A Study on the Correlation Between Age-Related Macular Degeneration and Alzheimer's Disease Based on the Application of Artificial Neural Network.

Age-related Macular Degeneration (AMD) is a kind of irreversible vision loss or disease caused by retinal pigment epithelial cells and neuroretinal degeneration, which has become the main cause of vision loss and blindness of the elderly over 65 years old in developed countries. The main clinical manifestations are cognitive decline, mental symptoms and behavioral disorders, and the gradual decline of daily living ability. In this paper, a feature extraction method of electroencephalogram (EEG) signal based on multi-spectral image fusion of multi-brain regions is proposed based on artificial neural network (ANN). In this method, the brain is divided into several different brain regions, and the EEG signals of different brain regions are transformed into several multispectral images by combining with the multispectral image transformation method. Using Alzheimer's disease (AD) classification algorithm, the depth residual network model pre-trained in ImageNet was transferred to sMRI data set for fine adjustment, instead of training a brand-new model from scratch. The results show that the proposed method solves the problem of few available medical image samples and shortens the training time of ANN model.

FUNDC1 Induces Apoptosis and Autophagy Under Oxidative Stress via PI3K/Akt/mTOR Pathway in Cataract Lens Cells.

PURPOSE: The purpose of the study is to explore the mRNA and protein expression of FUNDC1 in cataract cells and tissues, and clarify the function and mechanism of FUNDC1 in cataract cells under oxidative stress. METHODS: We used bioinformatic analysis to screen differentially expressed genes in cataract cells from GSE153933. The expression of FUNDC1 in cataract specimens and cells was measured by reverse transcription quantitative polymerase chain reaction and western blotting. MethPrimer was used to predict CpG island of FUNDC1 promoter. The methylation of FUNDC1 in cataract specimens and cells was determined by methylation-specific polymerase chain reaction assay. Flow cytometry assay was used to measure cell apoptosis in FUNDC1-knockdown and -overexpression SRA01/04 cells. The expression of LC3 was analyzed by immunofluorescence assay. The expression of apoptosis-related proteins, autophagy, and PI3K/Akt/mTOR-related proteins was determined by western blotting. RESULTS: The results of bioinformatic analysis revealed that FUNDC1 was upregulated in cataract. FUNDC1 was high expression in SRA01/04 cells with H2O2 treatment, whereas hypomethylation of FUNDC1 in cataract lens cells under oxidative stress. The knockdown of FUNDC1 decreased cell apoptosis and autophagy in comparison with the negative control of SRA01/04 cells. While the overexpression of FUNDC1 elevated cell apoptosis and autophagy compared to the empty vector group in SRA01/04 cells. Mechanically, FUNDC1 reduced the phosphorylation of PI3K/Akt/mTOR pathway under oxidative stress in SRA01/04 cells. CONCLUSION: Our study suggested that FUNDC1 deficiency restrains cell apoptosis and autophagy by inhibiting PI3K/Akt/mTOR signal pathway.

Sodium hyaluronate combined with rhEGF contributes to alleviate clinical symptoms and Inflammation in patients with Xerophthalmia after cataract surgery.

BACKGROUND: To determine the effect of sodium hyaluronate combined with recombinant human epidermal growth factor (rhEGF) on clinical symptoms and inflammation in patients with newly diagnosed xerophthalmia after cataract surgery. METHODS: A total of 106 patients who underwent cataract surgery and were newly diagnosed with xerophthalmia in our hospital between June 2018 and August 2019 were enrolled. Of these, 50 patients who were treated with sodium hyaluronate (0.1%) were assigned to the monotherapy group (MG) and the remaining 56 patients who were treated with sodium hyaluronate (0.1%) combined with rhEGF (20 µg/ml) were assigned to the combination group (CG). The 2 groups were compared based on ocular surface disease index (OSDI) score, break-up time (BUT), fluorescein corneal staining level, Schirmer I test (SI) level, clinical efficacy (disappearance of typical symptoms, including eyes drying, burning sensation, foreign body sensation, etc), and interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) levels. Spearman correlation analysis was conducted to analyze the relationship between IL-1, IL-6, TNF-α and clinical efficacy. In addition, receiver operating characteristic curves were drawn to analyze the predictive value of IL-1, IL-6, and TNF-α in efficacy on xerophthalmia. RESULTS: After treatment, the CG showed reduced OSDI score compared with the MG. The CG showed increased BUT (s) and SI (mm) levels compared with MG. After treatment, the CG exhibited decreased levels of IL-1(ng/mL), IL-6 (ng/mL), and TNF-α (ng/mL) compared with the MG. Spearman correlation analysis revealed that IL-1, IL-6, and TNF-α were negatively correlated with clinical efficacy. The areas under the curves of IL-1, IL-6, and TNF-α were 0.801, 0.800, and 0.736 respectively. CONCLUSIONS: Sodium hyaluronate combined with rhEGF is helpful to alleviate clinical symptoms and inflammation in patients with xerophthalmia undergoing cataract surgery.

SP1-induced upregulation of lncRNA PANDAR predicts adverse phenotypes in retinoblastoma and regulates cell growth and apoptosis in vitro and in vivo.

Retinoblastoma (RB) is an intraocular malignancy for children and has a high mortality rate. Long non-coding RNAs (lncRNAs) are emerging as gene regulators and biomarkers in various malignancies. PANDAR is a novel cancer-related lncRNA that dysregulated in several types of cancers. However, its clinical value and potential effects on RB remains unclear. RT-qPCR was used to assess the relative expression of PANDAR in RB tissues and cells. Additionally, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were performed to investigate whether SP1 could bind to the promoter region of PANDAR and activate its transcription. Furthermore, in vitro and in vivo studies were induced to elucidate the biological functions of PANDAR. The results indicated that PANDAR was increased in RB tissues and cells, and this upregulation was associated with advanced IIRC stage, positive optic nerve invasion, and lower differentiation grade in RB patients. In addition, SP1 could bind directly to the PANDAR promoter region and activate its transcription. Furthermore, PANDAR silencing yielded tumor suppressive effects both in vitro and in vivo. Importantly, PANDAR protects against apoptosis partly by affecting Bcl-2/caspase-3 pathway. Ultimately, our work first illustrate that PANDAR plays an oncogenic role in RB and may offer a potential therapeutic target for treating this devastating disease.