Automatic detection of adenoid hypertrophy on cone-beam computed tomography based on deep learning.

INTRODUCTION: This study proposed an automatic diagnosis method based on deep learning for adenoid hypertrophy detection on cone-beam computed tomography. METHODS: The hierarchical masks self-attention U-net (HMSAU-Net) for segmentation of the upper airway and the 3-dimensional (3D)-ResNet for diagnosing adenoid hypertrophy were constructed on the basis of 87 cone-beam computed tomography samples. A self-attention encoder module was added to the SAU-Net to optimize upper airway segmentation precision. The hierarchical masks were introduced to ensure that the HMSAU-Net captured sufficient local semantic information. RESULTS: We used Dice to evaluate the performance of HMSAU-Net and used diagnostic method indicators to test the performance of 3D-ResNet. The average Dice value of our proposed model was 0.960, which was superior to the 3DU-Net and SAU-Net models. In the diagnostic models, 3D-ResNet10 had an excellent ability to diagnose adenoid hypertrophy automatically with a mean accuracy of 0.912, a mean sensitivity of 0.976, a mean specificity of 0.867, a mean positive predictive value of 0.837, a mean negative predictive value of 0.981, and a F1 score of 0.901. CONCLUSIONS: The value of this diagnostic system lies in that it provides a new method for the rapid and accurate early clinical diagnosis of adenoid hypertrophy in children, allows us to look at the upper airway obstruction in three-dimensional space and relieves the work pressure of imaging doctors.

Targeted expression of receptor-associated late transducer inhibits maladaptive hypertrophy via blocking epidermal growth factor receptor signaling.

Receptor-associated late transducer (RALT) is a feedback inhibitor of epidermal growth factor receptor signaling. RALT has been shown previously to be induced in the ischemic heart and to promote cardiomyocyte apoptosis in vitro. However, the role of RALT in cardiac hypertrophy remains unclear. We hypothesized that forced expression of RALT in the murine heart would protect the heart against cardiac hypertrophy in vivo. We investigated the effect of cardiac overexpression of rat RALT on cardiac hypertrophy induced by angiotensin II and isoproterenol in RALT transgenic mice and wild-type littermates. The extent of cardiac hypertrophy was assessed by 2D and M-mode echocardiography as well as by molecular and pathological analyses of cardiac samples. Constitutive expression of rat RALT in cardiac myocytes of murine heart attenuated both hypertrophic and inflammatory responses and preserved cardiac function. These beneficial effects were associated with the attenuation of the epidermal growth factor receptor-dependent cascade that was triggered by angiotensin II and isoproterenol stimulation. Additional evidence demonstrated that RALT expression blocked fibrosis in vivo and collagen synthesis in vitro. Therefore, cardiac overexpression of RALT improves cardiac function and inhibits maladaptive hypertrophy, inflammation, and fibrosis through attenuating epidermal growth factor receptor-dependent signaling.