Correlation between facial asymmetry, shoulder imbalance, and adolescent idiopathic scoliosis.

We conducted a prospective cross-sectional study to examine the correlation between facial asymmetry, shoulder imbalance, and adolescent idiopathic scoliosis. Sixty-nine adolescent idiopathic scoliosis patients and 29 healthy volunteers were enrolled in this study. All patients underwent whole-spine standing anteroposterior radiographs and frontal cephalograms. Patients were divided into mild, moderate, and severe groups depending on Cobb angle (10°-25°, 25°-40°, and >40°, respectively). Facial measurements included maxilla height difference, ramus length difference, and anterior nasal spine-menton angle. Shoulder measurements included coracoid height difference, clavicular angle, clavicle-rib intersection difference, and radiographic shoulder height.The anterior nasal spine-menton angle in the severe group (>40°) was higher than in the other groups (P<.05), as was the clavicle-rib intersection difference (P<.05). In addition, the magnitude of the curve showed a possible correlation with the anterior nasal spine-menton angle and clavicle-rib intersection difference in scoliosis patients (r=0.433 and r=0.511, respectively). According to different curve patterns, the anterior nasal spine-menton angle and clavicle-rib intersection difference were significantly higher in the double thoracic group than in the other groups (P<.05). In the correlation analysis, the ramus length difference and anterior nasal spine-menton angle had a possible correlation with the coracoid height difference, clavicular angle, radiographic shoulder height, and clavicle-rib intersection difference (P<.05).

Toll-like receptor 9-mediated inhibition of apoptosis occurs through suppression of FoxO3a activity and induction of FLIP expression.

Synthetic oligodeoxynucleotides (ODN) with a CpG-motif are recognized by Toll-like receptor 9 (TLR9) and pleiotropic immune responses are elicited. Stimulation of macrophages with TLR9 agonist prevented apoptosis induced by serum deprivation through increased expression of FLICE-like inhibitory protein (FLIP). CpG ODN-mediated anti-apoptosis depended on the TLR9-Akt-FoxO3a signaling pathway. Inhibition of TLR9 by small interfering (si) RNA or an inhibitor suppressed CpG ODN-mediated anti-apoptosis. Analysis of signaling pathways revealed that the anti-apoptotic effect of CpG ODN required phosphorylation of FoxO3a and its translocation from the nucleus to the cytosol. Overexpression of FoxO3a increased apoptosis induced by serum deprivation and CpG ODN blocked these effects through FLIP expression. In contrast, siRNA knock-down of FoxO3a decreased apoptosis by serum deprivation. In addition, Akt activation was involved in CpG ODN-induced phosphorylation of FoxO3a, expression of FLIP, and anti-apoptosis. Taken together, these results demonstrate the involvement of Akt-FoxO3a in TLR9-mediated anti-apoptosis and indicate that FoxO3a is a distinct regulator for FLIP expression.