristics of the data: a double exponential decay, an increase in both the likelihood and lifetime of the high-binding state with shear stress, and a biphasic effect of force on detachment rates. The model parameters estimated from the data are consistent with the force-induced structural changes shown earlier in FimH. This strongly suggests that FimH forms allosteric catch bonds. The model advances our understanding of both catch bonds and the role of allostery in regulating protein activity.

Adhesins, Escherichia coli↗
PubMed2001

What do computer models of cognition explain: a reply to Gobet.

The differences between Gobet's views and ours call attention to some points concerning the argumentative status of computational models. If we have two fundamentally different models which reasonably accurately simulate a phenomenon, we must ask, what is the argumentative status of the models in psychological terms. Moreover, if it is possible to present different models of same phenomena, what is the general argumentative power of models in psychology? As the kind of differences between our views and the ones of Gobet's are common in modelling, we briefly call attention to these foundational issues in our paper.

Cognition↗
PubMed1999

Computing measures of explained variation for logistic regression models.

The proportion of explained variation (R2) is frequently used in the general linear model but in logistic regression no standard definition of R2 exists. We present a SAS macro which calculates two R2-measures based on Pearson and on deviance residuals for logistic regression. Also, adjusted versions for both measures are given, which should prevent the inflation of R2 in small samples.

Computer Simulation↗
PubMed2002

Birth and death of protein domains: a simple model of evolution explains power law behavior.

BACKGROUND: Power distributions appear in numerous biological, physical and other contexts, which appear to be fundamentally different. In biology, power laws have been claimed to describe the distributions of the connections of enzymes and metabolites in metabolic networks, the number of interactions partners of a given protein, the number of members in paralogous families, and other quantities. In network analysis, power laws imply evolution of the network with preferential attachment, i.e. a greater likelihood of nodes being added to pre-existing hubs. Exploration of different types of evolutionary models in an attempt to determine which of them lead to power law distributions has the potential of revealing non-trivial aspects of genome evolution. RESULTS: A simple model of evolution of the domain composition of proteomes was developed, with the following elementary processes: i) domain birth (duplication with divergence), ii) death (inactivation and/or deletion), and iii) innovation (emergence from non-coding or non-globular sequences or acquisition via horizontal gene transfer). This formalism can be described as a birth, death and innovation model (BDIM). The formulas for equilibrium frequencies of domain families of different size and the total number of families at equilibrium are derived for a general BDIM. All asymptotics of equilibrium frequencies of domain families possible for the given type of models are found and their appearance depending on model parameters is investigated. It is proved that the power law asymptotics appears if, and only if, the model is balanced, i.e. domain duplication and deletion rates are asymptotically equal up to the second order. It is further proved that any power asymptotic with the degree not equal to -1 can appear only if the hypothesis of independence of the duplication/deletion rates on the size of a domain family is rejected. Specific cases of BDIMs, namely simple, linear, polynomial and rational models, are considered in details and the distributions of the equilibrium frequencies of domain families of different size are determined for each case. We apply the BDIM formalism to the analysis of the domain family size distributions in prokaryotic and eukaryotic proteomes and show an excellent fit between these empirical data and a particular form of the model, the second-order balanced linear BDIM. Calculation of the parameters of these models suggests surprisingly high innovation rates, comparable to the total domain birth (duplication) and elimination rates, particularly for prokaryotic genomes. CONCLUSIONS: We show that a straightforward model of genome evolution, which does not explicitly include selection, is sufficient to explain the observed distributions of domain family sizes, in which power laws appear as asymptotic. However, for the model to be compatible with the data, there has to be a precise balance between domain birth, death and innovation rates, and this is likely to be maintained by selection. The developed approach is oriented at a mathematical description of evolution of domain composition of proteomes, but a simple reformulation could be applied to models of other evolving networks with preferential attachment.

Animals↗
PubMed1983

Computer modelling of haemodialysis/ultrafiltration explaining the pathogenesis of the disequilibrium syndrome.

Based on the hypothesis that rapid corrections of pH, Na+ and osmolality give rise to disequilibrium (DES) during efficient haemodialysis (HD), a 14 compartment model has been designed for dynamic analysis of the induced fluid shifts and the resulting haemodynamic reactions. Simulated HD and ultrafiltration (UF) on the model were based on data from 11 steady state dialysis (RDT) patients (diffusion coefficients for urea, body fluid compartments, haemodynamic monitoring by Swan-Ganz catheters). The model reactions correlated remarkably with clinical findings and indicate how far a patient's haemodynamic compensation can prevent circulatory collapse and hypovolaemia, mainly through lowering the mean pressure in a major portion of the capillaries. Steady weight dialysis causes reduction of blood volume up to 65 per cent before circulatory collapse occurs.

Blood↗
PubMed2003

A rate-dependent microcrack-bridging model that can explain the strain rate dependency of cortical bone apparent yield strength.

Although there are empirical correlations between strain rate, cortical and cancellous bone apparent stiffness, apparent yield strength, apparent ultimate strength and cortical bone fracture toughness, a mechanistic description for these phenomena is lacking. Microcracking is a major mechanism in cortical and cancellous bone failure, however, microdamage content alone cannot explain the strain rate dependence of bone strength without considering time-dependent behavior of the crack. Using a rate-dependent model of a fiber-bridged microcrack and data from the literature, we demonstrate that the experimental apparent yield strength of bone can be predicted directly from measurements of apparent moduli of elasticity of bone constituents and failure strain of the collagenous matrix. Yield strength predictions for estrogen depleted bone were made using the model and data from ovariectomized sheep. It was predicted that the yield strength of estrogen-deficient bone is comparable to that of normal bone within strain rates associated with physiological activities. For high strain rates, however, the strength of estrogen-depleted bone was predicted to be much weaker than normals suggesting a higher fracture risk due to impact from falls, for individuals with estrogen-depleted bones such as in post-menopausal osteoporosis.

Bone and Bones↗
PubMed1970

Comparison of physical models used to explain condensation effects in lecithin-cholesterol mixed films.

The apparent condensation effect observed with mixed monolayers of lecithin and cholesterol has been examined with respect to both molecular interaction and molecular cavity models. For each, model equations are presented which predict the surface areas of the film components as a function of the mole fraction of each component. For mixed monolayers where linearity does not exist in plots of mean surface area vs. mole fraction, and where there are breaks in the curve at mole fraction values other than 0.5, the size of the cavities are not invariant with respect to mole fraction.

Chemical Phenomena↗
PubMed1985

Will a three-allele model of inheritance explain the HLA data for type 1 (insulin-dependent) diabetes?

The HLA data from nine published studies on Type 1 (insulin-dependent) diabetes were examined to see whether a three-allele model for the inheritance of Type 1 diabetes at the HLA-associated locus could be rejected. None of the data rejected the three-allele model. The data were also examined to see whether they would reject a recessive model. Out of the nine data sets, five rejected a recessive and four did not. The p value for all studies together rejected a recessive. Two of the data sets allowed us to test the hypothesis that multiplex and simplex families would exhibit different modes of inheritance. Multiplex data from both data sets rejected recessive inheritance while the multiplex data from only one data set also rejected three-allele inheritance. The results of assuming a recessive model and analyzing the data from simplex families led to different results from the two data sets. In addition, data from a non-European population were examined and found to reject both recessive and three-allele inheritance for Type 1 diabetes at the HLA-associated locus.

Alleles↗
PubMed2001

The effect of physical abuse on children's social and affective status: a model of cognitive and behavioral processes explaining the association.

This study proposes a model explaining the association between physical abuse of children and children's social and affective status as one in which children's social expectations and behavior, developed within the context of abusive parenting, mediate current functioning in these two outcome domains. Subjects included one hundred 9 to 12-year-old physically abused children recruited from consecutive entries onto the New York State Register for Child Abuse for New York City and 100 case-matched classmate nonabused comparison children. Sociometric assessments were carried out in classrooms, interviews were conducted with the children and their parents, and teachers, parents, and classmates rated the children's behavior. Path analysis was utilized to test the conceptually derived models. Children's social expectations regarding peers, and two social behaviors--aggressive behavior and prosocial behavior--were found to mediate between abuse and positive and negative social status, as well as between abuse and positive and negative reciprocity. Social expectations and withdrawn behavior mediated between abuse and positive social status, but only where withdrawn behavior was a function of social expectations. Social expectations were generally found to mediate between abuse and internalizing problems. Negative social status (peer rejection) added to social expectations in producing internalizing problems. Identification of these mediating pathways can serve to guide secondary preventive intervention efforts so that they best address the problems abused children face in the absence of adequate parental and peer support as the children enter adolescence.

Affective Symptoms↗
PubMed1994

Model phylogenies to explain the real world.

Phylogenetic trees based on gene sequence data contain information about the evolutionary processes responsible for their genesis. Methods have now been developed which help to reveal those processes. The methods are based on simple models of evolutionary change but, when applied across individuals in a population, rather than across species in a higher-level taxon, they can reveal the past history of population change. Examples from salamanders and viruses are used to illustrate how the past history of changes in speciation rate and the origin of epidemics can be inferred in the absence of fossil material or historical documentation.

Animals↗
PubMed2007

Resolving the paradox of stasis: models with stabilizing selection explain evolutionary divergence on all timescales.

We tested the ability of six quantitative genetic models to explain the evolution of phenotypic means using an extensive database compiled by Gingerich. Our approach differs from past efforts in that we use explicit models of evolutionary process, with parameters estimated from contemporary populations, to analyze a large sample of divergence data on many different timescales. We show that one quantitative genetic model yields a good fit to data on phenotypic divergence across timescales ranging from a few generations to 10 million generations. The key feature of this model is a fitness optimum that moves within fixed limits. Conversely, a model of neutral evolution, models with a stationary optimum that undergoes Brownian or white noise motion, a model with a moving optimum, and a peak shift model all fail to account for the data on most or all timescales. We discuss our results within the framework of Simpson's concept of adaptive landscapes and zones. Our analysis suggests that the underlying process causing phenotypic stasis is adaptation to an optimum that moves within an adaptive zone with stable boundaries. We discuss the implication of our results for comparative studies and phylogeny inference based on phenotypic characters.

Animals↗