Oseteoid osteoma is a well-known type of benign bone-forming tumor, which has previously been diagnosed using plain radiograph imaging. However, diagnosis of osteoid osteoma may be delayed due to ambiguities on plain radiograph images; despite the increasing use of magnetic resonance imaging (MRI), this type of misdiagnosis is not uncommon. The aim of the present study was to evaluate the effectiveness of radionuclide imaging scans for the diagnosis of osteoid osteoma, as this form of imaging was proposed to be a more sensitive test. The characteristics of 18 cases of osteoid osteoma were analyzed based on diagnostic imaging and the time from initial recognition of symptoms by the patient to diagnosis. Diagnostic modalities included plain radiograph, computed tomography (CT), MRI and radionuclide imaging. Among the 18 patients, 14 patients had unique positive findings in plain radiographs. The mean duration between initial cognition of symptoms to the diagnosis for these patients was 5.2 months (range, 3.8‑9.3 months). A total of 4 patients exhibited no radiographic abnormalities in the initial plain radiographs and were diagnosed a mean of 18.5 months (range, 17‑20 months) following the onset of symptoms. Overall, radionuclide imaging was performed on 16 patients and all of the cases demonstrated positive findings. In these cases, 28.6% of osteoid osteoma patients with clinical indications revealed no abnormal findings in plain radiographs. Therefore, in situations such as these, radionuclide imaging may be a useful indicator for diagnosis, as these results have demonstrated that it positively identified all cases of osteoid osteoma. In addition, the results of the present study indicated that if the radionuclide imaging was positive, CT scan was a more valuable diagnostic tool, whereas if the radionuclide imaging was negative, MRI should be recommended for the diagnosis of other undiscovered disease entities.

Obesity is known to increase breast cancer risk and aggressiveness in postmenopausal luminal breast cancer and obesity-driven dysfunctional metabolic activity in visceral adipose tissue (VAT) is considered as one of the principal underlying mechanism. We aimed to investigate the relationship between VAT metabolic activity evaluated by preoperative ¹⁸F-FDG PET/CT and axillary lymph node (ALN) metastasis in postmenopausal luminal breast cancer patients. In total, 173 patients were enrolled in study. They all underwent preoperative ¹⁸F-FDG PET/CT and surgery. VAT metabolic activity was defined as the maximum standardized uptake value (SUVmax) of VAT divided by the SUVmax of subcutaneous adipose tissue (V/S ratio). In luminal breast cancer, the patients with ALN metastasis showed significantly higher V/S ratio than the patients without ALN metastasis. Furthermore, V/S ratio was significantly associated with ALN metastasis in luminal breast cancer patients. Erythrocyte sedimentation rate, which reflect the systemic inflammation, was significantly higher in ALN metastasis group than the negative ALN metastasis group in luminal breast cancer patients and showed significant positive correlation with V/S ratio. V/S ratio significantly affects the ALN metastasis status in postmenopausal luminal breast cancer patients and it may be useful as a potential biomarker of obesity-driven systemic inflammation associated with tumor aggressiveness.

Interactions between CD147 and cyclophilin A (CypA) promote plaque rupture that causes atherosclerosis-related cardiovascular events, such as myocardial infarction and stroke. Here, we investigated whether SP-8356 ((1S,5R)-4-(3,4-dihydroxy-5-methoxystyryl)-6,6-dimethylbicyclo[3.1.1]hept-3-en-2-one), a novel drug, can exert therapeutic effects against plaque progression and instability through disruption of CD147-CypA interactions in apolipoprotein E-deficient (ApoE KO) mice. Immunocytochemistry and immunoprecipitation analyses were performed to assess the effects of SP-8356 on CD147-CypA interactions. Advanced plaques were induced in ApoE KO mice via partial ligation of the right carotid artery coupled with an atherogenic diet, and SP-8356 (50 mg/kg) orally administrated daily one day after carotid artery ligation for three weeks. The anti-atherosclerotic effect of SP-8356 was assessed using histological and molecular approaches. SP-8356 interfered with CD147-CypA interactions and attenuated matrix metalloproteinase-9 activation. Moreover, SP-8356 induced a decreased in atherosclerotic plaque size in ApoE KO mice and stabilized plaque vulnerability by reducing the necrotic lipid core, suppressing macrophage infiltration, and enhancing fibrous cap thickness through increasing the content of vascular smooth muscle cells. SP-8356 exerts remarkable anti-atherosclerotic effects by suppressing plaque development and improving plaque stability through inhibiting CD147-CypA interactions. Our novel findings support the potential utility of SP-8356 as a therapeutic agent for atherosclerotic plaque.

Synthetic vascular smooth muscle cells (VSMCs) play important roles in atherosclerosis, in-stent restenosis, and transplant vasculopathy. We investigated the synthetic activity of VSMCs in the atherosclerotic carotid artery using ¹⁸F-fluorodeoxyglucose (FDG) positron emission tomography (PET). Atherosclerosis was induced in rats by partial ligation of the right carotid artery coupled with an atherogenic diet and vitamin D injections (2 consecutive days, 600,000 IU/day). One month later, rats were imaged by F-18 FDG PET. The atherosclerotic right carotid arteries showed prominent luminal narrowing with neointimal hyperplasia. The regions with neointimal hyperplasia were composed of α-smooth muscle actin-positive cells with decreased expression of smooth muscle myosin heavy chain. Surrogate markers of synthetic VSMCs such as collagen type III, cyclophilin A, and matrix metallopeptidase-9 were increased in neointima region. However, neither macrophages nor neutrophils were observed in regions with neointimal hyperplasia. F-18 FDG PET imaging and autoradiography showed elevated FDG uptake into the atherosclerotic carotid artery. The inner vessel layer showed higher tracer uptake than the outer layer. Consistently, the expression of glucose transporter 1 was highly increased in neointima. The present results indicate that F-18 FDG PET may be a useful tool for evaluating synthetic activities of VSMCs in vascular remodeling disorders.

Neointimal hyperplasia and its related arterial stiffness are the crucial pathophysiological features in atherosclerosis and in-stent restenosis. Cluster of differentiation 147 (CD147), a member of the immunoglobulin super family that induces the expression of matrix metalloproteinase-9 (MMP-9) by dimerization, may play important roles in neointimal hyperplasia and may therefore be an effective target for the treatment of this condition. Here, we investigated whether a novel CD147 inhibitor SP-8356 ((1S,5R)-4-(3,4-dihydroxy-5-methoxystyryl)-6,6-dimethylbicyclo[3.1.1]hept-3-en-2-one) reduces neointimal hyperplasia and arterial stiffness in a rat model of partial carotid artery ligation. Neointimal hyperplasia was induced in Sprague–Dawley rats by partial ligation of the right carotid artery combined with a high fat diet and vitamin D injection. Rats were subdivided into vehicle, SP-8356 (50 mg/kg), and rosuvastatin (10 mg/kg) groups. The drugs were administrated via intraperitoneal injections for 4 weeks. The elasticity of blood vessels was assessed by measuring pulse wave velocity using Doppler ultrasonography before sacrifice. Histomolecular analysis was carried out on harvested carotid arteries. SP-8356 significantly reduced MMP activity by inhibiting CD147 dimerization. SP-8356 reduced neointimal hyperplasia and prevented the deterioration of vascular elasticity. SP-8356 had a greater inhibitory effect on neointimal hyperplasia than did rosuvastatin. Furthermore, rosuvastatin did not improve vascular elasticity. SP-8356 increased the expression of smooth muscle myosin heavy chain (SM-MHC), but decreased the expression of collagen type III and MMP-9 in the neointimal region. In contrast to SP-8356, rosuvastatin did not alter the expression of SM-MHC or MMP-9. The ability of SP-8356 to reduce neointimal hyperplasia and improve arterial stiffness in affected carotid artery suggests that SP-8356 could be a promising therapeutic drug for vascular remodeling disorders involving neointimal hyperplasia and arterial stiffness.