scholarly journals Mechanism and Micro Kinetic Model for Electroreduction of CO2 on Pd/C: The Role of Different Palladium Hydride Phases

ACS Catalysis ◽  
2021 ◽  
pp. 6883-6891
Author(s):  
Martijn J. W. Blom ◽  
Wim P. M. van Swaaij ◽  
Guido Mul ◽  
Sascha R. A. Kersten
Keyword(s):  
Kinetic Model ◽  
Palladium Hydride ◽  
Hydride Phases

Kinetic Aspects of the Interplay of Cancer and the Immune System

2019 ◽  
Vol 14 (02) ◽  
pp. 101-114 ◽  
Author(s):  
Vladimir P. Zhdanov
Keyword(s):  
Stem Cells ◽  
Immune System ◽  
Kinetic Model ◽  
Human Population ◽  
Lifetime Risk ◽  
Risk Of Cancer

The understanding of the interplay between cancer and the immune system is still limited. Herein, I focus on two aspects of this interplay. First, I propose a kinetic model describing the likely role of the immune system in the lifetime risk of cancer at the level of the whole human population. For each tissue, the risk is predicted to be influenced by the heterogeneity of the population and to depend exponentially on time. The expression for the risk does not, however, depend explicitly on the total number of divisions of the corresponding stem cells. For this reason, the correlation with the latter number can only be indirect. Second, using another kinetic framework, I describe how the growth of a few tumors can depend on their interaction via the immune system. The analysis shows that depending on specific details, the tumors of different sizes tend either to reach the same size or remain to be of different sizes.

Impact of non-thermal electrons on spatial damping: a kinetic model for the parallel propagating modes

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Muhammad Sarfraz ◽  
Gohar Abbas ◽  
Hashim Farooq ◽  
I. Zeba
Keyword(s):  
Kinetic Model ◽  
Wave Spectrum ◽  
Field Approximation ◽  
Weak Field ◽  
Distribution Functions ◽  
Global Perspective ◽  
Energetic Electrons ◽  
Thermal Anisotropy ◽  
Spatial Damping

Abstract A sequence of in situ measurements points the presence of non-thermal species in the profile of particle distributions. This study highlights the role of such energetic electrons on the wave-spectrum. Using Vlasov–Maxwell’s model, the dispersion relations of the parallel propagating modes along with the space scale of damping are discussed using non-relativistic bi-Maxwellian and bi-Kappa distribution functions under the weak field approximation, i.e., ω − k . v > Ω 0 $\left\vert \omega -\mathbf{k}.\mathbf{v}\right\vert { >}{{\Omega}}_{0}$ . Power series and asymptotic expansions of plasma dispersion functions are performed to derive the modes and spatial damping of waves, respectively. The role of these highly energetic electrons is illustrated on real frequency and anomalous damping of R and L-modes which is in fact controlled by the parameter κ in the dispersion. Further, we uncovered the effect of external magnetic field and thermal anisotropy on such spatial attenuation. In global perspective of the kinetic model, it may be another step.

Pulmonary reduction of an intravascular redox polymer

2001 ◽  
Vol 280 (6) ◽  
pp. L1290-L1299 ◽  
Author(s):  
Said H. Audi ◽  
Robert D. Bongard ◽  
Yoshiyuki Okamoto ◽  
Marilyn P. Merker ◽  
David L. Roerig ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Superoxide Dismutase ◽  
Electron Transport ◽  
Kinetic Model ◽  
Electron Acceptors ◽  
Redox Polymer ◽  
Pulmonary Endothelial Cells ◽  
Equilibrium Level ◽  
A Cell

Pulmonary endothelial cells in culture reduce external electron acceptors via transplasma membrane electron transport (TPMET). In studying endothelial TPMET in intact lungs, it is difficult to exclude intracellular reduction and reducing agents released by the lung. Therefore, we evaluated the role of endothelial TPMET in the reduction of a cell-impermeant redox polymer, toluidine blue O polyacrylamide (TBOP+), in intact rat lungs. When added to the perfusate recirculating through the lungs, the venous effluent TBOP+concentration decreased to an equilibrium level reflecting TBOP+ reduction and autooxidation of its reduced (TBOPH) form. Adding superoxide dismutase (SOD) to the perfusate increased the equilibrium TBOP+ concentration. Kinetic analysis indicated that the SOD effect could be attributed to elimination of the superoxide product of TBOPH autooxidation rather than of superoxide released by the lungs, and experiments with lung-conditioned perfusate excluded release of other TBOP+ reductants in sufficient quantities to cause significant TBOP+ reduction. Thus the results indicate that TBOP+ reduction is via TPMET and support the utility of TBOP+ and the kinetic model for investigating TPMET mechanisms and their adaptations to physiological and pathophysiological stresses in the intact lung.

scholarly journals A kinetically defined Na+/H+ antiporter within a mathematical model of the rat proximal tubule.

1995 ◽  
Vol 105 (5) ◽  
pp. 617-641 ◽  
Author(s):  
A M Weinstein
Keyword(s):  
Kinetic Model ◽  
Proximal Tubule ◽  
Membrane Vesicles ◽  
Model Calculations ◽  
Kinetic Formulation ◽  
Luminal Membrane ◽  
Least Squares Fit ◽  
Velocity Effect ◽  
Rat Proximal Tubule

The luminal membrane antiporter of the proximal tubule has been represented using the kinetic formulation of E. Heinz (1978. Mechanics and Engergetics of Biological Transport. Springer-Verlag, Berlin) with the assumption of equilibrium binding and 1:1 stoichiometry. Competitive binding and transport of NH+4 is included within this model. Ion affinities and permeation velocities were selected in a least-squares fit to the kinetic parameters determined experimentally in renal membrane vesicles (Aronson, P.S., M.A. Suhm, and J. Nee. 1983. Journal of Biological Chemistry. 258:6767-6771). The modifier role of internal H+ to enhance transport beyond the expected kinetics (Aronson, P.S., J. Nee, and M. A. Suhm. 1982. Nature. 299:161-163) is represented as a velocity effect of H+ binding to a single site. This kinetic formulation of the Na+/H+ antiporter was incorporated within a model of the rat proximal tubule (Weinstein, A. M. 1994. American Journal of Physiology. 267:F237-F248) as a replacement for the representation by linear nonequilibrium thermodynamics (NET). The membrane density of the antiporter was selected to yield agreement with the rate of tubular Na+ reabsorption. Simulation of 0.5 cm of tubule predicts that the activity of the Na+/H+ antiporter is the most important force for active secretion of ammonia. Model calculations of metabolic acid-base disturbances are performed and comparison is made among antiporter representations (kinetic model, kinetic model without internal modifier, and NET formulation). It is found that the ability to sharply turn off Na+/H+ exchange in cellular alkalosis substantially eliminates the cell volume increase associated with high HCO3- conditions. In the tubule model, diminished Na+/H+ exchange in alkalosis blunts the axial decrease in luminal HCO3- and thus diminishes paracellular reabsorption of Cl-. In this way, the kinetics of the Na+/H+ antiporter could act to enhance distal delivery of Na+, Cl-, and HCO3- in acute metabolic alkalosis.

FEASIBILITY OF THE NON-CODING RNA GRADIENTS IN CELLS

2009 ◽  
Vol 04 (03) ◽  
pp. 267-272 ◽  
Author(s):  
VLADIMIR P. ZHDANOV
Keyword(s):  
Kinetic Model ◽  
Gene Transcription ◽  
Eukaryotic Cells ◽  
Model Parameters ◽  
Protein Association ◽  
Non Coding Rna ◽  
A Cell ◽  
Non Coding Rnas ◽  
Spatio Temporal

In eukaryotic cells, the gene transcription often results in the formation of non-coding RNAs (ncRNAs). The key function of such RNAs is to bind to and modulate the activity of mRNAs and/or proteins. To scrutinize this ncRNA function in a cell, the author (i) proposes a spatio-temporal kinetic model, including ncRNA–protein association and degradation, (ii) derives a criterion of feasibility of the ncRNA gradients, and (iii) shows that this criterion can be satisfied with physically reasonable values of the model parameters. Thus, the ncRNA gradients are feasible. For the ncRNA–mRNA association and degradation, the situation is similar. The likely biological role of such gradients is open for debate.

Mathematical modelling of Wnt/β-catenin signalling

2010 ◽  
Vol 38 (5) ◽  
pp. 1281-1285 ◽  
Author(s):  
Bente Kofahl ◽  
Jana Wolf
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Kinetic Model ◽  
Mathematical Modelling ◽  
Theoretical Models ◽  
Theoretical Approaches ◽  
Canonical Wnt ◽  
Plos Biol ◽  
Transcriptional Feedback

The Wnt/β-catenin pathway plays an important role in development and disease. Theoretical approaches have been used to describe this pathway and have provided intriguing insights into its signalling characteristics. In the present paper, we review mathematical models of the pathway. We focus on a quantitative kinetic model for canonical Wnt/β-catenin signalling describing the reactions of the pathway's core compounds [Lee, Salic, Krüger, Heinrich and Kirschner (2003) PLoS Biol. 1, 116–132]. Numerous modifications and further analyses with respect to signalling characteristics, transcriptional feedback and cross-talk were performed. In addition, the role of β-catenin in gene expression and cell–cell adhesion as well as spatial aspects of signalling are investigated in various theoretical models.

scholarly journals The Role of the Cytoplasmic Pore in Inward Rectification of Kir2.1 Channels

2007 ◽  
Vol 130 (2) ◽  
pp. 145-155 ◽  
Author(s):  
Harley T. Kurata ◽  
Wayland W. Cheng ◽  
Christine Arrabit ◽  
Paul A. Slesinger ◽  
Colin G. Nichols
Keyword(s):  
Steady State ◽  
Kinetic Model ◽  
Cytoplasmic Domain ◽  
Inward Rectification ◽  
Kir Channels ◽  
Voltage Dependent ◽  
Pore Lining ◽  
Blocking Kinetics

Steeply voltage-dependent block by intracellular polyamines underlies the strong inward rectification properties of Kir2.1 and other Kir channels. Mutagenesis studies have identified several negatively charged pore-lining residues (D172, E224, and E299, in Kir2.1) in the inner cavity and cytoplasmic domain as determinants of the properties of spermine block. Recent crystallographic determination of the structure of the cytoplasmic domains of Kir2.1 identified additional negatively charged residues (D255 and D259) that influence inward rectification. In this study, we have characterized the kinetic and steady-state properties of spermine block in WT Kir2.1 and in mutations of the D255 residue (D255E, A, K, R). Despite minimal effects on steady-state blockade by spermine, D255 mutations have profound effects on the blocking kinetics, with D255A marginally, and D255R dramatically, slowing the rate of block. In addition, these mutations result in the appearance of a sustained current (in the presence of spermine) at depolarized voltages. These features are reproduced with a kinetic model consisting of a single open state, two sequentially linked blocked states, and a slow spermine permeation step, with residue D255 influencing the spermine affinity and rate of entry into the shallow blocked state. The data highlight a “long-pore” effect in Kir channels, and emphasize the importance of considering blocker permeation when assessing the effects of mutations on apparent blocker affinity.

Role of gastric inhibitory polypeptide in postprandial hyperinsulinemia of obesity

1988 ◽  
Vol 254 (6) ◽  
pp. E767-E774 ◽  
Author(s):  
L. R. Roust ◽  
M. Stesin ◽  
V. L. Go ◽  
P. C. O'Brien ◽  
R. A. Rizza ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Kinetic Model ◽  
Healthy Subjects ◽  
Gastric Inhibitory Polypeptide ◽  
Volume Of Distribution ◽  
Insulin Clearance ◽  
C Peptide ◽  
Obese Subjects ◽  
Secretion Rates

To assess the contribution of gastric inhibitory polypeptide (GIP) to the postprandial hyperinsulinemia of obesity, secretion rates of GIP (generated from kinetic analyses from infusions of porcine GIP) and insulin (from C-peptide applied to a validated kinetic model) to meals of 3 sizes were determined in 10 obese (5 male and 5 female) and 10 lean, sex- and age-matched healthy subjects. Although the postprandial secretion rates of GIP were greater in obese subjects (P = 0.03), postprandial concentrations of GIP were not. The latter may be explained by the greater volume of distribution of GIP in obese subjects (P = 0.036). Secretion rates and volume of distribution of GIP were correlated (r = 0.652, P less than 0.01). Despite excessive integrated postprandial (P = 0.010) insulin concentrations, insulin secretion was not significantly different between obese and lean subjects. We conclude that 1) although postprandial plasma GIP concentrations are normal, GIP secretion is increased in obesity, 2) the postprandial hyperinsulinemia of obesity is not due to excessive insulin secretion but is likely secondary to altered insulin clearance, and 3) GIP cannot account for the hyperinsulinemia of obesity through its insulinotropic action.

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