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The study sought to evaluate the utility of a single supine radiograph in determining curve flexibility in early-onset scoliosis (EOS) patients.EOS patients with upright (standing/seated), supine, and side-bending radiographs who underwent spinal deformity surgery were identified. Coronal parameters included: proximal thoracic (PT) curve, main thoracic (MT) curve, and thoracolumbar/lumbar (TL/L) curve. Each radiograph was measured twice by 2 different raters. Correlation coefficients were utilized to investigate associations between the different radiographs. Interrater Correlation Coefficient (ICC) assessed intrarater and interrater reliability.Thirty-seven EOS patients were identified (age at diagnosis: 7.0±2.9 y, preoperative age: 13.0±2.9 y; 73% female; etiologies: 54% idiopathic, 30% syndromic, and 16% neuromuscular). Supine PT and MT curve measurements were highly associated with corresponding side-bending measurements (PT: r=0.75, P0.001; MT: r=0.80, P0.001), and TL/L curves were very highly associated (TL/L: r=0.92, P0.001). The mean absolute differences between supine and side-bending measurements were PT: 11.3±7.8 degrees, MT: 14.8±8.3 degrees, and TL/L: 16.2±7.6 degrees, where the side-bending was on average smaller than the supine measurement. The intrarater reliabilities were excellent, with an ICC ranging from 0.93 to 0.96 for side-bending films and 0.94 to 0.97 for supine films. The interrater reliability was excellent with ICC value of 0.88 for side-bending films and 0.93 for supine films.A single, preoperative supine radiograph was highly predictive of side-bending radiographs in patients with EOS. Supine curves measured an average of 15 degrees larger than bending curves in the MT and TL/L region. A single supine film may eliminate the need for effort-related, dual side-bending radiographs.Level II-retrospective study.

Continual efferocytic clearance of apoptotic cells (ACs) by macrophages prevents necrosis and promotes injury resolution. How continual efferocytosis is promoted is not clear. Here, we show that the process is optimized by linking the metabolism of engulfed cargo from initial efferocytic events to subsequent rounds. We found that continual efferocytosis is enhanced by the metabolism of AC-derived arginine and ornithine to putrescine by macrophage arginase 1 (Arg1) and ornithine decarboxylase (ODC). Putrescine augments HuR-mediated stabilization of the mRNA encoding the GTP-exchange factor Dbl, which activates actin-regulating Rac1 to facilitate subsequent rounds of AC internalization. Inhibition of any step along this pathway after first-AC uptake suppresses second-AC internalization, whereas putrescine addition rescues this defect. Mice lacking myeloid Arg1 or ODC have defects in efferocytosis in vivo and in atherosclerosis regression, while treatment with putrescine promotes atherosclerosis resolution. Thus, macrophage metabolism of AC-derived metabolites allows for optimal continual efferocytosis and resolution of injury.

Summary Regulatory T (Treg) cell responses and apoptotic cell clearance (efferocytosis) represent critical arms of the inflammation resolution response. We sought to determine whether these processes might be linked through Treg-cell-mediated enhancement of efferocytosis. In zymosan-induced peritonitis and lipopolysaccharide-induced lung injury, Treg cells increased early in resolution, and Treg cell depletion decreased efferocytosis. In advanced atherosclerosis, where defective efferocytosis drives disease progression, Treg cell expansion improved efferocytosis. Mechanistic studies revealed the following sequence: (1) Treg cells secreted interleukin-13 (IL-13), which stimulated IL-10 production in macrophages; (2) autocrine-paracrine signaling by IL-10 induced Vav1 in macrophages; and (3) Vav1 activated Rac1 to promote apoptotic cell engulfment. In summary, Treg cells promote macrophage efferocytosis during inflammation resolution via a transcellular signaling pathway that enhances apoptotic cell internalization. These findings suggest an expanded role of Treg cells in inflammation resolution and provide a mechanistic basis for Treg-cell-enhancement strategies for non-resolving inflammatory diseases.