BackgroundAngiomatous nasal polyps (ANPs), also known as angiectatic polyps, have rarely been reported in the literature. ANPs are characterized by extensive vascular proliferation and ectasia. ANPs can grow rapidly and exhibit aggressive clinical behavior that could simulate malignancy preoperatively, and they are easily confused with other diseases. In the present study, we analyzed the correlation between the computed tomography (CT) findings of nasal angiomatous polyps and their pathological features.MethodsWe evaluated CT findings and pathological features of 31 surgically proven ANPs.ResultsThe study population included 16 males and 15 females aged between 27 and 81 years (mean age, 53.5 years). On CT, the masses were heterogeneous; they had a soft tissue density and filled the maxillary and/or nasal cavities. Calcifications were found in 2 of the 31 cases. The lesions showed a clear boundary (15/31). The low-density shading on CT was related to the inflammatory, necrotic, and cystic changes, and the high-density shading on CT was related to hemorrhagic areas of the mass. On contrast-enhanced CT, the center of the lesions was non-enhanced with peripheral intensification due to occlusion or compression of feeder vessels of the polyp center, and the inflammatory cells and neovascularization around the edge of the mass. The most common site of maxillary wall erosion was the medial wall (21/31), followed by the posterior lateral wall (3/31), upper wall (2/31), and septum (3/31). Of these, the nasal cavity and/or maxillary sinus were enlarged in 28 cases. These findings were associated with the chronic progress of nasal angiomatous changes.ConclusionsCT of ANPs may demonstrate benign bone changes associated with the lesions and may also reflect the fact that ANPs do not invade peripheral soft tissue. CT demonstrated these lesions consistently and provided information useful for surgical planning.

Background This study is to explore the role of curcumin and GLUT‐1 antisense oligodeoxynucleotides (AS‐ODN) on autophagy modulation‐initiated radiosensitivity. Methods BALB/c mice were employed to establish xenograft model using Tu212 cell. The expression of autophagy‐ and apoptosis‐related proteins was determined by WB. Autophagosome was observed under transmission electron microscope. Apoptosis of tumor tissue were detected by TUNEL staining. Results Combinations of curcumin and GLUT‐1 AS‐ODN with 10 Gy inhibited the tumor growth by inducing apoptosis of laryngeal cancer cells followed with the enhancement of autophagy. 3‐MA also had a promotion effect on irradiation‐mediated growth inhibition possibly by depressing PI3K and on curcumin/GLUT‐1 AS‐ODN‐mediated growth inhibition potentially by regulating autophagic events. Of note, a de‐escalation of radiotherapy dose (5 Gy) along with curcumin, GLUT‐1 AS‐ODN or 3‐MA produced a stronger effect than high dosage of radiotherapy (10 Gy) alone. Conclusions Curcumin and GLUT‐1 AS‐ODN improve the radiosensitivity of laryngeal carcinoma through regulating autophagy and inducing apoptosis.

Hypoxic resistance is the main obstacle to radiotherapy for laryngeal carcinoma. Our previous study indicated that hypoxia‐inducible factor 1α (HIF‐1α) and glucose transporter 1 (Glut‐1) double knockout reduced tumour biological behaviour in laryngeal carcinoma cells. However, their radioresistance mechanism remains unclear. In this study, cell viability was determined by CCK8 assay. Glucose uptake capability was evaluated by measurement of 18F‐fluorodeoxyglucose radioactivity. A tumour xenograft model was established by subcutaneous injection of Tu212 cells. Tumour histopathology was determined by haematoxylin and eosin staining, immunohistochemical staining, and TUNEL assays. Signalling transduction was evaluated by Western blotting. We found that hypoxia induced radioresistance in Tu212 cells accompanied by increased glucose uptake capability and activation of the PI3K/Akt/mTOR pathway. Inhibition of PI3K/Akt/mTOR activity abolished hypoxia‐induced radioresistance and glucose absorption. Mechanistic analysis revealed that hypoxia promoted higher expressions of HIF‐1α and Glut‐1. Moreover, the PI3K/Akt/mTOR pathway was a positive mediator of HIF‐1α and/or Glut‐1 in the presence of irradiation. HIF‐1α and/or Glut‐1 knockout significantly reduced cell viability, glucose uptake and PI3K/Akt/mTOR activity, all of which were induced by hypoxia in the presence of irradiation. In vivo analysis showed that knockout of HIF‐1α and/or Glut‐1 also inhibited tumour growth by promoting cell apoptosis, more robustly compared with the PI3K inhibitor wortmannin, particularly in tumours with knockout of both HIF‐1α and Glut‐1. HIF‐1α and/or Glut‐1 knockout also abrogated PI3K/Akt/mTOR signalling transduction in tumour tissues, in a manner similar to wortmannin. HIF‐1α and/or Glut‐1 knockout facilitated radiosensitivity in laryngeal carcinoma Tu212 cells by regulation of the PI3K/Akt/mTOR pathway.

Tong Qiao nose drops alleviated the symptoms of allergic rhinitis in a rat model and lowered the expression levels of eotaxin, IL-5, and IL-13.

In this study, we investigated the ability of curcumin alone or in combination with GLUT1 siRNA to radiosensitize laryngeal carcinoma (LC) through the induction of autophagy. Protein levels in tumour tissues and LC cells were measured by immunohistochemistry and Western blotting. In vitro, cell proliferation, colony formation assays, cell death and autophagy were detected. A nude mouse xenograft model was established through the injection of Tu212 cells. We found that GLUT1 was highly expressed and negatively associated with autophagy‐related proteins in LC and that curcumin suppressed radiation‐mediated GLUT1 overexpression in Tu212 cells. Treatment with curcumin, GLUT1 siRNA, or the combination of the two promoted autophagy. Inhibition of autophagy using 6‐amino‐3‐methypourine (3‐MA) promoted apoptosis after irradiation or treatment of cells with curcumin and GLUT1 siRNA. 3‐MA inhibited curcumin and GLUT1 siRNA‐mediated non‐apoptotic programmed cell death. The combination of curcumin, GLUT1 siRNA and 3‐MA provided the strongest sensitization in vivo. We also found that autophagy induction after curcumin or GLUT1 siRNA treatment implicated in the AMP‐activated protein kinase‐mTOR‐serine/threonine‐protein kinase‐Beclin1 signalling pathway. Irradiation primarily caused apoptosis, and when combined with curcumin and GLUT1 siRNA treatment, the increased radiosensitivity of LC occurred through the concurrent induction of apoptosis and autophagy.