Background.The utility of ultrasound imaging in the screening of soft-part tumours (SPTs) has been reported. We classified SPTs according to their blood flow pattern on Doppler ultrasound and re-evaluated the efficacy of this imaging modality as a screening method. Additionally, we combined Doppler ultrasound with several values to improve the diagnostic efficacy and to establish a new diagnostic tool.Patients and methods.This study included 189 cases of pathologically confirmed SPTs (122 cases of benign disease including SPTs and tumour-like lesions and 67 cases of malignant SPTs). Ultrasound imaging included evaluation of vascularity by colour Doppler. We established a scoring system to more effectively differentiate malignant from benign SPTs (ultrasound-based sarcoma screening [USS] score).Results.The mean scores in the benign and malignant groups were 1.47 ± 0.93 and 3.42 ± 1.30, respectively. Patients with malignant masses showed significantly higher USS scores than did those with benign masses (p < 1 × 10−10). The area under the curve was 0.88 by receiver operating characteristic (ROC) analysis. Based on the cut-off value (3 points) calculated by ROC curve analysis, the sensitivity and specificity for a diagnosis of malignant SPT was 85.1% and 86.9%, respectively.Conclusions.Assessment of vascularity by Doppler ultrasound alone is insufficient for differentiation between benign and malignant SPTs. Preoperative diagnosis of most SPTs is possible by combining our USS score with characteristic clinical and magnetic resonance imaging findings.
Adult bone structural integrity is maintained by remodeling via the coupling of osteoclastic bone resorption and osteoblastic bone formation. Osteocytes or osteoblasts express receptor activator of nuclear factor κ-B ligand (Rankl) or osteoprotegerin (Opg) to promote or inhibit osteoclastogenesis, respectively. Bone morphogenetic protein (BMP) is a potent bone inducer, but its major role in adult bone is to induce osteocytes to upregulate sclerostin (Sost) and increase the Rankl/Opg expression ratio, resulting in promotion of osteoclastogenesis. However, the precise effect of BMP-target gene(s) in osteoblasts on the Rankl/Opg expression ratio remains unclear. In the present study, we identified atonal homolog 8 (Atoh8), which is directly upregulated by the BMP-Smad1 axis in osteoblasts. In vivo, Atoh8 was detected in osteoblasts but not osteocytes in adult mice. Although global Atoh8knockout mice showed only a mild phenotype in the neonate skeleton, the bone volume was decreased and osteoclasts were increased in the adult phase. Atoh8-null marrow stroma cells were more potent than wild-type cells in inducing osteoclastogenesis in marrow cells. Atoh8 loss in osteoblasts increased Runx2 expression and the Rankl/Opg expression ratio, while Runx2 knockdown normalized the Rankl/Opg expression ratio. Moreover, Atoh8 formed a protein complex with Runx2 to inhibit Runx2 transcriptional activity and decrease the Rankl/Opg expression ratio. These results suggest that bone remodeling is regulated elaborately by BMP signaling; while BMP primarily promotes bone resorption, it simultaneously induces Atoh8 to inhibit Runx2 and reduce the Rankl/ Opg expression ratio in osteoblasts, suppressing osteoclastogenesis and preventing excessive BMP-mediated bone resorption.
Extracranial vertebral artery aneurysm is uncommon, and the common cause is penetrating trauma. Rupture of extracranial vertebral artery aneurysm into the thoracic cavity is extremely rare and fatal due to haemorrhagic shock by massive haemothorax. We report an intrathoracic rupture of the extracranial vertebral artery aneurysm with neurofibromatosis Type 1, successfully treated by coil and liquid embolisation.
Background:The mechanisms by which Hivep3 regulates the osteochondrogenesis remain elusive. Results: Knockdown of Hivep3 down-regulated Alg2 expression. Alg2 suppressed osteoblast differentiation by inhibiting the activity of Runx2. Alg2 silencing suppressed the expression of Creb3l2 and chondrogenesis. Conclusion: Alg2 may be a modulator of osteochondrogenesis. Significance: This is the first report to describe the association of an Alg gene with osteochondrogenesis.
Histological distinction between enchondroma and chondrosarcoma is difficult because of a lack of definitive biomarkers. Here, we found highly active transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP) signalling in human chondrosarcomas compared with enchondromas by immunohistochemistry of phosphorylated SMAD3 and SMAD1/5. In contrast, the chondrogenic master regulator SOX9 was dramatically down-regulated in grade 1 chondrosarcoma. Paternally expressed gene 10 (PEG10) was identified by microarray analysis as a gene overexpressed in chondrosarcoma SW1353 and Hs 819.T cells compared with C28/I2 normal chondrocytes, while TGF-β1 treatment, mimicking higher grade tumour conditions, suppressed PEG10 expression. Enchondroma samples exhibited stronger expression of PEG10 compared with chondrosarcomas, suggesting a negative association of PEG10 with malignant cartilage tumours. In chondrosarcoma cell lines, application of the TGF-β signalling inhibitor, SB431542, increased the protein level of PEG10. Reporter assays revealed that PEG10 repressed TGF-β and BMP signalling, which are both SMAD pathways, whereas PEG10 knockdown increased the level of phosphorylated SMAD3 and SMAD1/5/9. Our results indicate that mutually exclusive expression of PEG10 and phosphorylated SMADs in combination with differentially expressed SOX9 is an index to distinguish between enchondroma and chondrosarcoma, while PEG10 and TGF-β signalling are mutually inhibitory in chondrosarcoma cells.
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