Real-Time Monitoring of Intraocular Pressure in Glaucoma Patients Using Wearable Mobile Medicine Devices.

Glaucoma is caused by excessive aqueous humor in the eye, resulting in a continuous or intermittent increase of intraocular pressure, which exceeds the tolerance of the eyeball and damages the optic nerve. Existing treatments for glaucoma do not work well or have significant side effects. Intraocular pressure signal is a very important physiological signal that needs real-time and accurate monitoring in glaucoma patients, especially in severe glaucoma patients. Therefore, long-term, real-time, and accurate monitoring of intraocular pressure is of great significance for the diagnosis and treatment of glaucoma patients. The use of wearable devices for real-time ocular diagnosis and treatment of glaucoma patients is an effective approach. However, the current commonly used intraocular pressure measurement and monitoring technology is difficult to meet the diagnosis and monitoring needs of glaucoma patients in terms of size, measurement accuracy, power consumption, and intelligence. Therefore, facing the needs of glaucoma disease treatment, this topic studies an implantable flexible intraocular pressure sensor for long-term continuous monitoring of intraocular pressure in glaucoma patients and mainly focuses on the working principle, structural design, process fabrication, measurement and control system, characterization, and performance test of the intraocular pressure sensor. It is of great significance for personalized and accurate treatment of glaucoma patients.

Knockdown of lncRNA HOTTIP Inhibits Retinoblastoma Progression by Modulating the miR-101-3p/STC1 Axis.

OBJECTIVE: Retinoblastoma (RB) is a frequent eye cancer in children. Long non-coding RNA (LncRNA) HOXA transcript at the distal tip (HOTTIP) is aberrantly expressed in cancer tissues. This study explores the underlying mechanism of lncRNA HOTTIP in RB. METHODS: HOTTIP expression in normal retinal cells and RB cell lines was detected using qRT-PCR. The proliferation of RB cells was measured using CCK-8 and EdU assays, and apoptosis was detected using flow cytometry and Western blotting after the transfection of si-HOTTIP into Y79 cells and pc-HOTTIP into HXO-RB-44 cells. The target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1 were predicted by bioinformatics website and verified using dual-luciferase reporter gene assay. The binding of HOTTIP and miR-101-3p was verified using RNA pull-down assay. STC1 mRNA and protein in RB cells were measured using qRT-PCR and Western blotting. Moreover, si-HOTTIP and in-miR-101-3p/in-NC, and si-HOTTIP and pc-STC1/pcDNA were co-transfected into Y79 cells respectively to evaluate cell proliferation and apoptosis. Xenograft study was conducted, and Ki67-positive expression was detected using immunohistochemical staining. RESULTS: HOTTIP expression was promoted in RB tissues and cells. Downregulation of HOTTIP inhibited proliferation and promoted apoptosis of Y79 cells, while upregulation of HOTTIP promoted proliferation and inhibited apoptosis of HXO-RB-44 cells. There were target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1. Inhibition of miR-101-3p or overexpression of STC1 reversed the effect of si-HOTTIP on the proliferation and apoptosis of RB cells. Xenograft study showed that knockdown of HOTTIP suppressed the growth of RB in vitro. CONCLUSION: It could be concluded that HOTTIP sponged miR-101-3p to upregulate STC1 expression, thereby promoting RB cell proliferation and inhibiting apoptosis.