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Background: There have been no reports on the relationship between wedging of vertebral bodies at the thoracolumbar spine and disc herniation in healthy individuals on magnetic resonance imaging (MRI). Purpose: To investigate the degree of wedging of vertebral bodies at the thoracolumbar spine in healthy individuals who underwent whole-body (WB) MRI. We also assessed the correlation between wedging and adjacent disc pathology. Material and Methods: This retrospective study comprised 200 healthy patients who underwent WB MRI as part of a regular health check from January 2019 to February 2019. We measured anterior and posterior vertical heights of each vertebral body between T10 and L2. The ratio of anterior height to posterior height (APR) was calculated, and we evaluated disc degeneration or disc herniation using WB MRI. Results: The APR of T10 was significantly higher than at the other levels (P < 0.05), and the APR of L1 was significantly lower (P < 0.05). Men had a significantly smaller APR than women at T12 to L2 (P < 0.05). Regarding the relationship between APR and disc degeneration, the group without disc degeneration had a higher APR, with statistical significance at T12, L1, and L2. Regarding the relationship between APR and disc herniation, the group without disc herniation had a higher APR, with statistical significance at T11, T12, L1, and L2. Conclusion: Wedging of vertebral bodies is most prominent at L1. Although the values were statistically significant only at some levels, the patients with disc degeneration or herniation had more prominent wedge deformity of thoracolumbar spine. [ABSTRACT FROM AUTHOR]

A major difference between experimental ischemic preconditioning (IPC), induced by brief ischemic episodes, and the clinical situation is that patients generally have repetitive episodes of ischemia. We used a swine model to examine differences in genes regulated by classical second-window IPC (SWOP) [two 10-min episodes of coronary artery occlusion (CAO) followed by 24 h reperfusion] compared with repetitive CAO/reperfusion (RCO), i.e., two 10-min CAO 12 h apart, and to repetitive coronary stenosis (RCS), six episodes of 90 min coronary stenosis 12 h apart (n = 5/group). All three models reduced infarct size by 60-85%, which was mediated by nitric oxide in SWOP but not in the other two models. We employed microarray analyses to discover additional molecular pathways intrinsic to models of repetitive ischemia and different from classical SWOP. There was an 85% homology in gene response between the RCO and RCS models, whereas SWOP was qualitatively different. Both RCO and RCS, but not SWOP, showed downregulation of genes encoding proteins involved in oxidative metabolism and upregulation of genes involved in protein synthesis, unfolded protein response, autophagy, heat shock response, protein secretion, and an activation of the NF-[kappa]B signaling pathway. Therefore, the regulated genes mediating IPC with repetitive ischemia differ radically from SWOP both quantitatively and qualitatively, showing that a repetitive pattern of ischemia, rather than the difference between no-flow vs. low-flow ischemia, dictates the genomic response of the heart. These findings illustrate new cardio-protective mechanisms developed by repetitive IPC, which are potentially more relevant to patients with chronic ischemic heart disease, who are subjected to repetitive episodes of ischemia. coronary occlusion; gene expression; myocardial infarction; ischemia; preconditioning doi: 10.1152/ajpheart.00147.2010.