Ectopic thyroid in the hepatoduodenal ligament: a case report and literature review.

Ectopic thyroid arises from abnormal development of thyroid primordial tissues as it migrates to the lower interstitium during the embryonic period, which can occur at various locations during the descent process. However, ectopic thyroid in the subdiaphragmatic area is extremely rare. In this case, we report a case of ectopic thyroid located in the hepatoduodenal ligament. The 60-year-old female patient was admitted to hospital with gallbladder stones and cholecystitis. Preoperative imaging showed a mass in the hepatoduodenal ligament. As the patient declined a needle biopsy of the mass, the nature of the mass remained unclear prior to surgery. The patient subsequently underwent laparoscopic cholecystectomy and exploratory resection of the mass. The histopathology of the resected mass showed the characteristics of ectopic thyroid, and immunohistochemical staining revealed positive expression of thyroid transcription factor-1 and thyroglobulin. The diagnosis of ectopic thyroid was established. Upon confirming the diagnosis, comprehensive neck examination revealed the presence of a normally functioning thyroid gland. Throughout the four-year follow-up period, the patient's thyroid ultrasonography and thyroid function tests indicated no abnormalities. Ectopic thyroid in the hepatoduodenal ligament and surrounding areas is an extremely rare clinical abnormality, achieving a clear diagnosis before initiating treatment offers diagnostic and treatment insights and clues for clinicians when differentiating masses within this region.

CircSOS2 promotes cervical squamous cell carcinoma by regulation of proliferation, cell cycle, apoptosis, migration, invasion, and glycolysis by targeting miR-543/FNDC3B axis.

BACKGROUND: Cervical squamous cell carcinoma (SCC) is a common subtype of cervical cancer. Circular RNAs (circRNAs) have been demonstrated as vital regulators in gene regulation and malignant tumor progression. Therefore, the precise role of circular RNA salt overly-sensitive 2 (circSOS2) was investigated in SCC. METHODS: The relative expression levels of circSOS2, microRNA-543 (miR-543), and Fibronectin type III domain containing 3B (FNDC3B) were determined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assays. The correlation between percent survival times of SCC patients and circSOS2 level was presented by Kaplan-Meier Plotter analysis. The cell proliferation was measured by MTT and colony-forming assays. Flow cytometry assay was used to assess apoptosis and cell cycle distribution. The migration and invasion were measured by transwell assay. The glycolysis was analyzed by extracellular acidification rate (ECAR) assay, Glucose Assay Kit, and Lactate Assay Kit. The interaction relationship between miR-543 and circSOS2 or FNDC3B was analyzed by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. A xenograft experiment was established to clarify the functional role of circSOS2 inhibition in viv. RESULTS: CircSOS2 was highly expressed in SCC tissues and cells; besides, its expression level was closely associated with poor prognosis. Loss-of-functional experiments revealed that suppression of circSOS2 repressed proliferation, cell cycle process, migration, invasion, and glycolysis while induced apoptosis in SCC cells, which was overturned by inhibition of miR-543. In addition, miR-543 was downregulated and negatively correlated with circSOS2 expression in SCC tissues. We also found that overexpression of miR-543 impeded proliferation, cell cycle process, migration, invasion, and glycolysis while induced apoptosis in SCC cells by targeting FNDC3B. The silencing of circSOS2 impeded tumorigenesis in vivo. CONCLUSION: CircSOS2 conferred an oncogenic function in SCC by regulation of proliferation, cell cycle, apoptosis, migration, invasion, and glycolysis of SCC cells, which was contributed to its interactions with miR-543 and FNDC3B.

Multivariate weighted recurrence network analysis of EEG signals from ERP-based smart home system.

Smart home has been widely used to improve the living quality of people. Recently, the brain-computer interface (BCI) contributes greatly to the smart home system. We design a BCI-based smart home system, in which the event-related potentials (ERP) are induced by the image interface based on the oddball paradigm. Then, we investigate the influence of mental fatigue on the ERP classification by the Fisher linear discriminant analysis. The results indicate that the classification accuracy of ERP decreases as the brain evolves from the normal stage to the mental fatigue stage. In order to probe into the difference of the brain, cognitive process between mental fatigue and normal states, we construct multivariate weighted recurrence networks and analyze the variation of the weighted clustering coefficient and weighted global efficiency corresponding to these two brain states. The findings suggest that these two network metrics allow distinguishing normal and mental fatigue states and yield novel insights into the brain fatigue behavior resulting from a long use of the ERP-based smart home system. These properties render the multivariate recurrence network, particularly useful for analyzing electroencephalographic recordings from the ERP-based smart home system.

Celastrol inhibits migration and invasion through blocking the NF-κB pathway in ovarian cancer cells.

Metastatic ovarian cancer is a major clinical challenge with poor prognosis and high mortality. Celastrol is a natural compound that has exhibits antiproliferative activity; however, its effects on metastasis-related phenotypes in ovarian cancer models are unclear. In the current study, the anti-invasive activities and associated signaling pathways of celastrol were determined in ovarian cancer cells. Cell proliferation was tested by MTT assay. Cell migration was detected by wound healing and Transwell assays, while cell invasion was detected by a Matrigel-coated Transwell method. In addition, nuclear factor (NF)-κB and matrix metalloproteinase (MMP) expression was examined by western blotting, and MMP-2/-9 activities were determined by gelatin zymography. At sub-toxic concentrations (<0.5 µM), celastrol inhibited migration and invasion in a concentration-dependent manner in SKOV-3 and OVCAR-3 cells. At the molecular level, celastrol blocked the canonical NF-κB pathway by inhibiting IκBα phosphorylation, and preventing IκBα degradation and p65 accumulation. Furthermore, the expression and activity of the NF-κB target protein MMP-9, but not MMP-2, were inhibited by celastrol. Furthermore, celastrol showed no synergistic effect with MG132, an NF-κB inhibitor. In conclusion, celastrol exhibited significant anti-invasive activities in ovarian cancer cells. Such functions may be mediated via NF-κB pathway blockade. The results of this in vitro study strengthen the value of applying celastrol as a potential clinical intervention modality for delaying ovarian cancer metastasis. This, celastrol warrants further preclinical investigation.