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In addition, the phenotype of pain behaviors induced by oxalate differs significantly from oxaliplatin-induced neuropathy, which is characterized by cold allodynia and a lack of spontaneous nocifensive behavior (Deuis et al., 2013)

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doi: 10.1016/0026-0495(92)90061-E

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R02, was activated by urea, but inhibited by Triton X-100 and SDS, with 50% maximum activity observed at an SDS concentration of 0.5% (w/v)