Nonsurgical correction of straight back syndrome (thoracic hypokyphosis), increased lung capacity and resolution of exertional dyspnea by thoracic hyperkyphosis mirror image® traction: a CBP® case report.

[Purpose] To present the increase in thoracic kyphosis in a patient suffering from exertional dyspnea, reduced lung capacity, and spinal pains related to straight back syndrome (SBS). [Subject and Methods] A 33-year-old male patient was put on a CBP® corrective care program involving mirror image® traction procedures designed to increase the thoracic kyphosis. [Results] This patient had a 10° improvement in thoracic kyphosis in 16-weeks that was maintained 7-months later. There was a simultaneous reduction of pain, resolved exertional dyspnea, and a greater than 2 liter increase in lung capacity. [Conclusion] This case illustrates that nonsurgical improvement in thoracic kyphosis in a patient with SBS is possible and that this may positively influence lung capacity, health and function.

The proliferative status of thyrotropes is dependent on modulation of specific cell cycle regulators by thyroid hormone.

In this report we have examined changes in cell growth parameters, cell cycle effectors, and signaling pathways that accompany thyrotrope growth arrest by thyroid hormone (TH) and growth resumption after its withdrawal. Flow cytometry and immunohistochemistry of proliferation markers demonstrated that TH treatment of thyrotrope tumors resulted in a reduction in the fraction of cells in S-phase that is restored upon TH withdrawal. This is accompanied by dephosphorylation and rephosphorylation of retinoblastoma (Rb) protein. The expression levels of cyclin-dependent kinase 2 and cyclin A, as well as cyclin-dependent kinase 1 and cyclin B, were decreased by TH, and after withdrawal not only did these regulators of Rb phosphorylation and mitosis increase in their expression but so too did the D1 and D3 cyclins. We also noted a rapid induction and subsequent disappearance of the type 5 receptor for the growth inhibitor somatostatin with TH treatment and withdrawal, respectively. Because somatostatin can arrest growth by activating MAPK pathways, we examined these pathways in TtT-97 tumors and found that the ERK pathway and several of its upstream and downstream effectors, including cAMP response element binding protein, were activated with TH treatment and deactivated after its withdrawal. This led to the hypothesis that TH, acting through increased type 5 somatostatin receptor, could activate the ERK pathway leading to cAMP response element binding protein-dependent decreased expression of critical cell cycle proteins, specifically cyclin A, resulting in hypophosphorylation of Rb and its subsequent arrest of S-phase progression. These processes are reversed when TH is withdrawn, resulting in an increase in the fraction of S-phase cells.