IONM system implemented in transoral thyroid surgery was feasible and serviceable in preventing RLN injury. The method of TOETVA shows promise for thyroidectomy with CND due its ideal cosmetic results.

Abstract. Primary thyroid paraganglioma (TP) is an uncommon tumor, and in rare cases, this disease tends to mimic medullary thyroid carcinoma (MTC). The present study reports a rare case of primary TP mimicking thyroid carcinoma, accompanied by hyperthyroidism. A 30-year-old female presented with an anterior cervical mass. Pre-operative radiological studies and operative frozen section analysis indicated an atypical MTC. Primary TP was finally diagnosed by pathology and immunohistochemical staining. Laboratory examinations (thyroid hormones tests) and Tc99m emission computed tomography revealed hyperthyroidism. Gene analysis of TP-associated gene mutations was negative. Surgical resection was performed as a curative approach and there is currently no metastasis after 36 months of follow-up. Surgeons must be aware of this disease in order to ensure a correct diagnosis and to prevent them from performing unnecessary procedures. The current study presents a case of primary TP mimicking MTC, discusses the radiographic results and histological characteristics, and provides a review of the associated literature.

Study has shown that long noncoding RNA (lncRNA) prostate androgen‐regulated transcript 1 (PART1) was elevated in colorectal cancer tissues and cells, and the proliferation and metastasis of colorectal cancer cells were reduced after its downregulation. The tumor‐suppressive role of microRNA‐150‐5p (miR‐150‐5p) has been shown in colorectal cancer. In this study, the association between PART1 and miR‐150‐5p in colorectal cancer was analyzed. Results revealed an increase of PART1, but a decrease of miR‐150‐5p in 56 colorectal cancer tissues. And there was a strong negative correlation between levels of PART1 and miR‐150‐5p in these cancer samples. Also, compared with 10 healthy controls, the level of PART1 was increased, whereas miR‐150‐5p expression was diminished in the serum of 10 colorectal cancer patients. Cell proliferation and migration, along with epithelial‐mesenchymal transition, was promoted by PART1 overexpression. However, this lncRNA mitigated apoptosis of colorectal cancer cells. Whereas miR‐150‐5p mimic abrogated these effects caused by PART1 overexpression. The influences of PART1 knockdown on the above malignant characteristics of colorectal cancer cells were contrary to its overexpression. miR‐150‐5p inhibitor ablated the effects induced by PART1 knockdown. In xenograft mouse models, silencing of PART1 decreased tumor volume and weight. Our data supported that lncRNA PART1 may regulate leucine‐rich α‐2‐glycoprotein‐1 (LRG1) expression through a competing interaction mechanism that hindering miR‐150‐5p function. In conclusion, PART1 facilitates the malignant progression of colorectal cancer via miR‐150‐5p/LRG1 pathway. The study further clarified the molecular mechanism of PART1 in colorectal cancer. This study may provide a new approach to diagnose and treat colorectal cancer.

Background: The role of circular RNA (circRNA) in papillary thyroid cancer (PTC) is largely unknown. This study aims to determine the function and mechanism of circPRMT5 in the regulation of PTC development. Methods: PTC tissues and cell lines were used to determine circPRMT5 expression via quantitative real-time polymerase chain reaction. Small interfering RNA (siRNA) was utilized to knock down circPRMT5. Proliferation was analyzed through CCK8 and colony formation assays. Transwell assay was performed to determine cell migration and invasion. Luciferase assay and RIP assay were carried out to analyze the interaction between circPRMT5 and miR-30c. Results: CircPRMT5 expression was upregulated in PTC tissues and cell lines. And circPRMT5 level was positively linked with advanced stage and lymph node metastasis. CircPRMT5 knockdown inhibited proliferation, migration and invasion while inducing apoptosis. CircPRMT5 worked as a competing endogenous RNA for miR-30c. By inhibiting miR-30c, circPRMT5 promoted the expression of E2F3. Conclusion: Our findings demonstrate that circPRMT5 acts as an oncogenic circRNA to promote PTC progression via regulating miR-30c/E2F3 axis.

Abstract:We have investigated comprehensively the effects of thyroid function on gallstone formation in a mouse model. Gonadectomized gallstone-susceptible male C57BL/6 mice were randomly distributed into three groups each of which received an intervention to induce hyperthyroidism, hypothyroidism, or euthyroidism. After 5 weeks of feeding a lithogenic diet of 15% (w/w) butter fat, 1% (w/w) cholesterol, and 0.5% (w/w) cholic acid, mice were killed for further experiments. The incidence of cholesterol monohydrate crystal formation was 100% in mice with hyperthyroidism, 83% in hypothyroidism, and 33% in euthyroidism, the differences being statistically significant. Among the hepatic lithogenic genes, Trβ was found to be up-regulated and Rxr down-regulated in the mice with hypothyroidism. In contrast, Lxrα, Rxr, and Cyp7α1 were up-regulated and Fxr down-regulated in the mice with hyperthyroidism. In conclusion, thyroid dysfunction, either hyperthyroidism or hypothyroidism, promotes the formation of cholesterol gallstones in C57BL/6 mice. Gene expression differences suggest that thyroid hormone disturbance leads to gallstone formation in different ways. Hyperthyroidism induces cholesterol gallstone formation by regulating expression of the hepatic nuclear receptor genes such as Lxrα and Rxr, which are significant in cholesterol metabolism pathways. However, hypothyroidism induces cholesterol gallstone formation by promoting cholesterol biosynthesis.