Ranjan K. Dash

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New mathematical model equations for O2 and CO2 saturations of hemoglobin ( $$ S_{{{\text{HbO}}_{ 2} }} $$ and $$ S_{{{\text{HbCO}}_{ 2} }} $$ ) are developed here from the equilibrium binding of O2 and CO2 with hemoglobin inside RBCs. They are in the form of an invertible Hill-type equation with the apparent Hill coefficients $$ K_{{{\text{HbO}}_{ 2} }} $$(More)
Calcium is a key ion and is known to mediate signalling pathways between cytosol and mitochondria and modulate mitochondrial energy metabolism. To gain a quantitative, biophysical understanding of mitochondrial Ca(2+) regulation, we developed a thermodynamically balanced model of mitochondrial Ca(2+) handling and bioenergetics by integrating kinetic models(More)
BACKGROUND The alterations in skeletal muscle structure and function after prolonged periods of unloading are initiated by the chronic lack of mechanical stimulus of sufficient intensity, which is the result of a series of biochemical and metabolic interactions spanning from cellular to tissue/organ level. Reduced activation of skeletal muscle alters the(More)
A detailed nonlinear four-region (red blood cell, plasma, interstitial fluid, and parenchymal cell) axially distributed convection-diffusion-permeation-reaction-binding computational model is developed to study the simultaneous transport and exchange of oxygen (O $$_{2}$$ ) and carbon dioxide (CO $$_{2}$$ ) in the blood–tissue exchange system of the heart.(More)
Skeletal muscle can maintain ATP concentration constant during the transition from rest to exercise, whereas metabolic reaction rates may increase substantially. Among the key regulatory factors of skeletal muscle energy metabolism during exercise, the dynamics of cytosolic and mitochondrial NADH and NAD+ have not been characterized. To quantify these(More)
Cardiac mitochondrial matrix (m) free Ca(2+) ([Ca(2+)]m) increases primarily by Ca(2+) uptake through the Ca(2+) uniporter (CU). Ca(2+) uptake via the CU is attenuated by extra-matrix (e) Mg(2+) ([Mg(2+)]e). How [Ca(2+)]m is dynamically modulated by interacting physiological levels of [Ca(2+)]e and [Mg(2+)]e and how this interaction alters bioenergetics are(More)
Assessment of the rate of muscle oxygen consumption, UO2m, in vivo during exercise involving a large muscle mass is critical for investigating mechanisms regulating energy metabolism at exercise onset. While UO2m is technically difficult to obtain under these circumstances, pulmonary oxygen uptake, VO2p, can be readily measured and used as a proxy to UO2m.(More)
While the theory of enzyme kinetics is fundamental to analyzing and simulating biochemical systems, the derivation of rate equations for complex mechanisms for enzyme-catalyzed reactions is cumbersome and error prone. Therefore, a number of algorithms and related computer programs have been developed to assist in such derivations. Yet although a number of(More)
NADH-ubiquinone oxidoreductase (Complex I, European Commission No. 1.6.5.3) is one of the respiratory complexes that generate the proton-motive force required for the synthesis of ATP in mitochondria. The catalytic mechanism of Complex I has not been well understood, due to the complicated structure of this enzyme. Here, we develop a kinetic model for(More)