long non-coding rnas (lncrnas) are a group of non-coding transcripts of >200 nucleotides. They can act as competing endogenous rnas (cernas) and suppress microrna (mirna) function by preventing them from binding to and interacting with target mrnas. However, the specific role of the lncRNA-associated ceRNA network in the pathogenesis of glaucoma has not yet been elucidated. To study this, data were downloaded from the Gene expression omnibus database (GSe126170), which contained three human trabecular meshwork cell (HTMC) samples treated with 300 µm hydrogen peroxide and three control samples treated with vehicle. differentially expressed lncrnas and mrnas of HTMCs were obtained using the R package limma. Gene ontology and Kyoto encyclopedia of Genes and Genomes pathway analyses of differentially expressed mrnas were performed using the R package clusterProfiler. Finally, the ceRNA network was constructed using the mircode, miRDB, miRTarBase and TargetScan databases, and visualized using cytoscape v3.6.1. The results showed that 70 lncrnas and 558 mRNAs were identified to be significantly dysregulated (|log2FoldChange| >1 and adjusted P<0.05) in HTMCs under oxidative stress compared to those in HTMcs under control conditions. Moreover, 24 lncrnas, 24 mirnas and 40 mrnas were closely connected, and were part of the ceRNA network. Among these, the expression levels of 19 lncrnas were upregulated, and those of 5 lncrnas were downregulated. To conclude, using bioinformatics analysis, the differential expression profiles of lncRNAs were reported and a lncRNA-associated ceRNA network in HTMCs under oxidative stress was constructed. These results may bring to light a new pathological mechanism or a potential therapeutic target for glaucoma.

The aim of this study was to analyze the long non-coding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) network in human retinal tissues following detachment with proliferative vitreoretinopathy (PVR). Material/Methods:Expression data of 19 human detached retinas with PVR and 19 normal retinas from postmortem donors were downloaded from Gene Expression Omnibust (GEO) database (GSE28133). The R package "limma" was utilized to discriminate the dysregulated lncRNA and mRNA profiles. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of differentially expressed mRNAs were performed using R packages "Clusterprofiler." The ceRNA network of dysregulated genes was constructed by using mircode, miRDB, miRTarBase and TargetScan databases, and was visualized by Cytoscape v3.6.1. Results:A total of 23 lncRNAs and 994 mRNAs were identified significantly expressed between the human detached retinas with PVR and the normal retina tissues, with thresholds of |log 2 FoldChange| >1.0 and adjusted P-value <0.05. The constructed ceRNA network (lncRNA-miRNA-mRNA regulatory axis) included 9 PVR-specific lncRNAs, as well as 27 miRNAs and 73 mRNAs. Conclusions:We demonstrated the differential lncRNA expression profile and constructed a lncRNA-associated ceRNA network in human detached retinas with PVR. This may ferret out an unknown ceRNA regulatory network in human retinal detachment with PVR.

Purpose: To examine the effect of nicorandil on high glucose-induced cardiomyocyte inflammation and oxidative stress.Methods: H9C2 cardiomyocytes were divided into control group, high glucose group and nicorandil group. The survival rate of cardiomyocytes was determined using the CCK-8 method. The contents of reactive oxygen species (ROS) of cardiomyocytes were determined by flow cytometry. The contents of MDA and LDH in cell supernatant were determined by kit. Western blot and real-time PCR were used to assess oxidative stress, inflammation and apoptosis related factors in each group of cardiomyocytes. The expression levels of IL-1β were determined by immunofluorescence. Tunnel staining was used to determine the apoptosis level of each group.Results: The expressions of SOD1 and SOD2 in the high glucose group were significantly decreased (p < 0.05). Also, the contents of MDA and LDH were significantly increased (p < 0.05). Furthermore, IL-1β, TNF-α, caspase 3 and Bax expressions were increased, while Bcl-2 expression was inhibited. IL-1β and Tunnel fluorescence also increased significantly. NF-κB and Ikkα were significantly increased, while IκB-α was inhibited. Furthermore, nicorandil inhibited oxidative stress and apoptosis, as well as NF-κB pathway and downstream factor Ikkα.Conclusion: Nicorandil ameliorates the inflammation and oxidative damage of cardiomyocytes induced by high glucose, by inhibiting NF-κB pathway, thereby lowering apoptosis. Thus, the findings provide new insight into the development of new agents for the treatment of diabetic cardiomyopathy.

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Purpose: To examine the effect of nicorandil on high glucose-induced cardiomyocyte inflammation and oxidative stress.Methods: H9C2 cardiomyocytes were divided into control group, high glucose group and nicorandil group. The survival rate of cardiomyocytes was determined using the CCK-8 method. The contents of reactive oxygen species (ROS) of cardiomyocytes were determined by flow cytometry. The contents of MDA and LDH in cell supernatant were determined by kit. Western blot and real-time PCR were used to assess oxidative stress, inflammation and apoptosis related factors in each group of cardiomyocytes. The expression levels of IL-1β were determined by immunofluorescence. Tunnel staining was used to determine the apoptosis level of each group.Results: The expressions of SOD1 and SOD2 in the high glucose group were significantly decreased (p < 0.05). Also, the contents of MDA and LDH were significantly increased (p < 0.05). Furthermore, IL-1β, TNF-α, caspase 3 and Bax expressions were increased, while Bcl-2 expression was inhibited. IL-1β and Tunnel fluorescence also increased significantly. NF-κB and Ikkα were significantly increased, while IκB-α was inhibited. Furthermore, nicorandil inhibited oxidative stress and apoptosis, as well as NF-κB pathway and downstream factor Ikkα.Conclusion: Nicorandil ameliorates the inflammation and oxidative damage of cardiomyocytes induced by high glucose, by inhibiting NF-κB pathway, thereby lowering apoptosis. Thus, the findings provide new insight into the development of new agents for the treatment of diabetic cardiomyopathy.

To explore the application value of quantitative susceptibility mapping (QSM) based on Laplace algorithm in the diagnosis of Parkinson’s disease, 48 Parkinson’s disease patients admitted to our hospital were included as the research objects. They were randomly divided into control group (24 cases) and experimental group (24 cases). All patients underwent quantitative magnetic susceptibility imaging scan. In the experimental group, the improved Laplace algorithm was used for QSM diagnosis, while in the control group, conventional QSM diagnosis was used. Through calculations of precision, recall, dice similarity coefficient, intersection-over-union (IoU), and area under the curve (AUC), the quality improvement effect of the improved Laplace algorithm for QSM image was assessed. Then, the diagnostic accuracy of the algorithm was verified by comparing with the results of QSM image diagnosis in Parkinson’s patients without algorithm processing. The results showed that compared with the traditional Laplace algorithm, the improved Laplace algorithm can considerably reduce the image noise level ( P < 0.05 ). The dice, IoU, precision, and recall rate of image quality evaluation indicator were considerably improved ( P < 0.05 ), and the AUC reached 0.896. There were no significant differences in fraction anisotropy (FA) and mean diffusivity (MD) between the two groups ( P > 0.05 ) and no significant differences in magnetic susceptibility of brain nuclei between the two groups ( P > 0.05 ). However, they all showed high magnetic susceptibility in the substantia nigra region of the brain. Compared with the control group, the diagnostic accuracy of the experimental group was 97.5 ± 1.23%, which was considerably higher than that of the control group (86.5 ± 3.56%) ( P < 0.05 ). In short, the image quality of QSM based on Laplace improved algorithm was greatly improved, and the diagnostic accuracy of PD was also greatly improved, which was worthy of promotion in the field of clinical QSM imaging diagnosis of PD.