Hepatic encephalopathy (HE) is frequently accompanied by visual dysfunction, yet the mechanisms underlying the liver-brain-eye axis remain unclear. We established mouse models of acute hepatic encephalopathy (AHE) using thioacetamide and chronic hepatic encephalopathy (CHE) using bile duct ligation, confirming hyperammonemia and visual impairment by electroretinogram (ERG) and visual evoked potentials (VEPs). Retinal analyses revealed preserved structure in AHE, whereas CHE induced significant thinning of the ganglion cell layer (GCL), inner nuclear layer (INL), and outer plexiform layer (OPL). Viral anterograde tracing identified aberrant activation of medial substantia nigra pars reticulata glutamate decarboxylase 2-positive (mSNrGAD2) projections to the superior colliculus (SC) under AHE conditions. Chemogenetic inhibition of this pathway restored retinal function, normalized visual signal transmission, and reduced retinal γ-aminobutyric acid (GABA) release. These findings identify SNr-SC signaling as a key neural mechanism driving liver-brain-eye axis dysfunction in HE.

To elucidate the contributions of M-cone to the negative off-response of rat Electroretinogram (ERG) using specific drugs and spontaneous mutation rat models. The ON/OFF responses of ERG were evoked by long duration flash (200 ms) pre or post the application of 2-amino-4-phosphonobutyric acid (APB), cis-piperidine-2,3-dicarboxylic acid (PDA) or BaCl2 to the Sprague-Dawley (SD) rats. Furthermore, the ON/OFF responses of other two types of mutation rats, the middle-wavelength opsin cone dysfunction (MCD) rats and congenital stationary night blindness (CSNB) rats, were recorded. Typical scotopic and photopic ON/OFF responses were recorded in SD rats. At light offset, the OFF response showed a rapid negative deflection, then the retinal potential slowly returned to baseline from the trough of the negative off-response. The negative off-response was completely eliminated by the intravitreal injection of 400 µM APB. The amplitude of the negative off-response was reduced by the application of 5 mM PDA. However, the off component was not blocked by the application of 50 µM BaCl2. In addition, distinct differences of OFF response were found among MCD, CSNB and SD rats. The scotopic ON/OFF ERG of the MCD and CSNB rats showed no obvious negative off component at light offset, while the negative off component of photopic ON/OFF ERG was found in the CSNB rats, though with lower amplitude. The negative off-response of rat ERGs is not the off component of M-wave: a negative potential change at stimulus onset or offset. M-cone and the depolarizing bipolar cell play a central role in the signal transmission of this negative off-response.

Long-term spaceflight can lead to changes in eye structure and decreased visual function. At present, there are almost no effective methods to prevent and treat eye damage caused by microgravity environments. Oxidative stress has been identified as one of the contributing mechanisms of spaceflight-associated neuro-ocular syndrome (SANS), and hydrogen (H2) has demonstrated significant antioxidant and anti-inflammatory effects. The aim of this study was to determine whether hydrogen-rich water (HRW) has a protective effect against eye injury induced by tail-suspension simulated weightlessness in rats, and to elucidate the underlying mechanisms. In this experiment, we utilized an 8-week tail-suspension model to simulate weightlessness, and employed histopathology, visual electrophysiology, and biochemical indices to evaluate retinal structure, function, and related molecular mechanisms leading to retinal damage. We also assessed the therapeutic efficacy of HRW treatment. Results demonstrated that tail-suspension simulated weightlessness induced thinning of the retinal outer nuclear layer, decreased visual function, and promoted retinal inflammation, oxidative stress, and mitochondrial dysfunction in rats. HRW treatment effectively alleviated the degenerative changes in the retinal outer nuclear layer, improved retinal function, and reduced retinal inflammation in treated rats. Our findings revealed that HRW reduced the retinal oxidative stress response and enhanced mitochondrial function through the PI3K/Akt/Nrf2 signaling pathway. Overall, HRW may be a promising candidate for the treatment of eye injuries in simulated microgravity environments.

Noise-induced hidden hearing loss (HHL) is a type of hearing dysfunction caused by moderate noise exposure. It is clinically manifested as speech recognition impairment in noisy environments while the hearing threshold remains within the normal range. The mechanism by which noise exposure causes speech recognition impairment remains unclear. This study aimed to investigate the excitation-inhibition status in the auditory cortex of HHL mice and its roles in sound recognition disability in noisy environments. A model of HHL in mice was induced using 110 decibels (dB) of helicopter noise for 2 h, the sound recognition-avoidance decision (SRAD) behavioral test was used to evaluate sound recognition ability. The activation level of excitatory neurons and the expression of vesicular glutamate transporter 1 (VGluT1) and glutamate decarboxylase 67 (GAD67) in the auditory cortex were observed. Mice were administered α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist NBQX. The results showed increased cFos expression in the auditory cortex of HHL mice and an upregulated ratio of activated CaMKⅡ+ neurons. Furthermore, the expression of VGluT1 and GAD67 increased in an imbalanced manner under an 80 dB noise stimulus for 2 h. The SRAD behavioral tests showed the HHL mice maintained normal sound recognition ability under quiet conditions but not in a noisy environment. The NBQX treatment improved sound recognition but did not restore normal status. This study suggested that the excitation-inhibition imbalance in the auditory cortex of mice with HHL might be the direct cause of sound recognition disorders.

Photoreceptor cell death, primarily through apoptosis, related to retinal disorders like retinitis pigmentosa (RP), would result in vision loss. The pathological processes and crucial mutant conditions preceding photoreceptor cell demise are not well understood. This study aims to conduct an in-depth examination of early-stage changes in the widely utilized Pde6b rd1/rd1 (rd1) mouse model, which has Pde6b gene mutations representing autosomal recessive RP disorder. We investigated the morphology and ultrastructure of retinal cells, including second-order neurons, during the initial phase of disease progression. Our findings revealed that mitochondrial alterations in rod photoreceptors were present as a predeath mutant state as early as postnatal day 3 (P3). The bipolar and horizontal cells from the rd1 mouse retina exhibited significant morphological changes in response to loss of photoreceptor cells, indicating that second-order neurons rely on these cells for their structures. Subsequent oral administration of idebenone, a mitochondria-protective agent, enhanced retinal function and promoted both photoreceptor cell survival and inner retinal second-order synaptogenesis in rd1 mice at P14. Our findings offer a mechanistic framework, suggesting that mitochondrial damage acts as an early driver for photoreceptor cell death in retinal degeneration.

Cellular senescence is a complex process involving multiple factors, such as genetics, environment, and behavior. However, recent studies have shown that stress also plays a crucial role in inducing cellular senescence. Stress can affect cellular function and structure through various pathways, leading to accelerated aging. Exposure to stressful conditions can alter the neuroendocrine system, activate the hypothalamus-pituitary-adrenal axis and sympathetic adrenal medullary axis, and release cortisol and catecholamines, causing mitochondrial dysfunction, generating excessive reactive oxygen species, and inducing oxidative stress, DNA damage, and inflammatory reactions, ultimately resulting in accelerated cellular senescence. The process of stress-induced cellular senescence has been implicated in a number of chronic diseases, including age-related macular degeneration, chronic kidney disease, type 2 diabetes, cardiovascular disease and obstructive sleep apnea. In this review, we integrate recent progress research progress in our understanding of the mechanisms of stress-induced cellular senescence and discuss its underlying mechanisms from the perspective of stress hormones. We review potential therapeutic targets for stress-induced premature senescence and discuss the advantages and limitations of existing pharmacological agents capable of ameliorating stress-induced premature senescence.

Background: Previously, we discovered a strain of Kunming mice, referred to as the KMush/ush strain, that exhibited notably abnormal electroretinogram (ERG) readings and elevated thresholds for auditory brainstem responses (ABRs), which resembled the characteristics of Usher Syndrome (USH). We successfully identified the pathogenic genes, Pde6b and Adgrv1, after KMush/ush crossbred with CBA/CaJ mice, referred to as CBA-1ush/ush, CBA-2ush/ush or CBA-2ush/ush. In this investigation, we crossbred KMush/ush and CBA/J mice to establish novel recombinant inbred lines and analysed their phenotypic and genotypic characteristics. Methods: ERG readings, ABR testing, fundus morphology, histological examination of the retina and inner ear, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis, western blotting, DNA sequence analysis and behavioural experiments were performed to assess the phenotypes and genotypes of the progeny lines. Results: No obvious waveforms in the ERG were detected in F1 hybrid mice while normal ABR results were recorded. The F2 hybrids, which were called J1ush/ush or J2ush/ush, exhibited segregated hearing-loss phenotypes. J1ush/ush mice had a retinitis pigmentosa (RP) phenotype with elevated ABR thresholds, whereas J2ush/ush mice exhibited only the RP phenotype. Interestingly, J1ush/ush mice showed significantly higher ABR thresholds than wild-type mice at 28 days post born (P28), and RT-qPCR and DNA-sequencing analysis showed that Adgrv1 gene expression was significantly altered in J1ush/ush mice, but histological analysis showed no significant structural changes in the organ of Corti or spiral ganglia. Further elevation of ABR-related hearing thresholds by P56 manifested only as a reduced density of spiral ganglion cells, which differed significantly from the previous pattern of cochlear alterations in CBA-2ush/ush mice. Conclusions: We successfully introduced the hearing-loss phenotype of inbred mice with USH into CBA/J mice, which provides a good animal model for future studies on the important physiological roles of the Adgrv1 gene in inner-ear structure and for therapeutic studies targeting Adgrv1-mutated USH.

JOURNAL/nrgr/04.03/01300535-202507000-00032/figure1/v/2024-09-09T124005Z/r/image-tiff A microgravity environment has been shown to cause ocular damage and affect visual acuity, but the underlying mechanisms remain unclear. Therefore, we established an animal model of weightlessness via tail suspension to examine the pathological changes and molecular mechanisms of retinal damage under microgravity. After 4 weeks of tail suspension, there were no notable alterations in retinal function and morphology, while after 8 weeks of tail suspension, significant reductions in retinal function were observed, and the outer nuclear layer was thinner, with abundant apoptotic cells. To investigate the mechanism underlying the degenerative changes that occurred in the outer nuclear layer of the retina, proteomics was used to analyze differentially expressed proteins in rat retinas after 8 weeks of tail suspension. The results showed that the expression levels of fibroblast growth factor 2 (also known as basic fibroblast growth factor) and glial fibrillary acidic protein, which are closely related to Müller cell activation, were significantly upregulated. In addition, Müller cell regeneration and Müller cell gliosis were observed after 4 and 8 weeks, respectively, of simulated weightlessness. These findings indicate that Müller cells play an important regulatory role in retinal outer nuclear layer degeneration during weightlessness.

Objective: Microgravity contributes to ocular injury yet the underlying mechanism remains unclear. This study aims to elucidate the mechanism behind choroidal circulation disorder and outer retinal degeneration in rats with simulated weightlessness.Methods: Optical coherence tomography angiography (OCTA) was used to evaluate choroidal circulation and retinal morphological alterations in rats with weightlessness simulation. Electroretinogram and transmission electron microscopy were used to examine the ultrastructure and function of the choroid and outer retina. Furthermore, histological and terminal deoxynucleotidyl transferase deoxyuridine dUTP nick-end labeling (TUNEL) staining was used to monitor retinal morphology. Western blotting was performed to analyze the expressions of blood-retinal outer barrier function-related proteins (Cx43, ZO-1, and occludin).Results: The choroidal thickening was observed from the fourth week of simulated weightlessness (p < 0.05), and choroidal capillary density started to decline by the fifth week (p < 0.05). Transmission electron microscopy revealed that the choroidal vessels were open and operating well by the fourth week. However, most of the mitochondria within the vascular endothelium underwent mild swelling, and by the fifth week, the choroidal vessels had various degrees of erythrocyte aggregation, mitochondrial swelling, and apoptosis. Additionally, ERG demonstrated a decline in retinal function beginning in the fifth week (p < 0.05). TUNEL staining revealed a significantly higher apoptotic index in the outer nuclear layer of the retina (p < 0.05). At the sixth week weeks of simulated weightlessness, OCTA and hematoxylin and eosin (HE) staining of retinal sections revealed that the outer nuclear layer of the retina started to become thin (p < 0.05). Results from western blotting revealed that Cx43, ZO-1, and occludin exhibited decreased expression (p < 0.05).Conclusion: Based on our findings in a rat model of simulated weightlessness, choroidal circulation disturbance induced by choroidal congestion is the initial cause of outer retinal degeneration. Blood-retinal barrier disruption is significant in this process.

Age-related macular degeneration (AMD) is the most common blindness-causing disease among the elderly. Under oxidative stress, low-density lipoprotein in the outer layer of the retina is easily converted into oxidized low-density lipoprotein (OxLDL), which promotes the development of choroidal neovascularization (CNV), the main pathological change in wet AMD. Liver X receptor (LXR), a ligand-activated nuclear transcription factor, regulates various processes related to CNV, including lipid metabolism, cholesterol transport, inflammation, and angiogenesis. In this study, we evaluated the effects of the LXR agonist TO901317 (TO) on CNV. Our results demonstrated that the TO could inhibit OxLDL-induced CNV in mice as well as inflammation and angiogenesis in vitro. Using siRNA transfection in cells and Vldlr−/− mice, we further confirmed the inhibitory effects of TO against the inflammatory response and oxidative stress. Mechanistically, the LXR agonist reduces the inflammatory response via the nuclear translocation of NF-κB p65 in the pathway for NF-κB activation and by enhancing ABCG1-dependent lipid transportation. Therefore, an LXR agonist is a promising therapeutic candidate for AMD, especially for wet AMD.

目的:基于网络药理学及实验验证探讨枸杞子治疗干眼(DE)的作用机制.方法:以"枸杞子"为关键词,通过采用TCMSP数据库与分析平台,搜索枸杞子的药物活性成分及作用靶点,以GeneCards和OMIM数据库搜索Dry eye(DE)相关的基因靶点,将枸杞子与DE的靶点基因导入Venn软件,可获得两者交集的靶点图,后将数据导入String数据库获得PPI蛋白与蛋白相互作用网络图,借助于Cytoscape3.7.2软件构建枸杞子活性成分-作用靶点-相关疾病的网络图;再利用Bioconductor平台及R语言GO富集分析、KEGG富集分析;通过实验验证干眼发病机制中的关键靶标.结果:通过TCMSP数据库与分析平台筛选得到枸杞子的有效化学成分45种,活性成分对应的靶点基因174个,与DE共同的靶点基因131个,根据"药物-成分-疾病-靶点"网络拓扑图,枸杞子治疗DE的主要有效成分27个.分析PPI网络,根据度值较高,即枸杞子治疗DE的关键靶点主要包括AKT1、VEGFA、CASP3、IL1B、JUN、PTGS2、CXCL8等,根据GO富集分析获得枸杞子治疗DE的166种生物学功能与过程,KEGG富集分析显示涉及31条信号通路,此外,通过实验验证发现DE模型组的结膜组织中AKT1、IL-6、TNF-α及IL-17蛋白表达量显著升高.结论:枸杞子治疗DE是多成分-多靶点-多途径的复杂过程,且枸杞子治疗DE主要通过抗炎及抑制细胞凋亡相关分子参与调控.

目的 研究不同模拟飞行光环境下,不同视力受试者动态视力(DVA)的差异,为保障飞行安全提供试验依据.方法 招募24名受试者,其中6名视力正常者为1.0/1.0视力组(小数视力),18名近视受试者随机分为0.8/0.8视力组、0.6/0.6视力组和0.4/0.4视力组,每组6人.在模拟日光、迎光、背光、曙暮光和云上光环境下,通过观察3.0、4.5、6.0、7.5 km/h运动速度的视标检测DVA.采用具有2个重复测量因素的三因素重复测量方差分析,比较不同光环境对不同视力者DVA的影响.结果 光环境、静态视力和运动速度3个因素间不存在交互作用(P>0.05).通过进一步两因素交互作用检验,分析发现光环境和静态视力存在交互作用(P<0.05),运动速度和静态视力存在交互作用(P<0.05),光环境和运动速度不存在交互作用(P>0.05).与日光环境相比,所有视力组受试者在背光下的DVA显著提高(P<0.001),在曙暮光、迎光下的DVA均显著下降(P<0.001).除0.4/0.4视力组外,其余视力组在云上光环境下的DVA显著低于日光(P<0.05).在相同的模拟光环境下,1.0/1.0视力组DVA最高,0.8/0.8视力组高于0.6/0.6视力组,0.4/0.4视力组最低,差异有统计学意义(P<0.05).对于3.0、4.5、6.0 km/h运动速度的视标,1.0/1.0视力组DVA最高,0.8/0.8视力组高于0.6/0.6视力组,0.4/0.4视力组最低,差异有统计学意义(P<0.05).1.0/1.0视力组观察7.5 km/h运动速度视标的DVA显著高于低视力组(P<0.05),0.4/0.4视力组低于0.8/0.8和0.6/0.6视力组,差异有统计学意义(P<0.05).所有视力组受试者DVA均随目标运动速度的增加而显著下降(P<0.05).结论 光环境和静态视力水平、运动速度和静态视力水平对DVA水平的作用相互影响.近视者在不利光环境(如迎光、云上光和曙暮光)下观察快速运动目标时,DVA严重下降,应引起飞行人员和航空医学工作者的重视.

目的 比较同一体质量区间不同品系大鼠、小鼠眼轴的差别.方法 选用野生型(SD)大鼠、实验室现有的不同品系大鼠和小鼠:先天性静止性夜盲(CSNB)大鼠、卷毛(HL)大鼠、视网膜锥细胞失功能(RCD)大鼠、C57BL/6小鼠、锥体光感受器功能丧失 1(cpfl1)小鼠、锥体光感受器功能丧失 3(cpfl3)小鼠、先天性静止性夜盲(Nob2)小鼠,按照体质量划分为不同组别(大鼠以 50 g为一区间分为 10 组,小鼠以 10 g为一区间共分为两组),测量其眼轴,在同一体质量区间比较不同品系大鼠和小鼠之间的眼轴区别.结果 大鼠与小鼠眼轴长度随体质量增加而增长,在不同品系之间存在差异.其中 100～150 g体质量的 CSNB大鼠眼轴长度大于 SD大鼠(P<0.05).150～200 g体质量的 RCD大鼠眼轴长度大于 SD 大鼠(P<0.01),但 SD 与 CSNB 大鼠之间不具有统计学差异;200～250 g、450～500 g、500～550 g体质量的 HL与 RCD大鼠眼轴较 SD大鼠长(P<0.05),但 SD 与 CSNB 大鼠之间没有统计差异;250～300 g与 300～350 g体质量的三种品系大鼠眼轴均长于 SD 大鼠(P<0.01);350～400 g 体质量的 CSNB与 RCD大鼠眼轴长于 SD大鼠(P<0.01),但 SD大鼠与 HL 大鼠之间无统计学差异;400～450 g 体质量的四种品系大鼠眼轴均无统计学差异;550～600 g体质量的 HL大鼠眼轴较 SD大鼠长(P<0.05),CSNB与 SD 大鼠之间无统计差异.全部体质量的 C57BL/6 小鼠眼轴长度短于其余 3 个品系的小鼠(P<0.01);结论 不同体质量区间,各基因突变大鼠或小鼠眼轴长于对照鼠(SD大鼠 C57BL/6 小鼠)眼轴,且在大鼠中,此差异在发育期更为明显.

Background To develop machine learning models for objectively evaluating visual acuity (VA) based on pattern-reversal visual evoked potentials (PRVEPs) and other related visual parameters. Methods Twenty-four volunteers were recruited and forty-eight eyes were divided into four groups of 1.0, 0.8, 0.6, and 0.4 (decimal vision). The relationship between VA, peak time, or amplitude of P100 recorded at 5.7°, 2.6°, 1°, 34′, 15′, and 7′ check sizes were analyzed using repeated-measures analysis of variance. Correlations between VA and P100, contrast sensitivity (CS), refractive error, wavefront aberrations, and visual field were analyzed by rank correlation. Based on meaningful P100 peak time, P100 amplitude, and other related visual parameters, four machine learning algorithms and an ensemble classification algorithm were used to construct objective assessment models for VA. Receiver operating characteristic (ROC) curves were used to compare the efficacy of different models by repeated sampling comparisons and ten-fold cross-validation. Results The main effects of P100 peak time and amplitude between different VA and check sizes were statistically significant (all P < 0.05). Except amplitude at 2.6° and 5.7°, VA was negatively correlated with peak time and positively correlated with amplitude. The peak time initially shortened with increasing check size and gradually lengthened after the minimum value was reached at 1°. At the 1° check size, there were statistically significant differences when comparing the peak times between the vision groups with each other (all P < 0.05), and the amplitudes of the vision reduction groups were significantly lower than that of the 1.0 vision group (all P < 0.01). The correlations between peak time, amplitude, and visual acuity were all highest at 1° ( r s = − 0.740, 0.438). VA positively correlated with CS and spherical equivalent (all P < 0.001). There was a negative correlation between VA and coma aberrations ( P < 0.05). For different binarization classifications of VA, the classifier models with the best assessment efficacy all had the mean area under the ROC curves (AUC) above 0.95 for 500 replicate samples and above 0.84 for ten-fold cross-validation. Conclusions Machine learning models established by meaning visual parameters related to visual acuity can assist in the objective evaluation of VA.

The traditional methods for the control of myopia development are optical correction, orthokeratology lens, defocus glasses and other methods, however, these approaches are poor. At present, it has been demonstrated that outdoor activities and the application of low concentration atropine had a positive effect on preventing the occurrence of myopia and controlling the growth of myopia diopter. The occurrence and development of axial myopia was related to scleral remodeling toward myopic direction, but the mechanism remains unclear. In addition, true myopia caused by the axial growth was irreversible. After long-term spaceflight, astronauts had posterior eyeball flattening, axial shortening, and hyperopic displacement of refractive state, indicating that stress environment could cause sclera remodeling. Therefore, the combination of appropriate exercise to promote the transfer of blood head and increase the hydrostatic pressure gradient of the head and eye tissue might affect the local scleral remodeling and shorten the axial direction of the eye, or delay the trend of axial growth, which could provide a new idea for the prevention and control of myopia.

AIM: To study the effects of the specific simulated luminous environment on the visual performance of people with different vision, so as to provide an experimental basis for revising pilots' vision standards. METHODS: A controlled randomized trial was conducted. Twenty-four volunteers were recruited and divided into four groups(1.0/1.0, 0.8/0.8, 0.6/0.6 and 0.4/0.4, decimal vision)according to right/left eye visual acuity, with six subjects in each group. Each subject was tested for static distant vision, kinetic visual acuity, color vision, depth perception error and visual search time under the simulated luminous environments of sunlight, twilight, and on-cloud, respectively, to compare changes in the impact of distinctive luminous surroundings on the visual performance indicators of human beings with different vision.RESULTS: There were main effect differences in static distant vision, kinetic visual acuity, color error, depth perception error and visual search time under different light environments(all P<0.01). The binocular static distant visual acuity, abilities of color discrimination, depth perception and visual search in simulated sunlight environment were higher than those in simulated twilight and on-cloud environments. In the 0.4/0.4 vision group, kinetic vision in simulated twilight and on-cloud environments were significantly lower than that in simulated sunlight environment(P<0.01). There were main effect differences in binocular static distant vision, kinetic visual acuity, depth perception error and visual search time among subjects with different vision(all P<0.05). Compared with 1.0/1.0 vision group, those with 0.6/0.6 and 0.4/0.4 vision had significant decrease in kinetic visual acuity, depth perception ability and visual search ability(all P<0.05). CONCLUSION: Different luminous environments have a great impact on the visual performance of people with low vision, which poses a potential threat to flight safety.

目的 探索一种制作大鼠全眼球石蜡组织切片的改进方法.方法 18只SD大鼠,随机分为3组,每组6只;取双眼眼球,分别固定于4％多聚甲醛、10％中性福尔马林和混合固定液中;2 h后左眼眼球于角膜中央用注射器扎一小孔,右眼眼球使用刀片在巩膜处剖一长约0.5 cm小开口;继续固定24 h;制作石蜡组织切片,并行苏木精-伊红染色,应用光学显微镜观察全眼球石蜡组织切片制作效果.结果 采用4％多聚甲醛和10％中性福尔马林组眼球皱缩变形,晶状体结构存留少,存在视网膜脱离,细胞层细胞核连续性差.混合固定液组眼球结构较完整,未见明显视网膜脱离,细胞层细胞核连续性较好;相对于左眼,右眼晶状体结构较完整.结论 采用混合固定液结合眼球侧壁纵剖制作大鼠全眼球石蜡组织切片,结构较完整,方法简便,可在一定范围推广适用.

Purpose:To explore the temporal topography of the chorioretinopathy in an animal model of central serous chorioretinopathy (CSC) induced by intravenous injection of adrenalin in the Chinchilla rabbits. Methods:Ten Chinchilla rabbits received a daily intravenous injection of adrenaline at 0.04 mg/kg for 8 weeks. Fluorescence fundus angiography (FFA) and electroretinogram (ERG) were performed every week afterwards to see whether there was fluorescence leakage in the fundus and to evaluate the retinal function. Indocyanine green angiography (ICGA) and optical coherence tomography (OCT) were also conducted to detect the change of choroidal vessels. Finally, the eyes of the rabbits were enucleated to make the retinal sections for histological examination with hematoxylin-eosin (HE) staining. Results:Within 8 weeks of the adrenalin administration, 7 out of the 10 rabbits showed different degrees of fluorescence leakage on FFA. The leakage was more obvious during 2-3 weeks after the adrenalin administration. With the progress of disease, the leakage subsided gradually and a scar-like lesion formed. ICGA revealed the local choroidal ischemia and the dilated choroidal vessels. An obvious detachment of retina and an increased thickness of the choroid were found on OCT, which was most obvious 2 weeks after the adrenalin administration (P<0.01). ERG revealed no obvious decline of the b-wave amplitude before and after the adrenalin administration (P>0.05). A circumscribed retinal detachment, the depigmentation of retinal pigment epithelium and enlarged choroidal vessels were shown by the histological examination. Conclusion:The temporal topography of the chorioretinopathy in the Chinchilla rabbits by intravenous injection of adrenaline somewhat mimicked that of the human CSC, which could enhance its application in the exploration for the pathogenesis and the therapeutic measures for human CSC.

BACKGROUND: Modafinil, as a wake-promoting agent, is commonly used to relieve fatigue during military operations. However, there is a lack of clarity regarding the effects of modafinil on the equilibrium and vestibular organs, especially when prescribing this drug to flight crewmembers. The objective of this study was to evaluate the equilibrium- and vestibular-related safety effects of modafinil.METHODS: In a randomized, double-blind, placebo-controlled, crossover study, 10 healthy male volunteers received a single 200-mg oral dose of modafinil or placebo. Equilibrium and vestibular functions were assessed 2 h after oral administration by the sensory organization test (SOT), adaptation test (ADT), and video head impulse test (v-HIT).RESULTS: There was no change in the equilibrium scores of the six SOT conditions or the composite scores between the modafinil and placebo groups. Statistically significant differences were not observed for the sway energy score (SES) in the toe-down test. In the toe-up test, the SES decreased by 16.7% in the modafinil group relative to the placebo group in trial 2, while the differences in other trials were not statistically significant. In the v-HIT, there was no significant difference in the gain of each semicircular canal between the two groups.DISCUSSION: A single 200-mg dose of modafinil did not cause any impairment to vestibular function, equilibrium ability, or adaptive balance response; in fact, modafinil might have a positive effect on adaptation function in healthy volunteers. These findings preliminarily suggest that there is no hidden risk of vestibular dysfunction among aviation employees using modafinil.Liu F, Zhang M, Chen T, Zhai L, Zhang Z, Xue J. Equilibrium and vestibular safety of modafinil in healthy volunteers. Aerosp Med Hum Perform. 2022; 93(6):487-492.

AIM To explore the effects of laser-activated remote phosphors (LARP) on visual function in guinea pigs. METHODS Electroretinogram (ERG) of guinea pigs were observed after LARP irradiation at different frequencies and irradiation times. We evaluated the expression of rhodopsin, β-catenin, connexin36, calretinin, and calbindin in the retina of guinea pigs and measured the density of photoreceptor cells after high-frequency LARP irradiation. RESULTS After LARP irradiation, the ERG results showed that the amplitude of the dark-adapted 3.0 b-wave of the model eye was lower than that of the control eye after high-frequency irradiation (P<0.05). The expression of rhodopsin, β-catenin, connexin36, calretinin, and calbindin in the retina of guinea pig declined. CONCLUSION There is frequency cumulative damage effect on the retina that relates to LARP illumination frequency. This has significance for staff visual protection policies under LARP lighting conditions.