We reported an 8-year-old boy with panscleritis in left eye and right epididymitis after falling on the ground.Etiologic diagnosis played a key role in this case.Systemic examinations ruled out systemic autoimmune dis...We reported an 8-year-old boy with panscleritis in left eye and right epididymitis after falling on the ground.Etiologic diagnosis played a key role in this case.Systemic examinations ruled out systemic autoimmune diseases,tumors,and infections as the cause of scleritis and suggested that the disease was caused by a local delayedtype hypersensitivity(DTH)induced by ocular trauma and was non-infectious.Still,the right epididymitis was infectious.Both conditions were treated successfully using steroids and antibiotics,respectively.Thus,early etiologic diagnosis and reasonable treatment are crucial to prevent visual loss.展开更多
Retinal injury after blunt ocular trauma may directly affect prognosis and lead to vision loss.To investigate the pathological changes and molecular mechanisms involved in retinal injury after blunt ocular trauma,we e...Retinal injury after blunt ocular trauma may directly affect prognosis and lead to vision loss.To investigate the pathological changes and molecular mechanisms involved in retinal injury after blunt ocular trauma,we established a weight drop injury model of blunt ocular trauma in male Beagle dogs.Hematoxylin-eosin staining,immunofluorescence staining,western blotting,and TUNEL assays were performed to investigate retinal injury within 14 days after blunt ocular trauma.Compared with the control group,the thicknesses of the inner and outer nuclear layers,as well as the number of retinal ganglion cells,gradually decreased within 14 days after injury.The number of bipolar cells in the inner nuclear layer began to decrease 1 day after injury,while the numbers of cholinergic and amacrine cells in the inner nuclear layer did not decrease until 7 days after injury.Moreover,retinal cell necroptosis increased with time after injury;it progressed from the ganglion cell layer to the outer nuclear layer.Visual electrophysiological findings indicated that visual impairment began on the first day after injury and worsened over time.Additionally,blunt ocular trauma induced nerve regeneration and Müller glial hyperplasia;it also resulted in the recruitment of microglia to the retina and polarization of those microglia to the M1 phenotype.These findings suggest that necroptosis plays an important role in exacerbating retinal injury after blunt ocular trauma via gliosis and neuroinflammation.Such a role has important implications for the development of therapeutic strategies.展开更多
Dear Editor,We are writing to present a case report of central retinal artery occlusion（CRAO）and traumatic optic neuropathy（TON）with immediate visual loss caused by blunt facial trauma with a soccer ball.CRAO is a...Dear Editor,We are writing to present a case report of central retinal artery occlusion（CRAO）and traumatic optic neuropathy（TON）with immediate visual loss caused by blunt facial trauma with a soccer ball.CRAO is an ophthalmic emergency with an estimated incidence of 10 in 1 million.展开更多
基金Supported by Beijing Natural Science Foundation(7202229).
文摘We reported an 8-year-old boy with panscleritis in left eye and right epididymitis after falling on the ground.Etiologic diagnosis played a key role in this case.Systemic examinations ruled out systemic autoimmune diseases,tumors,and infections as the cause of scleritis and suggested that the disease was caused by a local delayedtype hypersensitivity(DTH)induced by ocular trauma and was non-infectious.Still,the right epididymitis was infectious.Both conditions were treated successfully using steroids and antibiotics,respectively.Thus,early etiologic diagnosis and reasonable treatment are crucial to prevent visual loss.
基金supported by the National Natural Science Foundation of China,No.81600738the Youth Development Project of Air Force Medical University,No.21QNPY072(both to FF)。
文摘Retinal injury after blunt ocular trauma may directly affect prognosis and lead to vision loss.To investigate the pathological changes and molecular mechanisms involved in retinal injury after blunt ocular trauma,we established a weight drop injury model of blunt ocular trauma in male Beagle dogs.Hematoxylin-eosin staining,immunofluorescence staining,western blotting,and TUNEL assays were performed to investigate retinal injury within 14 days after blunt ocular trauma.Compared with the control group,the thicknesses of the inner and outer nuclear layers,as well as the number of retinal ganglion cells,gradually decreased within 14 days after injury.The number of bipolar cells in the inner nuclear layer began to decrease 1 day after injury,while the numbers of cholinergic and amacrine cells in the inner nuclear layer did not decrease until 7 days after injury.Moreover,retinal cell necroptosis increased with time after injury;it progressed from the ganglion cell layer to the outer nuclear layer.Visual electrophysiological findings indicated that visual impairment began on the first day after injury and worsened over time.Additionally,blunt ocular trauma induced nerve regeneration and Müller glial hyperplasia;it also resulted in the recruitment of microglia to the retina and polarization of those microglia to the M1 phenotype.These findings suggest that necroptosis plays an important role in exacerbating retinal injury after blunt ocular trauma via gliosis and neuroinflammation.Such a role has important implications for the development of therapeutic strategies.
文摘Dear Editor,We are writing to present a case report of central retinal artery occlusion（CRAO）and traumatic optic neuropathy（TON）with immediate visual loss caused by blunt facial trauma with a soccer ball.CRAO is an ophthalmic emergency with an estimated incidence of 10 in 1 million.
