Acute Intraocular Pressure Research Articles

Intraocular Pressure as an Indicator of the Level of Induced Anxiety in Basketball.

Our data demonstrate that intraocular pressure (IOP) is sensitive to anxiety manipulation in sport scenarios, specifically in a basketball free throw task. The present outcomes may be of special relevance because of its practical advantages for the objective control of athletes' anxiety levels. Athletes experience high levels of anxiety during sport competition, and IOP has demonstrated to reflect autonomous nervous system changes during mentally demanding situations. We tested whether different levels of induced anxiety during basketball free throw shooting alter IOP. We followed a repeated-measures design to test the effects of anxiety-induced manipulation during basketball free throw shooting on IOP, shooting performance, and perceived anxiety. Eighteen amateur basketball players performed three experimental sessions consisting of 100 free throws each. However, we gave three different instructions to participants regarding the score assigned to each free throw, allowing us to manipulate the level of induced anxiety (low, medium, and high). Confirming a successful anxiety manipulation, basketball players reported more perceived anxiety with higher levels of induced anxiety (P < .001, η = 0.37). Our data show that higher levels of induced anxiety provoke an acute IOP rise (P < .001, η = 0.44), with the low-, medium-, and high-anxiety-induced conditions promoting an average IOP rise of 0.21, 1.63, and 18.46%, respectively. Also, there was a linear IOP rise over time in the high-anxiety-induced condition (r = 0.82). Nevertheless, we found no effect of anxiety-induced manipulation on basketball free throw performance (P = .93). Intraocular pressure is sensitive to anxiety-induced manipulation during basketball free throw shooting, showing an increase in parallel with accumulated anxiety. Based on these findings, IOP may be considered a promising tool for the assessment of the level of anxiety in certain sport situations. Future studies are required to explore the generalizability of these results in other scenarios with different physical and mental demands.

Effect of Acute Increases in Intraocular Pressure on Corneal Pachymetry in Rabbit Eyes Treated with Timolol Maleate

Objective: To evaluate in an in vivo rabbit model, the effect of topical timolol maleate therapy on the central corneal thickness response to acute intraocular pressure increases. Method: In this prospective and interventional controlled study, the central corneal thickness and intraocular pressure were measured in vivo in 12 rabbit eyes treated with topical timolol maleate for 1 month and in 12 controls at baseline, and after the intraocular pressure (measured by direct cannulation of the anterior chamber) was increased to 15 and 30 mmHg using a forced saline infusion into the anterior chamber. Results: There were no significant differences in the basal central corneal thickness values (control group, 373.2±12.9 µm; study group, 377.5±19.2 µm, p=0.5) or the central corneal thickness values when the intraocular pressure was increased to 15 mmHg (control group, 335.2±14.3 µm; study group, 330.0±32.1 µm, p=0.6) and to 30 mmHg (study group, 318.8±25.3 µm; control group, 329.8±21.0 µm, p=0.3). Conclusion: Rabbit corneas treated with topical timolol maleate for 1 month did not show a strain response to acute intraocular pressure increases that differed from control eyes. This is in contrast to a previous finding in which rabbit eyes treated with prostaglandin analogues had a greater decrease in central corneal thickness in response to a sudden intraocular pressure increase compared with untreated corneas.

Acute intraocular pressure responses to high-intensity interval-training protocols in men and women

ABSTRACTWe aimed (1) to test the acute impact of two high-intensity interval-training (HIIT) protocols differing in the level of effort on intraocular pressure (IOP) responses, and (2) to elucidate whether the IOP responses differ between men and women. Twenty-four physically active collegiate (12 men and 12 women) performed three protocols: low-fatigue HIIT (eight 30-m sprints with 60-s of rest), high-fatigue HIIT (eight 30-m sprints with 30-s of rest), and control (walking). IOP was taken at baseline, after sprints and recovery by rebound tonometry. Our data revealed an acute IOP reduction during both HIIT protocols compared to the control condition (effect size [ES]:0.81–1.65). The differences between both HIIT protocols were generally negligible (ES<0.30), however, the reduction of IOP was moderately higher for the low-fatigue HIIT protocol after the 7th (ES: 0.67) and 8th (ES: 0.74) sprints. Women showed a more prominent lowering effect on IOP during the control condition (ES: 0.42–1.02), and during the two first sprints of both HIIT protocols (ES: 0.54–1.03). These findings highlight that a time-efficient HIIT protocol may acutely reduce IOP levels, while low-fatigue HIIT protocol could be recommended since it induced a higher reduction on IOP than the high-fatigue HIIT protocol.

Reduced Annexin A1 Secretion by ABCA1 Causes Retinal Inflammation and Ganglion Cell Apoptosis in a Murine Glaucoma Model.

Variants near the ATP-binding cassette transporter A1 (ABCA1) gene are associated with elevated intraocular pressure and newly discovered risk factors for glaucoma. Previous studies have shown an association between ABCA1 deficiency and retinal inflammation. Using a mouse model of ischemia-reperfusion (IR) induced by acute intraocular pressure elevation, we found that the retinal expression of ABCA1 protein was decreased. An induction of ABCA1 expression by liver X receptor agonist TO901317 reduced retinal ganglion cell (RGC) apoptosis after IR and promoted membrane translocation and secretion of the anti-inflammatory factor annexin A1 (ANXA1). Moreover, ABCA1 and ANXA1 co-localized in cell membranes, and the interaction domain is amino acid 196 to 274 of ANXA1 fragment. TO901317 also reduced microglia migration and activation and decreased the expression of pro-inflammatory cytokines interleukin (IL)-17A and IL-1β, which could be reversed by the ANXA1 receptor blocker Boc2. Overexpression of TANK-binding kinase 1 (TBK1) increased ABCA1 degradation, which was reversed by the proteasome inhibitor carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG132). Silencing Tbk1 with siRNA increased ABCA1 expression and promoted ANXA1 membrane translocation. These results indicate a novel IR mechanism, that leads via TBK1 activation to ABCA1 ubiquitination. This degradation decreases ANXA1 secretion, thus facilitating retinal inflammation and RGC apoptosis. Our findings suggest a potential treatment strategy to prevent RGC apoptosis in retinal ischemia and glaucoma.

In vivo optic nerve head mechanical response to intraocular and cerebrospinal fluid pressure: imaging protocol and quantification method

This study presents a quantification method for the assessment of the optic nerve head (ONH) deformations of the living human eye under acute intraocular pressure (IOP) elevation and change of cerebrospinal fluid pressure (CSFP) with body position. One eye from a brain-dead organ donor with open-angle glaucoma was imaged by optical coherence tomography angiography during an acute IOP and CSFP elevation test. Volumetric 3D strain was computed by digital volume correlation. With increase in IOP the shear strain consistently increased in both sitting and supine position (p < 0.001). When CSFP was increased at constant IOP by changing body position, a global reduction in the ONH strain was observed (−0.14% p = 0.0264). Strain in the vasculature was significantly higher than in the structural tissue (+0.90%, p = 0.0002). Retinal nerve fiber layer (RNFL) thickness strongly associated (ρ = −0.847, p = 0.008) with strain in the peripapillary sclera (ppScl) but not in the retina (p = 0.433) and lamina (p = 0.611). These initial results show that: CSFP independently to IOP modulates strain in the human ONH; ppScl strains are greater than strains in lamina and retina; strain in the retinal vasculature was higher than in the structural tissue; In this glaucoma eye, higher ppScl strain associated with lower RNFL thickness.

Ubiquinol promotes retinal ganglion cell survival and blocks the apoptotic pathway in ischemic retinal degeneration

Coenzyme Q10 (CoQ10) protects retinal ganglion cells (RGCs) in experimental retinal ischemia and glaucoma by scavenging reactive oxygen species. We tested whether a diet supplemented with ubiquinol, the reduced form of CoQ10, promotes RGC survival and blocks the apoptotic pathway in ischemic mouse retina induced by acute high intraocular pressure (IOP) elevation. Ubiquinol (1%) treatment significantly promoted RGC survival at 2 weeks after ischemia/reperfusion. The ubiquinol treatment significantly blocked activation of astroglial and microglial cells in the ischemic retina at 2 weeks. While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage. These results suggest that the ubiquinol enhances RGC survival by modulating the Bax/Bad/Bcl-xL-mediated apoptotic pathway in the ischemic retina. Ubiquinol has therapeutic potential for ameliorating elevated IOP-induced ischemic retinal degeneration.

Morphological and functional changes in the rat retina associated with 2 months of intermittent moderate intraocular pressure elevation

Morphological and functional changes in the rat retina and optic nerve head (ONH), associated with 8 weeks of intermittent moderately elevated intraocular pressure (IOP) were measured with a combined ultrahigh resolution optical coherence tomography (UHR-OCT) and electroretinography (ERG) system. The IOP of male Sprague-Dawley rats was raised in one eye to ~35 mmHg for 1 hour/day on 6 days each week using vascular loops. Single-flash ERG traces and volumetric UHR-OCT images of the ONH were acquired from both eyes before, during and after IOP elevations at weeks 1, 5 and 9 of the study. The UHR-OCT images showed depression of the posterior eye around the ONH during the IOP elevations, the magnitude of which increased significantly from week 1 to week 9 (p = 0.01). The ERG a-wave and b-wave amplitudes increased temporarily during IOP elevations and returned to normal ~30 minutes after loop removal. Recurrent intermittent IOP spikes caused > 30% decrease in the ERG a-wave and b-wave amplitudes measured during the IOP elevations over the course of 2 months. This study suggests that recurrent, relatively short-duration IOP spikes for extended period of time are associated with peri-ONH tissue hypercompliance and reduced retinal functional response to visual stimulation during acute IOP elevation.

Optical Coherence Tomography Angiography Vessel Density Changes after Acute Intraocular Pressure Elevation

To investigate changes in retinal vessel density in optic nerve head (ONH) and macula after acute intraocular pressure (IOP) elevation, we conducted a prospective observational study. Eyes with IOP rise ≥5 mmHg after 2-hour dark room prone provocative test (DRPPT) were included. Vasculature of ONH and macula was examined by optical coherence tomography angiography (OCTA) at baseline and after DRPPT. Among the 65 eyes of 42 individuals, 40 eyes with qualified images were enrolled. Mean IOP rise was 9.6 ± 4.2 mmHg (5.0–23.3 mmHg) after DRPPT. Retinal vessel density did not differ after IOP rise for either the papillary region (optic nerve head and radial peripapillary capillary layer) or the macula region (superficial, deep and outer retinal layer) (P > 0.05). Vessel density in each subregion did not change either. If only enrolled eyes with IOP rise ≥10 mmHg, similar results were obtained in condition of IOP increase by 15.0 ± 3.6 mmHg. To conclude, eyes with an acute IOP elevation by 10 or 15 mmHg for two hours, while the blood pressure remained constant, the vessel density in both ONH and macula region examined by OCTA did not show significant changes. The observations fit with an IOP-related autoregulation in retinal blood flow for a moderate elevation of IOP.

Effect of a Short-term Cycle Ergometer Sprint Training Against Heavy and Light Resistances on Intraocular Pressure Responses.

The purpose of this study is to determinate the long-term effect of a cycle ergometer sprint training program against heavy and light resistances on baseline intraocular pressure (IOP), and on the acute IOP response to cycling sprints. A total 27 physically active males were randomly assigned to a heavy loads group (HLG, n=9), low loads group (LLG, n=9), and control group (CG, n=9). Participants performed 12 training sessions during 6 weeks (2 sessions per week), and each training session consisted in performing 8 cycling sprints against either heavy (HLG) or light (LLG) resistances. Before and after intervention, they performed an identical protocol, which consisted in performing maximal cycling sprints against 5 different resistances in random order. In these protocols, IOP was measured before and after each sprint by rebound tonometry. A Bayesian analysis revealed that baseline IOP was reduced in the LLG after the intervention [Bayes factor (BF01)=0.043 and effect size (ES)=1.255; pretest=15.22±0.94 mm Hg and posttest=15.39±1.02 mm Hg], whereas the HLG did not manifest any baseline IOP change (BF01=2.363 and ES=-0.205; pretest=15.28±1.44 mm Hg and posttest=14.17±1.77 mm Hg). The acute IOP response to maximal sprints was modified for the HLG, showing a more stable IOP response with heavier loads (resistance, 4 and 5) after the intervention (BF01<0.01 in both cases, and ESs=1.847 and 1.920, respectively). A short-term cycle ergometer sprint training impacts long-term IOP depending on the level of resistance imposed, showing that training with low loads permits to reduce baseline IOP, whereas training with heavy loads attenuates the acute IOP changes after sprinting against heavy loads.

In vivo assessment of changes in corneal hysteresis and lamina cribrosa position during acute intraocular pressure elevation in eyes with markedly asymmetrical glaucoma.

PurposeTo investigate the biomechanical response of the cornea, lamina cribrosa (LC), and prelaminar tissue (PT) to an acute intraocular pressure (IOP) increase in patients with markedly asymmetrical glaucoma and in healthy controls.Patients and methodsA total of 24 eyes of 12 patients with markedly asymmetrical primary open-angle glaucoma (POAG) and 12 eyes of 12 healthy patients were examined with spectral-domain optical coherence tomography (SD-OCT) and ocular response analyzer (ORA) at baseline and during acute IOP elevation by means of an ophthalmodynamometer. The displacement of the LC and PT and the change in corneal hysteresis (CH) and corneal resistance factor (CRF) were evaluated.ResultsFollowing a mean IOP increase of 12.3±2.4 mmHg, eyes with severe glaucoma demonstrated an overall mean anterior displacement of the LC (−6.58±26.09 µm) as opposed to the posterior laminar displacement in eyes with mild glaucoma (29.08±19.28 µm) and in healthy eyes (30.3±10.9; p≤0.001 and p=0.001, respectively). The PT displaced posteriorly during IOP elevation in all eyes. The CH decreased in eyes with severe glaucoma during IOP elevation (from 9.30±3.65 to 6.92±3.04 mmHg; p=0.012), whereas the CRF increased markedly in eyes with mild glaucoma (from 8.61±2.30 to 12.38±3.64; p=0.002) and in eyes with severe glaucoma (from 9.02±1.48 to 15.20±2.06; p=0.002). The increase in CRF correlated with the anterior displacement of the LC in eyes with severe glaucoma.ConclusionEyes with severe glaucoma exhibited a mean overall anterior displacement of the anterior laminar surface, while eyes with mild glaucoma and healthy eyes showed a posterior displacement of the LC during IOP elevation. The CH decreased significantly from baseline only in eyes with severe glaucoma, but the CRF increased significantly in all glaucomatous eyes. The CRF increase correlated with the anterior displacement of the LC in eyes with severe glaucoma.

Muscular Strength Is Associated with Higher Intraocular Pressure in Physically Active Males.

The positive association between intraocular pressure (IOP) and relative maximum force may have relevance for exercise recommendations when IOP is a concern. The relationship between exercise and IOP has been approached in several studies. However, the influence of muscle function on IOP remains underexplored. This study aimed to determine the relationship between the maximal mechanical capabilities of muscles to generate force, velocity, and power with IOP. Sixty-five physically active males participated in this cross-sectional study. Baseline IOP measures were obtained by rebound tonometry, and participants performed an incremental loading test in the ballistic bench press. Baseline IOP showed a strong positive correlation with relative maximum force (r65 = 0.85, P < .001) relative maximum power (r65 = 0.85, P < .001), and relative one-repetition maximum (r65 = 0.91, P < .001). Also, a moderate positive association was obtained between baseline IOP and maximum force (r65 = 0.74, P < .001), maximum power (r65 = 0.72, P < .001), and maximum dynamic strength (r65 = 0.80, P < .001). No significant correlations between IOP and maximal velocity were obtained (all P > .05). There is a positive association between greater upper-body power and strength with higher baseline IOP, which might have important implications in the management of ocular health and especially in individuals constantly involved in resistance training programs (e.g., military personnel, weightlifters). The possible protective effect of high fitness level on the acute IOP response to strength exercise needs to be addressed in future studies.

Visual recovery as the target for glaucoma

Visual recovery is an established but poorly studied phenomenon in glaucoma. To provide insights into functional recovery of retinal ganglion cells (RGCs) with aview to providing information on the development of forms of treatment that improve RGC function after injury. Amodel of recoverable RGC function in the mouse eye, induced by short-term elevation of intraocular pressure (IOP). The RGCs manifest near complete functional recovery after aprolonged period of dysfunction following acute IOP elevation. Increasing age and ahigh fat diet were subsequently found to impair recovery, whereas exercise substantially improved recovery such that older mice recovered in asimilar way to young mice. Injured RGCs have the capacity to restore function after periods of functional impairment. Therapies that specifically target injured RGCs and enhance their capacity to recover function may provide anew approach for treating glaucoma.

Fitness Level Modulates Intraocular Pressure Responses to Strength Exercises

ABSTRACTPurpose/Aim: The execution of strength exercises has demonstrated to increase the intraocular pressure (IOP) levels, and it may have a negative impact on the ocular health. We aimed to explore the influence of fitness level on the acute IOP response to strength exercises performed under different loading conditions, as well as to test whether the IOP responses differ between the bench press and jump squat when performed against the same relative loads.Materials and Methods: Forty military personnel males were divided in two subgroups (20 high-fit and 20 low-fit) based on their relative to body mass one-repetition maximum (1-RM). Participants performed an incremental loading test in the bench press and jump squat exercises, and IOP was assessed before and after each repetition by rebound tonometry.Results: IOP increased immediately after executing both exercises (p < 0.01 in both cases), being the magnitude of the IOP increment positively and linearly associated with the increment of the load in both groups (i.e., high-fit and low-fit) and in both exercises (R2 range: 0.81–1.00). Higher fitness level attenuated the IOP rise produced by both exercises (p < 0.01 in both cases). The bench press induced higher IOP increments than the jump squat for both groups at relative loads of ~50%1-RM and ~60%1-RM (p < 0.01 in all cases).Conclusions: These data indicate that IOP increases as a consequence of performing strength exercises, being the increment accentuated with the increase of the load and in the bench press compared to the jump squat exercise. Of special importance would be that the IOP responses were significantly reduced in high-fit individuals. These findings should be addressed in glaucoma patients.

In Vivo Three-Dimensional Lamina Cribrosa Strains in Healthy, Ocular Hypertensive, and Glaucoma Eyes Following Acute Intraocular Pressure Elevation.

To compare in vivo lamina cribrosa (LC) strains (deformations) following acute IOP elevation in healthy, glaucoma, and ocular hypertensive subjects. There were 20 healthy, 20 high-tension primary open-angle glaucoma (POAG), 16 primary angle-closure glaucoma (PACG), and 20 ocular hypertensive (OHT; with normal visual fields) eyes studied. For each test eye, the optic nerve head was imaged three times (at baseline IOP, following an acute elevation of IOP to approximately 35 then 45 mm Hg using an ophthalmodynamomter) using optical coherence tomography (OCT). A three-dimensional (3D) strain-mapping algorithm was applied to both sets of baseline and IOP-elevated OCT volumes to extract IOP-induced 3D strains. Octant-wise LC strains were also extracted to study the pattern of local deformation. The average LC strain in OHT subjects (3.96%) was significantly lower than that measured in healthy subjects (6.81%; P < 0.05). On average, POAG subjects experienced higher strain than the PACG subjects (4.05%), healthy subjects experienced higher strains than the POAG and PACG subjects, but these difference were not statistically significant. Local LC deformations showed lowest strain in the infero-temporal and temporal octant in the POAG and OHT subjects. We demonstrate measurable LC strains in vivo in humans as a response to acute IOP elevation. In this population, our data suggest that OHT LCs experience lower IOP-induced strains than healthy LCs.

Association of Functional Loss With the Biomechanical Response of the Optic Nerve Head to Acute Transient Intraocular Pressure Elevations

The acute biomechanical response of the optic nerve head (ONH) to intraocular pressure (IOP) elevations may serve as a biomarker for the development and progression of glaucoma. To evaluate the association between visual field loss and the biomechanical response of the ONH to acute transient IOP elevations. In this observational study, 91 Chinese patients (23 with primary open-angle glaucoma [POAG], 45 with primary angle-closure glaucoma, and 23 without glaucoma) were recruited from September 3, 2014, through February 2, 2017. Optical coherence tomography scans of the ONH were acquired at baseline and at 2 sequential IOP elevations (0.64 N and then 0.90 N, by applying forces to the anterior sclera using an ophthalmodynamometer). In each optical coherence tomography volume, lamina cribrosa depth (LCD) and minimum rim width (MRW) were calculated. The mean deviation (MD) and the visual field index (VFI), as assessed by automated perimetry, were correlated with IOP-induced changes of LCD and MRW globally and sectorially. The LCD, MRW, MD, and VFI. Among the 91 patients, 39 (42.9%) were women; the mean (SD) age was 65.48 (7.23) years. In POAG eyes, a greater change in LCD (anterior displacement) was associated with worse MD and VFI (R = -0.64; 95% CI, -0.97 to -0.31; P = .001; and R = -0.57; 95% CI, -0.94 to -0.19; P = .005, respectively) at the first IOP elevation, and a greater reduction in MRW was also associated with worse MD and VFI (first IOP elevation: R = -0.48; 95% CI, -0.86 to -0.09; P = .02; and R = -0.57; 95% CI, -0.94 to -0.20; P = .004, respectively; second IOP elevation: R = -0.56; 95% CI, -0.98 to -0.13; P = .01; and R = -0.60; 95% CI, -1.03 to -0.17; P = .008, respectively), after adjusting for age, sex, and baseline IOP. A correlation was found between the reduction in MRW in the inferior-temporal sector and the corresponding visual field cluster in POAG eyes at the second elevation (ρ = -0.55; 95% CI, -0.78 to -0.18; P = .006). The biomechanical response of the ONH to acute IOP elevations was associated with established visual field loss in POAG eyes, but not in primary angle-closure glaucoma eyes. This suggests that ONH biomechanics may be related to glaucoma severity in POAG and that the 2 glaucoma subgroups exhibit inherently different biomechanical properties.

The Effect of Acutely Elevated Intraocular Pressure on the Functional and Blood Flow Responses of the Rat Retina to Flicker Stimulation.

To evaluate the effect of acutely elevated intraocular pressure (IOP) on the functional and blood flow responses of the rat retina to flicker stimulation. Brown Norway (n = 15) rats were dark-adapted before ketamine/xylazine anesthesia. IOP was raised acutely in one eye to ∼45 mm Hg with a vascular loop. In 11 rats, white light flicker stimulus (10 Hz, 2 seconds duration, 0.80 log scotopic cd·s/m2) was applied before and during IOP elevation, and 10 minutes after loop removal. Changes in the total retinal blood flow (TRBF) and retinal function induced by the visual stimulus were measured simultaneously with a combined optical coherence tomography (OCT) + electroretinography (ERG) system. Systemic blood pressure was measured in the remaining four rats frequently from 10 to 90 minutes post anesthesia injection. The systemic blood pressure remained at 99 ± 4 mm Hg throughout the measurements (n = 4). Under normal IOP, the TRBF was 5.6 ± 1.9 μL/min, and the average retinal blood vessel size (BVS) in the vicinity of the optic nerve head (ONH) was 44.1 ± 4.5 μm. During IOP elevation, the TRBF was significantly lower (3.8 ± 1.2 μL/min, P < 0.01) and the BVS was significantly smaller (35.1 ± 2.6 μm, P < 0.01). Both TRBF and BVS returned to baseline within ∼10 minutes from removal of the vascular loop. The flicker-induced TRBF change measured under normal IOP (6.0 ± 3.3%) was reduced significantly to 0.1 ± 0.3% (P < 0.01) during IOP elevation, and recovered to 5.9 ± 1.7% within 10 minutes after loop removal. During IOP elevation, the magnitude of the ERG second harmonic component (SHC) decreased to 55% of its baseline value (P < 0.01) and remained significantly smaller than baseline (P < 0.01). Acute IOP elevation to 45 mm Hg caused suppression of the retinal functional and TRBF response to flicker stimulation.

Integrated microarray analysis provided novel insights to the pathogenesis of glaucoma.

Glaucoma is characterized as a visual field defect, which is the second most common cause of blindness. The present study performed an integrated analysis of microarray studies of glaucoma derived from Gene Expression Omnibus (GEO). Following the identification of the differentially expressed genes (DEGs) in glaucoma compared with normal control (NC) tissues, the functional annotation, glaucoma-specific protein-protein interaction (PPI) network and transcriptional regulatory network constructions were performed. The acute intraocular pressure (IOP) elevation rat models were established and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed for DEGs expression confirmation. Three datasets were downloaded from GEO. A total of 97 DEGs, 82 upregulated and 15 downregulated were identified in glaucoma compared with NC groups with false discovery rate <0.05. Response to virus and immune response were two significantly enriched GO terms in glaucoma. Valine, leucine and isoleucine degradation was a significantly enriched pathway of DEGs in glaucoma. According to the PPI network, HDAC1, HBN, UBR4 and PDK1 were hub proteins in glaucoma. FOXD3, HNF-4 and AP-1 were the three transcription factors (TFs) derived from top 10 TFs which covered the majority of downstream DEGs in glaucoma. Based on the RT-qPCR results, the expression levels of 3 DEGs, raftlin, lipid raft linker 1 (RFTN1), PBX homeobox 1 (PBX1), HDAC1 were significantly upregulated and the expression of GEM was significantly downregulated in acute IOP elevation rat model at the first and fifth day. These four DEGs had the same expression pattern with our integrated analysis. Therefore, the current study concluded that 6 DEGs, including HEPH, SELENBP1, RFTN1, ID1, HDAC-1 and PBX1 and three TFs, including FOXD3, HNF-4 and AP-1 may be involved with the pathogenesis of glaucoma. The findings of the current study may improve diagnosis and drug design for glaucoma.

A novel RIPK1 inhibitor that prevents retinal degeneration in a rat glaucoma model

In glaucoma, retinal ganglion cells (RGCs) are exposed to ischemic stress with elevation of the intraocular pressure and are subsequently lost. Necroptosis, a type of regulated necrosis, is known to play a pivotal role in this loss. We observed that receptor-interacting protein kinase 1 (RIPK1), the key player of necroptosis, was activated by diverse ischemic stresses, including TCZ, chemical hypoxia (CH), and oxygen glucose deprivation (OGD). In this study, we introduce a RIPK1-inhibitory compound (RIC) with a novel scaffold. RIC inhibited downstream events following RIPK1 activation, including necrosome formation and mitochondrial dysfunction in RGC5 cells. Moreover, RIC protected RGCs against ischemic injury in the rat glaucoma model, which was induced by acute high intraocular pressure. However, RIC displayed biochemical characteristics that are distinct from those of previous RIPK1 inhibitors (necrostatin-1; Nec-1 and Compound 27; Cpd27). RIC protected RGCs against OGD insult, while Nec-1 and Cpd27 did not. Conversely, Nec-1 and Cpd27 protected RGCs from TNF-stimulated death, while RIC failed to inhibit the death of RGCs. This implies that RIPK1 activates alternative pathways depending on the context of the ischemic insults.

Implantable Collamer Lens in the Management of Pseudophakic Ametropia.

To assess Visian Implantable Collamer Lens (ICL) (STAAR Surgical, Monrovia, CA) implantation in the ciliary sulcus to correct pseudophakic ametropia in patients who are not candidates for a keratorefractive procedure. The authors performed a prospective non-comparative case series study of 18 patients (age: 48 to 61 years) with refractive surprise after phacoemulsification. Patients underwent implantation of a piggyback collagen copolymer lens: V4C design in 16 myopic eyes and V4B design in 2 hyperopic eyes. The position and vault of the ICLs were documented at all control visits clinically and with Pentacam (Oculus Optikgeräte, Wetzlar, Germany). Uncorrected distance visual acuity (UDVA), corrected distance visual acuity (CDVA), manifest refraction spherical equivalent (MRSE), intraocular pressure (IOP), and endothelial cell count were recorded at baseline and 1 week and 1, 6, 12, and 18 months postoperatively. The MRSE improved from -3.08 ± 2.37 diopters (D) preoperatively to -0.44 ± -0.23 D postoperatively, corrected with a mean ICL power of -3.20 ± 2.90 D. The mean UDVA improved from 1.03 ± 0.12 logMAR preoperatively to 0.05 ± 0.06 logMAR postoperatively (P = .00), whereas CDVA improved from 0.47 ± 0.03 logMAR preoperatively to -0.006 ± 0.02 logMAR (P = .001) postoperatively. None of the cases developed interlenticular opacification throughout the 18-month follow-up. The mean ICL vault measured by Scheimpflug tomography was 451.27 ± 178.5 µm. Acute IOP elevation with anterior uveitis developed in 2 eyes and was controlled by topical steroids and a beta-blocker. Sulcus implantation of the secondary ICL to correct pseudophakic refractive error was safe, predictable, and well tolerated in all studied eyes. [J Refract Surg. 2017;33(8):532-537.].

Acute ocular hypertension disrupts barrier integrity and pump function in rat corneal endothelial cells

Acute ocular hypertension (AOH) frequently compromises corneal endothelial cell (CEC) function in clinical practice. This type of stress induces corneal oedema and a decrease in the corneal endothelial cell density (ECD). The anterior chamber of the right eye of Sprague-Dawley rats was irrigated with Balanced Salt Solution (BSS) for two hours, and the left eye served as a control to determine the time-dependent effects of AOH on endothelial cell morphology and function. The average intraocular pressure (IOP) increased to 82.6 ± 2.3 mmHg (normal range: 10.2 ± 0.4 mmHg) during anterior irrigation. Very soon after initiating irrigation, corneal oedema became evident and the cornea exhibited a significant increase in permeability to FITC-dextran. The peripheral ECD was significantly reduced, and the morphology of CECs became irregular and multiform. The structures of the zonula occludens-1 (ZO-1) and F-actin were severely disrupted. In addtion, Na,K-ATPase exhibited a dispersed expression pattern. Two days after irrigation, obvious CEC proliferation was observed, the ECD recovered to a normal level, and F-actin was dispersed throughout the cytoplasm. Seven days later, the CEC structure and function were nearly normalized. Based on the results obtained using this model, an acute IOP crisis exerts transient deleterious effects on CEC structure and function in rats.