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Emma Levine
Researcher at University of California, San Francisco
Publications - 11
Citations - 268
Emma Levine is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Nociceptor & Hyperalgesia. The author has an hindex of 6, co-authored 7 publications receiving 219 citations. Previous affiliations of Emma Levine include Wolfson Centre for Age-Related Diseases.
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Journal ArticleDOI
Defining the nociceptor transcriptome.
Matthew Thakur,Megan Crow,Natalie Richards,Gareth I. J. Davey,Emma Levine,Jayne H. Kelleher,Chibeza C. Agley,Franziska Denk,Stephen D. R. Harridge,Stephen B. McMahon +9 more
TL;DR: Using genome-wide RNA-sequencing, an unprecedented insight is given into the molecular composition of small nociceptive neurons in the DRG, potentially altering the interpretation of previous studies performed at the tissue level, and indicating a number of novel markers of this widely-studied population of cells.
Journal ArticleDOI
Effect of Sex, Age, and Positivity Threshold on Fecal Immunochemical Test Accuracy: A Systematic Review and Meta-analysis.
Kevin Selby,Kevin Selby,Emma Levine,Cecilia Doan,Anton Gies,Hermann Brenner,Charles P. Quesenberry,Jeffrey K. Lee,Douglas A. Corley +8 more
TL;DR: In a meta-analysis of studies that analyzed detection of CRC and advanced adenomas at different FIT positivity thresholds, the sensitivity and specificity of detection to vary with positive cut-off value is found.
Journal ArticleDOI
Transient decrease in nociceptor GRK2 expression produces long–term enhancement in inflammatory pain
Luiz F. Ferrari,Oliver Bogen,Nicole Alessandri-Haber,Emma Levine,Robert W. Gear,Jon D. Levine +5 more
TL;DR: Rats treated with GRK2 AS-ODN exhibited enhanced and prolonged hyperalgesia induced by direct activation of second messengers, adenyl cyclase, Epac or PKA, suggesting changes downstream of G-protein-coupled receptors.
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Role of a novel nociceptor autocrine mechanism in chronic pain
TL;DR: The hypothesis that the delayed onset, PKCε‐mediated, component of PGE2 hyperalgesia is generated by the active release of a nucleotide from the peripheral terminal of the primed nociceptor and this nucleotide is then metabolized to produce adenosine is tested.
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Mitochondrial dependence of nerve growth factor-induced mechanical hyperalgesia
TL;DR: Inhibition of 3 major mitochondrial functions—oxidation of nutrients, adenosine triphosphate (ATP) production, and generation of reactive oxygen species—markedly attenuated NGF‐induced mechanical hyperalgesia in the rat.