Thyroid cancer (THCA) is a leading endocrine cancer and becomes the fifth most commonly diagnosed malignancy in females. It is confirmed that circular RNAs (circRNAs) perform regulatory potencies in the pathological progress of THCA. Our purpose was to certify the trait of hsa_circ_0000285 (circ_0000285) and investigate its modulatory mechanism in THCA progression. We identified the expression profile of hsa_circ_0000285 in THCA by conducting qRT‐PCR assay. Therewith, the potential of hsa_circ_0000285 in THCA development was determined with a set of functional experiments, including CCK‐8, wound healing assay, Western blot, and xenograft model. The molecular mechanism underlying hsa_circ_0000285 was investigated with bioinformatic analysis, RIP and dual‐luciferase reporter experiments. As opposed to normal samples and cells, hsa_circ_0000285 level was overtly increased in THCA specimens and cells. The downregulation of hsa_circ_0000285 weakened the proliferative and migratory capacity of THCA cells and promoted cell apoptosis. In addition, hsa_circ_0000285 silence suppressed the tumor growth of xenograft model mice in vivo. Notably, we demonstrated that hsa_circ_0000285 might target miR‐127‐5p/CDH2 axis in THCA. Afterward, our findings manifested that miR‐127‐5p attenuation blocked the function of hsa_circ_0000285 depletion in THCA cells. In the final step, CDH2 was proven to mediate the repressive potency of miR‐127‐5p in the malignant behaviors of THCA. Mechanistically, hsa_circ_0000285 induced the development of THCA via functioning as a competing endogenous RNA (ceRNA) of miR‐127‐5p to enhance CDH2 expression, which provided a new perspective for THCA therapy.

Choosing reaction time as dependent variable, the paper discussed the effects of object independent vibration on visual identification efficiency, which was under different vibration frequency, amplitude, direction and the position of target gap. The major experiment results indicated that the reaction time increase exponentially with the increasing of vibration frequency and amplitude within a certain range. This will provide a scientific basis for design optimization and vibration control of human-machine system.

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The cancer-promoting function of the long non-coding RNA (lncRNA) LPP-AS2 has been documented in different cancers. Nonetheless, its role in thyroid carcinoma (THCA) remains unestablished. Reverse transcription quantitative polymerase chain reaction and Western blotting were conducted to estimate the expressions of lncRNA LPP-AS2, miR-132-3p, and OLFM1. The THCA cells' functions were assessed through CCK8 assays, Transwell invasion assays, scratch wound-healing migration assays, and quantification of caspase-3 activity. The in vivo assays were also implemented to assess tumor growth. Luciferase reporter and RNA immuno-precipitation assay (RIPA) experiments were executed to elucidate the interactions of miR-132-3p with lncRNA LPP-AS2 and OLFM1. THCA tissues and cells exhibited poor lncRNA LPP-AS2 and OLFM1 expressions and a robust expression of miR-132-3p. Overexpressing lncRNA LPP-AS2 constrained THCA cell proliferation, migration, and invasion and improved caspase-3 activity. The anti-tumor function of lncRNA LPP-AS2 was also validated <i>in vivo</i>. miR-132-3p had an interplay with lncRNA LPP-AS2 and OLFM1. Functionally, overexpressing miR-132-3p promoted the malignant THCA cell phenotypes. However, that tumor promotion was abolished by the additional overexpression of lncRNA LPP-AS2. The <i>in vitro</i> experiments also demonstrated that the repressive effect of OLFM1 overexpression on THCA cell malignant action could be offset by the miR-132-3p mimic. lncRNA LPP-AS2 impedes THCA progression via the miR-132-3p/OLFM1 axis. Our findings contribute a potential strategy in interfering with THCA progression.

Objective. To investigate the relationship between changes in blood glucose and blood lipid levels and the risk of thyroid cancer in patients with type 2 diabetes mellitus. Methods. A total of 159 patients with type 2 diabetes who were treated in our hospital between June 2018 and February 2021 were recruited and assigned into the observation group, including 136 patients with type 2 diabetes without thyroid cancer (nonthyroid cancer group) and 23 patients with type 2 diabetes complicated with thyroid cancer (thyroid cancer group), and 120 healthy subjects during the same period were selected as the control group. Glycated hemoglobin (HbAlc), total cholesterol (TC), triacylglycerol (TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) were detected and compared. Pearson’s method was conducted to analyze the correlation between serum HbAlc level and TC, TG, HDL-C, and LDL-C levels in patients with type 2 diabetes mellitus; multivariate logistic regression analysis was performed to analyze the influencing factors of thyroid cancer in patients with type 2 diabetes mellitus. Results. The serum HbAlc level and the incidence of thyroid cancer in patients with type 2 diabetes mellitus in the observation group were significantly higher than those in the control group ( P < 0.05 ). The levels of TC, TG, and LDL-C in patients with type 2 diabetes mellitus in the observation group were significantly higher than those in the control group, and the level of HDL-C was significantly lower than that in the control group ( P < 0.05 ). The correlation analysis showed that serum HbAlc levels in patients with type 2 diabetes were positively correlated with TC and TG levels and negatively correlated with HDL-C levels ( P < 0.05 ) and not correlated with LDL-C levels ( P > 0.05 ). Compared with the type 2 diabetes patients without thyroid cancer, the serum HbAlc, TC, and TG levels of the patients with type 2 diabetes mellitus in the thyroid cancer group were significantly higher, and the levels of HDL-C were significantly lower ( P < 0.05 ). There was no significant change in the level of LDL-C ( P > 0.05 ). Multivariate logistic regression analysis showed that serum HbAlc, TC, and TC levels were all risk factors for thyroid cancer in patients with type 2 diabetes mellitus ( P < 0.05 ), while serum HDL-C level was a protective factor for thyroid cancer in patients with type 2 diabetes mellitus ( P < 0.05 ). Conclusion. Thyroid cancer in type 2 diabetes patients may be linked to elevated levels of blood HbAlc, TC, and TG. HbAlc may raise the risk of thyroid cancer in type 2 diabetes patients by modulating blood lipid levels, which might serve as a marker to assess the risk of thyroid cancer in type 2 diabetes mellitus patients. However, since this study did not conduct in vitro and in vivo experiments, how HbAlc affects the pathogenesis of thyroid cancer has not been described in this study, which is also our future research direction. It is expected to provide new ideas for the prevention and treatment of thyroid cancer.