Myopia is a substantial global public health concern primarily linked to the elongation of the axial length of the eyeball. While numerous animal models have been employed to investigate myopia, the specific contributions of genetic factors and the intricate signaling pathways involved remain incompletely understood. In this study, we conducted RNA-seq analysis to explore genes and pathways in two distinct myopia-inducing mouse models: form-deprivation myopia (FDM) and lens-induced myopia (LIM). Comparative analysis with a control group revealed significant differential expression of 2362 genes in FDM and 503 genes in LIM. Gene Set Enrichment Analysis (GSEA) identified a common immune-associated pathway between LIM and FDM, with LIM exhibiting more extensive interactions. Notably, downregulation was observed in OxPhos complex III of FDM and complex IV of LIM. Subunit A of complex I was downregulated in LIM but upregulated in FDM. Additionally, complex V was upregulated in LIM but downregulated in FDM. These findings suggest a connection between alterations in energy metabolism and immune cell activation, shedding light on a novel avenue for understanding myopia’s pathophysiology. Our research underscores the necessity for a comprehensive approach to comprehending myopia development, which integrates insights from energy metabolism, oxidative stress, and immune response pathways.

Hyun S, et al. Ann Surg Treat Res. 2023 Jan;104(1):34-42. https://doi.org/10.4174/astr.2023.104.1.34

Background: Effusion-based lymphoma (EBL) is a rare and aggressive large B-cell lymphoma. It presents as a body cavity effusion without a solid mass, lacks HHV-8 association, and typically expresses CD20. Objectives: To better understand the biology of this entity, we performed transcriptomic profiling of eight EBL cases. Methods: We analyzed the cases with the NanoString PanCancer Immune Profiling Panel and compared the results with publicly available datasets representing follicular lymphoma (FL), mantle cell lymphoma (MCL), and large B-cell lymphoma (LBCL) subtypes. Results: Unsupervised clustering and differential expression analysis revealed that EBL cases cluster transcriptionally with the LBCL group. Lymphoma-specific signaling pathway enrichment (SignatureDB) predominantly identified non-germinal center (activated B-cell-type) pathways. In addition, KEGG pathway analyses revealed enrichment in specific inflammatory and immune response pathways that are associated with B-cell lymphoma development in the setting of chronic inflammation, including those linked to Toll-like receptor and NF-κB signaling. Conclusions: These findings support a post-germinal center origin for EBL, which arises in a background of chronic inflammation and persistent antigen stimulation.

ABO-incompatible living donor liver transplantation (ABO-I LDLT) is limited by the risk of antibody-mediated rejection (AMR) from preformed anti-A/B antibodies. Conventional desensitization with therapeutic plasma exchange (TPE) and rituximab (RTX) has procedural and logistical drawbacks. We conducted a retrospective analysis of patients who underwent ABO-I LDLT at our center between January 2022 and December 2023. All were managed with eculizumab (ECU) at a dose of 900 mg IV on preoperative day - 1 and again within two weeks, without preoperative TPE or RTX. Median recipient age was 49.5 years (MELD 14). All achieved prompt graft function. No biopsy-proven AMR was identified in the patients in whom biopsy was performed. Complement activity normalized by POD 30 in all cases. At a mean follow-up of 17 months, three patients had stable graft function; one died at one year from a cerebrovascular event unrelated to rejection. ECU-based complement inhibition may offer a simplified, potentially AMR-reducing approach in ABO-I LDLT; these findings are preliminary and hypothesis-generating, requiring validation in larger studies.