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Purpose: To describe the subretinal hyporeflective globule in cases of central serous chorioretinopathy (CSC). Methods: A retrospective analysis of consecutive cases of CSC presenting to a tertiary eye care center in eastern India was conducted. Subretinal hyporeflective globules were identified as small globular lesions below the external limiting membrane/ellipsoid zone, but above the RPE layer. They had a hyperreflective border with a hyporeflective core and a clear posterior tail of hyper-transmission. Results: The present study analyzed 137 eyes of 137 patients. Eighty (58.4%) eyes had acute disease at presentation, 48 (35%) eyes had chronic disease, and eight (5.8%) eyes had resolved CSC. Subretinal hyporeflective globules were seen in 27 (21.8%) eyes, of which choroidal caverns were seen in seven (5.1%) eyes. Twenty-five eyes with chronic CSC and only two eyes with acute CSC had subretinal hyporeflective globules. Three eyes with resolved CSC had subretinal hyporeflective globules. Conclusion: We describe subretinal hyporeflective globule as a novel optical coherence tomography (OCT) finding in cases of CSC and describe its clinical correlates. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor‐α (TNF‐α)‐induced keratinocyte inflammation plays a key role in the pathogenesis of multiple inflammatory skin diseases. Here we investigated the anti‐inflammatory effect of S‐allyl cysteine (SAC) on TNF‐α‐induced HaCaT keratinocyte cells and the mechanism behind its anti‐inflammatory potential. SAC was found to inhibit TNF‐α‐stimulated cytokine expression. Further, SAC was found to inhibit TNF‐α‐induced activation of p38, JNK and NF‐κB pathways. Interestingly, SAC was found to differentially regulate ERK MAP kinase in cells. TNF‐α‐induced transient ERK activation and SAC treatment resulted in sustained ERK activation both in the presence and absence of TNF‐α. Additionally, SAC failed to inhibit the TNF‐α‐induced expression of the pro‐inflammatory cytokines TNF‐α and IL‐1β when cells were treated with the MEK inhibitor PD98059, suggesting that the anti‐inflammatory effect of SAC is via sustained activation of the ERK pathway. Since ERK activation has been reported to negatively regulate NF‐κB‐driven gene expression and we find that SAC activates ERK and negatively regulates NF‐κB, we investigated whether there existed any crosstalk between the ERK and the NF‐κB pathways. NF‐κB‐dependent reporter assay, visualization of the nuclear translocation of NF‐κB‐p65 subunit and determination of the cellular levels of I‐κB, the inhibitor of NF‐κB, revealed that SAC inhibited TNF‐α‐induced NF‐κB activation, and PD98059 treatment reversed this effect. These results collectively suggest that SAC inhibits TNF‐α‐induced inflammation in HaCaT cells via a combined effect entailing the inhibition of the p38 and the JNK pathways and NF‐κB pathway via the sustained activation of ERK. [ABSTRACT FROM AUTHOR]