PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Models, Biological”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed2001

Can robots make good models of biological behaviour?

UNLABELLED: How should biological behaviour be modelled? A relatively new approach is to investigate problems in neuroethology by building physical robot models of biological sensorimotor systems. The explication and justification of this approach are here placed within a framework for describing and comparing models in the behavioural and biological sciences. First, simulation models--the representation of a hypothesis about a target system--are distinguished from several other relationships also termed "modelling" in discussions of scientific explanation. Seven dimensions on which simulation models can differ are defined and distinctions between them discussed: 1. RELEVANCE: whether the model tests and generates hypotheses applicable to biology. 2. Level: the elemental units of the model in the hierarchy from atoms to societies. 3. Generality: the range of biological systems the model can represent. 4. Abstraction: the complexity, relative to the target, or amount of detail included in the model. 5. Structural accuracy: how well the model represents the actual mechanisms underlying the behaviour. 6. Performance match: to what extent the model behaviour matches the target behaviour. 7. Medium: the physical basis by which the model is implemented. No specific position in the space of models thus defined is the only correct one, but a good modelling methodology should be explicit about its position and the justification for that position. It is argued that in building robot models biological relevance is more effective than loose biological inspiration; multiple levels can be integrated; that generality cannot be assumed but might emerge from studying specific instances; abstraction is better done by simplification than idealisation; accuracy can be approached through iterations of complete systems; that the model should be able to match and predict target behaviour; and that a physical medium can have significant advantages. These arguments reflect the view that biological behaviour needs to be studied and modelled in context, that is, in terms of the real problems faced by real animals in real environments.

Behavior↗
PubMed1992

Biologically based modeling in toxicology research.

Biologically based modeling can be described as the process by which the specific mechanistic steps governing tissue disposition and toxic action of chemicals are expressed in quantitative terms by a set of equations leading to prediction of the outcome of specific toxicological experiments by computer simulation. These models are useful in risk assessment because their mechanistic biological basis permits the high-to-low dose, route to route and interspecies extrapolation of the tissue disposition and toxic action of chemicals. By far their greatest utility is not as "finished" risk assessment models, but as research tools that convey a quantitative expression of our hypotheses of tissue disposition and toxic action of a chemical. A structured modeling approach to toxicology problems helps identify the data gaps in the areas of chemical disposition and toxic action, thus prioritizing on-going research to obtain critical information required to conduct quantitative risk assessment. This paper examines progress in developing comprehensive biologically based models for cancer induction by non-genotoxic carcinogens that are cytotoxic in target tissues. The strategies for linking the models on dosimetry, cytotoxicity, and carcinogenicity are described in detail. The basic concepts and approaches discussed here can be applied to many other toxic chemicals and to toxicity endpoints other than cancer.

Animals↗
PubMed2004

Development and validation of computational models of cellular interaction.

In this paper we take the view that computational models of biological systems should satisfy two conditions - they should be able to predict function at a systems biology level, and robust techniques of validation against biological models must be available. A modelling paradigm for developing a predictive computational model of cellular interaction is described, and methods of providing robust validation against biological models are explored, followed by a consideration of software issues.

Animals↗
PubMed2004

Development of a biological filtration model applied for advanced treatment of sewage.

A mathematical model of biological filtration process is developed in this paper. A biological filtration process has advantages that filtration action and biological activities are combined in a single reactor with aid of filter media. Both physical and biological functions are incorporated in this developed model to simulate both mechanisms. Backwashing is expressed by the assumption that a mean captured solids concentration is input as data, and a captured solids concentration is kept at that value during each filtration run. The developed model is applied to explain the experimental performance with biological filtration reactors, in which batch cultivation of autotrophic bacteria and continuous treatment of actual sewage are carried out. Its applicability is discussed by comparing the simulated results with the experimental data. This model can favourably estimate maximum accumulation of autotrophic bacteria on the medium in batch cultivation, long-term treatment performance in continuous treatment, details of water quality profiles through the filter bed, and biomass. Required hydraulic retention time for nitrification and an appropriate recirculation ratio in a winter season are discussed with this model. This model predicts that a HRT of 1.1 h or above is required to achieve nitrification with remaining NH4(+)-N of less than 1 mgN/L and that an appropriate recirculation ratio is 2-3.

Bioreactors↗
PubMed2000

Modelling in tumour biology part 1: modelling concepts and structures.

Our strategies for the treatment of cancer are constrained by our incomplete understanding of tumour biology and behaviour, and by the enormous complexity and resilience to therapeutic perturbation found in the biological world. We are obliged to simplify this complexity through the use of models and mechanistic explanations. In the first of these papers, we consider the nature of modelling mechanisms available to clinical researchers and the extent to which we rely upon them in our understanding of the nature and behaviour of tumours. In the second part, we will consider specifically how models help us to develop more effective strategies for cancer therapy.

Algorithms↗
PubMed1981

A model for biological oscillations.

A model and computation for oscillatory phenomena observed in some biological processes that utilize ion gradients across a membrane is presented. The model contains two main features: (i) active H+ transport pathways in the membrane and (ii) key enzymes having a pH-dependent activity profile and either translocating H+ from outside or producing H+ as a product. With this model a very long period of oscillations, as observed in mitochondrial and circadian rhythms, could be quantitatively demonstrated.

Biological Transport, Active↗
PubMed1986

Bulimia: clinical characteristics, development, and etiology.

Bulimia is characterized by recurrent episodes of binge eating and severe self-deprecation, often accompanied by self-induced vomiting and/or laxative abuse. It is most often found among young women in their late teens to mid-30s. Estimates of the disorder's prevalence vary widely, depending on the diagnostic criteria used, but usually range from 5% to 20% of college age women. Binge eating typically begins in late adolescence, frequently after a period of dieting to lose weight. Self-induced vomiting usually follows the onset of binge eating by about a year. To date, theories of the disorder's etiology have included several biological models, a psychosocial model, and a biopsychosocial model. The biological models proposed have viewed bulimia as a form of biological depression, neurological disturbance, or metabolic disturbance. The psychosocial model suggests that society's pressure on young women for extreme thinness leads to excessive dietary restraint, deprivation, and, paradoxically, binge eating. The presence of anxiety or depression exacerbates the process. The biopsychosocial model appears to be the most promising. It proposes that young women with biological predispositions toward overweight, depression, or metabolic disturbance are particularly vulnerable to social pressure for thinness, the binge eating that may result from excessive dieting, and, hence, bulimia. The complex nature of bulimia suggests that a multidisciplinary team approach treatment is appropriate.

Adolescent↗
PubMed1989

Variability in biological monitoring of solvent exposure. I. Development of a population physiological model.

Biological indicators of exposure to solvents are often characterised by a high variability that may be due either to fluctuations in exposure or individual differences in the workers. To describe and understand this variability better a physiological model for differing workers under variable industrial environments has been developed. Standard statistical distributions are used to simulate variability in exposure concentration, physical workload, body build, liver function, and renal clearance. For groups of workers exposed daily, the model calculates air monitoring indicators and biological monitoring results (expired air, blood, and urine). The results obtained are discussed and compared with measured data, both physiological (body build, cardiac output, alveolar ventilation) and toxicokinetic for six solvents: 1,1,1-trichloroethane, trichloroethylene, tetrachloroethylene, benzene, toluene, styrene, and their main metabolites. Possible applications of this population physiological model are presented.

Adipose Tissue↗
PubMed1989

[Substitute model for in-vitro biological testing. II. Quantitative evaluation of the biocompatibility of dental products].

A biological model for evaluating pulpo-dentinal capping materials is described. The model uses cultures of human pulp cells which are explanted to form cell monolayers. Four products already tested in vivo on teeth subsequently extracted for orthodontic reasons were laid directly over these cultures and observed after 7, 14, 21 and 28 days, corresponded to the in vivo test periods. The growth and morphology of the cells were similar for both test systems, indicating comparability between the two biological models as well as the validity of the developed in vitro method. A preliminary scale of biological activity is proposed which could be useful for preliminary screening of materials.

Biocompatible Materials↗
PubMed2003

Punctuated equilibria and 1/f noise in a biological coevolution model with individual-based dynamics.

We present a study by linear stability analysis and large-scale Monte Carlo simulations of a simple model of biological coevolution. Selection is provided through a reproduction probability that contains quenched, random interspecies interactions, while genetic variation is provided through a low mutation rate. Both selection and mutation act on individual organisms. Consistent with some current theories of macroevolutionary dynamics, the model displays intermittent, statistically self-similar behavior with punctuated equilibria. The probability density for the lifetimes of ecological communities is well approximated by a power law with exponent near -2, and the corresponding power spectral densities show 1/f noise (flicker noise) over several decades. The long-lived communities (quasisteady states) consist of a relatively small number of mutualistically interacting species, and they are surrounded by a "protection zone" of closely related genotypes that have a very low probability of invading the resident community. The extent of the protection zone affects the stability of the community in a way analogous to the height of the free-energy barrier surrounding a metastable state in a physical system. Measures of biological diversity are on average stationary with no discernible trends, even over our very long simulation runs of approximately 3.4 x 10(7) generations.

Journal Article↗
PubMed2003

Using models to enhance the intellectual content of learning in developmental biology.

Models have been particularly useful in developmental biology over the last 30 years. At first, underlying control mechanisms were poorly understood, but over time a wealth of detailed information became available to provide an increasingly detailed knowledge of underlying mechanisms, at levels from genes through cells to organs, organisms and populations. Models are also of great value in teaching developmental biology, as they allow students to explore phenomena hard to perceive directly because of their scale, accessibility, expense or other considerations. A model may allow students to "experiment" in ways which would be impractical in real life, as well as give them a deep understanding of competing hypotheses of development. Lastly, students can be challenged to produce models of their own, whereas only rarely are they able to carry out original experiments. I discuss two main kinds of models and their uses in generating, testing and expounding hypotheses and point out dangers in the use of models in education. Models may draw upon and reflect the consensus paradigm in the field: a researcher may be able to appreciate that models are interim conditional statements of probability and use them to generate new knowledge. A student may be less able to do so and may fail to appreciate where new knowledge will come from. And unlike physics, biology is stochastic and contingent and can never be entirely deduced from first principles, implying that models can never be as perfect in any biological field as they can be in some other fields.

Developmental Biology↗
PubMed1995

Effects of solutes on optical properties of biological materials: models, cells, and tissues.

Perturbations of scattering background for absorbance measurements by photon diffusion techniques complicate algorithms used for determining the concentration of blood and the saturation of hemoglobin in tissues. In order to better define these perturbations, we have undertaken a study of the effect of solutes, some of physiological importance, upon the scattering of three types of model systems: a lipid vessel suspension (Intralipid), a cell suspension (Baker's yeast), and a tissue (perfused liver). A simple formula relates absorbancy change to proportional changes of the input/output separation rho and the square root of mu a and mu's in relation to a relevant model system. Thus, absorbance changes at 850 nm slopes and intercepts are measured as a function of rho; the absorption and reduced scattering coefficient, mu a and mu's, are calculated. We studied each of these cases as a function of the perturbation induced by low-molecular-weight polyhydroxy solutes, generally sugars (mannitol, fructose, sucrose, and glucose), alcohols (propanediol and methanol), and electrolytes (sodium and potassium chloride). Dilatometric studies indicate volume changes of the solvent system and afford correction factors. The slopes are approximately +/- 0.5 x 10(-4) OD/mM solute per centimeter separation of input/output per percent scatter (yeast or Intralipid) and indicate possible physiological detection of solutes in tissues in the millimolar range. The large optical effects of temperature upon the solute effect on model systems and of osmotic and perfusion pressures on the perfused liver further complicate the possibility of quantitative in vivo studies of these solutes.

Animals↗
PubMed1994

Ultrastructural studies of complement mediated cell death: a biological reaction model to plasma membrane injury.

Complement-mediated nucleated cell death has been shown to be independent of colloid-osmotic swelling. In contrast, other factors (e.g. Ca2+ influx) are of importance in the induction of cell death. In this communication, the sequential morphological features of complement-mediated cell injury have been studied by electron microscopy and compared with biochemical data (ATP content and LDH release). It was observed that immediately after C5b-8 lesion formation, although the overall cell, morphology is well preserved, the mitochondria display an "ultracondensed" appearance. Upon addition of C9, the mitochondria remain initially condensed, but swell progressively with final formation of flocculent densities. The nuclei become progressively edematous, with concurrent disappearance of heterochromatin. The nucleoli lose their associated chromatin and display segregation of their components with formation of markedly electron-dense filamentous deposits. The nuclear envelope remains initially intact, but subsequently progressive dilatation of the associated perinuclear RER cisterna and distention of the nuclear pores associated with leakage of chromatin into the cytoplasm are seen. The larger cell organelles (including mitochondria, ER, Golgi apparatus, etc.) become clustered around the nucleus, concurrently with marked edema of the outer cytoplasm and bleb formation. The RER cisternae become dilated, whereas the Golgi complex disappears. Relatively early on the plasma membrane shows breaks in continuity. The pattern of these changes--potentially related to Ca2+ influx, ATP efflux and overall metabolic depletion--corresponds to the previously described model of cell reaction to injury, confirming the dynamic nature of the process. The morphology of cell death in this model shares some features, e.g., the nucleolar changes, with "apoptosis" (programmed cell death). However, the overall pattern appears to correspond more to "necrosis," characterized by loss of volume control and mitochondrial abnormalities.

Adenosine Triphosphate↗
PubMed2004

Lung tumour risk in radon-exposed rats from different experiments: comparative analysis with biologically based models.

Data sets of radon-exposed male rats from Wistar and Sprague-Dawley strains have been investigated with two different versions of the two-step clonal expansion (TSCE) model of carcinogenesis. These so-called initiation-promotion (IP) and initiation-transformation (IT) models are named after the cell-based processes that are assumed to be induced by radiation. The analysis was done with all malignant lung tumours taken to be incidental and with fatal tumours alone. For all tumours treated as incidental, both models could explain the tumour incidence data equally well. Owing to its better fit, only the IP model was applied in the analysis of fatal tumours that carry additional information on the time when they cause death. A statistical test rejected the hypothesis that a joint cohort of Wistar and Sprague-Dawley rats can be described with the same set of model parameters. Thus, the risk analysis has been carried out for the Wistar rats and the Sprague-Dawley rats separately and has been restricted to fatal tumours alone because of their similar effect in humans. Using a refined technique of age-adjustment, the lifetime excess absolute risk has been standardised with the survival function from competing risks in the control population. The age-adjusted excess risks for both strains of rats were of similar size, for animals with first exposure later in life they decreased markedly. For high cumulative exposure the excess risk increased with longer exposure duration, for low cumulative exposure it showed the opposite trend. In addition, high cumulative exposure exerted lethal effects other than lung cancer on the rats.

Administration, Inhalation↗
PubMed2005

Comment on "Studies of radon-exposed miner cohorts using a biologically based model: comparison of current Czech and French data with historic data from China and Colorado" by W.F. Heidenreich, L. Tomasek, A. Rogel, D. Laurier, M. Tirmarche (2004) Radiat Environ Biophys 43:247-256, and "Radon-induced lung cancer in French and Czech miner cohorts described with a two-mutation cancer model" by M.J.P. Brugmans, S.M. Rispens, H. Bijwaard, D. Laurier, A. Rogel, L. Tomasek, M. Tirmarche (2004) Radiat Environ Biophys 43:153-163.

Explore the source record for details and available documents.

Humans↗