We analyze an open quantum system under the influence of more than one environment: a dephasing bath and a probability-absorbing bath that represents a decay channel, as encountered in many models of quantum networks. In our case, dephasing is modeled by random fluctuations of the site energies, while the absorbing bath is modeled with an external lead attached to the system. We analyze under which conditions the effects of the two baths can enter additively the quantum master equation. When such additivity is legitimate, the reduced master equation corresponds to the evolution generated by an effective non-Hermitian Hamiltonian and a Haken-Strobl dephasing super-operator. We find that the additive decomposition is a good approximation when the strength of dephasing is small compared to the bandwidth of the probability-absorbing bath.

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In this paper we formulate a poroelastic model starting from a model of species diffusion in an elastic material. The model is applied to study the mechanics of the lamina cribrosa (LC) in the eye. The LC is a porous tissue at the head of the optic nerve. Deformation of this tissue and impairment of blood flow induced by tissue deformation are considered to be related to the pathogenesis of glaucoma.The governing equations are derived from general thermomechanical principles. We carefully revise the role of the energy-stress Eshelby tensor, mutuated from the framework of tissue growth, in describing the hemo-mechanical behaviour of the tissue.The model accounts for non-linear deformations of the solid matrix and deformation-induced changes in porosity and permeability. The model provides a qualitative better undertanding of the phatophysiology and pathogenesis of glaucoma in terms of coupling between tissue deformation and the resulting impaired hemodynamics inside the LC.

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