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We demonstrate that the maximum entropy production principle (MEPP) serves as a physical selection principle for the description of the most probable non-equilibrium steady states in simple enzymatic reactions. A theoretical approach is developed, which enables maximization of the density of entropy production with respect to the enzyme rate constants for the enzyme reaction in a steady state. Mass and Gibbs free energy conservations are considered as optimization constraints. In such a way computed optimal enzyme rate constants in a steady state yield also the most uniform probability distribution of the enzyme states. This accounts for the maximal Shannon information entropy. By means of the stability analysis it is also demonstrated that maximal density of entropy production in that enzyme reaction requires flexible enzyme structure, which enables rapid transitions between different enzyme states. These results are supported by an example, in which density of entropy production and Shannon information entropy are numerically maximized for the enzyme Glucose Isomerase.

The authors developed a mathematical model of arachidonic acid (AA) degradation to prostaglandins (PGs) and leukotrienes (LTs), which are implicated in the processes of inflammation and hypersensitivity to non‐steroidal anti‐inflammatory drugs (NSAIDs). The model focuses on two PGs (PGE(2) and PGD(2)) and one LT (LTC(4)), their % increases and their ratios. Results are compared with experimental studies obtained from non‐asthmatics (NAs), and asthmatics tolerant (ATA) or intolerant (AIA) to aspirin. Simulations are carried out for predefined model populations NA, ATA and three AIA, based on the differences of two enzymes, PG E synthase and/or LTC(4)‐synthase in two states, that is, no‐inflammation and inflammation. Their model reveals that the model population with concomitant malfunctions in both enzymes is the most sensitive to NSAIDs, since the duration and the capacity for bronchoconstriction risk are highest after simulated oral dosing of indomethacin. Furthermore, inflammation prolongs the duration of the bronchoconstriction risk in all AIA model populations, and the sensitivity analysis reveals multiple possible scenarios leading to hypersensitivity, especially if inflammatory processes affect the expression of multiple enzymes of the AA metabolic pathway. Their model estimates the expected fold‐changes in enzyme activities and gives valuable information for further targeted transcriptomic/proteomic and metabolomic studies.

It is shown that Onsager's principle of the least dissipation of energy is equivalent to the maximum entropy production principle. It is known that solutions of the linearized Boltzmann equation make extrema of entropy production. It is argued, in the case of stationary processes, that this extremum is a maximum rather than a minimum., 12 pages, revtex4

A procedure for maximization of the density of entropy production in a single stationary two-step enzyme reaction is developed. Under the constraints of mass conservation, fixed equilibrium constant of a reaction and fixed products of forward and backward enzyme rate constants the existence of maximum in the density of entropy production is demonstrated. In the state with maximal density of entropy production the optimal enzyme rate constants, the stationary concentrations of the substrate and the product, the stationary product yield as well as the stationary reaction flux are calculated. The test, whether these calculated values of the reaction parameters are consistent with their corresponding measured values, is performed for the enzyme Glucose Isomerase. It is found that calculated and measured rate constants agree within an order of magnitude, whereas the calculated reaction flux and the product yield differ from their corresponding measured values for less than 20 % and 5 %, respectively. This indicates that the enzyme Glucose Isomerase, considered in a non-equilibrium stationary state, as found in experiments using the continuous stirred tank reactors, possibly operates close to the state with the maximum in the density of entropy production.

Ovaj rad obrađuje problem predviđanja mehaničkog odziva dijela zajedničke arterije glave (ZAG). Zaostala naprezanja u arteriji uzeta su u obzir uporabom termo-mehaničke analogije (TMA), koja se primjenjuje u ovom radu za potrebe modeliranja mehaničkog odziva dvoslojne strukture stijenke arterije. Obično se modeliranju zaostalih naprezanja u arteriji pristupi s uzdužno otvorenim modelom arterije, tzv. cut-open section, koji u slučaju bolesnikove arterije nije poznat. S TMA pristupom, umjesto uporabe uzdužno prerezane stijenke arterije, koja doduše osigurava početno stanje bez zaostalih naprezanja, u termo-mehaničkom modelu zajedničke arterije glave također je postignuto početno stanje bez zaostalih naprezanja ali na modelu stvarne, in vivo arterije. Tim pristupom, zaostalo naprezanje u ZAG aproksimirano je podvrgavanjem ZAG modela obujamskom deformacijom, t.j. primjenom odgovarajućih termičkih dilatacija. Takav pristup potvrđen je na modelu arterije kružnog presjeka i postizanjem stanja bez naprezanja u slučaju uzdužnog rezanja stijenke., This work deals with the prediction of the mechanical response of a section of a human common carotid artery (CCA). The arterial residual stress state is accounted for using the thermomechanical analogy (TMA) approach, which is applied in this work to model the mechanical response of a two-layered arterial structure. The starting point to model the arterial residual stress state is normally the cut-open section, which is in the case of patient-specific artery not known. With TMA approach, however, instead of using the arterial zero-stress cut-open configuration to predict the arterial residual stress state, a thermomechanical model of the CCA is considered with its zero-stress geometry defined based on the actual CCA in vivo configuration. The approximation to the CCA residual stress state is then obtained by exposing the auxiliary CCA model to a volumetric deformation, enforced via adequate thermal dilatations. The approach is validated on a circular arterial model and by predicting the CCA cut-open zero-stress state.

The purpose of this work is to predict the effect of impaired red blood cells (RBCs) deformability on blood flow conditions in human carotid artery bifurcation. First, a blood viscosity model is developed that predicts the steady-state blood viscosity as a function of shear rate, plasma viscosity, and mechanical (and geometrical) properties of RBC's. Viscosity model is developed by modifying the well-known Krieger and Dougherty equation for monodisperse suspensions by using the dimensional analysis approach. With the approach, we manage to account for the microscopic properties of RBC's, such as their deformability, in the macroscopic behavior of blood via blood viscosity. In the second part of the paper, the deduced viscosity model is used to numerically predict blood flow conditions in human carotid artery bifurcation. Simulations are performed for different values of RBC's deformability and analyzed by investigating parameters, such as the temporal mean wall shear stress (WSS), oscillatory shear index (OSI), and mean temporal gradient of WSS. The analyses show that the decrease of RBC's deformability decrease the regions of low WSS (i.e., sites known to be prevalent at atherosclerosis-prone regions); increase, in average, the value of WSS along the artery; and decrease the areas of high OSI. These observations provide an insight into the influence of blood's microscopic properties, such as the deformability of RBC's, on hemodynamics in larger arteries and their influence on parameters that are known to play a role in the initiation and progression of atherosclerosis.

The prediction of the arterial zero-stress state is as of yet an unresolved problem in the field of modelling the mechanical response of patientspecific arteries. This is because the configuration associated with arterial zero-stress state is impossible to obtain experimentally. However, the zero-stress configuration (or, equivalently, the residual stresses related to this configuration) represents the crucial data of any numerical analysis. In this study, the mechanical response of a pre-stressed, pressurised, hyperelastic tube (representing the artery) is determined without knowing the initial zero-stress configuration of the artery. Instead, to predict the arterial residual (bending and stretching) stresses, a corresponding thermomechanical analogy is used. As shown in the paper, the arterial residual stress state can equally be obtained by thermally loading a properly defined closed tube. Thus, based on the loaded state of the corresponding thermomechanical model, the arterial residual stress sate is constructed, from where the arterial loaded state can be obtained. The initial configuration of the thermomechanical model is defined on the basis of the arterial loaded configuration. The methodology is validated by predicting the zero-stress state of the artery. The predicted equilibrium state of the artery, when cut longitudinally and transversally, has the form of an opened-up tube with a relatively low stress state in comparison to the arterial residual stresses. The results thus demonstrate that arterial residual stresses that are predicted with the corresponding thermomechanical model exhibited the bending distribution, which proves the methodology to be adequate. Določitev breznapetostnega stanja arterij predstavlja še vedno nerazrešen problem na področju numeričnega modeliranja mehanskega odziva realnih arterij. Breznapetostno stanje arterije, ki ima v splošnem obliko krožnega sektorja, je namreč eksperimentalno nemogoče določiti. Oblika breznapetostnega stanja (oziroma temu pripadajoče zaostalo napetostno stanje) pa je pomembno zato, ker predstavlja začetno stanje in tako ključen podatek sleherne numerične analize. Arterije se za karakterizacijo njihovega mehanskega odziva običajno obravnava kot idealno krožne cevi, to pomeni idealno krožne in ravne. Takšna poenostavitev omogoča določitev zaostalih napetosti arterije brez poznavanja njihovega breznapetostnega stanja. Prisotnost zaostalih napetosti je posledica homogenizacije odziva arterij in vivo. Napetostno stanje arterije in vivo bi bilo namreč izrazito nehomogeno z velikim transmuralnim gradientom brez upoštevanja zaostalih napetosti. Zaradi njihove porazdelitve skozi debelino žilne stene se jih običajno asociira z upogibnimi napetostmi. Na notranji površini kolobarja so zaostale napetosti tlačne, medtem ko so na zunanji površini natezne.