Elvin Irihamye

Elvin Irihamye

Oxford, England, United Kingdom
5K followers 500+ connections

About

Builder & Promoter of Beautiful Technologies in Healthcare- Intuitive, Data-Driven and…

Experience

  • University of Oxford Graphic
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    Oxford, England, United Kingdom

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    South San Francisco, California, United States

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Education

  • University of Oxford Graphic

    University of Oxford

    - Present

    Dissertation: "Navigating the Market Complexities of Commercializing AI- Enabled Digital Health Innovations in LMIC’s"

  • - Present

    Activities and Societies: 2022 Rhodes Scholar (Indiana & Jesus College)

    Thesis: "Scoping Review of the Use of Provider-facing Chatbots for Healthcare Triage, Diagnosis, Treatment & Administrative workflows"

    Modules: Foundations of Digital Health, Harnessing Big Data to Improve Care, Remote Monitoring and Digital Diagnostics, Clinical Informatics for Trials and Health Surveillance, Supporting health behaviour change using digital tools, Digital Transformation of Primary Care, Economics of Digital Health, User focused design and the lifecycle of digital health…

    Thesis: "Scoping Review of the Use of Provider-facing Chatbots for Healthcare Triage, Diagnosis, Treatment & Administrative workflows"

    Modules: Foundations of Digital Health, Harnessing Big Data to Improve Care, Remote Monitoring and Digital Diagnostics, Clinical Informatics for Trials and Health Surveillance, Supporting health behaviour change using digital tools, Digital Transformation of Primary Care, Economics of Digital Health, User focused design and the lifecycle of digital health innovation

  • Areas of Focus: Social Entrepreneurship, Medical Informatics, Computational Neuroscience

Licenses & Certifications

Publications

  • Cisplatin and phenanthriplatin modulate long-noncoding RNA expression in A549 and IMR90 cells revealing regulation of microRNAs, Wnt/β-catenin and TGF-β signaling

    Scientific Reports

    Abstract: The monofunctional platinum(II) complex, phenanthriplatin, acts by blocking transcription, but its regulatory effects on long-noncoding RNAs (lncRNAs) have not been elucidated relative to traditional platinum-based chemotherapeutics, e.g., cisplatin. Here, we treated A549 non-small cell lung cancer and IMR90 lung fibroblast cells for 24 h with either cisplatin, phenanthriplatin or a solvent control, and then performed microarray analysis to identify regulated lncRNAs. RNA22 v2…

    Abstract: The monofunctional platinum(II) complex, phenanthriplatin, acts by blocking transcription, but its regulatory effects on long-noncoding RNAs (lncRNAs) have not been elucidated relative to traditional platinum-based chemotherapeutics, e.g., cisplatin. Here, we treated A549 non-small cell lung cancer and IMR90 lung fibroblast cells for 24 h with either cisplatin, phenanthriplatin or a solvent control, and then performed microarray analysis to identify regulated lncRNAs. RNA22 v2 microRNA software was subsequently used to identify microRNAs (miRNAs) that might be suppressed by the most regulated lncRNAs. We found that miR-25-5p, -30a-3p, -138-5p, -149-3p, -185-5p, -378j, -608, -650, -708-5p, -1253, -1254, -4458, and -4516, were predicted to target the cisplatin upregulated lncRNAs, IMMP2L-1, CBR3-1 and ATAD2B-5, and the phenanthriplatin downregulated lncRNAs, AGO2-1, COX7A1-2 and SLC26A3-1. Then, we used qRT-PCR to measure the expression of miR-25-5p, -378j, -4516 (A549) and miR-149-3p, -608, and -4458 (IMR90) to identify distinct signaling effects associated with cisplatin and phenanthriplatin. The signaling pathways associated with these miRNAs suggests that phenanthriplatin may modulate Wnt/β-catenin and TGF-β signaling through the MAPK/ERK and PTEN/AKT pathways differently than cisplatin. Further, as some of these miRNAs may be subject to dissimilar lncRNA targeting in A549 and IMR90 cells, the monofunctional complex may not cause toxicity in normal lung compared to cancer cells by acting through distinct lncRNA and miRNA networks.

    Other authors
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  • RNA-Seq Analysis of Cisplatin and The Monofunctional Platinum(II) Complex, Phenanthriplatin, in A549 Non-Small Cell Lung Cancer and IMR90 Lung Fibroblast Cell Lines

    Cells

    Abstract: Phenanthriplatin is a new monofunctional platinum(II) complex that binds only one strand of DNA and acts by blocking gene transcription, but its effect on gene regulation has not been characterized relative to the traditional platinum-based complex, cisplatin. A549 non-small cell lung cancer and IMR90 lung fibroblast cells were treated with cisplatin, phenanthriplatin, or a control and then their RNA transcripts were subjected to next generation sequencing analysis. DESeq2 and…

    Abstract: Phenanthriplatin is a new monofunctional platinum(II) complex that binds only one strand of DNA and acts by blocking gene transcription, but its effect on gene regulation has not been characterized relative to the traditional platinum-based complex, cisplatin. A549 non-small cell lung cancer and IMR90 lung fibroblast cells were treated with cisplatin, phenanthriplatin, or a control and then their RNA transcripts were subjected to next generation sequencing analysis. DESeq2 and CuffDiff2 were used to identify up- and downregulated genes and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases were used to identify pathways and functions. We found that phenanthriplatin may regulate the genes GPRC5a, TFF1, and TNFRSF10D, which act through p53 to control apoptosis, differently or to a greater extent than cisplatin, and that it, unlike cisplatin, could upregulate ATP5MD, a gene which signals through the Wnt/β catenin pathway. Furthermore, phenanthriplatin caused unique or enhanced effects compared to cisplatin on genes regulating the cytoskeleton, cell migration, and proliferation, e.g., AGAP1, DIAPH2, GDF15, and THSD1 (p < 0.05; q < 0.05). Phenanthriplatin may modulate some oncogenes differently than cisplatin potentially leading to improved clinical outcome, but this monofunctional complex should be carefully matched with cancer gene data to be successfully applied in chemotherapy.

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  • Effects of L-Serine Against Cisplatin-Mediated Reactive Oxygen Species Generation in Zebrafish Vestibular Tissue Culture and HEI-OC1 Auditory Hybridoma Cells

    Neurotoxicity Research

    Abstract: Cisplatin is a platinum-based chemotherapy compound effective against a variety of cancers. However, it can cause increased reactive oxygen species (ROS) production in auditory and vestibular tissue leading to permanent hearing and balance loss. The amino acid, L-serine, has been shown to reduce ROS in some tissue types. In this project, we first investigated whether L-serine could reduce cisplatin-mediated ROS generation in zebrafish utricular tissue culture using spectrophotometry…

    Abstract: Cisplatin is a platinum-based chemotherapy compound effective against a variety of cancers. However, it can cause increased reactive oxygen species (ROS) production in auditory and vestibular tissue leading to permanent hearing and balance loss. The amino acid, L-serine, has been shown to reduce ROS in some tissue types. In this project, we first investigated whether L-serine could reduce cisplatin-mediated ROS generation in zebrafish utricular tissue culture using spectrophotometry and the fluorescent ROS detector dye, H2DCFDA. Then, we examined whether L-serine could prevent the effect of cisplatin against cellular viability in the mouse auditory hybridoma cell line, HEI-OC1, using the spectrophotometric (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay. As a final step, we used H2DCFDA dye and flow cytometry analysis to determine if L-serine could counteract the effect of cisplatin on ROS production in this cell line. We found that cisplatin and L-serine treatment may influence ROS production in utricular tissue. Further, although L-serine did not counteract the effect of cisplatin against HEI-OC1 cellular viability, the amino acid did prevent the platinum compound’s effect to increase ROS in these cells. These results suggest that L-serine may act in auditory and vestibular tissues as an effective protectant against cisplatin-mediated toxicity.

    Other authors
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Honors & Awards

  • Wells Scholar

    Indiana University - Bloomington

    Named in honor of Herman B Wells, Indiana University’s beloved 11th president, the Wells Scholars Program guarantees the full cost of attendance for four years of undergraduate study on IU’s Bloomington campus.

  • 1st Place Finish Research Oral Presentation

    Western Kentucky University

    First place Oral Presentation finish at the Western Kentucky University Student Research Conference for “Analyzing the efficiency of reforestation efforts in a Costa Rican Cloudforest in regaining Carbon Storage"

  • State of Kentucky Citation of Achievement

    Kentucky House of Representatives

    Awarded by the State of Kentucky House of Representatives and State Representative Patti Minter for research achievement at the 2019 Poster-at-the-Capitol event.

  • Gatton Academy Research Internship Grant ($3,300)

    The Gatton Academy of Mathematics and Science

    Competitive research grant to support summer undergraduate research

  • WKU FUSE Research Grant

    Western Kentucky University

    Competitive research grant to support WKU Faculty-mentored undergraduate research

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