Raymond Hickey

ORCID: 0000-0003-2354-0205
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About
Contact & Profiles
Research Areas
  • Linguistic Variation and Morphology
  • Linguistics, Language Diversity, and Identity
  • Lexicography and Language Studies
  • Linguistics and language evolution
  • Multilingual Education and Policy
  • Phonetics and Phonology Research
  • Syntax, Semantics, Linguistic Variation
  • Gender Studies in Language
  • Language, Discourse, Communication Strategies
  • Virus-based gene therapy research
  • Liver physiology and pathology
  • Historical Linguistics and Language Studies
  • Natural Language Processing Techniques
  • Spanish Linguistics and Language Studies
  • Metabolism and Genetic Disorders
  • Pancreatic function and diabetes
  • CRISPR and Genetic Engineering
  • Viral gastroenteritis research and epidemiology
  • Linguistic research and analysis
  • Xenotransplantation and immune response
  • linguistics and terminology studies
  • Irish and British Studies
  • Swearing, Euphemism, Multilingualism
  • Historical Studies of British Isles
  • Philippine History and Culture

University of Limerick
2023-2024

University of Duisburg-Essen
2011-2024

Mayo Clinic in Arizona
2014-2022

Mayo Clinic
2013-2021

WinnMed
2015-2021

Essen University Hospital
2002-2020

Oregon Health & Science University
2009-2013

Uppsala University
2011

Roslin Institute
2010

University of Edinburgh
2010

Mammals have limited regenerative capacity, whereas some vertebrates, like fish and salamanders, are able to regenerate their organs efficiently. The regeneration in these species depends on cell dedifferentiation followed by proliferation. We generate a mouse model that enables the inducible expression of four Yamanaka factors (Oct-3/4, Sox2, Klf4, c-Myc, or 4F) specifically hepatocytes. Transient vivo 4F induces partial reprogramming adult hepatocytes progenitor state concomitantly...

10.1016/j.celrep.2022.110730 article EN cc-by Cell Reports 2022-04-01

We previously showed that fusion between hepatocytes lacking a crucial liver enzyme, fumarylacetoacetate hydrolase (FAH), and wild-type blood cells resulted in hepatocyte reprogramming. FAH expression was restored hybrid and, upon vivo expansion, ameliorated the effects of deficiency. Here, we show fusion-derived polyploid can undergo ploidy reductions to generate daughter with one-half chromosomal content. Fusion hybrids are, by definition, at least tetraploid. demonstrate reduction diploid...

10.1371/journal.pgen.1000385 article EN cc-by PLoS Genetics 2009-02-19

Hereditary tyrosinemia type I (HT1) results in hepatic failure, cirrhosis, and hepatocellular carcinoma (HCC) early childhood is caused by a deficiency the enzyme fumarylacetoacetate hydrolase (FAH). In novel approach we used chimeric adeno-associated virus DJ serotype (AAV-DJ) homologous recombination to target disrupt porcine Fah gene. AAV-DJ an artificial AAV vector containing hybrid capsid sequences from three naturally occurring serotypes (AAV2, 8, 9). The was deliver knockout construct...

10.1002/hep.24490 article EN Hepatology 2011-06-14

Hereditary tyrosinemia type I (HT1) is caused by deficiency in fumarylacetoacetate hydrolase (FAH), an enzyme that catalyzes the last step of tyrosine metabolism. The most severe form disease presents acutely during infancy, and characterized liver involvement, commonly resulting death if untreated. Generation FAH+/− pigs was previously accomplished adeno-associated virus-mediated gene knockout fibroblasts somatic cell nuclear transfer. Subsequently, these animals were outbred crossed to...

10.1016/j.scr.2014.05.003 article EN cc-by-nc-nd Stem Cell Research 2014-05-14
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