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.

A high sensitivity analog front-end is presented for semi-passive HF RFID tag for implantable devices. The design is compatible with the ISO/IEC 14443 Type-A. A rectifier with high power conversion efficiency is presented to provide stable rectified voltage. Novel tag system architecture with wake-up circuit is proposed to improve the sensitivity. Other Key circuits are studied and designed to make the system work effectively. Simulation results show that the AFE has realized much longer recognition distance than passive tags. Its sensitivity is 5.7 dBm and can work properly when the magnetic field is 0.3A/m. The AFE was fabricated with HHNEC 0.13 1P4M CMOS technology with an area of . The AFE is also measured with FPGA based digital baseband. Measurement results show that the proposed AFE can support the 100% ASK demodulation and a modulation depth of 16.4%. The AFE can also accommodate a data rates from 106 Kbps to 848 Kbps are supported. Its power consumption is as low as 129. 6 . This chip meets the demands of a semi-passive HF RFID tag and has great potential for implantable devices.

VIP regulates the distribution of F-actin in SCEs via the VPAC2 receptor in order to induce a decrease in IOP. VIP may represent a new target for antiglaucoma drugs.

A RF powering circuit used in radio-frequency identification (RFID) tags and other batteryless embedded devices is presented in this paper. The RF powering circuit harvests energy from electromagnetic waves and converts the RF energy to a stable voltage source. Analysis of a NMOS gate-cross connected bridge rectifier is conducted to demonstrate relationship between device sizes and power conversion efficiency (PCE) of the rectifier. A rectifier with 38.54% PCE under normal working conditions is designed. Moreover, a stable voltage regulator with a temperature and voltage optimizing strategy including adoption of a combination resistor is developed, which is able to accommodate a large input range of 4 V to 12 V and be immune to temperature variations. Latch-up prevention and noise isolation methods in layout design are also presented. Designed with the HJTC 0.25 μm process, this regulator achieves 0.04 mV/°C temperature rejection ratio (TRR) and 2.5 mV/V voltage rejection ratio (VRR). The RF powering circuit is also fabricated in the HJTC 0.25 μm process. The area of the RF powering circuit is 0.23 × 0.24 mm2. The RF powering circuit is successfully integrated with ISO/IEC 15693-compatible and ISO/IEC 14443-compatible RFID tag chips.

Glaucoma is a leading cause of irreversible blindness worldwide and is characterized by progressive optic nerve degeneration and retinal ganglion cell loss. Axonal transport deficits have been demonstrated to be the earliest crucial pathophysiological changes underlying axonal degeneration in glaucoma. Here, we explored the role of the tetraspanin superfamily member CD82 in an acute ocular hypertension model. We found a transient downregulation of CD82 after acute IOP elevation, with parallel emergence of axonal transport deficits. The overexpression of CD82 with an AAV2/9 vector in the mouse retina improved optic nerve axonal transport and ameliorated subsequent axon degeneration. Moreover, the CD82 overexpression stimulated optic nerve regeneration and restored vision in a mouse optic nerve crush model. CD82 exerted a protective effect through the upregulation of TRAF2, which is an E3 ubiquitin ligase, and activated mTORC1 through K63-linked ubiquitylation and intracellular repositioning of Raptor. Therefore, our study offers deeper insight into the tetraspanin superfamily and demonstrates a potential neuroprotective strategy in glaucoma treatment.

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.

Drug resistance is the main cause of chemotherapy failure in ovarian cancer (OC), and identifying potential druggable targets of autophagy is a novel and promising approach to overcoming drug resistance. In this study, 131 genes associated with autophagy were identified from three autophagy-related databases, and of these, 14 were differentially expressed in 90 drug-resistant OC tissues versus 197 sensitive tissues according to the Cancer Genome Atlas ovarian cancer cohort. Among these 14 genes, SLC7A11 was significantly decreased in two paclitaxel-resistant OC cells (HeyA8-R and SKOV3-R) and in 90 drug-resistant tissues compared with their controls. In vitro overexpression of SLC7A11 significantly increased the sensitivity of HeyA8-R cells to paclitaxel, inhibited colony formation, induced apoptosis, and arrested cell cycle. Further, low SLC7A11 expression was correlated with poor overall survival (OS), progression-free survival (PFS), and post-progression survival (PPS) in 1815 OC patients. Mechanistically, SLC7A11 strongly regulated cell autophagy as a competing endogenous RNA (ceRNA) based on pan-cancer analyses of 32 tumor types. Specifically, as a ceRNA for autophagy genes STX17, RAB33B, and UVRAG, SLC7A11 was strongly and positively co-expressed with these three genes in 20, 12, and 12 different tumors, respectively, in 379 OC tissues and in 90 drug-resistant OC tissues, and the former two were significantly upregulated in SLC7A11-overexpressed HeyA8-R cells. Further, SLC7A11 induced the protein expression of other autophagy genes, such as LC3, Atg16L1, and Atg7, and the expression of the respective proteins was further increased when the cells were treated with paclitaxel. The results strongly suggest that SLC7A11 regulates autophagy via ceRNA interactions with the three abovementioned genes in pan-cancer and in drug-resistant OC. Moreover, low expression of STX17 and UVRAG also significantly predicted low OS, PFS, and PPS. The combination of SLC7A11 with STX17 was more predictive of OS and PFS than either individually, and the combination of SLC7A11 with UVRAG was highly predictive of OS and PPS. The above results indicated that decreased SLC7A11 resulted in drug resistance and effected low rates of survival in OC patients, probably via ceRNA interactions with autophagy genes, and thus the gene could serve as a therapeutic target and potential biomarker in OC.

Purpose Optic nerve injury (ONI) causes neuroinflammation and neurodegeneration leading to visual deficits. The response of microglia has emerged as an impactful component of etiology in neurodegeneration. This study aimed to investigate the effect of SIRT1-mTORC1 signaling pathway in microglia regulation after ONI. Methods Cx3Cr1-Cre ERT2 / Raptor F/F and Cx3Cr1-Cre ERT2 / Sirt1 F/F mice were used to delete Raptor and Sirt1 in microglia, respectively. Optic nerve crush (ONC) model was established to mimic ONI. PLX5622, a highly specific inhibitor of the colony-stimulating factor 1 receptor (CSF1R), is used to eliminate microglia in optic nerve. Ionized calcium binding adaptor molecule 1 (Iba1) immunostaining was used to detect microglial activation. Retinal ganglion cells (RGCs) were quantified by Nissl staining and retinal whole-mount immunostaining with RNA-binding protein with multiple splicing (RBPMS). Axonal damage was valued by transmission electron microscopy (TEM). Results Microglial activation emerged on day 3 post ONC and was earlier than RGCs loss which occurred at day 5 after injury. Depleting microglia with PLX5622 could attenuate the loss of RGCs and axon damage after ONC. Gain- and loss-of-function studies revealed that SIRT1 determined the activation of microglia in optic nerve. In addition, microglia-specific deletion of Raptor resulted in decreased microglial activation. Interestingly, activating mTORC1 with CCT007093 could reverse the function of SIRT1 in regulating the process of microglial activation mediated RGCs loss. Conclusion Our study reveals a potential novel mechanism of SIRT1-mTORC1 pathway in microglia regulation, and indicates a therapeutic potential for the protection of RGCs in ONI.