A novel ultrasound image diagnostic method for thyroid nodules

Abstract The incidence of thyroid nodules is increasing year by year. Accurate determination of benign and malignant nodules is an important basis for formulating treatment plans. Ultrasonography is the most widely used methodology in the diagnosis of benign and malignant nodules, but diagnosis by doctors is highly subjective, and the rates of missed diagnosis and misdiagnosis are high. To improve the accuracy of clinical diagnosis, this paper proposes a new diagnostic model based on deep learning. The diagnostic model adopts the diagnostic strategy of localization-classification. First, the distribution laws of the nodule size and nodule aspect ratio are obtained through data statistics, a multiscale localization network structure is a priori designed, and the nodule aspect ratio is obtained from the positioning results. Then, uncropped ultrasound images and nodule area image are correspondingly input into a two-way classification network, and an improved attention mechanism is used to enhance the feature extraction performance. Finally, the deep features, the shallow features, and the nodule aspect ratio are fused, and a fully connected layer is used to complete the classification of benign and malignant nodules. The experimental dataset consists of 4021 ultrasound images, where each image has been labeled under the guidance of doctors, and the ratio of the training set, validation set, and test set sizes is close to 3:1:1. The experimental results show that the accuracy of the multiscale localization network reaches 93.74%, and that the accuracy, specificity, and sensitivity of the classification network reach 86.34%, 81.29%, and 90.48%, respectively. Compared with the champion model of the TNSCUI 2020 classification competition, the accuracy rate is 1.52 points higher. Therefore, the network model proposed in this paper can effectively diagnose benign and malignant thyroid nodules

Resveratrol and caloric restriction prevent hepatic steatosis by regulating SIRT1-autophagy pathway and alleviating endoplasmic reticulum stress in high-fat diet-fed rats

<div><p>Background</p><p>Studies have demonstrated that resveratrol (a natural polyphenol) and caloric restriction activate Sirtuin-1 (SIRT1) and induce autophagy. Furthermore, autophagy is induced by the SIRT1-FoxO signaling pathway and was recently shown to be a critical protective mechanism against non-alcoholic fatty liver disease (NAFLD) development. We aimed to compare the effects of resveratrol and caloric restriction on hepatic lipid metabolism and elucidate the mechanism by which resveratrol supplementation and caloric restriction alleviate hepatosteatosis by examining the molecular interplay between SIRT1 and autophagy.</p><p>Methods and results</p><p>Eight-week-old male Wistar rats (40) were divided into four groups: the STD group, which was fed a standard chow diet; the HFD group, which was fed a high-fat diet; HFD-RES group, which was fed a high-fat diet plus resveratrol (200 mg/kg.bw); and the HFD-CR group, which was fed a high-fat diet in portions containing 70% of the mean intake of the HFD group rats. The groups were maintained for 18 weeks. Metabolic parameters, Oil Red O and hematoxylin-eosin staining of the liver, and the mRNA and protein expression of SIRT1, autophagy markers and endoplasmic reticulum(ER) stress-associated genes in the liver were assessed after the 18-week treatment. We found that resveratrol (200 mg/kg bw) and caloric restriction (30%) partially prevented hepatic steatosis and hepatocyte ballooning, increased the expression of SIRT1 and autophagy markers while decreasing ER stress markers in the liver and alleviated lipid metabolism disorder. Moreover, caloric restriction provided superior protection against HFD-induced hepatic fatty accumulation compared with resveratrol and the effects were associated with decreased total energy intake and body weight.</p><p>Conclusion</p><p>We conclude that the SIRT1-autophagy pathway and decreased ER stress are universally required for the protective effects of moderate caloric restriction (30%) and resveratrol (a pharmacological SIRT1 activator) supplementation against HFD-induced hepatic steatosis.</p></div

Hematoxylin and eosin staining observation of rat liver tissue (original magnification: ×400, scale bars = 50 μm).

<p>(A) STD group. (B) HFD group. (C) HFD-RES group. (D) HFD-CR group. (E) Volume density of quantitation of hepatic steatosis (n = 5 per group). **, <i>P</i><0.01 compared with the STD group; ^#, <i>P</i><0.05 and ^##, <i>P</i><0.01 compared with the HFD group.</p

Changes of expression autophagy relative genes, ER stress genes and SIRT1 gene in the rat liver (n = 3 per group).

<p>(A) <i>LC3</i>. (B) <i>Beclin 1</i>. (C) <i>p62</i>. (D) <i>SIRT1</i>. (E) <i>PERK</i>. (F) <i>GRP78</i>. (G) <i>CHOP</i>. ^<b>*</b>, <i>P</i><0.05 and **, <i>P</i><0.01 compared with the STD group; ^#, <i>P</i><0.05 and ^##, <i>P</i><0.01 compared with the HFD group; ^△, <i>P</i><0.05 compared with the HFD-RES group. Data are expressed as the mean ± SD.</p

Effects of RES and CR on the protein levels of autophagy markers and SIRT1 in the liver (n = 3 per group).

<p>(A) Western blotting results for LC3 protein. (B) Quantitative analysis of LC3-II band densities. (C) Western blotting results for SIRT1 protein. (D) Quantitative analysis of SIRT1 band densities. (E) Western blotting results for p62 protein. (F) Quantitative analysis of p62 band densities. ^<b>*</b>, <i>P</i><0.05 and **, <i>P</i><0.01 compared with the STD group; ^#, <i>P</i><0.05 and ^##, <i>P</i><0.01 compared with the HFD group. Data are expressed as the mean ± SD.</p

Lipid parameters in the serum and liver of rats (n = 8–10 per group).

<p>(A) Serum total triglycerides. (B) Serum total cholesterol. (C) Serum HDL. (D) Serum LDL. (E) Hepatic total triglycerides. (F) Hepatic total cholesterol. ^<b>*</b>, <i>P</i><0.05 and **, <i>P</i><0.01 compared with the STD group; ^#, <i>P</i><0.05 and ^##, <i>P</i><0.01 compared with the HFD group. Data are expressed as the mean ± SD.</p

Effects of RES and CR on the protein levels of endoplasmic reticulum stress markers in the liver (n = 3 per group).

<p>(A) Western blotting results for CHOP protein. (B) Quantitative analysis of CHOP band densities. (C) Western blotting results for GRP78 protein. (D) Quantitative analysis of GRP78 band densities. ^<b>*</b>, <i>P</i><0.05 and **, <i>P</i><0.01 compared with the STD group; ^#, <i>P</i><0.05 and ^##, <i>P</i><0.01 compared with the HFD group. Data are expressed as the mean ± SD.</p