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Hisashi Shirakawa

Researcher at Kyoto University

Publications -  97
Citations -  2306

Hisashi Shirakawa is an academic researcher from Kyoto University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 26, co-authored 78 publications receiving 1933 citations.

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Acute cold hypersensitivity characteristically induced by oxaliplatin is caused by the enhanced responsiveness of TRPA1 in mice

TL;DR: It is suggested that a brief treatment with oxaliplatin or its metabolite oxalate is sufficient to enhance the responsiveness of TRPA1 but not that of TRPM8 and TRPV1 expressed by DRG neurons, which may contribute to the characteristic acute peripheral neuropathy induced by oxali Platin.
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TRPM2 Contributes to Inflammatory and Neuropathic Pain through the Aggravation of Pronociceptive Inflammatory Responses in Mice.

TL;DR: The results of the present study suggest that TRPM2 expressed in macrophages and microglia aggravates peripheral and spinal pronociceptive inflammatory responses and contributes to the pathogenesis of inflammatory and neuropathic pain.
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Endogenous d-Serine Is Involved in Induction of Neuronal Death by N-Methyl-d-aspartate and Simulated Ischemia in Rat Cerebrocortical Slices

TL;DR: Exogenous supply of d-serine as a glycine site agonist is important for neuronal injury involving NMDA receptor overactivation in the cerebral cortex, using rat brain slices maintained in a defined salt solution.
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Activation of mitochondrial transient receptor potential vanilloid 1 channel contributes to microglial migration.

TL;DR: The role of TRP vanilloid 1 (TRPV1), a channel opened by capsaicin, heat, protons, and endovanilloids, in microglia is explored and it is indicated that mitochondrial TRPV 1 plays an important role in inducing microglial migration.
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Transient Receptor Potential Canonical 3 (TRPC3) Mediates Thrombin-Induced Astrocyte Activation and Upregulates Its Own Expression in Cortical Astrocytes

TL;DR: Thrombin dynamically upregulates TR PC3 and that TRPC3 contributes to the pathological activation of astrocytes in part through a feedforward upregulation of its own expression are suggested.