## 2 Materials and Methods
In this context, the role played by the H\({}^{+}\)-ATPase is fundamental, because it moves positive charges into the cell, while it generates large membrane voltage (inside negative and outside positive) and a pH gradient [30; 31; 32; 33]. Protein phosphorylation is an important cellular regulatory mechanism, because many enzymes and receptors [28; 34; 35] are activated or deactivated by phosphorylation by involving kinases and phosphatases. Moreover, kinases are responsible for cellular transduction signalling [7; 36; 37; 38]. When ion fluxes occur, a variation in the concentration of the ions on both side of the membrane occurs [39; 40]:  
\[\frac{dc_{i}}{dt}=-\
abla\cdot\mathbf{J}_{i} \tag{6}\]  
where \(c_{i}\) is the concentration of the \(i\)-th ion (Na\({}^{+}\), K\({}^{+}\), Ca\({}^{2+}\), Cl\({}^{-}\), etc.) in C m\({}^{-3}\), \(t\) is the time and \(\mathbf{J}_{i}\) is the current density of the \(i\)-th ion. However, as a consequence of these cellular fluxes and processes, a specific entropy rate is generated [41; 42]:  
\[T\,\frac{ds}{dt}=\
abla\cdot\left(\mathbf{J}_{u}-\sum_{i=1}^{3}\mu_{i}\, \mathbf{J}_{i}\right)-\sum_{i=1}^{3}\mathbf{J}_{i}\cdot\
abla\mu_{i} \tag{7}\]  
where \(s\) is the specific entropy, \(T\) is the temperature, \(\mathbf{J}_{5}=\mathbf{J}_{u}-\sum_{i=1}^{3}\mu_{i}\,\mathbf{J}_{i}\) is the contribution of the inflows and outflows, with \(i=1,2,3\) meaning Cl\({}^{-}\), Na\({}^{+}\)-, K\({}^{+}\)-fluxes, \(T\sigma=-\sum_{i=1}^{3}\mathbf{J}_{i}\cdot\
abla\mu_{i}\) is the dissipation function [40], and \(\mu\) is the chemical potential, defined as:  
\[\mu_{i}=\left(\frac{\partial G}{\partial n_{i}}\right)_{T,p,n_{k}\
eq i} \tag{8}\]  
where \(G\) is the Gibbs energy, \(n\) is the number of moles, and \(p\) is the pressure. In relation to the ion fluxes, we also wrote the Equation (7) in a different way [15]:  
\[T\,\frac{ds}{dt}=-\
abla\cdot\left(\mathbf{J}_{u}-\sum_{i=1}^{3}\mu_{i}\, \mathbf{J}_{i}\right) \tag{9}\]which, considering \(T\) constant and following Prigogine (\(ds/dt=0\)) [43], becomes:  
\[\
abla\cdot\left(\mathbf{J}_{u}-\sum_{i=1}^{3}\mu_{i}\,\mathbf{J}_{i}\right)=0 \tag{10}\]  
So, taking into account the change in the internal energy, we obtained [15]:  
\[c_{N}=c_{N,0}\,\exp\left(\frac{N\,e_{N}}{k_{B}\,T}\right) \tag{2}\]0  
where \(u\) is the specific internal energy, \(\mathbf{J}_{u}\) is the heat flux in W m\({}^{-2}\), \(V\) is the cell volume in m\({}^{3}\), and \(\dot{Q}\) is the heat power in W, represented also by the power of the electromagnetic waves flowing into the eyes. Now, we describe the following experimental approach. In chronic glaucoma, the Retinal Nerve Fibre Layer (RNFL) tends to gradually reduce, until the connection between the retina and the nervous system disappears. Indeed, the first glaucomatous lesions seem to occur in the brain, and they are quite similar to other neurodegenerative diseases lesions. The nervous system also reacts by processing a compensatory response to maintain the signal between the eye and brain regions, slowing the progression of the disease, which can be interpreted as a balance between the disease and a brain adaptation. Moreover, recently, some degree of regeneration has been achieved by the optic nerve by factors associated with intraocular inflammation, as our thermodynamic model suggests. So, in relation to Equations (1) and (6), specific energy fluxes could allow the retinal ganglion cells to regenerate axons, from the eye through the entire length of the optic nerve. Progress in optic nerve regeneration holds promise for visual restoration [44; 45]. Indeed, retinal ganglion cell activity has been shown to increase, if stimulated by visual stimulation, with a consequent axons regeneration, due to the neural activity [21; 46]. Consequently, the rationale of our analysis consists in verifying the effectiveness of the visible light phototherapy in relation to rehabilitation.