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Retinal vessel segmentation is generally grounded in image-based datasets collected with bench-top devices. The static images naturally lose the dynamic characteristics of retina fluctuation, resulting in diminished dataset richness, and the usage of bench-top devices further restricts dataset scalability due to its limited accessibility. Considering these limitations, we introduce the first video-based retinal dataset by employing handheld devices for data acquisition. The dataset comprises 635 smartphone-based fundus videos collected from four different clinics, involving 415 patients from 50 to 75 years old. It delivers comprehensive and precise annotations of retinal structures in both spatial and temporal dimensions, aiming to advance the landscape of vasculature segmentation. Specifically, the dataset provides three levels of spatial annotations: binary vessel masks for overall retinal structure delineation, general vein-artery masks for distinguishing the vein and artery, and fine-grained vein-artery masks for further characterizing the granularities of each artery and vein. In addition, the dataset offers temporal annotations that capture the vessel pulsation characteristics, assisting in detecting ocular diseases that require fine-grained recognition of hemodynamic fluctuation. In application, our dataset exhibits a significant domain shift with respect to data captured by bench-top devices, thus posing great challenges to existing methods. In the experiments, we provide evaluation metrics and benchmark results on our dataset, reflecting both the potential and challenges it offers for vessel segmentation tasks. We hope this challenging dataset would significantly contribute to the development of eye disease diagnosis and early prevention.

Purpose: To evaluate the intraocular pressure (IOP)-lowering efficacy and safety of 10- and 15-μg bimatoprost implant in subjects with open-angle glaucoma (OAG) and ocular hypertension (OHT) after initial and repeated administrations. Design: Randomized, 20-month, multicenter, subject- and efficacy evaluator-masked, parallel-group, phase 3 clinical study. Participants: Adults with OAG or OHT in each eye, open iridocorneal angle inferiorly in the study eye, and study eye baseline IOP (hour 0; 8 AM) of 22–32 mmHg after washout. Methods: Study eyes received bimatoprost implant 10 μg (n = 198) or 15 μg (n = 198) on day 1 with readministration at weeks 16 and 32, or twice-daily topical timolol maleate 0.5% (n = 198). Intraocular pressure was measured at hours 0 and 2 at each visit. Main Outcome Measures: Primary end points were IOP and change from baseline IOP through week 12. Safety measures included treatment-emergent adverse events (TEAEs) and corneal endothelial cell density (CECD). Results: Both dose strengths of bimatoprost implant were noninferior to timolol in IOP lowering after each administration. Mean diurnal IOP was 24.0, 24.2, and 23.9 mmHg at baseline and from 16.5–17.2, 16.5–17.0, and 17.1–17.5 mmHg through week 12 in the 10-μg implant, 15-μg implant, and timolol groups, respectively. The incidence of corneal and inflammatory TEAEs of interest (e.g., corneal endothelial cell loss, iritis) was higher with bimatoprost implant than timolol and highest with the 15-μg dose strength. Incidence of corneal TEAEs increased after repeated treatment; with 3 administrations at fixed 16-week intervals, incidence of ≥20% CECD loss was 10.2% (10-μg implant) and 21.8% (15-μg implant). Mean best-corrected visual acuity (BCVA) was stable; 3 implant-treated subjects with corneal TEAEs had >2-line BCVA loss at their last visit. Conclusions: Both dose strengths of bimatoprost implant met the primary end point of noninferiority to timolol through week 12. One year after 3

Cellular responses to changes in pressure are implicated in numerous disease processes. In glaucoma apoptosis of retinal ganglion cells (RGCs) is associated with elevated intra-ocular pressure (IOP), however the exact cellular basis of this link remains unclear. This research aimed to examine the direct response of neuronal cells to elevated hydrostatic pressure in terms of apoptosis. We developed an in vitro model consisting of a pressure chamber to adjust ambienthydrostatic pressure, a source of neuronal cells and methods to measure apoptosis in these cells. The neural cells examined were primary retinal cultures, four neuronal cell lines (B35, PC12, C17, NT2), and the RGC-5 cell line. Pressure conditions selected were within physiological limits; 100 mmHg above atmospheric pressure (as seen clinically in severe acute glaucoma) and extended in RGC-5 neurons to 30 mmHg (chronic glaucoma) and 15 mmHg (normal IOP). Apoptosis was detected by cell morphology and specific immunochemical markers: TUNEL and Annexin V. Caspase-3 activation, a known pathway of apoptosis, was also investigated in RGC-5 neurons. These fluorescent markers were detected and quantified by automated Laser Scanning Cytometry. Negative controls were treated identicallyexcept for the application of pressure, while positive controls were generated by treatment with a known apoptotic stimulus. The results showed that neurons responded to elevated hydrostatic pressure directly and that an apoptotic process was induced. There was a greater level of apoptosis in pressurised cells compared to the negative controls. This apoptotic effect at highpressures was seen in primary rat retinal cultures and in both undifferentiated (B35, C17, NT2, RGC-5) and differentiated (PC12, RGC-5) neuronal cell lines. RGC-5 neurons showed a graded response, proportionate to the level of pressure elevation, representative of the severity of analogous clinical settings (acute, chronic glaucoma & normal). RGC-5 neurons also show