Thermodynamics and dynamics of flowing polymer solutions and blends

Passem revista a les idees bàsiques i els principals resultats dels nostres estudis sobre els efectes induïts per gradients de velocitat en dissolucions i mescles de polímers, en què es combinen les descripcions hidrodinàmica i termodinàmica. La contribució del flux hidrodinàmic a l'energia lliure de la dissolució és descrita en el marc de la termodinàmica irreversible estesa, que estableix una relació entre les equacions constitutives viscoelàstiques i una entropia de noequilibri que depèn del tensor de pressions viscoses. Per diferenciació d'aquesta, s'obté l'equació d'estat per al potencial químic de no-equilibri, el qual, en presència de gradients de velocitat, acobla el flux de difusió amb la pressió viscosa. En certes condicions, aquesta influència fa que un sistema que en repòs seria unifàsic esdevingui inestable i es descompongui en dues fases, tot provocant, així, un desplaçament de la línia espinodal en el diagrama de fases. L'anàlisi teòrica està basada en l'estabilitat de les equacions de balanç de massa i de quantitat de moviment, de les equacions constitutives per al flux de difusió i el tensor de pressions viscoses, i de l'equació d'estat per al potencial químic de no-equilibri. Les prediccions concorden qualitativament amb les observacions experimentals conegudes. Presentem resultats per a dissolucions polimèriques diluïdes i concentrades i per a mescles de polímers.We review the basic ideas and main results of our analysis of shear-induced effects in polymer solutions and blends. The analysis combines thermodynamic and hydrodynamic descriptions. The flow contribution to the free energy of the solution is described in the framework of extended irreversible thermodynamics, which relates the viscoelastic constitutive equations to a non-equilibrium entropy that depends on the viscous pressure tensor. This yields, by differentiation, the corresponding non-equilibrium equation of state for the chemical potential, which couples diffusion flux to viscous pressure in the presence of a flow. In some conditions, the one-phase system becomes unstable and splits into two phases, leading to a shift in the spinodal line. The theoretical analysis is based on the stability of the mass and momentum balance equations, the constitutive equations for viscous pressure tensor and diffusion flux, and the equation of state for the chemical potential. The resulting predictions corroborate qualitatively the known experimental observations. Results for dilute and entangled polymer solutions and for polymer blends are given

Entropy and Entropy Production in Some Applications

By using entropy and entropy production, we calculate the steady flux of some phenomena. The method we use is a competition method, $S_S/\tau+\sigma={\it maximum}$, where $S_S$ is system entropy, $\sigma$ is entropy production and $\tau$ is microscopic interaction time. System entropy is calculated from the equilibrium state by studying the flux fluctuations. The phenomena we study include ionic conduction, atomic diffusion, thermal conduction and viscosity of a dilute gas

Legendre transform in the thermodynamics of flowing polymer solutions

We propose a Legendre transform linking two different choices of nonequilibrium variables (viscous pressure tensor and configuration tensor) in the thermodynamics of flowing polymer solutions. This may avoid some current confusions in the analysis of thermodynamic effects in polymer solutions under flow

Shear-induced shift of spinodal line in entangled polymer blends

We study the shear-flow effects on phase separation of entangled polymer blends by incorporating into the chemical potential a nonequilibrium contribution due to the flow. The results are compared with those of a previous analysis by other authors which did not modify the chemical potential but used a different assumption for the stress tensor of the blend

Thermodynamics and dynamics of flowing polymer solutions and blends

We review the basic ideas and main results of our analysis of shear-induced effects in polymer solutions and blends. The analysis combines thermodynamic and hydrodynamic descriptions. The flow contribution to the free energy of the solution is described in the framework of extended irreversible thermodynamics, which relates the viscoelastic constitutive equations to a non-equilibrium entropy that depends on the viscous pressure tensor. This yields, by differentiation, the corresponding non-equilibrium equation of state for the chemical potential, which couples diffusion flux to viscous pressure in the presence of a flow. In some conditions, the one-phase system becomes unstable and splits into two phases, leading to a shift in the spinodal line. The theoretical analysis is based on the stability of the mass and momentum balance equations, the constitutive equations for viscous pressure tensor and diffusion flux, and the equation of state for the chemical potential. The resulting predictions corroborate qualitatively the known experimental observations. Results for dilute and entangled polymer solutions and for polymer blends are given

O(N)O(N) fluctuations and lattice distortions in 1-dimensional systems

Statistical mechanics harmonizes mechanical and thermodynamical quantities, via the notion of local thermodynamic equilibrium (LTE). In absence of external drivings, LTE becomes equilibrium tout court, and states are characterized by several thermodynamic quantities, each of which is associated with negligibly fluctuating microscopic properties. Under small driving and LTE, locally conserved quantities are transported as prescribed by linear hydrodynamic laws, in which the local material properties of the system are represented by the transport coefficients. In 1-dimensional systems, on the other hand, the transport coefficients often appear to depend on the global state, rather than on the local state of the system at hand. We interpret these facts within the framework of boundary driven 1-dimensional Lennard-Jones chains of $N$ oscillators, observing that they experience non-negligible $O(N)$ lattice distortions and fluctuations. This implies that standard hydrodynamics and certain expressions of energy flow do not apply in these cases. One possible modification of the energy flow is considered.Comment: 8 pages, 7 figure

Possible experiment to check the reality of a nonequilibrium temperature

An experiment is proposed to check the physical reality of a nonequilibrium absolute temperature previously proposed from theoretical grounds in the framework of extended irreversible thermodynamics

Influence of elevated-CRP level-related polymorphisms in non-rheumatic Caucasians on the risk of subclinical atherosclerosis and cardiovascular disease in rheumatoid arthritis

Association between elevated C-reactive protein (CRP) serum levels and subclinical atherosclerosis and cardiovascular (CV) events was described in rheumatoid arthritis (RA). CRP, HNF1A, LEPR, GCKR, NLRP3, IL1F10, PPP1R3B, ASCL1, HNF4A and SALL1 exert an influence on elevated CRP serum levels in non-rheumatic Caucasians. Consequently, we evaluated the potential role of these genes in the development of CV events and subclinical atherosclerosis in RA patients. Three tag CRP polymorphisms and HNF1A, LEPR, GCKR, NLRP3, IL1F10, PPP1R3B, ASCL1, HNF4A and SALL1 were genotyped in 2,313 Spanish patients by TaqMan. Subclinical atherosclerosis was determined in 1,298 of them by carotid ultrasonography (by assessment of carotid intima-media thickness-cIMT-and presence/absence of carotid plaques). CRP serum levels at diagnosis and at the time of carotid ultrasonography were measured in 1,662 and 1,193 patients, respectively, by immunoturbidimetry. Interestingly, a relationship between CRP and CRP serum levels at diagnosis and at the time of the carotid ultrasonography was disclosed. However, no statistically significant differences were found when CRP, HNF1A, LEPR, GCKR, NLRP3, IL1F10, PPP1R3B, ASCL1, HNF4A and SALL1 were evaluated according to the presence/absence of CV events, carotid plaques and cIMT after adjustment. Our results do not confirm an association between these genes and CV disease in RA