AIM:To detect whether Toxoplasma gondii(T.gondii)infection of mice can induce retinal DNA damage.METHODS:A total of 20 laboratory-bred male Swiss albino mice were used and divided into four groups:control group(non-in...AIM:To detect whether Toxoplasma gondii(T.gondii)infection of mice can induce retinal DNA damage.METHODS:A total of 20 laboratory-bred male Swiss albino mice were used and divided into four groups:control group(non-infected animals);T.gondii infected group;immunosuppressed infected group;and infected group treated with sulfadiazine and pyrimethamine.Mice eyes were collected 6wk post infection and retinas were obtained.Each retina was immediately processed for comet assay and the frequency of tailed nuclei(DNA damage)was calculated.In addition,retinal DNA damage was revealed by various comet assay parameters that were provided by the image analysis software including tail length,percentage of DNA in the tail,percentage of tailed cells and tail moment.RESULTS:The obtained results showed that T.gondii infection induced a statistically significant increase in the frequency of tailed nuclei,tail length,percentage of DNA in the tail,and tail moment in mice retinal cells compared to the control group(which showed some degree of DNA damage).In immunosuppressed infected group,retinal DNA damage was severing and there was significant increase in various comet assay parameters compared to both control and infected groups.After treatment with sulfadiazine and pyrimethamine,retinal DNA damage decreased and all comet assay parameters showed a statistical significant decrease compared to infected groups.CONCLUSION:T.gondii infection can induce DNA damage in mice retinal cells.展开更多
Report a case of a male patient with a macular scar compatible with ocular toxoplasmosis (OT) in right eye (RE) and review the relevant literature on this disease. A patient, who attended for a routine contact lens fo...Report a case of a male patient with a macular scar compatible with ocular toxoplasmosis (OT) in right eye (RE) and review the relevant literature on this disease. A patient, who attended for a routine contact lens follow up, presented with amblyopic exotropia without any ocular disease. Best-corrected visual acuity of the affected eye was 20/40 with constant and mono-fixation exotropia. Ophthalmoscopic assessment revealed a macular scar compatible with OT. OT is the leading cause of infection in the posterior segment. Inactive cases could be asymptomatic and diagnosis requires a complete eye examination, providing a correct diagnosis and patient management.展开更多
Objective:: To investigate retinochoroidal changes and establish eye damage model after brain impact injury. Methods: An eye damage model after brain impact injury was established by striking the frontoparietal zone i...Objective:: To investigate retinochoroidal changes and establish eye damage model after brain impact injury. Methods: An eye damage model after brain impact injury was established by striking the frontoparietal zone in rabbits with BIM-Ⅱ bioimpact machine. Seventeen rabbits were killed at 4 different intervals after injury. The pathological characteristics of the retinal and choroid damages were observed. Results: All the rabbits had severe brain injury with subarachnoid hemorrhage and brain contusion. The eye damage occurred in all of the 17 rabbits. Hemorrhage in optic nerve sheaths was observed and retinal edema and bleeding was discovered with ophthalmoscope. Histopathologic study displayed subarachnoid hemorrhage in the retrobulbar portion of the retinal nerve, general choroid blood vessel dilatation, retinal nerve fibre swelling within 6 hours after injury, and flat retinal detachment with subretinal proteinoid exudation, and degeneration and disappearance of the outer segment of the optic cell over 6 hours after injury. Conclusions: The pathological characteristic of the eye damage at early stage following brain impact injury is local circulation disturbance. At late stage, it features in retinal detachment, and optic cellular degeneration and necrosis.展开更多
文摘AIM:To detect whether Toxoplasma gondii(T.gondii)infection of mice can induce retinal DNA damage.METHODS:A total of 20 laboratory-bred male Swiss albino mice were used and divided into four groups:control group(non-infected animals);T.gondii infected group;immunosuppressed infected group;and infected group treated with sulfadiazine and pyrimethamine.Mice eyes were collected 6wk post infection and retinas were obtained.Each retina was immediately processed for comet assay and the frequency of tailed nuclei(DNA damage)was calculated.In addition,retinal DNA damage was revealed by various comet assay parameters that were provided by the image analysis software including tail length,percentage of DNA in the tail,percentage of tailed cells and tail moment.RESULTS:The obtained results showed that T.gondii infection induced a statistically significant increase in the frequency of tailed nuclei,tail length,percentage of DNA in the tail,and tail moment in mice retinal cells compared to the control group(which showed some degree of DNA damage).In immunosuppressed infected group,retinal DNA damage was severing and there was significant increase in various comet assay parameters compared to both control and infected groups.After treatment with sulfadiazine and pyrimethamine,retinal DNA damage decreased and all comet assay parameters showed a statistical significant decrease compared to infected groups.CONCLUSION:T.gondii infection can induce DNA damage in mice retinal cells.
文摘Report a case of a male patient with a macular scar compatible with ocular toxoplasmosis (OT) in right eye (RE) and review the relevant literature on this disease. A patient, who attended for a routine contact lens follow up, presented with amblyopic exotropia without any ocular disease. Best-corrected visual acuity of the affected eye was 20/40 with constant and mono-fixation exotropia. Ophthalmoscopic assessment revealed a macular scar compatible with OT. OT is the leading cause of infection in the posterior segment. Inactive cases could be asymptomatic and diagnosis requires a complete eye examination, providing a correct diagnosis and patient management.
文摘Objective:: To investigate retinochoroidal changes and establish eye damage model after brain impact injury. Methods: An eye damage model after brain impact injury was established by striking the frontoparietal zone in rabbits with BIM-Ⅱ bioimpact machine. Seventeen rabbits were killed at 4 different intervals after injury. The pathological characteristics of the retinal and choroid damages were observed. Results: All the rabbits had severe brain injury with subarachnoid hemorrhage and brain contusion. The eye damage occurred in all of the 17 rabbits. Hemorrhage in optic nerve sheaths was observed and retinal edema and bleeding was discovered with ophthalmoscope. Histopathologic study displayed subarachnoid hemorrhage in the retrobulbar portion of the retinal nerve, general choroid blood vessel dilatation, retinal nerve fibre swelling within 6 hours after injury, and flat retinal detachment with subretinal proteinoid exudation, and degeneration and disappearance of the outer segment of the optic cell over 6 hours after injury. Conclusions: The pathological characteristic of the eye damage at early stage following brain impact injury is local circulation disturbance. At late stage, it features in retinal detachment, and optic cellular degeneration and necrosis.
