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  1. Fulltext Effect of surgical intraocular pressure lowering on retinal structures - nerve fibre layer, foveal avascular zone, peripapillary and macular vessel density: 1 year results
    Ch'ng TW, Gillmann K, Hoskens K, Rao HL, Mermoud A, Mansouri K
    Eye (Lond), 2020 03;34(3):562-571.
    PMID: 31409906 DOI: 10.1038/s41433-019-0560-6
    OBJECTIVES: To determine the effect of surgical intraocular pressure (IOP) lowering on peripapillary retinal nerve fibre layer thickness (RNFL), fovea avascular zone (FAZ), peripapillary and macular vessel density (VD) in glaucoma using with optical coherence tomography angiography (OCT-A).

    METHODS: This was a prospective observational study performed at the Glaucoma Research Centre, Montchoisi Clinic, Lausanne. In total 40 eyes with open-angle glaucoma were included. OCT-A scans were performed before glaucoma surgery, and at 1-month, 3-month, 6-month, and 12-month post-operatively. AngioVue AngioAnalytic (Optovue Inc, Fremont, CA) software was used to analyse the RNFL, FAZ, peripapillary and macular VD. Changes were analysed using analysis of variance (ANOVA) models.

    RESULTS: Mean IOP dropped from 19.4 (±7.0) mmHg pre-surgery and stabilized at 13.0 (±3.1) mmHg at 12 months (p 

  2. Fulltext JAK-STAT and G-protein-coupled receptor signaling pathways are frequently altered in epitheliotropic intestinal T-cell lymphoma
    Nairismägi ML, Tan J, Lim JQ, Nagarajan S, Ng CC, Rajasegaran V, et al.
    Leukemia, 2016 06;30(6):1311-9.
    PMID: 26854024 DOI: 10.1038/leu.2016.13
    Epitheliotropic intestinal T-cell lymphoma (EITL, also known as type II enteropathy-associated T-cell lymphoma) is an aggressive intestinal disease with poor prognosis and its molecular alterations have not been comprehensively characterized. We aimed to identify actionable easy-to-screen alterations that would allow better diagnostics and/or treatment of this deadly disease. By performing whole-exome sequencing of four EITL tumor-normal pairs, followed by amplicon deep sequencing of 42 tumor samples, frequent alterations of the JAK-STAT and G-protein-coupled receptor (GPCR) signaling pathways were discovered in a large portion of samples. Specifically, STAT5B was mutated in a remarkable 63% of cases, JAK3 in 35% and GNAI2 in 24%, with the majority occurring at known activating hotspots in key functional domains. Moreover, STAT5B locus carried copy-neutral loss of heterozygosity resulting in the duplication of the mutant copy, suggesting the importance of mutant STAT5B dosage for the development of EITL. Dysregulation of the JAK-STAT and GPCR pathways was also supported by gene expression profiling and further verified in patient tumor samples. In vitro overexpression of GNAI2 mutants led to the upregulation of pERK1/2, a member of MEK-ERK pathway. Notably, inhibitors of both JAK-STAT and MEK-ERK pathways effectively reduced viability of patient-derived primary EITL cells, indicating potential therapeutic strategies for this neoplasm with no effective treatment currently available.
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