Retinitis pigmentosa (RP) is a kind of inherited retinal degenerative diseases characterized by the progressive loss of photoreceptors. RP has been a conundrum without satisfactory countermeasures in clinic until now. Acetaldehyde dehydrogenase 2 (ALDH2), a major enzyme involved in aldehyde detoxification, has been demonstrated to be beneficial for a growing number of human diseases, such as cardiovascular dysfunction, diabetes mellitus and neurodegeneration. However, its protective effect against RP remains unknown. Our study explored the impact of ALDH2 on retinal function and structure in N-methyl-N-nitrosourea (MNU)-induced RP rats. Rats were gavaged with 5 mg/kg Alda-1, an ALDH2 agonist, 5 days before and 3 days after MNU administration. Assessments of retinal function and morphology as well as measurement of specific proteins expression level were conducted. Electroretinogram recordings showed that Alda-1 administration alleviated the decrease in amplitude caused by MNU, rendering protection of retinal function. Mitigation of photoreceptor degeneration in MNU-treated retinas was observed by optical coherence tomography and retinal histological examination. In addition, Western blotting results revealed that ALDH2 protein expression level was upregulatedwith increased expression of SIRT1 protein after the Alda-1 intervention. Besides, endoplasmic reticulum stress (ERS) was reduced according to the significant downregulation of GRP78 protein, while apoptosis was ameliorated as shown by the decreased expression of PARP1 protein. Together, our data demonstrated that ALDH2 could provide preservation of retinal function and morphology against MNU-induced RP, with the underlying mechanism at least partly related to the modulation of SIRT1, ERS and apoptosis.

Rationale: Ischemic optic neuropathy (ION), due to diseases of the arteries supplying the optic nerve, is an ischemic damage of the optic nerve. This report highlights a case with monocular decreasing visual acuity caused by dissection of the internal carotid artery (ICA), which is a relatively rare cause for ION. Patient concerns: A 44-year-old woman presented with a decreasing visual acuity and defected visual field in the right eye for 1 week. The best corrected visual acuity (BCVA) was 20/400 in the right eye, and 20/20 in the left eye. In the right eye, the pupil showed little reaction to light with a relative afferent pupillary defect. The visual field test disclosed a defect in the inferior field connecting to the blind spot. Electroretinogram recording showed no obviously declined retinal function. No recognizable waveforms were presented in pattern visual–evoked potential (PVEP) examination, whereas the flash visual–evoked potential result revealed a delayed peak time and a reduced amplitude of P2-wave. Diagnosis: The patient was diagnosed as ION with the aid of computed tomographic angiography of the brain and neck, which revealed a stenosis in the right ICA and an occlusion in the right cerebral middle artery. The stenosis was verified as dissection of the ICA by digital subtraction angiography. Interventions: Based on the clinical findings, stent implantation inside the right ICA was performed. Outcomes: The ICA was recanalized soon and the BCVA of the right eye was improved to be 20/25 five months later. A second PVEP examination revealed a recognizable waveform in the right eye, although the peak time and amplitude of the P100-wave was a bit abnormal compared to that of the left eye. Lessons: ION with the sign of decreasing monocular visual acuity could occur due to dissection of the ICA, with no obvious neurologic symptom at the beginning. The present case emphasizes the importance of suspicion of ICA problems as the underlying cause for ION, which could help to take in-time measure to save the vision and avoid further complications.

Upregulation of Sirtuin Type 1 (SIRT1), a nicotinamide adeninedinucleotide (NAD⁺)-dependent deacetylase, has been proved to protect against ample ocular diseases, while its effect on retinitis pigmentosa (RP) has not been illustrated. The study was aimed to explore the impacts of resveratrol (RSV), a SIRT1 activator, on the photoreceptor degeneration in a rat model of RP induced by N-methyl-N-nitrosourea (MNU), an alkylation. The rats were induced RP phenotypes via the intraperitoneal injection of MNU. The electroretinogram was conducted and revealed that RSV could not prevent the decline of retinal function in the RP rats. The optical coherence tomography (OCT) and the retinal histological examination were performed and showed that the reduced thickness of the outer nuclear layer (ONL) was not preserved by RSV intervention. The immunostaining technique was applied. Afther the MNU administration, the number of the apoptotic photoreceptors in the ONL throughout the retinasand the number of microglia cells present among the outer part throughout the retinas were not significantly reduced by RSV. Western blotting was also performed. The data showed that the level of SIRT1 protein was decreased after MNU administration, while RSV was not able to obviously alleviate the downregulation. Our data together indicated that RSV was not able to rescue the photoreceptor degeneration in the MNU-induced RP rats, which might be due to the MNU-induced consumption of the NAD⁺.

To investigate the prevalence and influencing factors of Demodex folliculorum (DF) in the eyelashes of healthy young males. An epidemiological cross-sectional prevalence study was conducted. We conducted visual acuity, eye-related examination, eyelash microscopic examination and DF count of recruits in Fujian Province in 2019. The presence of DF was analyzed according to age, keratorefractive surgery, annual household income, educational level, long-term residence, sleep time, time of using electronic products, smoking and drinking habit. A total of 2253 healthy young males (aged 17–24 years) were studied for the presence of DF within eyelash follicles. The total prevalence of DF was 20.73% in our study. Subjects with history of keratorefractive surgery had a statistically significant increase in the prevalence of DF (P < 0.001). The prevalence of DF was higher in subjects with ocular symptoms than in those without symptoms (P < 0.05). Factors such as the educational level and so on we analyzed had no significant correlation with the prevalence of DF (all P > 0.05). According to the multivariate logistic regression analysis, the history of keratorefractive surgery was the risk factors of DF infection (P < 0.001), and the risk of infection was 1.437 times higher in the population with the history of keratorefractive surgery than in the population without. There was no correlation between ocular discomfort and DF infection (P > 0.05). The prevalence of DF in eyelash follicles in healthy young males was relatively high. The history of keratorefractive surgery was an important risk factor for the infection.

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.

This report describes a patient who had acute lymphocytic leukemia with exudative retinal detachment (RD), which mimicked Vogt–Koyanagi–Harada disease (VKH). A 61-year-old woman presented with painless loss of vision in the left eye. Fundus examination revealed RD in her left eye. B-scan ultrasonography confirmed localized RD and choroidal thickening. Fundus fluorescein angiography revealed stippled pinpoint hyperfluorescence in the upper macula. One week later, reduced visual acuity was noted in the right eye. B-scan ultrasonography and optical coherence tomography revealed serous RD in both eyes. A provisional diagnosis of VKH was made. However, subsequent hematologic analysis detected an extremely high leukocyte count. Elevated numbers of leukocytes and tumor cells were found in cerebrospinal fluid. Bone marrow biopsy revealed 77% primary atypical blood cells, 89% of which were immature lymphocytes. The patient was subsequently diagnosed with acute lymphocytic leukemia and transferred to the Department of Hematology. However, the patient and her family refused chemotherapy; she eventually died. Our findings suggest that exudative RD, similar to VKH, could be a sign of leukemia. Pinpoint hyperfluorescence leakage is important for differential diagnosis, particularly with respect to VKH.