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Masahiro Kondo

Researcher at Nihon University

Publications -  53
Citations -  2515

Masahiro Kondo is an academic researcher from Nihon University. The author has contributed to research in topics: Trigeminal ganglion & Nociception. The author has an hindex of 22, co-authored 48 publications receiving 2294 citations. Previous affiliations of Masahiro Kondo include Harvard University.

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Extensive Diversity of Ig-Superfamily Proteins in the Immune System of Insects

TL;DR: Evidence is presented that Drosophila immune-competent cells have the potential to express more than 18,000 isoforms of the immunoglobulin-superfamily receptor Down syndrome cell adhesion molecule (Dscam), and the molecular diversity of Dscam transcripts generated through a mechanism of alternative splicing is highly conserved across major insect orders, suggesting an unsuspected molecular complexity of the innate immune system of insects.
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Homophilic Dscam Interactions Control Complex Dendrite Morphogenesis

TL;DR: Overexpression of the same Dscam isoforms in two da neurons with overlapping dendritic fields forced a spatial segregation of the two fields, supporting the model that d endritic branches of da neurons use isoform-specific homophilic interactions to ensure minimal overlap.
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The Molecular Diversity of Dscam Is Functionally Required for Neuronal Wiring Specificity in Drosophila

TL;DR: The role of Dscam in neuron-target recognition of single mechanosensory neurons, which connect with different target cells through multiple axonal branches, is examined and a very large number of structurally unique receptor isoforms is required to ensure fidelity and precision of neuronal connectivity.
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Astroglia in medullary dorsal horn (trigeminal spinal subnucleus caudalis) are involved in trigeminal neuropathic pain mechanisms.

TL;DR: Findings provide the first documentation that astroglia is involved in the enhanced nociceptive responses of functionally identified Vc nocICEptive neurons and in the associated orofacial hyperalgesia following trigeminal nerve injury.
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The JAK inhibitor, tofacitinib, reduces the T cell stimulatory capacity of human monocyte-derived dendritic cells

TL;DR: Tofacitinib, a JAK1/JAK3 inhibitor, affected the activities of human DCs and decreased CD80/CD86 expression and T cell stimulatory capability through suppression of type I IFN signalling, suggesting a novel mode of action and a pivotal role for JAKs in the differentiation of DCs.