Auxiliary diagnostic method of Parkinson's disease based on eye movement analysis in a virtual reality environment.

Eye movement dysfunction is one of the non-motor symptoms of Parkinson's disease (PD). An accurate analysis method for eye movement is an effective way to gain a deeper understanding of the nervous system function of PD patients. However, currently, there are only a few assistive methods available to help physicians conveniently and consistently assess patients suspected of having PD. To solve this problem, we proposed a novel visual behavioral analysis method using eye tracking to evaluate eye movement dysfunction in PD patients automatically. This method first provided a physician task simulation to induce PD-related eye movements in Virtual Reality (VR). Subsequently, we extracted eye movement features from recorded eye videos and applied a machine learning algorithm to establish a PD diagnostic model. Then, we collected eye movement data from 66 participants (including 22 healthy controls and 44 PD patients) in a VR environment for training and testing during visual tasks. Finally, on this relatively small dataset, the results reveal that the Support Vector Machine (SVM) algorithm has better classification potential.

Circular RNA circBNC2 facilitates glycolysis and stemness of hepatocellular carcinoma through the miR-217/high mobility group AT-hook 2 (HMGA2) axis.

Hepatocellular cancer (HCC) accounts for approximately 90% of primary liver carcinoma and is a significant health threat worldwide. Circular RNA basonuclin 2 (circBNC2) is implicated with the progression of several cancers. However, its roles in carcinogenesis and glycolysis are still unclear in HCC. In this study, the levels of circBNC2 and high mobility group AT-hook 2 (HMGA2) were highly expressed, while these of miR-217 were poorly expressed in HCC tissues and cells. Upregulation of circBNC2 was related to poor prognosis and tumor node metastasis (TNM) stage. Knockdown of circBNC2 inhibited the HCC progression. Moreover, knockdown of circBNC2 suppressed the levels of Ras, ERK1/2, PCNA, HK2, and OCT4. Notably, circBNC2 functioned as a molecular sponge of microRNA 217 (miR-217) to upregulate the HMGA2 expression. The inhibitory effects of the circBNC2 silence on the growth and stemness of HCC cells, and levels of PCNA, HK2 and OCT4 were aggravated by the miR-217 overexpression, but neutralized by the HMGA2 overexpression. Besides, silencing of circBNC2 blocked the tumor growth through upregulating the expression of miR-217 and downregulating the levels of HMGA2, PCNA2, HK2 and OCT4 in vivo. Thus, the current data confirmed that circBNC2 sponged miR-217 to upregulate the HMGA2 level, thereby contributing to the HCC glycolysis and progression. These findings might present novel insight into the pathogenesis and treatment of HCC.

STAT1 Mediates the Transcription of CircIFI30 and Promotes the Progression of Triple-Negative Breast Cancer by Up-Regulating CDCA4.

Signal transducers and activators of transcription 1 (STAT1) is an important transcription factor that regulates the growth, survival, differentiation and apoptosis of various tumor cells. However, the biological roles of STAT1 and potential mechanisms in triple-negative breast cancer (TNBC) remain largely unknown. The expression levels of STAT1, CircIFI30, CDCA4, and epithelial-mesenchymal transition (EMT)-associated molecules (MM2, MMP9, E-cadherin, and N-cadherin) were evaluated using quantitative reverse transcription polymerase chain reaction (RT-qPCR). Furthermore, cell-counting kit-8 assay, Transwell assay, flow cytometry, and immunofluorescence staining were performed to investigate the biological functions of STAT1 and CircIFI30 in TNBC cells. In addition, Dual luciferase activity assay and chromatin immunoprecipitation qPCR were used to predict the interaction between STAT1 and CircIFI30 promoter. The effects of CircIFI30 on the stability of CDCA4 mRNA were also confirmed in further function study. Up-regulation of STAT1 was detected in TNBC tissues and cells, which were positively correlated with tumor metastasis, advanced clinical stage and poor survival rate. Up-regulated STAT1 could promote the proliferation, invasion, migration, EMT and inhibit the apoptosis of TNBC cells. RNA-seq indicated has_circ_0005571 (CircIFI30) was significantly down-regulated in TNBC cells after knockdown of STAT1. Moreover, STAT1 could be novel transcription factor that binds to CircIFI30 promoter to enhance its transcription. Additionally, knockdown of CirclFl30 down regulated the expression of cell division cycleassociated protein 4 (CDCA4) through reducing the stability of its mRNA. Our data revealed the STAT1/CircIFI30/CDCA4 axis could regulate the proliferation, invasion, migration, EMT and apoptosis of TNBC cells. Therefore, STAT1 may be a putative therapeutic candidate for targeted treatment of TNBC.

Development of a Multi-Channel Wearable Heart Sound Visualization System.

A multi-channel wearable heart sound visualization system based on novel heart sound sensors for imaging cardiac acoustic maps was developed and designed. The cardiac acoustic map could be used to detect cardiac vibration and heart sound propagation. The visualization system acquired 72 heart sound signals and one ECG signal simultaneously using 72 heart sound sensors placed on the chest surface and one ECG analog front end. The novel heart sound sensors had the advantages of high signal quality, small size, and high sensitivity. Butterworth filtering and wavelet transform were used to reduce noise in the signals. The cardiac acoustic map was obtained based on the cubic spline interpolation of the heart sound signals. The results showed the heart sound signals on the chest surface could be detected and visualized by this system. The variations of heart sounds were clearly displayed. This study provided a way to select optimal position for auscultation of heart sounds. The visualization system could provide a technology for investigating the propagation of heart sound in the thoracic cavity.

HDAC3-Mediated Repression of LncRNA-LET Regulates Gastric Cancer Cell Growth Proliferation, Invasion, Migration, and Apoptosis via MiR-548k.

Emerging studies have indicated the aberrant expression of histone deacetylases (HDACs) is closely associated with the development of tumors. However, the regulatory roles of HDACs-regulated long noncoding RNAs (lncRNA) in gastric cancer (GC) remain largely unknown. In this study, the effects of HDAC3 and HDAC3-mediated lncRNA-LET on the progression of GC were investigated. The expressions of HDAC3, lncRNA-LET, and miR-548k in GC cell lines were analyzed. The biological functions of HDAC3 and lncRNA-LET were measured by CCK-8 assay, Transwell assay, Western blot analysis, and cell apoptosis assays. Chromatin immunoprecipitation and luciferase reporter assay verified the regulatory relationship between HDAC3 and lncRNA-LET, and lncRNA-LET and miR-548 in GC cells. HDAC3 was significantly overexpressed in GC cell lines compared to GES-1. Knockdown of HDAC3 suppressed the proliferation, invasion, and migration of AGS and SGC-7901 cells, while cell apoptosis was promoted. Silenced HDAC3 promoted histone acetylation in the promoter region of lncRNA-LET, subsequently upregulating the expression of lncRNA-LET in AGS and SGC-7901 cells. In addition, overexpressed lncRNA-LET notably inhibited the proliferation, invasion, and migration of GC cells, whereas apoptosis was enhanced. LncRNA-LET could function as the sponge of miR-548k. HDAC3 was able to regulate the progression of GC cells via the lncRNA-LET/miR-548k signaling pathway. We confirmed that the HDAC3/lncRNA-LET/miR-548k signal axis mediated the occurrence and development of GC, and HDAC3 could be a novel therapeutic target for the treatments of GC.