Clinical and Imaging Features of Longus Colli Calcific Tendinitis: An Analysis of Ten Cases

BACKGROUND: Longus colli calcific tendinitis (LCCT) exhibits characteristic clinical features; thus, misidentification can be avoided once it is learned. There is a lack of reports on this disease. In this study, we analyzed the imaging and clinical features of LCCT in 10 patients. METHODS: We retrospectively reviewed the radiolographic findings, laboratory data and clinical features of 10 patients diagnosed with LCCT between January 2015 and June 2017. All patients were treated with medical treatment consisting of intravenous methylprednisolone 125 mg twice and oral nonsteroidal anti-inflammatory drug administration. RESULTS: On clinical findings, all 10 patients complained of severe posterior neck pain and cervical motion limitation. Odynophagia was present in nine patients. The mean time from symptom onset to hospital visit was 2.9 days. The mean time to symptom relief was 4.6 days. Of the 10 patients, three patients were admitted through the emergency room. There were five patients in the medical records who were transferred from another hospital. On the laboratory data, the mean value of C-reactive protein and erythrocyte sedimentation rate were 2.08 mg/dL (reference range, < 0.30 mg/dL) and 36.9 mm/hr (reference range, < 20 mm/hr), respectively. Leukocytosis was found in only two patients and fever was not present all patients. On radiographic findings, calcification was present on computed tomography images of all patients. The calcification was located at the lower part of the C1 arch, except for one case where calcification occurred in the anterolateral aspect of the C4–5 disc space. The mean value of the retropharyngeal space was 7.2 mm. CONCLUSIONS: LCCT, a rare disease, has characteristic radiographic findings and clinical features. Understanding such characteristics of this disease can prevent unnecessary testing and misdiagnosis.

Ctbp2-mediated β-catenin regulation is required for exit from pluripotency

The canonical Wnt pathway is critical for embryonic stem cell (ESC) pluripotency and aberrant control of β-catenin leads to failure of exit from pluripotency and lineage commitments. Hence, maintaining the appropriate level of β-catenin is important for the decision to commit to the appropriate lineage. However, how β-catenin links to core transcription factors in ESCs remains elusive. C-terminal-binding protein (CtBP) in Drosophila is essential for Wnt-mediated target gene expression. In addition, Ctbp acts as an antagonist of β-catenin/TCF activation in mammals. Recently, Ctbp2, a core Oct4-binding protein in ESCs, has been reported to play a key role in ESC pluripotency. However, the significance of the connection between Ctbp2 and β-catenin with regard to ESC pluripotency remains elusive. Here, we demonstrate that C-terminal-binding protein 2 (Ctbp2) associates with major components of the β-catenin destruction complex and limits the accessibility of β-catenin to core transcription factors in undifferentiated ESCs. Ctbp2 knockdown leads to stabilization of β-catenin, which then interacts with core pluripotency-maintaining factors that are occupied by Ctbp2, leading to incomplete exit from pluripotency. These findings suggest a suppressive function for Ctbp2 in reducing the protein level of β-catenin, along with priming its position on core pluripotency genes to hinder β-catenin deposition, which is central to commitment to the appropriate lineage.