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AIM: To investigate the features of retinal ischemic injuries in a novel mouse model with bilateral carotid artery stenosis (BCAS). METHODS: BCAS was induced with microcoil implantation in 6-8-week-old C57BL6 mice. Cerebral blood flow was monitored at 2, 7, and 28d postoperatively. Retinal morphological changes were evaluated by fundus photography and hematoxylin-eosin staining. Fluorescein fundus angiography (FFA) was performed to detect retinal vascular changes and circulation. The levels of apoptosis, activation of neurogliosis, and expression of hypoxia-inducible factor (HIF)-1α in the retina were assessed by Western blotting and immunofluorescence staining, followed by retinal ganglion cell (RGC) density detection. Additionally, electrophysiological examinations including photopic negative response (PhNR) was also performed. RESULTS: The mice demonstrated an initial rapid decrease in cerebral blood flow, followed by a 4-week recovery period after BCAS. The ratio of retinal artery and vein was decreased under fundus photography and FFA. Compared with the sham mice, BCAS mice showed thinner retinal thickness on day 28. Additionally, apoptosis was increased and RGC density was decreased mainly in peripheral retinal region. Neurogliosis was mainly located in the inner retinal layers, with a stable increase in HIF-1α expression. The dark-adapted electroretinogram showed a notable reduction in the a-, b-, and oscillatory potential (OP) wave amplitudes between days 2 and 7; this gradually recovered over the following 4wk. However, the b- and OP-wave amplitudes were still significantly decreased on PhNR examination on day 28. CONCLUSION: BCAS can result in relatively mild retinal ischemia injuries in mice, mainly in the inner layer and peripheral region. Our study provides a novel animal model for investigating retinal ischemic diseases.

The adsorption isotherm of n -perfluorohexane on BAM-P109 activated carbon was predicted using an ab initio force field and a slit-like pore model representing the activated carbon. The force field parameters were derived from data calculated using quantum mechanics density functional theory with dispersion energy correction, and the total adsorption amount was calculated as the sum of the adsorption amounts of microscopic and mesoscopic pores. It was found that the Grand Canonical Monte Carlo method can efficiently calculate adsorption on microscopic pores but not on mesoscopic pores. Thus, we divided the mesoscopic pores into surface and free-volume regions and calculated the density and thickness of the adsorbed layers and the density of the vapor phase using canonical ensemble simulations. Using this protocol, we can calculate the adsorption isotherms in good agreement with the experimental data.

AIM: To compare the three-dimensional choroidal vascularity index (CVI) and choroidal thickness between fellow eyes of acute primary angle-closure (F-APAC) and chronic primary angle-closure glaucoma (F-CPACG) and the eyes of normal controls. METHODS: This study included 37 patients with unilateral APAC, 37 with asymmetric CPACG without prior treatment, and 36 healthy participants. Using swept-source optical coherence tomography (SS-OCT), the macular and peripapillary choroidal thickness and three-dimensional CVI were measured and compared globally and sectorally. Pearson's correlation analysis and multivariate regression models were used to evaluate choroidal thickness or CVI with related factors. RESULTS: The mean subfoveal CVIs were 0.35±0.10, 0.33±0.09, and 0.29±0.04, and the mean subfoveal choroidal thickness were 315.62±52.92, 306.22±59.29, and 262.69±45.55 μm in the F-APAC, F-CPACG, and normal groups, respectively. All macular sectors showed significantly higher CVIs and choroidal thickness in the F-APAC and F-CPACG eyes than in the normal eyes (P

For mobile robots working in the power inspection environment, navigation algorithms and collaborative path planning are the keys to understanding and reproducing human power inspection’s thinking mode. Firstly, the paper proposed a hybrid navigation algorithm of reflector and laser based on the generalized inverse of the least squares solution. Secondly, to solve the problem of multi-robot inspection cooperative path planning, the traffic rule reservation table generated a dynamic weighted map representing traffic congestion in power inspection to prevent multi-robot collision. Thirdly, through the distributed control method, the robot used the dynamic weighted map to improve the RRT (Rapidly-Exploring Random Trees)algorithm to achieve the purpose of active cooperative path planning, reducing the trajectory’s critical path points and solving the cooperative congestion. Finally, the positioning and calibration compensation can be carried out through the experiment by the reflector navigation algorithm in a large-scale complex environment. Comparing the path planning methods of the A* algorithm and the dynamic weighted RRT algorithm, the dynamic weighted RRT algorithm reduces the number of extended nodes. It solves the multi-robot planning collision problem while ensuring the search path’s completeness. Meanwhile, the dynamic weighted RRT algorithm can save the running time of the multi-robot system and effectively improve the efficiency of the power inspection system.

This paper proposes a solution to the problem of mobile robot navigation and trajectory interpolation in dynamic environments with large scenes. The solution combines a semantic laser SLAM system that utilizes deep learning and a trajectory interpolation algorithm. The paper first introduces some open-source laser SLAM algorithms and then elaborates in detail on the general framework of the SLAM system used in this paper. Second, the concept of voxels is introduced into the occupation probability map to enhance the ability of local voxel maps to represent dynamic objects. Then, in this paper, we propose a PointNet++ point cloud semantic segmentation network combined with deep learning algorithms to extract deep features of dynamic point clouds in large scenes and output semantic information of points on static objects. A descriptor of the global environment is generated based on its semantic information. Closed-loop completion of global map optimization is performed to reduce cumulative error. Finally, T-trajectory interpolation is utilized to ensure the motion performance of the robot and improve the smooth stability of the robot trajectory. The experimental results indicate that the combination of the semantic laser SLAM system with deep learning and the trajectory interpolation algorithm proposed in this paper yields better graph-building and loop-closure effects in large scenes at SIASUN large scene campus. The use of T-trajectory interpolation ensures vibration-free and stable transitions between target points.

AIM: To perform a bibliometric analysis in the field of primary angle-closure disease (PACD) research to characterize current global trends and compare contributions from different countries, institutions, journals, and authors. METHODS: All PACD-related publications from 1991 to 2022 from the Web of Science Core Collection database were extracted. Microsoft Excel and VOSviewer were used to collect publication data, analyze publication trends, and visualize relevant results. RESULTS: A total of 1721 publications with 34 591 citations were identified. China produced the most publications (554) while ranking third in citations (8220 times). The United States contributed the most citations (12 315 times) with publications (362) ranking second. The Investigative Ophthalmology Visual Science was the most productive journal concerning PACD, and Aung Tin was the author with the highest number of publications in the field. Keywords were classified into three clusters, epidemiology and pathogenesis research, optical coherence tomography (OCT) and other imaging examinations, and glaucoma surgery treatment. Genome-wide association, susceptibility loci, OCT, and combined phacoemulsification have become new hot research topics in recent years since 2015. CONCLUSION: China, the United States, and Singapore make the most outstanding contributions in the field of PACD research. OCT, combined phacoemulsification, and gene mutation-related study, are considered the potential focus for future research.

Retinal ganglion cell apoptotic death is the main pathological characteristic of glaucoma, which is the leading cause of irreversible blindness. Disruption of Ca2+ homeostasis plays an important role in glaucoma. Voltage-gated Ca2+ channel blockers have been shown to improve vision in patients with glaucoma. However, whether and how voltage-gated Ca2+ channels are involved in retinal ganglion cell apoptotic death are largely unknown. In this study, we found that total Ca2+ current densities in retinal ganglion cells were reduced in a rat model of chronic ocular hypertension experimental glaucoma, as determined by whole-cell patch-clamp electrophysiological recordings. Further analysis showed that L-type Ca2+ currents were downregulated while T-type Ca2+ currents were upregulated at the later stage of glaucoma. Western blot assay and immunofluorescence experiments confirmed that expression of the CaV1.2 subunit of L-type Ca2+ channels was reduced and expression of the CaV3.3 subunit of T-type Ca2+ channels was increased in retinas of the chronic ocular hypertension model. Soluble tumor necrosis factor-α, an important inflammatory factor, inhibited the L-type Ca2+ current of isolated retinal ganglion cells from control rats and enhanced the T-type Ca2+ current. These changes were blocked by the tumor necrosis factor-α inhibitor XPro1595, indicating that both types of Ca2+ currents may be mediated by soluble tumor necrosis factor-α. The intracellular mitogen-activated protein kinase/extracellular signal-regulated kinase pathway and nuclear factor kappa-B signaling pathway mediate the effects of tumor necrosis factor-α. TUNEL assays revealed that mibefradil, a T-type calcium channel blocker, reduced the number of apoptotic retinal ganglion cells in the rat model of chronic ocular hypertension. These results suggest that T-type Ca2+ channels are involved in disrupted Ca2+ homeostasis and apoptosis of retinal ganglion cells in glaucoma, and application of T-type Ca2+ channel blockers, especially a specific CaV3.3 blocker, may be a potential strategy for the treatment of glaucoma.

This paper studies the AWC (Active Wafer Centering) algorithm for the movement control and wafer calibration of the handling robot in semiconductor manufacturing to prevent wafer surface contact and contamination during the transfer process. The mechanical and software architecture of the wafer-handling robot is analyzed first, which is followed by a description of the experimental platform for semiconductor manufacturing methods. Secondly, the article utilizes the geometric method to analyze the kinematics of the semiconductor robot, and it decouples the motion control of the robot body from the polar coordinates and joint space. The wafer center position is calibrated using the generalized least-square inverse method for AWC correction. The AWC algorithm is divided into calibration, deviation correction, and retraction detection. These are determined by analyzing the robot’s wafer calibration process. In conclusion, the semiconductor robot’s motion control and AWC algorithm are verified through experiments for correctness, feasibility, and effectiveness. After the wafer correction, the precision of AWC is

AIM: To measure the depths of different regions of the anterior chamber (AC) in healthy Chinese adults, and to explore possible correlations with age or gender. METHODS: The AC was imaged by swept-source optical coherence tomography in healthy Chinese adults. The horizontal scan of the right eye was used to measure the anterior chamber depth (ACD) at 199 points. RESULTS: A total of 309 images from 309 subjects were analyzed. The ACD values at nearly all locations were negatively correlated with age (all P

Abstract It was previously shown that EphB/ephrinB reverse signaling in retinal ganglion cells (RGCs) is activated and involved in RGC apoptosis in a rat chronic ocular hypertension (COH) model. In the present work, we first show that ephrinB/EphB forward signaling was activated in COH retinas, and RGC apoptosis in COH retinas was reduced by PP2, an inhibitor of ephrinB/EphB forward signaling. We further demonstrate that treatment of cultured Müller cells with ephrinB1-Fc, an EphB1 activator, or intravitreal injection of ephrinB1-Fc in normal rats induced an increase in phosphorylated EphB levels in these cells, indicating the activation of ephrinB/EphB forward signaling, similar to those in COH retinas. The ephrinB1-Fc treatment did not induce Müller cell gliosis, as evidenced by unchanged GFAP expression, but significantly up-regulated mRNA and protein levels of tumor necrosis factor-α (TNF-α) in Müller cells, thereby promoting RGC apoptosis. Production of TNF-α induced by the activation of ephrinB/EphB forward signaling was mediated by the NR2B subunit of NMDA receptors, which was followed by a distinct PI3K/Akt/NF-κB signaling pathway, as pharmacological interference of each step of this pathway caused a reduction of TNF-α production, thus attenuating RGC apoptosis. Functional analysis of forward and reverse signaling in such a unique system, in which ephrin and Eph exist respectively in a glial element and a neuronal element, is of theoretical importance. Moreover, our results also raise a possibility that suppression of ephrinB/EphB forward signaling may be a new strategy for ameliorating RGC apoptosis in glaucoma.

AIM: To determine whether glaucoma patients exhibit an abnormal melatonin concentration in serum and the effects of psychiatric disorders caused by glaucoma in melatonin secretion. METHODS: A sample of 80 primary angle-closure glaucoma (PACG) patients, 120 primary open angle glaucoma (POAG) patients, and 120 normal controls were enrolled in this study. All the participants were asked to complete the following questionnaires: Pittsburgh sleep quality index (PSQI), self-rating anxiety scale (SAS), and self-rating depression scale (SDS). Variance analysis was used to compare the subscores between the groups. After that, we chose 58 patients with primary glaucoma and 20 non-glaucoma control patients to collect their serum samples at 7-10 a.m. Serum melatonin levels were measured using enzyme linked immunosorbent assay (ELISA). RESULTS: Of all participants, the scores of PSQI, SAS, and SDS in PACG and POAG group were 9.38±0.40, 46.08±8.99, 51.11±10.72 and 7.43±0.35, 45.42±9.87, 49.04±12.24 respectively, significantly higher than those in control group (4.16±0.28, 35.49±9.18, 40.31±13.08). The serum melatonin levels in PACG (37.29±2.99 pg/mL) and POAG (35.97±3.64 pg/mL) were significantly higher than the controls (29.96±3.94 pg/mL) (P

Glaucoma is a progressive neuropathy characterized by the loss of retinal ganglion cells (RGCs). Strategies that delay or halt RGC loss have been recognized as potentially beneficial for rescuing vision in glaucoma patients. Quercetin (Qcn) is a natural and important dietary flavonoid compound, widely distributed in fruits and vegetables. Mounting evidence suggests that Qcn has numerous neuroprotective effects. However, whether Qcn exerts neuroprotective effects on RGC in glaucoma is poorly understood. In this study, we investigated the protective effect of Qcn against RGC damage in a rat chronic ocular hypertension (COHT) model invivo and hypoxia-induced primary cultured RGC damage in vitro, and we further explored the underlying neuroprotective mechanisms. We found that Qcn not only improved RGC survival and function from a very early stage of COHT invivo, it promoted the survival of hypoxia-treated primary cultured RGCs invitro via ameliorating mitochondrial function and preventing mitochondria-mediated apoptosis. Our findings suggest that Qcn has direct protective effects on RGCs that are independent of lowering the intraocular pressure (IOP). Qcn may be a promising therapeutic agent for improving RGC survival and function in glaucomatous neurodegeneration.

AIM: To evaluate the efficacy of a registration system for the blind people and to monitor the blindness due to uncorrected refractive error and cataract in Jing’an district, Shanghai, China.METHODS: Five hundred and ten blind people, based on visual acuity screening in a population aged 70 or older were enrolled into the study. Four hundred and forty subjects were interviewed. The following data were collected on each patient: demographic data, number of hospital visits for eye related problems, distance visual acuity, visual fields, ophthalmic diagnoses, education and registration status. If the eligible subject was not registered as blind, the reason for non-registration was recorded.RESULTS: Ten point nine one percent blindness was due to cataract, 27.5% due to uncorrected refractive error, and only 61.59% met the eligible blindness criteria (uncorrected refractive error and cataract are not considered as eligible blindness). The first four leading causes of eligible blindness were age related macular degeneration (25.09%), myopic macular degeneration (21.40%), glaucoma (18.82%) and corneal disease (8.12%). Only 68.27% eligible blind people were registered. The patients with macular degeneration and glaucoma tended not to register. Blind people with an above primary school education were 2.59 times more likely to be registered than those who were illiterate or had only a primary school education (OR=2.59, 95%CI: 1.49-4.48, P

Purpose: Our previous study indicated that mitochondrial DNA (mtDNA) damage and mutations are crucial to the progressive loss of retinal ganglion cells (RGCs) in a glaucomatous rat model. In this study, we examined whether high pressure could directly cause mtDNA alterations and whether the latter could lead to mitochondrial dysfunction and RGC death.Methods: Primary cultured rat RGCs were exposed to 30 mm Hg of hydrostatic pressure (HP) for 12, 24, 48, 72, 96, and 120 hours. mtDNA alterations and mtDNA repair/replication enzymes OGG1, MYH and POLG expressions were also analyzed. The RGCs were then infected with a lentiviral small hairpin RNA (shRNA) expression vector targeting POLG (POLG-shRNA), and mtDNA alterations as well as mitochondrial function, including complex I/III activities and ATP production were subsequently studied at appropriate times. Finally, RGC apoptosis and the mitochondrial-apoptosis pathway-related protein cleaved caspase-3 were detected using a Terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) assay and western blotting, respectively. Results: mtDNA damage was observed as early as 48 hours after the exposure of RGCs to HP. At 120 h after HP, mtDNA damage and mutations significantly increased, reaching >40% and 4.8±0.3-fold, respectively, compared with the control values. Twelve hours after HP, the expressions of OGG1, MYH and POLG mRNA in the RGCs were obviously increased 5.02±0.6-fold (p

BACKGROUND: Cataract and geographic atrophy (GA, also called advanced "dry" age-related macular degeneration) are the two major causes of visual impairment in the developed world. The association between cataract surgery and the development of GA was controversial in previous studies. METHODS/PRINCIPAL FINDINGS: We performed a meta-analysis by pooling the current evidence in literature and found that cataract is associated with an increased risk of geographic atrophy with a summary odds ratio (OR) of 3.75 (95% CI: 95% CI: 1.84-7.62). However, cataract surgery is not associated with the risk of geographic atrophy (polled OR=3.23, 95% CI: 0.63-16.47). Further experiments were performed to analyze how the αA-crystallin, the major component of the lens, influences the development of GA in a mouse model. We found that theαA-crystallin mRNA and protein expression increased after oxidative stress induced by NaIO(3) in immunohistochemistry of retinal section and western blot of posterior eyecups. Both functional and histopathological evidence confirmed that GA is more severe in αA-crystallin knockout mice compared to wild-type mice. CONCLUSIONS: Therefore, αA-crystallin may protect against geographic atrophy. This study provides a better understanding of the relationship between cataract, cataract surgery, and GA.

AIM: To investigate the treatment pattern and safety of tafluprost for glaucoma and ocular hypertension (OH) in clinical practice in China. METHODS: This post-marketing observational study included patients who received tafluprost to lower intraocular pressure (IOP) within 30d between September 2017 and March 2020 in 20 hospitals in China. Adverse drug reactions (ADRs) during tafluprost treatment and within 30d after the treatment were collected. RESULTS: A total of 2544 patients were included in this study, of them 58.5% (1488/2544) had primary open angle glaucoma (POAG), 21.9% (556/2544) had OH and 19.7% (500/2544) used tafluprost for other reasons. Of 359 ADRs occurred in 10.1% (258/2544) patients, and no serious adverse event occurred. The most common ADR was conjunctival hyperemia (128 ADRs in 124 patients, 4.9%). Totally 1670 participants (65.6%) combined tafluprost with carbonic anhydrase inhibitors (CAIs; 37.1%, 620/1670), sympathomimetics (33.5%, 559/1670), β-blockers (33.2%, 555/1670), other prostaglandin analogs (PGAs; 15.6%, 260/1670) and other eye drops (15.1%, 253/1670). The highest incidence of conjunctival hyperemia was noted in patients who received tafluprost in combination with other PGAs (23 ADRs in 23 patients, 8.8%, 23/260) and the lowest was in combination with CAIs (16 ADRs in 16 patients, 2.6%, 16/620). Tafluprost was applied in primary angle-closure glaucoma (41.6%, 208/500), after glaucoma surgery (17.8%, 89/500) and after non-glaucoma surgery (15.8%, 79/500). CONCLUSION: Tafluprost is safe for POAG and OH, and tolerable when combined with other eye drops and under various clinical circumstances.

With the rapid development of molecular biology technologies such as whole-genome testing in the past decade, non-coding RNA has been deeply explored. Circular RNA(circRNA)gradually becomes a hot topic in recent years, which plays an important role in the occurrence and development of a variety of diseases, and relevant studies have been carried out in ophthalmological diseases. This article will review the mechanism, basic research, and clinical findings of circRNA in various ophthalmic diseases, and briefly discuss the potential clinical significance of circRNA in ophthalmic diseases.

AIM: To study the changes of the red blood cell volume distribution width(RDW)level and the correlation between them in patients with primary angle-closure glaucoma(PACG).METHODS: Retrospective case-control study was conducted. A total of 306 PACG patients in Eye & ENT Hospital of Fudan University from February 2019 to October 2020 were selected as the case group and 126 healthy patients who received physical examination at the hospital during the same period were selected as the control group. The PACG patients were divided into three subgroups according to the mean defect of visual field(MD): mild(MD≤6dB), moderate(612dB). The detailed eye and physical examinations information of the two groups were collected from the medical data platform of Eye & ENT Hospital of Fudan University. The blood sample parameters were detected by automated hematology and biochemistry analyzers. Independent sample t-test, Chi-square test, one-way ANOVA test, Pearson correlation analyses and multiple linear regression analyses were performed in this research. RESULTS: There was no significant difference between the PACG group and the control group in age, gender, body mass index and blood pressure(P>0.05). Based on the laboratory results, the mean RDW level was significantly higher(t=2.132, P=0.034)in the PACG group(12.64%±0.96%)than that in the control group(12.45%±0.49%). Moreover, the mean RDW level and the mean hemoglobin(HG)level was significantly lower(P

Abstract Our previous studies have demonstrated that activation of group I metabotropic glutamate receptors downregulated Kir channels in chronic ocular hypertension (COH) rats, thus contributing to Müller cell gliosis, characterized by upregulated expression of glial fibrillary acidic protein (GFAP). In the present study, we explored possible signaling pathways linking Kir channel inhibition and GFAP upregulation. In normal retinas, intravitreal injection of BaCl2 significantly increased GFAP expression in Müller cells, which was eliminated by co-injecting mitogen-activated protein kinase (MAPK) inhibitor U0126. The protein levels of phosphorylated extracellular signal-regulated protein kinase1/2 (p-ERK1/2) and its upstream regulator, p-MEK, were significantly increased, while the levels of phosphorylated c-Jun N-terminal kinase (p-JNK) and p38 kinase (p-p38) remained unchanged. Furthermore, the protein levels of phosphorylated cAMP response element binding protein (p-CREB) and c-fos were also increased, which were blocked by co-injecting ERK inhibitor FR180204. In purified cultured rat Müller cells, BaCl2 treatment induced similar changes in these protein levels apart from p-p38 levels and the p-p38:p38 ratio showing significant upregulation. Moreover, intravitreal injection of U0126 eliminated the upregulated GFAP expression in COH retinas. Together, these results suggest that Kir channel inhibition-induced Müller cell gliosis is mediated by the MEK-ERK/p38-CREB/c-fos signaling pathway.

Glaucoma is a chronic neurodegenerative disease characterized by the progressive loss of retinal ganglion cells (RGCs). Mitochondrial DNA (mtDNA) alterations have been documented as a key component of many neurodegenerative disorders. However, whether mtDNA alterations contribute to the progressive loss of RGCs and the mechanism whereby this phenomenon could occur are poorly understood. We investigated mtDNA alterations in RGCs using a rat model of chronic intraocular hypertension and explored the mechanisms underlying progressive RGC loss. We demonstrate that the mtDNA damage and mutations triggered by intraocular pressure (IOP) elevation are initiating, crucial events in a cascade leading to progressive RGC loss. Damage to and mutation of mtDNA, mitochondrial dysfunction, reduced levels of mtDNA repair/replication enzymes, and elevated reactive oxygen species form a positive feedback loop that produces irreversible mtDNA damage and mutation and contributes to progressive RGC loss, which occurs even after a return to normal IOP. Furthermore, we demonstrate that mtDNA damage and mutations increase the vulnerability of RGCs to elevated IOP and glutamate levels, which are among the most common glaucoma insults. This study suggests that therapeutic approaches that target mtDNA maintenance and repair and that promote energy production may prevent the progressive death of RGCs.