Objective: To evaluate, using multislice computed tomography (MSCT), the morphologic changes in the upper airway after large incisor retraction in adult bimaxillary protrusion patients. Materials and Methods: Thirty adult patients with bimaxillary protrusion had four first premolars extracted, and then miniscrews were placed to provide anchorage. A CT scan was performed before incisor retraction and again posttreatment. Three-dimensional (3D) reconstruction of the pre-(T1) and post-(T2) CT data was used to assess for morphological changes of the upper airway. A paired t-test was used to compare changes from T1 to T2. The relationship among the three variables (upper incisor retraction amount, upper airway size, and hyoid position) was analyzed by Pearson correlation coefficient. Results: The amounts of upper incisor retraction at the incisal edge and apex were 7.64 6 1.68 mm and 3.91 6 2.10 mm, respectively. The hyoid was retracted 2.96 6 0.54 mm and 9.87 6 2.92 mm, respectively, in the horizontal and vertical directions. No significant difference was observed in the mean cross-sectional area of the nasopharynx (P . .05) between T1 and T2, while significant differences between T1 and T2 were found in the mean cross-sectional areas of the palatopharynx, glossopharynx, and hypopharynx (P , .05); these mean cross-sectional areas were decreased by 21.02% 6 7.89%, 25.18% 6 13.51%, and 38.19% 6 5.51%, respectively. The largest change in the cross-sectional area is always noted in the hypopharynx. There was a significant correlation among the retraction distance of the upper incisor at its edge, the retraction distance of the hyoid in the horizontal direction, and the decrease of the hypopharynx. Conclusion: Large incisor retraction leads to narrowing of the upper airway in adult bimaxillary protrusion patients. (Angle Orthod. 2012;82:964-970.)

The cellular prion protein (PrPC), a protein most noted for its link to prion diseases, has been found to play a protective role in ischemic brain injury. To investigate the role of PrPC in the kidney, an organ highly prone to ischemia/reperfusion (IR) injury, we examined wild-type (WT) and PrPC knockout (KO) mice that were subjected to 30-min of renal ischemia followed by 1, 2, or 3 days of reperfusion. Renal dysfunction and structural damage was more severe in KO than in WT mice. While PrP was undetectable in KO kidneys, Western blotting revealed an increase in PrP in IR-injured WT kidneys compared to sham-treated kidneys. Compared to WT, KO kidneys exhibited increases in oxidative stress markers heme oxygenase-1, nitrotyrosine, and Nε-(carboxymethyl)lysine, and decreases in mitochondrial complexes I and III. Notably, phosphorylated extracellular signal-regulated kinase (pERK) staining was predominantly observed in tubular cells from KO mice following 2 days of reperfusion, a time at which significant differences in renal dysfunction, histological changes, oxidative stress, and mitochondrial complexes between WT and KO mice were observed. Our study provides the first evidence that PrPC may play a protective role in renal IR injury, likely through its effects on mitochondria and ERK signaling pathways.

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