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 559 records · Page 31Linked to original sources

Investigation of the conditions for oscillations in two-variable models of biological processes.

A procedure is presented for the direct determination of possible limit cycles that might occur in two-coupled differential equations that can arise in the modeling of certain biological phenomena. Mathematical expressions are given so that for a particular pair of differential equations the possible limit cycles, their parameters, and stability properties can be calculated by a purely algebraic process. Several examples are used to illustrate the procedure.

Biological Clocks↗

Movable Finite Automata (MFA) models for biological systems. I: Bacteriophage assembly and operation.

A new class of models, called Movable Finite Automata (MFA) models, is introduced. MFA models are physically realistic, but still share some of the features of cellular automata that make the latter easy to handle mathematically and computationally. They are found to be quite versatile in modeling the self-organization of biological systems. Their use in simulating the interaction of protein molecules in the self-assembly and operation of the T4 bacteriophage is described. The results of these simulations carried out on a microcomputer, are given.

Bacteriophages↗

A return to time, cells, systems, and aging: III. Gompertzian models of biological aging and some possible roles for critical elements.

In this paper, I continue my investigation into the modeling of senescence in biological hierarchies. Making use of my previous discussion on non-reestablishable biological components, I derive a mathematical model which has Gompertzian-like dynamics. I show how this model may be approximated, in certain instances, by a Gompertzian equation. I then demonstrate how our approach yields a biological interpretation for the parameters in the Gompertzian equation. I then demonstrate how changes in the parameter values may be interpreted in light of the biology. Subsequently, I review the literature on the allometry of aging, and I demonstrate how my reliability model may be used to obtain--in a qualitative manner--some of the lifespan curves found in the literature. I close my discussion by constructing a more complex reliability model which incorporates the deterministic failure of biological components with stochastic aspects of senescence.

Aging↗

A biological-based model that links genomic instability, bystander effects, and adaptive response.

This paper links genomic instability, bystander effects, and adaptive response in mammalian cell communities via a novel biological-based, dose-response model called NEOTRANS3. The model is an extension of the NEOTRANS2 model that addressed stochastic effects (genomic instability, mutations, and neoplastic transformation) associated with brief exposure to low radiation doses. With both models, ionizing radiation produces DNA damage in cells that can be associated with varying degrees of genomic instability. Cells with persistent problematic instability (PPI) are mutants that arise via misrepair of DNA damage. Progeny of PPI cells also have PPI and can undergo spontaneous neoplastic transformation. Unlike NEOTRANS2, with NEOTRANS3 newly induced mutant PPI cells and their neoplastically transformed progeny can be suppressed via our previously introduced protective apoptosis-mediated (PAM) process, which can be activated by low linear energy transfer (LET) radiation. However, with NEOTRANS3 (which like NEOTRANS2 involves cross-talk between nongenomically compromised [e.g., nontransformed, nonmutants] and genomically compromised [e.g., mutants, transformants, etc.] cells), it is assumed that PAM is only activated over a relatively narrow, dose-rate-dependent interval (D(PAM),D(off)); where D(PAM) is a small stochastic activation threshold, and D(off) is the stochastic dose above which PAM does not occur. PAM cooperates with activated normal DNA repair and with activated normal apoptosis in guarding against genomic instability. Normal repair involves both error-free repair and misrepair components. Normal apoptosis and the error-free component of normal repair protect mammals by preventing the occurrence of mutant cells. PAM selectively removes mutant cells arising via the misrepair component of normal repair, selectively removes existing neoplastically transformed cells, and probably selectively removes other genomically compromised cells when it is activated. PAM likely involves multiple pathways to apoptosis, with the selected pathway depending on the type of cell to be removed, its cellular environment, and on the nature of the genomic damage.

Animals↗

Transport of spin-labeled tetracycline across model and biological membranes.

Electron spin resonance spectra of spin labeled tetracycline (TC-SL) do not show any recognizable partitioning into a lipid bilayer or bulk hydrocarbon solvent, paraffin oil. TC-SL, however, penetrates through the model and biological membranes. It is shown that the rate of permeation depends on membrane composition and increases with temperature. In fluid phase, the rate is greater for saturated dimyristoylphosphatidylcholine than for unsaturated egg yolk phosphatidylcholine membranes. Cholesterol significantly decreases the rate, 30 mol% cholesterol decreases the rate of TC-SL permeation across egg yolk phosphatidylcholine bilayer 8 times at 37 degrees C. The rate of permeation of TC-SL across model membranes is much smaller than the rate for TEMPONE--a compound which slightly partitions into lipid bilayer, and much greater than the rate for TEMPO--choline-a positively charged compound. After addition to the suspension of Ehrlich's ascites tumor cells, the TC-SL is reduced to a non-paramagnetic form. Reduction rate is independent of oxygen concentrations, which led us to suggest that the permeation of TC-SL across the cell plasma membrane is the limiting step of reduction reaction.

Animals↗

Sulfur ligation in copper enzymes and models.

Biological copper-sulfur entities display versatile and unusual coordination chemistry. The role of the sulfur ligation is briefly reviewed through examples from selected copper enzymes and relevant biomimetic models. Copper thiolate complexes are of particular interest because of their key roles in a number of ubiquitous metalloenzymes such as Type I (blue copper proteins) or in the binuclear Cu(A) electrons transfer site found in both cytochrome c oxidase (CcO) and nitrous oxide reductase (N2OR). The possible roles of the S(Met) ligand in monoxygenases are described in relation to recently proposed pathways. Some prospective regarding the biological relevance of disulfide copper ligation and possible radical copper bonds in catalytic cycle are also discussed.

Biomimetic Materials↗

Molecular and cell models of biological effects of heavy ion radiation.

Many quantitative models have been developed for the biological effectiveness of radiation of different quality. They differ substantially in their assumptions, and a lack of firm knowledge remains as to the detailed nature of the critical early molecular damage. Analyses of microscopic features of the stochastic structures of radiation tracks have led to hypotheses on the importance of clustered damage in DNA and associated molecules. Clustered damage of greater complexity or severity is suggested to be less repairable and therefore to dominate the biological consequences.

Animals↗

Trends in primary breast cancer management. Where are we going?

The treatment of cancer during any period has been based not on the whim of a clinician but on the therapeutic consequences of the dominant biologic model of the disease. Until the 1960s, the dominant model of breast cancer was of a disease that spread centrifugally along anatomic pathways, with time being the only determinant of prognosis. An alternative model, that of biologic determinism, posits that the outcomes of treatment are determined by the extent of microscopic dissemination that occurred before the tumor became detectable. This model, too, has flaws, and the author suggests that it is time for a Kuhnian paradigm shift. Breast cancer exhibits a heterogeneity of phenotypes resulting from one or perhaps two mutations. The multiple prognostic variables may be epiphenomena, expressing different degrees of amplification of a limited domain of the genome.

Breast Neoplasms↗

Hydrolysis of phosphates, esters and related substrates by models of biological catalysts.

Why study hydrolases, and why model them? First, hydrolases themselves are of fundamental importance and utility. Examples of their utility in organic synthesis include kinetic resolutions of optical isomers. Restriction endonucleases (DNA hydrolases) are key tools for biotechnology and are vital biological catalysts. Peptidases are necessary for protein digestion and can be harnessed to perform the reverse reaction (peptide synthesis). Thus, for these and many other reasons, hydrolases receive the attention of fundamental and applied research. Models of hydrolases can contribute to our understanding of reaction mechanisms and may also supplant the enzymes as useful catalysts under some conditions. Altering or even increasing the specificity of natural catalysts are also goals of these model studies.

Catalysis↗

Identifying constraints that govern cell behavior: a key to converting conceptual to computational models in biology?

Cells must abide by a number of constraints. The environmental constrains of cellular behavior and physicochemical limitations affect cellular processes. To regulate and adapt their functions, cells impose constraints on themselves. Enumerating, understanding, and applying these constraints leads to a constraints-based modeling formalism that has been helpful in converting conceptual models to computational models in biology. The continued success of the constraints-based approach depends upon identification and incorporation of new constraints to more accurately define cellular capabilities. This review considers constraints in terms of environmental, physicochemical, and self-imposed regulatory and evolutionary constraints with the purpose of refining current constraints-based models of cell phenotype.

Adaptation, Physiological↗

Phenomenological and molecular models of biological proton transfers.

In this paper, the main models describing the transfer of a proton in a molecular system are presented. Models valid when the intersite coupling is weak (non-adiabatic and electronically adiabatic regimes) and strong (adiabatic regime) are described. We distinguish molecular models in which the rate constant is obtained by considering explicitly various degrees of freedom of the system and simpler, phenomenological models built to account for the kinetic isotope effect. The relations between the various models are discussed. Their application to specific systems is illustrated by several studies reported in the literature, with a special emphasis on biological systems.

Ion Transport↗

Comparisons of the interaction of propranolol and timolol with model and biological membrane systems.

The nonspecific interaction of the beta-adrenergic blocking drugs, propranolol and timolol, with model and biological membranes has been investigated. Radioisotope measurements of the association of these drugs with dimyristoyl lecithin (DMPC) bilayers showed that both propranolol and timolol had a significantly greater molar association (mole of drug per mole of lipid) with DMPC above its phase transition temperature than below. Timolol had a much lower molar association with DMPC as compared with propranolol both above and below the phase transition temperature. For the DMPC model membrane system, the molar association of propranolol as measured by radioisotope and inferred from calorimetric studies was similar. Neutron diffraction utilizing propranolol deuterated in the naphthalene moiety showed that the naphthalene moiety of propranolol partitions into the hydrocarbon core of the DMPC lipid bilayer, and that the charged amine side chain is most likely positioned in the aqueous phospholipid head group region. For timolol, the association as measured by radioisotope methods was apparently greater than the partitioning inferred from calorimetric studies using freezing point depression analysis, suggesting a more complex interaction of timolol as compared with propranolol with the DMPC lipid bilayer. The association of propranolol and timolol with sarcoplasmic reticulum vesicles (SR) was similar to that with highly purified protein-depleted SR lipids, and DMPC above its phase transition. The association of propranolol with the SR membrane (mole of propranolol per mole of SR phospholipid) correlated with its ability to inhibit calcium uptake, whereas only a fraction of the total association of timolol with the SR membrane appeared to lead to inhibition of calcium uptake. These results suggest that the major nonspecific interactions of propranolol and timolol are with the SR membrane lipids, and that the magnitude of their interactions depends on both the lipid solubility of the drug and the physical state of the fatty acyl chains of the membrane. Both propranolol and timolol appear to perturb the functional properties of the calcium pump protein in the SR membrane (inhibition of ATP-induced calcium uptake) indirectly by partitioning into the bulk lipid matrix of the SR lipid bilayer, although other sites of interaction cannot be excluded.

Animals↗

Human sexuality in biological perspective: theoretical and methodological considerations.

An increasing number of observers are claiming that a biological model is more appropriate to an understanding of human sexuality than the conventional social-learning one. Such claims have prompted a perusal of the biological literature to ascertain whether the relevant evidence is convincing. The results of this review suggest that claims for the biological model are questionable since the evidence for that model either derives from animal studies (and is thus not generally applicable to human behavior) or is inconclusive, contradictory, or methodologically deficient. It is concluded, therefore, that behavioral scientists are at present on firm ground in using a social-learning, in preference to a biological, model to interpret most aspects of human sexual behavior.

Adolescent↗