The purposes of this study were to investigate the potential roles of long noncoding RNA (lncRNA) PVT1 in thyroid cancer cell proliferation and to explore their possible mechanisms. A total of 84 patients who were diagnosed as having thyroid cancer (papillary thyroid carcinoma (PTC), follicular thyroid carcinoma (FTC), and anaplastic thyroid carcinoma (ATC)) in Renji Hospital were enrolled in this study. Expressions of lncRNA PVT1 in thyroid cancer tissues and cell lines (IHH-4, FTC-133, and 8505C) were analyzed using RT-polymerase chain reaction (PCR) and western blotting analysis. The effects of lncRNA PVT1 expression on thyroid cancer cell proliferation and cell cycle were analyzed using flow cytometry. Furthermore, the effects of lncRNA expression on thyroid-stimulating hormone receptor (TSHR) expression and polycomb enhancer of zeste homolog 2 (EZH2) were also analyzed using RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay, respectively. Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues, as well as in three kinds of tumor cell lines (P < 0.05). Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions (P < 0.05). Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2. This study suggested that lncRNA PVT1 may contribute to tumorigenesis of thyroid cancer through recruiting EZH2 and regulating TSHR expression.

This study suggested that countries with higher economic status tend to present a higher prevalence of NAFLD. It is believed to provide a distinctive epidemiologic perspective to global situation of NAFLD.

With the development of socioeconomic status, as measured by the Human Development Index, the prevalence of coronary heart disease is growing in developing countries, while declining in developed countries. Future research needs to pay more attention to the reasonable allocation of medical resources and control of coronary heart disease risk factors.

This study reveals a correlation between the economy and the prevalence of FLD in mainland China.

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Abstract. Mental fatigue is considered to be a contributing factor responsible for numerous road accidents and various medical conditions and the efficiency and performance could be impaired during fatigue. Hence, determining how to evaluate mental fatigue is very important. In the present study, ten subjects performed a long-term visual search task with electroencephalogram recorded, and self-assessment and reaction time (RT) were combined to verify if mental fatigue had been induced and were also used as confirmatory tests for the proposed measures. The changes in relative energy in four wavebands į ș Į and ȕ), four ratio formulas [(D + T)/E, D/E, (D + T)/(D + E), and T/E], and Shannon's entropy (SE) were compared and analyzed between the beginning and end of the task. The results showed that a significant increase occurred in alpha activity in the frontal, central, posterior temporal, parietal, and occipital lobes, and a dip occurred in the beta activity in the pre-frontal, inferior frontal, posterior temporal, and occipital lobes. The ratio formulas clearly increased in all of these brain regions except the temporal region, where only D/E changed obviously after finishing the 60-min visual search task. SE significantly increased in the posterior temporal, parietal, and occipital lobes. These results demonstrate some potential indicators for mental fatigue detection and evaluation, which can be applied in the future development of countermeasures to fatigue.

The availability of algorithms to create three-dimensional (3D) models from medical images has made it possible to render and build patient-specific reconstructions of individual body parts. In the present study, this technology was used to create 3D models of pediatric hearts for use in medical device development. Digital models were created using CT datasets of pediatric hearts and commercially available 3D image processing software. Using this software, stacked CT data were viewed, and pixels representing the heart and rib cage were selected and rendered as 3D models. Stereolithography and 3D printing technology were used to create rigid and flexible physical heart models (biomodels) from the digital models. Twelve on-screen models of the thorax and cardiac structures were created from cardiac CT scans obtained from 11 patients with and without congenital heart disease (median age, 3 years; range, 2 days to 13 years). Rigid and flexible physical heart models were generated from the digital models to provide tactile and visual information. 3D models of pediatric cardiac and chest anatomy provide enhanced understanding and tactile representation of complex anatomy. Precise representation of the spatial relationships between anatomic structures is particularly useful during the development and placement of medical devices.

Long noncoding RNAs (lncRNAs) are emerging as important regulators in the development of cancer cells. However, the role and mechanisms of most lncRNAs in papillary thyroid carcinoma (PTC) remain unknown. In this study, we investigated lncRNA expression profiles of PTC using RNA-seq in two groups of PTC tissues and adjacent normal tissues, and validated by real-time PCR analysis in another 53 pairs of tissues. We identified a novel lncRNA, n384546, which is highly expressed in PTC tissues and cell lines. n384546 expression was associated with clinicopathological features of PTC patients, such as tumor size, lymph node metastasis, and TNM stage. Functionally, knockdown of n384546 inhibited PTC cell proliferation, invasion, and migration both in vitro and in vivo. In addition, we identified miR-145-5p as a key miRNA target of n384546 using online bioinformatics tools. Anti-miR-145 could partially reverse the effects of n384546 knockdown. Furthermore, we found that n384546 could regulate the expression of AKT3 by sponging miR-145-5p, which was confirmed using an in vitro luciferase assay. In conclusion, we validated n384546 as a novel oncogenic lncRNA in PTC and determined that the n384546/miR-145-5p/AKT3 pathway contributes to PTC progression, which might be used as potential therapeutic targets for PTC patients.