Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Kinetic modeling”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 235 records · Page 13Linked to original sources
PubMed1999

Effect of tetramethylammonium, choline and edrophonium on insect acetylcholinesterase: test of a kinetic model.

Cholinesterases display a non-Michaelian behaviour with respect to substrate concentration. With the insect enzyme, there is an activation at low substrate concentrations and an inhibition at high concentrations. Previous studies allow us to propose a kinetic model involving a secondary non-productive binding site for the substrate. Unexpectedly, this secondary site has a very high affinity for the substrate when the enzyme is free. On the contrary, when the catalytic site of the enzyme is occupied a strong decrease of this affinity was observed. Moreover, a substrate molecule bound to the peripheral site results in a global decrease of the acylation and/or the deacylation step. Kinetic studies with three reversible inhibitors, tetramethylammonium, edrophonium and choline supported the kinetic model and enable its further refinement.

Acetylcholinesterase↗
PubMed2003

Comparison of three kinetic models of HIV-1 infection: implications for optimization of treatment.

Clinical markers in the peripheral blood guide the treatment of human immunodeficiency virus type 1 (HIV-1). Likewise, many of the theoretical models developed to simulate infection only incorporate variables in the blood. To test the suitability of blood-only models, three distinct models of HIV infection kinetics are compared: "full model" including latently and actively infected cells and virus in the peripheral blood and lymphoid tissue (LT); "reduced model", including peripheral blood and LT without latent cells; and "blood model" including only actively infected cells and virus in the peripheral blood. Using the same parameter values for all three, qualitative differences are demonstrated between the blood model and its more inclusive counterparts. Additionally, optimization studies show that the reduced and blood models generate progressively lower optimal treatment levels relative to the full model when constant-level treatment is considered. These findings indicate that including the lymphoid tissue and latently infected cells into kinetic models may lead to differing conclusions with regard to optimal treatment and could be useful in guiding therapy even when plasma viral levels are below detectable limits.

Anti-HIV Agents↗
PubMed1982

A kinetic model for the pathogenesis of radiation lung damage.

The development of radiation-induced lung damage can be explained by a kinetic model, based on the assumption that this damage becomes manifest only when a critical proportion (K) of essential cells have ceased to function, and that the rate of loss of these cells following irradiation is linear and dose-dependent. The kinetic model relates the surviving fraction to the time to manifestation of radiation-induced lung damage and to constants, K and the cell cycle time, T. Predictions made from the model about the nature of the response to irradiation are, for the most part, fulfilled. The model can also be used to interpret the response to combined treatment with irradiation and cytotoxic drugs, including the much earlier manifestation of lung damage sometimes seen with such treatment.

Dose-Response Relationship, Radiation↗
PubMed2006

Photocatalytic degradation of gaseous benzene over TiO2/Sr2CeO4: kinetic model and degradation mechanisms.

Photocatalytic oxidation of benzene in air was carried out over TiO2/Sr2CeO4 catalysts. The prepared photocatalyst was characterized by SBET, UV-vis diffuse reflectance and XPS. TiO2/Sr2CeO4 absorbs much more visible light than TiO2 in the visible light region. The XPS spectrum shows that the binding energy value of Ti 2p3/2 transfers to a lower value. The main purpose was to investigate the kinetic model and degradation mechanisms. The kinetic data matched well with the Langmuir-Hinshelwood (L-H) kinetic model with the limiting rate constant and the adsorption constant in this case were 0.0064 mg l-1 min-1 and 9.2078 l mg-1, respectively. No gas-phase intermediates were detected by direct GC/FID analysis under the conditions despite the high benzene concentration. Ethyl acetate and (3-methyl-oxiran-2-yl)-methanol were two major identified intermediates which were accompanied by butylated hydroxytoluene, 2,6-bis(1,1-dimethylethyl)-4,4-dimethylycyclohe, 2,5-cyclohexadiene-1,4,dione,2,6-bis(1,1-dim). It is plausible that at least one of these less-reactive intermediates caused the deactivation of the photocatalyst. Finally, the photocatalytic oxidation mechanisms were speculated.

Benzene↗
PubMed2006

Mutual sensitization of the oxidation of nitric oxide and a natural gas blend in a JSR at elevated pressure: experimental and detailed kinetic modeling study.

The mutual sensitization of the oxidation of NO and a natural gas blend (methane-ethane 10:1) was studied experimentally in a fused silica jet-stirred reactor operating at 10 atm, over the temperature range 800-1160 K, from fuel-lean to fuel-rich conditions. Sonic quartz probe sampling followed by on-line FTIR analyses and off-line GC-TCD/FID analyses were used to measure the concentration profiles of the reactants, the stable intermediates, and the final products. A detailed chemical kinetic modeling of the present experiments was performed yielding an overall good agreement between the present data and this modeling. According to the proposed kinetic scheme, the mutual sensitization of the oxidation of this natural gas blend and NO proceeds through the NO to NO2 conversion by HO2, CH3O2, and C2H5O2. The detailed kinetic modeling showed that the conversion of NO to NO2 by CH3O2 and C2H5O2 is more important at low temperatures (ca. 820 K) than at higher temperatures where the reaction of NO with HO2 controls the NO to NO2 conversion. The production of OH resulting from the oxidation of NO by HO2, and the production of alkoxy radicals via RO2 + NO reactions promotes the oxidation of the fuel. A simplified reaction scheme was delineated: NO + HO2 --> NO2 + OH followed by OH + CH4 --> CH3 + H2O and OH + C2H6 --> C2H5 + H2O. At low-temperature, the reaction also proceeds via CH3 + O2 (+ M) --> CH3O2 (+ M); CH3O2 + NO --> CH3O + NO2 and C2H5 + O2 --> C2H5O2; C2H5O2 + NO --> C2H5O + NO2. At higher temperature, methoxy radicals are produced via the following mechanism: CH3 + NO2 --> CH3O + NO. The further reactions CH3O --> CH2O + H; CH2O + OH --> HCO + H2O; HCO + O2 --> HO2 + CO; and H + O2 + M --> HO2 + M complete the sequence. The proposed model indicates that the well-recognized difference of reactivity between methane and a natural gas blend is significantly reduced by addition of NO. The kinetic analyses indicate that in the NO-seeded conditions, the main production of OH proceeds via the same route, NO + HO2 --> NO2 + OH. Therefore, a significant reduction of the impact of the fuel composition on the kinetics of oxidation occurs.

Journal Article↗
PubMed1987

Kinetic models for predicting bioaccumulation of pollutants in ecosystems.

Steady state kinetic models, which may be useful for the prediction from simple data, of the bioaccumulation of liophilic pollutants in ecosystems are discussed. For some aquatic species, such as Mytilus edulis, bioconcentration factors (BCFs) are closely related to water solubilities, and octanol: water partition coefficients (Kows). In other cases, more complex models are necessary to take account of metabolism and/or uptake from food. Somewhat different considerations apply in the estimation of bioaccumulation factors (BFs) for terrestrial organisms that cannot excrete lipophilic compounds by diffusion into ambient water. The relationship between half-lives and BFs is discussed. Metabolism is necessary for the effective elimination of lipophilic pollutants by terrestrial animals, and a model is proposed for the prediction of BFs from kinetic data obtained from in vitro metabolism studies. If such a model can be successfully developed it will make possible the prediction of bioaccumulation of pollutants by a wide range of species which cannot be studied by present methods.

Journal Article↗
PubMedDate not supplied

Urea kinetic modelling: comparison of three methods.

It has been claimed that computed urea kinetic (UK) modelling in haemodialysed patients for the estimation of protein intake and of the relation between total dialyser urea clearance and distribution volume (Kt/V) leads to an overestimation of protein catabolic rate (PCR). In the present study three different methods of kinetic modelling for the determination of PCR and Kt/V are compared in 15 patients. The first method (MI) is the direct quantification method based on the collection of all urea eliminated from the body. The two other methods are based on an iterative computed calculation. The second method (MII) is the urea kinetic modelling method as described by Sargent. Dialyser clearances were measured directly and not estimated by theoretical extrapolation. The third method described here (MIII), is based on the indirect calculation of urea distribution volume (Vw) according to Watson and of dialyser clearances from this Vw and from pre- and post-dialysis urea concentrations. All three methods result in PCRs that are not significantly different (MI: 1.04 +/- 0.29; MII: 1.07 +/- 0.28; MIII: 1.05 +/- 0.24 mg/kg BW per 24 h; p greater than 0.05). When the results are correlated, the following results are obtained: MI vs MII: r = 0.76, p less than 0.001; MI vs MIII: r = 0.78, p less than 0.001; MII vs MIII: r = 0.90, p less than 0.001. For Kt/V virtually identical results were obtained for each of the methods under study. In conclusion, all methods under study seem equally reliable in determining mean PCR.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1992

A kinetic model of the agglutination process.

We propose a kinetic model of the aggregation process in a system consisting of two different types of particles. Aggregating particles (cells) are polyvalent and bear on the surface a huge number of binding sites for the other type of particles, ligands. The ligand is bivalent and has two identical active sites for binding to cells. The cross-linking of the cells by the ligands causes the aggregation phenomenon called agglutination. We obtained the analytical solution of this model task describing the time dependence of the aggregate mean size versus the composition of the system. The comparison of the analytical solution with the experimental data for the agglutination of bacterial cells by bivalent antibodies shows that the main factors affecting agglutination were correctly taken into account.

Bacterial Adhesion↗
PubMed2005

Towards a quantitative understanding of horizontal gene transfer: a kinetic model.

In this work, we present a simple kinetic model of horizontal gene transfer. It describes the processes of gene duplication, mutation, gene transfer and the regulation of the total size of the genome for genetically homogeneous prokaryotic species or strains. The emerging nonlinear system of first-order differential equations can be linearized at the stationary point. For selected models, we give an analytical solution for the number of foreign and native genes within a species. We identify a regime characterized by a fast gene transfer rate and species with a mixed genome, a slow gene transfer regime with pure organisms, and a crossover region. The data are compared to experiments, and the biological implications of our model are discussed.

Animals↗
PubMedDate not supplied

Bedside formulas for K.t/V. A kinder, gentler approach to urea kinetic modeling.

Based on an empiric analysis of urea kinetic modeling equations, three formulas were derived for use at the bedside: (F1) Ob.t = 14.W.(K.t/V); (F2) target R = e-K.t/V + 0.03 + UF/W; (F3) K.t/V = -In (R - 0.03 - UF/W); where Qb = blood flow (ml/min); t = session length (h); R = post/pre BUN; UF = ultrafiltrate volume (L/session); and W = postdialysis weight (kg). When a particular K.t/V is desired, F1 is used to estimate Qb for a given W and t. Qb, t, and/or dialyzer type are then adjusted until R = target R calculated by F2 (based on target K.t/V, UF, and W). F3 estimates delivered K.t/V from R, UF, and W. These formulas were validated against 336 conventional 3-point modeling sessions in 256 patients. The multiplier "14" in F1 actually averaged 12.5 +/- 2.8, the large standard deviation suggesting that use of F1 would often result in K.t/V values substantially above or below the target K.t/V. The main causes of error were unusual V/W or K/Qb. On the other hand, F2 and F3 were highly accurate: target R estimated by F2 predicted actual R (at a given K.t/V, UF, and W) very well (% error = 0.65 +/- 2.3); K.t/V estimated by F3 predicted actual K.t/V (% error = 0.74 +/- 2.7). The results suggest that attainment of a target R (F2) will ensure that the target K.t/V is being delivered; F3 is useful to estimate K.t/V.F1 is an initial estimate only of the dialysis Rx; it must be followed by adjustment of t, Qb, or dialyzer until target R (from F2) is attained.

Blood Flow Velocity↗
PubMed1993

Abbreviated method for urea kinetic modeling in continuous ambulatory peritoneal dialysis patients.

Urea kinetic modeling (UKM) is an established method for quantitating hemodialysis, with target values clearly defined. Precise methods for measuring continuous ambulatory peritoneal dialysis (CAPD) prescriptions are less well-defined, and 24-hour collections of dialysate effluent are logistically impractical. UKM parameters derived from an abbreviated (4-hour) collection period were compared with simultaneously obtained 24-hour collections of urine and dialysate effluent in 22 CAPD patients. Daily Kt/V was calculated from total (residual renal and peritoneal) urea clearance and an anthropometric-derived total body water volume. Results yielded from the 24-hour collection included a mean Kt/V of 0.29 +/- 0.09, and mean protein catabolic rate (PCR) of 0.84 +/- 0.24 g/kg/day. Daily Kt/V values were calculated from each individual dialysate cycle. The first morning cycle after an overnight dwell correlated best with results obtained using 24-hour collections (r = 0.921; p < 0.0001) with no significant differences in Kt/V found (p = 0.454) between the short and 24-hour methods. Daily Kt/V values converted by exponential transformation to a thrice-weekly hemodialysis value yielded a Kt/V equivalent of 1.02 +/- 0.40. UKM using an abbreviated collection period is an accurate and practical tool for quantitating CAPD adequacy in a routine clinical setting.

Blood Urea Nitrogen↗
PubMed1985

A kinetic model describing the interaction of bovine prothrombin fragment 1 with calcium ions.

A kinetic model is derived for the interaction of bovine prothrombin fragment 1 with calcium ions. The model requires binding of a minimum of two calcium ions for induction of the observed biphasic fluorescence decrease as a function of time. The model is shown to be consistent with experimental kinetic and equilibrium data by fitting theoretical curves for the biphasic fluorescence change to the data through exact solution of the nonlinear differential rate equations derived from the model. The rate constants for the binding of these two required calcium ions are calculated from the solutions as best fit parameters. The thermodynamic equilibrium constants, K1 and K2, for the binding of these two calcium ions are calculated from ratios of the forward and reverse rate constants as 0.6 X 10(4) and 5.4 X 10(4), respectively. Thus, the model correctly predicts positively cooperative calcium ion binding for at least the two calcium ions required to induce fluorescence quenching.

Animals↗
PubMed2001

Kinetic modeling of pyruvic acid ozonation in aqueous solutions catalyzed by Mn(II) and Mn(IV) ions.

The ozonation of pyruvic acid (2-ketopropionic acid) in aqueous solutions, catalyzed by Mn(II) and Mn(IV) ions, has been studied at three different pH values (pH = 1.1, 2.0 and 3.0). A mathematical model of the unsteady operation of the experimental reactor has been developed, which takes into account the reactions occurring in the liquid phase and the ozone mass transfer from the gas bubbles. Those reactions have been described with two alternative kinetic models, both made out of four elementary steps. The two kinetic models correlate the experimental data with a fair accuracy, respectively at the lowest and at the highest pH examined. In particular, at pH = 3.0, the ozonation results are inhibited by the acetate ions produced by the reaction itself. This effect has been correctly described in the terms of a complex formed with the low oxidation-state manganese, which successively reacts with the dissolved ozone.

Hydrogen-Ion Concentration↗
PubMed2006

Kinetic modeling of adsorption of di-2-pyridylketone salicyloylhydrazone on silica gel.

The kinetics of DPKSH (di-2-pyridylketone salicyloylhydrazone) adsorption onto silica gel has been investigated at (25+/-1) degrees C and pH 1 and 4.7. The kinetics of adsorption of DPKSH is discussed using three kinetic models, the first-order Lagergren model, the pseudo-second-order model, and the intraparticle diffusion model. The adsorption of DPKSH, at pH 1 and 4.7, onto silica gel proceeds according to the pseudo-second-order model and the correlation coefficients were very close to 1. The intraparticle diffusion of DPKSH molecules within the silica gel particles was identified as the rate-limiting step. The parameters of the pseudo-second-order model are q(max,calc)=1.02 x 10(-4) and 1.5 x 10(-4) g DPKSH/g silica; k(2)=3.01 x 10(4) and 9.67 x 10(4) h(-1)g silica/g DPKSH, respectively, for pH 1 and 4.7.

Adsorption↗
PubMed2006

Kinetic modelling of phenol co-oxidation using horseradish peroxidase.

Phenol is an industrial pollutant and its removal from industrial wastewaters is of great importance. In order to design optimised phenol removal procedures by using horseradish peroxidase-based systems, there are some points that have to be dealt with. One of the most important issues is the need for reliable kinetics as this is one of the difficulties found during process scale-up. Although simplified kinetics can be used for limited ranges of operating conditions, they are not usually reliable for the description of varying process conditions. The present work describes the implementation of a kinetic model, based on a mechanism, for the co-oxidation of phenol and 4-aminoantipyrine (Am-NH2), which is used as a chromogen agent, with hydrogen peroxide as the oxidant. The model covers not only the variation of the concentrations of all the species involved, but also the effect of temperature in the reaction. The estimation of kinetic rate constants and activation energies for the various steps in the mechanism is performed with a single optimisation procedure, and all the experimental results are described using a unique set of parameters, which, thus, is valid over an extended range of operating conditions. The mechanism allowed the determination of a reliable kinetic model which is appropriate for the range of experimental conditions used. The computational model was also tested with an independent set of experiments with different conditions from the ones for which the parameters were estimated.

Ampyrone↗
PubMedDate not supplied

[Kinetic model and mechanism of regulation of a multienzyme system of thromboxane synthesis].

A kinetic model has been suggested for the thromboxane synthesis polyenzyme system, taking into account the inactivation of a limiting enzyme, prostaglandin H-synthetase, in the course of the reaction. The model also includes the effect of phospholipase, adenylate cyclase, as well as the "outflows" of the components from the system, and basic regulatory effects in the system. A mathematical description of the model is given, and numerical solutions of the system of equations obtained for a wide variety of parameters. An analysis of the kinetic responses of the polyenzyme system shows that: 1) the system is highly conserved with respect to thromboxane concentration changes; 2) two cardinally different modes of the system are registered; they correspond to two insignificantly differing thromboxane steady-state levels; 3) transition of the system from one mode to the other is controlled by the phospholipase activity level which is sensitive to a change in the concentration of the regulator (cyclo-AMP or Ca ions) in the system. It is presumed that the two thromboxane steady-state levels are of physiological significance.

Arachidonic Acid↗
PubMed1996

[Use of urea kinetic modeling for evaluating the efficacy of reusing capillary dialyzers].

The aim of the study was to evaluate the influence of follow fiber dialyzers reprocessing procedure on urea kinetic modeling parameters, dialysis effectiveness for small molecules and effective clearance/predicted clearance ratio. Fifty patients (27 F, 23 M) aged 18-61 years (mean 47) being on maintenance hemodialysis due to end stage renal failure for 4-136 months were included into the study. Patients were treated 3 times a week with blood flow 160-290 ml/min and dialysate flow 500 ml/min. The dialysis time was calculated individually based on urea kinetic modeling parameters. Reprocessing of dialyzers was performed using Renatron RS 8300 and Renalin as sterilized agent. Dialysers with ppr below 80% were excluded from the use. Mean values of dialysis index Kt/V, TAC and dialysis effectiveness (Ct/C0) for urea, creatinine, uric acid and kalium as well as values of effective/predicted clearance ratio for consecutive reprocessing procedures were compared with the results obtained for the new dialyzers. There was no significant influence of reprocessing procedure on Kt/V, TAC and Ct/C0 for tested substances and studied clearances. The obtained results indicates that dialysers reprocessing procedure performed according to the described protocol was safe and didn't decrease dialysis effectiveness.

Adolescent↗
PubMedDate not supplied

A computational procedure for optimal engineering interventions using kinetic models of metabolism.

The identification of optimal intervention strategies is a key step in designing microbial strains with enhanced capabilities. In this paper, we propose a general computational procedure to determine which genes/enzymes should be eliminated, repressed or overexpressed to maximize the flux through a product of interest for general kinetic models. The procedure relies on the generalized linearization of a kinetic description of the investigated metabolic system and the iterative application of mixed-integer linear programming (MILP) optimization to hierarchically identify all engineering interventions allowing for reaction eliminations and/or enzyme level modulations. The effect of the magnitude of the allowed changes in concentrations and enzyme levels is investigated, and a variant of the method to explore high-fold changes in enzyme levels is also analyzed. The proposed framework is demonstrated using a kinetic model modeling part of the central carbon metabolism of E. coli for serine overproduction. The proposed computational procedure is a general approach that can be applied to any metabolic system for which a kinetic description is provided.

Computer Simulation↗