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Background: Computed tomography angiography (CTA) is a reliable, non-invasive screening method for diagnosing panvascular disease. By using low contrast agent volume, CTA imaging enables one-stop multi-organ scanning, thereby minimizing the potential risk of contrast-induced nephropathy in patients with impaired renal function. Purpose: To evaluate the feasibility of one-stop CTA following a heart rate (HR)-based protocol using a low volume of contrast medium (CM) for examination of the coronary, carotid and cerebrovascular arteries. Material and Methods: Sixty patients undergoing coronary carotid, and cerebrovascular CTA after a single injection of CM were recruited and randomly divided into two groups. Group A (n = 30) underwent CTA following a traditional protocol. The timing of the scans in Group B (n = 30) was determined according to the patient's HR. Results: The CT values for the thoracic aorta (432.2 ± 104.28 HU), anterior cerebral artery (303.96 ± 99.29 HU), and right coronary artery (366.70 ± 85.10 HU) in Group A did not differ significantly from those in Group B (445.80 ± 106.13, 293.73 ± 75.25 and 344.13 ± 111.04 HU, respectively). The qualities of most of the scanned images for both groups were scored as 3 or 4 (on a five-point scale). The radiation dose and the volume of CM were significantly higher in Group A (303.05 ± 110.95 mGy) (100 mL) than in Group B (239.46 ± 101.12 mGy) (50 mL). Conclusion: The radiation dose and volume of CM were significantly reduced in CTA following the HR-based protocol. The personalized administration of CM also simplified the scanning process. [ABSTRACT FROM AUTHOR]

Osteosarcoma is among the commonly observed malignancies worldwide. High-mobility group box 1 protein (HMGB1) is a highly conserved protein and is involved in the progression of various types of human cancer. The aim of the present study was to explore whether the level of HMGB1 was involved in the necrosis of osteosarcoma cells. Doxorubicin (DXR), as an inducer of necrosis, was administered to human osteosarcoma cell lines (MG63, Saos-2 and U2OS), and the results indicated that 0.5 µg/ml DXR significantly induced the necrosis of MG63 cells (P<0.01), while 0.5 and 1.0 µg/ml DXR suppressed the viability of MG63 and U2OS cells (P<0.05), relative to untreated controls. Additionally, treatment with DXR was observed by western blot analysis to markedly increase the expression levels of HMGB1 in MG63 cells, and to significantly increase the levels of secreted HMGB1 in the supernatants of MG63 and U2OS cells (P<0.01). In conclusion, cell necrosis increased the level of HMGB1 in osteosarcoma cells, as well as the level of secreted HMGB1 in cell supernatants. Therefore, HMGB1 may be a potential target in molecular therapy for patients with osteosarcoma. [ABSTRACT FROM AUTHOR]

C-Met receptor and its ligand hepatocyte growth factor (HGF) are overexpressed in a variety of osteosarcoma cell lines and osteosarcoma pathological samples. It is suggested that c-Met/HGF plays an important role in the development of osteosarcoma. This study aimed to explore the anticancer effect of the c-Met-targeted drug crizotinib on osteosarcoma (OS) cells. The effects of crizotinib on the proliferation of osteosarcoma cells (SaOS2, MG-63 and MNNG) at different concentrations were detected by CCK8. Human osteosarcoma cell line MG-63 was used as an in vitro model to evaluate the effects of 2.5 μM crizotinib, 5.0 μM crizotinib and DMSO on cell apoptosis, cell cycle, migration and invasion. The expression of the c-Met signaling pathway in osteosarcoma cells was detected by western blot. The results showed that crizotinib inhibited the proliferation of cell lines in a concentration-dependent manner. Crizotinib significantly increased the number of apoptotic cells compared with the control group. Compared with the control group, crizotinib increased G0/G1 phase cells and decreased S phase cells. Compared with the control group, crizotinib inhibited the migration and invasion of osteosarcoma cells and decreased the expression of c-Met/Gab1/STAT5. This study will provide a promising therapeutic target and theoretical basis for the clinical application of crizotinib in osteosarcoma.