As a rule, it is accepted that free energies of unfolded states of proteins are equal and that unfolded conformations of different proteins are the same and represent statistical coils. The SS-bond introduced into the protein changes the conformation of the protein unfolded state. Therefore, the disulfide bridge inserted in apomyoglobin has undoubtedly changed the entropy component of the free energy of the unfolded state of this protein ; therefore, it would be more correct to level the energy free profiles of apomyoglobin and its mutant form with the SS-bond by the energy of native states of these proteins. This means that to make the comparison more convenient we have attributed the zero value of the free energy in Fig. 7 to the protein native states. Another important moment that ensues from the impossibility to estimate absolute free energies values for different states of the protein is as follows. In the analysis of intricate energy schemes, it is impossible to estimate the stability of a definite state of protein; it is probable to estimate its stability relative to the other state of protein. So it is more correct to speak about the stability of transition between the two states rather than the stability of the state. To understand the details of the influence of the SS-bond on apomyoglobin, using Fig. 7 it can be analyzed how the mutation affected the mutual arrangement of different protein states. Bronchopulmonary dysplasia is an acquired form of chronic lung disease that is unique to the preterm infant. BPD is clinically diagnosed at 36 weeks postmenstrual age or later if there is a persistent need for oxygen reflecting underlying abnormal lung development. BPD is multifactorial in its pathogenesis and, in general, is a consequence of chronic lung injury with a failure to repair and resume normal lung development. Infants with BPD experience significant clinical sequelae even after discharge from the neonatal intensive care unit including persistently altered lung function and poor neurocognitive outcomes in early childhood. Reducing the incidence of BPD would have a significant impact on quality of life as well as long term health expenditures. Multiple therapies have been tested including a variety of ventilatory strategies and pharmacotherapies, but little has proved to effectively reduce BPD with some, such as postnatal steroids, resulting in potential harm. The pathogenesis of BPD is multifactorial but is characterized by several major disease-rendering pathways: pulmonary injury, inflammation, and altered lung development, most notably alveolar simplification. During fetal development the fetus is exposed to multiple biologic factors that facilitate organ development. With early delivery there is an abrupt termination in exposure to these biologic factors, many of which cannot be replaced at a rate or level that the fetus was exposed to while in utero.