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Objective: To investigate the mechanisms of ocular injuries in astronauts due to gravity deficit by examining changes in retinal microcirculation and visual electrophysiology in macaques subjected to simulated weightlessness. Methods: The head-down recumbency of macaques was used to simulate the movement of blood to the side of the head that occurs without microgravity. Head-down recumbency was performed with the head tilted downwards at a recommended angle of 10°. The macaques in the control group were similarly tethered to the rope but could be held in a normal position. The whole experiment lasted for 6 weeks and retinal microcirculation and visual electrophysiology information was collected at weeks 0, 3 and 6. Results: The retinal microcirculation of macaques was affected by 3 weeks of weightlessness. This includes morphological changes, such as dilation and tortuosity of the retinal microvasculature in macaques at day 21. OCT and OCTA results showed an increase in retinal and choroidal thickness and a significant decrease in vessel length density within 6×6 mm of the macula. Sustained simulated weightlessness (42 days) significantly exacerbated retina-related damage. This was evidenced by a significant decrease in the perfusion density of microcirculatory vessels, such as the macular 3×3 mm mesial vessels and the macular 6*6 mm central and medial vessels. The FAZ density in the macula 3×3 mm area began to increase. Retinal oxygen saturation testing showed a slight increase in arterial oxygen saturation. Simultaneous changes in visual electrophysiology occurred, including a significant decrease in a- and b-wave amplitudes on the dark-vision electroretinogram and a significant decrease in the amplitude of the bright-vision negative wave response. The peak timing of the flash visual evoked potential component P1 was significantly delayed compared to its baseline and time-matched control. Conclusions: Sustained simulated weightlessness (42 days) significantly exacerbated retina-related damage, with both reduced macular blood supply and increased FAZ density suggesting the development of retinal ischemic changes, which disrupt visual electrophysiology. Retinal damage in human astronauts under long-term outer space conditions may be prevented by intervening in ischemic changes in the retina during the early stages of weightlessness.
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BACKGROUND: Congenital anomalies of the pupil are quite varied, including abnormal size, shape, color, response to stimulus, and function. We are here reporting an unusual case presented with the absence of pupillary opening with folds of iris tissue at the center. Only an extremely small pupil (diameter < 0.5 mm) could be observed during the operation. CASE PRESENTATION: A 15-year-old male patient visited our outpatient clinic due to vision difficulty in his right eye for more than ten years. The best-corrected visual acuity was 2.0 logMAR and 0 logMAR for the right and left eye, respectively. There were amblyopia, astigmatism and constant exotropia in his right eye. Ophthalmic examination of the right eye showed flat iris root, minimal iris pigmentation, and the pupil area was entirely covered by iris tissue. Lens status and fundus evaluation could not be commented. The left eye was found to be within normal limit. Based on ophthalmic examination, the admission diagnosis was given as acorea. Pupilloplasty was performed on the right eye due to the situation that the iris tissue blocked the visual axis, which led to visual impairment and stimulus deprivation amblyopia. However, an extremely small pupil at the center of his pupillary area was observed during the operation. The postoperative course was favorable, and a normal pupil was secured. Hospital discharge diagnosis was given as microcoria, and amblyopia treatment was followed. CONCLUSIONS: We report a rare case of congenital pupillary abnormality. The further diagnosis was given as microcoria, which should be differentiated from acorea. For this kind of pupil disorder which blocks the visual axis, early diagnosis and treatment can help prevent the development of stimulus deprivation amblyopia.