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Results for “quantitative model”

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At least 181 records · Page 10Linked to original sources
PubMed1996

Comparison of ultrafast dipyridamole magnetic resonance imaging with dipyridamole SestaMIBI SPECT for detection of perfusion abnormalities in patients with one-vessel coronary artery disease: assessment by quantitative model fitting.

The value of ultrafast MRI for detection of myocardial perfusion abnormalities in patients with coronary artery disease (CAD) was assessed in 10 patients with stable angina pectoris and angiographically proven one-vessel CAD using double-level short-axis ultrafast MRI with bolus injection of gadolinium-DTPA and tomographic technetium-99m SestaMIBI imaging (SPECT) during dipyridamole-induced coronary hyperemia. Abnormally perfused regions were assessed with SPECT and MRI in all (100%) patients. Agreement in localization between arteriography and SPECT was 80%; between arteriography and MR, 70%; and between SPECT and MR, 90%. The signal intensity increase after the bolus injection of gadolinium-DTPA using a linear fit, and the slope of gadolinium-DTPA wash-in using double exponential model fitting were significantly different between abnormally and normally perfused regions. These preliminary results demonstrate the potential of dipyridamole ultrafast MR to monitor stress-induced flow maldistribution in patients with single vessel CAD.

Aged↗
PubMedDate not supplied

Characterization of BOLD activation in multi-echo fMRI data using fuzzy cluster analysis and a comparison with quantitative modeling.

A combination of multiple gradient-echo imaging and exploratory data analysis (EDA), i.e. fuzzy cluster analysis (FCA), is proposed for separation and characterization of BOLD activation in single-shot spiral functional magnetic resonance imaging (fMRI) experiments at 3 T. Differentiation of functional activation using FCA is performed by clustering pixel signal changes (DeltaS) as a function of echo time (TE). Further vascular classification is supported by the localization of activation and the comparison with a single-exponential decay model. In some subjects, an additional indication for large vessels within a voxel was found as oscillation of the fMRI signal difference vs echo time (TE). Such large vessels may be separated from small vessel activation and, therefore, our proposed procedure might prove useful if a more specific functional localization is desired in fMRI. In addition to the signal change DeltaS, DeltaT(2)*/T(2)* is significantly different between activated regions. Averaged over all eight subjects DeltaT(2)* is 1.7 +/- 0.2 ms in ROIs with the highest signal change characterized as containing large vessels, whereas in ROIs corresponding to microvascular environment average DeltaT(2)* values are 0.8 +/- 0.1 ms.

Brain↗
PubMed2000

Tyrosinase kinetics: a semi-quantitative model of the mechanism of oxidation of monohydric and dihydric phenolic substrates.

A mathematical model of phase I melanogenesis is described based on the differential reactivity of tyrosinase according to the redox status of the active site copper atoms shown by Lerch and co-workers (see Lerch, 1981, Metal Ions in Biological Systems (Sigel, H., ed.) Vol. 13, pp. 143-186. New York: Marcel Dekker) in combination with the indirect formation of the catecholic intermediate substrate. In this model the unusual autoactivation kinetics of tyrosinase are explained by recruitment of enzyme from the met -form, in which the active-site copper atoms are in the oxidized (Cu(II)) state, by 2-electron donation from catechol oxidation. Using estimates of the values for the rate constants of the six reactions involved, the general characteristics of the model are shown to be consistent with the kinetic behaviour of tyrosinase in vitro. These include a lag period which is sensitive to catechol addition.

Animals↗
PubMed1999

A novel, quantitative model for study of endothelial cell migration and sprout formation within three-dimensional collagen matrices.

Interactions between migratory endothelial cells (ECs) and surrounding extracellular matrix (ECM) are of central importance to vascular growth. Here, we present a new model of EC migration and morphogenesis within three-dimensional ECM termed "radial invasion of matrix by aggregated cells" (RIMAC). In the RIMAC model, single aggregates of defined numbers of bovine aortic ECs were embedded within small, lenticular gels of type I collagen supported by annuli of nylon mesh. Culture of the gels in nutrient media resulted in quantifiable, reproducible, radial migration of ECs into the collagen. The angiogenic proteins basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) each stimulated migration of ECs in a concentration-dependent manner. In combination, bFGF and VEGF stimulated migration synergistically. In contrast, transforming growth factor-beta1 inhibited migration of ECs. Low concentrations (0.1-0.5 ng/ml) of VEGF induced ECs to form multicellular sprouts, some of which possessed lumen-like spaces. Mitomycin C, an inhibitor of cell proliferation, did not affect the migration of ECs into collagen induced by 0.5 ng/ml VEGF but moderately inhibited migration induced by 5 ng/ml VEGF. Increasing the density (concentration) of the collagen gel inhibited the migration of single ECs and increased the branching and anastomosis of multicellular sprouts. We conclude that the RIMAC model is a highly efficacious assay for the screening of potentially angiogenic and angiostatic compounds and, moreover, is advantageous for mechanistic studies of vascular morphogenesis.

Animals↗
PubMed1992

A quantitative model for spontaneous bone metastasis: evidence for a mitogenic effect of bone on Walker 256 cancer cells.

A new model for the study of spontaneous bone metastasis has been developed which allows for the quantification of metastatic tumor burden and cancer cell growth rate, and which describes the progressive changes in bone morphology. Walker 256 (W256) cells or vehicle were injected into the left upper thigh muscle of male Fischer rats, which were killed 7, 10 or 14 days later. By day 7, metastases had appeared in the distal femur, in the glomeruli of the kidney, and diffusely throughout the liver and lungs. The extent of tumor burden in these organs increased over time. In the femur, 14 days of tumor burden was associated with a 53 +/- 10% decrease in trabecular bone content, a 61 +/- 15% increase in osteoclast surface, and a 95 +/- 10% decrease in osteoblast surface, as compared with non-tumor-bearing controls. By autoradiography, metastatic tumor cells in all organs were determined to have greater growth rates than did cells in the primary tumor. However, within the femur, W256 cells located adjacent to trabecular bone surfaces had a 33 +/- 7% greater growth rate than did W256 cells located > 50 microns from bone surfaces (P < 0.05), suggesting a mitogenic effect of bone.

Animals↗
PubMed1975

Interpretation of invertebrate photoreceptor potentials in terms of a quantitative model.

It is known from voltage-clamp experiments on visual cells of Limulus and Balanus that the total membrane current can be separated approximately into a dark current JD and a light-induced current JL such that each part has a time-and intensity-independent reversal potential. In addition JL can be represented approximately as a product of a nonlinear, time independent current-voltage characteristics J0L (v) and an "activation factor" xa which depends on light intensity and time. J0L(V) can be described by a simple electro-diffusion membrane model (for JD we use the same model). A set of kinetic equations including amplification, latency and light adaptation leads to a determination of xa for photoisomerization of single rhodospin molecules and for arbitrary light signals. The receptor potentials calculated show many features of the experiments on Limulus, Balanus and Astacus.

Adaptation, Physiological↗
PubMed1991

Quantitative model for Schädler's isometric oscillations in insect flight and cardiac muscle.

Schädler and colleagues (1969, 1971) and Steiger (1977a) have found that tetanized insect fibrillar and cardiac muscles exhibit damped isometric oscillations in tension following a quick stretch. This behaviour cannot be explained by the conventional sliding filament model at full activation, or by including stretch activation in the obvious way. However, it is predicted by a sliding filament model which allows these muscles to be further activated by an increase in thin-filament tension even at high calcium levels (above 10(-5) M), providing the strength gamma of strain-activation coupling exceeds a critical value. Calculations from a comprehensive model of the actin-myosin contraction cycle suggest that this can be achieved if the phosphate release and head rotation steps are both regulated by calcium and thin-filament tension. The model also predicts a delayed tension rise following a quick release for subcritical values of gamma. Current knowledge of sarcomere structure and regulation of contractility in striated muscle indicates that this strain-activation mechanism alone cannot account for all stretch-activation phenomena, although many can be predicted if the regulatory filament is allowed to carry passive tension.

Actinin↗
PubMed1989

A quantitative model for lifespan curves.

"This paper addresses the issue of a model for the total lifespan survival curve, with particular interest in the later life or geriatric years. This new model is based upon the basic premise that the population under study is a mixture of individuals comprising three major subgroups: (1) neonatal deaths, (2) standard Gompertzian-like survival, (3) geriatric survival. It is demonstrated that a standard mixture model, mixing three survival distributions, more than adequately describes survival over the entire lifespan of the population. Further, this newer model has the desirable added virtue that the model parameters may be interpreted in a biological manner."

Adult↗
PubMed1999

Quantitative modelling of DNA damage using Monte Carlo track structure method.

This paper presents data on modelling of DNA damage induced by electrons, protons and alpha-particles to provide an insight into factors which determine the biological effectiveness of radiations of high and low linear energy transfer (LET). These data include the yield of single- and double-strand breaks (ssb, dsb) and base damage in a cellular environment. We obtain a ratio of 4-15 for ssb:dsb for solid and cellular DNA and a preliminary ratio of about 2 for base damage to strand breakage. Data are also given on specific characteristics of damage at the DNA level in the form of clustered damage of varying complexity, that challenge the repair processes and if not processed adequately could lead to the observed biological effects. It is shown that nearly 30% of dsb are of complex form for low-LET radiation, solely by virtue of additional breaks, rising to about 70% for high-LET radiation. Inclusion of base damage increases the complex proportion to about 60% and 90% for low- and high-LET radiation, respectively. The data show a twofold increase in frequencies of complex dsb from low-LET radiation when base damage is taken into account. It is shown that most ssb induced by high-LET radiation have associated base damages, and also a substantial proportion is induced by low-energy electrons.

DNA↗
PubMed1998

Brain temperature and limits on transcranial cooling in humans: quantitative modeling results.

Selective brain cooling (SBC) of varying strengths has been demonstrated in a number of mammals and appears to play a role in systemic thermoregulation. Although primates lack obvious specialization for SBC, the possibility of brain cooling in humans has been debated for many years. This paper reports on the use of mathematical modeling to explore whether surface cooling can control effectively the temperature of the human cerebrum. The brain was modeled as a hemisphere with a volume of 1.33 1 and overlying layers of cerebrospinal fluid, skull, and scalp. Each component was assigned appropriate dimensions, physical properties and physiological characteristics that were determined from the literature. The effects of blood flow and of thermal conduction were modeled using the steady-state form of the bio-heat equation. Input parameters included core (arterial) temperature: normal (37 degrees C) or hyperthermic (40 degrees C), air temperature: warm (30 degrees C) or hot (40 degrees C), and sweat evaporation rate: 0, 0.25, or 0.50 l x m(-2) x h(-1). The resulting skin temperatures of the model ranged from 31.8 degrees C to 40.2 degrees C, values which are consistent with data obtained from the literature. Cerebral temperatures were generally insensitive to surface conditions (air temperature and evaporation rate), which affected only the most superficial level of the cerebrum (< or =1.5 mm) The remaining parenchymal temperatures were 0.2-0.3 degrees C above arterial temperatures, regardless of surface conditions. This held true even for the worst-case conditions combining core hyperthermia in a hot environment with zero evaporative cooling. Modeling showed that the low surface-to-volume ratio, low tissue conductivity, and high rate of cerebral perfusion combine to minimize the potential impact of surface cooling, whether by transcranial venous flow or by conduction through intervening layers to the skin or mucosal surfaces. The dense capillary network in the brain assures that its temperature closely follows arterial temperature and is controlled through systemic thermoregulation independent of head surface temperature. A review of the literature reveals several independent lines of evidence which support these findings and indicate the absence of functionally significant transcranial venous flow in either direction. Given the fact that humans sometimes work under conditions which produce face and scalp temperatures that are above core temperature, a transcranial thermal link would not necessarily protect the brain, but might instead increase its vulnerability to environmentally induced thermal injury.

Body Temperature↗
PubMed2005

A quantitative model to evaluate solubility relationship of polymorphs from their thermal properties.

PURPOSE: The objective of the study is to develop a model to estimate the solubility ratio of two polymorphic forms based on the calculation of the free energy difference of two forms at any temperature. This model can be used for compounds with low solubility (a few mole percent) in which infinite dilution can be approximated. METHODS: The model is derived using the melting temperature and heat of fusion for apparent monotropic systems, and the solid-solid transition temperature and heat of transition for apparent enantiotropic systems. A rigorous derivation also requires heat capacity (Cp) measurement of liquid and two solid forms. This model is validated by collecting thermal properties of polymorphs for several drugs using conventional or modulated differential scanning calorimetry. From these properties the solubility ratio of two polymorphs is evaluated using the model and compared with the experimental value at different temperatures. RESULTS: The predicted values using the full model agree well with the experimental ones. For the purpose of easy measurement, working equations without Cp terms are also applied. Ignoring Cp may result in an error of 10% or less, suggesting that the working equation is applicable in practice. Additional error may be generated for the apparent enantiotropic systems due to the inconsistency between the observed solid-solid transition temperature and the true thermodynamic transition temperature. This inconsistency allows the predicted solubility ratios (low melt/high melt) to be smaller. Therefore, a correction factor of 1.1 is recommended to reduce the error when the working equation is used to estimate the solubility ratio of an enantiotropic system. CONCLUSIONS: The study of the free energy changes of two crystalline forms of a drug allows for the development of a model that successfully predicts the solubility ratio at any temperature from their thermal properties. This model provides a thermodynamic foundation as to how the free energy difference of two polymorphs is reflected by their equilibrium solubilities. It also provides a quick and practical way of evaluating the relative solubility of two polymorphs from single differential scanning calorimetry runs.

Calorimetry, Differential Scanning↗
PubMed1981

Control of energy transformation of mitochondria. Analysis by a quantitative model.

A mathematical model of control of energy transformation in mitochondria is presented. The considered processes are: the proton translocation by the respiratory chain, the production of ATP by ATPase, the translocation of adenine nucleotides and of phosphate by their translocators, and a passive backflow of protons through the mitochondrial membrane. The mathematical equations expressing the steady-state kinetics of these processes and the relations between them were derived on the basis of current experimental data. The model predicts fairly well the values of the proton electrochemical gradient, of the ATP/ADP ratios within and outside mitochondria and of the distribution of phosphate between both compartments in different metabolic states of mitochondria. From the general agreement of model computations with experimental data, it is suggested that the electron flux through the respiratory chain is immediately controlled by the energy back-pressure of the proton electrochemical gradient, that the ATPase reaction is near equilibrium in phosphorylating mitochondria but that the adenine nucleotide exchange across the mitochondrial membrane requires some loss of energy. The latter is caused by an inhibition of the translocator by ATP from the outer side or by ADP from the inner side depending on the actual ATP/ADP in both compartments. It explains that no fixed relation exists between the rate of respiration and the phosphorylation state of extramitochondrial adenine nucleotides. The relation is modified by the concentration of phosphate and by intramitochondrial energy utilization.

Adenine Nucleotides↗