Bilateral retinal nerve fiber layer thickness reduction in a 9-year-old myopic boy suffering from unilateral optic neuritis:A case report

BACKGROUND In this paper,we present a 9-year-old boy who demonstrates a complex interplay between myopia progression,axial length(AL)extension,and retinal nerve fiber layer(RNFL)thickness loss in both eyes.Additionally,concurrent optic neuritis has directly impacted RNFL thickness in his right eye,and its potential indirect influence on RNFL and macular ganglion cell layer(mGCL)thickness in his left eye is also noteworthy.CASE SUMMARY A 9-year-old boy with bilateral myopia presented with diminished vision and pain in his right eye due to optic neuritis,while his left eye showed pseudopapilledema.Steroid therapy improved his vision in the right eye,and 16-mo follow-up revealed recovery without recurrence despite myopia progression.Follow-up optical coherence tomography conducted 16 mo later revealed a notable thinning of the RNFL in both eyes,especially along with a reduction in mGCL thickness in the left eye.This intricate interaction between optic neuritis,myopia,and retinal changes underscores the need for comprehensive management,highlighting potential long-term visual implications in young patients.CONCLUSION The progression of myopia and AL extension led to the loss of RNFL thickness in both eyes in a 9-year-old boy.Concurrently,optic neuritis directly affected RNFL thickness in his right eye and may indirectly play a role in the thickness of RNFL and mGCL in his left eye.

TIMP-1 Production in Human Retinal Pigment Epithelial Cells after Laser Exposure

Purpose: To investigate changes in the production of tissue inhibitor of metalloproteinase type 1 (TIMP-1) by human retinal pigment epithelial (RPE) cells following argon laser exposure.Methods: Human cultured ARPE19 cells were exposed to argon green laser at four different energy levels ranging from 60mW to 360mW. After laser exposure, the culture media were sampled at 0, 24, 72 and 144 hours for TIMP-1 concentration produced by the RPE cells. The levels of TIMP-1 in the cells treated with different laser energy levels were compared with a control group not exposed to laser application.Immunocytochemistry for proliferating cell nuclear antigen (PCNA) was performed to detect any adverse effects on the RPE cells caused by laser exposure.Results: Immediately after laser exposure, the concentration of TIMP- 1 was not detectable. At 24 hours after laser exposure, the concentration of TIMP-1 increased significantly in RPE cells treated with 120mW and 240mW at 24 hours (P=0.006 and P=0.001respectively) compared with control cells. At 72 hours after treatment, RPE cells treated at 120mW, 240mW and 360mW demonstrated significantly increase in TIMP-1production compared with control (P=0.003, P ＜ 0.001 and P ＜ 0.001, respectively).No significant reduction in cell viability was observed following laser application as detected by PCNA expression.Conclusions: Our results demonstrated that early TIMP-1 production by RPE cells in cell cultures was enhanced following laser exposure.

Genome-wide analysis identified 17 new loci influencing intraocular pressure in Chinese population

Intraocular pressure(IOP) is a major risk factor for glaucoma. Genetic determinants of intraocular pressure can provide critical insights into the genetic architecture of glaucoma and, as a result, open new avenues for therapeutic intervention. We performed a genome-wide association study and replication analysis of 8,552 Chinese participants. In the genome-wide association study, we identified 51 loci that surpassed the significance of P<9×10^(-7), and we formally replicated these loci. A combined discovery and replication meta-analysis identified 21 genome-wide loci that surpassed the genome-wide significance of P<5×10^(-8), including 4 previously reported loci: rs145063132(7 p21.2, ETV1/DGKB), rs548030386(7 q31.2, ST7 near CAV1/CAV2), rs7047871(9 p24.2, GLIS3), and rs2472494(9 q31.1, ABCA1/SLC44 A1). Of the 17 newly identified loci, five were reported to have ocular related phenotypes: PTCH2(rs7525308 in 1 p34.1), LRIF1/DRAM2(rs1282146 in 1 p13.3), COLEC11(rs201143466 in 2 p25.3),SPTBN1(rs4514918 in 2 p16.2), and CRK(rs11078446 in 17 p13.3). The genetic loci identified in this study not only increase our understanding of the genes involved in intraocular pressure but also provide important genetic markers to improve future genetic screening and drug discovery for intraocular pressure disorders.

Glial cells and glaucomatous neuropathy

Glaucomatous optic neuropathy is characterized by progressive loss of retinal ganglion cells associated with visual functional deficits. As the ganglion cells die in glaucoma, there is a progressive thinning of the nerve fibre layer （NFL）.l The underlying pathophysiological mechanisms, however, remain unclear. Many mechanisms are involved in the initiation and process of irreversible ganglionic cell death in glaucoma. These include reduced axoplasmic transport, accumulation of toxic levels of neurotransmitter, increased nitric oxide and endothelin syntheses, and remodelling of the extracellular matrix, among others.